Federal Register / Vol. 62, No. 148 / Friday, August 1, 1997 / Notices 41379

ENVIRONMENTAL PROTECTION

AGENCY

[ER–FRL–5482–8]

Environmental Impact Statements and

Regulations; Availability of EPA

Comments

Availability of EPA comments

prepared July 7, 1997 Through July 11,

1997 pursuant to the Environmental

Review Process (ERP), under Section

309 of the Clean Air Act and Section

102(2)(c) of the National Environmental

Policy Act as amended. Requests for

copies of EPA comments can be directed

to the OFFICE OF FEDERAL

ACTIVITIES AT (202) 564–7167. An

explanation of the ratings assigned to

draft environmental impact statements

(EISs) was published in FR dated April

4, 1997 (62 FR 16154).

Draft EISs

ERP No. D–BOP–E80001–KY Rating

EC2, United States Penitentiary Martin

County, Construction and Operation,

Possible Sites, Bizwell and Honey

Branch Sites, located in Martin and

Johnson Counties, KY.

Summary: EPA expressed

environmental concerns due to potential

wetland impacts and requested addition

information on this issues.

Final EISs

ERP No. F–AFS–L65263–ID, Targhee

National Forest, Forest Plan Revision,

Bonneville, Butte, Clark, Fremont,

Jefferson, Lemhi, Madison and Teton

Counties, ID and Lincoln and Teton

Counties, WY.

Summary: Review of the Final EIS

was not deemed necessary. No formal

comment letter was sent to the

preparing agency.

ERP No. F–FAA–C51016–00, John F.

Kennedy International Airports, Light

Rail System, Implementation of

Automated Guideway Transit System by

the Port Authority Program, Funding,

Airport Layout Plan Approval, COE

Section 10 and 404 Permits, NY and NJ.

Summary: EPA had no objection to

the project as proposed, therefore the

project would not result in significant

environmental impacts.

ERP No. FS–NOA–E64007–00,

Fishery Management Plan (FMP) for the

Shrimp Fishery of the Gulf of Mexico

portions of the Exclusive Economic

Zone (EEZ), Amendment 9 Concerning

Reduction of Unwanted Bycatch of

Juvenile Red Snapper with Ancillary

Benefits to Other Finfish Species,

adjacent to State Waters of TX, LA, MS,

AL and FL.

Summary: EPA had no objection to

the action as proposed. EPA stated its

support for mandatory use of Bycatch

Reduction Devices.

Other

ERP No. LD–AFS–L61209–00 Rating

LO, Wallowa-Whitman National Forest,

Wild and Scenic River Study, Eight

Rivers for Suitability and inclusion in

the National Wild and Scenic Rivers

System, Baker, Union and Umatilla

Counties, OR and Adams and Idaho

Counties, ID.

Summary: EPA’s abbreviated review

has revealed no concerns on this

project.

Dated: July 29, 1997.

B. Katherine Biggs,

Associate Director, NEPA Compliance

Division, Office of Federal Activities.

[FR Doc. 97–20381 Filed 7–31–97; 8:45 am]

BILLING CODE 6560–50–P

ENVIRONMENTAL PROTECTION

AGENCY

[PF–751; FRL–5732–4]

Notice of Filing of Pesticide Petitions

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–751, must be

received on or before September 2,

1997.

ADDRESSES: By mail submit written

comments to: Public Information and

Records Integrity Branch (7506C),

Information Resources and Services

Division, 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 by following

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.,

Monday through Friday, excluding legal

holidays.

FOR FURTHER INFORMATION CONTACT: By

mail: Mary Waller, Acting (PM 21),

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) 308–9354; email: waller.mary@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–751]

(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–751] and

appropriate petition number. Electronic
41380 Federal Register / Vol. 62, No. 148 / Friday, August 1, 1997 / Notices

comments on this 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: July 22, 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.

1. AgrEvo USA Company

PP 4E4384

EPA has received a pesticide petition

(PP 4E4384)from AgrEvo USA

Company, Little Falls Centre One, 2711

Centerville Rd., Wilmington, DE 19808,

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 by establishing a tolerance for

residues of the fungicide (N-4,6-

dimethylpyrimidin-2-yl) aniline

expressed as pyrimethanil in or on the

raw agricultural commodity (RAC)

grapes at 5.0 ppm, and the processed

food, raisins at 8.0 ppm.

A. Residue Chemistry

1. Metabolism. Numerous studies

have been conducted to evaluate the

absorption, distribution, metabolism

and/or excretion of pyrimethanil in rats.

These studies indicate that pyrimethanil

is rapidly absorbed, metabolized and

excreted primarily through the kidneys;

rats given an oral dose of 1,000 mg/kg

excrete over 95% of compound related

products in urine within 6 to 8 hours,

studies in other species including the

dog and mouse show similar rapid and

quantitative excretion profiles. There is

no evidence of any significant

accumulation in tissues on repeat

dosing in rats.

2. Analytical method. The nature of

the residue in grapes is adequately

understood. The residue of concern is

the parent compound only. The

proposed analytical method for

determining residues of pyrimethanil is

high-pressure liquid chromatography,

with a UV detector. This method has

adequate accuracy, precision and

sensitivity for this purpose. This

method has been confirmed through an

independent laboratory validation.

3. Magnitude of residues. Field

residue and processing studies were

submitted from trials from the various

countries of proposed use including

France, Germany, Italy, South Africa,

Spain and Greece. These data

demonstrate that the proposed tolerance

of 5.0 ppm will be adequate to cover the

residues in grapes or wine. Processing

data show that pyrimethanil residues in

wine will not exceed the tolerance in

the RAC grapes. Data from residue trials

in Chile reflecting the proposed use

pattern on table grapes also demonstrate

that the proposed tolerance of 5.0 ppm

is adequate to cover the residues on

fresh table grapes. Processing data on

raisins indicates that there is a

concentration factor of 1.6 and a

tolerance of 8.0 ppm is proposed to

cover the residues of pyrimethanil in

raisins. Residues in juice were

determined to be 70% of the residues in

fresh grapes; therefore, the tolerance on

fresh grapes is sufficient to cover the

potential residues of pyrimethanil in

grape juice.

B. Toxicological Profile

1. Acute toxicity. The acute rat oral

LD50 of pyrimethanil was 4.15 g/kg in

males and 5.97 g/kg in females. The

acute rat dermal LD50 was  ́ 5.0 g/kg in

both sexes. The 4-hour rat inhalation

LC50 was >1.98 mg/L in males and in

females. Pyrimethanil was not irritating

to rabbit skin and slightly irritating to

the rabbit eyes. Pyrimethanil did not

cause skin sensitization in guinea pigs.

Based on these data, EPA has classified

pyrimethanil as Tox Category III for

inhalation and oral toxicity, and Tox

Category IV for dermal toxicity, skin and

eye irritation.

2. Genotoxicty. No evidence of

genotoxicity was noted in an extensive

battery of in vitro and in vivo studies.

Negative studies determined acceptable

by EPA included an Ames Assay (S.

typhimurium), Gene mutation (E. coli),

In vivo mouse micronucleus, in-vitro

chromosome analysis of cultured

human lymphocytes and Unscheduled

DNA synthesis.

3. Reproductive and developmental

toxicity. A developmental toxicity study

was conducted in rats. The NOEL s for

maternal and developmental effects

were determined by the EPA to be 85

mg/kg/day for maternal toxicity and

1,000 mg/kg/day (limit dose) for

developmental effects. There were no

teratogenetic or embryotoxic effects in

fetuses at 1,000 mg/kg/day.

A developmental toxicity study in

rabbits with a maternal NOEL of 7 mg/

kg/day. The developmental NOEL was

determined by the EPA to be 45 mg/kg/

day.

A 2-generation rat reproduction study

was determined by the EPA to have a

reproductive and developmental NOEL

of 23.1 mg/kg/day in males and 27.4

mg/kg/day in females.

4. Subchronic toxicity. A 90-day

feeding study was conducted in CRL:CD

(SD) BR strain rats with a NOEL of 5.4

mg/kg/day.

A 90-day study was conducted in

beagle dogs with a NOEL of 6 mg/kg/day

and a LOEL of 80mg/kg/day.

5. Chronic toxicity. A 12-month dog

study was determined by EPA to have

a NOEL of 30 mg/kg/day.

A 2-year mouse oncogenicity study in

CRL: CD-1 (ICR) BR with a NOEL for

systemic effects of 211 and 253 mg/kg/

day for males and females, respectively.

At doses up to 1,600 ppm there was no

evidence of oncogenicity. The EPA

concluded that the highest dose did not

achieve an MTD, however the EPA Peer

Review Committee concluded that the

data were sufficient to classify the

compound with respect to

carcinogenicity at this time.

A combined chronic toxicity/

oncogenicity study was conducted in

CRL:CD (SD) BR strain rats with a NOEL

of 17 and 22 mg/kg/day for males and

females, respectively. Findings included

increased thyroid follicular cell

adenomas in male and female rats. The

EPA Peer Review Committee concluded

on February 11, 1997 that there was

sufficient evidence from the data

provided to conclude that the thyroid

tumors were a result of disruption of the

thyroid-pituitary status.

6. Endocrine effects. There is no

evidence from the data or chemical

structure that pyrimethanil causes

endocrine effects other than those

already noted for the thyroid-pituitaryliver axis.

C. Aggregate Exposure

Dietary exposure. The aggregate

exposure to pyrimethanil is limited to

dietary exposure only because no U.S.

registrations are being sought. A worst

case estimate of the dietary exposure

from the tolerance on grapes results in

a maximum theoretical exposure of

0.55% of the reference dose for the U.S.

population and a worst case estiimate of

1.29% of the ADI for children 1-6 years

old. This worst case estimate assumes
Federal Register / Vol. 62, No. 148 / Friday, August 1, 1997 / Notices 41381

that all diets contain grapes and grape

products with the maximum theoretical

residue. In reality this will not be the

case because in commerce, only

imported grapes and grape products

have the potential for residues. In

addition, only a portion of the crop will

actually be treated and, under actual use

conditions the residue will be much

smaller that the residue trials indicate.

It can therefore be estimated that the

actual exposure to pyrimethanyl in the

diet will be less than 0.1% of the ADI,

or negligible from a dietary point of

view.

D. Cumulative Effects

There is no evidence that the

mechanism of toxicity of pyrimethanil

shares a common mechanism with any

other pesticides. In addition, the dietary

exposure in grapes or grape products is

negligible and therefore, AgrEvo

believes that even if it did share a

common mechanism with another

product, pyrimethanil would not

contribute in a significant way to the

overall risk.

E. Safety Determination

1. U.S. population —Reference dose.

Based upon the results of the

oncogenicity studies, genotoxicity

studies, structure-activity analysis and

studies on the effects of pyrimethanil on

the thyroid-pituitary-liver axis, the EPA

Peer Review Committee has concluded

that pyrimethanil should be classified as

a category C with respect to

carcinogenicity and that a threshold

methodology (MOE) should be

considered in conducting the risk

assessment. The appropriate reference

dose is .3 mg/kg/day based upon the

NOEL in the chronic oral dog study

with a 100 fold safety factor. This

reference dose is adequate to protect

infants and children and based upon the

data there is no need for an additional

safety factor.

2. Infants and children. It is proposed

that an additional 10X safety factor is

not required for pyrimethanil. The

toxicology data are complete and there

is no evidence of increased sensitivity to

young animals. Therefore, a 100X safety

factor should be sufficient and

protective of the health of adults, infants

and children.

F. International Tolerances

At the present time there are no

Mexican, Canadian or Codex maximum

residue limits for pyrimethanil in or on

grapes. Therefore compatibility is not an

issue.

2. Griffin Corporation

PP 5F4582

EPA has received a pesticide petition

(PP 5F4582) from Griffin Corporation,

P.O. Box 1847, 2509 Rocky Ford Road,

Valdosta, GA 31603-1847 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 by

establishing a tolerance for residues of

maneb, mancozeb and their metabolite

ethylenethiourea (ETU) in or on the raw

agricultural commodity walnuts at 0.05

parts per million (ppm). An adequate

analytical method is available for

enforcement purposes. 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. Residue

tolerances are established for maneb and

mancozeb at 40 CFR 180.110 and 40

CFR 180.176, respectively. It is well

known that the key metabolite of

toxicological concern is

ethylenethiourea (ETU).

Ethylenebisdithiocarbamate (EBDC),

including maneb and mancozeb are not

systemic in plants; therefore, EBDC and

ETU residues that might be found on

walnut nutmeats would then occur as a

surface residue transferred at the time of

harvesting or shelling operations.

2. Analytical method. An adequate

analytical method is available for

enforcement purposes. The method

describes gas chromatographic

procedures and appropriate limits of

quantitation. In general, maneb and

mancozeb residues are measured by

digesting the crop component with acid,

which converts the EBDC to carbon

disulfide. The carbon disulfide residues

are measured to determine the level of

EBDC residue. ETU residues are

measured by extraction from the crop

and analysis by high pressure liquid

chromatography or by extraction,

formation of a derivative, and

measurement of the derivative by gas

chromatography.

3. Magnitude of residues. Residues of

maneb and mancozeb in walnut meat

samples ranged from just below to just

above the limit of quantitation (0.01

ppm). The ETU metabolite was not

detected in any samples analyzed (limit

of quantitation was 0.01 ppm).

B. Toxicological Profile

1. Acute toxicity. Maneb and

mancozeb are virtually non-toxic after

administration by the oral, dermal and

respiratory routes.

i. Maneb. The acute oral LD50 for rats

is 6,750 mg/kg. The acute dermal LD50

for rabbits > 2,000 mg/kg and for rats >

5,000 mg/kg. Acute inhalation LC50 for

rats > 1.30 mg/l. Maneb is classified as

a slight irritant to skin and eye irritation

in rabbits clears in 7 days. Maneb has

been classified as a sensitizer in guinea

pigs.

ii. Mancozeb. The acute oral LD50 in

mice and rats is >5,000 mg/kg. The

acute dermal LD50 in rats is >5,000 mg/

kg. Mancozeb was not significantly toxic

to rats after a 4-hour inhalation

exposure, with an LD50 value of > 5.14

mg/L. Mancozeb is classified as not

irritating to skin on initial contact and

is a moderate eye irritant. It has been

classified as not a sensitizer in the

Buehler test.

iii. ETU. The mouse acute oral LD50

is 4,000 mg/kg/day and the rat acute

oral LD50 is 545 mg/kg/day. ETU is a

moderate to weak sensitizer.

2. Genotoxicty. Regarding

genotoxicity, maneb and mancozeb have

been adequately tested in a wide variety

of in vitro and in vivo mutagenicity

tests. Although EPA believes maneb and

mancozeb have some genotoxic

potential, and the World Health

Organization (WHO) has said the

evidence for genotoxicity is equivocal,

Griffin is informed that the wellconducted scientifically valid studies

demonstrate mancozeb is not genotoxic

in mammalian systems. Mancozeb is

negative in the Ames test and negative

in vitro and in vivo somatic and germ

cell tests. It did not induce unscheduled

DNA synthesis (UDS). These same

conclusions would be expected to apply

to maneb. In fact, the FAO and WHO

concluded ‘‘that maneb is not

genotoxic.’’

The WHO reviewed the genotoxicity

of ETU in 1993 and concluded that ETU

is not genotoxic in mammalian systems.

EPA has classified ETU as being weakly

genotoxic, at most.

3. Reproductive and developmental

toxicity. Maneb and mancozeb do not

produce birth defects and are not toxic

to the developing fetus at doses below

those which are toxic to the mother.

i. Maneb. The 1993 FAO/WHO

Toxicology Evaluations summarized

two rat studies as follows: NOAEL - 20

mg/kg/day, LOAEL - 100 mg/kg/day

(LOAEL effects being decreased

maternal body weight gain and food

consumption; embryofetoxicity);

NOAEL - 100 mg/kg/day, LOAEL 500
41382 Federal Register / Vol. 62, No. 148 / Friday, August 1, 1997 / Notices

mg/kg/d (LOAEL effects being decreased

maternal body weight gain and food

consumption, embryofetotoxicity and

teratogenicity).

ii. Mancozeb. The mancozeb maternal

no observable effect level (NOEL) was

established at 30-32 mg/kg/day in rats

and rabbits. The fetal NOEL is 128 mg/

kg/day in rats and > 80 mg/kg/day in

rabbits. The parental no observable

adverse effect level (NOAEL) was 120

ppm (7.0 mg/kg/day) in a 2-generation

reproduction study in rats. Mancozeb

had no effect on reproduction, on the

microscopic appearance of the

reproductive organs, or on neonatal

survival or growth below adult toxic

levels in appropriate studies.

iii. ETU. In a 2-generation rat

reproduction study, the ETU parental

NOEL was 2.5 ppm, or 0.11-0.43 mg/kg/

day, and there were no reproductive

effects. The developmental toxicity of

ETU has been studied in six species and

the results are species-specific. ETU did

not produce developmental effects in

mice (NOEL-100 mg/kg/day), rabbits

(NOEL-40 mg/kg/day), guinea pigs, or

cats. In hamsters, the NOEL was 100

mg/kg/day. In rats, the maternal NOEL

was 50 mg/kg/day, with a fetal NOEL of

5-15 mg/kg/day.

4. Chronic toxicity. The chronic

toxicity of the EBDCs is driven by its

metabolite ETU. The primary effects are

on the pituitary-thyroid-liver axis.

i. Maneb. While the EPA Maneb

Chemical Fact Sheet does not include

chronic toxicology information due to

data gaps at the time of publication,

combined chronic-oncogenic long-term

studies are summarized in the 1993

FAO/WHO Toxicology Evaluations:

NOAEL - 20 mg/kg/day, LOAEL - 67

mg/kg/day (LOAEL effects: decreased

body weight, T4; increased 131I halflife, thyroid weight).

ii. Mancozeb. In a 2-year combined

chronic toxicity/oncogenicity study in

the rat, the NOEL was 125 ppm (4.8 mg/

kg/day) based on thyroid effects. An

increased incidence of thyroid tumors

was seen at the highest dose of 750

ppm. These effects are likely due to ETU

exposure resulting from bioconversion

of mancozeb in the rat. This is

consistent with the toxicology of ETU,

which is described below. In

comparison with laboratory animals,

humans are expected to exhibit a lesser

degree of sensitivity to thyroid

inhibitors because humans possess a

substantial reserve supply of thyroid

hormone, much of it carried in serum

bound to thyroxine-binding globulin.

This protein is missing in rodents.

Additionally, there is a threshold effect

for thyroid tumors and the levels of

human exposure are well below those

that produced tumors in the rat study.

The WHO concluded that the data

support an RfD for mancozeb of 0.05

mg/kg/day based on this study. An

EBDC group ADI of 0.03 mg/kg/day was

established by the WHO in 1993.

In an 18-month mancozeb combined

chronic toxicity/oncogenicity study in

the mouse, the NOEL was 1,000 ppm, or

13 mg/kg/day. No tumors were seen in

any dose in this study. In a 1-year dog

feeding study, the NOEL was 200 ppm,

or 7.8 mg/kg/day.

In a 21-day mancozeb dermal toxicity

study in the rat, the NOEL was 1,000

mg/kg/day, with no effects seen at the

limit dose. Respiratory administration to

rats for 13 weeks decreased body

weights and serum T4 levels, and

induced thyroid hyperplasia. All effects

were reversible after 13 weeks of postexposure recovery.

iii. ETU. In an 18-month mouse

feeding study for ETU by the National

Toxicology Program (NTP), the NOEL

was 100 ppm, or 17 mg/kg/day. Tumors

of the liver, thyroid, and pituitary were

seen at 330 and 1,000 ppm. A 2-year rat

feeding chronic/oncogenicity study

established a NOEL of 5 ppm, or 0.37

mg/kg/day. Tumors were seen in the

thyroid and pituitary. The WHO

established an RfD of 0.004 mg/kg/day

based on these data.

5. Carcinogenicity. Prolonged

ingestion of ETU at very high levels has

caused thyroid and pituitary tumors in

rats and mice and an increase in liver

tumors in mice. Thyroid tumors were

also formed when mancozeb was fed to

rats at high doses (750 ppm) for long

periods of time. It is generally accepted

that these tumors result from ETU

formation in the rat from feeding high

doses of mancozeb. Because 7.5 percent

of EBDC is converted to ETU in rats,

feeding 750 ppm of EBDC can produce

enough ETU to cause tumors in these

animals. No carcinogenic effects were

seen from feeding maneb and mancozeb

to mice.

ETU is classified as a B2 oncogen with

a Q* of 0.06 (mg/kg/day)-1. Maneb and

mancozeb are also classified as B2

oncogens because of ETU.

C. Aggregate Exposure

1. Dietary exposure. The consumer

exposure to EBDC and ETU residues

was measured in a market basket survey

during an EPA Special Review which

concluded in 1992. The data showed

that aggregate ETU exposure from all

current uses is less than 50% of the RfD.

More specifically, Griffin residue data

show no detectable residues of ETU on

walnuts. Even if low levels of residues

were present, mean per capita

consumption of walnuts is negligible.

USDA dietary consumption data from

1977-78 indicates that it is 0.0048243 g/

kg bw/day for the U.S. general

population. Moreover, there is no

concern with identifiable

subpopulations (see infants and

children consumption).

FQPA requires EPA to use ‘‘available

information’’ to consider risks to infants

and children before establishing a

tolerance. Available information

demonstrates that dietary exposures to

infants and children from walnuts is

immaterial; furthermore, there are also

no processed food uses for walnuts.

2. Drinking water. Maneb and

mancozeb have no tendency to

contaminate groundwater or drinking

water because they degrade rapidly in

soil and water, have low solubility in

water, and are absorbed to soil.

Although the water solubility of ETU is

relatively high, ETU is not expected to

contaminate groundwater for several

reasons. First, ETU is only present in

the soil as the result of degradation of

the parent EBDCs (maneb or mancozeb),

and it is being degraded at the same

time it is being formed. Thus, the ETU

concentration will always be low.

Second, the degradation of ETU is rapid,

thus it will degrade before it can move.

Data from laboratory studies and field

dissipation studies have been integrated

in computer modeling studies to predict

the movement of maneb and mancozeb

and ETU in California from EBDC

applications on tomatoes and pears

(mancozeb only) using the USDA

GLEAMS model, which accounts for

degradation products as well as the

parent. The model predicts that there

would be no measurable residues near

the bottom of the rooting zone of

tomatoes and pears, even with a heavy

amount of simulated rainfall. Therefore,

the model predicts that maneb,

mancozeb and ETU will not leach into

groundwater. The modeling predictions

are consistent with the fact that EBDCs

and ETU degrade rapidly in soil and

with the results of actual field

dissipation studies.

The most direct evidence that ETU

will not contaminate groundwater

comes from an extensive review of

actual groundwater samples that have

been analyzed for ETU. In EPA’s own

National Pesticide Survey, only one

well out of 1,295 samples had an ETU

residue. There were no measurable ETU

residues in community wells, with a

sensitivity of 0.0045 ppm. The one

residue was in an area where EBDC

fungicides are not heavily used.

Analysis of nearly 100 additional

samples in state surveys did not show

any confirmed residues of ETU, even in
Federal Register / Vol. 62, No. 148 / Friday, August 1, 1997 / Notices 41383

vulnerable areas such as Florida, Maine

and New York.

Specific to walnuts which are grown

almost exclusively in California, the

California Environmental Protection

Agency’s Pesticide Well Inventory

Database reveals extensive annual

sampling for maneb and ETU during the

period August 15, 1984 to September

29, 1994, but only one ETU detect (10

years ago in 1987) at 0.725 ppb. After

not finding ETU for decade, CDPR

ceased testing for EBDCs.

Additionally, maneb, mancozeb and

ETU degrade rapidly in natural water/

sediment systems. Thus, ETU is not

likely to be present in drinking water

from natural surface water systems.

3. Non-dietary exposure. Mancozeb is

labeled for application to residential

lawns only by commercial applicators,

and both maneb and mancozeb are

labelled for ornamentals and vegetables

by homeowners or professional

applicators. Mancozeb products are

commonly applied to golf course greens

to control a broad complex of turf

diseases. Application to golf course

fairways is less common. There are no

reliable data to assess the exposure from

these uses.

Any acute exposures to children

would come from oral or dermal

exposure. As previously discussed,

maneb and mancozeb are not orally or

dermally acutely toxic. Furthermore,

golf is not played by infants or children;

therefore, no exposure to infants and

children would be expected. Thus, there

is a reasonable certainty that no harm

would occur to infants or children from

these uses. Regardless, there are no nonoccupational exposures associated with

walnut uses.

D. Cumulative Effects

The toxicological effects from maneb

and mancozeb are due to ETU. Other

EBDC fungicides, including metiram

and zineb are also converted to ETU.

The EBDC fungicides have been

extensively reviewed by the US-EPA as

part of a Special Review which was

concluded in 1992 with publication of

the PD4 document. These fungicides

were regulated against their common

metabolite, ETU, and use restrictions

were enacted as part of the conclusion

of the Special Review. As a result,

common mode of action has received

considerable evaluation by the Agency

and currently approved risk levels have

already accommodated any potential

concerns.

E. Safety Determination

1. U.S. population. DRES analyses for

the U.S. general population show

vanishingly small oncogenic risks from

combined maneb and ETU residues on

walnuts (reflective of mancozeb, as well,

since 100% maneb application assumed

for calculation). The Combined

Oncogenic Risk for Maneb and ETU

Residues for the U.S. population 48

states subgroup is 1.7 x 10-9 (ETU

Oncogenic Risk). The general U.S.

population oncogenic risk with

consumption of walnuts is essentially

no different than the risk without

walnut consumption. An ETU

oncogenic risk of 10-9 is three orders of

magnitude below the FQPA standard,

again a negligible contribution.

The RfD of ETU will not be exceeded.

In concluding that EBDC Special

Review, EPA calculated that the 45

crops on the EBDC labels occupied 47%

of the RfD for the general population

using a safety factor of 3,000, resulting

in an RfD of 0.00008 mg/kg/day

(established in 1988). With a new

complete database, the WHO

established a reference dose of 0.004

mg/kg/day. Because the WHO

evaluation used all recently developed

data, Griffin believes their number is

appropriate. With this RfD and with

addition of turnips, mustard greens, and

collards to the maneb label since the

Special Review ended, the dietary

exposure to ETU will utilize less than

2% of the RfD. The incremental RfD

utilized for the U.S. general population

by walnut uses, a fractional 0.71x10-3, is

so minute it does not change this

number. The total percent RfD utilized

by all uses, including addition of

walnuts, is well below the 100% RfD

level, and is not perceptibly changed by

addition of walnut uses.

The sole acute risk would be for

women of childbearing age. In

concluding the EBDC special review,

EPA calculated that the Margin of

Exposure (MOE) for mancozeb would be

4, 985 based on field trial data and

concluded the margin would be

adequate. The MOE would be even

higher based on the consumer exposure

data from the market basket survey.

Thus, there is adequate safety for this

group. Because walnuts have such a low

dietary consumption, it will not add to

the exposure. Thus, there is a reasonable

certainly that no harm will result from

EBDC uses generally, and walnut uses

specifically.

EPA has previously determined that

the dietary risk from ‘‘all EBDC treated

crops combined’’ is acceptable; this

summary of exposure and toxicological

safety shows that use of maneb and

mancozeb on walnuts will not

materially increase that risk. FQPA

anticipates that tolerances will be

reviewed over the next decade. (See

FFDCA sections 408 (b)(2)(E)(ii) and

408(q)). The Agency should issue the

walnut time-limited tolerances on

maneb and mancozeb now, since this

process will provide the opportunity for

the Agency to visit any broader

questions that may arise in the future as

to the tolerances at issue.

2. Infants and children. As with the

U.S. general population, there is no

concern with identifiable

subpopulations. The consumption

figures for walnuts are: U.S. general

population -- 0.0048243 g/kg bw/day;

non-nursing infants -- 0.0029131 g/kg

bw/day, children 1-6 -- 0.0133432 g/kg

bw/day, and children 7-12 --- 0.0087970

g/kg bw/day. Available information

demonstrates that exposures to infants

and children from walnuts is

immaterial. In addition, there are no

processed food uses for walnuts. Thus,

the raw crop’s dietary impact for

children is de minimis. In fact, the PD4

separate dietary analysis for children

and infants that considered far more

extensive uses than walnuts found risks

no greater than those of the general

population, even when overstated by

calculations using an unrealistic

lifetime exposure. Specifically, EPA

calculated the dietary risk to infants and

children from the allowed 45 uses to be

3.7 x 10-9 and 2.6 x10-8, respectively,

adjusted for a revised Q* of 0.06 (mg/

kg/day)-1. [57 FR 7521 March 2, 1992]

With addition of the greens uses, the

risks to these subgroups is still less than

1x10-7.

DRES analyses for infants and

children show vanishingly small

oncogenic risks from combined maneb

and ETU residues on walnuts (reflective

of mancozeb, as well, since 100%

maneb application assumed for

calculation). The Combined Oncogenic

Risk for Maneb and ETU Residues (ETU

Oncogenic Risk) for the subgroups: U.S.

population 48 states -- 1.7 x 10-9; Nonnursing infants < 1 yr (1 yr lifetime

corrected) -- 1.4 x 10-11; Children 1-6

years (6 yr lifetime corrected) -- 4.0 x

10-10; Children 7-12 years (6 yr lifetime

corrected) -- 2.6 x 10-10. The incremental

oncogenic risk for infants and children

is well below the 1x10-6 FQPA standard

of ‘‘reasonable certainty of no harm.’’

Non-nursing infants at 10-11 are five

orders of magnitude below this

standard. Even the highest children’s

group (1-6 years old) at 10-10 is an

infinitesimal four orders of magnitude

lower than the standard.

The Agency also estimated that the 45

crops allowed at the end of the special

review occupied less than 50% of the

RfD of 0.00008 mg/kg/day for infants

and children. With addition of greens

and use of the WHO ETU ADI of 0.004
41384 Federal Register / Vol. 62, No. 148 / Friday, August 1, 1997 / Notices

mg/kg/day, ETU utilizes less than 2% of

the ADI for infants and children.

The reproductive and developmental

toxicity does not require additional

safety factors because the database for

maneb, mancozeb and ETU is complete.

Furthermore, the NTP evaluated the

toxicity of the ETU in utero in rats and

mice and found that there was no

significant increase in toxicity, with the

exception of a slight increase in rat

thyroid tumors, which have a threshold

effect. Thus, prenatal and postnatal

exposure does not lead to increased

sensitivity in infants and children, and

there is no evidence that ETU would

present only unusual or

disproportionate hazard to infants and

children. Therefore, there is no need to

impose an additional safety factor for

infants and children.

FQPA anticipates that tolerances will

be reviewed over the next decade. (See

FFDCA sections 408 (b)(2)(E)(ii) and

408(q)). This process will provide the

opportunity for the Agency to visit any

broader questions that may arise in the

future as to the tolerances at issue.

F. International Tolerances

There is no Codex MRL for walnuts.

Codex has established MRLs for the

dithiocarbamate group, including

maneb and mancozeb, on 21 crops and

proposed MRLs on 29 additional

substrates.

3. Rohm and Haas Company

PP 2E4141

EPA has received a pesticide petition

(PP 2E4141) from Rohm and Haas

Company, 100 Independence Mall West,

Philadelphia, PA 19106-2399 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 by

establishing an import tolerance for

residues of the fungicide myclobutanil

and free and bound forms of its

metabolite in or on the raw agricultural

commodity bananas at 4.0 parts per

million (ppm) in the whole fruit (0.8

ppm in edible portion). An adequate

analytical method is available for

enforcement purposes. 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 metabolism

of myclobutanil in plants is well

understood. The chemical identities of

probable plant residues resulting from

the use of myclobutanil on bananas

have been elucidated. The major

metabolite is alpha-(3-hydroxybutyl)-

alpha-(4-chlorophenyl)-1H-1,2,4-

triazole-1-propanenitrile. Analyses

indicate that the majority of the residue

is located on the banana peel.

2. Analytical method. Myclobutanil

residues, parent plus free and bound

alcohol metabolites, are measured at an

analytical sensitivity of 0.01 mg/kg in

most crops by extraction of samples,

partitioning into an organic solvent,

clean up on silica gel, and GLC using

nitrogen specific thermionic detection.

Myclobutanil residues in animal

commodities are measured in

essentially the same manner with the

additional diol metabolite in milk.

3. Magnitude of residues. The residue

levels found on banana peel ranged

between 1.02 and 1.62 ppm at a 200

ppm application rate and between 1.32

and 3.77 ppm at a 400 ppm application

rate. In general, the average total

residues in the edible pulp were a small

percentage (5.8 to 7.8%) of the average

total residues in the peel.

B. Toxicological Profile

1. Acute toxicity. Myclobutanil is

essentially non-toxic after

administration by the oral, dermal and

respiratory routes. Myclobutanil is not

irritating to skin (Draize score = 0),

slightly irritating to the eyes (mean

irritation score = 0), and it is not a

sensitizer. The highest EPA acute

toxicity category is III based on ocular

irritation. No evidence exists regarding

differential sensitivity of children and

adults to acute exposure.

2. Genotoxicity. A reverse mutation

assay (Ames), point mutation in CHO/

HGPRT cells, in vitro and in vivo

(mouse) cytogenetic assays,

unscheduled DNA synthesis, and a

dominant-lethal study in rats were

conducted. All were negative for

mutagenic effects.

3. Reproductive and developmental

toxicity. In assessing the potential for

additional sensitivity of infants and

children to residues of myclobutanil,

data were considered from

developmental toxicity studies in the rat

and rabbit and a 2-generation

reproduction study in the rat. The

developmental toxicity studies are

designed to evaluate adverse effects on

the developing organism resulting from

pesticide exposure during prenatal

development to one or both parents.

Reproduction studies provide

information relating to effects from

exposure to the pesticide on the

reproductive capability of mating

animals and data on systemic toxicity.

From the rat developmental study, the

maternal (systemic) no-observed-effect

level (NOEL) was 93.8 mg/kg/day, based

on rough hair coat, and salivation at the

lowest-observed effect level (LOEL) of

312.6 mg/kg/day. The developmental

(pup) NOEL was 93.8 mg/kg/day, based

on increased incidences of 14th

rudimentary and 7th cervical ribs at the

LOEL of 312.6 mg/kg/day. From the

rabbit developmental study, the

maternal (systemic) NOEL was 60 mg/

kg/day, based on reduced weight gain,

clinical signs of toxicity and abortions at

the LOEL of 200 mg/kg/day. The

developmental (pup) NOEL was 60 mg/

kg/day, based on increases in number of

resorptions, decreases in litter size, and

a decrease in the viability index at the

lowest effect level (LEL) of 200 mg/kg/

day.

From the rat reproduction study, the

maternal (systemic) NOEL was 2.5 mg/

kg/day, based on increased liver weights

and liver cell hypertrophy at the LOEL

of 10 mg/kg/day. The developmental

(pup) NOEL was 10 mg/kg/day, based

on decreased pup body weight during

lactation at the LEL of 50 mg/kg/day.

The reproductive (parental) NOEL was

10 mg/kg/day, based on increased

incidence of stillborns, and atrophy of

the testes, epididymides, and prostate at

the LEL of 50 mg/kg/day.

4. Chronic toxicity. In 2-year

combined chronic toxicity/oncogenicity

studies in rats and 18-month

oncogenicity studies in mice, the overall

NOEL was 80 ppm (2.49 mg/kg/day)

based on decreased body weight, and

liver and testicular atrophy. In a 1-year

chronic toxicity study in dogs, the

NOEL was 3.83 mg/kg/day based on

hepatotoxicity. The LOEL was 14.3 mg/

kg/day. The Reference Dose (RfD) of

0.025 mg/kg/day was established by the

Agency based on the chronic feeding

study in rats with a NOEL of 2.5 mg/kg/

day and an uncertainty factor of 100.

There was testicular atrophy at the

lowest effect level (LEL) of 9.9 mg/kg/

Twenty four-month rat and 18-month

mouse chronic feeding/carcinogenicity

studies with myclobutanil produced no

statistically significant increase in the

incidence of combined, benign or

malignant tumors. Worst-case estimates

of dietary intake of myclobutanil in

human adults and children indicate

effects on the liver will not occur, thus

there is a reasonable certainty of no

harm. Using its Guidelines for

Carcinogen Risk Assessment published

September 24, 1986, EPA has classified

myclobutanil as a Group E chemical (no

evidence of carcinogenicity for humans)

based on the results of carcinogenicity
Federal Register / Vol. 62, No. 148 / Friday, August 1, 1997 / Notices 41385

studies in two species. The doses tested

were adequate for identifying a cancer

risk.

5. Animal metabolism. The

metabolism of myclobutanil in animals

is adequately understood for the

purposes of this tolerance.

C. Aggregate Exposure

1. Dietary exposure. Established U.S.

tolerances for myclobutanil and its

metabolites are found in 40 CFR

180.443, and range from 0.02 ppm for

cotton seed and eggs to 5.0 ppm for

cherries (sweet and sour). There are no

livestock feed items associated with the

proposed use on bananas, so no

additional livestock dietary burden will

result from this registration. Therefore,

existing meat, milk and poultry

tolerances are adequate.

For the purposes of assessing the

potential dietary exposure under this

petition, the estimated aggregate

exposure was based on the theoretical

maximum residue contribution (TMRC)

from the tolerances for myclobutanil on

all registered uses plus banana pulp, the

edible portion of whole bananas, at 0.8

ppm. The tolerance for myclobutanil on

bananas (whole fruit) is 4.0 ppm. The

TMRC is obtained by multiplying the

tolerance level residues for banana pulp

by the consumption data which

estimates the amount of bananas and

other products eaten by various

population subgroups.

The RfD based on the 2-year rat

chronic feeding study (NOEL of 2.49

mg/kg bwt/day) and using a hundredfold uncertainty factor is calculated to

be 0.025 mg/kg bwt/day. The TMRC

from previously established tolerances

and tolerances established here is

0.003286 mg/kg bwt/day for the general

population and utilizes 13.1% of the

RfD. The percentage of the RfD for the

most highly exposed subgroup, nonnursing infants (less than 1 year old) is

72.3%. The TMRC was calculated based

on the assumption that myclobutanil

occurs at the maximum legal limit in all

of the dietary commodities for which

tolerances are proposed. Even with this

probable large overestimate of exposure/

risk, the TMRC is well below the RfD for

the population as a whole and for each

of the 22 subgroups considered.

Thus, the dietary risk from exposure

to myclobutanil appears to be minimal

for the use on bananas. In conducting

this exposure assessment, very

conservative assumptions (100% of

bananas will contain myclobutanil

residues and those residues would be at

the level of the tolerance) were made

which results in an overestimate of

human exposure. Thus, in making a

safety determination for these

tolerances, this conservative exposure

assessment is taken into account.

2. Drinking water. Myclobutanil will

not contaminate groundwater or

drinking water because of its adsorptive

properties on soil, solubility in water,

and degradation rate. Data from

laboratory studies and field dissipation

studies have been used in the USDA

PRZM/GLEAMS computer model to

predict the movement of myclobutanil.

The model predicts that myclobutanil

will not leach into groundwater, even if

heavy rainfall is simulated. The

modeling predictions are consistent

with the data from environmental

studies in the laboratory and the results

of actual field dissipation studies. There

are no data on passage of myclobutanil

through water treatment facilities and

there are no State water monitoring

programs which target myclobutanil.

Based on the available studies used in

the assessment of environmental risk, it

is not anticipated that there will be

exposure to residues of myclobutanil in

drinking water. Review of terrestrial

field dissipation data indicated that

myclobutanil did not leach into

groundwater in either sandy loam or

coastal soil. There is no established

Maximum Concentration Level for

residues of myclobutanil in drinking

water. No drinking water health

advisories have been issued for

myclobutanil. The ‘‘Pesticides in

Groundwater Database’’ has no

information concerning myclobutanil.

Based on the available data, the Agency

does not anticipate that there will be

significant exposure to the general

population from myclobutanil residues

in drinking water. Since myclobutanil is

unlikely to leach into groundwater,

there is no increased risk from this

source.

3. Non-dietary exposure. EPA has not

provided Rohm and Haas Company

with an estimate of non-occupational

exposure for myclobutanil, however,

there are no products registered in the

United States for home-owner use

which contain myclobutanil. While this

does not preclude potential exposure,

the market channels for home-owner

products do not contain myclobutanil.

This makes the potential for nonoccupational exposure to the general

population essentially nil and the

contribution from this source is not

expected to be significant.

D. Cumulative Effects

EPA is aware of and has considered

the potential for cumulative effects of

myclobutanil and other substances that

have a common mechanism of

fungicidal activity. These are commonly

designated as the DMI fungicides. The

Rohm and Haas Company, other

producers, University advisors,

economic consultants, and the EPA are

well aware of the existing national IPM

and resistance management programs

for these fungicides which strongly

discourage the use of multiple products

either concomitantly or in succession

within the same season. The activities

within these highly publicized programs

and the Fungicide Resistance Action

Committee, which monitors fungal

resistance on an annual basis, support

the conclusion that overlapping use of

DMI fungicides on the same crop are

unlikely. In addition, Rohm and Haas

Company is not aware of any

toxicological data available to EPA or to

the producers which suggest that there

is a common mechanism of mammalian

or ecological toxicity among these

fungicidal products. Therefore, it is

reasonable to conclude that EPA has

reliable information to indicate that

toxic effects produced by myclobutanil

should not be considered to be

cumulative with those of any other

chemical compounds. Thus,

consideration of a common mechanism

of toxicity for these fungicidal products

is not appropriate at this time. EPA

should consider only the potential risks

of myclobutanil in its aggregate

exposure assessment.

E. Safety Determination

1. U.S. population. Using the

conservative exposure assumptions

described above, based on the

completeness and reliability of the

toxicity data, it was concluded that

aggregate exposure to myclobutanil will

utilize 13.1% of the RfD for the U.S.

population. EPA generally has no

concern for exposures below 100% of

the RfD because the RfD represents the

level at or below which daily aggregate

dietary exposure over a lifetime will not

pose appreciable risks to human health.

It is therefore concluded that there is a

reasonable certainty that no harm will

result from aggregate exposure to

myclobutanil residues.

2. Infants and children. In assessing

the potential for additional sensitivity of

infants and children to residues of

myclobutanil, data were considered

from developmental toxicity studies in

the rat and rabbit and a 2-generation

reproduction study in the rat. The

developmental toxicity studies are

designed to evaluate adverse effects on

the developing organism resulting from

pesticide exposure during prenatal

development to one or both parents.

Reproduction studies provide

information relating to effects from

exposure to the pesticide on the
41386 Federal Register / Vol. 62, No. 148 / Friday, August 1, 1997 / Notices

reproductive capability of mating

animals and data on systemic toxicity.

FFDCA section 408 provides that EPA

may apply an additional safety factor for

infants and children in the case of

threshold effects to account for pre- and

post-natal toxicity and the completeness

of the database. Based on the current

toxicological data requirements, the

database relative to pre- and post-natal

effects for children is complete. Further,

for the chemical myclobutanil, the

NOEL at 2.5 mg/kg/day from the rat

study, which was used to calculate the

RfD, is already lower than the NOELs

from the developmental studies in rats

and rabbits by a factor of approximately

4-fold.

The effects observed in the

reproductive toxicity study suggest that

there is no unique sensitivity for infants

and children. Therefore, the data

support a conclusion that an additional

uncertainty factor is not warranted and

that the RfD at 0.025 mg/kg/day is

appropriate for assessing aggregate risk

to infants and children.

Using the conservative exposure

assumptions described above, it was

concluded that the percent of the RfD

that will be utilized by aggregate

exposure to residues of myclobutanil

ranges from 13.1% for adults up to

72.3% for non-nursing infants.

Therefore, based on the completeness

and reliability of the toxicity data and

the conservative exposure assessment,

EPA has already published a conclusion

which indicates that there is a

reasonable certainty that no harm will

result to infants and children from

aggregate exposure to myclobutanil

residues.

F. International Tolerances

There are Codex maximum residue

levels (MRL) established for residues of

myclobutanil for apricot, cherry, peach,

plum/prune (fresh), prune (dried),

grapes, apples, and pears. Rohm and

Haas company has proposed

modifications to the current CXL for

stone fruits only to accommodate US

GAP.

[FR Doc. 97–20216 Filed 7-31-97; 8:45 am]

BILLING CODE 6560–50–F

FEDERAL COMMUNICATIONS

COMMISSION

Notice of Public Information

Collection(s) Being Reviewed by the

Federal Communications Commission

for Extension Under Delegated

Authority, 5 CFR 1320 Authority;

Comments Requested

July 28, 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

following information collection(s), as

required by the Paperwork Reduction

Act of 1995, Pub. L. 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 does not

display a valid control number.

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 clarity 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 by September 30,

1997.

ADDRESSES: Direct all comments to Judy

Boley, Federal Communications

Commission, Room 234, 1919 M St.,

NW., Washington, DC 20554 or via

internet to jboley@fcc.gov.

FOR FURTHER INFORMATION CONTACT: For

additional information or copies of the

information collections contact Judy

Boley at 202–418–0214 or via internet at

jboley@fcc.gov.

SUPPLEMENTARY INFORMATION:

OMB Approval No.: 3060–0132.

Title: Supplemental Information—72–

76 MHz Operational Fixed Stations.

Form Number: FCC Form 1068–A.

Type of Review: Extension of a

currently approved collection.

Respondents: Individuals or

households; Business or other for-profit;

Not-for-profit institutions; State, Local

or Tribal Government.

Number of Respondents: 300.

Estimate Hour Per Response: .50

hours.

Frequency of Response: On occasion

reporting requirement.

Total Annual Burden: 150 hours.

Needs and Uses: FCC Rules require

that the applicant agrees to eliminate

any harmful interference caused by the

operation to TV reception on either

channel 4 or 5 that might develop. This

form is required by the Communications

Act of 1934, as amended; International

Treaties and FCC Rules, 47 CFR Part

90.257.

FCC staff will use the data to

determine if the information submitted

will meet the FCC rule requirements for

the assignment of frequencies in the 72–

76 MHz band.

OMB Approval No.: 3060–0021.

Title: Civil Air Patrol Radio Station

License.

Form Number: FCC Form 480.

Type of Review: Extension of a

currently approved collection.

Respondents: Not-for-profit

institutions.

Number of Respondents: 12.

Estimate Hour Per Response: .84

hours.

Frequency of Response: On occasion

reporting requirement.

Total Annual Burden: 1 hour.

Needs and Uses: FCC Rules require

that applicants file the FCC Form 480 to

apply for a new, renewed, or modified

Civil Air Patrol Radio Station License.

This form is required by the

Communications Act of 1934, as

amended; International Treaties and

FCC Rules, 47 CFR Parts 1.922, 87.21,

and 87.31.

The data will be used by Commission

personnel to evaluate the application to

issue licenses, to provide information

for enforcement and rulemaking

proceedings and to maintain a current

inventory of licensees.

Federal Communications Commission.

William F. Caton,

Acting Secretary.

[FR Doc. 97–20257 Filed 7–31–97; 8:45 am]

BILLING CODE 6712–01–P

FEDERAL COMMUNICATIONS

COMMISSION

[Report No. 2212]

Petitions for Reconsideration and

Clarification of Action in Rulemaking

Proceedings

July 29, 1997.

Petitions for reconsideration have

been filed in the Commission’s

rulemaking proceeding listed in this