34176 Federal Register / Vol. 63, No. 120 /Tuesday, June 23, 1998 / Notices

Pretreatment Pilot Program would meet

the eight Project XL criteria discussed

earlier in this notice.

EPA believes stakeholder involvement

in developing Local Pilot Pretreatment

Programs is crucial to the success of the

programs. Therefore, as part of the

application, the POTW must clearly

explain its process for involving

stakeholders in the design of the pilot

program. This process should be based

upon the guidance set out in the April

23, 1997, Federal Register document.

The support of parties that have a stake

in the program is very important.

Once EPA has accepted a candidate

based on its detailed proposal, the

POTW, EPA, the State and local

stakeholders should finalize a Final

Project Agreement (FPA). The FPA is a

non-binding agreement that enumerates

the conditions of the project. (In order

to expedite this process, EPA will

develop a FPA template for these

projects that will contain the elements

that are anticipated to be common

among these projects and shall make

this available to the candidates.) The

actual regulatory flexibility will be

granted by modifying 40 CFR part 403

to allow these specific POTWs to

operate Local Pilot Pretreatment

Programs.

After an opportunity for public

participation at the local level and the

development of the Final Project

Agreement, a selected POTW’s

Approval Authority would approve or

disapprove the pilot program using the

procedures in 40 CFR 403.18. The

POTW may implement its Local Pilot

Pretreatment Program once its NPDES

permit has been modified to incorporate

the program as an enforceable permit

element.

As with any XL Project, EPA intends

to work cooperatively with the POTWs

that submit applications for Local Pilot

Pretreatment Programs to develop and

fine tune the applications. Applicants

must recognize that EPA retains the

ultimate authority to select projects

based on a qualitative consideration of

the criteria described earlier. Since

these are pilot projects and there are a

limited number of pilots that can be

approved, projects that satisfy many or

all of the criteria may not be chosen for

Local Pilot Pretreatment Programs

status. The decision of which projects

will be selected will be based on an

Agency decision about which projects

are expected to best serve the objectives

of this program. No person is required

to submit a proposal or obtain approval

as a condition of commencing or

continuing a regulated activity.

Accordingly, there will be no formal

administrative review available for

proposals that are not selected, nor does

EPA believe there will be a right to

judicial review.

Dated: June 20, 1998.

Michael B. Cook,

Director, Office of Wastewater Management.

[FR Doc. 98–16399 Filed 6–22–98; 8:45 am]

BILLING CODE 6560–50–P

ENVIRONMENTAL PROTECTION

AGENCY

[PF–813; FRL–5795–1]

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–813, must be

received on or before July 23, 1998.

ADDRESSES: By mail submit written

comments to: Public Information and

Records Integrity Branch, Information

Resources and Services Division

(7502C), Office of Pesticides Programs,

Environmental Protection Agency, 401

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

person bring comments to: Rm. 119, 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: The

product manager listed in the table

below:

Product Manager Office location/telephone number Address

Mary Waller .................... Rm. 247, CM #2, 703–308–9354, e-mail:waller.mary@epamail.epa.gov. 1921 Jefferson Davis Hwy, Arlington, VA

James Tompkins ............ Rm. 239, CM #2, 703–305–5687, e-mail: tompkins.james@epamail.epa.gov.

Stephanie Willett ............ Rm. 202, CM #2, 703-305-5419, e-mail:willett.stephanie@epamail.epa.gov. Do.

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–813]

(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
Federal Register / Vol. 63, No. 120 /Tuesday, June 23, 1998 / Notices 34177

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 (insert docket

number) and appropriate petition

number. Electronic comments on notice

may be filed online at many Federal

Depository Libraries.

List of Subjects

Environmental protection,

Agricultural commodities, Food

additives, Feed additives, Pesticides and

pests, Reporting and recordkeeping

requirements.

Dated: June 12, 1998.

James Jones,

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 4F4380

EPA has received a pesticide petition

(PP [4F4380]) from AgrEvo USA

Company, 2711 Centerville Road,

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

flutolanil in or on the raw agricultural

commodity of rice grain at 2.0 parts per

million (ppm), rice straw at 12.0 ppm

and in or on the processed commodities

of rice hulls at 7.00 ppm and rice bran

at 3.0 ppm. EPA has determined that the

petition contains data or information

regarding the elements set forth in

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

however, EPA has not fully evaluated

the sufficiency of the submitted data at

this time or whether the data supports

granting of the petition. Additional data

may be needed before EPA rules on the

petition.

A. Residue Chemistry

1. Plant and animal metabolism. The

metabolism of flutolanil in plants and

animals is adequately understood for

the purposes of this petition. Animal

studies in rats, ruminants, and poultry

indicate that flutolanil is metabolized

primarily to desisopropylflutolanil and

its conjugates. Plant metabolism studies

have been conducted in rice, cucumber,

and peanuts. The metabolic profile for

flutolanil was similar in all three crops.

The major route of degradation was 4′-

0-dealkylation to desisopropylflutolanil,

followed by conjugation. Other

metabolites may occur at very low levels

due to hydroxylation and oxidation of

the side chain, hydroxylation of the

aniline ring, and methylation of the

hydroxyl groups. These minor

metabolites were also subject to

conjugation. The residues of concern are

the parent flutolanil and

desisopropylflutolanil.

2. Analytical method. The analytical

method designated as AU-95R-04 has

been independently validated and is

adequate for enforcement purposes. A

multi-residue method for flutolanil has

been previously submitted. It has the

following disclaimer: The method is for

use only by experienced chemists who

have demonstrated knowledge of the

principles of trace organic analysis and

have proven skills and abilities to run

a complex residue analytical method

obtaining accurate results at the part per

million level (PPML). Users of this

method are expected to perform

additional method validation prior to

using the method for either monitoring

or enforcement. The method can detect

gross misuse.

3. Magnitude of residues. 24 field

trials consisting of foliar applications to

rice were conducted in California,

Louisiana, Texas, Arkansas, Arizona,

Missouri, and Mississippi. Applications

of flutolanil formulated as 50WP or

70WP were made at a total seasonal rate

of 1.0 lb active ingredient (a.i) per acre

resulted in flutolanil-derived residues

ranging from below the limit of

detection (<0.05 ppm) to 1.66 ppm in

whole rice grain and hulled rice and

from 0.95 ppm to 11.28 ppm in rice

straw.

A processing study was also

conducted in Louisiana in which the

50WP formulation of flutolanil was

applied to rice following label

directions at a total rate of 1.0 lb active

ingredient per acre. Residues of

flutolanil were observed in all processed

commodities and ranged from <0.05

ppm in polished rice to 1.37 ppm in

grain dust below 420 microns.

B. Toxicological Profile

1. Acute toxicity. A battery of acute

studies was conducted: the acute oral

LD50 in rat and mice were >10,000

milligram/kilograms (mg/kg), Toxicity

category IV; acute dermal LD50 in rat

was >2,000 mg/kg, Toxicity category III;

and acute inhalation LC50 in rat was

>5.98 milligram/liter (mg/l), Toxicity

category III. There was slight eye

irritation; no dermal irritation; and no

dermal sensitization.

2. Genotoxicty. Flutolanil has been

tested in a battery of in-vitro and in-vivo

assays. No evidence of genotoxicity was

noted in gene mutation assays with

Salmonella, E. coli, or mouse lymphoma

cells; a mouse micronucleus assay or in

an in-vitro unscheduled DNA synthesis

assay. A weak positive response was

noted in an in-vitro cytogenetics assay

in Chinese hamster lung cells but no

evidence of clastogenicity was noted in

an in-vitro cytogenetics assay in human

lymphocytes. The overall weight of

evidence indicates that flutolanil is not

genotoxic.

3. Reproductive and developmental

toxicity. A 3-generation rat reproduction

study was conducted at dietary

concentrations of 0, 1,000 and 10,000

ppm. The NOEL for this study is

considered to be 1,000 ppm (63

milligram/kilograms/day (mg/kg/day),

based on reduced pup weights late in

lactation at 10,000 ppm. Because the

Agency considered this study

supplementary, a 2-generation rat

reproduction study subsequently was

conducted at dietary concentrations of

200, 2,000, and 20,000 ppm. No adverse

findings were noted at any dose level

and the NOEL was considered to be

20,000 ppm 1,936 mg/kg/day. The

Agency, however, has concluded that

the NOEL of the original study 63 mg/

kg/day should continue to be used for

risk assessment.

Developmental toxicity (teratology)

studies were conducted in both rats and

rabbits at dose levels of 0, 40, 200, and

1,000 mg/kg/day. No significant

maternal or developmental toxicity was

noted in either study. Thus, both the

maternal and developmental NOEL’s for

both rats and rabbits were considered to

be 1,000 mg/kg/day highest dose tested

(HDT).

4. Subchronic toxicity. A 90-day rat

feeding study was conducted at dose

levels of 500, 4,000 and 20,000 ppm.

The NOEL in this study was considered

to be 500 ppm (37 mg/kg/day for males

and 44 mg/kg/day for females) based on

increased liver weights at 4,000 ppm

and slightly decreased body weights at

20,000 ppm.
34178 Federal Register / Vol. 63, No. 120 /Tuesday, June 23, 1998 / Notices

In a 90-day oral toxicity study in dogs,

flutolanil was administered via capsule

at dose levels of 0, 80, 400 and 2,000

mg/kg/day. The NOEL was determined

to be 80 mg/kg/day based on enlarged

livers and increased glycogen

deposition at 400 and 2,000 mg/kg/day,

and increased alkaline phosphatase and

cholesterol levels and thyroid/

parathyroid organ weights at 2,000 mg/

kg/day.

In a 21-day dermal toxicity study,

flutolanil was applied dermally to rats

for 15-days over a 21-day interval at

dose levels of 0 and 1,000 mg/kg/day.

No evidence of dermal irritation or

systemic toxicity was observed. Thus,

the NOEL was considered to be 1,000

mg/kg/day.

5. Chronic toxicity. In a 2-year chronic

toxicity/oncogenicity study, flutolanil

was administered to rats at dietary

levels of 0, 40, 200, 2,000 and 10,000

ppm. The NOEL was considered to be

2,000 ppm (86.9 mg/kg/day for males

and 103.1 mg/kg/day for females) based

on reduced body weight gain in males

and increased liver weights in females

at 10,000 ppm. No evidence of

carcinogenicity was observed.

In a 78-week carcinogenicity study,

flutolanil was administered to mice at

dietary concentrations of 0, 300, 1,500,

7,000 and 30,000 ppm. The NOEL was

considered to be 7,000 ppm (735 mg/kg/

day for males) and 1,500 ppm (162 mg/

kg/day for females) based on decreased

body weight gains at the higher level(s).

No evidence of carcinogenicity was

observed.

A 2-year chronic toxicity study was

conducted in beagle dogs at dose levels

of 0, 50, 250, and 1,250 mg/kg/day. The

NOEL was considered to be 250 mg/kg/

day based on decreased weight gain at

1,250 mg/kg/day.

6. Animal metabolism. Studies in rats,

ruminants, and poultry suggest that

flutolanil is not well-absorbed following

oral administration. Once absorbed,

however, it is rapidly metabolized,

primarily to desisopropylflutolanil and

its conjugates, and rapidly excreted via

urine and feces.

7. Endocrine disruption. No special

studies have been conducted to

investigate the potential of flutolanil to

induce estrogenic or other endocrine

effects. However, no evidence of such

effects has been observed in the

subchronic, chronic, or reproductive

studies previously discussed. Thus, the

potential for flutolanil to cause

endocrine effects is considered to be

minimal.

C. Aggregate Exposure

1. Dietary exposure. Includes food

and drinking water—i. Food. Timelimited tolerances have been previously

established for flutolanil in or on rice

commodities, and tolerances with no

time limitations are established for

peanut commodities, meat, milk, and

eggs. Potential dietary exposures to

flutolanil from these food commodities

were assessed using the exposure one

software system (TAS, Inc.) and food

consumption data from the 1977-1978

USDA Continuing Surveys of Food

Consumption by Individuals (CSFCI).

For the purposes of this assessment, it

was assumed that 100% of all of the

above commodities were at the existing

tolerance levels for flutolanil.

ii. Drinking water. The potential for

flutolanil to leach into groundwater has

been assessed in two terrestrial field

dissipation studies, a long-term

terrestrial field dissipation study, and

an aquatic field dissipation study.

Under field conditions, the half-life of

flutolanil varied from 101 to 123 days in

the long-term field soil dissipation

study, which was consistent with the

other field studies, and was

approximately 180 days in the aquatic

environment. Flutolanil strongly

adsorbs to soil following application

and did not exhibit mobility under

either terrestrial or aquatic conditions.

The water solubility of flutolanil is quite

low ( 5.0 ppm). Based on these

environmental fate data and the

conditions of use, the potential for

movement of flutolanil into

groundwater is very low, and as such

the potential contribution of any such

residues to the total dietary intake of

flutolanil will be negligible. No

maximum contaminant level (MCL) or

Health Advisory Level for residues of

flutolanil in drinking water has been

established.

2. Non-dietary exposure. As prostar

50WP (EPA Reg No. 45639-153) is a

professional turf and ornamental

fungicide, flutolanil is used primarily

(>95%) on golf courses for control of

brown patch disease (Rhizoctonia

solani). Very limited use of prostar

50WP may occur on commercial

ornamental turf by professional lawn

care applicators or on sod farms. The

product is rarely, if ever, used on

homeowner turf due to the fact that the

diseases it controls (Brown patch, Fry

ring, snow molds) occur in highfertility, high-maintenance turf (e.g. golf

courses), not in homeowner lawns.

Thus, non-dietary exposure to flutolanil

would be minimal. Furthermore, no

dermal toxicity endpoints of concern

have been identified for flutolanil. Thus,

an assessment of non-dietary exposure

and risk is not considered to be

necessary.

D. Cumulative Effects

Flutolanil has demonstrated only

minimal toxicity in animal studies. The

mechanism of this toxicity is unknown.

Furthermore, there are no available data

to indicate that flutolanil has a common

mechanism of toxicity with other

substances. Thus, only the potential

risks from flutolanil are being

considered in this document.

E. Safety Determination

1. U.S. population. Based on the

existing and proposed tolerances in rice,

peanuts, and secondary commodities,

the Theoretical Maximum Residue

Contribution (TMRC) of the current

action is estimated to be 0.001124 mg/

kg/day for the U.S. population in

general. This exposure would utilize

less than 1% of the RfD. There is

generally no concern for exposures

below 100% of the RfD since the RfD

represents the exposure level at or

below which daily exposure over a

lifetime will not pose any appreciable

risks to human health. Therefore, there

is a reasonable certainty that no harm

will result to the U.S. population in

general from aggregate exposure to

flutolanil.

2 Infants and children. Data from

reproductive and developmental

toxicity studies are generally used to

assess the potential for increased

sensitivity of infants and children. No

evidence of developmental toxicity was

noted in rats or rabbits, even at the limit

dose of 1,000 mg/kg/day. Reduced pup

weights in the absence of parental

toxicity were noted at the HDL (10,000

ppm) in a 3-generation rat reproduction

study. However, no such effects were

noted in a subsequent reproduction

study, even at a HDT (20,000 ppm).

Furthermore, the reduced weight gain in

the first study began late in the lactation

period, at a time when the pups were

likely ingesting significant quantities of

diet. Feed intake is much higher in

young animals than in adults and the

apparent increase in sensitivity may

simply reflect the higher test material

intake in these pups on a mg/kg basis

compared to the adults. Thus, AgrEvo

believes that the overall weight of

evidence does not indicate any special

concern for infants and children, and

that no additional safety factor is

necessary.

Based on the existing and proposed

tolerances in rice, peanuts, and

secondary commodities, the Theoretical

Maximum Residue Contribution

(TMRC) from the current petition is

estimated to be 0.006218 mg/kg/day for

the most highly exposed subpopulation, non-nursing infants (less
Federal Register / Vol. 63, No. 120 /Tuesday, June 23, 1998 / Notices 34179

than 1-year old).. This exposure would

utilize less than 1 % of the RfD.

Therefore, there is a reasonable certainty

that no harm will result to infants or

children from aggregate exposure to

flutolanil.

F. International Tolerances

No CODEX tolerances have been

established or proposed for residues of

flutolanil. (Mary Waller).

2. Bayer Corporation

PP 6F4631

EPA has received a pesticide petition

(PP 6F4631) from Bayer Corporation,

8400 Hawthorn Road, P.O. Box 4913,

Kansas City, MO 64120–0013 proposing

pursuant to section 408(d) of the Federal

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

346a(d), to amend 40 CFR 180.527 by

establishing tolerances for inadvertent

residues of N-(4-fluorophenyl)-N-(1-

methylethyl)-2- [[5-(trifluoromethyl)-

1,3,4-thiadiazol-2-yl]oxy]acetamide

[hereafter referred to as flufenacet, the

proposed common chemical name] and

metabolites containing the 4-fluoro-Nmethylethyl benzenamine moiety in or

on the raw agricultural commodities of

Crop Group 15 (cereal grains), Crop

Group 16 (forage, stover and hay of

cereal grains), Crop Group 17 (grass

forage, and grass hay), alfalfa forage,

alfalfa hay, alfalfa seed, clover forage,

and clover hay at 0.1 parts per million

(ppm) when present therein as a result

of the application of flufenacet to field

corn and soybeans as a herbicide. EPA

has determined that the petition

contains data or information regarding

the elements set forth in section

408(d)(2) of the FFDCA; however, EPA

has not fully evaluated the sufficiency

of the submitted data at this time or

whether the data supports granting of

the petition. Additional data may be

needed before EPA rules on the petition.

A. Residue Chemistry

1. Plant metabolism. The nature of the

residue in field corn, soybeans,

livestock and rotational crops is

adequately understood. The residues of

concern for the tolerance expression are

N-(4-fluorophenyl)-N-(1-methylethyl)-2-

[[5-(trifluoromethyl)-1,3,4-thiadiazol-2-

yl]oxy]acetamide parent and its

metabolites containing the 4-fluoro-Nmethylethyl benzenamine moiety. Based

on the results of animal metabolism

studies it is unlikely that secondary

residues would occur in animal

commodities from the use of flufenacet

on field corn and soybeans.

2. Analytical method. An adequate

analytical method, gas chromatography/

mass spectrometry with selected ion

monitoring, is available for enforcement

purposes. Because of the long lead time

from establishing these tolerances to

publication of the enforcement

methodology in the Pesticide Analytical

Manual, Vol. II, the analytical

methodology is being made available in

the interim to anyone interested in

pesticide enforcement when requested

from: Calvin Furlow, Public Information

and Records Integrity Branch,

Information Resources and Services

Division (7502C), Office of Pesticide

Programs, Environmental Protection

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

DC 20460. Office location and telephone

number: Room 119E, CM #2, 1921

Jefferson Davis Highway, Arlington, VA

22202, (703–305–5937).

3. Magnitude of residues. Time

limited tolerances exist for the

combined residues of flufenacet, N-(4-

fluorophenyl)-N-(1-methylethyl)-2-[[5-

(trifluoromethyl)-1,3,4-thiadiazol-2-

yl]oxy]acetamide and its metabolites

containing the 4-fluoro-N-methylethyl

benzenamine moiety in or on field corn

grain at 0.05 ppm, field corn forage at

0.4 ppm, field corn stover at 0.4 ppm,

and soybean seed at 0.1 ppm. The

petitioner, Bayer Corporation has

amended its petition (PP 6F4631) to

include tolerances for residues of N-(4-

fluorophenyl)-N-(1-methylethyl)-2-[[5-

(trifluoromethyl)-1,3,4-thiadiazol-2-

yl]oxy]acetamide and its metabolites

containing the 4-fluoro-N-methylethyl

benzenamine moiety at 0.1 ppm for

residues in or on the raw agricultural

commodities of Crop Group 15 (cereal

grains), Crop Group 16 (forage, stover

and hay of cereal grains), Crop Group 17

(grass forage and grass hay), alfalfa

forage, alfalfa hay, alfalfa seed, clover

forage, and clover hay. The proposed

tolerance levels are adequate to cover

residues likely to be present in

rotational crops planted after corn or

soybeans which were treated with

flufenacet.

B. Toxicological Profile

1. Acute toxicity. A rat acute oral

study with a LD50 of 1,617 milligrams/

kilograms for males and 589 mg/kg for

females.

2. Genotoxicty. Flufenacet was

negative for mutagenic/genotoxic effects

in a Gene mutation/In vitro assay in

bacteria, a Gene mutation/In vitro assay

in chinese hamster lung fibroblasts

cells, a Cytogenetics/In vitro assay in

chinese hamster ovary cells, a

Cytogenetics/In vivo mouse

micronucleus assay, and an In vitro

unscheduled DNA synthesis assay in

primary rat hepatocytes.

3. Reproductive and developmental

toxicity. A two-generation rat

reproduction study with a parental

systemic no observed effect level

(NOEL) of 20 ppm [1.4 mg/kg/day in

males and 1.5 mg/kg/day in females]

and a reproductive NOEL of 20 ppm [1.3

mg/kg/day] and a parental systemic

lowest observed effect level (LOEL) of

100 ppm [7.4 mg/kg/day in males and

8.2 mg/kg/day in females] based on

increased liver weight in F1 females and

hepatocytomegaly in F1 males and a

reproductive LOEL of 100 ppm [6.9 mg/

kg/day] based on increased pup death in

early lactation (including cannibalism)

for F1 litters and the same effects in

both F1 and F2 pups at the high dose

level of 500 ppm [37.2 mg/kg/day in F1

males and 41.5 mg/kg/day in F1

females, respectively]. A rat

developmental study with a maternal

NOEL of 25 mg/kg/day and with a

maternal LOEL of 125 mg/kg/day based

on decreased body weight gain initially

and a developmental NOEL of 25 mg/

kg/day and a developmental LOEL of

125 mg/kg/day based on decreased fetal

body weight, delayed development

[mainly delays in ossification in the

skull, vertebrae, sternebrae, and

appendages], and an increase in the

incidence of extra ribs. A rabbit

developmental study with a maternal

NOEL of 5 mg/kg/day and a maternal

LOEL of 25 mg/kg/day based on

histopathological finds in the liver and

a developmental NOEL of 25 mg/kg/day

and a developmental LOEL of 125 mg/

kg/day based on increased skeletal

variations.

4. Subchronic toxicity. A 84–day rat

feeding study with a No Observed Effect

Level ( NOEL) less than 100 ppm [6.0

mg/kg/day] for males and a NOEL of 100

ppm [7.2 mg/kg/day] for females and

with a Lowest Observed Effect Level

(LOEL) of 100 ppm [6.8 mg/kg/day] for

males based on suppression of

thyroxine (T4) level and a LOEL of 400

ppm [28.8 mg/kg/day] for females based

on hematology and clinical chemistry

findings. A 13–week mouse feeding

study with a NOEL of 100 ppm [18.2

mg/kg/day for males and 24.5 mg/kg/

day for females] and a LOEL of 400 ppm

[64.2 mg/kg/day for males and 91.3 mg/

kg/day for females] based on

histopathology of the liver, spleen and

thyroid. A 13–week dog dietary study

with a NOEL of 50 ppm [1.70 mg/kg/day

for males and 1.67 mg/kg/day for

females] and a LOEL of 200 ppm [6.90

mg/kg/day for males and 7.20 mg/kg/

day for females] based on evidence that

the bio-transformation capacity of the

liver has been exceeded, (as indicated

by increase in LDH, liver weight, ALK

and hepatomegaly), globulin and spleen

pigment in females, decreased T4 and
34180 Federal Register / Vol. 63, No. 120 /Tuesday, June 23, 1998 / Notices

ALT values in both sexes, decreased

albumin in males, and decreased serum

glucose in females. A 21–day rabbit

dermal study with the dermal irritation

NOEL of 1,000 mg/kg/day for males and

females and a systemic NOEL of 20 mg/

kg/day for males and 150 mg/kg/day for

females and a systemic LOEL of 150 mg/

kg/day for males and 1,000 mg/kg/day

for females based on clinical chemistry

data (decreased T4 and FT4 levels in

both sexes) and centrilobular

hepatocytomegaly in females.

5. Chronic toxicity. A 1–year dog

chronic feeding study with a NOEL was

40 ppm [1.29 mg/kg/day in males and

1.14 mg/kg/day in females] and a LOEL

of 800 ppm [27.75 mg/kg/day in males

and 26.82 mg/kg/day in females] based

on increased alkaline phosphatase,

kidney, and liver weight in both sexes,

increased cholesterol in males,

decreased T2, T4 and ALT values in

both sexes, and increased incidences of

microscopic lesions in the brain, eye,

kidney, spinal cord, sciatic nerve and

liver. A rat chronic feeding/

carcinogenicity study with a NOEL less

than 25 ppm [1.2 mg/kg/day in males

and 1.5 mg/kg/day in females] and a

LOEL of 25 ppm [1.2 mg/kg/day in

males and 1.5 mg/kg/day in females]

based on methemoglobinemia and

multi-organ effects in blood, kidney,

spleen, heart, and uterus. Under

experimental conditions the treatment

did not alter the spontaneous tumor

profile. In a mouse carcinogenicity

study the NOEL was less than 50 ppm

[7.4 mg/kg/day] for males and the NOEL

was 50 ppm [9.4 mg/kg/day] for females

and the LOEL was 50 ppm [7.4 mg/kg/

day] for males and the LOEL was 200

ppm [38.4 mg/kg/day] for females based

on cataract incidence and severity.

There was no evidence of

carcinogenicity for flufenacet in this

study.

6. Animal metabolism. A rat

metabolism study showed that radiolabeled flufenacet was rapidly absorbed

and metabolized by both sexes. Urine

was the major route of excretion at all

dose levels and smaller amounts were

excreted via the feces. A 55–day dog

study with subcutaneous administration

of Thiadone [flufenacet metabolite]

supports the hypothesis that

limitationsin glutathione

interdependent pathways and

antioxidant stress result in metabolic

lesions in the brain and heart following

flufenacet exposure.

7. Endocrine disruption. EPA is

required to develop a screening program

to determine whether certain substances

(including all pesticides and inerts) may

have an effect in humans that is similar

to an effect produced by a naturally

occurring estrogen, or such other effect.

The Agency is currently working with

interested stakeholders, including other

government agencies, public interest

groups, industry and research scientists

in developing a screening and testing

program and a priority setting scheme to

implement this program. Congress has

allowed 3 years from the passage of

FQPA (August 3, 1999) to implement

this program. At that time, EPA may

require further testing of this active

ingredient and end use products for

endocrine disrupter effects. Based on

the toxicological findings for flufenacet

relating to endocrine disruption effects,

flufenacet should be considered as a

candidate for evaluation as an endocrine

disrupter when the criteria are

established.

C. Aggregate Exposure

In examining aggregate exposure,

FFDCA section 408 requires that EPA

take into account available and reliable

information concerning exposure from

the pesticide residue in the food in

question, residues in other foods for

which there are tolerances, residues in

groundwater or surface water that is

consumed as drinking water, and other

non-occupational exposures through

pesticide use in gardens, lawns, or

buildings (residential and other indoor

uses).

1. Dietary exposure—i. Food. Dietary

exposure to residues of a pesticide in a

food commodity are estimated by

multiplying the average daily

consumption of the food forms of that

commodity by the tolerance level or the

anticipated pesticide residue level. The

Theoretical Maximum Residue

Contribution (TMRC) is an estimate of

the level of residues consumed daily if

each food item contained pesticide

residues equal to the tolerance. In

evaluating food exposures, varying

consumption patterns of major

identifiable subgroups of consumers,

including infants and children is taken

into account. The TMRC is a ‘‘worst

case’’ estimate since it is based on the

assumptions that food contains

pesticide residues at the tolerance level

and that 100% of the crop is treated by

pesticides that have established

tolerances. Using tolerance levels and

percent crop treated, the residues in the

diet (food only) are calculated to be

0.0001 milligrams/kilogram of body

weight per day (mg/kg bwt/day) or 2.6%

of the RfD for the general U.S.

population and 0.00023 mg/kg bwt/day

or 5.8% of the RfD for children aged 1–

6 years.

ii. Drinking water. Residues of

flufenacet in drinking water may

comprise up to 0.0039 mg/kg bwt/day

(0.0040–0.0001 mg/kg bwt/day) for the

U.S. population and 0.0038 mg/kg bwt/

day (0.00400–0.00023 mg/kg bwt/day)

for children 1–6 years old (the group

exposed to the highest level of

flufenacet residues in both food and

water). The drinking water levels of

concern (DWLOCs) for chronic exposure

to flufenacet in drinking water

calculated for the U.S. population was

136 parts per billion (ppb) assuming

that an adult weighs 70 kg and

consumes a maximum of 2 liters of

water per day. For children (1–6 years

old), the DWLOC was 37.7 ppb

assuming that a child weighs 10 kg and

consumes a maximum of 1 liter of water

per day. The drinking water estimated

concentration (DWECs) for groundwater

(parent flufenacet and degradate

thiadone) calculated from the

monitoring data is 0.03 ppb for chronic

concentrations which does not exceed

DWLOC of 37.7 ppb for children (1–6

years old). The DWEC for surface water

based on the computer models PRZM

2.3 and EXAMS 2.97.5 was calculated to

be 14.2 ppb for chronic concentration

(parent flufenacet and degradate

thiadone) which does not exceed the

DWLOC of 37.7 ppb for children (1–6

years old).

2. Non-dietary exposure. There are no

non-food uses of flufenacet currently

registered under the Federal Insecticide,

Fungicide and Rodenticide Act, as

amended. No non-dietary exposures are

expected for the general population.

D. Cumulative Effects

Flufenacet is structurally a

thiadiazole. EPA is not aware of any

other pesticides with this structure. For

flufenacet, EPA has not yet conducted a

detailed review of common mechanisms

to determine whether it is appropriate,

or how to include this chemical in a

cumulative risk assessment. After EPA

develops a methodology to address

common mechanism of toxicity issues

to risk assessments, the Agency will

develop a process (either as part of the

periodic review of pesticides or

otherwise) to reexamine these tolerance

decisions. Unlike other pesticides for

which EPA has followed a cumulative

risk approach based on a common

mechanism of toxicity, flufenacet does

not appear to produce a toxic metabolite

produced by other substances. For the

purposes of these tolerance actions;

therefore, EPA has not assumed that

flufenacet has a common mechanism of

toxicity with other substances.

E. Safety Determination

1. U.S. population—i. Acute risk. The

acute endpoint for flufenacet and its

metabolites is 75 mg/kg/day. The acute
Federal Register / Vol. 63, No. 120 /Tuesday, June 23, 1998 / Notices 34181

exposure for flufenacet and its

metabolites is 0.0015 mg/kg/day for the

general U.S. population and 0.002 mg/

kg/day for children 1–6 years of age.

The DWLOC for acute exposure to

flufenacet in drinking water calculated

for the U.S. population was 2.87 ppm

and for children (1–6 years old) was 813

ppb. These figures were calculated as

follows. First, the acceptable acute

exposure to flufenacet in drinking water

was obtained by subtracting the acute

dietary food exposures from the ratio of

the acute LOEL to the acceptable margin

of exposure (MOE) for aggregate

exposure. Then, the DWLOCs were

calculated by multiplying the acceptable

exposure to flufenacet in drinking water

by estimated body weight (70 kg for

adults, 10 kg for children) and then

dividing by the estimated daily drinking

water consumption (2 L/day for adults,

1 L/day for children). The Agency’s SCIGrow model estimates peak levels of

flufenacet and its metabolite thiadone in

groundwater to be 15.3 ppb. PRZM/

EXAMS estimates peak levels of

flufenacet and its metabolite thiadone in

surface water to be 17 ppb. EPA’s acute

drinking water level of concern is well

above the estimated exposures for

flufenacet in water for the U.S.

population and subgroup with highest

estimated exposure.

ii. Chronic risk. The chronic endpoint

for flufenacet is 0.004 mg/kg bwt/day.

Using tolerance levels and percent crop

treated, the residues in the diet (food

only) are calculated to be 0.0001 mg/kg

bwt/day or 2.6% of the Reference dose

(RfD) for the general U.S. population

and 0.00023 mg/kg bwt/day or 5.8% of

the RfD for children aged 1–6 years.

Therefore, residues of flufenacet in

drinking water may comprise up to

0.0039 mg/kg bwt/day (0.0040–0.0001

mg/kg bwt/day) for the U.S. population

and 0.0038 mg/kg bwt/day (0.00400–

0.00023 mg/kg bwt/day) for children 1–

6 years old (the group exposed to the

highest level of flufenacet residues in

both food and water). The DWLOCs for

chronic exposure to flufenacet in

drinking water calculated for the U.S.

population was 136 ppb assuming that

an adult weighs 70 kg and consumes a

maximum of 2 liters of water per day.

For children (1–6 years old), the

DWLOC was 37.7 ppb assuming that a

child weighs 10 kg and consumes a

maximum of 1 liter of water per day.

The drinking water estimated

concentration (DWECs) for groundwater

(parent flufenacet and degradate

thiadone) calculated from the

monitoring data is 0.03 ppb for chronic

concentrations which does not exceed

the DWLOC of 37.7 ppb for children (1–

6 years old). The DWEC for surface

water based on the computer models

PRZM 2.3 and EXAMS 2.97.5 was

calculated to be 14.2 ppb for chronic

concentration (parent flufenacet and

degradate thiadone) which does not

exceed the DWLOC of 37.7 ppb for

children (1–6 years old). EPA concludes

that there is a reasonable certainty that

no harm will result from aggregate

exposure to flufenacet residues.

2. Infants and children. In assessing

the potential for additional sensitivity of

infants and children to residues of

flufenacet, EPA considered data from

developmental toxicity studies in the rat

and rabbit and a two-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.

FFDCA section 408 provides that EPA

shall apply an additional tenfold margin

of safety for infants and children in the

case of threshold effects to account for

pre- and post-natal toxicity and the

completeness of the database unless

EPA determines that a different margin

of safety will be safe for infants and

children. Although there is no

indication of increased sensitivity to

young rats or rabbits following pre- and/

or post-natal exposure to flufenacet in

the standard developmental and

reproductive toxicity studies, an

additional developmental neurotoxicity

study, which is not normally required,

is needed to access the susceptibility of

the offspring in function/neurological

development. Therefore, EPA has

required that a developmental

neurotoxicity study be conducted with

flufenacet and a threefold safety factor

for children and infants will be used in

the aggregate dietary acute and chronic

risk assessment. Although there is no

indication of additional sensitivity to

young rats or rabbits following pre- and/

or post-natal exposure to flufenacet in

the developmental and reproductive

toxicity studies; the Agency concluded

that the FQPA safety factor should not

be removed but instead reduced

because:

(i) There was no assessment of

susceptibility of the offspring in

functional/neurological developmental

and reproductive studies.

(ii) There is evidence of neurotoxicity

in mice, rats, and dogs.

(iii) There is concern for thyroid

hormone disruption.

F. International Tolerances

There are no Codex Alimentarius

Commission (Codex) Maximum Residue

Levels (MRLs) for flufenacet. (James A.

Tompkins).

3. FMC Corporation

PP 8F4970

EPA has received pesticide petitions

(PP 8F4970) from FMC Corporation,

1735 Market Street,Philadelphia, PA

19103, proposing pursuant to section

408 (d) of the Federal Food, Drug, and

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

amend 40 CFR 180.418 by establishing

a tolerance for residues of the

insecticide zeta-cypermethrin (±αCyano(3-phenoxyphenyl)methyl ( ±) cis,

trans 3-(2,2-dichloroethenyl)-2,2-

dimethylcyclopropanecarboxylate)in or

on the raw agricultural commodity

Brassica vegetables, head and stem at

2.0 ppm and Brassica vegetables, leafy

at 14.0 ppm; and the leafy vegetables

(except Brassica vegetables) group at

10.0 ppmn. 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 cypermethrin in plants is adequately

understood. Studies have been

conducted to delineate the metabolism

of radio labelled cypermethrin in

various crops all showing similar

results. The residue of concern is the

parent compound only.

2. Analytical method. There is a

practical analytical method for detecting

and measuring levels of cypermethrin in

or on food with a limit of detection that

allows monitoring of food with residues

at or above the levels set in these

tolerances (Gas Chromatography with

Electron Capture Detection (GC/ECD).

3. Magnitude of residues. Crop field

trial residue data from studies

conducted at the maximum label rates

for head and stem Brassica vegetables,

leafy Brassica greens, and leafy

vegetables (except Brassica vegetables)

group, show that the proposed zetacypermethrin tolerances on Brassica

vegetables, head and stemat 2.0 ppm

and Brassica vegetables, leafy at 14.0

ppm; and the leafy vegetables (except

Brassica vegetables) group at 10.0 ppm

will not be exceeded when the zetacypermethrin products labeled for these

uses are used as directed.
34182 Federal Register / Vol. 63, No. 120 /Tuesday, June 23, 1998 / Notices

B. Toxicological Profile

1. Acute toxicity. For the purposes of

assessing acute dietary risk, FMC has

used the no-observed-effected label

(NOEL) of 3.8 mg/kg/day based on the

NOEL of 7.5 mg/kg/day from the

cypermethrin chronic feeding/

oncogenicity study in rats and a

correction factor of two to account for

the differences in the percentage of the

biologically active isomer. The LOEL of

50.0 mg/kg/day was based on

neurological signs which were

displayed during week one of the study.

This acute dietary end point is used to

determine acute dietary risks to all

population subgroups.

2. Genotoxicity. The following

genotoxicity tests were all negative: in

vivo chromosomal aberration in rat bone

marrow cells; in vitro cytogenic

chromosome aberration; unscheduled

DNA synthesis;CHO/HGPTT mutagen

assay; weakly mutagenic: gene mutation

(Ames).

3. Reproductive and developmental

toxicity. No evidence of additional

sensitivity to young rats was observed

following pre- or postnatal exposure to

zeta-cypermethrin.

i. A 2-generation reproductive toxicity

study with zeta-cypermethrin in rats

demonstrated a NOEL of 7.0 mg/kg/day

and a LOEL of 27.0 mg/kg/day for

parental/systemic toxicity based on

body weight, organ weight, and clinical

signs. There were no adverse effects in

reproductive performance. The NOEL

for reproductive toxicity was considered

to be > 45.0 mg/kg/day the highest dose

tested (HDT).

ii. A developmental study with zetacypermethrin in rats demonstrated a

maternal NOEL of 12.5 mg/kg/day and

a LOEL of 25 mg/kg/day based on

decreased maternal body weight gain,

food consumption and clinical signs.

There were no signs of developmental

toxicity at 35.0 mg/kg/day, the higest

dose level tested (HDLT).

iii. A developmental study with

cypermethrin in rabbits demonstrated a

maternal NOEL of 100 mg/kg/day and a

LOEL of 450 mg/kg/day based on

decreased body weight gain. There were

no signs of developmental toxicity at

700 mg/kg/day, the HDLT.

4. Subchronic toxicity— Short- and

intermediate-term toxicity. The NOEL of

3.8 mg/kg/day based on the NOEL 7.5

mg/kg/day from the cypermethrin

chronic feeding/oncogenicity study in

rats and a correction factor of two to

account for the biologically active

isomer would also be used for short-and

intermediate-term MOE calculations (as

well as acute, discussed in (1) above).

The LOEL of 50.0 mg/kg/day was based

on neurological signs which were

displayed during week one of the study.

5. Chronic toxicity. The reference dose

(RfD) of 0.0125 mg/kg/day for zetacypermethrin is based on a NOEL of 2.5

mg/kg/day from a cypermethrin rat

reproduction study and an uncertainty

factor of 200 (used to account for the

differences in the percentage of the

biologically active isomer). The

endpoint effect of concern was based on

consistent decreased body weight gain

in both sexes at the LOEL of 7.5 mg/kg/

day.

Cypermethrin is classified as a Group

C chemical (possible human carcinogen

with limited evidence of carcinogenicity

in animals) based upon limited

evidence for carcinogenicity in

femalemice; assignment of a Q* has not

been recommended.

6. Animal metabolism. The

metabolism of cypermethrin in animals

is adequately understood. Cypermethrin

has been shown to be rapidly absorbed,

distributed, and excreted in rats when

administered orally. Cypermethrin is

metabolized by hydrolysis and

oxidation.

7. Metabolite toxicology. The Agency

has previously determined that the

metabolites of cypermethrin are not of

toxicological concern and need not be

included in the tolerance expression.

8. Endocrine disruption. No special

studies investigating potential

estrogenic or other endocrine effects of

cypermethrin have been conducted.

However, no evidence of such effects

were reported in the standard battery of

required toxicology studies which have

been completed and found acceptable.

Based on these studies, there is no

evidence to suggest that cypermethrin

has an adverse effect on the endocrine

system.

C. Aggregate Exposure

1. Dietary exposure—i. Food.

Permanent tolerances, in support of

registrations, currently exist for residues

of zeta-cypermethrin on cottonseed;

pecans; lettuce, head; onions, bulb; and

cabbage and livestock commodities of

cattle, goats, hogs, horses, and sheep.

For the purposes of assessing the

potentialdietary exposure for these

existing and the subject proposed

tolerances, FMC has utilized available

information on anticipated residues,

monitoring data and percent crop

treated as follows:

ii. Acute exposure and risk. Acute

dietary exposure risk assessments are

performed for a food-use pesticide if a

toxicological study has indicated the

possibility of an effect of concern

occurring as a result of a 1-day or single

exposure. For the purposes of assessing

acute dietary risk for zeta-cypermethrin,

FMC has used the NOEL of 3.8 mg/kg/

day based on the NOEL of 7.5 mg/kg/

day from the cypermethrin chronic

feeding/oncogenicity study in rats and a

correction factor of two to account for

the differences in the percentage of the

biologically active isomer. The LOEL of

50.0 mg/kg/day was based on

neurological signs which were

displayed during week one of this

study. This acute dietary endpoint is

used to determine acute dietary risks to

all population subgroups. Available

information on anticipated residues,

monitoring data and percent crop

treated was incorporated into a Tier 3

analysis, using Monte Carlo modeling

for commodities that may be consumed

in a single serving. These assessments

show that the margins of exposure

(MOE) are significantly greater than the

EPA standard of 100 for all

subpopulations. The 95th percentile of

exposure for the overall U. S.

population was estimated to be

0.000708 mg/kg/day (MOE of 5364);

99th percentile 0.002677 mg/kg/day

(MOE of 1420); and 99.9th percentile

0.012098 mg/kg/day (MOE of 314). The

95th percentile of exposure for all

infants <1- year old was estimated to be

0.000264 mg/kg/day (MOE of 14394);

99th percentile 0.00189 mg/kg/day

(MOE of 2011); and 99.9th percentile

0.018164 mg/kg/day (MOE of 209). The

95th percentile of exposure for nursing

infants <1-year old was estimated to be

0.000026 mg/kg/day (MOE of 147540);

99th percentile 0.000484 mg/kg/day

(MOE of 7843); and 99.9th percentile

0.002004 mg/kg/day (MOE of 1896).The

95th percentile of exposure for nonnursing infants < 1- year old was

estimated to be 0.000367mg/kg/day

(MOE of 10342); 99th percentile

0.005649 mg/kg/day (MOE of 673); and

99.9th percentile 0.019823 mg/kg/day

(MOE of 192). The 95th percentile of

exposure for children 1 to 6-years old

(the most highly exposed population

subgroup) and children 7 to 12-years old

was estimated to be, respectively,

0.000742 mg/kg/day (MOE of 5120) and

0.00748 mg/kg/day (MOE of 5077); 99th

percentile 0.003061 mg/kg/day (MOE of

1241) and 0.002638 (MOE of 1440); and

99.9th percentile 0.031769 mg/kg/day

(MOE of 120) and 0.013432 (MOE of

283). Therefore, FMC concludes that the

acute dietary risk of zeta-cypermethrin,

as estimated by the dietary risk

assessment, does not appear to be of

concern.

iii. Chronic exposure and risk. RfD of

0.0125 mg/kg/day for zeta-cypermethrin

is based on a NOEL of 2.5 mg/kg/day

from a cypermethrin rat reproduction
Federal Register / Vol. 63, No. 120 /Tuesday, June 23, 1998 / Notices 34183

study and an uncertainty factor of 200

(used to account for the differences in

the percentage of the biologically active

isomer). The endpoint effect of concern

was based on consistent decreased body

weight gain in both sexes at the LOEL

of 7.5 mg/kg/day. A chronic dietary

exposure/risk assessment has been

performed for zeta-cypermethrin using

the above RfD. Available information on

anticipated residues, monitoring data

and percent crop treated was

incorporated into the analysis to

estimate the anticipated residue

contribution (ARC). The ARC is

generally considered a more realistic

estimate than an estimate based on

tolerance level residues. The ARC are

estimated to be 0.000098 mg/kg body

weight/day (mg/kg/bwt/day) and utilize

0.8 % of the RfD for the overall U. S.

population. The ARC for non-nursing

infants (<1-year) and nursing infants

(<1-year) are estimated to be 0.00016

mg/kg/day and 0.00001 mg/kg/day and

utilizes 1.3 % and 0.1 % of the RfD,

respectively. The ARC for children 1-6

years old (subgroup most highly

exposed) and children 7-12 years old are

estimated to be 0.000172 mg/kg bwt/day

and 0.000092 mg/kg bwt/day and

utilizes 1.4 % and 0.7 % of the RfD,

respectively. Generally speaking, the

EPA has no cause for concern if the total

dietary exposure from residues for uses

for which there are published and

proposed tolerances is less than 100 %

of the RfD. Therefore, FMC concludes

that the chronic dietary risk of zetacypermethrin, as estimated by the

dietary risk assessment, does not appear

to be of concern.

2. Drinking water. Laboratory and

field data have demonstrated that

cypermethrin is immobile in soil and

will not leach into groundwater. Other

data show that cypermethrin is virtually

insoluble in water and extremely

lipophilic. As a result, FMC concludes

that residues reaching surface waters

from field runoff will quickly adsorb to

sediment particles and be partitioned

from the water column. Further, a

screening evaluation of leaching

potential of a typical pyrethroid was

conducted using EPA’s Pesticide Root

Zone Model (PRZM3). Based on this

screening assessment, the potential

concentrations of a pyrethroid in

groundwater at depths of 1 and 2 meters

are essentially zero (<0.001 part per

billion (PPB). Surface water

concentrations for pyrethroids were

estimated using PRZM3 and Exposure

Analysis Modeling System (EXAMS)

using standard EPA cotton runoff and

Mississippi pond scenarios. The

maximum concentration predicted in

the simulated pond was 0.052 PPB.

Concentrations in actual drinking water

would be much lower than the levels

predicted in the hypothetical, small,

stagnant farm pond model since

drinking water derived from surface

water would normally be treated before

consumption. Based on these analyses,

the contribution of water to the dietary

risk estimate is negligible. Therefore,

FMC concludes that together these data

indicate that residues are not expected

to occur in drinking water.

3. Non-dietary exposure. Zetacypermethrin is registered for

agricultural crop applications only,

therefore non-dietary exposure

assessments are not warranted.

D. Cumulative Effects

In consideration of potential

cumulative effects of cypermethrin and

other substances that may have a

common mechanism of toxicity, to our

knowledge there are currently no

available data or other reliable

information indicating that any toxic

effects produced by cypermethrin

would be cumulative with those of other

chemical compounds; thus only the

potential risks of cypermethrin have

been considered in this assessment of its

aggregate exposure. FMC intends to

submit information for the EPA to

consider concerning potential

cumulative effects of cypermethrin

consistent with the schedule established

by EPA at 62 FR 42020 (August 4, 1997)

(FRL 5734-6) and other EPA

publications pursuant to the Food

Quality Protection Act.

E. Safety Determination

1. U.S. population. Based on a

complete and reliable toxicology

database, the RfD for zeta-cypermethrin

is 0.0125 mg/kg/day, based on a NOEL

of 2.5 mg/kg/day and a LOEL of 7.5 mg/

kg/day from the cypermethrin rat

reproduction study and an uncertainty

factor of 200. Available information on

anticipated residues, monitoring data

and percent crop treated was

incorporated into an analysis to estimate

the ARC for 26 population subgroups.

The ARC is generally considered a more

realistic estimate than an estimate based

on tolerance level residues. The ARC are

estimated to be 0.000098 mg/kg/bwt/day

and utilize 0.8 of the RfD or the overall

U. S. population. The ARC for nonnursing infants (<1-year) and nursing

infants (<1- year) are estimated to be

0.00016 mg/kg/day and 0.00001 mg/kg/

day and utilizes 1.3 % and 0.1 % of the

RfD, respectively. The ARC for children

1-6 years old (subgroup most highly

exposed) and children 7-12 years old are

estimated to be 0.000172 mg/kg bwt/day

and 0.000092 mg/kg bwt/day and

utilizes 1.4 % and 0.7 % of the RfD,

respectively. Generally speaking, the

EPA has no cause for concern if the total

dietary exposure from residues for uses

for which there are published and

proposed tolerances is less than 100 %

of the RfD. Therefore, FMC concludes

that the chronic dietary risk of zetacypermethrin, as estimated by the

aggregate risk assessment, does not

appear to be of concern.

For the overall U.S. population, the

calculated margins of exposure (MOE) at

the 95th percentile was estimated to be

5364; 1420 at the 99th percentile; and

314 at the 99.9th percentile. For all

infants < 1-year old, the calculated MOE

at the 95th percentile was estimated to

be 14394; 2011 at the 99th percentile;

and 209 at the 99.9th percentile. For

nursing infants < 1-year old, the

calculated MOE at the 95th percentile

was estimated to be 147540; 7843 at the

99th percentile; and 1896 at the 99.9th

percentile. For non-nursing infants < 1-

year old, the calculated MOE at the 95th

percentile was estimated to be 10342;

673 at the 99th percentile; and 192 at

the 99.9th percentile. For the most

highly exposed population subgroup,

children 1- 6 years old, and for children

7-12 years old, the calculated MOEs at

the 95th percentile were estimated to be,

respectively, 5120 and 5077; 1241 and

1440 at the 99th percentile; and 120 and

283 at the 99.9th percentile. Therefore,

FMC concludes that there is reasonable

certainty that no harm will result from

acute exposure to zeta-cypermethrin.

2. Infants and children—i. General. In

assessing the potential for additional

sensitivity of infants and children to

residues of zeta-cypermethrin, FMC

considered data from developmental

toxicity studies in the rat and rabbit,

and a 2-generation reproductive study

in the rat. The data demonstrated no

indication of increased sensitivity of

rats to zeta-cypermethrin or rabbits to

cypermethrin in utero and/or postnatal

exposure to zeta-cypermethrin or

cypermethrin. 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.

FFDCA section 408 provides that EPA

may apply an additional margin of

safety for infants and children in the

case of threshold effects to account for

pre- and post-natal toxicity and the

completeness of the database.
34184 Federal Register / Vol. 63, No. 120 /Tuesday, June 23, 1998 / Notices

ii. Developmental toxicity studies. In

the prenatal developmental toxicity

studies in rats and rabbits, there was no

evidence of developmental toxicity at

the HDT (35.0 mg/kg/day in rats and

700 mg/kg/day in rabbits). Decreased

body weight gain was observed at the

maternal LOEL in each study; the

maternal NOEL was established at 12.5

mg/kg/day in rats and 100 mg/kg/day in

rabbits.

iii. Reproductive toxicity study. In the

2-generation reproduction study in rats,

offspring toxicity (body weight) and

parental toxicity (body weight, organ

weight, and clinical signs) was observed

at 27.0 mg/kg/day and greater. The

parental systemic NOEL was 7.0 mg/kg/

day and the parental systemic LOEL was

27.0 mg/kg/day. There were no

developmental (pup) or reproductive

effects up to 45.0 mg/kg/day, HDT.

iv. Pre- and post-natal sensitivity—a.

Pre-natal. There was no evidence of

developmental toxicity in the studies at

the HDT in the rat (35.0 mg/kg/day) or

in the rabbit (700 mg/kg/day). Therefore,

there is no evidence of a special dietary

risk (either acute or chronic) for infants

and children which would require an

additional safety factor.

b. Post-natal. Based on the absence of

pup toxicity up to dose levels which

produced toxicity in the parental

animals, there is no evidence of special

post-natal sensitivity to infants and

children in the rat reproduction study.

c. Conclusion. Based on the above,

FMC concludes that reliable data

support use of the standard 100-fold

uncertainty factor, and that an

additional uncertainty factor is not

needed to protect the safety of infants

and children. As stated above, aggregate

exposure assessments utilized

significantly less than 1 % of the RfD for

either the entire U. S. population or any

of the 26 population subgroups

including infants and children.

Therefore, it may be concluded that

there is reasonable certainty that no

harm will result to infants and children

from aggregate exposure to

cypermethrin residues.

3. Subchronic toxicity— Short- and

intermediate-term toxicity. The NOEL of

3.8 mg/kg/day based on the NOEL 7.5

mg/kg/day from the cypermethrin

toxicity/oncogenicity study in rats and a

correction factor of two to account for

the biologically active isomer would

also be used for short- and intermediateterm MOE calculations (as well as acute,

discussed in (E.1.) above). The LOEL of

this study of 50.0 mg/kg/day was based

on neurological signs observed in the

first week of the study.

F. International Tolerances

There are no Codex, Canadian, or

Mexican residue limits for residues of

zeta-cypermethrin in or on Brassica,

head and stem vegetables; Brassica,

leafy vegetables; and leafy vegetables

(except Brassica vegetables) group.

(Stephaine Willette).

[FR Doc. 98–16673 Filed 6–22–98; 8:45 am]

BILLING CODE 6560–50–F

ENVIRONMENTAL PROTECTION

AGENCY

[FRL–6114–3]

Proposed CERCLA Prospective

Purchaser Agreement and Proposed

CERCLA Section 122(h)(1)

Administrative Cost Recovery

Settlement Agreement for the IngramRichardson Site

AGENCY: Environmental Protection

Agency (EPA).

ACTION: Proposal of CERCLA

Prospective Purchaser Agreement and

Proposal of CERCLA section 122(h)(1)

Administrative Cost Recovery

Settlement Agreement for the IngramRichardson site.

SUMMARY: In accordance with the

Comprehensive Environmental

Response, Compensation, and Liability

Act of 1980 (CERCLA), 42 U.S.C. 9601

et seq., as amended by the Superfund

Amendments and Reauthorization Act

of 1986 (SARA), Pub. L. 99–499,

notification is hereby given that a

proposed Agreement and Covenant Not

to Sue (Agreement) for the IngramRichardson Site (the Site) located near

Frankfort, in Clinton County, Indiana,

has been executed by Clinton County,

Indiana (the County), Frankfort Market

Place, Inc. (Frankfort Market Place), and

Kelly Strange (Mr. Strange). The

proposed Agreement has been

submitted to the Attorney General for

approval. The proposed Agreement

would resolve certain potential claims

of the United States under sections 106

and 107 of CERCLA, 42 U.S.C. 9606 and

9607, against the County, as the

prospective purchaser of the Site. The

proposed Agreement also would resolve

the potential liability of Frankfort

Market Place and Mr. Strange (who are

alleged to be past and current owners

and operators of the Site) under

CERCLA section 107 for certain past

response costs incurred in connection

with the Site, pursuant to the

administrative cost recovery settlement

authority conferred by CERCLA section

122(h)(1), 42 U.S.C. 9622(h)(1).

The components of the proposed

Agreement relating to the County would

require the County to pay $7,500 to the

United States and to demolish unusable

buildings on the Site before

redeveloping the Site for use as a

residential treatment center for

juveniles. The United States would

remove the CERCLA lien currently

placed on the Site property. The components of the proposed

Agreement relating to Frankfort Market

Place and Mr. Strange provide that: (1)

Frankfort Market Place and Mr. Strange

will pay $7,500 to the United States, to

be applied toward more than $2.789

million in unreimbursed past response

costs incurred in connection with

removal action undertaken at the Site;

(2) Frankfort Market Place and Mr.

Strange will convey their ownership

interest in the Site to the County, at no

cost to the County; and (3) the United

States will grant Frankfort Market Place

and Mr. Strange a covenant not to sue

for past response costs incurred in

connection with the removal action (and

will dismiss without prejudice a

pending, unanswered civil judicial

complaint filed by the United States

against Frankfort Market Place under

CERCLA section 107), and those parties

will obtain contribution protection as

provided by CERCLA sections 113(f)(2)

and 122(h)(4) upon satisfactory

completion of their obligations under

the Agreement. The Site is not on the NPL, and no

further response activities at the Site are

anticipated at this time.

DATES: Comments on the proposed

Agreement must be received by July 23,

1998.

ADDRESSES: A copy of the proposed

Agreement is available for review at

U.S. EPA, Region 5, 77 West Jackson

Boulevard, Chicago, Illinois 60604.

Please contact Karen Peaceman at (312)

353–5751 prior to visiting the Region 5

office.

Comments on the proposed

Agreement should be addressed to

Karen Peaceman, Office of Regional

Counsel, U.S. EPA, Region 5, 77 West

Jackson Boulevard, (Mail Code C–14J),

Chicago, Illinois 60604.

FOR FURTHER INFORMATION CONTACT:

Karen Peaceman at (312) 353–3751 of

the U.S. EPA Region 5 Office of

Regional Counsel. A 30-day period, commencing on the

date of publication of this notice, is

open for comments on the proposed

Agreement. Comments should be sent to

the addressee identified in this

document.

Doug Ballotti,

Acting Director, Superfund Division, Region

#5.

[FR Doc. 98–16670 Filed 6–22–98; 8:45 am]

BILLING CODE 6560–50–M