Federal Register / Vol. 62, No. 209 / Wednesday, October 29, 1997 / Notices 56173

statement that this chemical

demonstrates the properties associated

with chemicals detected in

groundwater, the Registrant is not aware

of imidacloprid being detected in any

wells, ponds, lakes, streams, etc. from

its use in the United States. In studies

conducted in 1995, imidacloprid was

not detected in seventeen wells on

potato farms in Quebec, Canada. In

addition, groundwater monitoring

studies are currently underway in

California and Michigan. Therefore,

contributions to the dietary burden from

residues of imidacloprid in water would

be inconsequential.

4. Non-dietary exposure— a.

Residential turf. Bayer Corporation has

conducted an exposure study to address

the potential exposures of adults and

children from contact with imidacloprid

treated turf. The population considered

to have the greatest potential exposure

from contact with pesticide treated turf

soon after pesticides are applied are

young children. Margins of safety (MOS)

of 7,587 - 41,546 for 10 year old

children and 6,859 - 45,249 for 5 year

old children were estimated by

comparing dermal exposure doses to the

imidacloprid no-observable effect level

of 1,000 mg/kg/day established in a 15-

day dermal toxicity study in rabbits.

The estimated safe residue levels of

imidacloprid on treated turf for 10 year

old children ranged from 5.6 - 38.2 g/

cm2 and for 5 year old children from 5.1

- 33.3 g/cm2. This compares with the

average imidacloprid transferable

residue level of 0.080 g/cm2 present

immediately after the sprays have dried.

These data indicate that children can

safely contact. Bayer Corporation has

conducted an exposure imidaclopridtreated turf as soon after application as

the spray has dried.

b. Termiticide. Imidacloprid is

registered as a termiticide. Due to the

nature of the treatment for termites,

exposure would be limited to that from

inhalation and was evaluated by EPA’s

Occupational and Residential Exposure

Branch (OREB) and Bayer Corporation.

Data indicate that the Margins of Safety

for the worst case exposures for adults

and infants occupying a treated building

who are exposed continuously (24

hours/day) are 8.0 x 107 and 2.4 x 108,

respectively, and exposure can thus be

considered negligible.

c. Tobacco smoke. Studies have been

conducted to determine residues in

tobacco and the resulting smoke

following treatment. Residues of

imidacloprid in cured tobacco following

treatment were a maximum of 31 ppm

(7 ppm in fresh leaves). When this

tobacco was burned in a pyrolysis study

only two percent of the initial residue

was recovered in the resulting smoke

(main stream plus side stream). This

would result in an inhalation exposure

to imidacloprid from smoking of

approximately 0.0005 mg per cigarette.

Using the measured subacute rat

inhalation NOEL of 5.5 mg/m3, it is

apparent that exposure to imidacloprid

from smoking (direct and/or indirect

exposure) would not be significant.

d. Pet treatment. Human exposure

from the use of imidacloprid to treat

dogs and cats for fleas has been

addressed by EPA’s Occupational and

Residential Exposure Branch (OREB)

who have concluded that due to the fact

that imidacloprid is not an inhalation or

dermal toxicant and that while dermal

absorption data are not available,

imidacloprid is not considered to

present a hazard via the dermal route.

D. Cumulative Effects

No other chemicals having the same

mechanism of toxicity are currently

registered, therefore, there is no risk

from cumulative effects from other

substances with a common mechanism

of toxicity.

E. Safety Determination

1. U.S. population. Using the

conservative exposure assumptions

described above and based on the

completeness and reliability of the

toxicity data, it can be concluded that

total aggregate exposure to imidacloprid

from all current uses including those

currently proposed will utilize little

more than 15% of the RfD for the U.S.

population. EPA generally has no

concerns for exposures below 100% of

the RfD, because the RfD represents the

level at or below which daily aggregate

exposure over a lifetime will not pose

appreciable risks to human health.

Thus, it can be concluded that there is

a reasonable certainty that no harm will

result from aggregate exposure to

imidacloprid residues.

2. Infants and children. In assessing

the potential for additional sensitivity of

infants and children to residues of

imidacloprid, the data from

developmental studies in both rat and

rabbit and a 2-generation reproduction

study in the rat have been considered.

The developmental toxicity studies

evaluate potential adverse effects on the

developing animal resulting from

pesticide exposure of the mother during

prenatal development. The reproduction

study evaluates effects from exposure to

the pesticide on the reproductive

capability of mating animals through

two generations, as well as any observed

systemic toxicity.

FFDCA Section 408 provides that the

EPA may apply an additional safety

factor for infants and children in the

case of threshold effects to account for

pre- and post-natal effects and the

completeness of the toxicity database.

Based on current toxicological data

requirements, the toxicology database

for imidacloprid relative to pre- and

post-natal effects is complete. Further

for imidacloprid, the NOEL of 5.7 mg/

kg/bwt from the 2-year rat feeding/

carcinogenic study, which was used to

calculate the RfD (discussed above), is

already lower than the NOELs from the

developmental studies in rats and

rabbits by a factor of 4.2 to 17.5 times.

Since a 100-fold uncertainty factor is

already used to calculate the RfD, it is

surmised that an additional uncertainty

factor is not warranted and that the RfD

at 0.057 mg/kg/bwt/day is appropriate

for assessing aggregate risk to infants

and children. Using the conservative

exposure assumptions described above,

EPA has concluded that the TMRC from

use of imidacloprid from published uses

is 0.008358 mg/kg/bwt/day utilizing

14.7% of the RfD for the general

population. For the most highly exposed

subgroup in the population, nonnursing infants (less than 1 year old),

the TMRC for the published tolerances

is 0.01547 mg/kg/day. This is equal to

27.1% of the RfD. Therefore, dietary

exposure from the existing uses

including the currently proposed

tolerances will not exceed the reference

dose for any subpopulation (including

infants and children).

F. International Tolerances

No CODEX Maximum Residue Levels

(MRLs) have been established for

residues of imidacloprid on any crops at

this time.

[FR Doc. 97–28663 Filed 10–28–97; 8:45 am]

BILLING CODE 6560–50–F

ENVIRONMENTAL PROTECTION

AGENCY

[PF–771; FRL–5749–7]

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–771, must be

received on or before November 28,

1997.
56174 Federal Register / Vol. 62, No. 209 / Wednesday, October 29, 1997 / Notices

ADDRESSES: By mail submit written

comments to: Public Information and

Records Integrity Branch, Information

Resources and Services Division

(7502C), Office of Pesticides Programs,

Environmental Protection Agency, 401

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

person bring comments to: Rm. 1132,

CM #2, 1921 Jefferson Davis Highway,

Arlington, VA.

Comments and data may also be

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

instructions under ‘‘SUPPLEMENTARY

INFORMATION.’’ No confidential

business information should be

submitted through e-mail.

Information submitted as a comment

concerning this document may be

claimed confidential by marking any

part or all of that information as

‘‘Confidential Business Information’’

(CBI). CBI should not be submitted

through e-mail. Information marked as

CBI will not be disclosed except in

accordance with procedures set forth in

40 CFR part 2. A copy of the comment

that does not contain CBI must be

submitted for inclusion in the public

record. Information not marked

confidential may be disclosed publicly

by EPA without prior notice. All written

comments will be available for public

inspection in Rm. 1132 at the address

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

Monday through Friday, excluding legal

holidays.

FOR FURTHER INFORMATION CONTACT: By

mail: Sidney C. Jackson, Registration

Division (7505C), Office of Pesticide

Programs, 401 M St., SW., Washington,

DC 20460. Office location and telephone

number, Rm. 274, Crystal Mall #2, 1921

Jefferson Davis Hwy., Arlington, VA.,

703–305–7610, e-mail:

jackson.sidney@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–771]

(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 6.1 or ASCII file format. All

comments and data in electronic form

must be identified by the docket number

[PF-771] and appropriate petition

number. Electronic 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: October 22, 1997

Peter Caulkins,

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. IR-4 Project

PP 2E4044 and 3E4164

EPA has received pesticide petitions

(PP 2E4044 and 3E4164) from the

Interregional Research Project number 4

(IR-4), 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

tolerances for residues of Triadimefon,

1-(4-Chlorophenoxy)-3,3-dimethyl-1-

(1H-1,2,4-triazol-1-yl)-2-butanone, and

its metablolites containing

chlorophenoxy and triazole moieties

expressed as the fungicide in or on the

raw agricultural commodities artichoke,

globe at 0.6 parts per million (ppm) and

pome fruits group (Crop Group 11) at

0.2 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 support

granting of the petition. Additional data

may be needed before EPA rules on the

petition. This notice includes a

summary of each petition prepared by

the Bayer Corporation(Bayer), the

registrant.

A. Residue Chemistry

1. Plant metabolism. The nature of the

residue in plants and animals is

adequately understood. The residue of

concern is triadimefon and its triazole

and chlorophenoxy metabolites.

Triadimefon is rapidly absorbed by

plants and translocated systemically in

the young growing tissue.

2. Analytical method. Adequate

analytical methods are available for

analysis of triadimefon and its triazole

and chlorophenoxy metabolites in or on

artichokes. These methods are available

in PAM II as Method I.

3. Magnitude of residues. Three

separate residue trials have been

conducted on globe artichokes and

submitted to the EPA. The EPA has

determined that these data show that

residues of triadimefon and its

metabolites containing chlorophenoxy

and triazole moieties (expressed as the

fungicide) in the raw agricultural

commodity artichokes, globe will not

exceed the proposed tolerance of 0.6

ppm.

For pome fruits and as part of the

reregistration requirements for

triadimefon, Bayer has submitted nine

trials on apples and six trials on pears

to the EPA. EPA’s Chemistry Branch

Tolerance Support has concluded that

these data are adequate to support the

requested crop group tolerance for

triadimefon and its metabolites

containing chlorophenoxy and triazole

moieties expressed as the fungicide in

or on pome fruit at 0.2 ppm.

There are no livestock feed stuffs from

globe artichokes and pome fruits,

therefore, secondary residues in meat,

milk, poultry and eggs are not expected.

B. Toxicological Profile

1. Acute toxicity. A rat acute oral

study resulted in a lethal dose (LD50) of

568 ± 61 milligrams (mg)/kilogram (kg)
Federal Register / Vol. 62, No. 209 / Wednesday, October 29, 1997 / Notices 56175

for males and 363 ± 41 mg/kg for

females. In a rabbit acute dermal study

a LD50 of >2,000 mg/kg was determined.

A rat acute inhalation study produced a

lethal concentration (LC50) of >3.570

mg/liter(l). A primary eye irritation

study in the rabbit showed practically

no irritation. A primary dermal

irritation study showed practically no

irritation and a primary dermal

sensitization study indicated that

triadimefon is a skin sensitizer.

2. Genotoxicity. Triadimefon has been

found to be negative in the Ames

reverse mutation test and in the

Structural Chromosome Aberration Test.

3. Reproductive and developmental

toxicity. A rat developmental toxicity

study showed a maternal systemic noobserved-effect level (NOEL) of 30 mg/

kg/day and the lowest-observed-effect

level (LOEL) 90 mg/kg/day. The NOEL

for developmental toxicity was 30 mg/

kg/day and the LOEL was 90 mg/kg/day.

In the developmental toxicity study in

rabbits, the maternal systemic NOEL

was 50 mg/kg/day and the LOEL 120

mg/kg/day. The NOEL for

developmental toxicity was 20 mg/kg/

day and the LOEL was 50 mg/kg/day.

Effects seen at the developmental lowest

effect level(LEL) in the rabbit study

were irregular spinous process and

ossification of various bones.

A 3-generation rat reproduction study

showed decreases in maternal body

weight gain, fertility, and in litter size,

pups survival during the lactation

phase, and pups weights. The maternal

NOEL was 300 ppm and the

reproductive NOEL was 50 ppm.

A 2-generation rat reproductive study

showed reductions in litter size, pups

viability, birth and lactational weights.

The reproductive NOEL was 50 ppm.

4. Subchronic toxicity. A 3-month

feeding study in the rat produced a

NOEL of 2,000 ppm based on decreased

body weight gain and food consumption

attributed to palatability. A rat 30-day

feeding study showed a NOEL of 10 mg/

kg. A 13-week dog-feeding study

resulted in a NOEL of 2,400 ppm based

on decreased body weight gain and food

consumption due to palatability. Test

results also showed a decreased

hematocrit, RBC count, hemoglobin

volume and microsomal induction. A

28-day rabbit dermal study produced a

NOEL >250 mg/kg and a 21-day

inhalation study in rats showed a NOEL

of 78.7 mg/cubic meters(m3)/6 hrs. per

day/ 15 exposures.

5. Chronic toxicity. A 2–year rat

chronic feeding study defined a NOEL

for systemic effect as 300 ppm (males =

16.4 mg/kg/day; females = 22.5 mg/kg/

day). The systemic LOEL was 1,800

ppm (males = 114.0 mg/kg/day; females

= 199.0 mg/kg/day) based on neoplastic

and systemic effects. A dog feeding

study showed only minimal toxic effects

decrease in body weight, increase in

liver weight and in hepatic Ndemethylase activity, and an increase in

serum alkaline phosphatase activity.

The NOEL was established at 100 ppm.

A mouse oncogenicity study showed

hepatocellular adenomas in both sexes

of NMRI mice. The NOEL was

established for males at 50 ppm. No

NOEL was reached for females. A mouse

carcinogenicity study using CF1-W74

mice was negative for carcinogenicity.

6. Animal metabolism. In a general rat

metabolism study triadimefon was

initially converted by reduction of its

carbonyl group. This conversion was

more rapid in males. The major

metabolites were the acid and alcohol of

triadimefon. In males radioactivity was

found mainly in feces, whereas, in

females, radioactivity was equally

distributed between urine and feces. No

radioactivity was recovered in the

expired air. Peak tissue levels were

found in 2 to 4 hours and were highest

in fat, liver and kidney.

7. Endocrine effects. No special

studies investigating potential

estrogenic or endocrine effects of

triadimefon have been conducted.

However, the standard battery of

required studies has been completed.

These studies include an evaluation of

the potential effects on reproduction

and development, and an evaluation of

the pathology of the endocrine organs

following repeated or long-term

exposure. No adverse effects were noted

in any of the studies with either

triadimefon or its metabolites.

C. Aggregate Exposure

1. Dietary exposure. For purposes of

assessing the potential dietary exposure

from food under the proposed

tolerances, the EPA estimates exposure

based on the Theoretical Maximum

Residue Contribution (TMRC). The

TMRC is obtained by using a model

which multiplies the tolerance level

residue for each commodity by

consumption data which estimates the

amount of each commodity and

products derived from the commodities

that are eaten by the U.S. population

and various population subgroups. The

model uses a reference dose (RfD) which

the EPA has determined to be 0.04

milligrams(mg)/ kilogram(kg)/day. This

RfD is based on a 2–year dog feeding

study with a NOEL of 11.4 mg/kg/day

and an uncertainty factor of 300. An

uncertainty factor of 300 was applied to

account for inter-species extrapolation

(10), intra-species variability (10), and

the lack of an adequate reproduction

study (3). Decreased food intake,

depression in weight gain, and

significantly (p >0.05) increased

alkaline phosphatase activity in both

sexes were the effects observed at the

lowest effect level (LEL). This

assessment assumes 100% of all

commodities will contain triadimefon

residues, and those residues would be at

the level of the tolerance for estimating

potential human exposure.

2. Food. Using assumptions discussed

above, it was determined that the TMRC

for existing tolerances plus the proposed

uses on globe artichokes and pome

fruits. For globe artichokes, the TMRC is

equivalent to 17% of the RfD for the US

general population (48 states) and 74%

of the RfD for the highest population

subgroup (non-nursing infants >1 year

old).

For pome fruits, the TMRC for

triadimefon derived from the previously

established tolerances plus the proposed

0.2 ppm tolerance for this crop group

(pome fruit) would be 0.003782 mg/kg

body weight(bwt)/day (9.5% of the RfD)

for the U.S. population 48 states and

0.009549 mg/kg bwt/day (23.9% of the

RfD) for the most highly exposed

population subgroup, children (1-6 year

old). Therefore, Bayer concludes that

dietary exposure from the existing and

proposed uses will not exceed the

reference dose for any subpopulation

including infants and children.

For globe artichoke, the estimated

acute dietary exposure is based on a

maternal NOEL of 10 mg/kg/day. The

calculated Margin of Exposure (MOE)

for the general US population is 100 (at

the 99th percentile); for infants (>1 year

old) 100 (at the 95th percentile); for

children (1-6 year old) 200 (at the 96th

percentile); and for both females (13+

years) and males (13+ years) 333 (at the

99th percentile). These values are all at

or above the MOE level EPA considers

to provide an adequate safety margin

(100).

3. Drinking water. Available data

show that triadimefon and its

metabolites are mobile and persistent

and have the potential to leach into

groundwater. There is no established

Maximum Concentration Level for

residues of triadimefon in drinking

water. No drinking water health

advisory levels have been issued for

triadimefon or its metabolite

triadimefon. The ‘‘Pesticides in

Groundwater Database’’ (EPA 734–12–

92–001, September 1992) indicated that

triadimefon was monitored for in 14

wells in California from 1984 to 1989.

There were no detectable residues (limit

of detection was not stated).

Previous experience with more

persistent and mobile pesticides for
56176 Federal Register / Vol. 62, No. 209 / Wednesday, October 29, 1997 / Notices

which there have been available data to

perform quantitative risk assessments

have demonstrated that drinking water

exposure is typically a small percentage

of the total exposure when compared to

the total dietary exposure. This

observation holds even for pesticides

detected in wells and drinking water at

levels nearing or exceeding established

maximum residue levels (MCL’s). Best

scientific judgement from available data

suggests that the potential exposure

from residues of triadimefon in drinking

water, added to the current dietary

exposure, will not result in an exposure

which exceeds the RfD.

4. Non-dietary exposure. Triadimefon

is currently registered for use on turf

and ornamentals. Studies were

conducted by Bayer designed to

measure the upper bound acute

exposure potential of adults and

children from contact with triadimefon

treated turf. The population considered

to have the greatest potential exposure

from contact with pesticide treated turf

soon after pesticides are applied are

young children. The estimated safe

residue levels for triadimefon on treated

turf for 10-year old children ranged from

1.3 - 6.4 micro gram(μg)/centimeter(cm)2

and for 5-year old children from 1.1 -

5.6 μg/cm2. This compares with the

average triadimefon transferable residue

level of 1.0 μg/cm2 present immediately

after the sprays have dried. Bayer

concludes from these studies that

children can safely contact triadimefontreated turf as soon after application as

the spray has dried.

D. Cumulative Effects

At this time, the Agency has not made

a determination that triadimefon and

other substances that may have a

common mode of toxicity would have

cumulative effects. For purposes of this

tolerance, only the potential risks of

triadimefon in its aggregate exposure are

being considered.

E. Safety Determination

1. U.S. population. Using the

exposure assumptions described above

under aggregate exposure and based on

the toxicity data, Bayer concludes that

aggregate dietary exposure to

triadimefon from the previously

established tolerances plus the proposed

use on globe artichoke will utilize 17%

of the RfD for the U.S. population (48

states) and 74% of the RfD for the most

highly exposed population subgroup

(non-nursing infants >1 year old). In

comparison, pome fruit will vitilize

9.5% and 23.9% of the RfD for the same

U.S. population and for children (1-6

yrs), respectively. There is generally no

concern for exposures below 100

percent of the RfD because the RfD

represents the level at or below which

daily aggregate exposure over a lifetime

will not pose appreciable risks to

human health. Bayer concludes that

there is a reasonable certainty that no

harm will result from aggregate

exposure to triadimefon.

Bayer estimated acute dietary

exposure using the maternal NOEL of 10

mg/kg/day and determined that the

calculated MOE for each population

group is at or above the MOE level EPA

considers to provide an adequate safety

margin.

2. Infants and children. In assessing

the potential for additional sensitivity of

infants and children to residues of

triadimefon, the data from

developmental studies in both rat and

rabbit and a 2-generation reproduction

study in the rat were considered. The

developmental toxicity studies evaluate

any potential adverse effects on the

developing animal resulting from

pesticide exposure of the mother during

prenatal development. The reproduction

study evaluates any effects from

exposure to the pesticide on the

reproductive capability of mating

animals through 2-generations, as well

as any observed systemic toxicity.

Results of a rat and rabbit

developmental toxicity studies and a 2-

generation and 3-generation rat

reproduction studies conducted with

triadimefon have been reviewed.

Maternal and developmental toxicity

NOELs of 30 mg/kg/day were

determined in the rat developmental

toxicity studies. In the rabbit

developmental toxicity study, the

maternal NOEL was 50 mg/kg body

weight(bwt)/day and the developmental

NOEL was 20 mg/kg bwt/day. The rat

reproduction studies were inconclusive.

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 effects and the completeness

of the toxicity database. Therefore, EPA

has incorporated an additional 3-fold

uncertainty factor into the calculation of

the RfD because of the absence of an

acceptable reproduction study.

There is approximately a two-fold

difference between the developmental

NOEL of 20 mg/kg/day from the rabbit

developmental toxicity study and the

NOEL of 11.4 mg/kg/day from the 2–

year dog feeding study which was the

basis of the RfD. It is further noted that

in the rabbit developmental toxicity

study, the developmental NOEL of 20

mg/kg/day is lower than the maternal

systemic NOEL of 50 mg/kg/day,

suggesting the possibility of increased

sensitivity for the pre-natal child.

The TMRC value for the most highly

exposed infant and children subgroup

(non-nursing infants >1 year old)

occupies 74% of the RfD. However, this

calculation also assumes 100% crop

treated and uses tolerance level residues

for all commodities. Refinement of the

dietary risk assessment by using percent

of crop treated and anticipated residue

data would likely greatly reduce the

dietary exposure estimate and result in

an anticipated residue contribution

(ARC) which would occupy a percent of

the RfD that is substantially lower than

the currently calculated TMRC value.

Should an additional uncertainty

factor be deemed appropriate, when

considered in conjunction with a

refined exposure estimate, Bayer

believes it is unlikely that the dietary

risk will exceed 100 percent of the RfD.

Due to the completeness and reliability

of the toxicity data and the exposure

assessment, Bayer believes there is a

reasonable certainty that no harm will

result to infants and children from

aggregate exposure to triadimefon

residues.

Bayer estimated acute dietary

exposure using the maternal NOEL of 10

mg/kg/day and determined that the

calculated MOE for infants and children

population groups is at or above the

MOE level EPA considers to provide an

adequate safety margin.

F. International Tolerances

There are no CODEX, Canadian, or

Mexican MRLs for triadimefon residues

in/on globe artichokes. A CODEX MRL

for triadimefon residues in/on pome

fruits has been established at 0.5 ppm.

2. IR-4 Project

PP 6E4652

EPA has received a pesticide petition

(PP 6E4652) from the Interregional

Research Project number 4 (IR-4),

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

the combined residues of quizalofop-p

ethyl ester [ethyl (R)-(2-[4-((6-

chloroquinoxalin-2-yl) oxy)phenoxy])-

propanoate), and its acid metabolite

quizalofop-p [R-(2-[4-((6-

chloroquinoxalin-2-yl)oxy)phenoxy])

propanoic acid), and the S enantiomers

of both the ester and the acid, all

expressed as quizalofop-p ethyl ester in

or on the raw agricultural commodities

spearmint tops and peppermint tops at

3.0 parts per million(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
Federal Register / Vol. 62, No. 209 / Wednesday, October 29, 1997 / Notices 56177

evaluated the sufficiency of the

submitted data at this time or whether

the data support granting of the petition.

Additional data may be needed before

EPA rules on the petition. This notice

includes a summary of the petition

prepared by the DuPont Agricultural

Products(DuPont), the registrant.

A. Residue Chemistry

1. Plant metabolism. The registrant

has provided plant metabolism studies

for soybeans, cotton, tomatoes, potatoes,

and sugar beets. These studies have

been previously reviewed in PP 3F4268.

In summary, quizalofop-p ethyl ester is

metabolized by cleavage at three sites as

follows: (a) Primary pathway is

hydrolysis of the ethyl ester to form the

quizalofop-p acid, then (b) cleavage of

the enol ether linkage in the acid,

between the phenyl and quinoxalinyl

rings, to form phenols, and (c) cleavage

of the ether linkage between the

isopropanic group and the phenyl ring

to form a phenol.

The plant metabolism data show that

quizalofop-p ethyl ester does not

translocate, but is rapidly hydrolyzed to

the corresponding acid; then the

phenols conjugate with the plant sugars.

Metabolism studies in soybeans using

the racemic mixture quizalofop ethyl

ester and the resolved D+ isomer show

nearly identical pathways.

The nature of the quizalofop-p ethyl

ester residue in cottonseed, potatoes,

tomatoes, soybeans, and sugar beets is

adequately understood. The residues of

concern are quizalofop-p ethyl ester and

its acid metabolite, quizalofop-p, and

the S enantiomers of both the ester and

the acid, all expressed as quizalofop-p

ethyl ester. EPA is translating these data

to mint.

2. Analytical method. An adequately

validated residue analytical method,

LAN-1, was used to gather the

magnitude of the quizalofop-p, its acid

metabolite, and residue data on mint

hay and mint oil. Samples were

analyzed using MS30.00, an adaptation

of Analytical Method for the

Quantification of Quizalofop (IN-YE945)

and Quizalofop-Ethyl (DPX-79379) in

Raw and Processed Agricultural

Commodities, Protocol No. Lan-1,

Enviro-Test Laboratory. (Reference

Method: Determination of DPX-79376,

DPX-79376 Acid and Conjugates as

DPX-79376 as Acid in Cottonseed and

Fractions Treated with Assure (II

Herbicide. DuPont Report No. AMR

1853–90).

3. Magnitude of residues. The

maximum residues detected on fresh

mint foliage at the proposed labeled

level of DuPont’s product, Assure, of 0.2

pounds(lbs) active ingredient(ai) acre

(1x) applied 30 days before harvest were

0.22, 0.46, and 1.0 ppm for Indiana,

Oregon and Washington, respectively.

The largest residue found on fresh mint

foliage, 2.6 ppm, was detected in a

Washington sample treated with 0.4 lbs.

acre (2x) 29 days before harvest, twice

the maximum yearly rate allowed. At

the Level of Quantitation of 0.05 ppm,

there were no detectable residues in the

mint oil, either at the proposed label

rate of 0.2 lbs. ai/acre(A), or at the

exaggerated rate of 0.4 lbs. ai/A,

indicating that quizalofop-p ethyl and

its acid metabolite are not concentrated

during the oil distillation process.

Results of a freezer storage stability

study demonstrated that the two

compounds, quizalofop-p ethyl ester

and quizalofop acid, were stable in

frozen storage at -20 degrees centigrade

for 592 to 593 days in mint hay, and 597

days in oil. Field samples were stored

a maximum of 654 days.

The residues detected in this study

are well below the proposed tolerances

of 3.0 ppm for the raw agricultural

commodity mint. The nature of the

residues is adequately understood and

an adequate analytical method is

available for enforcement purposes.

Based on the information presented

above, Dupont believes the

establishment of the proposed tolerance

would protect the public health and

would not expose man or the

environment to unreasonable adverse

effects.

B. Toxicological Profile

1. Acute toxicity. Several acute

toxicology studies were conducted and

the overall results placed technical

grade quizalofop ethyl in toxicity

Category III. These include the

following studies in Category III: acute

oral toxicity (LD50s 1,480 and 1,670 for

female and male rats, respectively) and

eye irritation (mild effects; reversible

within 4 days). Dermal toxicity (lethal

dose) LD50 >5,000 milligram(mg)/

kilogram(kg); rabbit), inhalation toxicity

(lethal concentration) LC50 >5.8 mg/

liter(L); rat) and dermal irritation were

classified within Category IV. Technical

quizalofop ethyl was not a dermal

sensitizer.

2. Genotoxicity. Technical quizalofop

ethyl was negative in the following

genotoxicity tests: bacterial gene

mutation assays with E. coli and S.

typhimurium; gene mutation assays in

Chinese hamster ovary(CHO) cells ; in

vitro DNA damage assays with B.

subtillis and in rat hepatocytes; and an

in vitro chromosomal aberration test in

CHO cells.

3. Reproductive and developmental

toxicity. Studies supporting the

registration include: A developmental

toxicity study in rats administered

dosage levels of 0, 30, 100, and 300 mg/

kg/day (HDT). The maternal toxicity noobserved-effect level (NOEL) was 30 mg/

kg/day and a developmental toxicity

NOEL was greater than 300 mg/kg/day

(HDT). The maternal NOEL was based

on reduced food consumption and

increased liver weights.

A developmental toxicity study in

rabbits administered dosage levels of 0,

7, 20, and 60 mg/kg/day with no

developmental effects noted at 60 mg/

kg/day (HDT). The maternal toxicity

NOEL was 20 mg/kg/day based on

decreases in food consumption and

body weight gain at 60/mg/kg/day

(HDT).

A 2-generation reproduction study in

rats fed diets containing 0, 25, 100 or

400 ppm (or approximately 1, 1.25, 5,

and 20 mg/kg/day, respectively) with a

developmental (systemic effects) NOEL

of 1.25 mg/kg/day for F2B weanlings

based on increased liver weights and

increased incidence of eosinophilic

changes in the livers at 5.0 mg/kg/day.

These liver changes were considered to

be physiological or adaptive changes to

compound exposure among weanlings.

When access to the mother’s feed is

available, it is a common observation

that young rats will begin consuming

chow prior to complete weaning at 21-

days of age. Consumption could not be

quantified; therefore, the maternal

consumption was assumed as the NOEL

(if normalized on a body weight basis,

exposures to the weanling rats were

likely higher). The parental NOEL of 5.0

mg/kg/day was based on decreased body

weight and premating weight gain in

males at 20 mg/kg/day (HDT).

4. Subchronic toxicity. A 90-day study

was conducted in rats fed diets

containing 0, 40, 128, 1,280 ppm (or

approximately 0, 2, 6.4 and 64 mg/kg/

day, respectively). The NOEL was 2 mg/

kg/day. This was based on increased

liver weights at 6.4 mg/kg.

A 90–day feeding study in mice was

conducted with diets that contained 0,

100, 316 or 1,000 ppm (or

approximately 0, 15, 47.4, and 150 mg/

kg/day, respectively). The NOEL was

>15 mg/kg/day Lowest Dose Tested

(LDT) based on increased liver weights

and reversible histopathological effects

in the liver at the LDT. A 6-month

feeding study in dogs was conducted

with diets that contained 0, 25, 100 or

400 ppm (or approximately 0, 0.625, 2.5,

and 10 mg/kg/day, respectively). The

NOEL was 2.5 mg/kg/day based on

increased blood urea nitrogen at 10 mg/

kg/day. A 21–day dermal study was

conducted in rabbits at doses of 0, 125,
56178 Federal Register / Vol. 62, No. 209 / Wednesday, October 29, 1997 / Notices

500 or 2,000 mg/kg/day. The NOEL was

2,000 mg/kg/day (HDT).

5. Chronic toxicity. An 18-month

carcinogenicity study was conducted in

CD-1 mice fed diets containing 0, 2, 10,

80 or 320 ppm (or approximately 0, 0.3,

1.5, 12, and 48 mg/kg/day, respectively).

There were no carcinogenic effects

observed under the conditions of the

study at levels up to and including 12

mg/kg/day. A marginal increase in the

incidence of hepatocellular tumors was

observed at 48 mg/kg/day, the highest

dose tested (HDT) which exceeded the

maximum tolerated dose (MTD).

A 2–year chronic toxicity/

carcinogenicity study was conducted in

rats fed diets containing 0, 25, 100 or

400 ppm (or 0, 0.9, 3.7, and 15.5 mg/kg/

day for males and 0, 1.1, 4.6, and 18.6

mg/kg/day for females, respectively).

There were no carcinogenic effects

observed under the conditions of the

study at levels up to and including 18.6

mg/kg/day (HDT). The systemic NOEL

was 0.9 mg/kg/day based on altered red

cell parameters and slight/minimal

centrilobuler enlargement of the liver at

3.7 mg/kg/day.

A 1–year feeding study was

conducted in dogs fed diets containing

0, 25, 100 or 400 ppm (or approximately

0, 0.625, 2.5, and 10 mg/kg/day,

respectively). The NOEL was 10 mg/kg/

day (HDT).

The Carcinogenicity Peer Review

Committee (CPRC) of the EPA has

evaluated the rat and mouse cancer

studies on quizalofop along with other

relevant short-term toxicity studies,

mutagenicity studies, and structure

activity relationships. The CPRC

concluded, after three meetings and an

evaluation by the EPA Science Advisory

panel, that the classification should be

a Category D (not classifiable as to

human cancer potential). No new cancer

studies were required.

The first CPRC review tentatively

concluded that quizalofop should be

classified as a Category B2 (probable

human carcinogen). That classification

was based on liver tumors in female

rats, ovarian tumors in female mice, and

liver tumors in male mice. This

classification was downgraded to a

Category C (possible human carcinogen)

at a second CPRC review. The change in

classification was due to a

reexamination of the liver tumors in

female rats and ovarian tumors in

female mice. The first peer review had

found a statistically significant positive

trend for liver carcinomas in female rats.

Subsequent to this conclusion the tumor

data were reevaluated, and the

revaluation showed a reduced number

of carcinomas. Although there remained

a statistically significant positive trend

for carcinomas in the study, the CPRC

concluded that the carcinomas were not

biologically significant given the few

carcinomas identified (one at the middose and two at the high dose). Noting

that this level of carcinomas was within

historical levels, the CPRC concluded

that administration of quizalofop did

not appear to be associated with the

liver carcinomas.

As to the ovarian tumors in female

mice, the CPRC had first attached

importance to the fact that these tumors

were statistically significant at the high

dose as compared to historical control

values although statistically significant

when compared to concurrent controls.

However, review of further historical

control data showed that the level of

ovarian tumors in the quizalofop study

was similar to the background rate in

several other studies. Given this

information and that the quizalofop

study showed no hyperplasia of the

ovary, no signs of endocrine activity

related to ovarian function, and no dose

response relationship, the CPRC

concluded that the ovarian tumors were

probably not compound-related.

The findings of the second CPRC

review were presented to EPA’s

Scientific Advisory Panel (SAP). The

SAP concurred with the CPRC

conclusion that the liver tumors in

female rats and the ovary tumors in

female mice showed no evidence of

carcinogenicity. However, the SAP

disagreed with CPRC’s classification of

quizalofop as a Category C based on the

liver tumors in male mice. The SAP

concluded that the mouse liver tumors

did not support such a classification

because the tumors occurred at a dose

above the maximum-tolerated dose

(MTD) and because they were not

statistically significant if a ‘‘p’’value of

less than 0.05. The SAP believed that

such greater statistical rigor was

appropriate for variable tumor

endpoints such as male mouse liver

tumors.

Following the SAP review, the CPRC

changed the classification for quizalofop

to Category D. The Category D

classification is based on an

approximate doubling in the incidence

of male mice liver tumors between

controls an the high dose. This finding

was not considered strong enough to

warrant the finding of a Category C

(possible human carcinogen) since the

increase was of marginal statistical

significance, occurred at a high dose

which exceeded the predicted MTD,

and occurred in a study in which the

concurrent control for liver tumors was

somewhat low as compared to the

historical controls, while the high dose

control group was at the upper end of

previous historical control-groups.

EPA has found the evidence on the

carcinogenicity of quizalofop-p ethyl

ester in animals to be equivocal and

therefore concludes that quizalofop-p

ethyl ester does not induce cancer in

animals within the meaning of the

Delaney clause. Important to this

conclusion was the following evidence:

(a) The only statistically significant

tumor response that appears compoundrelated was seen at a single dose in a

single sex in a single species; (b) the

response was only marginally

statistically significant; (c) the response

was only significant when benign and

malignant tumors were combined; (d)

the tumors were in the male mouse

liver; (e) the tumors were within

historical controls; and (f) the

mutagenicity studies were negative.

Although in some circumstances a

finding of animal carcinogenicity would

be made despite any one, or even

several, of the six factors noted, the

combination of all of these factors here

cast sufficient doubt on the

reproducibility of the response in the

high dose male mouse that EPA

concludes the evidence on

carcinogenicity is equivocal.

6. Animal metabolism. The

metabolism of quizalofop ethyl in

animals (rat, goat and poultry) is well

understood. 14C-phenyl and 14Cquinoxaline quizalofop ethyl ester

metabolism studies have been

conducted in each species. There are

similarities among these species with

respect to metabolism. Quizalofop ethyl

is rapidly and extensively metabolized

and rapidly excreted by rats. The

principal metabolites were the

quizalofop-p acid and two

dechlorinated hydroxylated forms of the

acid. Tissue residues were minimal and

there was no evidence of accumulation

of quizalofop ethyl or its metabolites in

the rat.

The primary pathway in ruminants is

hydrolysis of the ethyl ester to form the

quizalofop-p methyl ester. In poultry,

the primary metabolic pathway is also

the hydrolysis of the ethyl ester to form

the quizalofop-p acid, then the methyl

esterification to form the quizalofop

methyl ester becomes a minor pathway.

The nature of the quizalofop ethyl

ester residue in livestock is adequately

understood. The residues of concern are

quizalofop ethyl, quizalofop methyl,

and quizalofop, all expressed as

quizalofop ethyl.

7. Metabolite toxicology. There is no

evidence that the metabolites of

quizalofop ethyl as identified as either

the plant or animal metabolism studies

are of any toxicological significance.
Federal Register / Vol. 62, No. 209 / Wednesday, October 29, 1997 / Notices 56179

C. Aggregate Exposure

1. Dietary exposure. An analysis of

chronic dietary risk was conducted to

determine the impact of the possible

addition of peppermint and spearmint

to the Assure label. A Reference Dose

(RfD) of 0.009 mg/kg/day was used in

the analyses. Consumption data were

available for peppermint and spearmint

from previous studies.

2. Food. The first step in the analysis

was to run the TAS (Tolerance

Assessment System) program using

current tolerances with an RfD of 0.009

mg/kg/day. The Theoretical Maximum

Residue Concentration (TMRC), based

on the current tolerances, was 0.000288

mg/kg/day for the U.S. population (48

states) and 0.000759 mg/kg/day for the

population subgroup with the highest

estimated exposure (non-nursing infants

>1 year old). For the U.S. population

subgroup this represents approximately

3.2% of the RfD while for the most

exposed population this represents

approximately 8.4% of the RfD. Based

on the risk estimates arrived at in this

analysis, chronic dietary risk from the

current uses of Assure is minimal.

Consumption data for peppermint and

spearmint within the TAS database are

available only for the entire U.S.

population (48 states) and not for the

population subgroups. For peppermint

the consumption is listed as 0.000001

gram(g)/kg body weight(bw)/day for the

raw commodity and 0.000255 for the

flavoring oil. For spearmint the

consumption is 0.000001 g/kg bw/day

for the raw commodity and 0.000458 for

the flavoring oil. The TMRC, based on

the current tolerances and the potential

peppermint and spearmint tolerances,

was 0.000290 mg/kg/day for the U.S.

population (48 states). Since no

consumption data were available for

population subgroups, Theoretical

Maximum Residue Concentrations did

not change and the sub group with the

highest potential exposure had a TMRC

of 0.000759 g/kg/day (non-nursing

infants >1 year old). When expressed as

a percentage of the RfD, the U.S.

population (48 states) was

approximately 3.2% and that of the

population subgroup with the highest

potential exposure, i.e. infants and

children, was approximately 8.4%.

These results indicate that predicted

chronic exposure after the addition of a

peppermint tolerance is well below the

RfD. The lack of specific population

sub-group data for these commodities

should not be a problem since both

peppermint and spearmint are not likely

to be consumed in large quantities by

any population subgroup and the

difference between the TMRC and the

RfD is so great.

3. Drinking water. Another potential

source of dietary exposure to pesticides

is residues in drinking water. There is

no established Maximum Concentration

Level (MCL) for quizalofop ethyl in

water. Based on the low use rate of

quizalofop ethyl, and a use pattern that

is not widespread (since the current and

proposed uses are on minor crops),

DuPont does not anticipate residues of

quizalofop in drinking water and

exposure from this route is unlikely.

4. Non-dietary exposure. Quizalofop

ethyl is not registered for any use which

could result in non-occupational, nondietary exposure to the general

population.

D. Cumulative Effects

There is no evidence to indicate or

suggest that quizalofop p-ethyl has any

toxic effects on mammals that would be

cumulative with those of any other

chemicals.

E. Safety Determination

1. U.S. population. Using the

exposure assumptions described above

and based on the most sensitive species

chronic NOEL of 0.9 mg/kg and a

reference dose (RfD) of 0.009 mg/kg/day,

the existing tolerances and proposed use

of quizalofop ethyl on mint are expected

to utilize 3.2% of the RfD for the general

U.S. population. Generally, exposures

below 100% of the RfD are of no

concern because the RfD represents the

level at or below which daily aggregate

dietary exposure over a lifetime will not

pose risk to human health. Thus, there

is a reasonable certainty that no harm

will result from aggregate exposure to

quizalofop ethyl resulting from

proposed agricultural use on

peppermint and spearmint.

2. Infants and children. In assessing

the potential for additional sensitivity of

infants and children to residues of

quizalofop ethyl, data were considered

from developmental toxicity studies in

the rat and rabbit, and a multigeneration reproduction study in rats.

There were no developmental effects

observed in the absence of maternal

toxicity in the rat and rabbit

developmental studies. Minimal

adaptive or physiological effects were

observed in livers of weanlings in the 2-

generation rat reproduction study

described earlier. However, this effect

was only observed at a dose that far

exceeds any expected human exposure.

Further, the NOEL of 0.9 mg/kg/day

from the 2–year rat study with

quizalofop ethyl, which was used to

calculate the RfD(discussed above), is

already lower than any of the NOELs

defined in the developmental and

reproductive toxicity studies with

quizalofop ethyl.

Using the exposure assumptions

described above and based on the most

sensitive species chronic NOEL of 0.9

mg/kg and a reference dose (RfD) of

0.009 mg/kg/day, the existing tolerances

and proposed use of quizalofop ethyl on

mint are expected to utilize 8.4% of the

RfD for infants and children. Infants and

children have a low potential for

quizalofop ethyl exposure because of

both the low levels of mint in the diet

(mint is a low dietary intake crop used

primarily as an oil for flavoring, and is

diluted to a ratio of 1:250 or greater in

the finished food product), and the

absence of detectable residues in mint

oil. The toxicology profile of quizalofop

ethyl demonstrates low mammalian

toxicity. Because there was no evidence

that offspring were uniquely susceptible

to the toxic effects of quizalofop ethyl,

an additional 10-fold uncertainty factor

should not be required to protect infants

and children. Therefore, the registrant

believes that the RfD of 0.009 mg/kg/

day, which utilizes a 100-fold safety

factor, is appropriate to assure a

reasonable certainty of no harm to

infants and children from aggregate

exposure to quizalofop ethyl.

F. International Tolerances

Since there are no Mexican, Canadian,

or Codex MRLs/tolerances,

compatibility is not a problem at this

time.

3. IR-4 Project

PP 6E4658

EPA has received a pesticide petition

( PP 6E4658 ) from the Interregional

Research Project Number 4 (IR-4),

proposing pursuant to section 408(d) of

the Federal Food, Drug and Cosmetic

Act, 21 U.S.C. 346a(d), to amend 40 CFR

part 180 to establish an exemption from

the requirements of a tolerance for

copper-ethylenediamine complex

(Komeen) in or on the raw agricultural

commodity (RAC) potatoes. 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 support granting of the petition.

Additional data may be needed before

EPA rules on the petition. This notice

includes a summary of the petition

prepared by the Griffin Corporation

(Griffin), the registrant.
56180 Federal Register / Vol. 62, No. 209 / Wednesday, October 29, 1997 / Notices

A. Residue Chemistry

1. Analytical method. A practical

analytical method for copperethylenediamine complex is not

required for crop use since it is expected

that no residues will occur in RACs.

2. Magnitude of residues. Residues are

not expected in the RAC (potatoes) since

the potato tubers are underground and

only the vines which are above ground

are treated.

B. Toxicological Profile

The Agency does not require

subchronic, chronic, reproductive or

developmental toxicity studies for the

copper salts.

Copper-ethylenediamine(Komeen) is

slightly to moderately toxic upon acute

oral, dermal and inhalation exposure,

slightly irritating to the skin and

moderately irritating to the eye.

Acute toxicity. The acute oral lethal

dose LD50 (95% confidence limits) for

Komeen was 498 milligram(mg)/

kilogram(kg) (349–710 mg/kg).

The acute dermal LD50 for Komeen

was determined to be >2,000 mg/kg.

The acute inhalation lethal

concentration LC50 (95% confidence

limits) for Komeen was 0.81 mg/liter(l)

(0.26-1.37 mg/l).

Komeen was shown to be moderately

irritating to the eye with all signs of

ocular irritation cleared within 10 days

of treatment.

C. Aggregate Exposure

1. Dietary (food) exposure. Based on

the proposed used pattern of potato vine

desiccation, no copper residues are

expected to occur on potatoes and the

dietary exposure would be negligible by

comparison to the normal daily intake

of copper. A single day’s diet may

contain 10 mg or more of copper. The

daily recommended allowance of

copper for adults nutritional needs is 2

mg.

2. Drinking water. Copper is

ubiquitous in the environment and

found in natural water. In 1991, the

USEPA established a maximum

contamination level (MCL) for copper in

drinking water of 1.3 mg/l. No impact

on copper levels found naturally in

water would occur as a result of potato

vine desiccant use for this product.

3. Non-dietary exposure. Copper is

registered for use as an aquatic

herbicide for outdoor residential sites.

Any contributions to aggregate exposure

from this use would not be expected to

be significant.

4. Potential for endocrine effects.

Since copper is required for

homeostasis, low copper dietary

exposures would not be expected result

in any adverse endocrine effects.

D. Cumulative Effects

Griffin believes that no cumulative

adverse effects are expected from longterm exposure to copper salts. No other

elements are expected to produce

cumulative toxicity with copper.

E. Safety Determination

Copper compounds such as copper

sulfate pentahydrate are considered as

Generally Recognized as Safe (GRAS) by

the Food and Drug Administration and

as such are exempt from the

requirement of a tolerance when used as

aquatic herbicides (40 CFR 180.1021).

Copper compounds are also exempt

from the requirement of a tolerance

when applied to growing crops when

used as a plant fungicide in accordance

with good agricultural practices (40 CFR

180.1001(b)(1). Copper-ethylenediamine

complex is registered as an aquatic

herbicide under the trade name,

Komeen.

1. U.S. population. Copper is a

component of the human diet and an

essential element. Use of copperethylenediamine complex is not

expected to increase the amount of

copper in the diet as a result of potato

vine desiccation.

2. Infants and children. Infants and

children also require copper in their

diets and Griffin believes that no special

sensitivity for this population subgroup

would be expected as a result of the

proposed use.

F. International Tolerances

No international tolerances have been

established for copper-ethylenediamine

complex.

[FR Doc. 97–28640 Filed 10–28–97; 8:45 am]

BILLING CODE 6560–50–F

ENVIRONMENTAL PROTECTION

AGENCY

[OPP–181049; FRL 5751–6]

Bifenthrin; Receipt of Application for

Emergency Exemption, Solicitation of

Public Comment

AGENCY: Environmental Protection

Agency (EPA).

ACTION: Notice.

SUMMARY: EPA has received a specific

exemption request from the California

Department of Pesticide Regulations

(hereafter referred to as the

‘‘Applicant’’) to use the pesticide

bifenthrin (CAS #8657–04–3 cis and

83322–02–5 trans), formulated as

Capture 2EC, to treat up to 22,000 acres

of broccoli, cauliflower, cabbage, and

rapini; and 40,000 acres of lettuce, to

control silverleaf whitefly. An

emergency exemption has been

requested for this use for the previous

6 years. Since this request proposes a

use which has been requested or granted

in any 3 previous years, and a complete

application for registration and petition

for tolerance has not yet been submitted

to the Agency, EPA is soliciting public

comment before making the decision

whether or not to grant the exemption,

in accordance with 40 CFR 166.24(a)(6).

DATES: Comments must be received on

or before November 13, 1997.

ADDRESSES: Three copies of written

comments, bearing the identification

notation ‘‘OPP–181049,’’ should be

submitted by mail to: 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. In person, bring

comments to: Rm. 1132, Crystal Mall #2,

1921 Jefferson Davis Highway,

Arlington, VA.

Comments and data may also be

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

instructions under ‘‘SUPPLEMENTARY

INFORMATION.’’ No Confidential

Business Information (CBI) 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 CBI.

Information so marked will not be

disclosed except in accordance with

procedures set forth in 40 CFR part 2.

A copy of the comment that does not

contain CBI must be submitted for

inclusion in the public record.

Information not marked confidential

will be included in the public docket by

EPA without prior notice. The public

docket is available for public inspection

in Rm. 1132 at the Virginia address

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

Monday through Friday, excluding legal

holidays.

FOR FURTHER INFORMATION CONTACT: By

mail: Andrea Beard, Registration

Division (7505C), Office of Pesticide

Programs, Environmental Protection

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

DC 20460. Office location, telephone

number and e-mail: Crystal Mall #2, Rm.

267, 1921 Jefferson Davis Highway,

Arlington, VA, (703) 308–9356; e-mail:

beard.andrea@epamail.epa.gov.

SUPPLEMENTARY INFORMATION: Pursuant

to Section 18 of the Federal Insecticide,

Fungicide, and Rodenticide Act (FIFRA)

(7 U.S.C. 136p), the Administrator may,

at her discretion, exempt a state agency

from any registration provision of