Federal Register / Vol. 63, No. 77 /Wednesday, April 22, 1998 /Rules and Regulations 19829

TABLE 52.2381—EPA-APPROVED REGULATIONS—Continued

[Vermont SIP regulations 1972 to present]

State citation, title and subject Date adopted by State

Date approved by

EPA

Federal Register citation 52.2370 Comments and unapproved

sections

* * * * * * *

Section 5–253.1 Petroleum

Liquid Storage in Fixed Roof

Tanks.

10/29/92 4/22/98 [Insert FR citation from published date].(c)(25) ......

Section 5–253.2 Bulk Gasoline

Terminals

10/29/92 4/22/98 [Insert FR citation published

date].

(c)(25) ......

Section 5–253.3 Bulk Gasoline

Plants

10/29/92 4/22/98 [Insert FR citation from published date].(c)(25) ......

Section 5–253.4 Gasline Tank

Trucks.

10/29/92 4/22/98 [Insert FR citation from published date].(c)(25) ......

Section 5–253.5 Stage I vapor

recovery controls at gasoline

dispensing facilities.

10/29/92 4/22/98 [Insert FR citation from published date].(c)(25) ......

Section 5–253.10 Paper Coating.10/29/92 4/22/98 [Insert FR citation from published date].(c)(25) ......

Section 5–253.12 Coating of

Flatwood Paneling.

10/29/92 4/22/98 [Insert FR citation from published date].(c)(25) ......

Section 5–252.13 Coating of

Miscellaneous Metal Parts.

7/29/93 4/22/98 [Insert FR citation from published date].(c)(25) ......

Section 5–253.14 Solvent

Metal Cleaning.

7/29/93 4/22/98 [Insert FR citation from published date].(c) 25) ......

Section 5–253.15 Cutback and

Emulsified Asphalt.

8/2/94 4/22/98 [Insert FR citation from published date].(c)(25) ......

* * * * * * *

[FR Doc. 98–10724 Filed 4–21–98; 8:45 am]

BILLING CODE 6560–50–P

ENVIRONMENTAL PROTECTION

AGENCY

40 CFR Part 180

[OPP–300635; FRL–5782–1]

RIN 2070–AB78

Fenoxaprop-ethyl; Pesticide Tolerance

AGENCY: Environmental Protection

Agency (EPA).

ACTION: Final rule.

SUMMARY: This regulation establishes

tolerances for combined residues of

fenoxaprop-ethyl [ethyl 2-[4-[(6-chloro2-benzoxazolyl) oxy]phenoxy]

propanoate] and its metabolites [2-[4-]

(6-chloro-2-benzoxazolyl)oxy]phenoxy]

propanoic acid and 6-chloro-2,3-

dihydrobenzoxazol-2-one in or on the

following raw agricultural commodities

(RACs): barley, grain at 0.05 parts per

million (ppm), and barley straw at 0.1

ppm. AgrEvo USA Company requested

these tolerances under the Federal Food,

Drug and Cosmetic Act (FFDCA), as

amended by the Food Quality Protection

Act of 1996 (Pub. L. 104–170).

DATES: This regulation is effective April

22, 1998. Objections and requests for

hearings must be received by EPA on or

before June 22, 1998.

ADDRESSES: Written objections and

hearing requests, identified by the

docket control number, [OPP–300635],

must be submitted to: Hearing Clerk

(1900), Environmental Protection

Agency, Rm. M3708, 401 M St., SW.,

Washington, DC 20460. Fees

accompanying objections and hearing

requests shall be labeled ‘‘Tolerance

Petition Fees’’ and forwarded to: EPA

Headquarters Accounting Operations

Branch, OPP (Tolerance Fees), P.O. Box

360277M, Pittsburgh, PA 15251. A copy

of any objections and hearing requests

filed with the Hearing Clerk identified

by the docket control number, [OPP–

300635], must also be submitted 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

a copy of objections and hearing

requests to Rm. 119, CM #2, 1921

Jefferson Davis Hwy., Arlington, VA.

A copy of objections and hearing

requests filed with the Hearing Clerk

may also be submitted electronically by

sending electronic mail (e-mail) to: oppdocket@epamail.epa.gov. Copies of

objections and hearing requests must be

submitted as an ASCII file avoiding the

use of special characters and any form

of encryption. Copies of objections and

hearing requests will also be accepted

on disks in WordPerfect 5.1/6.1 or

ASCII file format. All copies of

objections and hearing requests in

electronic form must be identified by

the docket control number [OPP–

300635]. No Confidential Business

Information (CBI) should be submitted

through e-mail. Electronic copies of

objections and hearing requests on this

rule may be filed online at many Federal

Depository Libraries.

FOR FURTHER INFORMATION CONTACT: By

mail: Joanne I. Miller, Product Manager

(PM) 23, Registration Division (7505C),

Office of Pesticide Programs,

Environmental Protection Agency, 401

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

Office location, telephone number, and

e-mail address: Crystal Mall #2, 1921

Jefferson Davis Hwy., Arlington, VA,

(703) 305–6224, e-mail:

miller.joanne@epamail.epa.gov.

SUPPLEMENTARY INFORMATION: In the

Federal Register of September 17, 1997

(62 FR 48837) (FRL–5741–1), EPA,

issued a notice pursuant to section 408

of the Federal Food, Drug, and Cosmetic

Act (FFDCA), 21 U.S.C. 346a(e)

announcing the filing of a pesticide

petition (PP) for tolerance by AgrEvo

USA Company, Little Falls One, 2711

Centerville Road, Wilmington, DE

19808. This notice included a summary

of the petition prepared by AgrEvo USA

Company, the registrant. There were no
19830 Federal Register / Vol. 63, No. 77 /Wednesday, April 22, 1998 /Rules and Regulations

comments received in response to the

notice of filing.

The petition requested that 40 CFR

180.430 (b) be amended by establishing

tolerances for combined residues of the

herbicide fenoxaprop-ethyl [ethyl 2-[4-

[(6-chloro-2-

benzoxazolyl)oxy]phenoxy]propanoate]

and its metabolites [2-[4-](6-chloro-2-

benzoxazolyl)oxy]phenoxy]propanoic

acid and 6-chloro-2,3-

dihydrobenzoxazol-2-one, in or on the

following raw agricultural commodities:

barley, grain at 0.05 ppm; and barley

straw at 0.1 ppm.

I. Risk Assessment and Statutory

Findings

New section 408(b)(2)(A)(i) of the

FFDCA allows EPA to establish a

tolerance (the legal limit for a pesticide

chemical residue in or on a food) only

if EPA determines that the tolerance is

‘‘safe.’’ Section 408(b)(2)(A)(ii) defines

‘‘safe’’ to mean that ‘‘there is a

reasonable certainty that no harm will

result from aggregate exposure to the

pesticide chemical residue, including

all anticipated dietary exposures and all

other exposures for which there is

reliable information.’’ This includes

exposure through drinking water and in

residential settings, but does not include

occupational exposure. Section

408(b)(2)(C) requires EPA to give special

consideration to exposure of infants and

children to the pesticide chemical

residue in establishing a tolerance and

to ‘‘ensure that there is a reasonable

certainty that no harm will result to

infants and children from aggregate

exposure to the pesticide chemical

residue. . . .’’

EPA performs a number of analyses to

determine the risks from aggregate

exposure to pesticide residues. First,

EPA determines the toxicity of

pesticides based primarily on

toxicological studies using laboratory

animals. These studies address many

adverse health effects, including (but

not limited to) reproductive effects,

developmental toxicity, toxicity to the

nervous system, and carcinogenicity.

Second, EPA examines exposure to the

pesticide through the diet (e.g., food and

drinking water) and through exposures

that occur as a result of pesticide use in

residential settings.

A. Toxicity

1. Threshold and non-threshold

effects. For many animal studies, a dose

response relationship can be

determined, which provides a dose that

causes adverse effects (threshold effects)

and doses causing no observed effects

(the ‘‘no-observed effect level’’ or

‘‘NOEL’’).

Once a study has been evaluated and

the observed effects have been

determined to be threshold effects, EPA

generally divides the NOEL from the

study with the lowest NOEL by an

uncertainty factor (usually 100 or more)

to determine the Reference Dose (RfD).

The RfD is a level at or below which

daily aggregate exposure over a lifetime

will not pose appreciable risks to

human health. An uncertainty factor

(sometimes called a ‘‘safety factor’’) of

100 is commonly used since it is

assumed that people may be up to 10

times more sensitive to pesticides than

the test animals, and that one person or

subgroup of the population (such as

infants and children) could be up to 10

times more sensitive to a pesticide than

another. In addition, EPA assesses the

potential risks to infants and children

based on the weight of the evidence of

the toxicology studies and determines

whether an additional uncertainty factor

is warranted. Thus, an aggregate daily

exposure to a pesticide residue at or

below the RfD (expressed as 100% or

less of the RfD) is generally considered

acceptable by EPA. EPA generally uses

the RfD to evaluate the chronic risks

posed by pesticide exposure. For shorter

term risks, EPA calculates a margin of

exposure (MOE) by dividing the

estimated human exposure into the

NOEL from the appropriate animal

study. Commonly, EPA finds MOEs

lower than 100 to be unacceptable. This

100-fold MOE is based on the same

rationale as the 100-fold uncertainty

factor.

Lifetime feeding studies in two

species of laboratory animals are

conducted to screen pesticides for

cancer effects. When evidence of

increased cancer is noted in these

studies, the Agency conducts a weight

of the evidence review of all relevant

toxicological data including short-term

and mutagenicity studies and structure

activity relationship. Once a pesticide

has been classified as a potential human

carcinogen, different types of risk

assessments (e.g., linear low dose

extrapolations or MOE calculation based

on the appropriate NOEL) will be

carried out based on the nature of the

carcinogenic response and the Agency’s

knowledge of its mode of action.

2. Differences in toxic effect due to

exposure duration. The toxicological

effects of a pesticide can vary with

different exposure durations. EPA

considers the entire toxicity data base,

and based on the effects seen for

different durations and routes of

exposure, determines which risk

assessments should be done to assure

that the public is adequately protected

from any pesticide exposure scenario.

Both short and long durations of

exposure are always considered.

Typically, risk assessments include

‘‘acute,’’ ‘‘short-term,’’ ‘‘intermediate

term,’’ and ‘‘chronic’’ risks. These

assessments are defined by the Agency

as follows.

Acute risk, by the Agency’s definition,

results from 1-day consumption of food

and water, and reflects toxicity which

could be expressed following a single

oral exposure to the pesticide residues.

High end exposure to food and water

residues are typically assumed.

Short-term risk results from exposure

to the pesticide for a period of 1-7 days,

and therefore overlaps with the acute

risk assessment. Historically, this risk

assessment was intended to address

primarily dermal and inhalation

exposure which could result, for

example, from residential pesticide

applications. However, since enaction of

FQPA, this assessment has been

expanded to include both dietary and

non-dietary sources of exposure, and

will typically consider exposure from

food, water, and residential uses when

reliable data are available. In this

assessment, risks from average food and

water exposure, and high-end

residential exposure, are aggregated.

High-end exposures from all three

sources are not typically added because

of the very low probability of this

occurring in most cases, and because the

other conservative assumptions built

into the assessment assure adequate

protection of public health. However,

for cases in which high-end exposure

can reasonably be expected from

multiple sources (e.g. frequent and

widespread homeowner use in a

specific geographical area), multiple

high-end risks will be aggregated and

presented as part of the comprehensive

risk assessment/characterization. Since

the toxicological endpoint considered in

this assessment reflects exposure over a

period of at least 7 days, an additional

degree of conservatism is built into the

assessment; i.e., the risk assessment

nominally covers 1-7 days exposure,

and the toxicological endpoint/NOEL is

selected to be adequate for at least 7

days of exposure. (Toxicity results at

lower levels when the dosing duration

is increased.)

Intermediate-term risk results from

exposure for 7 days to several months.

This assessment is handled in a manner

similar to the short-term risk

assessment.

Chronic risk assessment describes risk

which could result from several months

to a lifetime of exposure. For this

assessment, risks are aggregated

considering average exposure from all

sources for representative population
Federal Register / Vol. 63, No. 77 /Wednesday, April 22, 1998 /Rules and Regulations 19831

subgroups including infants and

children.

B. 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). 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, EPA takes

into account varying consumption

patterns of major identifiable subgroups

of consumers, including infants and

children.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. If the TMRC exceeds the RfD

or poses a lifetime cancer risk that is

greater than approximately one in a

million, EPA attempts to derive a more

accurate exposure estimate for the

pesticide by evaluating additional types

of information (anticipated residue data

and/or percent of crop treated data)

which show, generally, that pesticide

residues in most foods when they are

eaten are well below established

tolerances.

Percent of crop treated estimates are

derived from federal and private market

survey data. Typically, a range of

estimates are supplied and the upper

end of this range is assumed for the

exposure assessment. By using this

upper end estimate of percent of crop

treated, the Agency is reasonably certain

that exposure is not understated for any

significant subpopulation group.

Further, regional consumption

information is taken into account

through EPA’s computer-based model

for evaluating the exposure of

significant subpopulations including

several regional groups, to pesticide

residues. For this pesticide, the most

highly exposed population subgroup

was not regionally based.

II. Aggregate Risk Assessment and

Determination of Safety

Consistent with section 408(b)(2)(D),

EPA has reviewed the available

scientific data and other relevant

information in support of this action,

EPA has sufficient data to assess the

hazards of fenoxaprop-ethyl and to

make a determination on aggregate

exposure, consistent with section

408(b)(2), for tolerances for combined

residues of fenoxaprop-ethyl [ethyl 2-[4-

[(6-chloro-2-

benzoxazolyl)oxy]phenoxy]propanoate]

and its metabolites [2-[4-](6-chloro-2-

benzoxazolyl)oxy]phenoxy]propanoic

acid and 6-chloro-2,3-

dihydrobenzoxazol-2-one in or on the

following raw agricultural commodities:

barley, grain at 0.05 ppm; and barley

straw at 0.1 ppm. EPA’s assessment of

the dietary exposures and risks

associated with establishing these

tolerances follows.

A. Toxicological Profile

EPA has evaluated the available

toxicity data and considered its validity,

completeness, and reliability as well as

the relationship of the results of the

studies to human risk. EPA has also

considered available information

concerning the variability of the

sensitivities of major identifiable

subgroups of consumers, including

infants and children. The nature of the

toxic effects caused by fenoxaprop-ethyl

are discussed below.

1. Acute toxicity. A battery of acute

toxicity studies is available, places

technical fenoxaprop-ethyl in Toxicity

Category III for acute oral (rat) ( LD50 =

2,357 milligram/kilograms (mg/kg) (M)

and 2,500 mg/kg (F) ), and acute

inhalation (rat) LC50 = >0.511 mg/L; in

Toxicity Category IV for acute dermal

(rat) = >2,000 mg/kg and rabbit =>1,000

mg/kg and skin irritation (slight irritant)

; and in Toxicity Category I for eye

irritation (rabbit) with non-reversible

corneal opacity at day 21. Fenoxapropethyl was determined to be a nonsensitizer in a dermal sensitization

study (guinea pig).

2. Genotoxicity . A battery of

genotoxicity studies, none of which

indicated any genotoxic potential. The

studies submitted included: in vitro

human lymphocyte chromosomal

aberration, mouse micronucleus, in vitro

unscheduled DNA synthesis, Ames

Salmonella bacterial point mutation and

yeast DNA repair assays.

3. In a subchronic feeding study with

rats (30/sex/dose), fenoxaprop-ethyl was

administered at doses of 0, 1, 4 or 16

mg/kg/day for 90 days. The NOEL was

1 mg/kg/day and the lowest observed

effect level (LOEL) was 4 mg/kg/day)

based on relative organ weight changes.

After the 4-week recovery period,

significantly decreased liver weights

were observed in males at the 1 mg/kg/

day dose and in females at 4 mg/kg/day.

4. In a subchronic feeding study in

dogs (6 dogs/sex/dose), fenoxapropethyl was administered at doses of 0,

0.4, 2, or 10 mg/kg /day were fed for 90

days. The NOEL was 0.4 mg/kg/day)

and the LOEL was 2 mg/kg/day based

on histological changes of the kidneys.

Inflammatory changes of the kidneys

(interstitial pyelonephritis) were

detected in the 2 mg/kg/day and in the

10 mg/kg/day dosed dogs.

5. In a 21–day dermal toxicity study,

Wistar rats (10/sex/dose) received

repeated dermal applications of

fenoxaprop-ethyl (96.5%, moistened

with sesame oil) at doses of 0, 5, 10, or

20 mg/kg, 6 hours/day, 5 days/week, for

21 total exposures. The LOEL was >5

mg/kg based on decreased liver weights.

A NOEL was not established.

6. In a second 21–day dermal toxicity

study, Wistar rats (10/sex/dose) received

repeated dermal applications of

fenoxaprop-ethyl (96.5%, vehicle not

specified) at doses of 0, 5, or 20 mg/kg,

6 hours/day, 5 days/week, for 21 total

exposures. The study author concluded

that the NOEL was >20 mg/kg; a LOEL

was not established.

7. In a subchronic inhalation toxicity

study, Wistar rats (10-15/sex/

concentration) were exposed by noseonly inhalation to fenoxaprop-ethyl

(96.5%) at target concentrations of 0,

0.075, 0.250, or 0.750 mg/L (analytically

-determined concentrations of 0, 0.073,

0.248, or 0.727 mg/L, respectively) for 6

hours/day, 5 days/week, for 6 weeks

(28-29 total exposures). An unequivocal

NOEL was not established in this study.

A second study using the same protocol

with target concentrations of 0 or 0.015

mg/L (analytically determined to be 0 or

0.0143 mg/L, respectively) was

conducted. The exposure period was

followed by a 4-week recovery period

for animals in all but the 0.750 mg/L

group. A NOEL for the repeated dose

inhalation was 0.015 mg/L.

8. In a chronic toxicity study in beagle

dogs (6/sex/dose) dogs were fed

fenoxaprop-ethyl (94%) at doses of 0,

0.075, 0.375 or 1.875 mg/kg/day for two

years. The NOEL was 0.375 mg/kg/day

and the LOEL was 1.875 mg/kg/day

based on decreases in body weight gain.

9. In a carcinogenicity study with

groups of 50 male and 50 female

NMRKF (SPF71) mice, fenoxaprop-ethyl

(94%) was administered at dose levels

of 0, 0.375, 1.5, or 6 mg/kg/day for 24

months. The NOEL was >6 mg/kg/day

(HDT). A LOEL was not established.
19832 Federal Register / Vol. 63, No. 77 /Wednesday, April 22, 1998 /Rules and Regulations

10. In a second carcinogenicity study,

fenoxaprop-ethyl (96.8%) was

administered to groups of 50 male and

50 female NMRI mice at doses of 0, 5.7,

16.6 or 44.6 mg/kg/day in males and 0,

6.8, 19.4 or 53.7 mg/kg/day in females

for 24 months. For chronic toxicity the

NOEL was 5.7 mg/kg/day and the LOEL

was 16.6 mg/kg/day based on

histopathological findings in the liver.

There was evidence of carcinogenicity

at the highest dose tested (HDT).

Statistically (p=0.05) significant

increases were seen in liver and adrenal

gland tumors. In males at the high dose,

the incidence of hepatocellular

adenomas (30%) and carcinomas (8%)

were increased when compared to

controls (2%, adenomas and 0%,

carcinomas). Also at this dose in males,

the incidence of subcapsular adenomas

of the adrenal glands was 43%

compared to 22% in controls. In

addition, microscopic pathology

indicated the hepatocellular

hypertrophy was observed in the

majority of all treated animals (both

sexes). Dosing was considered adequate

to assess the carcinogenic potential of

fenoxaprop-ethyl based on clinical

signs, increased liver weight, and

histopathology.

11. In a combined chronic/

oncogenicity study, Wistar rats (116/

sex/dose) were dosed with fenoxapropethyl (95.8%) at 0. 0.25, 1.5 or 9 mg/kg/

day for 28 months. For chronic toxicity,

the NOEL was 1.5 mg/kg/day) and the

LOEL was 9 mg/kg//day based on

decreased serum lipids and cholesterol

in the males. Under the conditions of

this study, there was no evidence of

carcinogenic potential.

12. In an oral developmental toxicity

study, pregnant Wistar rats (20/dose)

received fenoxaprop-ethyl (93% a.i.) in

sesame oil at doses of 0, 10, 32, or 100

mg/kg/day from days 7 through 16 of

gestation. For maternal toxicity, the

NOEL was 32 mg/kg/day and the LOEL

was 100 mg/kg/day, based on slight

initial reduction in body weight and

food consumption. There were no

treatment-related effects or clinical

signs, body weight gain, food

consumption, or development of the

conceptuses in the uterus at dose levels

of less than 32 mg/kg/day.

Developmental toxicity was

demonstrated at 100 mg/kg/day as

slightly impaired growth of the fetuses

(reduced body weights and placental

weights and reduced skeletal

ossification). For developmental

toxicity, the NOEL was 32 mg/kg/day

and the LOEL was 100 mg/kg/day, based

on reduced fetal body weights, reduced

placental weights, retarded skeletal

ossification of the cranium, sternebrae

and 5th metacarpals.

13. In a second oral developmental

toxicity study, pregnant Cr1:COBS CD

(SD) BR rats were dosed with

fenoxaprop-ethyl (96.2%) in corn oil at

doses of 0, 10, 32, or 100 mg/kg/day

from days 6 through 15 of gestation. For

maternal toxicity, the NOEL was 32 mg/

kg/day and the LOEL was 100 mg/kg/

day, based on decreased body weight

gain and increased liver weights. For

developmental toxicity, the NOEL was

32 mg/kg/day and the LOEL was 100

mg/kg/day base on increase

malformations, significant fetal weight

reduction and increase total visceral and

skeletal anomalies.

14. In an oral developmental toxicity

study with groups of Himalayan

[(Hoe:HIMK(SPFWiga)] rabbits were

dosed at doses of fenoxaprop-ethyl

(93%) in sesame oil at 0, 0.5, 12.5, 50.0

or 200 mg/kg/day from days 7 through

19 of gestation. For maternal toxicity,

the NOEL was 12.5 mg/kg/day and the

LOEL was 50.0 mg/kg/day, based on

decreased food consumption and body

weight gain. For developmental toxicity,

the NOEL was 50 mg/kg/day and the

LOEL was 200 mg/kg/day based on

reduced fetal weights, placental

weights, crown-rump lengths, and fetal

survival, and increased litter and fetal

incidence of rib anomalies and

diaphragmatic hernias. No

developmental toxicity was observed at

doses of less than 50.0 mg/kg/day.

15. In a dermal developmental

toxicity study, pregnant KFM-Han

Wistar rats (25/dose) received repeated

dermal applications of fenoxaprop-ethyl

(96.5%) in sesame oil at doses of 0, 100,

300, or 1,000 mg/kg/day for 6 hours/day

on days 6–15 of gestation. For maternal

toxicity, the NOEL was >1,000 mg/kg/

day (HDT); a LOEL was not observed.

For developmental toxicity, the NOEL

was 1,000 mg/kg/day; a LOEL was not

observed. There were no treatmentrelated malformations or variations

noted upon external, visceral, and

skeletal examination of the fetuses.

16. In a dermal developmental

toxicity study, fenoxaprop-ethyl (96.5%)

in sesame oil was administered

dermally to 16 Chinchilla rabbits (SPF

quality) at dose levels of 0,100, 300, or

1,000 mg/kg/day for 6 hours/day on

days 6–18 of gestation. For maternal

toxicity, the NOEL was 1,000 mg/kg/day

(HDT); a LOEL was not observed. There

was no developmental toxicity

demonstrated at any dose level. For

developmental toxicity, the NOEL was

1,000 mg/kg/day; a LOEL was not

observed.

17. In a 2-generation reproductive

toxicity study, fenoxaprop-ethyl (97.2%)

was administered to 30 WISTAR/HAN

rats/sex/dose in their diet at doses of 0,

0.25, 1.5, or 9.0 mg/kg/day. Exposure to

animals began at 7 weeks of age and

lasted for 80 days prior to mating to

produce F1a and F1b pups. At 21 days

of age, F1b pups were selected to

become the parents of the F2a and F2b

litters. There were no treatment-related

effects on mortality, clinical signs of

toxicity, body weight, food consumption

or reproductive parameters at any does

level. For parental/systemic toxicity, the

NOEL was 0.25 mg/kg/day) and the

LOEL was 1.5 mg/kg/day based on

decreased blood lipids. The NOEL for

systemic toxicity was 0.25 mg/kg/day.

For reproductive toxicity, the NOEL was

0.25 mg/kg/day and the LOEL was 1.5

mg/kg/day based on reduced pup body

weights (F1a).

18. No developmental neurotoxicity

data are required for fenoxaprop-ethyl.

No effects on histopathology of the brain

were observed in any of the studies in

which these parameters were measured.

There no evidence of developmental

anomalies of the fetal nervous system in

the prenatal developmental toxicity

studies with rats or rabbits or in the 2-

generation reproduction study in rats.

19. Studies on metabolism: In a rat

metabolism study fenoxaprop-ethyl(U14C-chlorophenyl; 98% radiochemical

purity) was administered to male and

female Wistar HOE: Wiskf (SPF 71)

strain of rats (10–15 animals/dose/sex)

by gavage as a single dose at levels of

2 or 10 mg/kg, or at a single dose at 2

mg/kg following a 4–day pretreatment

with unlabeled fenoxaprop-ethyl at 2

mg/kg/day. Within 6 hours of dosing

83–109% of the administered

radioactivity was recovered in the urine

and feces, with a majority of the dose

(51–65%) being recovered within 24

hours of dosing. Within 24 hours of

dosing, urinary excretion accounted for

39–48% of the dose for females and 22–

311% of the dose for males. The

primary metabolite in urine of both

sexes in each dose group was 6-

chlorobenzoxazole-2-mercapturic acid,

accounting for 22–50% of the total

radioactivity in the urine (15–26% of

the dose) The urine of female rats dosed

either once at 10 mg/kg or repeatedly at

2 mg/kg also contained high levels (23–

28% of dose) of 2-(4-(6-chloro-2-

benzoxazolyloxy)-phenoxy)-propionic

acid (the free acid of fenoxaprop-ethyl).

At the 10 mg/kg dose, unchanged parent

accounted for 24% of the fecal

radioactivity (15% of dose) for male rats

and 6% for female rats (1.7% of dose).

In a second rat metabolism study,

fenoxaprop-ethyl (1–14C-dioxyphenyl;

96% radiochemical purity) was

administered by gavage as a single dose
Federal Register / Vol. 63, No. 77 /Wednesday, April 22, 1998 /Rules and Regulations 19833

to male and female SPF Wistar strain

rats (10 animals /sex) at 10 mg/kg body

weight and to 15 females at 2 mg/kg

body weight. Within 96 hours of dosing,

101.3% and 87.4% of the 10 gm/kg dose

was recovered from male and female

rats, respectively, and 108.8% of the 2

mg/kg dose was recovered from female

rats. There were sex- and dose-related

differences in excretion. In the 0- to 24-

hour urine of male rats dosed at 10 mg/

kg, 99% of the radioactivity was

identified as 2-(4-hydroxyphenoxy)-

propionic acid (HPP-acid), accounting

for 47.5% of the administered dose. In

female rats dosed at 10 mg/kg, the

primary urinary metabolites were

identified as HPP acid (27.5% of dose)

and 2-(4-6-chloro-2-benzoxazolyloxy)-

phenoxy)-propionic acid (the free acid

of fenoxaprop-ethyl; 27% of dose). In

feces of the 10 mg/kg dose groups,

fenoxaprop-ethyl and its free acid

accounted for 20.1 and 16.6% of the

dose for males and 9.0 and 11.3% of the

dose for females.

B. Toxicological Endpoints

1. Acute toxicity. EPA has selected for

acute dietary risk assessment the NOEL

of 32 mg/kg/day from the rat

developmental toxicity study. The

effects were increased incidence of

fetuses with malformations (including

skeletal defects, eye defects, absent

innominate artery, diaphragmatic hernia

and umbilical hernia at 100 mg/kg/day

(LOEL). Population subgroup of concern

is females 13+ years old.

An acute dietary risk assessment for

the general population, including

infants and children, (excluding the

subgroup, females 13+ years old) is not

required because no treatment-related

effects attributable to a single exposure

(dose) were seen in oral studies

conducted with fenoxaprop-ethyl. A

MOE of 100 is adequate to ensure

protection for females 13+ years old.

2. Short - and intermediate - term

toxicity. No dermal or systemic toxicity

was seen in a dermal developmental

toxicity study in rats and rabbits

following repeated dermal applications

of fenoxaprop-ethyl at 1,000 mg/kg/day

(Limit-Dose). Also, no dermal or

systemic toxicity was seen at the HDT

(20 mg/kg/day) in a 21–day dermal

toxicity study in rats.

3. Intermediate-term inhalation

toxicity. A 6-week rat inhalation toxicity

study demonstrated a NOEL = 0.015 mg/

L based on decreases in total lipids,

increased triglycerides, increased

alkaline phosphatase, increased liver

and kidney weights, and liver

hypertrophy at 0.075 mg/L (LOEL).

C. Cancer Dietary/Inhalation

1. Chronic toxicity. EPA has

established the RfD for fenoxaprop-ethyl

at 0.0025 milligrams/kilogram/day (mg/

kg/day). This RfD is based on reduced

pup weights observed in a 2-generation

rat reproductive toxicity study with a

NOEL of 0.25 mg/kg/day. An

uncertainity factor of 100 was used in

calculating the RfD to account for both

inter- and intra-species variations.

2. Carcinogenicity. Characterization of

the carcinogenicity of fenoxaprop-ethyl

has been referred to EPA Health Effects

Division’s Cancer Peer Review

Committee. For the interim, a worst case

and protective risk assessment was

carried out by use of a linear low dose

extrapolation method (Q1*) based on

the increases in adrenal tumors in male

mice. The Q1* for the adrenal tumors is

9.1 x 10-2.

D. Exposures and Risks

1. From food and feed uses.

Tolerances have been established (40

CFR 180.430 (a)) for the combined

residues of fenoxaprop-ethyl [ethyl 2-[4-

[(6-chloro-2-

benzoxazolyl)oxy]phenoxy]propanoate]

and its metabolites [2-[4-](6-chloro-2-

benzoxazolyl)oxy]phenoxy]propanoic

acid, and 6-chloro-2,3-

dihydrobenzoxazol-2-one in or on a

variety of raw agricultural commodities.

Risk assessments were conducted by

EPA to assess dietary exposures and

risks from fenoxaprop-ethyl as follows:

i. Acute exposure and risk. Acute

dietary 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. The NOEL

for the acute dietary exposure was 32

mg/kg/day from a rat study. The Agency

has determined that the uncertainty

factor of 10 to account for enhanced

sensitivity of infants and children

should be removed for fenoxapropethyl, and that the MOE of 100 to

account for inter (10) and intra (10)

species variation is adequate to insure

protection for this population from

exposure to fenoxaprop-ethyl, because

in the rat developmental toxicity study,

the fetal effects (malformations) were

seen at maternally toxic doses (i.e., the

LOEL was the same for both adults and

fetuses).

From the acute dietary (food only)

risk assessment a high-end exposure

estimate of 0.001 mg/kg/day was

calculated. This exposure yields a

dietary (food only) MOE of 32,000 for

females 13+ years, the population

subgroup of concern. This risk estimate

was highly conservative because it

assume that 100% of barley and all

other commodities having tolerances for

residues of fenoxaprop-ethyl will

contain residues at tolerance levels.

Therefore, this is an overestimation of

human dietary exposure. Use of

anticipated residue values and percent

crop-treated data will result in a lower

acute dietary exposure estimate if

estimated by probabilistic techniques.

ii. Chronic exposure and risk. The

anticipated residues for existing

fenoxaprop-ethyl uses (including the

use on barley) result in Anticipated

Residue Contribution that varies

between 0.000009 and 0.000023 mg/kg/

day for the population subgroups ( the

U.S. Population, Nursing Infants (<1

year old), Non-Nursing Infants (> year

old), Children (1–6 years old) , Children

(7–12 years old) and Non-Hispanic

Others); and occupied between 0.4%

and 0.9% of the RfD.

Section 408(b)(2)(E) authorizes EPA to

use available data and information on

the anticipated residue levels of

pesticide residues in food and the actual

levels of pesticide chemicals that have

been measured in food. If EPA relies on

such information, EPA must require that

data be provided five years after the

tolerance is established, modified, or

left in effect, demonstrating that the

levels in food are not above the levels

anticipated. Following the initial data

submission, EPA is authorized to

require similar data on a time frame it

deems appropriate. Section 408(b)(2)(F)

states that the Agency may use data on

the actual percent of crop treated for

assessing chronic dietary risk only if the

Agency can make the following

findings: (1) that the data used are

reliable and provide a valid a basis for

showing the percentage of food derived

from a crop that is likely to contain

residues; (2) that the exposure estimate

does not underestimate the exposure for

any significant subpopulation and; (3)

where data on regional pesticide use

and food consumption are available,

that the exposure estimate does not

understate exposure for any regional

population. In addition the Agency

must provide for periodic evaluation of

any estimates used.

The percent of crop treated estimates

for fenoxaprop-ethyl were derived from

federal and market survey data. EPA

considers these data reliable. A range of

estimates are supplied by this data and

the upper end of this range was used for

the exposure assessment. By using this

upper end estimate of percent crop

treated, the Agency is reasonably certain

that exposure is not underestimated for

any significant subpopulation. Further,

regional consumption information is

taken into account through EPA’s
19834 Federal Register / Vol. 63, No. 77 /Wednesday, April 22, 1998 /Rules and Regulations

computer-based model for evaluating

the exposure of significant

subpopulations including several

regional groups. Review of this regional

data allows the Agency to be reasonably

certain that no regional population is

exposed to residue levels higher than

those estimated by the Agency. To

provide for the periodic evaluation of

these estimates of percent crop treated

as required by the section 408(b)(2)(F),

EPA may require fenoxaprop-ethyl

registrants to submit data on percent

crop treated. As required by section

408(b)(2)(E), EPA will issue a data callin for information relating to anticipated

residues to be submitted no later than

five years from the date of issuance of

this tolerance.

In the absence of an Agency Cancer

Assessment Review, the Health Effects

Division of the Office of Pesticide

Programs recommended a worst case

and protective risk assessment using a

linear low dose extrapolation method

(Q1*) based on the increases in adrenal

tumors in mice. The Q1* for the adrenal

tumors was determined to be 9.1 x 10-2.

Based on the US population chronic

dietary exposure of 0.00001 mg/kg/day,

this results in a cancer risk estimate of

9.1 x 10-7.

2. From drinking water. Based on the

acute and chronic dietary (food)

exposure and using default body

weights and water consumption figures,

acute and chronic drinking water levels

of concern (DWLOC) for drinking water

were calculated. To calculate the

DWLOC, the acute or chronic dietary

food exposure (from the DRES analysis)

was subtracted from the acute toxicity

NOEL or RfD, as appropriate. DWLOCs

were then calculated using the default

bodyweights and drinking water

consumption figures.

For acute drinking water exposure for

both adults and children, the level of

concern was 960 ppm. For chronic and

cancer exposure in drinking water the

levels of concern were 80 ppb and 110

ppt, respectively. For adults, the

estimate was based on a body weight of

70 kg and consumption of 2 liters of

water per day; for children, a body

weight of 10 kg and a consumption of

1 liter of water per day. Agency

estimates for contamination of drinking

water from the registered uses of

fenoxaprop-ethyl is less than 1 ppb for

acute exposure and less than 100 ppt for

chronic exposure. These levels are not

greater than levels of EPA concern.

3. From non-dietary exposure.

Fenoxaprop-ethyl is currently registered

for use on turfgrass including sod farms,

commercial and residential turf and

ornamentals. Applications to residential

turf are done by professional

applicators. There are no homeowner

uses. There is a potential dermal

exposure to infants to fenoxaprop-ethyl

from the registered uses for lawn and

turfgrass weed control but no dermal

toxicity has been shown in animal

studies. Potentially, infants and

children may have some inhalation

exposure due to residual residues of the

pesticide on lawns but such exposure

would be very low. Currently there are

no inhalation exposure data required for

post-application of pesticides to lawns

and turf uses. As inhalation exposure

for mixer/loaders is acceptable, the risk

to children and infants from inhalation

exposure under a much lower exposure

scenario is characterized qualitatively as

being extremely low. Exposure data are

required for hand to mouth movements

of infants and children; however, no

acute dietary toxicity endpoints have

been identified for fenoxaprop-ethyl for

infants and children. There is an acute

dietary toxicity endpoint; however, the

only population subgroup of concern is

females 13+ for developmental effects.

The risk to this subgroup will be

addressed later in this document under

‘‘Aggregate Risk and Determination of

Safety for Infants and Children.’’ No

acute dietary toxicity endpoints have

been identified for the general

populations.

4. Cumulative exposure to substances

with common mechanism of toxicity.

Section 408(b)(2)(D)(v) requires that,

when considering whether to establish,

modify, or revoke a tolerance, the

Agency consider ‘‘available

information’’ concerning the cumulative

effects of a particular pesticide’s

residues and ‘‘other substances that

have a common mechanism of toxicity.’’

The Agency believes that ‘‘available

information’’ in this context might

include not only toxicity, chemistry,

and exposure data, but also scientific

policies and methodologies for

understanding common mechanisms of

toxicity and conducting cumulative risk

assessments. For most pesticides,

although the Agency has some

information in its files that may turn out

to be helpful in eventually determining

whether a pesticide shares a common

mechanism of toxicity with any other

substances, EPA does not at this time

have the methodologies to resolve the

complex scientific issues concerning

common mechanism of toxicity in a

meaningful way. EPA has begun a pilot

process to study this issue further

through the examination of particular

classes of pesticides. The Agency hopes

that the results of this pilot process will

increase the Agency’s scientific

understanding of this question such that

EPA will be able to develop and apply

scientific principles for better

determining which chemicals have a

common mechanism of toxicity and

evaluating the cumulative effects of

such chemicals. The Agency anticipates,

however, that even as its understanding

of the science of common mechanisms

increases, decisions on specific classes

of chemicals will be heavily dependent

on chemical specific data, much of

which may not be presently available.

Although at present the Agency does

not know how to apply the information

in its files concerning common

mechanism issues to most risk

assessments, there are pesticides as to

which the common mechanism issues

can be resolved. These pesticides

include pesticides that are

toxicologically dissimilar to existing

chemical substances (in which case the

Agency can conclude that it is unlikely

that a pesticide shares a common

mechanism of activity with other

substances) and pesticides that produce

a common toxic metabolite (in which

case common mechanism of activity

will be assumed).

EPA does not have, at this time,

available data to determine whether

fenoxaprop-ethyl has a common

mechanism of toxicity with other

substances or how to include this

pesticide in a cumulative risk

assessment. Unlike other pesticides for

which EPA has followed a cumulative

risk approach based on a common

mechanism of toxicity, fenoxaprop-ethyl

does not appear to produce a toxic

metabolite produced by other

substances. For the purposes of this

tolerance action, therefore, EPA has not

assumed that fenoxaprop-ethyl has a

common mechanism of toxicity with

other substances.

E. Aggregate Risks and Determination of

Safety for U.S. Population

1. Acute risk. From the acute dietary

(food use) risk assessment a high-end

exposure estimate of 0.001 mg/kg/day

was determined for females 13+ years,

the population subgroup of concern for

acute toxicity. This exposure yields a

dietary MOE of 32,000. The potential

contribution to acute exposure from

residues in drinking water is minimal

(1,000-fold less than EPA’s level of

concern) and would not result in an

aggregate acute exposure that exceeds

EPA’s level of concern. EPA concludes

there is a reasonable certainty that no

acute harm will result from aggregate

exposure to fenoxapro-ethyl residues.

2. Chronic risk. Using the ARC

exposure assumptions described above,

EPA has concluded that aggregate

exposure to fenoxaprop-ethyl from food
Federal Register / Vol. 63, No. 77 /Wednesday, April 22, 1998 /Rules and Regulations 19835

will utilize less than 0.4% of the RfD for

the U.S. population. The major

identifiable subgroup with the highest

aggregate exposure is non-nursing

infants less than one year old. EPA

generally has no concern for exposures

below 100% of the RfD because the RfD

represents the level at or below which

daily aggregate dietary exposure over a

lifetime will not pose appreciable risks

to human health. Despite the potential

for exposure to fenoxaprop-ethyl in

drinking water and from non-dietary,

non-occupational exposure, EPA does

not expect the aggregate exposure to

exceed 100% of the RfD. EPA concludes

that there is a reasonable certainty that

no harm will result from aggregate

exposure to fenoxaprop-ethyl residues.

Short- and intermediate-term

aggregate exposure takes into account

chronic dietary food and water

(considered to be a background

exposure level) plus indoor and outdoor

residential exposure.

Fenoxaprop-ethyl is currently

registered for use on turfgrass including

sod production, commercial and

residential turf and landscape

ornamentals. No short- or intermediateterm dermal toxicity endpoints have

been identified for fenoxaprop-ethyl. An

inhalation endpoint has been identified,

however, as the uses are outdoors,

exposure from inhalation route should

be considerable less than that

determined for worker mixer/loaders,

who have an MOE of 2,800.

Additionally, based on the low level of

chronic dietary exposure, the Agency

concludes that aggregate short- and

intermediate-term exposure is at a level

below EPA’s level of concern.

F. Aggregate Cancer Risk for U.S.

Population

Based on a upper bound potency

factor (Q1*) of 9.1 x 10-2 (mg/kg/day)-1,

the lifetime cancer risk from residues of

fenoxaprop-ethyl in food commodities

is 9.1 x 10-7. Taking into accoutn the

exposure from residues in food, EPA has

caluculated a drinking water level of

concern which would not result in a

greater negligible total cancer risk from

chronic exposure to fenoxaprop-ethyl

residues in food and water. The

Agency’s GENEEC screening model was

then used to estimate maximum

residues in surface water. This model

estimates potential residues in surface

water for use in ecological risk

assessment. As such, it provides highend values on the concentrations of

pesticides that might be found in

ecologically sensitive environments.

The residue levels obtained for

fenoxaprop-ethyl plus its acid

metabolite in water using GENEEC do

not exceed the drinking water level of

concern. Therefore, EPA doen not

expect there to be a greater than

negligible cancer risk from chronic

exposures to fenoxaprop-ethyl in

drinking water and food.

G. Aggregate Risks and Determination of

Safety for Infants and Children

1. Safety factor for infants and

children— a. In general. In assessing the

potential for additional sensitivity of

infants and children to residues of

fenoxaprop-ethyl, 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

maternal pesticide exposure gestation.

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. Margins of safety are

incorporated into EPA risk assessments

either directly through use of a MOE

analysis or through using uncertainty

(safety) factors in calculating a dose

level that poses no appreciable risk to

humans. EPA believes that reliable data

support using the standard uncertainty

factor (usually 100 for combined interand intra-species variability)) and not

the additional tenfold MOE/uncertainty

factor when EPA has a complete data

base under existing guidelines and

when the severity of the effect in infants

or children or the potency or unusual

toxic properties of a compound do not

raise concerns regarding the adequacy of

the standard MOE/safety factor.

b. Developmental toxicity studies. In a

oral developmental toxicity study with

Wistar rats, the maternal NOEL was 32

mg/kg/day, based on reduction in body

weight and food consumption. The

developmental NOEL was 32 mg/kg/

day, based on reduced fetal body

weights, reduced placental weights and

retarded skeletal ossification of the

cranium, sternebrae and 5th

metacarpals.

In a second oral developmental

toxicity study with Crl:COBS CD (SD)

BR rats, the maternal NOEL was 32 mg/

kg/day, based on decreased body weight

gain and increased liver weights. The

developmental NOEL was 32 mg/kg/

day, based on increase malformations,

significant fetal weight reduction and

increase total visceral and skeletal

anomalies.

In a oral developmental toxicity study

with Himalayan rabbits, the maternal

NOEL was 12.5 mg/kg/day, based on

decreased food consumption and body

weight gain. The developmental NOEL

was 50mg/kg/day, based on reduced

fetal weights, placental weights, crownrump lengths, fetal survival and

increased litter and fetal incidence of rib

anomalies and diaphragmatic hernias.

c. Reproductive toxicity study. In a rat

reproduction study, the parental

(systemic) NOEL was 0.25 mg/kg/day,

based on decreased blood lipids. The

reproductive (pup) NOEL was 0.25 mg/

kg/day, based on reduced pup body

weights.

d. Pre- and post-natal sensitivity. The

toxicological data base is complete and

adequate to determine pre- and postnatal toxicity. The prenatal

developmental toxicity data

demonstrated no indication of increased

sensitivity of rats or rabbits to in utero

exposure or repeated dermal

applications of fenoxaprop-ethyl. The

rat reproduction study did not identify

any increased sensitivity of rats to in

utero or postnatal exposure. Maternal

and parental NOELs were equivalent to

developmental or offspring NOELs.

e. Conclusion. Based on the above

data, EPA determined that the standard

safety factor would be adequate to

protect the safety of infants and children

thus the additional children’s safety

factor was removed.

2. Acute risk. The acute dietary (food

only) MOE for females 13+ years old

(accounts for both maternal and fetal

exposure) was determined to be 32,000.

This MOE was based on the

developmental NOEL in rats of 32 mg/

kg/day. This risk assessment assumed

100% crop-treated and tolerance level

residues on all treated crops consumed,

resulting in a significant over-estimate

of dietary exposure. Despite the

potential for exposure to fenoxapropethyl in drinking water, EPA does not

expect the acute aggregate exposure to

exceed level of concern. The large acute

dietary MOE determined for females

13+ years old provides assurance that

there is a reasonable certainty of no

harm from both females 13+ years and

the pre-natal development of infants.

3. Chronic risk. Using the exposure

assumptions described in this rule, the

percentage of the RfD that will be

utilized by chronic dietary (food only)

exposure to residues of fenoxapropethyl ranges from 0.4% for nursing

infants less than one year old, up to

0.9% for non-nursing infants less than
19836 Federal Register / Vol. 63, No. 77 /Wednesday, April 22, 1998 /Rules and Regulations

one year old. Despite the potential for

exposure to fenoxaprop-ethyl in

drinking water, EPA does not expect the

chronic aggregate exposure to exceed

100% of the RfD. Based on the nature

of the residential uses, no chronic

residential exposure is anticipate. EPA

concludes that there is a reasonable

certainty that no harm will result to

infants and children from chronic

aggregate exposure to fenoxaprop-ethyl

regulable residues.

III. Other Considerations

A. Metabolism In Plants and Animals

The metabolism of fenoxaprop-ethyl

in plants and animals is adequately

understood for purposes of these

tolerances.

B. Analytical Enforcement Methodology

An adequate analytical method for

determining the magnitude of residues

in the raw agricultural commodities

listed in this Final Rule has been

evaluated by EPA and is published in

the Pesticide Analytical Manual (PAM

II). The method may be requested from:

Calvin Furlow, Public Information

Branch, Field Operations Division

(7502C), Office of Pesticide Programs,

Environmental Protection Agency, 401

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

Office location and telephone number:

Rm. 1130A, CM #2, 1921 Jefferson Davis

Hwy., Arlington, VA, (703–305–5937).

C. Magnitude of Residues

The nature of the residue in plants is

adequately understood for the purposes

of these tolerances.

D. International Residue Limits

No CODEX Maximum Residue Levels

(MRLs) have been established for

fenoxaprop-ethyl. Canadian MRLs for

combined residues of fenoxaprop-ethyl,

its free acid metabolite [2-[4-[(6-chloro2-benzoxazolyl)oxy]propanoic acid] and

6-chloro-2,3-dihydrobenzoxazol-2-one

have been established at 0.02 ppm for

milk. This tolerance expression and

level for milk is in harmony with

subject tolerances of the final rule.

IV. Conclusion

Therefore, the tolerances are

established for combined residues of

fenoxaprop-ethyl [ethyl 2-[4-[(6-chloro2-benzoxazolyl) oxy]phenoxy]

propanoate] and its metabolites [2-[4-]

(6-chloro-2-benzoxazolyl)oxy]phenoxy]

propanoic acid and 6-chloro-2,3-

dihydrobenzoxazol-2-one, in or on the

following raw agricultural commodities:

barley, grain at 0.05 ppm; and barley

straw at 0.1 ppm.

V. Objections and Hearing Requests

The new FFDCA section 408(g)

provides essentially the same process

for persons to ‘‘object’’ to a tolerance

regulation issued by EPA under new

section 408(e) and (l)(6) as was provided

in the old section 408 and in section

409. However, the period for filing

objections is 60 days, rather than 30

days. EPA currently has procedural

regulations which govern the

submission of objections and hearing

requests. These regulations will require

some modification to reflect the new

law. However, until those modifications

can be made, EPA will continue to use

those procedural regulations with

appropriate adjustments to reflect the

new law.

Any person may, by June 22, 1998,

file written objections to any aspect of

this regulation and may also request a

hearing on those objections. Objections

and hearing requests must be filed with

the Hearing Clerk, at the address given

above (40 CFR 178.20). A copy of the

objections and/or hearing requests filed

with the Hearing Clerk should be

submitted to the OPP docket for this

rulemaking. The objections submitted

must specify the provisions of the

regulation deemed objectionable and the

grounds for the objections (40 CFR

178.25). Each objection must be

accompanied by the fee prescribed by

40 CFR 180.33(i). If a hearing is

requested, the objections must include a

statement of the factual issues on which

a hearing is requested, the requestor’s

contentions on such issues, and a

summary of any evidence relied upon

by the requestor (40 CFR 178.27). A

request for a hearing will be granted if

the Administrator determines that the

material submitted shows the following:

There is genuine and substantial issue

of fact; there is a reasonable possibility

that available evidence identified by the

requestor would, if established, resolve

one or more of such issues in favor of

the requestor, taking into account

uncontested claims or facts to the

contrary; and resolution of the factual

issues in the manner sought by the

requestor would be adequate to justify

the action requested (40 CFR 178.32).

Information submitted in connection

with an objection or hearing request

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 information 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.

VI. Public Docket

EPA has established a record for this

rulemaking under docket control

number [OPP–300635] (including any

comments and data submitted

electronically). A public version of this

record, including printed, paper

versions of electronic comments, which

does not include any information

claimed as CBI, is available for

inspection from 8:30 a.m. to 4 p.m.,

Monday through Friday, excluding legal

holidays. The public record is located in

Room 119 of the Public Information and

Records Integrity Branch, Information

Resources and Services Division

(7502C), Office of Pesticide Programs,

Environmental Protection Agency,

Crystal Mall #2, 1921 Jefferson Davis

Highway, Arlington, VA.

Electronic comments may be sent

directly to EPA at:

opp-docket@epamail.epa.gov.

Electronic comments must be

submitted as an ASCII file avoiding the

use of special characters and any form

of encryption.

The official record for this

rulemaking, as well as the public

version, as described above will be kept

in paper form. Accordingly, EPA will

transfer any copies of objections and

hearing requests received electronically

into printed, paper form as they are

received and will place the paper copies

in the official rulemaking record which

will also include all comments

submitted directly in writing. The

official rulemaking record is the paper

record maintained at the Virginia

address in ‘‘ADDRESSES’’ at the

beginning of this document.

VII. Regulatory Assessment

Requirements

This final rule establishes tolerances

under FFDCA section 408(d) in

response to a petition submitted to the

Agency. The Office of Management and

Budget (OMB) has exempted these types

of actions from review under Executive

Order 12866, entitled Regulatory

Planning and Review (58 FR 51735,

October 4, 1993). This final rule does

not contain any information collections

subject to OMB approval under the

Paperwork Reduction Act (PRA), 44

U.S.C. 3501 et seq., or impose any

enforceable duty or contain any

unfunded mandate as described under

Title II of the Unfunded Mandates

Reform Act of 1995 (UMRA) (Pub. L.

104–4). Nor does it require any prior

consultation as specified by Executive

Order 12875, entitled Enhancing the
Federal Register / Vol. 63, No. 77 /Wednesday, April 22, 1998 /Rules and Regulations 19837

Intergovernmental Partnership (58 FR

58093, October 28, 1993), or special

considerations as required by Executive

Order 12898, entitled Federal Actions to

Address Environmental Justice in

Minority Populations and Low-Income

Populations (59 FR 7629, February 16,

1994), or require OMB review in

accordance with Executive Order 13045,

entitled Protection of Children from

Environmental Health Risks and Safety

Risks (62 FR 1985, April 23, 1997).

In addition, since these tolerances and

exemptions that are established on the

basis of a petition under FFDCA section

408(d), such as the tolerances in this

final rule, do not require the issuance of

a proposed rule, the requirements of the

Regulatory Flexibility Act (RFA) (5

U.S.C. 601 et seq.) do not apply.

Nevertheless, the Agency has previously

assessed whether establishing

tolerances, exemptions from tolerances,

raising tolerance levels or expanding

exemptions might adversely impact

small entities and concluded, as a

generic matter, that there is no adverse

economic impact. The factual basis for

the Agency’s generic certification for

tolerance actions published on May 4,

1981 (46 FR 24950) and was provided

to the Chief Counsel for Advocacy of the

Small Business Administration.

VIII. Submission to Congress and the

Comptroller General

The Congressional Review Act, 5

U.S.C. 801 et seq., as added by the Small

Business Regulatory Enforcement

Fairness Act of 1996, generally provides

that before a rule may take effect, the

Agency promulgating the rule must

submit a rule report, which includes a

copy of the rule, to each House of the

Congress and to the Comptroller General

of the United States. EPA will submit a

report containing this rule and other

required information to the U.S. Senate,

the U.S. House of Representatives, and

the Comptroller General of the United

States prior to publication of this rule in

the Federal Register. This rule is not a

‘‘major rule’’ as defined by 5 U.S.C.

804(2).

List of Subjects in 40 CFR Part 180

Environmental protection,

Administrative practice and procedure,

Agricultural commodities, Pesticides

and pests, Reporting and recordkeeping

requirements.

Dated: April 8, 1998.

James Jones,

Director, Registration Division, Office of

Pesticide Programs.

Therefore, 40 CFR chapter I is

amended as follows:

PART 180—[AMENDED]

1. The authority citation for part 180

continues to read as follows:

Authority: 21 U.S.C. 346a and 371.

2. In § 180.430, in paragraph (a) by

alphabetically adding the following

commodities to the table to read as

follows:

§ 180.430 Fenoxaprop-ethyl; tolerances for

residues.

(a) * * *

Commodity Parts per

million

Barley, grain .............................. 0.05

Barley, straw ............................. 0.1

* * * * *

* * * * *

[FR Doc. 98–10395 Filed 4–21–98; 8:45 am]

BILLING CODE 6560–50–F

ENVIRONMENTAL PROTECTION

AGENCY

40 CFR Parts 264 and 265

[FRL–6001–8]

Removal of Direct Final Rule for XL

Project at OSi Specialties, Inc.,

Sistersville, WV

AGENCY: Environmental Protection

Agency (EPA).

ACTION: Removal of direct final rule

amendments.

SUMMARY: On March 6, 1998, EPA

published a direct final rule entitled

‘‘Project XL Site-Specific Rulemaking

for OSi Specialties, Inc., Sistersville,

West Virginia’’ at 63 FR 11124–11147.

That Federal Register notice provided

that the direct final rule would be

withdrawn if relevant adverse

comments were received by March 27.

Because EPA received such comments,

EPA is now removing the amendments

made by the direct final rule.

EFFECTIVE DATE: April 22, 1998.

ADDRESSES: Docket. A docket containing

documents relevant to this action is

available for public inspection and

copying at the EPA’s docket office

located at Crystal Gateway, 1235

Jefferson Davis Highway, First Floor,

Arlington, Virginia. The public is

encouraged to phone in advance to

review docket materials. Appointments

can be scheduled by phoning the Docket

Office at (703) 603–9230. Refer to RCRA

docket number F–98–MCCP–FFFFF.

A duplicate copy of the docket is

available for inspection and copying at

U.S. EPA, Region 3, 841 Chestnut Street,

Philadelphia, PA 19107–4431, during

normal business hours. Persons wishing

to view the duplicate docket at the

Philadelphia location are encouraged to

contact Mr. Tad Radzinski in advance,

by telephoning (215) 566–2394.

FOR FURTHER INFORMATION CONTACT:

Mr. Tad Radzinski, U.S. Environmental

Protection Agency, Region 3 (3WC11),

Waste Chemical Management Division,

841 Chestnut Street, Philadelphia, PA

19107–4431, (215) 566–2394.

SUPPLEMENTARY INFORMATION: A

companion proposal to the direct final

rule was published in the March 6, 1998

Federal Register (63 FR 11200–11202).

EPA will address the comments

received in response to that proposal

but will not institute a second comment

period.

However, persons who stil wish to

comment on the companion proposal

may do so by attending the hearing

announced in the proposed rule section

of today’s Federal Register. In a

subsequent final rule EPA will address

the comments received on the proposed

rule.

The Congressional Review Act, 5

U.S.C. Section 801 et seq., as added by

the Small Business Regulatory

Enforcement Fairness Act of 1996,

generally provides that before a rule

may take effect, the Agency

promulgating the rule must submit a

rule report, which includes a copy of

the rule, to each House of the Congress

and the Comptroller General of the

United States. Section 804, however,

exempts from Section 801 the following

types of rules: rules of particular

applicability; rules relating to Agency

management or personnel; and rules of

Agency organization, procedure, or

practice that do not substantially affect

the rights or obligations of non-Agency

parties, 5 U.S.C. Section 804(3). EPA is

not required to submit a rule report

regarding today’s action under Section

801 because this is rule of particular

applicability.

Because the rule now being

withdrawn is currently effective, EPA

also finds that good cause exists under

section 3010(b)(3) of RCRA (42 U.S.C.

6903(b)(3)) to publish this removal of

the site-specific regulation with an

immediate effective date, rather than

having it take effect in 30 days. See 5

U.S.C. 553(d)(3). Today’s removal of the

direct final rule affects only one facility,

and is limited in its scope to a removal

of a temporary conditional deferral of a

relatively narrow set of RCRA

regulations. As such, the deferral was