Federal Register / Vol. 65, No. 121 / Thursday, June 22, 2000 / Rules and Regulations 38765

ENVIRONMENTAL PROTECTION

AGENCY

40 CFR Part 180

[OPP–301009; FRL–6590–7]

RIN 2070–AB78

Clodinafop-propargyl; Pesticide

Tolerance

AGENCY: Environmental Protection

Agency (EPA).

ACTION: Final rule.

SUMMARY: This regulation establishes

tolerances for combined residues of

clodinafop-propargyl and its acid

metabolite in or on wheat, grain; wheat,

forage; wheat, hay; and wheat, straw.

Novartis Crop Protection, Inc. requested

these tolerances under the Federal Food,

Drug, and Cosmetic Act, as amended by

the Food Quality Protection Act of 1996.

DATES: This regulation is effective June

22, 2000. Objections and requests for

hearings, identified by docket control

number OPP–301009, must be received

by EPA on or before August 21, 2000.

ADDRESSES: Written objections and

hearing requests may be submitted by

mail, in person, or by courier. Please

follow the detailed instructions for each

method as provided in Unit VI. of the

‘‘SUPPLEMENTARY INFORMATION.’’

To ensure proper receipt by EPA, your

objections and hearing requests must

identify docket control number OPP–

301009 in the subject line on the first

page of your response.

FOR FURTHER INFORMATION CONTACT By

mail: Joanne I. Miller, Registration

Division (7505C), Office of Pesticide

Programs, Environmental Protection

Agency, 1200 Pennsylvania Ave.,

NW.,Washington, DC 20460; telephone

number: 703–305–6224; and e-mail

address: miller.joanne@epa.gov.

SUPPLEMENTARY INFORMATION:

I. General Information

A. Does this Action Apply to Me?

You may be affected by this action if

you are an agricultural producer, food

manufacturer, or pesticide

manufacturer. Potentially affected

categories and entities may include, but

are not limited to:

Categories NAICS Examples of potentially affected entities

Industry 111 Crop production

112 Animal production

311 Food manufacturing

32532 Pesticide manufacturing

This listing is not intended to be

exhaustive, but rather provides a guide

for readers regarding entities likely to be

affected by this action. Other types of

entities not listed in the table could also

be affected. The North American

Industrial Classification System

(NAICS) codes have been provided to

assist you and others in determining

whether or not this action might apply

to certain entities. If you have questions

regarding the applicability of this action

to a particular entity, consult the person

listed under ‘‘FOR FURTHER

INFORMATION CONTACT.’’

B. How Can I Get Additional

Information, Including Copies of this

Document and Other Related

Documents?

1. Electronically. You may obtain

electronic copies of this document, and

certain other related documents that

might be available electronically, from

the EPA Internet Home Page at http://

www.epa.gov/. To access this

document, on the Home Page select

‘‘Laws and Regulations’’ and then look

up the entry for this document under

the ‘‘Federal Register—Environmental

Documents.’’ You can also go directly to

the Federal Register listings at http://

www.epa.gov/fedrgstr/.

2. In person. The Agency has

established an official record for this

action under docket control number

OPP–301009. The official record

consists of the documents specifically

referenced in this action, and other

information related to this action,

including any information claimed as

Confidential Business Information (CBI).

This official record includes the

documents that are physically located in

the docket, as well as the documents

that are referenced in those documents.

The public version of the official record

does not include any information

claimed as CBI. The public version of

the official record, which includes

printed, paper versions of any electronic

comments submitted during an

applicable comment period is available

for inspection in the Public Information

and Records Integrity Branch (PIRIB),

Rm. 119, Crystal Mall #2, 1921 Jefferson

Davis Hwy., Arlington, VA, from 8:30

a.m. to 4 p.m., Monday through Friday,

excluding legal holidays. The PIRIB

telephone number is (703) 305–5805.

II. Background and Statutory Findings

In the Federal Register of April 26,

2000 (65 FR 24471–24477) (FRL– 6554–

2), EPA issued a notice pursuant to

section 408 of the Federal Food, Drug,

and Cosmetic Act (FFDCA), 21 U.S.C.

346a as amended by the Food Quality

Protection Act of 1996 (FQPA) (Public

Law 104–170) announcing the amended

filing of a pesticide petition (PP) for

tolerance by Novartis Crop Protection,

Inc., P.O. Box 18300, Greensboro, NC

27419. This notice included a summary

of the petition prepared by Novartis

Crop Protection, Inc., the registrant.

There were no comments received in

response to the notice of filing.

The petition requested that 40 CFR

part 180 be amended by establishing

tolerances for combined residues of the

herbicide clodinafop-propargyl

(propanoic acid, 2-[4-[(5-chloro-3-

fluoro-2-pyridinyl)oxy]phenoxy]-,2-

propynyl ester, (2R)-) and its acid

metabolite, CGA–193469, (propanoic

acid, 2-[4-[(5-chloro-3-fluoro-2-

pyridinyl)oxy]phenoxy]-, (2R)-), in or on

wheat, grain at 0.1 part per million

(ppm); wheat, forage at 0.1 ppm; wheat,

hay at 0.1 ppm; and wheat, straw at 0.5

ppm.

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. For

further discussion of the regulatory

requirements of section 408 and a

complete description of the risk

assessment process, see the final rule on

Bifenthrin Pesticide Tolerances (62 FR

62961, November 26, 1997) (FRL–5754–

7).

III. 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 and to make a determination

on aggregate exposure, consistent with

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

38766 Federal Register / Vol. 65, No. 121 / Thursday, June 22, 2000 / Rules and Regulations

combined residues of clodinafoppropargyl and its acid metabolite on

wheat, grain at 0.1 ppm; wheat, forage

at 0.1 ppm; wheat, hay at 0.1 ppm; and

wheat, straw at 0.5 ppm. EPA’s

assessment of exposures and risks

associated with establishing the

tolerance 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 clodinafoppropargyl are discussed in this unit as

well as the no observed adverse effect

level (NOAEL) and the lowest observed

adverse effect level (LOAEL) from the

toxicity studies reviewed.

TABLE 1.—SUBCHRONIC, CHRONIC AND OTHER TOXICITY

Guideline No./ Study Type Results

870.3100 28-Day Oral Gavage ............... NOAEL <5 mg/kg

LOAEL = 5 mg/kg for M and F based on liver toxicity (enzyme changes),

870.3100 13-Week Oral Toxicity in Rodent.NOAEL = M: 0.9 mg/kg; F: 8.2 mg/kg/day

LOAEL = M: 120 ppm (8.2 mg/kg/day); F: 1000 ppm (71.1 mg/kg/day) decreased body weight; based

on increased liver weights and enzymes (AlPtase); decreased thymus weight (atrophy). Reversed

after 28 day recovery period.

870.3100 13-Week Oral Toxicity in Mice NOAEL = M: 0.9 mg/kg/day; F: 1.1 mg/kg/day

LOAEL = M: 7.3 mg/kg/day ; F: 8.6 mg/kg/day based on clinical chemistry; glucose, sodium, and

chloride increases and hepatocellular hypertrophy in males and females.

870.3150 90-Day Oral Toxicity in Dogs .. The NOAEL = M: 0.346 mg/kg/day, F: 1.89 mg/kg/day.

The LOAEL = M: 1.73 mg/kg/day ; F: 7.16 mg/kg/day based on occurrence of skin lesions.

870.3200 28-Day Dermal Toxicity in

Rats.

Systemic NOAEL = 50 mg/kg/day

Systemic LOAEL = 200 mg/kg based on dose-related increases in liver weights and clinical signs

(piloerection and hunched posture) in male rats.

Dermal NOAEL = 1000 mg/kg/day.

870.3700a Prenatal Developmental in

Rats.

Maternal NOAEL = 160 mg/kg/day

Maternal LOAEL > 160 mg/kg/day based on lack of effect.

Developmental NOAEL = 5 mg/kg/day

Developmental LOAEL = 40 mg/kg/day based on increased incidences of bilateral distension and torsion of the ureters, unilateral 14th ribs, and incomplete ossification of the metacarpals and various

cranial bones (parietals, interparietals, occipital, and squamosal).

870.3700b Prenatal Developmental in

Rabbits.

Maternal NOAEL = 25 mg/kg/day pMaternal LOAEL = 125 mg/kg/day based on mortality, clinical

signs and body weight loss

Developmental NOAEL = 125 mg/kg/day

Developmental LOAEL > 125 mg/kg/day

870.3800 Two Generation Reproduction Parental/Systemic NOAEL = 3.2 mg/kg/day.

Parental/Systemic LOAEL = 31.7 mg/kg/day based on decrease in body weight gain, reduced food

consumption, increased liver and kidney weights and histopathological changes in the liver and

renal tubules.

Offspring NOAEL = 3.2 mg/kg/day

Offspring LOAEL = 31.7 mg/kg/day based on reduced viability, decreased pup body weight and dilatation of renal pelvis.

Reproductive NOAEL = 64.2 mg/kg/day.

Reproductive LOAEL  ́ 64.2 mg/kg/day

870.4100b Chronic Toxicity Nonrodent .. NOAEL = M: 3.38 mg/kg/day; F: 3.37 mg/kg/day

LOAEL = M: 15.2 mg/kg/day; F: 16.7 mg/kg/day based on occurrence of skin lesions, clinical signs,

and reduced body weight gain and food consumption.

870.4200b Carcinogenicity Mice ............. NOAEL = M: 1.10 mg/kg/day; F: 1.25 mg/kg/day

LOAEL = M: 11.0 mg/kg/day; F: 12.6 mg/kg/day based on increase in liver enzyme activity and liver

weights. Under the conditions of this study, clodinafop-propargyl induced hepatocellular tumors at

29.6 mg/kg. The chemical was tested at doses sufficient to measure its carcinogenic potential.

870.4300 Chronic/Oncogenicity in the

Rat.

NOAEL = M:0.03 mg/kg/day ; F: 0.03 mg/kg/day

LOAEL = M: 0.3 mg/kg/day; F: 0.4 mg/kg/day based on hepatocytic hypertrophy, chronic progressive

nephropathy, and tubular pigmentation.

Under the conditions of this study, treatment with clodinafop-propargyl increased the incidence of

prostate and ovarian tumors in rats at 750 ppm. For males, an increased incidence of prostate adenoma was seen in the high-dose group. The chemical was administered at a dose sufficient to test

its carcinogenic potential.

Federal Register / Vol. 65, No. 121 / Thursday, June 22, 2000 / Rules and Regulations 38767

TABLE 1.—SUBCHRONIC, CHRONIC AND OTHER TOXICITY—Continued

Guideline No./ Study Type Results

870.5100 Gene Mutation Salmonella

and Escherichia/Liver Microsome Test.

Negative for mutagenicity.

870.5200 Gene Mutation Mutation Test

with Chinese Hamster cells V79.

Negative for mutagenicity.

870.5315 Chromosome Studies; Human

Lymphocytes in vitro.

Owing to the conflicting results from the cytotoxicity assessment and the presence of rare complex

chromosome aberrations both with and without S9 activation, the study is considered inconclusive.

870.5395 Micronucleus Test (Chinese

Hamster).

No clear evidence that clodinafop-propargyl induced a clastogenic or aneugenic effect in either sex at

any dose or sacrifice time.

870.5550 DNA Repair Human Fibroblasts.Compound precipitation was seen at doses  ́ 320 μg/mL: there was, however, no indication of a

cytotoxic effect at any dose. The positive control induced the expected marked increases in unscheduled DNA synthesis (UDS). There was, however, no evidence that CGA–184927 in the absence of S9 activation induced a genotoxic response in either trial.

870.5550 DNA Repair Rat Hepatocytes Compound precipitation was noted at levels  ́ 4000 μ/mL. Lethality was apparent in the preliminary

cytotoxicity test at 94.8 μg/mL. The positive control induced the expected marked increases in

UDS. There was, however, no evidence that clodinafop-propargyl induced a genotoxic response in

either trial.

870.7485 Metabolism and Pharmacokinetics.The main metabolite was CGA–193469 (76% in male urine). Additional 5% was in the form of taurine

conjugate of CGA–193469. Similar distribution was found in feces.

870.7485 Metabolism and Pharmacokinetics.The major metabolite in urine and feces was determined to be CGA–193469, accounting for about

36% to 47% of the administered dose (AD) for males, and 80% to 85% of the AD for females. In

addition, 11 minor metabolite fractions were isolated from urine and feces. Three were further identified as reference materials CGA– 193468, CGA–214111 and unchanged clodinofop-propargyl.

Special Study: Determination Of Residues As CGA–193469 in Abdominal

Fat After A 3-Month Oral Toxicity

Study in Rat.

There was a dose-dependent increase in clodinofop-propargyl residues in fat samples from both

sexes taken at the end of treatment (14 weeks) and after the 4-week recovery period (18 weeks).

Concentrations of clodinofop-propargyl were higher in male rats at all dose levels tested. With the

exception of low-dose group males, for all remaining groups, residues in the fat at 18 weeks had

decreased by between 40%—51.5% of the 14 week value.

Special Study Determination of Residues as CGA–193469 in Abdominal

Fat After 12 Months in Study.

1 ppm and 10 ppm, the concentration of CGA–184927 in the abdominal fat was higher in males when

compared to females. At 300 and 750 ppm, the concentration of CGA–184927 in the abdominal fat

was comparable between males and females. The results of this study also indicate that the

clodinafop-propargyl residue in fat is reduced after 1 year of treatment compared to 3 month treatment.

Special Study: The Effect Of CGA–

184927 on Selected Biochemical Parameters in the Rat Liver Following

Subchronic Administration.

The effects of clodinafop-propargyl on selected liver enzymes in the rat were similar to the effects

seen after subchronic treatment with known peroxisome proliferators (hypolipidemic compounds,

phenoxyacetic acid derivatives). Hence, clodinafop-propargyl was considered to most likely be a

peroxisome proliferator in the rat liver.

Special Study: Apparently Clonal Thyroid Adenomas May Contain Heterogeneously Growing and Functioning

Cell Subpopulations. New Frontiers in

Thyroidology, p. 901–905, 1986.

The asynchronous growth rate of subsets of cells within the old adenomas as well as the intercellular

heterogeneity of the endocytotic response to TSH suggests that clonal thyroid adenomas may acquire new qualities and can modify gene expression via much debated mechanism. The author

concludes that the growth of benign thyroid tumors and progression does not require a change in

genomic expression in any cell. The apparent heterogeneity of a tumor does not necessarily exclude its monoclonal origin.

Special Study: Assessment of

Hyperplastic and Neoplastic Lesions

of the Thyroid Gland. TIPS, Vol. 8, p.

511–514.

In cell cultures, TSH does not induce proliferation of human thyroid cells, but does stimulate the

growth of cells obtained from rat and dog thyroids. Conventional procedures of evaluating carcinogenicity tests by simply counting tumors in rodents treated with high doses, and by mathematical

extrapolation to the low doses to which humans are exposed, are not suitable for the proliferative

reactions of the thyroid gland. In assessing the human risk, relevant conclusions can only be drawn

if the physiological factors of growth control are known, and if the biological mechanisms by which

chemicals initiate focal proliferation and support their progression to tumors are considered.

Special Study: Stott, W.T. Chemically Induced Proliferation of Peroxisomes:

Implications for Risk Assessment.

Regulatory Toxicology and Pharmacology, Vol. 8, p. 125–159, 1988.

The author concludes that a more appropriate maximum tolerated dose (MTD) of a peroxisome proliferative agent in sensitive species would appear to be based upon evidence of the proliferation of

peroxisomes and the induction of peroxisomal enzymes capable of producing an increased

intracellular oxidative stress. Exceeding these dosages will only result in a predictable sequence of

events leading, ultimately, to tumor formation due to physiological adaptation of the animal to the

administered compound rather than from the direct effects of the compound itself.

38768 Federal Register / Vol. 65, No. 121 / Thursday, June 22, 2000 / Rules and Regulations

TABLE 1.—SUBCHRONIC, CHRONIC AND OTHER TOXICITY—Continued

Guideline No./ Study Type Results

Special Study Bieri, F. The Effect of

CGA–193469, the Free Acid Derivative of CGA–184927, on Peroxisomaloxidation in Primary Cultures of Rat,

Mouse, Marmoset and Guinea Pig

Hepatocytes.

This study characterized and compared the in vitroeffects of clodinafop-propargyl on selected parameters (i.e., cytotoxicity and induction of peroxisomal beta-oxidation) in primary hepatocytes from various species.

The monolayer cultures were treated with medium containing clodinafop-propargyl, CGA–193469 or

propargyl alcohol at the appropriate concentrations (0.1 to 100 μg/mL), or solvent controls and incubated for three days. Hepatocytes were then examined for morphological alterations and cell viability. The lactate dehydrogenase (LDH) activity was measured as an indicator of cytotoxicity. In addition, protein content of hepatocytes were measured to determine the membrane damage.

Peroxisomal beta-oxidation was measured in hepatocyte homogenates treated with [1-14]palmitoylCoA, a peroxisomal enzyme marker. Clodinafop-propargyl-induced cytotoxicity through propargyl alcohol.

Special Study Guyomard, C. (1992). Effects of CGA–193469, the Acid Derivative of CGA–184927, on the

Peroxisomal Beta-oxidation in Human

Hepatocytes.

Under the conditions of this study, neither CGA–193469 nor bezafibric acid induced peroxisomal

beta-oxidation in human hepatocytes, in vitro. However, in the absence of a known concurrent

human positive control to validate the test system, (i.e., a substance known to elicit peroxisomal

beta-oxidation in human hepatocytes,) this cannot be definitely concluded.

Special Study: Trendelenburg, C. Effects

on Selected Plasma Concentrations

and Biochemical Parameters in the

Liver upon Subchronic Administration

to Male Adult Rats.

Clodinafop-propargyl may act as a peroxisomal proliferating agent and alters monooxygenase activity

in subfamilies of cytochrome P450 which are known to be involved in the synthesis or catabolism of

steroid hormones.

B. Toxicological Endpoints

The dose at which no adverse effects

are observed (the NOAEL) from the

toxicology study identified as

appropriate for use in risk assessment is

used to estimate the toxicological level

of concern (LOC). However, the lowest

dose at which adverse effects of concern

are identified (the LOAEL) is sometimes

used for risk assessment if no NOAEL

was achieved in the toxicology study

selected. An uncertainty factor (UF) is

applied to reflect uncertainties inherent

in the extrapolation from laboratory

animal data to humans and in the

variations in sensitivity among members

of the human population as well as

other unknowns. An UF of 100 is

routinely used, 10X to account for

interspecies differences and 10X for

intra species differences.

For dietary risk assessment (other

than cancer) the Agency uses the UF to

calculate an acute or chronic reference

dose (acute RfD or chronic RfD) where

the RfD is equal to the NOAEL divided

by the appropriate UF (RfD=NOAEL/

UF). Where an additional safety factor is

retained due to concerns unique to the

FQPA, this additional factor is applied

to the RfD by dividing the RfD by such

additional factor. The acute or chronic

Population Adjusted Dose (aPAD or

cPAD) is a modification of the RfD to

accommodate this type of FQPA Safety

Factor.

For non-dietary risk assessments

(other than cancer) the UF is used to

determine the LOC. For example, when

100 is the appropriate UF (10X to

account for interspecies differences and

10X for intraspecies differences) the

LOC is 100. To estimate risk, a ratio of

the NOAEL to exposures (margin of

exposure (MOE) = NOAEL/exposure) is

calculated and compared to the LOC.

The linear default risk methodology

(Q*) is the primary method currently

used by the Agency to quantify

carcinogenic risk. The Q* approach

assumes that any amount of exposure

will lead to some degree of cancer risk.

A Q* is calculated and used to estimate

risk which represents a probability of

occurrence of additional cancer cases

(e.g., risk is expressed as 1 × 10-6 or one

in a million). Under certain specific

circumstances, MOE calculations will

be used for the carcinogenic risk

assessment. In this non-linear approach,

a ‘‘point of departure’’ is identified

below which carcinogenic effects are

not expected. The point of departure is

typically a NOAEL based on an

endpoint related to cancer effects

though it may be a different value

derived from the dose response curve.

To estimate risk, a ratio of the point of

departure to exposure (MOEcancer = point

of departure/exposures) is calculated.

TABLE 2. SUMMARY OF TOXICOLOGICAL DOSE AND ENDPOINTS FOR CLODINAFOP-PROPARGYL FOR USE IN HUMAN RISK

ASSESSMENT

Exposure Scenario Dose Used in Risk

Assessment, UF

FQPA SF 1 and Level of

Concern for Risk

Assessment

Study and Toxicological Effects

Acute Dietary females 13–

50 years of age.

NOAEL = 5 mg/kg/day

UF = 100 Acute RfD = 0.05 mg/kg/

day.

FQPA SF = 10X

aPAD = acute RfD ÷ FQPA

SF = 0.005 mg/kg/day.

Developmental Toxicity Study in Rats

LOAEL = 40 mg/kg/day based on increased

incidences of bilateral distension and torsion of the ureters, unilateral 14th ribs, and

incomplete ossification of the metacarpals

and various cranial bones (parietals,

interparietals, occipital, and squamosal) .

Federal Register / Vol. 65, No. 121 / Thursday, June 22, 2000 / Rules and Regulations 38769

TABLE 2. SUMMARY OF TOXICOLOGICAL DOSE AND ENDPOINTS FOR CLODINAFOP-PROPARGYL FOR USE IN HUMAN RISK

ASSESSMENT—Continued

Exposure Scenario Dose Used in Risk

Assessment, UF

FQPA SF 1 and Level of

Concern for Risk

Assessment

Study and Toxicological Effects

Acute Dietary infants and

children.

NOAEL = 25 mg/kg/day

UF = 100 ..........................................

Acute RfD = 0.25 mg/kg/day ............

FQPA SF = 3X aPAD =

acute RfD ÷ FQPA SF =

0.083 mg/kg/day

Developmental Toxicity Study in Rabbits

LOAEL = 125 mg/kg/day based on increased

mortality, clinical signs and body weight

loss

Acute Dietary general population.NOAEL = 25 mg/kg/day

UF = 100 ..........................................

Acute RfD = 0.25 mg/kg/day ............

FQPA SF = 1X

aPAD = acute RfD ÷ FQPA

SF = 0.25 mg/kg/day.

Developmental Toxicity Study in Rabbits

LOAEL = 125 mg/kg/day based on increased

mortality, clinical signs and body weight

loss

Chronic Dietary all populations.NOAEL = 0.03 mg/kg/day

UF = 100 ..........................................

Chronic RfD = 0.0003 mg/kg/day ....

FQPA SF = 10X

cPAD = chronic RfD ÷

FQPA SF = 0.00003 mg/

kg/day.

Chronic Toxicity Study in Rats

LOAEL = 0.3 mg/kg/day based on

Hepatocytic hypertrophy, chronic progressive nephropathy, and tubular pigmentation

1The reference to the FQPA Safety Factor refers to any additional safety factor retained due to concerns unique to the FQPA.

Carcinogenicity. In accordance with

the EPA Proposed EPA Weight-of-theEvidence Categories, August 1999, the

Agency’s Cancer Assessment Review

Committee (CARC) classified

clodinafop-propargyl as ‘‘likely to be

carcinogenic to humans’’ by the oral

route based on the occurrence of

prostate tumors in male rats, ovarian

tumors in female rats, and liver tumors

in both sexes of mice, as well as blood

vessel tumors in female mice. For the

quantification of human cancer risk, the

CARC recommended a linear low-dose

extrapolation approach based on the

most potent of these tumor types. This

approach is supported by possible

genotoxic potential and the lack of

confirmation of the mode of action of

clodinafop-propargyl. The most potent

unit risk, Q1

*(mg/kg/day)-1, of those

calculated for clodinafop-propargyl is

that for male mouse liver benign

hepatoma and/or carcinoma combined

tumor rates at 0.129 (mg/kg/day)-1 in

human equivalents.

C. Exposure Assessment

1. Dietary exposure from food and

feed uses. No tolerances have previously

been established for clodinafoppropargyl. Risk assessments were

conducted by EPA to assess dietary

exposures from clodinafop-propargyl in

food as follows:

i. Acute exposure. Acute dietary risk

assessments are performed for a fooduse pesticide if a toxicological study has

indicated the possibility of an effect of

concern occurring as a result of a one

day or single exposure. The Dietary

Exposure Evaluation Model (DEEM)

analysis evaluated the individual food

consumption as reported by

respondents in the USDA 1989–1992

nationwide Continuing Surveys of Food

Intake by Individuals (CSFII) and

accumulated exposure to the chemical

for each commodity. The following

assumptions were made for the acute

exposure assessments: (1) residues of

clodinafop-propargyl and its acid

metabolite would be present in/on

wheat at the tolerance level (0.1 ppm);

and (2) 100% of the wheat crop would

be treated.

ii. Chronic exposure. In conducting

this chronic dietary risk assessment the

Dietary Exposure Evaluation Model

(DEEM) analysis evaluated the

individual food consumption as

reported by respondents in the USDA

1989–1992 nationwide Continuing

Surveys of Food Intake by Individuals

(CSFII) and accumulated exposure to

the chemical for each commodity. The

following assumptions were made for

the chronic exposure assessments: (1)

residues of clodinafop-propargyl and its

acid metabolite would be present in/on

wheat at the anticipated residue level of

0.07 ppm; and (2) 4 percent of the wheat

crop would be treated. The anticipated

residue value of 0.07 ppm was derived

from the sum of the limit of quantitation

(LOQ) of clodinafop-propargyl (0.02

ppm) plus the LOQ of the acid

metabolite (0.05 ppm) in/on wheat

grain. The percent crop treated value of

4% assumes that the target pest, wild

oats, occurs on 10% of the wheat

acreage and that 40% of the affected

acreage could be treated.

iii. Cancer. A lifetime cancer risk

assessment was performed for the U.S.

total population. Lifetime cancer risk

was estimated by applying the Q1*

value of 0.129 (mg/kg/day)-1 to the

chronic dietary exposure estimate.

iv. Anticipated residue and percent

crop treated information. 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 5 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. 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 5

years from the date of issuance of this

tolerance.

Section 408(b)(2)(F) states that the

Agency may use data on the actual

percent of food treated for assessing

chronic dietary risk only if the Agency

can make the following findings:

Condition 1, that the data used are

reliable and provide a valid basis to

show what percentage of the food

derived from such crop is likely to

contain such pesticide residue;

Condition 2, that the exposure estimate

does not underestimate exposure for any

significant subpopulation group; and

Condition 3, if data are available on

pesticide use and food consumption in

a particular area, the exposure estimate

does not understate exposure for the

population in such area. In addition, the

Agency must provide for periodic

evaluation of any estimates used. To

provide for the periodic evaluation of

the estimate of percent crop treated

(PCT) as required by section

408(b)(2)(F), EPA may require

registrants to submit data on PCT.

The Agency used PCT information as

follows:

38770 Federal Register / Vol. 65, No. 121 / Thursday, June 22, 2000 / Rules and Regulations

A routine chronic dietary exposure

analysis for clodinafop-propargyl was

based on 4% of the wheat crop treated,

derived as follows. Of the

approximately 63 to 70 million acres of

wheat grown in the United States, about

6.5 million acres of wheat (or

approximately 10% of the total) are

treated to control the target pest, wild

oats. The petitioner expects to capture

up to 40% of the available market, or 2.5

million acres, representing 4% of the

total U.S. wheat crop (40% × 10% =

4%).

The Agency believes that the three

conditions previously discussed have

been met. With respect to Condition 1,

EPA finds that the PCT information

described above for clodinafoppropargyl used on wheat is reliable and

has a valid basis. The PCT information

is based on reliable estimates of the

potential market for clodinafoppropargyl and the petitioner’s estimate

of the market share it expects to capture.

EPA believes the petitioner’s estimate is

an overestimate. At the present time,

there are several competing products,

making it very unlikely that the

petitioner will gain 40% of the available

market when it enters the market. The

use of 4% in the chronic dietary

exposure assessment is, therefore,

considered conservative. As to

Conditions 2 and 3, regional

consumption information and

consumption information for significant

subpopulations is taken into account

through EPA’s computer-based model

for evaluating the exposure of

significant subpopulations including

several regional groups. Use of this

consumption information in EPA’s risk

assessment process ensures that EPA’s

exposure estimate does not understate

exposure for any significant

subpopulation group and allows the

Agency to be reasonably certain that no

regional population is exposed to

residue levels higher than those

estimated by the Agency. Other than the

data available through national food

consumption surveys, EPA does not

have available information on the

regional consumption of food to which

clodinafop-propargyl may be applied in

a particular area.

2. Dietary exposure from drinking

water. The Agency lacks sufficient

monitoring exposure data to complete a

comprehensive dietary exposure

analysis and risk assessment for

clodinafop-propargyl and its acid

metabolite in drinking water. Because

the Agency does not have

comprehensive monitoring data,

drinking water concentration estimates

are made by reliance on simulation or

modeling, taking into account data on

the physical characteristics of

clodinafop-propargyl and its acid

metabolite.

The Agency uses the Generic

Estimated Environmental Concentration

(GENEEC) or the Pesticide Root Zone/

Exposure Analysis Modeling System

(PRZM/EXAMS) to estimate pesticide

concentrations in surface water and

Screening Concentration in ground

water (SCI-GROW), which predicts

pesticide concentrations in

groundwater. In general, EPA will use

GENEEC (a tier 1 model) before using

PRZM/EXAMS (a tier 2 model) for a

screening-level assessment for surface

water. The GENEEC model is a subset of

the PRZM/EXAMS model that uses a

specific high-end runoff scenario for

pesticides. GENEEC incorporates a farm

pond scenario, while PRZM/EXAMS

incorporate an index reservoir

environment in place of the previous

pond scenario. The PRZM/EXAMS

model includes a percent crop area

factor as an adjustment to account for

the maximum percent crop coverage

within a watershed or drainage basin.

None of these models include

consideration of the impact processing

(mixing, dilution, or treatment) of raw

water for distribution as drinking water

would likely have on the removal of

pesticides from the source water. The

primary use of these models by the

Agency at this stage is to provide a

coarse screen for sorting out pesticides

for which it is highly unlikely that

drinking water concentrations would

ever exceed human health levels of

concern.

Since the models used are considered

to be screening tools in the risk

assessment process, the Agency does

not use estimated environmental

concentrations (EECs) from these

models to quantify drinking water

exposure and risk as a %RfD or %PAD.

Instead, drinking water levels of

comparison (DWLOCs) are calculated

and used as a point of comparison

against the model estimates of a

pesticide’s concentration in water.

DWLOCs are theoretical upper limits on

a pesticide’s concentration in drinking

water in light of total aggregate exposure

to a pesticide in food, and from

residential uses. Since DWLOCs address

total aggregate exposure to clodinafoppropargyl they are further discussed in

the aggregate risk sections below.

Based on the PRZM/EXAMS and SCIGROW models the estimated

environmental concentrations (EECs) of

clodinafop-propargyl in surface water

and ground water for acute exposures

are estimated to be 0.23 parts per billion

(ppb) for surface water and 5 × 10-6 ppb

for ground water. The EECs for chronic

exposures are estimated to be 0.0017

ppb for surface water and 5 × 10-6 ppb

for ground water. The estimated

environmental concentrations (EECs) of

the acid metabolite, CGA–193496, in

surface water and ground water for

acute exposures are estimated to be 1.1

ppb for surface water and 0.044 ppb for

ground water. The EECs for chronic

exposures are estimated to be 0.11 ppb

for surface water and 0.044 ppb for

ground water.

3. From non-dietary exposure. The

term ‘‘residential exposure’’ is used in

this document to refer to nonoccupational, non-dietary exposure

(e.g., for lawn and garden pest control,

indoor pest control, termiticides, and

flea and tick control on pets).

Clodinafop-propargyl is not registered

for use on any sites that would result in

residential exposure.

4. Cumulative exposure to substances

with a 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.’’

EPA does not have, at this time,

sufficient data to determine whether

clodinafop-propargyl has a common

mechanism of toxicity with other

substances or how to include this

pesticide in a cumulative risk

assessment. For the purposes of this

tolerance action, therefore, EPA has not

assumed that clodinafop-propargyl has a

common mechanism of toxicity with

other substances. For information

regarding EPA’s efforts to determine

which chemicals have a common

mechanism of toxicity and to evaluate

the cumulative effects of such

chemicals, see the final rule for

Bifenthrin Pesticide Tolerances (62 FR

62961, November 26, 1997).

D. Safety Factor for Infants and

Children

1. Safety factor for infants and

children i. In general. 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 prenatal

and postnatal toxicity and the

completeness of the data base on

toxicity and exposure 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 margin

of exposure (MOE) analysis or through

using uncertainty (safety) factors in

Federal Register / Vol. 65, No. 121 / Thursday, June 22, 2000 / Rules and Regulations 38771

calculating a dose level that poses no

appreciable risk to humans.

ii. Prenatal and postnatal sensitivity.

The Agency concluded that there is

concern for the increased susceptibility

of infants and children to exposure to

clodinafop-propargyl based on the

developmental toxicity study in rats

where increased skeletal effects were

observed at doses much lower (LOAEL

of 40 mg/kg/day) than the maternal

NOAEL (160 mg/kg/day). Although

there was no evidence of reproductive

toxicity, a fetotoxic effect was noted in

the two-generation reproduction study

in rats since reduced fetal viability,

decreased pup body weight, and

dilatation of renal pelvis were observed

in the offspring at doses that produced

relatively minimal parental toxicity

(decreased body weight gain, increased

liver and kidney weights with

histopathological changes).

iii. Conclusion. The toxicology

database for clodinafop-propargyl is

incomplete. Acute neurotoxicity,

subchronic neurotoxicity,

developmental neurotoxicity and in

vitro cytogenetics studies are required.

There is quantitative evidence of

increased susceptibility of the young

following in utero exposure to

clodinafop-propargyl in the prenatal

developmental study in rats, and there

is concern for qualitative increased

susceptibility in the 2-generation

reproduction study in rats. A

developmental neurotoxicity study has

been required based on the evidence of

potential endocrine disruption in the

mechanism studies with clodinafoppropargyl.

For the reasons given above, the

Agency concluded that the FQPA safety

factor be retained at 10x. When

assessing acute dietary exposure, the

safety factor is retained at 10x for the

females 13–50 years old population

subgroup since there are data gaps in

the toxicology database for clodinafoppropargyl including a developmental

neurotoxicity study and there is

quantitative evidence of increased

susceptibility following in utero

exposure to clodinafop-propargyl in the

prenatal developmental study in rats.

The safety factor can be reduced to 3x

for the infants and children population

subgroups when assessing acute dietary

exposure since the increased

susceptibility observed following in

utero exposure is only of concern for

females of childbearing age leaving only

the uncertainty due to the data gap for

the developmental neurotoxicity study.

The safety factor can be reduced to 1x

for all other populations subgroups not

included in females 13-50 years old and

infants and children when assessing

acute dietary exposure. The increased

susceptibility observed following in

utero exposure is only of concern for

females of childbearing age. The data

gap for developmental neurotoxicity is

of concern for infants and children.

When assessing the chronic dietary

exposure, the safety factor should be

retained at 10x for all population

subgroups since there is concern for

qualitative increased susceptibility of

the young demonstrated after repeated

oral exposures in the 2-generation

reproduction study and since there are

data gaps in the toxicology database

including a developmental

neurotoxicity study in rats.

E. Aggregate Risks and Determination of

Safety

To estimate total aggregate exposure

to a pesticide from food, drinking water,

and residential uses, the Agency

calculates DWLOCs which are used as a

point of comparison against the model

estimates of a pesticide’s concentration

in water (EECs). DWLOC values are not

regulatory standards for drinking water.

DWLOCs are theoretical upper limits on

a pesticide’s concentration in drinking

water in light of total aggregate exposure

to a pesticide in food and residential

uses. In calculating a DWLOC, the

Agency determines how much of the

acceptable exposure (i.e., the population

adjusted dose (PAD)) is available for

exposure through drinking water e.g.,

allowable chronic water exposure (mg/

kg/day) = cPAD—(average food +

residential exposure). This allowable

exposure through drinking water is used

to calculate a DWLOC.

A DWLOC will vary depending on the

toxic endpoint, drinking water

consumption, and body weights. Default

body weights and consumption values

as used by the USEPA Office of Water

are used to calculate DWLOCs: 2L/70 kg

(adult male), 2L/60 kg (adult female),

and 1L/10 kg (child). Default body

weights and drinking water

consumption values vary on an

individual basis. This variation will be

taken into account in more refined

screening-level and quantitative

drinking water exposure assessments.

Different populations will have different

DWLOCs. Generally, a DWLOC is

calculated for each type of risk

assessment used: acute, short-term,

intermediate-term, chronic, and cancer.

When EECs for surface water and

groundwater are less than the calculated

DWLOCs, OPP concludes with

reasonable certainty that exposures to

the pesticide in drinking water (when

considered along with other sources of

exposure for which OPP has reliable

data) would not result in unacceptable

levels of aggregate human health risk at

this time. Because OPP considers the

aggregate risk resulting from multiple

exposure pathways associated with a

pesticide’s use, levels of comparison in

drinking water may vary as those uses

change. If new uses are added in the

future, OPP will reassess the potential

impacts of residues of the pesticide in

drinking water as a part of the aggregate

risk assessment process.

1. Acute risk. Using the exposure

assumptions discussed in this unit for

acute exposure, the acute dietary

exposure from food to clodinafoppropargyl will occupy <1.0% of the

aPAD for the U.S. population, 7.5% of

the aPAD for nursing females 13 years

and older, the subgroup of adult females

with the highest estimated exposure,

and 1.0% of the aPAD for children 1 to

6 years old, the subgroup of infants and

children with the highest estimated

exposure. In addition, there is potential

for acute dietary exposure to clodinafoppropargyl in drinking water. After

calculating DWLOCs and comparing

them to the EECs for surface and ground

water, EPA does not expect the

aggregate exposure to exceed 100% of

the aPAD.

TABLE 3.—AGGREGATE RISK ASSESSMENT FOR ACUTE EXPOSURE TO CLODINAFOP-PROPARGYL

Population Subgroup aPAD

(mg/kg)

%

aPAD

(Food)

Surface Water EEC (ppb) Ground Water EEC (ppb) Acute DWLOC

(ppb)

U.S. Population ......................... 0.25 <1.0 0.23 ppb clodinafop-propargyl;

1.1 ppb CGA–193469

5 × 10-6 ppb clodinafop-propargyl; 0.044 ppb CGA–

193469

8.7 × 103

Females 13+ years old ............. 0.005 7.5 Same as above Same as above 1.4 × 102

Children, 1 to 6 years old ......... 0.083 1.0 Same as above Same as above 8.3 × 102

38772 Federal Register / Vol. 65, No. 121 / Thursday, June 22, 2000 / Rules and Regulations

2. Chronic risk. Using the exposure

assumptions described in this unit for

chronic exposure, EPA has concluded

that exposure to clodinafop-propargyl

from food will utilize 14% of the cPAD

for the U.S. population and 32% of the

cPAD for children 1 to 6 years old, the

subgroup of infants and children with

the highest estimated exposure. There

are no residential uses for clodinafoppropargyl that result in chronic

residential exposure to clodinafoppropargyl.

TABLE 4.—AGGREGATE RISK ASSESSMENT FOR CHRONIC (NON-CANCER) EXPOSURE TO CLODINAFOP-PROPARGYL

Population Subgroup

cPAD

mg/kg/

day

%

cPAD

(Food)

Surface Water EEC (ppb) Ground Water EEC (ppb) Chronic DWLOC

(ppb)

U.S. Population ......................... 0. 00003 14 0.0017 ppb clodinafop-propargyl; 0.11 ppb CGA–

193469

5 × 10-6 ppb clodinafop-propargyl; 0.044 ppb CGA–

193469

0.91

Children, 1 to 6 years old ......... 0. 00003 32 Same as above Same as above 0.21

3. Short-term risk. Short-term

aggregate exposure takes into account

residential exposure plus chronic

exposure to food and water (considered

to be a background exposure level).

Clodinafop-propargyl is not registered

for use on any sites that would result in

residential exposure. Therefore, the

aggregate risk is the sum of the risk from

food and water, which do not exceed

the Agency’s level of concern.

4. Intermediate-term risk.

Intermediate-term aggregate exposure

takes into account residential exposure

plus chronic exposure to food and water

(considered to be a background

exposure level).

Clodinafop-propargyl is not registered

for use on any sites that would result in

residential exposure. Therefore, the

aggregate risk is the sum of the risk from

food and water, which do not exceed

the Agency’s level of concern.

5. Aggregate cancer risk for U.S.

population. The DEEM analysis using

residues of 0.07 ppm for wheat and

assuming 4% crop treated estimates that

chronic exposure of the U.S. population

to clodinafop-propargyl will be

0.000004 mg/kg/day. Applying the Q1*

value of 0.129 (mg/kg/day)-1 results in a

food only risk of 5.3 × 10-7. Following

an aggregate dietary (food + water)

assessment for lifetime cancer risk, the

resulting DWLOC is 0.13 μg/L or ppb.

Using the models described above in

section C.2, the largest EEC value is for

surface water chronic exposure to the

acid metabolite, CGA–193469 (0.11

ppb). The cancer DWLOC is slightly

greater than the highest EEC.

Because the models used to obtain the

EECs for clodinafop-propargyl and

CGA–193469 are highly conservative

screening models not designed

specifically for estimating

concentrations in drinking water and

because of the conversative nature of the

food exposure assessment (anticipated

residues at LOQ for parent +

metabolite), EPA believes this aggregate

cancer dietary assessment will not

underestimate exposure and that

chronic dietary exposure from

clodinafop-propargyl residues in food

and drinking water will not exceed the

Agency’s level of concern for lifetime

aggregate cancer risk.

6. Determination of safety. Based on

these risk assessments, EPA concludes

that there is a reasonable certainty that

no harm will result to the general

population, and to infants and children

from aggregate exposure to clodinafoppropargyl residues.

IV. Other Considerations

A. Analytical Enforcement Methodology

The petitioner has proposed residue

analytical methods for tolerance

enforcement that use both normal and

reverse phase liquid chromatography

with UV detection (HPLC-UV). These

methods are currently being validated

by the Analytical Chemistry Branch

laboratories, BEAD (7503C), Office of

Pesticide Programs. Upon successful

completion of the EPA validation and

the granting of this registration these

methods will be forwarded to FDA for

publication in a future revision of the

Pesticide Analytical Manual, Vol-II

(PAM–II). Prior to publication in PAMII and upon request, the methods will be

available prior to the harvest season

from the Analytical Chemistry Branch

(ACB), BEAD (7503C), Environmental

Science Center, 701 Mapes Road, Fort

George G. Meade, MD 20755–5350;

contact Francis D. Griffith, Jr, telephone

(410) 305–2905, e-mail

griffith.francis@epa.gov. The analytical

standards for these methods are also

available from the EPA National

Pesticide Standard Repository at the

same location.

B. International Residue Limits

A default Maximum Residue Limit of

0.1 mg/kg has been established in

Canada for residues of clodinafoppropargyl on wheat. A Mexican limit

exists for clodinafop-propargyl on wheat

at 0.050 ppm. There are no Codex

tolerances for clodinafop-propargyl on

wheat. Therefore, no compatibility

issues exist with Codex in regard to the

proposed U.S. tolerances discussed in

this review.

C. Conditions

The registration of clodinafoppropargyl will be time-limited and

conditioned upon submission of

additional information/data to satisfy

certain toxicology, residue chemistry,

ecological effects and environmental

fate data deficiencies. Several guideline

requirements are either data gaps or are

only partially fulfilled, and the

additional information is required to

confirm and/or refine the parameters of

the Agency’s risk assessment.

Deficiencies exist in the following areas:

toxicology (neurotoxicity and

cytogenetics); residue chemistry (nature

of the residue in plants and animals,

analytical methods, storage stability,

magnitude of the residue in wheat and

processed commodities, and rotational

crop data); ecological effects (avian

reproduction and seedling emergence/

vegetative vigor); and environmental

fate (hydrolysis, photolysis in water,

anaerobic and aerobic soil metabolism,

adsorption/desorption and field

dissipation). Because of these

deficiencies, the Agency incorporated

several conservative assumptions into

the risk assessment for clodinafoppropargyl, including the use of the limit

of quantitation (0.07 ppm) as the

anticipated residue in wheat and the

assumption of 4% crop treated in the

chronic and cancer risk assessments.

Therefore, despite the data deficiencies

noted above, the Agency believes the

available data and risk assessment

support the determination that there is

a reasonable certainty that no harm will

result to the general population, and to

infants and children, from aggregate

exposure to clodinafop-propargyl

residues.

Federal Register / Vol. 65, No. 121 / Thursday, June 22, 2000 / Rules and Regulations 38773

V. Conclusion

Therefore, tolerances are established

for combined residues of clodinafoppropargyl (propanoic acid, 2-[4-[(5-

chloro-3-fluoro-2-

pyridinyl)oxy]phenoxy]-,2-propynyl

ester, (2R)-) and its acid metabolite

(propanoic acid, 2-[4-[(5-chloro-3-

fluoro-2-pyridinyl)oxy]phenoxy]-, (2R)-

)], in or on wheat, grain at 0.1 ppm;

wheat, forage at 0.1 ppm; wheat, hay at

0.1 ppm; and wheat, straw at 0.5 ppm.

VI. Objections and Hearing Requests

Under section 408(g) of the FFDCA, as

amended by the FQPA, any person may

file an objection to any aspect of this

regulation and may also request a

hearing on those objections. The EPA

procedural regulations which govern the

submission of objections and requests

for hearings appear in 40 CFR part 178.

Although the procedures in those

regulations require some modification to

reflect the amendments made to the

FFDCA by the FQPA of 1996, EPA will

continue to use those procedures, with

appropriate adjustments, until the

necessary modifications can be made.

The new section 408(g) provides

essentially the same process for persons

to ‘‘object’’ to a regulation for an

exemption from the requirement of a

tolerance issued by EPA under new

section 408(d), as was provided in the

old FFDCA sections 408 and 409.

However, the period for filing objections

is now 60 days, rather than 30 days.

A. What Do I Need to Do to File an

Objection or Request a Hearing?

You must file your objection or

request a hearing on this regulation in

accordance with the instructions

provided in this unit and in 40 CFR part

178. To ensure proper receipt by EPA,

you must identify docket control

number OPP–301009 in the subject line

on the first page of your submission. All

requests must be in writing, and must be

mailed or delivered to the Hearing Clerk

on or before August 21, 2000.

1. Filing the request. Your objection

must specify the specific provisions in

the regulation that you object to, and the

grounds for the objections (40 CFR

178.25). If a hearing is requested, the

objections must include a statement of

the factual issues(s) on which a hearing

is requested, the requestor’s contentions

on such issues, and a summary of any

evidence relied upon by the objector (40

CFR 178.27). 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.

Mail your written request to: Office of

the Hearing Clerk (1900), Environmental

Protection Agency, 1200 Pennsylvania

Ave., NW., Washington, DC 20460. You

may also deliver your request to the

Office of the Hearing Clerk in Rm. C400,

Waterside Mall, 401 M St., SW.,

Washington, DC 20460. The Office of

the Hearing Clerk is open from 8 a.m.

to 4 p.m., Monday through Friday,

excluding legal holidays. The telephone

number for the Office of the Hearing

Clerk is (202) 260–4865.

2. Tolerance fee payment. If you file

an objection or request a hearing, you

must also pay the fee prescribed by 40

CFR 180.33(i) or request a waiver of that

fee pursuant to 40 CFR 180.33(m). You

must mail the fee to: EPA Headquarters

Accounting Operations Branch, Office

of Pesticide Programs, P.O. Box

360277M, Pittsburgh, PA 15251. Please

identify the fee submission by labeling

it ‘‘Tolerance Petition Fees.’’

EPA is authorized to waive any fee

requirement ‘‘when in the judgement of

the Administrator such a waiver or

refund is equitable and not contrary to

the purpose of this subsection.’’ For

additional information regarding the

waiver of these fees, you may contact

James Tompkins by phone at (703) 305–

5697, by e-mail at

tompkins.jim@epa.gov, or by mailing a

request for information to Mr. Tompkins

at Registration Division (7505C), Office

of Pesticide Programs, Environmental

Protection Agency, 1200 Pennsylvania

Ave., NW., Washington, DC 20460.

If you would like to request a waiver

of the tolerance objection fees, you must

mail your request for such a waiver to:

James Hollins, Information Resources

and Services Division (7502C), Office of

Pesticide Programs, Environmental

Protection Agency, 1200 Pennsylvania

Ave., NW., Washington, DC 20460.

3. Copies for the Docket. In addition

to filing an objection or hearing request

with the Hearing Clerk as described in

Unit VI.A., you should also send a copy

of your request to the PIRIB for its

inclusion in the official record that is

described in Unit I.B.2. Mail your

copies, identified by docket control

number OPP–301009, to: Public

Information and Records Integrity

Branch, Information Resources and

Services Division (7502C), Office of

Pesticide Programs, Environmental

Protection Agency, 1200 Pennsylvania

Ave., NW., Washington, DC 20460. In

person or by courier, bring a copy to the

location of the PIRIB described in Unit

I.B.2. You may also send an electronic

copy of your request via e-mail to: oppdocket@epa.gov. Please use an ASCII

file format and avoid the use of special

characters and any form of encryption.

Copies of electronic objections and

hearing requests will also be accepted

on disks in WordPerfect 6.1/8.0 file

format or ASCII file format. Do not

include any CBI in your electronic copy.

You may also submit an electronic copy

of your request at many Federal

Depository Libraries.

B. When Will the Agency Grant a

Request for a Hearing?

A request for a hearing will be granted

if the Administrator determines that the

material submitted shows the following:

There is a 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(s) in the manner sought by the

requestor would be adequate to justify

the action requested (40 CFR 178.32).

VII. Regulatory Assessment

Requirements

This final rule establishes a tolerance

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) (Public

Law 104–4). Nor does it require any

prior consultation as specified by

Executive Order 13084, entitled

Consultation and Coordination with

Indian Tribal Governments (63 FR

27655, May 19, 1998); 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 or any

Agency action under Executive Order

13045, entitled Protection of Children

from Environmental Health Risks and

Safety Risks (62 FR 19885, April 23,

1997). This action does not involve any

38774 Federal Register / Vol. 65, No. 121 / Thursday, June 22, 2000 / Rules and Regulations

technical standards that would require

Agency consideration of voluntary

consensus standards pursuant to section

12(d) of the National Technology

Transfer and Advancement Act of 1995

(NTTAA), Public Law 104–113, section

12(d) (15 U.S.C. 272 note). Since

tolerances and exemptions that are

established on the basis of a petition

under FFDCA section 408(d), such as

the tolerance 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. In addition, the

Agency has determined that this action

will not have a substantial direct effect

on States, on the relationship between

the national government and the States,

or on the distribution of power and

responsibilities among the various

levels of government, as specified in

Executive Order 13132, entitled

Federalism (64 FR 43255, August 10,

1999). Executive Order 13132 requires

EPA to develop an accountable process

to ensure ‘‘meaningful and timely input

by State and local officials in the

development of regulatory policies that

have federalism implications.’’ ‘‘Policies

that have federalism implications’’ is

defined in the Executive Order to

include regulations that have

‘‘substantial direct effects on the States,

on the relationship between the national

government and the States, or on the

distribution of power and

responsibilities among the various

levels of government.’’ This final rule

directly regulates growers, food

processors, food handlers and food

retailers, not States. This action does not

alter the relationships or distribution of

power and responsibilities established

by Congress in the preemption

provisions of FFDCA section 408(n)(4).

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 final

rule in the Federal Register. This final

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: June 6, 2000.

Susan B. Hazen,

Acting Director, 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. 321(q), (346a) and

371.

2. Section 180.559 is added to read as

follows:

§ 180.559 Clodinafop-propargyl;

tolerances for residues.

(a) General. Tolerances are

established for combined residues of

clodinafop-propargyl (propanoic acid, 2-

[4-(5-chloro-3-fluoro-2-

pyridinyl)oxy]phenoxy]-,2-propynyl

ester, (2R)-) and its acid metabolite

(propanoic acid, 2-[4-[(5-chloro-3-

fluoro-2-pyridinyl)oxy]phenoxy]-, (2R)-

), in or on wheat, grain at 0.1 ppm ;

wheat, forage at 0.1 ppm; wheat, hay at

0.1 ppm; and wheat, straw at 0.50 ppm.

Commodity Parts per

million

Wheat, forage ........................... 0.1

Wheat, grain ............................. 0.1

Wheat, hay ............................... 0.1

Wheat, straw ............................. 0.5

(b) Section 18 emergency exemptions.

[Reserved]

(c) Tolerances with regional

registrations. [Reserved]

(d) Indirect or inadvertent residues.

[Reserved]

[FR Doc. 00–15715 Filed 6–21–00; 8:45 am]

BILLING CODE 6560–50–F

ENVIRONMENTAL PROTECTION

AGENCY

40 CFR Part 300

[FRL–6718–4]

National Oil and Hazardous

Substances Pollution Contingency

Plan; National Priorities List

AGENCY: Environmental Protection

Agency (EPA).

ACTION: Direct final rule and request for

comments.

SUMMARY: EPA Region 5 announces the

Partial Deletion of the Motor Wheel

Disposal Superfund Site from the

National Priorities List (NPL) and

requests public comment on this action.

Specifically, 3.45 acres of land would be

deleted from the Site. The NPL

constitutes Appendix B of 40 CFR part

300 to the National Oil and Hazardous

Substances Pollution Contingency Plan

(NCP), which EPA promulgated

pursuant to section 105 of the

Comprehensive Environmental

Response, Compensation, and Liability

Act of 1980 (CERCLA), as amended.

EPA is taking this action because the

Remedial Investigation (RI) has shown

that the release poses no significant

threat to public health or the

environment and, therefore, remedial

measures are not appropriate for the

3.45 acres of land. EPA, in consultation

with the State of Michigan, has

determined that no further response is

appropriate. Moreover, EPA and the

State have determined that remedial

activities conducted at the 3.45 acres of

land to date have been protective of

public health, welfare, and the

environment.

DATES: This ‘‘direct final’’ action will be

effective August 21, 2000 unless U.S.

EPA receives dissenting comments by

July 24, 2000. If written dissenting

comments are received, EPA will

publish a timely withdrawal of the rule

in the Federal Register informing the

public that the rule will not take effect.

ADDRESSES: Comments may be mailed to

Gladys Beard, Associate Remedial

Project Manager, Superfund Division,

U.S. EPA, Region 5 77 W. Jackson Blvd.

(SR–6J), Chicago, IL 60604.

Comprehensive information on the site

is available at U.S. EPA’s Region 5 office

and at the local information repository

located at: The Lansing Public Library,

Reference Section, 401 Capital Ave.,

Lansing, MI 48933. Requests for

comprehensive copies of documents

should be directed formally to the

Region 5 Docket Office. The address and

phone number for the Regional Docket

Officer is Jan Pfundheller (H–7J), U.S.

EPA, Region 5, 77 W. Jackson Blvd.,

Chicago, IL 60604, (312) 353–5821.

FOR FURTHER INFORMATION CONTACT:

Heather Nelson, Remedial Project

Manager, at (312) 353–0685 (SR–6J), or

Gladys Beard, Associate Remedial

Project Manager, Superfund Division

(SR–6J), U.S. EPA, Region 5, 77 W.

Jackson Blvd., Chicago, IL 60604, (312)

886–7253 or Jennifer Ostermeier (P–

19J), Office of Public Affairs, U.S. EPA,

Region 5 77 W. Jackson Blvd.,Chicago,

IL 60604, (312) 353–0618.

SUPPLEMENTARY INFORMATION: