Federal Register / Vol. 63, No. 91 /Tuesday, May 12, 1998 /Rules and Regulations 26089

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.

X. 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 the 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 27, 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. Section 180.507 is amended in

paragraph (b) by alphabetically adding

the following commodities to the table

to read as follows:

§ 180.507 Azoxystrobin; tolerances for

residues.

* * * * *

(b) * * *

Commodity Parts per million Expiration/Revocation Date

* * * * * * *

Cucurbits .............................................................................................. 1.0 6/30/99

* * * * * * *

Watercress ........................................................................................... 1.0 6/30/99

* * * * *

[FR Doc. 98–12578 Filed 5–11–98; 8:45 am]

BILLING CODE 6560–50–F

ENVIRONMENTAL PROTECTION

AGENCY

40 CFR Part 180

[OPP–300647; FRL–5787–7]

RIN 2070–AB78

Myclobutanil; Pesticide Tolerance.

AGENCY: Environmental Protection

Agency (EPA).

ACTION: Final rule.

SUMMARY: This regulation establishes a

tolerance for the fungicide myclobutanil

[alpha-butyl-alpha-(4-chlorophenyl)-1H1,2,4-triazole-1-propanenitrile] and its

metabolite alpha-(3-hydroxybutyl)-

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

triazole-1-propanenitrile (free and

bound) in or on bananas (post-harvest).

Rohm and Haas Company requested this

tolerance under the Federal Food, Drug

and Cosmetic Act (FFDCA), as amended

by the Food Quality Protection Act of

1996 (FQPA) (Pub. L. 104-170).

DATES: This regulation is effective May

12, 1998. Objections and requests for

hearings must be received by EPA on or

before July 13, 1998.

ADDRESSES: Written objections and

hearing requests, identified by the

docket control number, [OPP–300647],

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–

300647], 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 or 6.1 file

format or ASCII file format. All copies

of objections and hearing requests in

electronic form must be identified by

the docket control number [OPP–

300647]. 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: Mary L. Waller, 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, Rm 247, 1921 Jefferson Davis

Hwy., Arlington, VA, (703) 308-9354, email: waller.mary@epamail.epa.gov.

SUPPLEMENTARY INFORMATION: In the

Federal Register of August 1, 1997 (62

FR 41379)(FRL–5732–4), 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 pesticide petition (PP)

2E4141 for a tolerance by Rohm and

Haas Company, 100 Independence Mall
26090 Federal Register / Vol. 63, No. 91 /Tuesday, May 12, 1998 /Rules and Regulations

West, Philadelphia, PA 19106-2399.

This notice included a summary of the

petition prepared by Rohm and Haas

Company, the registrant. There were no

comments received in response to the

notice of filing.

The petition requested that 40 CFR

180.443 be amended by establishing a

tolerance for combined residues of the

fungicide myclobutanil [alpha-butylalpha-(4-chlorophenyl)-1H-1,2,4-

triazole-1-propanenitrile] and its

metabolite alpha-(3-hydroxybutyl)-

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

triazole-1-propanenitrile (free and

bound) in or on bananas (post-harvest)

at 4.0 parts per million (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
Federal Register / Vol. 63, No. 91 /Tuesday, May 12, 1998 /Rules and Regulations 26091

considering average exposure from all

sources for representative population

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 myclobutanil and to make a

determination on aggregate exposure,

consistent with section 408(b)(2), for a

tolerance for myclobutanil [alpha-butylalpha-(4-chlorophenyl)-1H-1,2,4-

triazole-1-propanenitrile] and its

metabolite alpha-(3-hydroxybutyl)-

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

triazole-1-propanenitrile (free and

bound) on bananas (post-harvest) at 4.0

ppm. EPA’s assessment of the dietary

exposures and risks associated with

establishing the tolerance follows.

A. Toxicological Data Base

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 myclobutanil are

discussed below.

1. Acute studies. The primary eye

irritation for the technical is classified

as toxicity category I. All other acute

studies on the technical were classified

as either toxicity category III or IV.

There was a positive sensitizing

reaction.

2. Subchronic toxicity testing— i.

Rats. A subchronic feeding study in rats

was conducted for 13 weeks. The NOEL

was determined to be 1,000 ppm and

the lowest observed effect level (LOEL)

was 3,000 ppm based on increased liver

and kidney weights, hypertrophy and

necrosis in the liver, pigmentation in

convoluted kidney tubules and

vacuolated adrenal cortex.

ii. Dogs. A subchronic feeding study

in dogs conducted for 13 weeks resulted

in a NOEL of 10 ppm and an LOEL of

200 ppm. Technical myclobutanil was

tested at 0, 10, 200, 800, and 1,600 ppm

(0, 0.34, 7.26, 29.13, and 56.80

milligrams/kilogram (mg/kg)/day for

males and 0, 0.42, 7.88, 32.43 and 57.97

mg/kg/day for females). At 200 ppm,

and above, hepatocellular centrilobular

or midzonal hypertrophy was observed

in males. At 800 ppm and above, the

same effect was observed in females. In

addition, increases in alkaline

phosphatase, in absolute liver weights

in both sexes and in relative liver

weights in males were observed. At

1,600 ppm, all the previous effects plus

increases in relative liver weights in

females, a suggestion of mild red cell

destruction or mild anemia, and

decreases in body weight and food

consumption (possibly related to

palatability) were observed.

Subchronic dermal studies using a

40% active ingredient (ai) formulation

(40WP) and a 24.99% emulsifiable

concentrate formulation (2EC) of

myclobutanil conducted in rats resulted

in a NOEL for systemic effects of ≤100

mg ai/kg/day, a NOEL for skin irritation

of 10 mg ai/kg/day and an LEL of 100

mg ai/kg/day. The 2EC was applied at

either 1, 10 or 100 mg ai/kg and the

40WP applied at 100 mg ai/kg once per

day for a total of 19-20 treatments over

a 4 week period. No systemic effects

were observed at any dose level for

either formulation. Microscopic

changes, indicating irritation, were

observed in the skin.

3. Chronic toxicity studies. A 1-year

dog feeding study was conducted using

doses of 0, 10, 100, 400 and 1,600 ppm

(equivalent to doses of 0, 0.34, 3.09,

14.28 and 54.22 mg/kg body weight

(bwt)/day in males and 0, 0.40, 3.83,

15.68 and 58.20 mg/kg bwt/day in

females). The NOEL is 100 ppm (3.09

mg/kg/day for males and 3.83 mg/kg/

day for females) based upon

hepatocellular hypertrophy, increases in

liver weights, ‘‘ballooned’’ hepatocytes

and increases in alkaline phosphatase,

SGPT and GGT, and possible slight

hematological effects. The LOEL is 400

ppm (14.28 mg/kg/day for males and

15.68 mg/kg/day for females).

4. Carcinogenicity— i. Mice. A

carcinogenicity study in mice was

conducted by administering 90.4% ai

test material in the diet at 0, 20, 100, or

500 ppm (0, 2.7, 13.7 or 70.2 mg/kg/day

for males and 0, 3.2, 16.5, or 85.2 mg/

kg/day for females) for 24 months. The

NOEL was determined to be 100 ppm

(systemic) and the LOEL was 500 ppm

(systemic) based on increased MFO

(male and female), increased SGPT

(male) and increased absolute and

relative liver weights (male and female,

increased incidences and severity of

centrilobular hepatocytic hypertrophy,

Kupffer cell pigmentation, periportal

punctate vacuolation and individual

hepatocellular necrosis (male), and

increased incidences of focal

hepatocellular alterations and

multifocal hepatocellular vacuolation

(male and female). In this test, dose

levels in females was not high enough.

In the following test, higher doses were

tested (2,000 ppm; 393.5 mg/kg/day). No

carcinogenic effects were observed.
26092 Federal Register / Vol. 63, No. 91 /Tuesday, May 12, 1998 /Rules and Regulations

A carcinogenicity study in mice was

conducted for 18 months in which

myclobutanil technical (92.9% ai) was

administered in the diet at 0 and 2,000

ppm (393.5 mg/kg/day). No NOEL was

established. The LOEL was 2,000 ppm

(393.5 mg/kg/day) based on decreases in

body weight and body weight gain,

increases in liver weights,

hepatocellular vacuolation, necrosis of

single hypertrophied hepatocytes,

yellow-brown pigment in the Kupffer

cells and cytoplasmic eosinophilia and

hypertrophy of the cells of the zona

fasciculata area of the adrenal cortex.

Myclobutanil was not carcinogenic

under the conditions of the study.

ii. Rats. A carcinogenicity study in

rats was conducted by administering

technical myclobutanil (92.9% ai) in the

diet at doses of 0 and 2,500 ppm (125

mg/kg/day). No NOEL was established

(refer to next study). The LOEL was

2,500 ppm based on testicular atrophy

and decreases in testes weights,

increases in the incidences of

centrilobular to midzonal hepatocellular

enlargement and vacuolization in the

liver of both sexes, increases in bilateral

aspermatogenesis in the testes, increases

in the incidence of hypospermia and

cellular debris in the epididymides, and

increased incidence of arteritis/

periarteritis in the testes. No

carcinogenic effects were observed.

A chronic feeding/carcinogenicity

study was conducted in rats. Technical

(90.4% and 91.4% pure) myclobutanil

was administered in the diet for 24

months at 25/35/50, 100/140/200 and

400/560/800 ppm (2 weeks/2 weeks/to

termination; 0, 2.49, 9.84 or 39.21 mg/

kg/day for males; 0, 3.23, 12.86, or 52.34

mg/kg/day for females). The NOEL was

2.49 mg/kg/day and the LOEL was 9.84

mg/kg/day based on a decrease in testes

weights and increase in testicular

atrophy. Dosage rates were not high

enough (refer to previous study). No

carcinogenic effects were observed.

5. Developmental toxicity— i. Rabbits.

A teratology study was conducted in

rabbits at doses of 0, 20, 60 or 200 mg

ai/kg/day (technical myclobutanil;

90.4% ai) administered by oral gavage

on days 7-19 of gestation which resulted

in a maternal NOEL of 60 mg/kg/day

and a maternal LOEL of 200 mg/kg/day

based on reduced body weight and body

weight gain during the dosing period

and clinical signs of toxicity and

possibly abortions. The developmental

NOEL was 60 mg/kg/day and the

developmental LOEL was 200 mg/kg/

day based on increases in number of

resorptions, decreases in litter size and

decrease in the viability index.

ii. Rats. In a teratology study, rats

were treated with dosages of 0, 31.26,

93.77, 312.58 and 468.87 mg/kg/day by

oral gavage from gestation days 6-15.

The maternal NOEL was 93.8 mg/kg/day

and the maternal LOEL was 312.6 mg/

kg/day based on observation of rough

hair coat and salivation at 312.6 mg/kg/

day and salivation, alopecia,

desquamation and red exudate around

mouth at 468.87 mg/kg/day. The

developmental NOEL was 93.8 mg/kg/

day. The developmental LOEL was

312.6 mg/kg/day based on increased

incidences of 14th rudimentary and 7th

cervical ribs.

6. Reproductive toxicity. A 2-

generation rat reproduction study was

conducted with dosage rates of 0, 50,

200 and 1,000 ppm (equivalent to 0, 2.5,

10 and 50 mg/kg/day). The parental

(systemic) NOEL was 50 ppm (2.5 mg/

kg/day) and the parental (systemic)

LOEL was 200 ppm (10 mg/kg/day)

based on hepatocellular hypertrophy

and increases in liver weights. The

reproductive toxicity NOEL was 200

ppm (10 mg/kg/day) and reproductive

toxicity LOEL was 1,000 ppm (50 mg/

kg/day) based on an increased incidence

in the number of stillborns and atrophy

of the testes, epididymides and prostate.

The developmental NOEL was 200 ppm

(10 mg/kg/day) and the developmental

LOEL was 1,000 ppm (50 mg/kg/day)

based on a decrease in pup body weight

gain during lactation.

7. Mutagenicity. A reverse mutation

assay (Ames), point mutation in CHO/

HGPRT cells, in vitro and in vivo

(mouse) cytogenetic assays,

unscheduled DNA synthesis and a

dominant lethal mutation study in rats,

were conducted, all of which were

negative for mutagenic effects.

8. Metabolism— i. Mice. A

metabolism study in mice demonstrated

that myclobutanil was rapidly absorbed

and excreted. It was completely

eliminated by 96 hours. The chemical

was extensively metabolized prior to

excretion with metabolic patterns

similar for both sexes. Disposition and

metabolism after pulse administration is

linear over the dose range.

ii. Rats. In a metabolism study in rats,

myclobutanil was completely and

rapidly absorbed. It was extensively

metabolized and rapidly and essentially

completely excreted. Elimination of

label from plasma was biphasic and

evenly distributed between urine and

feces. There was no tissue accumulation

after 96 hours.

In another metabolism study in rats,

at least 7 major metabolites of

myclobutanil were recovered and

identified. The highest amounts of

radioactivity were found in the liver,

kidneys, and large and small intestines.

There was no tissue accumulation.

9. Neurotoxicity. There have been no

clinical neurotoxic signs or other types

of neurotoxicity observed in any of the

evaluated toxicology studies. The

Hazard ID Assessment Review

Committee did not recommend that a

developmental neurotoxicity study be

required for myclobutanil. The

following information was considered

in the weight-of-evidence evaluation:

i. Myclobutanil does not appear to be

a neurotoxic chemical.

ii. The toxicology profile for this

chemical did not indicate that there

were any treatment-related effects on

the central or peripheral nervous

system. No acute or subchronic

neurotoxicity studies in rats or delayed

neuropathy studies in chickens were

available for review so there was no

evaluation of the nervous system

following perfusion.

iii. No evidence of developmental

anomalies of the fetal nervous system

were observed in the prenatal

developmental toxicity studies in either

rats or rabbits at maternally toxic oral

doses up to 468.9 and 200 mg/kg/day,

respectively.

10. Other toxicological

considerations. Myclobutanil has a

complete data base and no other

toxicological concerns have been

identified in the evaluated studies.

B. Toxicological Endpoints

1. Acute toxicity. EPA has determined

that data do not indicate the potential

for adverse effects after a single dietary

exposure.

2. Short - and intermediate - term

toxicity. EPA has determined that when

short- and intermediate-term risk

assessments are appropriate for

occupational and residential routes of

exposure, the following should be used.

OPP recommended that the NOEL of

100 mg/kg/day, taken from the 28-day

dermal toxicity study in rats, be used for

the short-term dermal MOE

calculations. This dose level was the

highest tested in the study. For

intermediate-term MOE calculations,

OPP recommended using the NOEL of

10 mg/kg/day from the 2-generation rat

study. Effects seen at the LOEL in this

study (50 mg/kg/day) were decreases in

pup body weight, an increased

incidence in number of stillborns, and

atrophy of the prostate and testes.

3. Chronic toxicity. EPA has

established the RfD for myclobutanil at

0.025 mg/kg/day. This RfD is based on

[the chronic feeding study in rats with

a NOEL of 2.5 mg/kg/day and an

uncertainty factor of 100. There was

testicular atrophy at the lowest observed

effect level (LOEL) of 9.9 mg/kg/day.
Federal Register / Vol. 63, No. 91 /Tuesday, May 12, 1998 /Rules and Regulations 26093

4. Carcinogenicity. Using its

Guidelines for Carcinogen Risk

Assessment published September 24,

1986 (51 FR 33992), EPA has classified

myclobutanil as a Group E chemical--

‘‘no evidence of carcinogenicity for

humans’’--based on the results of

carcinogenicity studies in two species.

The doses tested are adequate for

identifying a cancer risk.

B. Exposures and Risks

1. From food and feed uses.

Tolerances have been established (40

CFR 180.443) for myclobutanil [alphabutyl-alpha-(4-chlorophenyl)-1H-1,2,4-

triazole-1-propanenitrile] and its

metabolite alpha-(3-hydroxybutyl)-

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

triazole-1-propanenitrile (free and

bound) in or on a variety of raw

agricultural commodities. Commodities

include: almonds, apples, cherries,

cotton seed, grapes, stone fruits (except

cherries) and tolerances for meat, milk,

poultry and eggs. In today’s action, a

tolerance will be established for

combined residues of myclobutanil and

its metabolite in or on bananas (postharvest) at 4.0 ppm. Risk assessments

were conducted by EPA to assess

dietary exposures and risks from

myclobutanil 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 one day or single exposure. The

Toxicology Endpoint Selection

Committee did not identify an acute

dietary toxicological endpoint and

stated that an acute dietary risk

assessment is not required.

ii. Chronic exposure and risk. In

conducting the chronic dietary (food

only) risk assessment, EPA has made

several very conservative assumptions.

With the exceptions of bananas for

which a level representing residues in

pulp rather than the whole banana was

used and selected commodities which

were corrected for percent crop treated,

all commodities having myclobutanil

tolerances will contain myclobutanil

and metabolite residues and those

residues will be at the levels of the

established tolerances. For bananas, the

level of 0.8 ppm was used in the dietary

risk assessment rather than the

proposed tolerance of 4.0 ppm since

residues in the pulp will not exceed 0.8

ppm. Percent crop-treated estimates

were utilized for selected commodities

included in the assessment. Thus, in

making a safety determination for this

tolerance, EPA is taking into account

this partially refined exposure

assessment.

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: (a) that

the data used are reliable and provide a

valid basis for showing the percentage

of food derived from a crop that is likely

to contain residues; (b) that the

exposure estimate does not

underestimate the exposure for any

significant subpopulation and; (c) 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. To provide for the periodic

evaluation of these estimates of percent

food treated as required by the section

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

registrants to submit data on percent

crop treated.

As indicated above, the Agency is

required to determine the reliability of

the percent crop-treated data. Percent

crop-treated estimates are derived from

federal and private market survey data.

Typically, a range is assumed for the

exposure assessment. By using this

upper end estimate, the Agency is

reasonably certain that the exposure is

not understated for any significant

population sub-group. Additionally, the

DRES (Dietary Risk Evaluation System)

modeling used in estimating chronic

dietary risk uses regional consumption

groups that are geographically based

regions of the United States. None of

these subgroups exceeded the Agency’s

level of concern.

The existing myclobutanil tolerances

(published, pending, and including the

necessary Section 18 tolerances) for

crops other than bananas and the

anticipated residues on bananas result

in an Anticipated Residue Contribution

(ARC) that is equivalent to the following

percentages of the RfD.

Population Subgroup %RfD

U.S. Population (48

states) 17

Nursing Infants (<1 year

old) 25

Non-nursing Infants (<1

year old) 75

Children (1-6 years old) 46

Children (7-12 years old) 28

Northeast Region 18

Western Region 19

Hispanics 20

Non-Hispanic Others 18

The subgroups listed above are: (a) the

U.S. population (48 states), (b) those for

infants and children, and (c) the other

subgroups for which the percentage of

the RfD occupied is greater than that

occupied by the subgroup U.S.

population (48 states).

2. From drinking water. Based on

information in the EFED (Environmental

Fate and Effects Division) One-Liner

Database, myclobutanil is persistent and

not considered mobile in soils with the

exception of sandy soils. Data are not

available for its metabolite. There is no

established Maximum Contaminant

Level for residues of myclobutanil in

drinking water. No Health Advisory

Levels for myclobutanil in drinking

water have been established. The

‘‘Pesticides in Groundwater Database’’

has no information concerning

myclobutanil. Estimates of ground and

surface water concentrations for

myclobutanil were determined based on

the label rate of 0.65 lbs. a.i./acre and

assuming 15 applications per season.

Although the requested tolerance is for

bananas, these estimates were based on

turf since it would more realistically

estimate the concentrations in water.

The surface water numbers are based on

the results of a Generic Environmental

Concentration (GENEEC) model. The

ground water numbers are based on a

screening tool, SCI-GROW, which tends

to overestimate the true concentration in

the environment. For acute effects, the

surface water EEC was determined to be

0.14596 ppm or mg/L (maximum initial

concentration). For chronic effects the

surface water EEC was 0.1186 ppm or

mg/L (average 56-day concentration).

Current policy allows the 90/56-day

GENEEC value to be divided by 3 to

obtain a value for chronic risk

assessment calculations. Therefore, the

surface water value for use in the

chronic risk assessment would be 0.04

ppm or mg/L.

i. Acute exposure and risk. The

Toxicology Endpoint Selection

Committee did not identify an acute

dietary toxicological endpoint and

stated than an acute dietary risk

assessment is not required.

ii. Chronic exposure and risk. Chronic

exposure is calculated based on surface

water. Chronic exposure from ground

water is lower. Chronic exposure (mg/

kg/day) is calculated by multiplying the

concentration in water in mg/L by the

daily consumption (2L/day for male and

female adults and 1L/day for children)

and dividing this figure by average

weight (70 kg for males, 60 kg for

females and 10 kg for children). For

adult males, exposure is 1.1 x 10-3 mg/

kg/day; for adult females, 1.3 x 10-3 mg/

kg/day; and for children, 4.0 x 10-3 mg/

kg/day. Chronic risk (non-cancer) from

surface water was calculated to be 4.4%

of the Rfd for males, 5.2% for females

and 16% for children.
26094 Federal Register / Vol. 63, No. 91 /Tuesday, May 12, 1998 /Rules and Regulations

3. From non-dietary exposure.

Myclobutanil is currently registered for

use on the following non-food sites:

outdoor residential and greenhouse use

on annuals and perennials, turf, shrubs,

trees and flowers.

i. Acute exposure and risk. An acute

toxicological endpoint was not

identified for myclobutanil.

ii. Chronic exposure and risk. HED

has determined that these uses do not

constitute a chronic exposure scenario,

but may constitute a short- to

intermediate-term exposure scenario.

iii. Short- and intermediate-term

exposure and risk. The home use of

myclobutanil on turf has the greatest

potential for exposure and was used in

estimating short-term risk. HED

concluded that residential intermediateterm exposure is not expected for

handlers or persons re-entering treated

areas. Fungicide use on home lawns is

limited, restricted to certain parts of the

country, and considered to be a ‘‘rare,

extra treatment’’ in homeowner Do-ItYourself programs. The end-point

selected for short-term risk assessment

is from a 28-day dermal study in rats;

this dosing duration is expected to

adequately reflect the typical human

exposures for this use. Maximum

application rates are calculated from the

use directions on the label. Typical

lawn size of 13,000 ft2 is used in place

of the high-end lawn default value of

20,000 ft2. Post-application exposure

estimates assume that 10% of the

application rate is available as

dislodgeable residue since the label

states that the product is not washed

away by rain or sprinklers.

Currently there is no use/usage

information source available to HED for

residential end-use products. Therefore,

pertinent information is unknown and

assumptions are made for parameters

such as: amount of product applied,

how often treatment is actually

required; the number of applications

that are typically made; whether

applications are generally spot or full

lawn treatments, etc. Similarly, a

number of assumptions and best

estimates are made in assessing postapplication exposure, including: the

duration and degree of activity in the

treated area by children and adults; the

amount of product available to dislodge

and transfer to the skin during activity;

and the amount of product dissipation

over time.

HED determined that there is

potential for intermittent short-term

exposures to homeowners associated

with typical end-product use of

myclobutanil. Three exposure scenarios

with the greatest potential for exposure

are considered for application to home

lawns: (a) loading and application of

granular product by hand held rotary

granular spreader; (b) mixing, loading

and application of a soluble concentrate

product by low pressure handwand

sprayer; and (c) mixing, loading, and

application of a soluble concentrate

product by garden hose-end sprayer.

Short-term dermal exposure

assessments using the ‘‘Pesticide

Handlers Exposure Database’’ surrogate

data and risk calculations for

homeowners resulted in a short-term

MOE of 460 for scenario 1, 260 for

scenario 2 and 890 for scenario 3.

There is also the potential for postapplication homeowner exposure

following applications to lawn and

garden sites. There are no chemicalspecific data to use in assessing these

potential exposures. Post-application

exposure is estimated and risk

assessments performed using typical

transfer coefficients (Tc) and surrogate

dislodgeable foliar residues (DFR)

derived from the application rate. Shortterm post-application exposure

assessments and risk calculations for

adults and toddlers re-entering treated

areas on the day of application resulted

in a short-term MOE of 350 for adult

dermal exposure, 100 for toddler dermal

exposure, 1,600 for toddlers for nondietary ingestion and 100 for combined

dermal and non-dietary ingestion for

toddlers. Dietary ingestion is addressed

in the discussion of aggregate risk.

Using these exposure assumptions for

short-term risk assessments, it is

concluded that the MOEs that will

result from the residential use of

myclobutanil do not exceed the level of

concern.

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

myclobutanil 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,

myclobutanil 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 myclobutanil has a

common mechanism of toxicity with

other substances.

C. Aggregate Risks and Determination of

Safety for U.S. Population

1. Acute risk. No acute dietary risks

were identified.

2. Chronic risk. Using the partially

refined exposure assumptions described

above, EPA has concluded that

aggregate exposure to myclobutanil from

food will utilize 17% of the RfD for the

U.S. population. The major identifiable

subgroup with the highest aggregate

exposure is non-nursing infants (<1 year

old) which is discussed below. EPA

generally has no concern for exposures

below 100% of the RfD because the RfD
Federal Register / Vol. 63, No. 91 /Tuesday, May 12, 1998 /Rules and Regulations 26095

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 myclobutanil 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 myclobutanil residues.

3. Short- and intermediate-term risk.

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. Since short-term residential

exposure scenarios are present, shortterm aggregate MOEs for adults and

children from the turf use were

determined. The short-term aggregate

MOE for adults was 150 and for

children it was 94. Although an MOE of

94 was calculated, this MOE is

acceptable based on conservative

estimates of exposure. Since worst case

estimates were used in the calculations,

the MOE would be above 100 under

usual conditions of use. It was

concluded that short-term aggregate

MOEs for both adults and children are

acceptable. This is based on the

consideration of the conservative nature

of the default assumptions for duration

and degree of activity in treated areas by

children and adults, amount of product

available to dislodge and transfer to skin

during activity, and amount of product

dissipation over time which were used

in the derivation of exposure estimates.

The estimates were calculated using the

maximum application rate and the

assumption that 10% of the application

rate is available as dislodgeable residue.

Both of these factors are likely

overestimated. The fact that a LOEL was

not identified in the 28-day rat dermal

toxicity study used to determine the

MOE indicates an overestimate since the

level used was the highest dose tested.

Additionally there are no indoor

residential uses of myclobutanil; thus,

indoor residential exposure is not a

concern.

D. Aggregate Cancer Risk for U.S.

Population

Myclobutanil is classified as Category

E: not carcinogenic in two acceptable

animal studies.

E. Aggregate Risks and Determination of

Safety for Infants and Children

1. Safety factor for infants and

children— In general. In assessing the

potential for additional sensitivity of

infants and children to residues of

myclobutanil, 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.

2. Developmental toxicity studies— i.

Rats. In the developmental study in rats,

the maternal (systemic) NOEL was 93.8

mg/kg/day, based on rough hair coat

and salivation at the LOEL of 312.6 mg/

kg/day. The developmental (fetal) NOEL

was 93.8 mg/kg/day based on

incidences of 14th rudimentary and 7th

cervical ribs at the LOEL of 312.6 mg/

kg/day.

ii. Rabbits. In the developmental

toxicity study in rabbits, the maternal

(systemic) NOEL was 60 mg/kg/day,

based on reduced weight gain, clinical

signs of toxicity and abortions at the

LOEL of 200 mg/kg/day. The

developmental (fetal) NOEL was 60 mg/

kg/day, based on increases in number of

resorptions, decreases in litter size, and

a decrease in the viability index at the

LOEL of 200 mg/kg/day.

3. Reproductive toxicity study— Rats.

In the 2-generation reproductive toxicity

study in rats, the parental (systemic)

NOEL was 2.5 mg/kg/day, based on

increased liver weights and liver cell

hypertrophy at the LOEL of 10 mg/kg/

day. The developmental (pup) NOEL

was 10 mg/kg/day, based on decreased

pup body weight during lactation at the

LOEL of 50 mg/kg/day. The

reproductive NOEL was 10 mg/kg/day,

based on the increased incidences of

stillborns, and atrophy of the testes,

epididymides, and prostate at the LOEL

of 50 mg/kg/day.

4. Pre- and post-natal sensitivity. The

pre- and post-natal toxicology data base

for myclobutanil is complete with

respect to current toxicological data

requirements. Based on the

developmental and reproductive

toxicity studies discussed above, there

does not appear to be an extra

sensitivity for pre- or post-natal effects.

5. Acute risk. No acute dietary risk

has been identified.

6. Chronic risk. Using the

conservative exposure assumptions

described above, EPA has concluded

that exposure to myclobutanil from food

will utilize 25% (nursing infants < 1

year old) and 75% (non-nursing infants

< 1 year old) of the RfD. The percent of

the RfD that will be used by the food

and water exposure for children 1-6

years old is 62% and 21% for the U.S.

population. EPA generally has no

concern for exposures below 100% of

the RfD because the RfD represents the

level at or below which daily aggregate

dietary exposure over a lifetime will not

pose appreciable risks to human health.

Despite the potential for exposure to

myclobutanil 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 to infants and children from

aggregate exposure to myclobutanil

residues.

7. Short- or intermediate-term risk.

Intermediate-term risk is not expected

since there is no expectation of

intermediate-term exposure. Short-term

exposure scenarios are expected and the

MOEs which were determined for

aggregate short-term risk does not

exceed HED’s level of concern. It was

concluded that there is a reasonable

certainty that no harm will result from

aggregate exposure to myclobutanil

residues.

8. Conclusion. EPA concludes that

reliable data support use of the 100-fold

uncertainty factor and that an additional

10-fold factor is not needed to ensure

the safety of infants and children from

dietary exposure.

III. Other Considerations

A. Endocrine Disrupter Effects

EPA is required to develop a

screening program to determine whether

certain substances (including all

pesticides and inerts) ‘‘may have an
26096 Federal Register / Vol. 63, No. 91 /Tuesday, May 12, 1998 /Rules and Regulations

effect in humans that is similar to an

effect produced by a naturally occurring

estrogen, or such other endocrine effect

....’’ The Agency is currently working

with interested stakeholders, including

other government agencies, public

interest groups, industry and research

scientists in developing a screening and

testing program and a priority setting

scheme to implement this program.

Congress has allowed 3 years from the

passage of the FQPA (August 3, 1999) to

implement this program. At that time,

EPA may require further testing of this

active ingredient and end use products

for endocrine disrupter effects. Based on

the adverse testicular findings in the

chronic toxicity and reproduction

studies in rats, myclobutanil should be

considered as a candidate for evaluation

as an endocrine disrupter.

B. Metabolism In Plants and Animals

1. Plants. Based on the three

metabolism studies on wheat, apples

and grapes (which indicate a similar

metabolic route for crops in three

different crop groups), the nature of the

residue in bananas is adequately

understood. The residues of concern in

bananas are myclobutanil [alpha-butylalpha-(4-chlorophenyl)-1H-1,2,4-

triazole-1-propanenitrile] and its

metabolite alpha-(3-hydroxybutyl)-

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

triazole-1-propanenitrile (free and

bound).

2. Animals. The nature of the residue

in animals is adequately understood.

The residues of concern in animal

commodities except milk are

myclobutanil and its metabolite alpha-

(3-hydroxybutyl)-alpha-(4-

chlorophenyl)-1H-1,2,4-triazole-1-

propanenitrile (free). The residues of

concern in milk are myclobutanil and

its metabolites alpha-(3-hydroxybutyl)-

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

triazole-1-propanenitrile (free and

bound) and alpha-(4-chlorophenyl)-

alpha-(3,4-dihydroxybutyl)-1H-1,2,4-

triazole-1-propanenitrile.

C. Analytical Enforcement Methodology

An adequate enforcement method,

34S-88-10, is available to enforce the

tolerance on bananas. Quantitation is by

GLC using a nitrogen/phosphorus

detector for parent myclobutanil and an

electron capture detector (Ni63) for

residues measured as the alcohol

metabolite alpha-(3-hydroxybutyl)-

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

triazole-1-propanenitrile. Enforcement

methods for the established tolerances

on animal commodities are Methods

34S-88-22, 34S-88-15, 31S-87-02, and

34S-88-21. These methods have been

submitted for publication in PAM II.

The methods are available to anyone

who is interested in pesticide residue

enforcement from: By mail, Calvin

Furlow, Public Information and Records

Intregrity Branch, Information

Resources and Services Division

(7502C), Office of Pesticide Programs,

Environmental Protection Agency, 401

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

Office location and telephone number:

Crystal Mall #2, Rm. 119FF, 1921

Jefferson Davis Hwy., (703) 305–5229.

D. Magnitude of Residues

The combined residues of

myclobutanil and its metabolite alpha-

(3-hydroxybutyl)-alpha-(4-

chlorophenyl)-1H-1,2,4-triazole-1-

propanenitrile (free and bound)

resulting from the proposed use will not

exceed 4.0 ppm in bananas (postharvest). The tolerance on bananas is for

the raw agricultural commodity as

defined in 40 CFR 180.1(j)(1). Both peel

and pulp are included. Crown tissue or

stalk are excluded. For risk assessment

purposes, it was concluded that

residues resulting from the proposed

use will not exceed 0.8 ppm in banana

pulp.

E. Rotational Crop Restrictions.

Rotational crop studies are not

required for uses of pesticides on

bananas.

F. International Residue Limits

There are no Codex, Canadian or

Mexican residue limits established for

myclobutanil and its metabolites on

bananas. Therefore, no compatibility

problems exist for the proposed

tolerance on bananas.

IV. Conclusion

Therefore, the tolerance is established

for the combined residues of the

fungicide myclobutanil [alpha-butylalpha-(4-chlorophenyl)-1H-1,2,4-

triazole-1-propanenitrile] and its

metabolite alpha-(3-hydroxybutyl)-

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

triazole-1-propanenitrile (free and

bound) in or on the raw agricultural

commodity bananas (post-harvest) at 4.0

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 July 13, 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–300647] (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.,
Federal Register / Vol. 63, No. 91 /Tuesday, May 12, 1998 /Rules and Regulations 26097

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 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) (Pub. L.

104-4). Nor does it require any prior

consultation as specified by Executive

Order 12875, entitled Enhancing the

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 19885, 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 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.

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 was 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 the 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 23, 1998.

Peter Caulkins,

Acting 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. Section 180.443, is amended by

adding and alphabetically inserting into

the table of paragraph (a) the commodity

bananas (Post-H) at 4.0 ppm to read as

follows:

§ 180.443 Myclobutanil; tolerances for

residues.

(a) General. * * *

Commodity Parts per million

* * * * *

Bananas (Post-H) ........... 4.0

* * * * *

* * * * *

[FR Doc. 98–12577 Filed 5–11–98; 8:45 am]

BILLING CODE 6560–50–F

ENVIRONMENTAL PROTECTION

AGENCY

40 CFR Part 180

[OPP–300628A; FRL–5785–4]

RIN 2070–AB78

Imidacloprid; Pesticide Tolerance

Correction

AGENCY: Environmental Protection

Agency (EPA).

ACTION: Final rule; correction.

SUMMARY: EPA is correcting the final

rule issued in the Federal Register of

March 25, 1998 (63 FR 14371)(FRL–

5778–3), establishing permanent

tolerances for residues of the insecticide

1-[(6-chloro-3-pyridinyl)methyl]-Nnitro-2-imidazolidinimine and its

metabolites in or on sorghum grain at

0.05 parts per million (ppm), sorghum

forage at 0.10 ppm, and sorghum stover

at 0.10 ppm. Gustafson, Inc. submitted

a petition to EPA under the Federal

Food, Drug and Cosmetic Act (FFDCA),

as amended by the Food Quality

Protection Act of 1996 (Pub. L. 104-170)

requesting these tolerances.

DATES: This correction is effective May

12, 1998.

FOR FURTHER INFORMATION CONTACT: By

mail: Elizabeth T. Haeberer, 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) 308–2891, e-mail:

haeberer.elizabeth@epamail.epa.gov.

SUPPLEMENTARY INFORMATION:

I. Regulatory Assessment Requirements

This final rule does not impose any

requirements. It only implements a

technical correction to the Code of

Federal Regulations (CFR). As such, this

action does not require review by the

Office of Management and Budget

(OMB) under Executive Order 12866,

entitled Regulatory Planning and