Federal Register / Vol. 63, No. 144 /Tuesday, July 28, 1998 / Proposed Rules 40239

Comments received after the time

indicated under DATES or at locations

other than the Harrisburg Field Office

will not necessarily be considered in the

final rulemaking or included in the

Administrative Record.

IV. Procedural Determinations

Executive Order 12866

This proposed rule is exempted from

review by the Office of Management and

Budget (OMB) under Executive Order

12866 (Regulatory Planning and

Review).

Executive Order 12988

The Department of the Interior has

conducted the reviews required by

section 3 Executive Order 12988 (Civil

Justice Reform) and has determined

that, to the extent allowed by law, this

rule meets the applicable standards of

subsections (a) and (b) of that section.

However, these standards are not

applicable to the actual language of

State and Tribal abandoned mine land

reclamation plans and revisions thereof

since each such plan is drafted and

promulgated by a specific State or Tribe,

not by OSM. Decisions on proposed

abandoned mine land reclamation plans

and revisions thereof submitted by a

State or Tribe are based on a

determination of whether the submittal

meets the requirements of Title IV of

SMCRA (30 U.S.C. 1231–1243) and 30

CFR Parts 884 and 888.

National Environmental Policy Act

No environmental impact statement is

required for this rule since agency

decisions on proposed State and Tribal

abandoned mine land reclamation plans

and revisions thereof are categorically

excluded from compliance with the

National Environmental Policy Act (42

U.S.C. 4332) by the Manual of the

Department of the Interior (516 DM 6,

appendix 8, paragraph 8.4B(29)).

Paperwork Reduction Act

This rule does not contain

information collection requirements that

require approval by OMB under the

Paperwork Reduction Act (44 U.S.C.

3507 et seq.).

Regulatory Flexibility Act

The Department of the Interior has

determined that this rule will not have

a significant economic impact on a

substantial number of small entities

under the Regulatory Flexibility Act (5

U.S.C. 601 et seq.). The State submittal

which is the subject of this rule is based

upon corresponding Federal regulations

for which an economic analysis was

prepared and certification made that

such regulations would not have a

significant economic effect upon a

substantial number of small entities.

Accordingly, this rule will ensure that

existing requirements previously

promulgated by OSM will be

implemented by the State. In making the

determination as to whether this rule

would have a significant economic

impact, the Department relied upon the

data and assumptions in the analyses for

the corresponding Federal regulations.

Unfunded Mandates

This rule will not impose a cost of

$100 million or more in any given year

on any governmental entity or the

private sector.

List of Subjects in 30 CFR Part 938

Intergovernmental relations, Surface

mining, Underground mining.

Dated: July 21, 1998.

Allen D. Klein,

Regional Director, Appalachian Regional

Coordinating Center.

[FR Doc. 98–20163 Filed 7–27–98; 8:45 am]

BILLING CODE 4310–05–M

ENVIRONMENTAL PROTECTION

AGENCY

40 CFR Part 180

[OPP–300693; FRL–6020–6]

RIN 2070–AC18

Spinosad; Time-Limited Pesticide

Tolerance

AGENCY: Environmental Protection

Agency (EPA).

ACTION: Proposed rule.

SUMMARY: EPA proposes to establish a

time-limited tolerance for residues of

spinosad in or on coffee at 0.02 parts per

million (ppm). This action is being

initiated by EPA under the Federal

Food, Drug and Cosmetic Act (FFDCA),

as amended by the Food Quality

Protection Act of 1996 (Pub. L. 104–

170). The United States Department of

Agriculture/Agricultural Research

Service (USDA/ARS) has requested that

EPA establish a time-limited tolerance

on coffee in order for USDA/ARS to

conduct efficacy testing of spinosad to

control the Mediterranean Fruit Fly.

This testing will be conducted on 80

acres in Hawaii under an Experimental

Use Permit (EUP).

DATES: Comments, identified by the

docket conrol number [OPP–300693],

must be received by EPA on or before

August 11, 1998.

ADDRESSES: By mail, submit written

comments 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, deliver comments to: Rm. 119,

CM #2, 1921 Jefferson Davis Highway,

Arlington, VA.

Comments and data may also be

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

instructions under Unit VI of this

document. No Confidential Business

Information (CBI) should be submitted

through e-mail.

Information submitted as a comment

concerning this document may be

claimed confidential by marking any

part or all of that information as CBI.

Information so marked will not be

disclosed except in accordance with

procedures set forth in 40 CFR part 2.

A copy of the comment that does not

contain CBI must be submitted for

inclusion in the public record.

Information not marked confidential

will be included in the public docket by

EPA without prior notice. The public

docket is available for public inspection

in Rm. 119 at the Virginia address given

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

through Friday, excluding legal

holidays.

FOR FURTHER INFORMATION CONTACT: By

mail: Susan Lewis, Registration Division

[7505C], Office of Pesticide Programs,

Environmental Protection Agency, 401

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

Office location, telephone number, and

e-mail address: Crystal Mall #2, 1921

Jefferson Davis Hwy., Arlington, VA,

(703) 305–7448, e-mail:

lewis.susan@epamail.epa.gov.

SUPPLEMENTARY INFORMATION: In the

Federal Register of April 15, 1998 (63

FR 18329)(FRL–5785–7), EPA

established permanent tolerances by

removing the time limitation for the

tolerance for residues of the insecticide

spinosad in or on cottonseed at 0.02

ppm and by establishing tolerances in or

on almonds at 0.02 ppm; almond hulls

at 2.0 ppm; apples at 0.2 ppm; apple

pomace, wet at 0.5 ppm; citrus fruits

group at 0.3 ppm; dried citrus pulp at

0.5 ppm; citrus oil at 3.0 ppm; cotton

gin byproducts at 1.5 ppm; fruiting

vegetables (except cucurbits) group at

0.4 ppm; leafy vegetables (except

Brassica vegetables) group at 8.0 ppm;

Brassica (cole), leafy vegetables, head

and stem subgroup at 2.0 ppm; Brassica

(cole), leafy vegetables, greens subgroup

at 15.0 ppm; fat of cattle, goats, hogs,

horses, and sheep at 0.7 ppm; meat of

cattle, goats, hogs, horses, and sheep at

0.04 ppm; meat byproducts of cattle,

goats, hogs, horses, and sheep at 0.2
40240 Federal Register / Vol. 63, No. 144 /Tuesday, July 28, 1998 / Proposed Rules

ppm; milk fat at 0.5 ppm; and whole

milk at 0.04 ppm.

The USDA has requested that EPA

establish a time-limited tolerance for

residues of spinosad in or on coffee.

This tolerance will expire on August 28,

2000. USDA has requested this

tolerance in order to conduct efficacy

testing of spinosad for control of the

Mediterranean Fruit Fly. This testing

will be conducted on 80 acres in Hawaii

under an Experimental Use Permit

(EUP).

The Agency has concluded that a

tolerance of 0.02 ppm (which is the

Limit of Quantitation (LOQ) for the

analytical method) is adequate for

coffee. This is based on a very low

application rate and the fact that the

hull of the coffee bean is removed. No

residues are expected to be found on the

coffee beans.

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 percent

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 hundredfold MOE is

based on the same rationale as the

hundredfold 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.)
Federal Register / Vol. 63, No. 144 /Tuesday, July 28, 1998 / Proposed Rules 40241

Intermediate-term risk results from

exposure for 7 days to several months.

This assessment is handled in a manner

similar to the short-term risk

assessment.

Chronic risk assessment describes risk

which could result from several months

to a lifetime of exposure. For this

assessment, risks are aggregated

considering average exposure from all

sources for representative population

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.

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 the existing

uses of spinosad. EPA had sufficient

data to assess the hazards of spinosad

and to make a determination on

aggregate exposure, consistent with

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

residues of spinosad for those uses.

EPA’s assessment of the dietary

exposures and risks associated with

establishing the existing tolerances

follows.

A. Toxicological Profile

EPA has evaluated the available

toxicity data and considered its validity,

completeness, and reliability as well as

the relationship of the results of the

studies to human risk. EPA has also

considered available information

concerning the variability of the

sensitivities of major identifiable

subgroups of consumers, including

infants and children. The nature of the

toxic effects caused by spinosad are

discussed below.

1. Acute toxicity studies with

technical spinosad (88% – 90.4%): Oral

LD50 in the rat is > 5,000 milligram/

kilogram (mg/kg) for males and females

- Toxicity Category IV; dermal LD50 in

the rat is > 2,800 mg/kg for males and

females - Toxicity Category III;

inhalation LC50 in the rat is > 5.18 mg/

L - Toxicity Category IV; primary eye

irritation in the rabbit (slight

conjunctival irritation) - Toxicity

Category IV; primary dermal irritation in

the rabbit (no erythema and edema) -

Toxicity Category IV. Spinosad is not a

sensitizer.

2. Acute toxicity studies with the enduse (44% formulation) product for

spinosad: Oral LD50 in the rat is > 5,000

mg/kg for males and females - Toxicity

Category IV; dermal LD50 in the rat is >

2,800 mg/kg for males and females -

Toxicity Category III; inhalation LC50 in

the rat is > 5 mg/L - Toxicity Category

IV; primary eye irritation in the rabbit

(slight conjunctival irritation) - Toxicity

Category IV; primary dermal irritation in

the rabbit (slight transient erythema and

edema) - Toxicity Category IV; not a

sensitizer.

3. In a subchronic feeding study in

rats, the no-observed adverse effect level

(NOAEL) was 33.9 and 38.8 mg/kg/day

for males and females, respectively. The

lowest observed effect level (LOEL) was

68.5 and 78.1 mg/kg/day for males and

females, respectively based on

decreased body weight gain, anemia,

and vacuolation in multiple organs

(kidney, liver, heart, spleen, adrenals,

and thyroid).

4. In a subchronic feeding study in

mice, the no observed effect level

(NOEL) was 7.5 mg/kg/day and the

LOEL was 22.5 mg/kg/day based on

cytoplasmic vacuolation in multiple

organs (kidney, liver, heart, stomach,

lymphoid organs, and ovary).

5. In a subchronic feeding study in

dogs, the NOEL was 4.89 and 5.38 mg/

kg/day for males and females,

respectively. The LOEL was 9.73 mg/kg/

day and 10.5 mg/kg/day based on

decreased mean body weights and food

consumption, and anemia.

6. In a 21–day dermal study in rats,

the NOEL for systemic effects was >

1,000 mg/kg/day (limit dose). No

systemic toxicity was observed at any

dose tested.

7. In a chronic feeding study in dogs,

the NOEL was 2.68 mg/kg/day. The

LOEL was 8.22 mg/kg/day based on

increased liver enzymes (ALT, AST),

triglycerides; vacuolated cells

(parathyroid), and arteritis.

8. In an carcinogenicity study in mice,

the NOEL was 11.4 mg/kg/day. The

LOEL was 50.9 mg/kg/day based on

decreased body weight gains, increased

mortality, hematologic effects, increased

thickening of the gastric mucosa, and

histologic changes in the stomach of

males.

9. In a chronic feeding/

carcinogenicity/neurotoxicity study in

rats, the NOEL (systemic) was 9.5 and

12.0 mg/kg/day for males and females,

respectively. The LOEL (systemic) was

24.1 and 30.3 mg/kg/day for males and

females, respectively based on

vacuolation of epithelial follicular cells

of the thyroid. The neurological NOEL

was 46 and 57 mg/kg/day for males and

females, respectively. The neurological

LOEL was not determined.

10. In a developmental study in

rabbits, the maternal NOEL was  ́ 50

mg/kg/day. The maternal LOEL was not

established. The developmental NOEL

was  ́ 50 mg/kg/day. The

developmental LOEL was not

established.

11. In a developmental study in rats,

the maternal NOEL was > 200 mg/kg/

day. The maternal LOEL was not

established. The developmental NOEL

was > 200 mg/kg/day. The

developmental LOEL was not

established.

12. In a two-generation reproduction

toxicity study in rats, the systemic

NOEL was 10 mg/kg/day. The systemic

LOEL was 100 mg/kg/day based on

increased organ weights (heart, liver,

kidney, spleen, thyroid), histopath

lesions in the lungs and mesenteric

lymph nodes, stomach (F), and prostate.

The reproductive NOEL was 10 mg/kg/

day. The reproductive LOEL was 100

mg/kg/day based on decreased litter

size, decreased pup survival, decreased

body weight, increased incidence of

dystocia and/or vaginal bleeding postpartum with associated increased

mortality of dams.
40242 Federal Register / Vol. 63, No. 144 /Tuesday, July 28, 1998 / Proposed Rules

13. Studies on gene mutation and

other genotoxic effects: In a Gene

Mutation Assay (mouse forward

mutation) there was no forward

mutation induction in mouse lymphoma

L5178Y Tk +/- cells at concentrations of

0, 1, 5, 10, 15, 20, or 25 μg/ml without

metabolic activation or at

concentrations of 15 through 50 μg/ml

with metabolic activation. In a

Structural Chromosomal Aberration

Assay In vitro there was no increase in

the number of CHO (chinese hamster

ovary) cells with chromosomal

aberrations at concentrations from 20 to

35 μg/ml (without activation) or

concentrations from 100 to 500 μg/ml

(with activation). In a Micronucleus

Test in mice, there was no increase in

the frequencey of micronuclei in bone

marrow cells from mice treated at

concentrations from 500 to 2,000 μg/ml

for 2 days. In Other Genotoxicity

Assays, unscheduled DNA synthesis

was not induced in adult rat

hepatocytes in vitro at concentrations of

0.01 to 5 μg/ml tested.

14. The results of three metabolism

studies are as follows: i. Approximately

95% of technical spinosad was

eliminated by 24 hours mainly in the

urine (34%), bile (36%), and tissues and

carcass (21%). Metabolites include the

glutathione conjugates of the unchanged

form as well as N- and O-demethylated

forms of XDE-105 (Factor D).

ii. At 100 mg/kg/dose, the

radiolabeled XDE-105 (Factor D) was

primarily excreted in the feces (68%)

after 24–hours. The absorption,

distribution, and elimination of 14CXDE-105 (Factor A) demonstrated no

appreciable differences based on dose or

repeated dosing.

iii. At high (100 mg/kg) doses, there

are no major differences in the

bioavailability, routes or rates of

excretion or metabolism of 14C-XDE105 (Factor A) following oral

administration.

15. In an acute neurotoxicity study,

groups of Fischer 334 rats (10/sex/dose)

received a single oral (gavage)

administration of spinosad (87.9%) at

dose levels of 0, 200, 630, or 2,000 mg/

kg. There were no effects on

neurobehavioral endpoints or

histopathology of the nervous system.

For neurotoxicity, the NOEL was  ́

2,000 mg/kg/day (HDT). A LOEL was

not established.

16. In a subchronic neurotoxicity

study, groups of Fischer 344 rats (10/

sex/dose) were administered diets

containing spinosad at levels of 0, 0.003,

0.006, 0.012, or 0.06% (0, 2.2, 4.3, 8.6,

or 42.7 mg/kg/day for males and 2.6,

5.2, 10.4, or 52.1 mg/kg/day for females,

respectively). There were no effects on

neurobehavior endpoints or

histopathology of the nervous system.

For neurotoxicity, the NOEL was  ́ 42.7

and  ́ 52.1 mg/kg/day in males and

females, respectively (HDT).

17. In the 2–year chronic

neurotoxicity study, groups of Fischer

344 rats (65/sex/dose) received diets

containing spinosad at dose levels of 0,

0.005, 0.02, 0.05, or 0.1% (0, 2.4, 9.5,

24.1, or 49.4 mg/kg/day for males and 0,

3.0, 12.0, 30.3, or 62.2 mg/kg/day for

females, respectively). Neurobehavioral

testing performed at 3, 6, 9, and 12

months of study was negative, and

histopathological evaluation of perfused

tissues at study termination did not

identify pathology of the central or

peripheral nervous system. There was

no evidence of neurotoxicity. For

neuropathology, the NOEL was 0.1% ( ́

46 mg/kg/day for males and 57 mg/kg/

day for females (HDT).

B. Toxicological Endpoints

1. Acute toxicity. EPA did not select

a dose and endpoint for an acute dietary

risk assessment due to the lack of

toxicological effects attributable to a

single exposure (dose) in studies

available in the data base including oral

developmental toxicity studies in rats

and rabbits. In the acute neurotoxicity

study the NOEL was  ́ 2,000 mg/kg/

day.

2. Short - (1 day to 7 days),

intermediate- (1 week to several

months), and chronic - term

occupational and residential dermal

and inhalation toxicity. EPA did not

select a dose or endpoint for short-,

intermediate and long-term dermal risk

assessments because (i) lack of

appropriate endpoints; (ii) the

combination of molecular structure and

size as well as the lack of dermal or

systemic toxicity at 2,000 mg/kg/day in

a 21-day dermal toxicity study in rats

which indicates the lack of dermal

absorption; and (iii) the lack of longterm exposure based on the current use

pattern. Therefore, a dermal risk

assessment is not required. EPA also

determined that based on the current

use pattern and exposure scenario, and

inhalation risk assessment is not

required.

3. Chronic toxicity. EPA has

established the RfD for spinosad at

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

a chronic toxicity study in dogs using a

NOEL of 2.68 mg/kg/day. The LOEL was

8.46 mg/kg/day based on vacuolation in

glandular cells (parathyroid) and

lymphatic tissues, arteritis and increases

in serum enzymes such as alanine

aminotransferase, and aspartate

aminotransferase, and triglyceride levels

in dogs fed spinosad in the diet at dose

levels of 1.44, 2.68, or 8.46 mg/kg/day

for 52 weeks. A hundredfold

uncertainty factor (UF) was applied to

the NOEL of 2.68 mg/kg/day to account

for inter- and intra-species variation.

EPA determined that the 10X factor to

account for enhanced sensitivity of

infants and children (as required by

FQPA) should be removed. Thus, an

uncertainty factor of 100 is adequate

and the RfD remains at 0.027 mg/kg/

day. The FQPA factor is removed

because: (i) the data provided no

indication of increased susceptibility of

rats or rabbits to in utero and/or postnatal exposure to spinosad. In the

prenatal developmental toxicity studies

in rats and rabbits and the twogeneration reproduction study in rats,

effects in the offspring were observed

only at or below treatment levels which

resulted in evidence of parental toxicity.

(ii) No neurotoxic signs have been

observed in any of the standard required

studies conducted. (iii) The toxicology

data base is complete and there are no

data gaps.

4. Carcinogenicity. There is no

evidence of carcinogenicity in studies in

either the mouse or rat.

C. Exposures and Risks

1. From food and feed uses.

Tolerances have been established (40

CFR 180.495) for the residues of

spinosad in or on almonds at 0.02 ppm;

almond hulls at 2.0 ppm; apples at 0.2

ppm; apple pomace, wet at 0.5 ppm;

citrus fruits group at 0.3 ppm; dried

citrus pulp at 0.5 ppm; citrus oil at 3.0

ppm; cottonseed at 0.02 ppm; cotton gin

byproducts at 1.5 ppm; fruiting

vegetables (except cucurbits) group at

0.4 ppm; leafy vegetables (except

Brassica vegetables) group at 8.0 ppm;

Brassica (cole), leafy vegetables, head

and stem subgroup at 2.0 ppm; Brassica

(cole), leafy vegetables, greens subgroup

at 15.0 ppm; fat of cattle, goats, hogs,

horses, and sheep at 0.7 ppm; meat of

cattle, goats, hogs, horses, and sheep at

0.04 ppm; meat byproducts of cattle,

goats, hogs, horses, and sheep at 0.2

ppm; milk fat at 0.5 ppm; and whole

milk at 0.04 ppm.

For the existing uses referred to

above, risk assessments were conducted

by EPA to assess dietary exposures and

risks from spinosad as follows:

i. Acute exposure and risk. Acute

dietary risk assessments are performed

for a food-use pesticide if a toxicological

study has indicated the possibility of an

effect of concern occurring as a result of

a 1 day or single exposure. No acute

toxicological endpoints were identified

for spinosad due to the lack of

toxicological effects attributable to a

single exposure (dose). Therefore, the
Federal Register / Vol. 63, No. 144 /Tuesday, July 28, 1998 / Proposed Rules 40243

Agency concludes that there is a

reasonable certainty of no harm from

acute dietary exposure.

ii. Chronic exposure and risk. The RfD

used for the chronic dietary analysis is

0.027 mg/kg/day. In conducting this

chronic dietary risk assessment, EPA

made very conservative assumptions:

100% of citrus, almonds, apples,

fruiting (except cucurbit) vegetables,

Brassica leafy vegetables, leafy

vegetables, cottonseed, and ruminant

commodities having spinosad tolerances

will contain spinosad residues and

those residues will be at the level of the

established tolerance. This results in an

overestimate of human dietary

exposure. This chronic dietary risk

assessment used 10 ppm tolerances for

the leafy vegetables (except Brassica

vegetables) crop group and for the

Brassica leafy vegetables head and stem

subgroup from section 18 tolerances that

were established last year. For the

section 3 registrations on these groups,

EPA has recommended tolerances of 8

ppm (leafy vegetables) and 2 ppm

(Brassica head and stem leafy

vegetables). The use pattern for these

section 18 registrations is identical to

the section 3 registrations proposed in

this risk assessment, but due to an

incomplete data base at the time the

section 18 registrations were reviewed,

the tolerances were set high which

resulted in a conservative risk

assessment. With this action, these

section 18 tolerances are replaced by the

new section 3 tolerances. Thus, in

making a safety determination for this

tolerance, EPA is taking into account

this conservative exposure assessment.

The existing spinosad tolerances

resulted in a Theoretical Maximum

Residue Contribution (TMRC) that is

equivalent to the following percentages

of the RfD: U.S. population (24% of

RfD); nursing infants (< 1 year old)( 8%

of RfD); non-nursing infants (< 1 year

old) (24% of RfD); children (1–6 years

old) (34% of RfD); children (7–12 years

old) (29% of RfD); Northeast Region

(25% of RfD); Western Region (27% of

RfD); Non-Hispanic Blacks (27% of

RfD); Non-Hispanic others (37% of RfD);

females 13+ years, nursing (27% of

RfD).

The Agency believes that the addition

of a 0.02 ppm tolerance for spinosad on

coffee will only change the percent of

the RfD used for any of the categories

listed above by less than 1%. This is

based on the fact that the use will be

limited to 80 acres in Hawaii for

experimental purposes for period of

time not to exceed 2 years.

2. From drinking water. The Agency

has determined that spinosyns Factor A

and Factor D are immobile in soil and

will not leach into ground water. Based

on structure/activity relationships, the

Agency concluded that the spinosad

metabolites/fermentation impurities

(spinosyns Factor B, Factor B of D,

Factor K, and other related Factors)

were of no more toxicological concern

than the two parent compounds

(spinosyns Factor A and Factor D) and

therefore, only these were considered in

the drinking water assessment. EPA

used the ‘‘Interim Approach for

Addressing Drinking Water Exposure in

Tolerance Decision Making’’ issued on

11/17/97. Thus, the PRZM/EXAMS

Models were run to produce estimates

of spinosad in surface water. The

primary use of these models is to

provide a screen for sorting out

pesticides for which OPP has a high

degree of confidence that the true levels

of the pesticide in drinking water will

be less than the human health drinking

water levels of concern (DWLOCs). A

human health DWLOC is the

concentration of a pesticide in drinking

water which would result in acceptable

aggregate risk, after having already

factored in all food exposures and other

non-occupational exposures for which

OPP has reliable data. PRZM/EXAMS

was used to conduct a Tier 2 surface

water analysis. The Tier 2 estimated

drinking water concentration (EEC) of

spinosad from surface water sources is

not likely to exceed 0.059 μg/l from use

on apples, 0.092 μg/l from use on

Brassica vegetables, 0.065 μg/l from use

on cotton, and 0.075 μg/l from use on

citrus.

i. Acute exposure and risk. Because

no acute dietary endpoint was

determined, the Agency concludes that

there is a reasonable certainty of no

harm from acute exposure from drinking

water.

ii. Chronic exposure and risk. Based

on the chronic dietary (food) exposure

and using default body weights and

water consumption figures, chronic

drinking water levels of concern

(DWLOC) were calculated. The chronic

drinking water exposure and risk

estimates are 0.019890 mg/kg/day (690

μg/l DWLOC) for the overall U.S.

population; 0.01896 mg/kg/day (570 μg/

l DWLOC) for females 13+ years,

nursing; and 0.016865 mg/kg/day (170

μg/l DWLOC) for children age 1–6 years.

3. From non-dietary exposure. There

are no current residential uses for

spinosad. However, the proposed use of

a 0.5% spinosad product on structural

lumber may have residential uses. This

product is injected into drilled holes

and then sealed after treatment. Due to

the lack of toxicity endpoints (hazard)

and minimal contact with the active

ingredient during and after application,

exposure to residential occupants is not

expected.

4. Cumulative exposure to substances

with common mechanism of toxicity.

Spinosad has not yet been grouped with

any other insecticides into a class.

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
40244 Federal Register / Vol. 63, No. 144 /Tuesday, July 28, 1998 / Proposed Rules

spinosad 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,

spinosad does not appear to produce a

toxic metabolite produced by other

substances. For the purposes of these

tolerance actions, therefore, EPA has not

assumed that spinosad has a common

mechanism of toxicity with other

substances.

D. Aggregate Risks and Determination of

Safety for U.S. Population

Chronic risk. The following

information is based on the review of

the existing uses of spinosad: Using the

TMRC exposure assumptions described

above, EPA has concluded that

aggregate exposure to spinosad from

food will utilize 24% of the RfD for the

U.S. population. For the most highly

exposed populations subgroup, children

(1–6 years old), chronic dietary (food

only) exposure occupies 34% of the

RfD. This is a conservative risk estimate

for reasons described above. 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. The chronic DWLOC

for the infants and children subgroup is

170 parts per billion (ppb). The chronic

modeling estimates (EECs) for spinosad

residues in surface water are as high as

0.092 ppb from use on Brassica leafy

vegetables. The maximum estimated

concentrations of spinosad in surface

water are less than EPA’s levels of

concern for spinosad in drinking water

as a contribution to chronic aggregate

exposure. Taking into account present

uses and uses proposed in this risk

assessment, EPA concludes with

reasonable certainty that residues of

spinosad in drinking water (when

considered along with other sources of

exposure for which EPA has reliable

data ) would not result in unacceptable

levels of aggregate human health risk at

this time. Therefore, the Agency

concludes that there is a reasonable

certainty that no harm will result from

chronic aggregate exposure to spinosad

residues from food and water.

No dermal or inhalation endpoints

were identified. Due to the nature of the

non-dietary use, EPA believes that the

use of spinosad in treating structural

lumber will not result in any exposure

through the oral route. Therefore, the

chronic aggregate risk is the sum of food

and water.

Based on the above information, the

Agency concludes that there is a

reasonable certainty that no harm will

result from chronic aggregate exposure

to spinosad from food and water

resulting from the addition of the timelimited experimental use on coffee as

described above.

E. Aggregate Cancer Risk for U.S.

Population

The RfD Committee determined that

there is no evidence of carcinogenicity

in studies in either the mouse or rat.

Therefore, a carcinogenic risk

assessment is not required.

F. Aggregate Risks and Determination of

Safety for Infants and Children

1. Safety factor for infants and

children— a. In general. In assessing the

potential for additional sensitivity of

infants and children to residues of

spinosad, EPA considered data from

developmental toxicity studies in the rat

and rabbit and a two-generation

reproduction study in the rat. The

developmental toxicity studies are

designed to evaluate adverse effects on

the developing organism resulting from

pesticide exposure during prenatal

development to one or both parents.

Reproduction studies provide

information relating to effects from

exposure to the pesticide on the

reproductive capability of mating

animals and data on systemic toxicity.

FFDCA section 408 provides that EPA

shall apply an additional tenfold margin

of safety for infants and children in the

case of threshold effects to account for

pre-and post-natal toxicity and the

completeness of the database unless

EPA determines that a different margin

of safety will be safe for infants and

children. 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 MOE and

uncertainty factor (usually 100 for

combined inter- and intra-species

variability) and not the additional

tenfold MOE/uncertainty factor when

EPA has a complete data base under

existing guidelines and when the

severity of the effect in infants or

children or the potency or unusual toxic

properties of a compound do not raise

concerns regarding the adequacy of the

standard MOE/safety factor.

b. Developmental toxicity studies. i. In

a prenatal developmental toxicity study,

groups of pregnant Sprague-Dawley rats

(30/group) received oral (gavage)

administration of spinosad (88.6%) in

aqueous 0.5% methycellulose at dose

levels of 0, 10, 50, 200 mg/kg/day

during gestation days 6 through 17. For

maternal toxicity, the NOEL was  ́ 200

mg/kg/day (HDT); a LOEL was not

established. Marginal maternal toxicity

was reported at this dose level

(decreased body weight gain). Based

upon the results of a range-finding

study, which showed maternal toxicity

(body weight and food consumption

decreases at 100 and 300 mg/kg/day),

the dose level of 200 mg/kg/day in the

main study was considered adequate.

For developmental toxicity, the NOEL

was > 200 mg/kg/day; a LOEL was not

established. In the range-finding study,

fetal body weight decrements occurred

at 300 mg/kg/day.

ii. In a prenatal developmental

toxicity study, groups of pregnant New

Zealand White rabbits (20/group)

received oral (gavage) administration of

spinosad (88.6%) in 0.5% aqueous

methyl cellulose at doses of 0, 2.5, 10,

or 50 mg/kg/day during gestation days

7 through 19. For maternal toxicity, the

NOEL was  ́ 50 mg/kg/day (HDT); a

LOEL was not established. At this dose,

slight body weight loss was observed in

the first few days of dosing, but this

finding was not supported by other

signs. In the range-finding study,

inanition was observed at doses of 100,

200, and 400 mg/kg/day, with

significant decreases in body weight

gain during dosing. All does at these

dose levels were sacrificed prior to

scheduled termination; no fetal data

were available. No evidence of

developmental toxicity was noted. For

developmental toxicity, the NOEL was

 ́ 50 mg/kg/day; a LOEL was not

established. (No fetal effects were noted

for fetuses of the range-finding study at

doses up to 50 mg/kg/day).

c. Reproductive toxicity study. In a

two-generation reproduction study,

groups of Sprague-Dawley rats (30/sex/

group) received diets containing

spinosad (88%) at dose levels of 0,

0.005, 0.02, or 0.2% (3, 10, or 10 mg/

kg/day, respectively) for two successive

generations. For parental systemic

toxicity, the NOEL was 0.02% (10 mg/

kg/day) and the LOEL was 0.2% (100

mg/kg/day), based on increased heart,

kidney, liver, spleen, and thyroid

weights (both sexes), histopathology in

the spleen and thyroid (both sexes),

heart and kidney (males), and

histopathologic lesions in the lungs and

mesenteric lymph nodes (both sexes),

stomach (females), and prostate. For

offspring toxicity, the NOEL was 0.02%

(10 mg/kg/day) and the LOEL was 0.2%

(100 mg/kg/day) based on decreased

litter size, survival (F2), and body

weights. Reproductive effects at that
Federal Register / Vol. 63, No. 144 /Tuesday, July 28, 1998 / Proposed Rules 40245

dose level included increased incidence

of dystocia and/or vaginal bleeding after

parturition with associated increase in

mortality of dams.

d. Neurotoxicity. i. In an acute

neurotoxicity study, groups of Fischer

344 rats (10/sex/dose) received a single

oral (gavage) administration of spinosad

(87.9%) at dose levels of 0, 200, 630, or

2,000 mg/kg. There were no effects on

neurobehavioral endpoints or

histopathology of the nervous system.

For neurotoxicity, the NOEL was >

2,000 mg/kg (HDT); a LOEL was not

established.

ii. In a subchronic neurotoxicity

study, groups of Fisher 344 rats (10/sex/

dose) were administered diets

containing spinosad at levels of 0, 0.003,

0.006, 0.012, or 0.06% (0, 2.2, 4.3, 8.6,

or 42.7 mg/kg/day for males and 2.6,

5.2, 10.4, or 52.1 mg/kg/day for females,

respectively). There were no effects on

neurobehavioral endpoints or

histopathology of the nervous system.

For neurotoxicity, the NOEL was  ́ 42.7

for males and  ́ 52.1 mg/kg/day for

females (HDT).

iii. In the 2–year chronic toxicity

study, groups of Fischer 344 rats (65/

sex/dose) received diets containing

spinosad at dose levels of 0, 0.005, 0.02,

0.05, or 0.1% (0, 2.4, 9.5, 24.1, or 49.4

mg/kg/day for males and 0, 3.0, 12.0,

30.3, or 62.2 mg/kg/day for females,

respectively). Neurobehavioral testing

performed at 3, 6, 9, and 12 months of

study was negative, and

histopathological evaluation of perfused

tissues at study termination did not

identify pathology of the central or

peripheral nervous system. There was

no evidence of neurotoxicity. For

neuropathology, the NOEL was 0.1% (>

49.4 mg/kg/day for males and 62.8 mg/

kg/day for females).

e. Pre- and post-natal sensitivity.

There was no increased susceptibility to

rats or rabbits following in utero and/or

postnatal exposure to spinosad.

f. Conclusion. The data provided no

indication of increased susceptibility of

rats or rabbits to in utero and/or

postnatal exposure to spinosad. In the

prenatal developmental toxicity studies

in rats and rabbits and the twogeneration reproduction study in rats,

effects in the offspring were observed

only at or below treatment levels which

resulted in evidence of parental toxicity.

In addition, all neurotoxicity studies

were negative for effects on the central

or peripheral nervous system.

EPA determined that the 10X factor to

account for enhanced sensitivity of

infants and children (as required by

FQPA) should be removed. The FQPA

factor is removed because (i) the data

provided no indication of increased

susceptibility of rats or rabbits to in

utero and/or post natal exposure to

spinosad. In the prenatal developmental

toxicity studies in rats and rabbits and

the two-generation reproduction study

in rats, effects in the offspring were

observed only at or below treatment

levels which resulted in evidence of

parental toxicity. (ii) No neurotoxic

signs have been observed in any of the

standard required studies conducted.

(iii) The toxicology data base is

complete and there are no data gaps.

2. Acute risk. An acute risk

assessment is not required because no

acute toxicological endpoints were

identified for spinosad.

3. Chronic risk. Using the

conservative exposure assumptions

described above, EPA has concluded

that aggregate exposure to spinosad

from food will utilize 34% of the RfD for

children age 1–6 years old. EPA

generally has no concern for exposures

below 100% of the RfD because the RfD

represents the level at or below which

daily aggregate dietary exposure over a

lifetime will not pose appreciable risks

to human health. EPA concludes that

there is a reasonable certainty that no

harm will result to infants and children

from aggregate exposure to spinosad

residues.

Based on the above information, EPA

concludes that there is a resonable

certainty that no harm will result to

infants and children from aggregate

exposure to spinosad residues as a

result of the use on coffee in an

experimental use program in Hawaii.

G. Endocrine Disruption

EPA is required to develop a

screening program to determine whether

certain substances (including all

pesticides and inerts) ‘‘may have an

effect in humans that is similar to an

effect produced by a naturally occurring

estrogen, or such other 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 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.

III. Other Considerations

A. Metabolism In Plants and Animals

EPA has reviewed the results of plant

metabolism studies (apples, cabbage,

cotton, tomatoes, turnips) and livestock

metabolism studies (goat and hen). The

metabolism of spinosad in plants and

animals is adequately understood for

the purposes of these tolerances. Based

on structure/activity relationships, EPA

concluded that the spinosad

metabolites/fermentation impurities

(spinosyns Factor B, Factor B or D,

Factor K, and other related Factors)

were of no more toxicological concern

than the two parent compounds

(spinosyns Factor A and Factor D).

EPA focused on the following data/

information: the overall low toxicity of

spinosad; the low levels of metabolites/

fermentation impurities present; and

that spinosad appears to photodegrade

rapidly and become incorporated into

the general carbon pool. EPA concluded

that only 2 parent compounds

(spinosyns Factor A and Factor D) need

to be included in the tolerance

expression and used for dietary risk

assessment purposes.

B. Analytical Enforcement Methodology

Method GRM 94.02 (method for

determination of spinosad residues in

cottonseed and related commodities

using HPLC/UV) underwent successful

independent lab validation and EPA lab

validation and has been submitted to

FDA for inclusion in PAM II as Method

I. Additional methods have been

submitted for other crop matrices (leafy

vegetables - GRM 95.17; citrus - GRM

96.09; tree nuts - GRM 96.14; fruiting

vegetables - GRM 95.04; and cotton gin

byproducts - GRM 94.02.S1). All of

these methods are essentially similar to

GRM 94.02 and have been submitted to

FDA for inclusion in PAM II as letter

methods. These methods are adequate

for regulation of the tolerance

expression.

Method RES 94094 (method for

determination of spinosad residues in

ruminant commodities using HPLC/UV)

underwent successful independent lab

validation and EPA lab validation and

has been submitted to FDA for inclusion

in PAM II as Method I. This method is

adequate for regulation of the tolerance

expression.

Method RES 95114 (method for

determination of spinosad residues in

ruminant commodities using

immunoassay) underwent successful

independent lab validation and EPA lab

validation and has been submitted to

FDA for inclusion in PAM II as Method

I. This method is adequate for regulation

of the tolerance expression.

C. International Residue Limits

No CODEX, Canadian, or Mexican

MRLs have been established for residues

of spinosad on any crops.
40246 Federal Register / Vol. 63, No. 144 /Tuesday, July 28, 1998 / Proposed Rules

IV. Conclusion

A time-limited tolerance is being

proposed for residues of spinosad in

coffee at 0.02 ppm.

V. Public Comment Procedures

EPA invites interested persons to

submit written comments, information,

or data in response to this proposed

rule. After consideration of comments,

EPA will issue a final rule. Such rule

will be subject to objections. Failure to

file an objection within the appointed

period will constitute waiver of the right

to raise in future proceedings issues

resolved in the final rule.

The period for comments on this

proposed rule has been shortened to 14

days because the Agency believes that it

is in the public interest to do so. The

purpose of this temporary tolerance is to

allow for efficacy testing to determine

whether this reduced risk chemical will

control the Mediterranean Fruit Fly.

This quarantine insect is a serious

economic pest which is threatening

continental U.S. borders. The USDA/

ARS needs to begin their experimental

use program in Hawaii no later than

August 15, 1998 and therefore, the

Agency is allowing a 14 day public

comment period to accommodate this

need.

VI. Public Docket and Submission of

Electronic Comments

The official record for this

rulemaking, as well as the public

version, has been established for this

rulemaking under docket control

number [OPP–300693] (including

comments and data submitted

electronically as described below). A

public version of this record, including

printed, paper versions of electronic

comments, which does not include any

information claimed as CBI, is available

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

Monday through Friday, excluding legal

holidays. The official rulemaking record

is located at the Virginia address in

‘‘ADDRESSES’’ at the beginning of this

document.

Electronic comments can be sent

directly to EPA at:

opp-docket@epamail.epa.gov

Electronic comments must be

submitted as an ASCII file avoiding the

use of special characters and any form

of encryption. Comment and data will

also be accepted on disks in

Wordperfect 5.1/6.1 or ASCII file

format. All comments and data in

electronic form must be identified by

the docket control number [OPP–

300693]. Electronic comments on this

proposed rule may be filed online at

many Federal Depository Libraries.

VIII. Regulatory Assessment

Requirements

This action proposes a time-limited

tolerance under FFDCA section 408(e).

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). In addition, this

proposed 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 special 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, under the Regulatory

Flexibility Act (RFA) (5 U.S.C. 601 et

seq.), the Agency 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.

List of Subjects in 40 CFR Part 180

Environmental protection,

Administrative practice and procedure,

Agricultural commodities, Pesticides

and pests, Reporting and recordkeeping

requirements.

Dated: July 23, 1998.

James Jones,

Director, Registration Division, Office of

Pesticide Programs.

Therefore, it is proposed that 40 CFR

part 180 be amended as follows:

PART 180—[AMENDED]

1. The authority citation for part 180

continues to read as follows:

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

2. In § 180.495, by revising paragraph

(a) to read as follows:

§ 180.495 Spinosad; tolerances for

residues.

(a) General . Tolerances are

established for residues of the

insecticide Spinosad. Factor A is 2-[(6-

deoxy-2,3,4-tri-O-methyl-α-L-mannopyranosyl)oxy]-13-[[5-(dimethylamino)-

tetrahydro-6-methyl-2H-pyran-2-yl]oxy]-

9-ethyl2,3,3a,5a,5b,6,9,10,11,12,13,14,16a,6btetradecahydro-14-methyl-1H-asIndaceno[3,2-d]oxacyclododecin-7,15-

dione. Factor D is 2-[(6-deoxy-2,3,4-triO-methyl-α-L-manno-pyranosyl)oxy]-

13-[[5-(dimethylamino)-tetrahydri-6-

methyl-2H-pyran-2-yl]oxy]-9-ethyl2,3,3a,5a,5b,6,9,10,11,12,13,14,16a,16btetradecahydro-4,14-dimethyl-1H-asIndaceno[3,2-d]oxacyclododecin-7,15-

dione.

Commodity Parts per million Expiration/Revocation

Date

Almonds ............................................................................................................................................. 0.02 None

Almond hulls ....................................................................................................................................... 2.0 None

Apples ................................................................................................................................................ 0.2 None

Apple pomace, wet ............................................................................................................................ 0.5 None

Brassica (cole), leafy vegetables, greens subgroup .......................................................................... 10.0 None

Brassica (cole), leafy vegetables, head and stem subgroup ............................................................ 2.0 None

Cattle, fat ............................................................................................................................................ 0.6 None

Cattle, meat ........................................................................................................................................ 0.04 None

Cattle, meat byproducts ..................................................................................................................... 0.2 None
Federal Register / Vol. 63, No. 144 /Tuesday, July 28, 1998 / Proposed Rules 40247

Commodity Parts per million Expiration/Revocation

Date

Citrus fruits group ............................................................................................................................... 0.3 None

Citrus oil ............................................................................................................................................. 3.0 None

Citrus pulp, dried ................................................................................................................................ 0.5 None

Coffee ................................................................................................................................................. 0.02 8/28/00

Cotton gin byproducts ........................................................................................................................ 1.5 None

Cottonseed ......................................................................................................................................... 0.02 None

Fruiting vegetables (except cucurbits) group ..................................................................................... 0.4 None

Goat, fat ............................................................................................................................................. 0.6 None

Goat, meat ......................................................................................................................................... 0.04 None

Goat, meat byproducts ....................................................................................................................... 0.2 None

Hogs, fat ............................................................................................................................................. 0.6 None

Hogs, meat ......................................................................................................................................... 0.04 None

Hogs, meat byproducts ...................................................................................................................... 0.2 None

Horses, fat .......................................................................................................................................... 0.6 None

Horses, meat ...................................................................................................................................... 0.04 None

Horses, meat byproducts ................................................................................................................... 0.2 None

Leafy vegetables (except Brassica vegetables) group ...................................................................... 8.0 None

Milk, fat ............................................................................................................................................... 0.5 None

Milk, whole ......................................................................................................................................... 0.04 None

Sheep, fat ........................................................................................................................................... 0.6 None

Sheep, meat ....................................................................................................................................... 0.04 None

Sheep, meat byproducts .................................................................................................................... 0.2 None

* * * * *

[FR Doc. 98–20286 Filed 7–27–98; 8:45 am]

BILLING CODE 6560–50–F

ENVIRONMENTAL PROTECTION

AGENCY

40 CFR Part 300

[FRL–6131–1]

National Priorities List for Uncontrolled

Hazardous Waste Sites, Proposed Rule

No. 25

AGENCY: Environmental Protection

Agency.

ACTION: Proposed rule.

SUMMARY: The Comprehensive

Environmental Response,

Compensation, and Liability Act

(‘‘CERCLA’’ or ‘‘the Act’’), requires that

the National Oil and Hazardous

Substances Pollution Contingency Plan

(‘‘NCP’’) include a list of national

priorities among the known releases or

threatened releases of hazardous

substances, pollutants, or contaminants

throughout the United States. The

National Priorities List (‘‘NPL’’)

constitutes this list. The NPL is

intended primarily to guide the

Environmental Protection Agency

(‘‘EPA’’ or ‘‘the Agency’’) in determining

which sites warrant further

investigation to assess the nature and

extent of public health and

environmental risks associated with the

site and to determine what CERCLAfinanced remedial action(s), if any, may

be appropriate.

This rule proposes to add 14 new sites

to the NPL, 11 to the General Superfund

section and 3 to the Federal facilities

section.

DATES: Comments regarding any of these

proposed listings must be submitted

(postmarked) on or before September 28,

1998, EPA has changed its policy and

will normally no longer respond to late

comments.

ADDRESSES: By Postal Mail: Mail

original and three copies of comments

(no facsimiles or tapes) to Docket

Coordinator, Headquarters; U.S. EPA;

CERCLA Docket Office; (Mail Code

5201G); 401 M Street, SW; Washington,

DC 20460; 703/603–9232.

By Express Mail: Send original and

three copies of comments (no facsimiles

or tapes) to Docket Coordinator,

Headquarters; U.S. EPA; CERCLA

Docket Office; 1235 Jefferson Davis

Highway; Crystal Gateway #1, First

Floor; Arlington, VA 22202.

By E-Mail: Comments in ASCII format

only may be mailed directly to

SUPERFUND. DOCKET@EPA.GOV. Emailed comments must be followed up

by an original and three copies sent by

mail or Federal Express.

For additional Docket addresses and

further details on their contents, see

Section II, ‘‘Public Review/Public

Comment,’’ of the Supplementary

Information portion of this preamble.

FOR FURTHER INFORMATION CONTACT:

Terry Keidan, phone (703) 603–8852,

State, Tribal and Site Identification

Center, Office of Emergency and

Remedial Response (Mail Code 5204G),

U.S. Environmental Protection Agency,

401 M Street, SW, Washington, DC,

20460, or the Superfund Hotline, Phone

(800) 424–9346 or (703) 412–9810 in the

Washington, DC, metropolitan area.

SUPPLEMENTARY INFORMATION:

Contents

I. Background

What are CERCLA and SARA?

What is the NCP?

What is the National Priorities List (NPL)?

How are sites listed on the NPL?

What happens to sites on the NPL?

How are site boundaries defined?

How are sites removed from the NPL?

Can portions of sites be deleted from the

NPL as they are cleaned up?

What is the Construction Completion List

(CCL)?

II. Public Review/Public Comment

Can I review the documents relevant to this

proposed rule?

How do I access the documents?

What documents are available for public

review at the Headquarters docket?

What documents are available for public

review at the Regional dockets?

How do I submit my comments?

What happens to my comments?

What should I consider when preparing my

comments?

Can I submit comments after the public

comment period is over?

Can I view public comments submitted by

others?

Can I submit comments regarding sites not

currently proposed to the NPL?

III. Contents of This Proposed Rule

Proposed Additions to the NPL

Status of NPL

Withdrawal of 3 Sites from Proposal to the

NPL

IV. Executive Order 12866

What is Executive Order 12866?