Federal Register / Vol. 62, No. 185 / Wednesday, September 24, 1997 / Notices 49979

examination. The revised DOE

certification plan will continue to cover

only employees of the Bonneville Power

Administration. The DOE estimates that

there will be 100 applicators certified in

the new wood treatment category. There

are presently approximately 150

applicators certified in the right-of-way

category, whose certification will be

unaffected by this action.

No comments were received on EPA’s

notice of intention to approve the

revised DOE certification plan.

Therefore, EPA approves the revised

DOE certification plan.

List of Subjects

Environmental protection.

Dated: September 9, 1997.

Lynn R. Goldman,

Assistant Administrator for Prevention,

Pesticides and Toxic Substances.

[FR Doc. 97–25337 Filed 9–23–97; 8:45 am]

BILLING CODE 6560–50–F

ENVIRONMENTAL PROTECTION

AGENCY

[PF–764; FRL–5745–8]

E.I. DuPont de Nemours and Co., Inc.;

Pesticide Tolerance Petition Filing

AGENCY: Environmental Protection

Agency (EPA).

ACTION: Notice.

SUMMARY: This notice announces the

initial filing of a pesticide petition

proposing the establishment of

regulations for residues of a certain

pesticide chemical in or on various food

commodities.

DATES: Comments, identified by the

docket control number PF–764, must be

received on or before October 24, 1997.

ADDRESSES: By mail submit written

comments to: Information and Records

Integrity Branch, Public Information and

Services Division (7506C), Office of

Pesticides Programs, Environmental

Protection Agency, 401 M St., SW.,

Washington, DC 20460. In person bring

comments to: Rm. 1132, CM #2, 1921

Jefferson Davis Highway, Arlington, VA.

Comments and data may also be

submitted electronically by following

the instructions under

‘‘SUPPLEMENTARY INFORMATION.’’

No confidential business information

should be submitted through e-mail.

Information submitted as a comment

concerning this document may be

claimed confidential by marking any

part or all of that information as

‘‘Confidential Business Information’’

(CBI). CBI should not be submitted

through e-mail. Information marked as

CBI will not be disclosed except in

accordance with procedures set forth in

40 CFR part 2. A copy of the comment

that does not contain CBI must be

submitted for inclusion in the public

record. Information not marked

confidential may be disclosed publicly

by EPA without prior notice. All written

comments will be available for public

inspection in Rm. 1132 at the address

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

Monday through Friday, excluding legal

holidays.

FOR FURTHER INFORMATION CONTACT:

James Stone, PM-25 Team, 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: Rm. 257,

Crystal Mall #2 1921 Jefferson Davis

Highway, Arlington, VA 22202, (703)

305–7391; e-mail:

stone.james@epamail.epa.gov.

SUPPLEMENTARY INFORMATION: EPA has

received a pesticide petition as follows

proposing the establishment and/or

amendment of regulations for residues

of certain pesticide chemical in or on

various food commodities under section

408 of the Federal Food, Drug, and

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

EPA has determined that this petition

contains data or information regarding

the elements set forth in section

408(d)(2); however, EPA has not fully

evaluated the sufficiency of the

submitted data at this time or whether

the data supports granting of the

petition. Additional data may be needed

before EPA rules on the petition.

The official record for this notice of

filing, as well as the public version, has

been established for this notice of filing

under docket control number [PF–764]

(including comments and data

submitted electronically as described

below). A public version of this record,

including printed, paper versions of

electronic comments, which does not

include any information claimed as CBI,

is available for inspection from 8:30

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

excluding legal holidays. The official

record is located at the address in

‘‘ADDRESSES’’ at the beginning of this

document.

Electronic comments can be sent

directly to EPA at:

opp-docket@epamail.epa.gov

Electronic comments must be

submitted as an ASCII file avoiding the

use of special characters and any form

of encryption. Comment and data will

also be accepted on disks in

Wordperfect 5.1 file format or ASCII file

format. All comments and data in

electronic form must be identified by

the docket control number (PF–764) and

appropriate petition number. Electronic

comments on this notice may be filed

online at many Federal Depository

Libraries.

List of Subjects

Environmental protection,

Agricultural commodities, Food

additives, Feed additives, Pesticides and

pests, Reporting and recordkeeping

requirements.

Dated: September 11, 1997.

Peter Caulkins,

Acting Director, Registration Division, Office

of Pesticide Programs.

Summaries of Petitions

Petitioner summaries of the pesticide

petitions are printed below as required

by section 408(d)(3) of the FFDCA. The

summaries of the petitions were

prepared by the petitioners and

represent the views of the petitioners.

EPA is publishing the petition

summaries verbatim without editing

them in any way. The petition summary

announces the availability of a

description of the analytical methods

available to EPA for the detection and

measurement of the pesticide chemical

residues or an explanation of why no

such method is needed.

E.I. DuPont de Nemours and Co., Inc

PP 4F4391

EPA has received a pesticide petition

(PP 4F4391) from E.I. DuPont de

Nemours and Co., Inc (DuPont), Barley

Mill Plaza, P.O. Box 80083, Wilmington,

DE 19880–0038 proposing pursuant to

section 408(d) of the Federal Food, Drug

and Cosmetic Act, 21 U.S.C. 346a(d), to

amend 40 CFR part 180 by establishing

a tolerance for residues of pyrithiobac

sodium salt (sodium 2-chloro-6-[(4,6-

dimethoxypyrimidin-2-yl)thio]benzoate)

in or on the raw agricultural

commodities cottonseed at 0.02 part per

million (ppm) and cotton gin

byproducts at 0.10 (ppm). The proposed

analytical method involves

homogenization, filtration, partition and

cleanup with analysis by using

ultraviolet detection. EPA has

determined that the petition contains

data or information regarding the

elements set forth in section 408(d)(2) of

the FFDCA; however, EPA has not fully

evaluated the sufficiency of the

submitted data at this time or whether

the data supports granting of the

petition. Additional data may be needed

before EPA rules on the petition.
49980 Federal Register / Vol. 62, No. 185 / Wednesday, September 24, 1997 / Notices

A. Residue Chemistry

1. Plant metabolism. The qualitative

nature of the residues of pyrithiobac

sodium in cotton is adequately

understood. Metabolism studies with

pyrithiobac sodium indicate the major

metabolic pathway being o-dealkylation

of the parent compound resulting in odesmethyl pyrithiobac sodium (O-DPS).

O-DPS, both free and conjugated, was

the major metabolite identified in cotton

foliage. The results of a confined crop

rotation study with pyrithiobac sodium

revealed the presence of a metabolite 2-

chloro-6-sulfobenzoic acid (CSBA) not

seen in the cotton metabolism study.

This metabolite appeared to originate

from soil metabolism of pyrithiobac

sodium. Since preemergence

applications of pyrithiobac sodium are

allowed, crop residues of CSBA were

considered a possibility. In

consideration of PP 4F4391 CBTS, in

consultation with the HED Metabolism

Committee has previously concluded

that for the proposed use on cotton,

none of the pyrithiobac sodium

metabolites including O-DPS and CSBA

warrant inclusion in the tolerance

regulation, and that the only residue of

concern is the parent, pyrithiobac

sodium.

2. Analytical method. There are

independently validated practical

analytical methods available using

liquid chromatography (HPLC) with

column switching and ultraviolet (UV)

detection, to measure levels of

pyrithiobac sodium in or on cottonseed

and cotton gin byproducts, with limits

of quantitation that will allow for

monitoring of crop residues at or above

tolerance levels. EPA has previously

provided information on the method for

cottonseed to FDA for future publication

in PAM II.

3. Magnitude of residues. Crop field

trial residue data from 60 day PHI

studies show that the proposed

pyrithiobac sodium tolerances on these

raw agricultural commodities will not

be exceeded when pyrithiobac sodium

is used as directed. An adequate

cottonseed processing study shows that

pyrithiobac sodium does not

concentrate in cottonseed processed

commodities. No tolerances on

processed commodities are required.

B. Toxicological Profile

1. Acute toxicity. Pyrithiobac sodium

technical has been placed in EPA

Toxicity Category II for acute eye

irritation based on the test article

inducing irritation in the form of

corneal opacity, iritis and conjunctival

redness, and discharge in the eyes of

rabbits after receiving ocular doses of 36

mg (0.1 ml). Signs of irritation were

clear within 14 days of treatment.

Pyrithiobac sodium has been placed in

Toxicity Category III for acute dermal

toxicity based on the test article being

nonlethal and nonirritating at the limit

dose of 2,000 mg/kg, the highest dose

tested (HDT). Pyrithiobac sodium has

been placed in Toxicity Category III for

acute oral toxicity based on acute oral

LD50s of 3,200 mg/kg for both male and

female rats. Pyrithiobac sodium has

been placed in Category IV for the

remaining acute toxicity tests based on

the following: a rat acute inhalation

study with an LC50 of > 6.9 mg/l; and

a primary dermal irritation test that did

not induce a dermal irritation response.

A dermal sensitization test with

pyrithiobac sodium technical in guinea

pigs demonstrated no significant effects.

Based on these results, pyrithiobac

sodium does not pose an acute dietary

or exposure risk.

2. Genotoxicty. Pyrithiobac sodium

technical was negative (non-mutagenic

and non-genotoxic) in the following

tests: Ames microbial mutation assay;

the hypoxanthine-guanine

phosphoribosyl transferase gene

mutation assay using Chinese hamster

ovary cells; and induction of

unscheduled DNA synthesis (UDS) in

primary rat hepatocytes. Pyrithiobac

sodium was positive in an in vitro assay

for chromosome aberrations in human

lymphocytes. It was negative for the

induction of micronuclei in the bone

marrow cells of male and female CD-1

mice administered the test article by

oral gavage at 500, 1,000 or 2,000 mg/

kg. Based on the weight of these data,

pyrithiobac sodium is neither genotoxic

nor mutagenic.

3. Reproductive and developmental

toxicity. A two generation, 4 litter

reproduction study with CD rats treated

at dietary levels of 0, 25, 1,500, 7,500 or

20,000 ppm of pyrithiobac sodium

demonstrated a maternal NOEL of 1,500

ppm (103 mg/kg/day) and a maternal

LOEL of 7,500 ppm (508 mg/kg/day),

based on decreased body weight gain

and food efficacy. An offspring NOEL of

7,500 ppm (508 mg/kg/day) and LOEL

of 20,000 ppm (1,551 mg/kg/day) were

also demonstrated based on decreased

offspring body weight. Pyrithiobac

sodium was not teratogenic when

administered to rats or rabbits.

A developmental toxicity study with

pyrithiobac sodium in rats

demonstrated a maternal NOEL of 200

mg/kg and LOEL of 600 mg/kg due to

increased incidence of salivation. A

developmental NOEL of 600 mg/kg and

LOEL of 1,800 mg/kg were

demonstrated based on an increased

incidence of skeletal variations.

A developmental toxicity study with

pyrithiobac sodium in rabbits

demonstrated maternal and

developmental NOELs of 300 mg/kg and

a maternal LOEL of 1,000 mg/kg based

on mortality, decreased body weight

gain and feed consumption, increased

incidence of clinical signs, and an

increase in early resorptions. A

developmental LOEL of 1,000 mg/kg

was based on decreased fetal body

weight gain. Based on the weight of

these data, pyrithiobac sodium is not

considered a reproductive or

developmental hazard.

4. Subchronic toxicity. In a 90–day

feeding study in rats conducted with

pyrithiobac sodium at dietary levels of

0, 10, 50, 500, 7,000 and 20,000 ppm,

the NOEL was 500 ppm (31.8 and 40.5

mg/kg/day, m/f and the LOEL was 7,000

ppm (466 and 588 mg/kg/day, m/f)

based on decreased body weight gains

and increased rate of hepatic Boxidation in males.

In a 90–day feeding study in mice

conducted with pyrithiobac sodium at

dietary levels of 0, 10, 50, 500, 1,500

and 7,000 ppm, the NOEL was 500 ppm

(83.1 and 112 mg/kg/day, m/f) and the

L0EL was 1,500 ppm (263 and 384 mg/

kg/day, m/f) based on increased liver

weight and increased incidence of

hepatocellular hypertrophy in males

and decreased neutrophil count in

females.

In a 90–day feeding study in dogs

conducted with pyrithiobac sodium at

dietary levels of 0, 50, 5,000, or 20,000

ppm, the NOEL was 5,000 ppm (165

mg/kg/day) and the LOEL was 20,000

ppm (626 mg/kg/day) based on

decreased red blood cell count,

hemoglobin, and hematocrit in females

and increased liver weight in both

sexes.

In a 21–day dermal study with rats

conducted with pyrithiobac sodium at

exposure levels of 0, 50, 500, or 1,200

mg/kg/day, the dermal irritation NOEL

was 500 mg/kg/day and the dermal

irritation LOEL was 1,200 mg/kg/day.

There were no systemic effects observed

at this high dose; therefore, the systemic

NOEL is considered to be 1,200 mg/kg/

day.

5. Chronic toxicity. A 1–year feeding

study in dogs conducted with

pyrithiobac sodium at dietary levels of

0, 100, 5,000, and 20,000 ppm resulted

in a NOEL of 5,000 ppm (143 and 166

mg/kg/day, m/f) and a LOEL of 20,000

ppm (580 and 647 mg/kg/day, m/f)

based on decreases in body weight gain

and increased liver weight.

A 78–week oncogenicity study in

mice was conducted with pyrithiobac

sodium at dietary levels of 0, 10, 150,

1,500 and 5,000 ppm. The systemic
Federal Register / Vol. 62, No. 185 / Wednesday, September 24, 1997 / Notices 49981

NOEL is 1,500 ppm (217 and 319 mg/

kg/day, m/f) and the LEL is 5,000 ppm

(745 and 1,101 mg/kg/day, m/f), based

on decreased body weight gain and liver

lesions. Kidney effects were also

observed at 5,000 ppm; however, these

were present at low incidence and were

of minimal severity and were

considered to be of only minimal

biological significance. Increased

incidence of foci/focus of hepatocellular

alteration was observed in males fed

5,000 ppm diets. Increased incidences

of hepatocellular neoplasms (adenomas

or adenomas plus carcinomas) were

observed only in 150 and 1,500 ppm

males. The incidence of these liver

tumors was not significantly increased

in the 5,000 ppm males or in females at

any dose level; the 5,000 ppm male

tumor incidence was within the

historical control range.

A 2–year study in rats was conducted

at dietary pyrithiobac sodium levels of

0, 5, 25, 1,500 or 5,000 ppm for males

and 0, 5, 25, 5,000 or 15,000 ppm for

females. The NOEL for systemic effects

was 1,500 ppm (58.7 mg/kg/day) for

males and 5,000 ppm (278 mg/kg/day)

for females. The LEL was 5,000 ppm

(200 mg/kg/day for males)/15,000 ppm

(918 mg/kg/day) for females. The LEL

was based on the following: decreased

body weight, body weight gain and food

efficiency (for females); mild changes in

hematology and urinalysis, clinical

signs indicative of urinary tract

dysfunction (both sexes); increased

incidence of focal cystic degereration in

the liver and increased rate of hepatic

peroxisome beta-oxidation (males); and

an increased incidence of inflammatory

and degenerative microscopic lesions in

the kidney (females). There was

evidence of oncogenicity based on an

increased trend for kidney tubular

combined adenoma/carcinoma in male

rats and an increased trend for kidney

tubular adenomas in female rats.

Although the incidences were low, they

were statistically significant. The

highest dose level tested in male rats

(5,000 ppm) was considered adequate

for assessment of oncogenic potential,

that in female rats (15,000 ppm)

exceeded the Maximum Tolerated Dose

(MTD).

Carcinogenicity. In consideration of

PP 4F4391 the HED Carcinogenicity

Peer Review Committee has previously

concluded that the available data

provide limited evidence of the

carcinogenicity of pyrithiobac sodium

in mice and rats and has classified

pyrithiobac sodium as a Group C

(possible human carcinogen with

limited evidence of carcinogenicity in

animals) in accordance with Agency

guidelines published in the Federal

Register in 1986 (51 FR 33992, Sept. 24,

1986) and recommend that for the

purpose of risk characterization a lowdose extrapolation model should be

applied to the experimental animal

tumor data for quantification for human

risk (Q1*). This decision was based on

liver adenomas, carcinomas and

combined adenoma/carcinomas in the

male mouse and kidney tubular

adenomas, carcinomas and combined

adenoma/carcinomas in the male rat.

The unit risk, Q1* (mg/kg/day)-1, of

pyrithiobac sodium is 1.05 × 10-3 (mg/

kg/day)-1 in human equivalents based

on male kidney tumors.

6. Animal metabolism. Disposition

and metabolism of pyrithiobac sodium

were tested in male and female rats

using two radiolabeled forms of

pyrithiobac sodium. Either phenyllabeled or pryimidine-labeled

compounds were administered orally at

5 or 250 mg/kg. In addition, i.v.

administration was evaluated at 5 mg/

kg. Essentially all of the dose was

excreted in the urine and feces, with

greater than 90% being excreted within

48 hours. No label was detected in the

expired air. Only minute quantities of

radioactivity (at or near the limit of

detection) were detected in the major

organs of metabolism and excretion.

This study indicates that pyrithiobac

sodium has low toxicity and does not

accumulate within the body. The major

compound eliminated in urine and feces

was O-DPS (desmethyl metabolite),

formed by demethylation of the

pyrimidine ring. There was evidence

that conjugation with glucuronic acid

and 5-hydroxylation of the pyrimidine

ring of pyrithiobac sodium were

additional minor routes of metabolism

in the rat. The ruminant metabolism of

pyrithiobac sodium was studied in

lactating goats fed at a level of 15 mg/

kg for 5 consecutive days, equaling a

dose greater than 1000 times the

anticipated residues of pyrithiobac

sodium and its metabolites in

cottonseed, and greater than 100 times

the anticipated residues in cotton gin

byproducts. Of the total administered

dose 76–80% was recovered in the

excreta plus cagewashes. Concentrations

of radioactivity in milk, muscle, fat,

whole-blood, and plasma were

negligible. Biotransformation of the

parent compound was not substantial

with 90% of urine radioactivity and

40% of fecal extract corresponding to

parent test substance. The major

biotransformation pathway was Odemethylation. The results of this study

indicate low potential for transfer of

residues of pyrithiobac sodium and/or

its metabolites into edible tissues or

milk of ruminants, even at highly

exaggerated feeding levels.

7. Metabolite toxicology. There is no

evidence that the metabolites of

pyrithiobac sodium as identified in

either the plant metabolism, confined

crop rotation, or animal metabolism

studies are of any toxicological

significance.

i. Neurotoxicity. A 90–day rat

neurotoxicity screen battery conducted

with pyrithiobac sodium resulted in a

systemic no observed-effect level

(NOEL) of 7,000 ppm (466 and 588 mg/

kg/day, m/f) and a systemic lowestobserved-effect level (LOEL) of 20,000

ppm (1,376 and 1,609 mg/kg/day, m/f)

based on reduced body weight gain and

food efficiency and increased liver

weight. Slight reductions in hind-leg

grip strength and slightly increased foot

splay in males were observed in 20,000

ppm males. However, because these

were of small magnitude, lacked

statistical significance and

corresponding histopathology,

pyrithiobac sodium was not considered

a neurotoxin. The NOEL for

neurotoxicity was 20,000 ppm (HDT).

ii. Endocrine effects. No special

studies investigating potential

estrogenic or other endocrine effects of

pyrithiobac sodium have been

conducted. However, the standard

battery of required toxicology studies

has been completed and found

acceptable. These include an evaluation

of the potential effects on reproduction

and development, and an evaluation of

the pathology of the endocrine organs

following repeated or long-term

exposure to doses that far exceed likely

human exposures. Based on these

studies there is no evidence to suggest

that pyrithiobac sodium has an adverse

effect on the endocrine system.

C. Aggregate Exposure

1. Dietary exposure. It is proposed

that pyrithiobac sodium be defined as

the residue for enforcement purposes.

Monitoring for pyrithiobac sodium

residues in field samples will provide

an adequate estimate of this compound

in edible portions of treated crops.

2. Food—i. acute dietary exposure. A

Tier I acute dietary exposure analysis

was conducted using the Dietary

Exposure Evaluation Model (DEEM ver.

5.10) and assuming tolerance level

residues for cottonseed oil, cottonseed

meal, and a very conservative residue

value of 6 parts per billion (ppb) for all

sources of dietary water. Using the acute

endpoint of 200 mg/kg from a

developmental toxicity study in rats, the

margins of exposure were greater than

100,000 for all 22 population subgroups

at the 95th percentile exposure.
49982 Federal Register / Vol. 62, No. 185 / Wednesday, September 24, 1997 / Notices

ii. Chronic dietary exposure. For

purposes of assessing the potential

chronic dietary exposure under this

tolerance, an estimate of aggregate

exposure is made using the proposed

tolerance on cottonseed at 0.02 ppm,

cotton gin byproducts at 0.10 ppm, and

a very conservative contribution from

drinking water based on GENEEC

modeling. The potential exposure is

obtained by multiplying the tolerance

level residues by the consumption data

which estimates the amount of

cottonseed products translated as

cottonseed meal and cottonseed oil

eaten by various population subgroups.

Cottonseed and cotton gin byproducts

are fed to animals, thus exposure of

humans to residues of pyrithiobac

sodium might result if such residues are

transferred to meat, milk, poultry, or

eggs. However, in previous

consideration of PP 4F4391 CBTS has

concluded that secondary residues in

meat, milk, poultry and eggs are not

expected from the use of cottonseed as

an animal feed. A ruminant (goat)

metabolism study further demonstrates

that residues of pyrithiobac sodium in

cotton gin byproducts will not result in

secondary meat or milk residues when

this commodity is fed to livestock.

There are no other established

tolerances or registered uses for

pyrithiobac sodium in the United States.

Based on a NOEL of 58.7 mg/kg/day,

from the chronic rat toxicity study and

a 100-fold safety factor, the reference

dose (RfD) is 0.58 mg/kg/day. Assuming

residues at tolerance levels and that

100% of the crop is being treated, a

theoretical maximum residue

contribution (TMRC) of < 0.1 mg/kg/day

is calculated using the DEEM computer

software (version 5.1, Novigen Sciences,

Inc., 1997). With the above assumptions

which clearly overestimate potential

human exposure and are a most

conservative assessment of risk, dietary

(food) exposure to pyrithiobac sodium

will utilize significantly less than 1% of

the RfD for the overall U.S. population.

For the most highly exposed subgroup,

non-nursing infants less than 1 year old,

the TMRC is also < 0.1 mg/kg/day,

which is still less than 1% of the RfD.

The unit risk, Q1* (mg/kg/day)-1, of

pyrithiobac sodium is 1.05 × 10-3 (mg/

kg/day)-1 in human equivalents based

on male kidney tumors. Based on this

upper bound potency factor (Q*), a 70–

year lifespan, and the assumption that

100% of the crop is treated with

pyrithiobac sodium, the upper-bound

limit of a dietary carcinogenic risk is

calculated in the range of 1 incidence in

a billion (1.0 × 10-9).

3. Drinking water . Other potential

dietary sources of exposure of the

general population to pesticides are

residues in drinking water. There is no

Maximum Contaminant Level

established for residues of pyrithiobac

sodium. The petitioner has reported to

the Environmental Fate and

Groundwater Branch of EPA (EFGWB)

the results of a prospective groundwater

monitoring study conducted at a highly

vulnerable site. This study confirms the

previous interim conclusions of EFGWB

that pyrithiobac sodium may not be

stable enough to leach to groundwater at

most use sites, even in sandy soils. The

potential for pyrithiobac sodium to

enter surface water is also very low.

This is supported by modeling done

using GENEEC which under worst case

conditions (100% of area treated, long

half-life, etc.) predicted peak surface

water concentrations of only 6 ppb. All

environmental fate data requirements

for pyrithiobac sodium have now been

satisfied and based on these studies, the

conditions of use, and worst-case

modeling, the potential for finding

pyrithiobac sodium residues in drinking

water is minimal.

4. Non-dietary exposure. Pyrithiobac

sodium is not registered for any use

which could result in non-occupational,

non-dietary exposure to the general

population.

D. Cumulative Effects

Pyrithiobac sodium is based on a new

chemical class; there are no known

registered herbicides with similar

structure. Therefore, EPA should

consider only the potential risks of

pyrithiobac sodium in its exposure

assessment. The herbicidal activity of

pyrithiobac sodium is due to the

inhibition of acetolactate synthase

(ALS), an enzyme only found in plants.

ALS is part of the biosynthetic pathway

leading to the formation of branched

chain amino acids. Animals lack ALS

and this biosynthetic pathway. This lack

of ALS contributes to the low toxicity of

pyrithiobac sodium in animals. There is

no evidence to indicate or suggest that

pyrithiobac sodium has any toxic effects

on mammals that would be cumulative

with those of any other chemical.

E. Safety Determination

1. U.S. population. Based on a

complete and reliable toxicity database,

the EPA has adopted an RfD value of

0.58 mg/kg/day using the NOEL of 58.7

mg/kg/day, from the 2–year chronic

toxicity study in rats and a 100-fold

safety factor. Using crop tolerance levels

and assuming 100% of the crop treated,

a Theoretical Maximum Residue

Contribution (TMRC) was calculated for

the overall U.S. population and 22

population subgroups. This analysis

concluded that aggregate exposure to

pyrithiobac sodium will utilize

significantly less than 1% of the RfD for

either the entire U.S. population or any

subgroup population. The TMRC for the

most highly exposed subgroup

identified as non-nursing infants less

than 1 year old was also < 0.1 mg/kg/

day. EPA generally has no concern for

exposure 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 risk to human health. Thus,

there is a reasonable certainty that no

harm will result from aggregate

exposure to pyrithiobac sodium

residues. The unit risk, Q1* (mg/kg/

day)-1, of pyrithiobac sodium is 1.05 ×

10-3 (mg/kg/day)-1 in human equivalents

based on male kidney tumors. Based on

this upper bound potency factor (Q1*)

and assuming a 70 year lifetime

exposure an upper-bound limit of a

dietary carcinogenic risk is calculated in

the range of 1 incidence in a billion (1.0

× 10-9). This indicates a negligible cancer

risk.

2. Infants and children. In assessing

the potential for additional sensitivity of

infants and children to residues of

pyrithiobac sodium, data from the

previously discussed developmental

and reproduction toxicity studies were

considered. Developmental studies are

designed to evaluate adverse effects on

the developing organism resulting from

pesticide exposure during pre-natal

development. Reproduction studies

provide information relating to

reproductive and other effects on adults

and offspring from pre-natal and postnatal exposure to the pesticide. Based

on the weight of these data, pyrithiobac

sodium was not a reproductive toxicant.

Maternal and developmental effects

(NOEL’s, LOEL’s) were comparable

indicating no increase in susceptibility

of developing organisms. No evidence of

endocrine effects were noted in any

study. FFDCA section 408 provides that

EPA may apply an additional safety

factor for infants and children in the

case of threshold effects to account for

pre and post-natal toxicity and the

completeness of the database. Based on

current toxicological data requirements,

the database for pyrithiobac sodium

relative to pre- and post-natal effects for

children is complete. The NOEL of 58.7

mg/kg/day from the 2–year rat study

with pyrithiobac sodium, which was

used to calculate the RfD, is lower than

any of the NOEL’s defined in the

developmental and reproductive

toxicity studies with pyrithiobac
Federal Register / Vol. 62, No. 185 / Wednesday, September 24, 1997 / Notices 49983

sodium. When the weight of these facts

is considered an additional safety factor

is not warranted for developmental

effects. As stated above, aggregate

exposure assessments utilized

significantly less than 1% of the RfD for

either the entire U.S. population or any

of 22 population subgroups including

infants and children. Therefore, it may

be concluded that there is reasonable

certainty that no harm will result to

infants and children from aggregate

exposure to pyrithiobac sodium

residues.

F. International Tolerances

There are no established Codex MRLs

for pyrithiobac sodium on cottonseed.

An established Mexican tolerance for

pyrithiobac sodium on cottonseed is

identical to the U.S. tolerance.

Compatibility is not a problem at this

time.

[FR Doc. 97–25234 Filed 9-23-97; 8:45 am]

BILLING CODE 6560–50–F

ENVIRONMENTAL PROTECTION

AGENCY

[PF–761; FRL–5740–9]

Yoshitomi Fine Chemicals Ltd.;

Pesticide Tolerance Petition Filing

AGENCY: Environmental Protection

Agency (EPA).

ACTION: Notice.

SUMMARY: This notice announces the

initial filing of a pesticide petition

proposing the establishment of

tolerances for residues of 4,5-Dichloro1,2-Dithiol-3-one (CASRN 1192–52–5)

in or on paper and paperboard.

DATES: Comments, identified by the

docket control number PF–761, must be

received on or before October 24, 1997.

ADDRESSES: By mail submit written

comments to: Information and Records

Integrity Branch, Public Information and

Services Divison (7506C), Office of

Pesticides Programs, Environmental

Protection Agency, 401 M St., SW.,

Washington, DC 20460. In person bring

comments to: Rm. 1132, CM #2, 1921

Jefferson Davis Highway, Arlington, VA.

Comments and data may also be

submitted electronically by following

the instructions under

‘‘SUPPLEMENTARY INFORMATION.’’

No confidential business information

should be submitted through e-mail.

Information submitted as a comment

concerning this document may be

claimed confidential by marking any

part or all of that information as

‘‘Confidential Business Information’’

(CBI). CBI should not be submitted

through e-mail. Information marked as

CBI will not be disclosed except in

accordance with procedures set forth in

40 CFR part 2. A copy of the comment

that does not contain CBI must be

submitted for inclusion in the public

record. Information not marked

confidential may be disclosed publicly

by EPA without prior notice. All written

comments will be available for public

inspection in Rm. 1132 at the address

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

Monday through Friday, excluding legal

holidays.

FOR FURTHER INFORMATION CONTACT: By

mail: Portia Jenkins, Acting Product

Manager (34), Antimicrobials Division

(7510C), Office of Pesticide Programs,

Environmental Protection Agency, 401

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

Office location and telephone number:

Rm. 6C, Crystal Plaza #1, 2800 Crystal

Drive, Arlington, VA, (703) 308–6230; email: jenkins.portia@epamail.epa.gov.

SUPPLEMENTARY INFORMATION: EPA has

received a pesticide petition ((PP)

7F4902) from Yoshitomi Fine

Chemicals, Ltd., 6–9, Hiranomachi 2-

chome, Chuo-ku, Osaka, 541, Japan,

proposing pursuant to section 408(d) of

the Federal Food, Drug and Cosmetic

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

amend 40 CFR 185 ‘‘Tolerances for

Pesticides in Food’’ by establishing

Subpart D ‘‘Tolerance Exemptions for

Pesticides in Foods’’ and promulgating

therein section 185.9000 establishing a

tolerance exemption for residues of the

slimicide 4,5-Dichloro-1,2-Dithiol-3-one

(CASRN 1192–52–5) in or on paper and

paperboard resulting from its addition

to pulp and paper mill process water to

control slime forming organisms. EPA

has determined that the petition

contains data or information regarding

the elements set forth in section

408(d)(2); however, EPA has not fully

evaluated the sufficiency of the

submitted data at this time or whether

the data supports granting of the

petition. Additional data may be needed

before EPA rules on the petition.

The official record for this notice of

filing, as well as the public version, has

been established for this notice of filing

under docket control number [PF–761]

(including comments and data

submitted electronically as described

below). A public version of this record,

including printed, paper versions of

electronic comments, which does not

include any information claimed as CBI,

is available for inspection from 8:30

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

excluding legal holidays. The official

record is located at the address in

‘‘ADDRESSES’’.

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 file format or ASCII file

format. All comments and data in

electronic form must be identified by

the docket number (PF–761) and

appropriate petition number. Electronic

comments on this notice may be filed

online at many Federal Depository

Libraries.

List of Subjects

Environmental protection,

Administrative practice and procedure,

Paper and paperboard, Slimicides,

Pesticides and pests, Reporting and

recordkeeping requirements.

Dated: September 16, 1997.

Frank Sanders,

Director, Antimicrobials Division, Office of

Pesticide Programs.

Summary of Petition

Petitioner summary of the pesticide

petition is printed below as required by

section 408(d)(3) of the FFDCA. The

summary of the petition was prepared

by the petitioner and represent the

views of the petitioner. The petition

summary announces the availability of

a description of the analytical methods

available to EPA for the detection and

measurement of the pesticide chemical

residues or an explanation of why no

such method is needed.

Yoshitomi Fine Chemicals, Ltd.

A. Residue Chemistry

This petition is not for residues in or

on raw agricultural commodities. It is

for residues in or on food contact paper

or paperboard. Accordingly, the residue

chemistry data submitted are solely for

the residues remaining in food contact

paper and paperboard when the subject

slimicide (4,5-Dichloro-1,2-Dithiol-3-

one, CASRN 1192–52–5, hereafter

referred to as RYH–86) is used in pulp

and paper mill process water to control

slime forming organisms.

1. Residues in paper and paperboard.

GC-MS-SIM analysis of approximately

30 paper and paperboard samples

manufactured in a papermill which

used RYH–86 amended slurry water

revealed no RYH–86 detectable with a

detection limit of 100 μg/kilograms (Kg)

of paper (i.e., 100 parts per billion

(ppb)). Extraction of such samples with