36366 Federal Register / Vol. 63, No. 128 / Monday, July 6, 1998 /Rules and Regulations

notice also contains a correction of a

citation in the interim rule.

EFFECTIVE DATE: July 6, 1998.

FOR FURTHER INFORMATION CONTACT: H.

Edward Odom, Chief, Legislation and

Regulations Division, Visa Services,

Department of State, Washington, DC

20520–0106, (202) 663–1204.

SUPPLEMENTARY INFORMATION: An

interim rule implementing the new

subsection 222(g) of the Immigration

and Nationality Act (INA), and

requesting comments, was published on

January 7, 1998 [63 FR 669]. The period

for comments has expired; no comments

have been received. The rule will thus

stand as originally published, with a

correction of the reference to INA 214(k)

in 22 CFR 41.101(c)(1) which should

read 214(l). As there are now two

214(l)’s in the INA, this reference is to

the first one, i.e., the subsection relating

to a waiver of the 2-year foreign

residence requirement.

As the final regulation is identical to

the interim regulation other than for the

correction of a citation, it is not being

reprinted in full herein.

List of Subjects in 22 CFR Part 41

Aliens, Nonimmigrants, Passports,

Visas.

In view of the foregoing, the interim

rule amending 22 CFR parts 40 and 41

which was published at 63 FR 669 on

January 7, 1998, is adopted as a final

rule with the following change:

PART 41—[CORRECTED]

1. The authority citation for part 41

continues to read:

Authority: 8 U.S.C. 1104.

§ 41.101 [Corrected]

2. In § 41.101(c)(1), correct the

reference to ‘‘INA 214(k)’’ to read ‘‘INA

214(l)’’.

Dated: May 20, 1998.

Donna J. Hamilton,

Acting Assistant Secretary for Consular

Affairs.

[FR Doc. 98–17735 Filed 7–2–98; 8:45 am]

BILLING CODE 4710–06–P

ENVIRONMENTAL PROTECTION

AGENCY

40 CFR Part 180

[OPP–300666; FRL–5794–6]

RIN 2070–AB78

Pyriproxyfen (2-[1-methyl-2-(4-

phenoxyphenoxy)ethoxy]pyridine;

Pesticide Tolerance

AGENCY: Environmental Protection

Agency (EPA).

ACTION: Final rule.

SUMMARY: This regulation establishes a

tolerance for combined residues of

pyriproxfen in or on cotton seed and

cotton gin byproducts. Valent U.S.A.

Corporation requested this tolerance

under the Federal Food, Drug, and

Cosmetic Act (FFDCA), as amended by

the Food Quality Protection Act of 1996

(Pub. L. 104-170).

DATES: This regulation is effective July

6, 1998. Objections and requests for

hearings must be received by EPA on or

before September 4, 1998.

ADDRESSES: Written objections and

hearing requests, identified by the

docket control number, [OPP–300666],

must be submitted to: Hearing Clerk

(1900), Environmental Protection

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

Washington, DC 20460. Fees

accompanying objections and hearing

requests shall be labeled ‘‘Tolerance

Petition Fees’’ and forwarded to: EPA

Headquarters Accounting Operations

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

360277M, Pittsburgh, PA 15251. A copy

of any objections and hearing requests

filed with the Hearing Clerk identified

by the docket control number, [OPP–

300666], must also be submitted to:

Public Information and Records

Integrity Branch, Information Resources

and Services Division (7502C), Office of

Pesticide Programs, Environmental

Protection Agency, 401 M St., SW.,

Washington, DC 20460. In person, bring

a copy of objections and hearing

requests to Rm. 119, CM #2, 1921

Jefferson Davis Hwy., Arlington, VA.

A copy of objections and hearing

requests filed with the Hearing Clerk

may also be submitted electronically by

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

objections and hearing requests must be

submitted as an ASCII file avoiding the

use of special characters and any form

of encryption. Copies of objections and

hearing requests will also be accepted

on disks in WordPerfect 5.1/6.1 file

format or ASCII file format. All copies

of objections and hearing requests in

electronic form must be identified by

the docket control number [OPP–

300666]. No Confidential Business

Information (CBI) should be submitted

through e-mail. Electronic copies of

objections and hearing requests on this

rule may be filed online at many Federal

Depository Libraries.

FOR FURTHER INFORMATION CONTACT: By

mail: Joseph Tavano, 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) 305-6411, e-mail:

tavano.joseph@epamail.epa.gov.

SUPPLEMENTARY INFORMATION: In the

Federal Register of March 6, 1998 (63

FR 11240) (FRL–5777–5), EPA, issued a

notice pursuant to section 408 of the

Federal Food, Drug, and Cosmetic Act

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

the filing of a pesticide petition (PP

6F4737) for tolerance by Valent U.S.A.

Corporation, 1333 N. California Blvd.,

Walnut Creek, CA 94596. This notice

included a summary of the petition

prepared by Valent U.S.A. Corporation,

the registrant. There were no comments

received in response to the notice of

filing.

The petition requested that 40 CFR

180.534 be amended by establishing

tolerances for combined residues of the

insecticide, pyriproxfen, in or on cotton

seed and cotton gin byproducts at 0.05

and 2.0 parts per million (ppm)

respectively.

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. . . .’’
Federal Register / Vol. 63, No. 128 / Monday, July 6, 1998 /Rules and Regulations 36367

EPA performs a number of analyses to

determine the risks from aggregate

exposure to pesticide residues. First,

EPA determines the toxicity of

pesticides based primarily on

toxicological studies using laboratory

animals. These studies address many

adverse health effects, including (but

not limited to) reproductive effects,

developmental toxicity, toxicity to the

nervous system, and carcinogenicity.

Second, EPA examines exposure to the

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

drinking water) and through exposures

that occur as a result of pesticide use in

residential settings.

A. Toxicity

1. Threshold and non-threshold

effects. For many animal studies, a dose

response relationship can be

determined, which provides a dose that

causes adverse effects (threshold effects)

and doses causing no observed effects

(the ‘‘no-observed effect level’’ or

‘‘NOEL’’).

Once a study has been evaluated and

the observed effects have been

determined to be threshold effects, EPA

generally divides the NOEL from the

study with the lowest NOEL by an

uncertainty factor (usually 100 or more)

to determine the Reference Dose (RfD).

The RfD is a level at or below which

daily aggregate exposure over a lifetime

will not pose appreciable risks to

human health. An uncertainty factor

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

100 is commonly used since it is

assumed that people may be up to 10

times more sensitive to pesticides than

the test animals, and that one person or

subgroup of the population (such as

infants and children) could be up to 10

times more sensitive to a pesticide than

another. In addition, EPA assesses the

potential risks to infants and children

based on the weight of the evidence of

the toxicology studies and determines

whether an additional uncertainty factor

is warranted. Thus, an aggregate daily

exposure to a pesticide residue at or

below the RfD (expressed as 100% or

less of the RfD) is generally considered

acceptable by EPA. EPA generally uses

the RfD to evaluate the chronic risks

posed by pesticide exposure. For shorter

term risks, EPA calculates a margin of

exposure (MOE) by dividing the

estimated human exposure into the

NOEL from the appropriate animal

study. Commonly, EPA finds MOEs

lower than 100 to be unacceptable. This

100-fold MOE is based on the same

rationale as the 100-fold uncertainty

factor.

Lifetime feeding studies in two

species of laboratory animals are

conducted to screen pesticides for

cancer effects. When evidence of

increased cancer is noted in these

studies, the Agency conducts a weight

of the evidence review of all relevant

toxicological data including short-term

and mutagenicity studies and structure

activity relationship. Once a pesticide

has been classified as a potential human

carcinogen, different types of risk

assessments (e.g., linear low dose

extrapolations or MOE calculation based

on the appropriate NOEL) will be

carried out based on the nature of the

carcinogenic response and the Agency’s

knowledge of its mode of action.

2. Differences in toxic effect due to

exposure duration. The toxicological

effects of a pesticide can vary with

different exposure durations. EPA

considers the entire toxicity data base,

and based on the effects seen for

different durations and routes of

exposure, determines which risk

assessments should be done to assure

that the public is adequately protected

from any pesticide exposure scenario.

Both short and long durations of

exposure are always considered.

Typically, risk assessments include

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

term,’’ and ‘‘chronic’’ risks. These

assessments are defined by the Agency

as follows.

Acute risk, by the Agency’s definition,

results from 1-day consumption of food

and water, and reflects toxicity which

could be expressed following a single

oral exposure to the pesticide residues.

High end exposure to food and water

residues are typically assumed.

Short-term risk results from exposure

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

and therefore overlaps with the acute

risk assessment. Historically, this risk

assessment was intended to address

primarily dermal and inhalation

exposure which could result, for

example, from residential pesticide

applications. However, since enaction of

FQPA, this assessment has been

expanded to include both dietary and

non-dietary sources of exposure, and

will typically consider exposure from

food, water, and residential uses when

reliable data are available. In this

assessment, risks from average food and

water exposure, and high-end

residential exposure, are aggregated.

High-end exposures from all three

sources are not typically added because

of the very low probability of this

occurring in most cases, and because the

other conservative assumptions built

into the assessment assure adequate

protection of public health. However,

for cases in which high-end exposure

can reasonably be expected from

multiple sources (e.g. frequent and

widespread homeowner use in a

specific geographical area), multiple

high-end risks will be aggregated and

presented as part of the comprehensive

risk assessment/characterization. Since

the toxicological endpoint considered in

this assessment reflects exposure over a

period of at least 7 days, an additional

degree of conservatism is built into the

assessment; i.e., the risk assessment

nominally covers 1-7 days exposure,

and the toxicological endpoint/NOEL is

selected to be adequate for at least 7

days of exposure. (Toxicity results at

lower levels when the dosing duration

is increased.)

Intermediate-term risk results from

exposure for 7 days to several months.

This assessment is handled in a manner

similar to the short-term risk

assessment.

Chronic risk assessment describes risk

which could result from several months

to a lifetime of exposure. For this

assessment, risks are aggregated

considering average exposure from all

sources for representative population

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
36368 Federal Register / Vol. 63, No. 128 / Monday, July 6, 1998 /Rules and Regulations

of information (anticipated residue data

and/or percent of crop treated data)

which show, generally, that pesticide

residues in most foods when they are

eaten are well below established

tolerances.

Percent of crop treated estimates are

derived from federal and private market

survey data. Typically, a range of

estimates are supplied and the upper

end of this range is assumed for the

exposure assessment. By using this

upper end estimate of percent of crop

treated, the Agency is reasonably certain

that exposure is not understated for any

significant subpopulation group.

Further, regional consumption

information is taken into account

through EPA’s computer-based model

for evaluating the exposure of

significant subpopulations including

several regional groups, to pesticide

residues. For this pesticide, the most

highly exposed population subgroup

was not regionally based.

II. Aggregate Risk Assessment and

Determination of Safety

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

EPA has reviewed the available

scientific data and other relevant

information in support of this action,

EPA has sufficient data to assess the

hazards of pyriproxyfen (2-[1-methyl-2-

(4-phenoxyphenoxy)ethoxy]pyridine

and to make a determination on

aggregate exposure, consistent with

section 408(b)(2), tolerances for

combined residues of pyriproxfen on

cotton seed and cotton gin byproducts at

0.05 and 2.0 ppm respectively EPA’s

assessment of the dietary exposures and

risks associated with establishing the

tolerance follows.

A. Toxicological Profile

EPA has evaluated the available

toxicity data and considered its validity,

completeness, and reliability as well as

the relationship of the results of the

studies to human risk. EPA has also

considered available information

concerning the variability of the

sensitivities of major identifiable

subgroups of consumers, including

infants and children. The nature of the

toxic effects caused by pyriproxyfen (2-

[1-methyl-2-(4-

phenoxyphenoxy)ethoxy]pyridine are

discussed below.

1. Acute toxicity— Acute toxicity

studies with technical pyriproxyfen.

Oral LD50 in the rat is >5,000 milligram/

kilogram (mg/kg) for males and females

- Toxicity Category IV; dermal LD50 in

the rabbit at >2,000 mg/kg - Toxicity

Category IV; inhalation LC50 in the rat

is >1.3 mg/L (highest dose attainable) -

Toxicity Category III; primary eye

irritation in the rabbit (mild irritatant) -

Toxicity Category III; primary dermal

irritation in the rabbit (not an irritant:

non-irritating to the skin under

conditions of test))- Toxicity Category

IV. Pyriproxyfen is not a sensitizer.

2. Subchronic toxicity— i. Rats. In the

subchronic feeding study in rats, the noobserved effect level (NOEL) was 27.68

mg/kg/day. The lowest oberved effect

level (LOEL) was 141.28 mg/kg/day,

based upon higher mean total

cholesteral and phospholipids,

decreased mean RBCs, hematocrit and

hemoglobin counts and increased

relative liver weight.

ii. Dogs. In the subchronic feeding

study in dogs, the NOEL was 100 mg/

kg/day and the LOEL was 300 mg/kg/

day. The effects were based on

increased absolute and relative liver

weight in males and hepatocellular

hypertrophy in females. These findings

were also observed at 1,000 mg/kg/day

and may represent adaptive changes at

both 300 mg/kg/day and the limit dose

of 1,000 mg/kg/day.

iii. Dermal study - Rats. In a 21-day

dermal study in rats, the NOEL for

systemic effects was >1,000 mg/kg/day

(limit dose). The LOEL for systemic

effects was not established in this study.

No dermal or systemic toxicity was

observed at any dose tested.

3. Chronic toxicity/carcinogenicity—

i. Dogs. In a one-year chronic feeding

study in dogs, the NOEL was 100 mg/

kg/day. The LOEL was 300 mg/kg/day

based on decreased weight gain,

increased absolute and relative liver

weight, mild anemia, increased

cholesterol and triglycerides.

ii. Mice. The oncogenicity study in

mice the NOEL and LOEL for systemic

toxicity in males are 600 ppm and 3,000

ppm, respectively, based on an renal

lesions in males. The technical grade

test material was given to male and

female CD-1 mice in diet for 18 months

at 0, 120, 600, or 3,000 ppm. No

statistically significant increase in

tumor incidence relative to controls

were observed in either sex at any does

up to 3,000 ppm (highest dose tested).

iii. Rats. In the chronic feeding/

oncogenicity study in rats, the NOEL

(systemic) was 35.1 mg/kg/day and the

LOEL (systemic) was 182.7 mg/kg/day.

The technical grade test material was

administered to male and female

Sprague-Dawley rats in diet for 24

months at 0, 120, 600, or 3,000 ppm. A

decrease of 16.9% in bogy weight gain

in females at 3,000 ppm (182.7 mg/kg/

day) was basis for the systemic LOEL.

4. Developmental toxicity— i. Rabbits.

In the developmental study in rabbits,

the maternal NOEL/LOEL for maternal

toxicity were 100 and 300 mg/kg/day

based on premature delivery/abortions,

soft stools, emaciation, decreased

activity and bradypnea. The

developmental NOEL was determined to

be 300 mg/kg/day and developmental

LOEL was determined to be

undetermined; no dose related

anomalies occurred in the 4 remaining

litters studied at 1,000 mg/kg/day.

ii. Rats. In the developmental study in

rats, a maternal NOEL/LOEL were

determined to be 100 mg/kg/day and

300 mg/kg/day, respectively. These

findings were based on increased

incidences in mortality and clinical

signs at 1,000 mg/kg/day with decreases

in food consumption, body weight, and

body weight gain together with

increases in water consumption at 300

and 1,000 mg/kg/day. The

developmental NOEL/LOEL were 100

mg/kg/day and 300 mg/kg/day based on

the increase of skeletal variations at 300

mg/kg/day and above.

5. Reproductive toxicity. In a twogeneration reproduction study in rats,

the systemic NOEL was 1,000 ppm (87

mg/kg/day). The LOEL for sytemic

toxicity was 5,000 ppm (453 mg/kg/

day). Effects were based on decreased

body weight, weight gain and food

consumption in both sexes and both

generations, and increased liver weights

in both sexes associated with liver and

kidney histopathology in males. The

reproductive NOEL was 5,000 ppm. A

reproductive LOEL was not established.

6. Mutagenicity. Studies on gene

mutation and other genotoxic effects: In

a Gene Mutation Assay (Ames Test)/

Reverse Mutation, finding were

determined as negative for induction of

gene mutation measured as the

reversion to histine protrophy of 5

S.typhimurium strains and E.Coli WP2

uvra at doses from 10 to 5,000 μg/plate

with & without S-9 activation. The

highest dose was insoluble. A Gene

Mutation assay in Mammalian Cells was

found to be negative f or mutagencity in

CHO (Chinese hamster ovary) V79 cells

with and without metabolic activation

up to cytotoxic doses (300 μg/mL). In a

Structural Chromosomal Aberration

Assay in vivo, findings proved

nonclastogenic in CHO cells both with

and without S-9 activation up to

cytotoxic doses (300 μg/mL). In Other

Genotoxicity Assays, an increase in

unscheduled DNA synthesis was not

induced both with and without

activation in HeLa cells exposed up to

insoluble doses ranging to 6.4 μg/mL

(without activation) and 51.2 μg/mL

(with activation).

7. Metabolism. The results of the

metabolism studies are as follows:

Acceptable: Rats were orally dosed

with 14C-labeled pyriproxyfen at 2 or
Federal Register / Vol. 63, No. 128 / Monday, July 6, 1998 /Rules and Regulations 36369

1,000 mg/kg and at repeated oral doses

(14 daily doses) of unlabeled

pyriproxyfen at 2 mg/kg followed by

administration of a single oral dose of

labeled pyriproxyfen at 2 mg/kg. Most

radioactivity was excreted in the feces

(81-92%) and urine (5-12%) over a 7

day collection period. Expired air was

not detected. Tissue radioactivity levels

were very low (less than 0.3%) except

for fat. Examination of urine, feces,

liver, kidney, bile and blood metabolites

yielded numerous (>20) identified

metabolites when compared to synthetic

standards. The major biotransformation

reactions of pyriproxyfen include: (i)

Oxidation of the 4′ - position of the

terminal phenyl group; (ii) oxidation at

the 5′ - position of pyridine; and (iii)

cleavage of the ether linkage and

conjugation of the resultant phenols

with sulfuric acid.

8. Neurotoxicity. Neurotoxicity has

not been observed in any of the acute,

subchronic, chronic, developmental or

reproductive studies performed with

pyriproxyfen.

B. Toxicological Endpoints

1. Acute toxicity. An acute dietary

dose and endpoint was not identified in

the database. The Agency concludes

that there is a reasonable certainty of no

harm from acute dietary exposure.

2. Short - and intermediate - term

toxicity. Doses and endpoints were not

identified for short and intermediateterm dermal and inhalation exposure.

The Agency concludes that there are

reasonable certainties of no harm from

these exposures.

3. Chronic toxicity. EPA has

established the RfD for pyriproxyfen (2-

[1-methyl-2-(4-

phenoxyphenoxy)ethoxy]pyridine at

0.35 mg/kg/day. This RfD is based on a

NOEL of 35.1 mg/kg/day and an

uncertainty factor (UF) of 100. The

NOEL was established from the

combined chronic feeding/oncogenicity

study in rats where the LOEL was 3,000

ppm, based on a 16.9% decrease in

body weight gain in females when

compared to controls.

4. Carcinogenicity. Pyriproxyfen is

classified as Category E: not

carcinogenic in two acceptable animal

studies.

C. Exposures and Risks

1. From food and feed uses. In today’s

action tolerances will be established (40

CFR 180.534) for the combined residues

of pyriproxfen, in or on the raw

agricultural commodities: cotton seed

and cotton gin byproducts at 0.05 and

2.0 ppm respectively. Risk assessments

were conducted by EPA to assess

dietary exposures and risks from

pyriproxyfen (2-[1-methyl-2-(4-

phenoxyphenoxy)ethoxy]pyridine as

follows:

i. Acute exposure and risk. Acute

dietary risk assessments are performed

for a food-use pesticide if a toxicological

study has indicated the possibility of an

effect of concern occurring as a result of

a one day or single exposure. No acute

dietary endpoint and dose was

identified in the toxicology data base for

pyriproxyfen, therefore the Agency

concludes that there is a reasonable

certainty of no harm from acute dietary

exposure.

ii. Chronic exposure and risk. The

chronic dietary exposure analysis from

food sources was conducted using the

RfD of 0.35 mg/kg/day. The RfD is based

on the NOEL of 35.1 mg/kg/day in male

and female rats from the Chronic

Feeding/Oncogenicity study in rats, and

an uncertainty factor of 100 applicable

to all population subgroups.

In conducting this chronic dietary risk

assessment, EPA has made very

conservative assumptions: 100% of

cottonseed having pyriproxyfen

tolerances will contain pyriproxyfen

residues and those residues will be at

the level of the established tolerance.

This results in an overestimate of

human dietary exposure. Thus, in

making a safety determination for this

tolerance, EPA is taking into account

this conservative exposure assessment.

The existing pyriproxyfen tolerances

(published, pending, and including the

necessary Section 18 tolerances) result

in a Theoretical Maximum Residue

Contribution (TMRC) that is equivalent

to the following percentages of the RfD:

U.S. population (48 states) 0.00029%;

Nursing infants (< 1 year old) 0.00003%;

Non-nursing infants (< 1 year old)

0.00009%; Children (1-6 years old)

0.00053%; Children (7-12 years old)

0.00045%; Non-Hispanic Whites

0.00030%; Males (13-19 years old)

0.00032%.

The subgroups listed above are: (1)

the U.S. population (48 states); (2) those

for infants and children; and (3) the

other subgroups for which the

percentage of the RfD occupied is

greater than that occupied by the

subgroup U.S. population (48 states).

2. From drinking water— i. Acute

exposure and risk. As previously stated,

no acute dietary endpoint was identified

for assessment of acute dietary risk.

Thus the risk from acute exposure is

considered to be negligible.

ii. Chronic exposure and risk. No

monitoring data is available to perform

a quantitative drinking water risk

assessment for pyriproxyfen at this time.

Thus, the GENEEC model and the SCIGROW model were run to produce

estimates of pyriproxyfen

concentrations in surface and ground

water respectively. The primary use of

these models is to provide a coarse

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 unacceptable aggregate

risk, after having already factored in all

food exposures and other nonoccupational exposures for which OPP

has reliable data.

For chronic (non-cancer) exposure to

pyriproxyfen in surface and ground

water, the drinking water levels of

concern are 12,250 g/L for males (13

yrs+), 10,500 g/L for females (13 yrs+)

and 3,500 g/L for children (1-6 yrs). To

calculate the DWLOC for chronic (noncancer) exposure relative to a chronic

toxicity endpoint, the chronic dietary

food exposure (from DRES) was

subtracted from the RfD to obtain the

acceptable chronic (non-cancer)

exposure to pyriproxyfen in drinking

water. DWLOCs were then calculated

using default body weights and drinking

consumption figures.

Estimated average concentrations of

pyriproxyfen in surface and ground

water are 0.011 ppb (after adjustment for

the highly conservative nature of the

GENEEC model and 0.006 ppb,

respectively). The estimated average

concentrations of pyriproxyfen in

surface and ground water are less than

OPP’s level of concern for pyriproxyfen

in drinking water as a contribution to

chronic aggregate exposure. Therefore,

taking into account present uses and

uses proposed in this action, OPP

concludes with reasonable certainty that

residues of pyriproxyfen in drinking

water (when considered along with

other sources of exposure for which

OPP has reliable data) would not result

in unacceptable levels of aggregate

human health risk at this time.

3. From non-dietary exposure.

Pyriproxyfen is the active ingredient in

many registered residential (indoor,

non-food) products for flea and tick

control. Formulations include foggers,

aerosol sprays, emulsifiable

concentrates, and impregnated materials

(pet collars). Pyriproxyfen (2-[1-methyl2-(4-phenoxyphenoxy)ethoxy]pyridine

is currently registered for use on the

following residential non-food sites:

indoor premise, pet bedding, dogs and

cats.

i. Acute exposure and risk. An acute

dietary dose and endpoint was not
36370 Federal Register / Vol. 63, No. 128 / Monday, July 6, 1998 /Rules and Regulations

identified. Thus the risk from acute

aggregate exposure is considered to be

negligible.

ii. Chronic exposure and risk. Longterm exposure to pyriproxyfen in

residential use products is not expected.

Therefore there is no chronic risk.

Consumer use of these products

typically results in short-term,

intermittent exposures.

iii. Short- and intermediate-term

exposure and risk. The Agency

concludes that there is reasonable

certainty of no harm from short term

and intermediate-term dermal and

inhalation occupational and residential

exposure due to the lack of significant

toxicological effects observed.

4. Cumulative exposure to substances

with common mechanism of toxicity.

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

when considering whether to establish,

modify, or revoke a tolerance, the

Agency consider ‘‘available

information’’ concerning the cumulative

effects of a particular pesticide’s

residues and ‘‘other substances that

have a common mechanism of toxicity.’’

The Agency believes that ‘‘available

information’’ in this context might

include not only toxicity, chemistry,

and exposure data, but also scientific

policies and methodologies for

understanding common mechanisms of

toxicity and conducting cumulative risk

assessments. For most pesticides,

although the Agency has some

information in its files that may turn out

to be helpful in eventually determining

whether a pesticide shares a common

mechanism of toxicity with any other

substances, EPA does not at this time

have the methodologies to resolve the

complex scientific issues concerning

common mechanism of toxicity in a

meaningful way. EPA has begun a pilot

process to study this issue further

through the examination of particular

classes of pesticides. The Agency hopes

that the results of this pilot process will

increase the Agency’s scientific

understanding of this question such that

EPA will be able to develop and apply

scientific principles for better

determining which chemicals have a

common mechanism of toxicity and

evaluating the cumulative effects of

such chemicals. The Agency anticipates,

however, that even as its understanding

of the science of common mechanisms

increases, decisions on specific classes

of chemicals will be heavily dependent

on chemical specific data, much of

which may not be presently available.

Although at present the Agency does

not know how to apply the information

in its files concerning common

mechanism issues to most risk

assessments, there are pesticides as to

which the common mechanism issues

can be resolved. These pesticides

include pesticides that are

toxicologically dissimilar to existing

chemical substances (in which case the

Agency can conclude that it is unlikely

that a pesticide shares a common

mechanism of activity with other

substances) and pesticides that produce

a common toxic metabolite (in which

case common mechanism of activity

will be assumed).

EPA does not have, at this time,

available data to determine whether

pyriproxyfen (2-[1-methyl-2-(4-

phenoxyphenoxy)ethoxy]pyridine 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, pyriproxyfen (2-

[1-methyl-2-(4-

phenoxyphenoxy)ethoxy]pyridine does

not appear to produce a toxic metabolite

produced by other substances. For the

purposes of this tolerance action,

therefore, EPA has not assumed that

pyriproxyfen (2-[1-methyl-2-(4-

phenoxyphenoxy)ethoxy]pyridine has a

common mechanism of toxicity with

other substances.

D. Aggregate Risks and Determination of

Safety for U.S. Population

1. Acute risk. An acute dietary dose

and endpoint was not identified. Thus

the risk from acute aggregate exposure is

considered to be negligible.

2. Chronic risk. Using the TMRC

exposure assumptions described above,

EPA has concluded that aggregate

exposure to pyriproxyfen (2-[1-methyl2-(4-phenoxyphenoxy)ethoxy]pyridine

from food will utilize 0.0003% of the

RfD for the U.S. population. The major

identifiable subgroup with the highest

aggregate exposure is children (1-6 years

old). See discussion below. 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. There are currently no

chronic residential scenarios. The

estimated average concentrations of

pyriproxyfen in surface and ground

water are less than OPP’s level of

concern for pyriproxyfen in drinking

water as a contribution to chronic

aggregate exposure. Therefore, EPA

concludes with reasonable certainty that

residues of pyriproxyfen (2-[1-methyl-2-

(4-phenoxyphenoxy)ethoxy]pyridine in

drinking water do not contribute

significantly to the aggregate chronic

human health risk at the present time

when considering the present uses and

uses proposed by this action.

E. Aggregate Cancer Risk for U.S.

Population

Pyriproxyfen is classified as Category

E: not carcinogenic in two acceptable

animal studies.

F. Aggregate Risks and Determination of

Safety for Infants and Children

1. Safety factor for infants and

children— i. In general . In assessing the

potential for additional sensitivity of

infants and children to residues of

pyriproxyfen (2-[1-methyl-2-(4-

phenoxyphenoxy)ethoxy]pyridine, EPA

considered data from developmental

toxicity studies in the rat and rabbit and

a two-generation reproduction study in

the rat. The developmental toxicity

studies are designed to evaluate adverse

effects on the developing organism

resulting from maternal pesticide

exposure gestation. Reproduction

studies provide information relating to

effects from exposure to the pesticide on

the reproductive capability of mating

animals and data on systemic toxicity.

FFDCA section 408 provides that EPA

shall apply an additional tenfold margin

of safety for infants and children in the

case of threshold effects to account for

pre-and post-natal toxicity and the

completeness of the database unless

EPA determines that a different margin

of safety will be safe for infants and

children. Margins of safety are

incorporated into EPA risk assessments

either directly through use of a MOE

analysis or through using uncertainty

(safety) factors in calculating a dose

level that poses no appreciable risk to

humans. EPA believes that reliable data

support using the standard uncertainty

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

the additional tenfold MOE/uncertainty

factor when EPA has a complete data

base under existing guidelines and

when the severity of the effect in infants

or children or the potency or unusual

toxic properties of a compound do not

raise concerns regarding the adequacy of

the standard MOE/safety factor.

ii. Developmental toxicity studies. In

the rat developmental study, the

developmental NOEL was 100 mg/kg/

day and the maternal NOEL was 100

mg/kg/day. Therefore, there was no

prenatal developmental toxicity in the

presence of maternal toxicity. Similarly

in rabbits, the prenatal developmental

NOEL was 300 mg/kg/day and the

maternal NOEL was 300 mg/kg/day.

Therefore, prenatally exposed fetuses

were not more sensitive to the effects of

pyriproxyfen than maternal animals.
Federal Register / Vol. 63, No. 128 / Monday, July 6, 1998 /Rules and Regulations 36371

iii. Reproductive toxicity study. In the

rat reproduction study, the parental

NOEL of 1,000 ppm was identical to the

pup NOEL of 1,000 ppm and decreased

body weight was seen in both pup and

parental animals. This finding

demonstrates that there are no extra

sensitivities with respect to pre- and

post-natal toxicity between adult and

infant animals.

iv. Pre- and post-natal sensitivity. The

oral perinatal and prenatal data

demonstrated no indication of increased

sensitivity of rats or rabbits to in utero

and postnatal exposure to pyriproxyfen.

v. Conclusion. The 10x factor for

infants and children (as required by

FQPA) was removed, since there was no

special sensitivity for infants and

children and the data base is complete.

For chronic dietary risk assessment, a

UF of 100 is adequate for protection

from exposure to pyriproxyfen.

2. Acute risk. An acute dietary dose

and endpoint was not identified. Thus

the risk from acute aggregate exposure is

considered to be negligible.

3. Chronic risk. Using the

conservative exposure assumptions

described above, EPA has concluded

that aggregate exposure to pyriproxyfen

(2-[1-methyl-2-(4-

phenoxyphenoxy)ethoxy]pyridine from

food will utilize 0.00053% of the RfD

for infants and children. 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. There are currently no

chronic residential scenarios. The

estimated average concentrations of

pyriproxyfen in surface and ground

water are less than OPP’s level of

concern for pyriproxyfen in drinking

water as a contribution to chronic

aggregate exposure. Therefore, OPP

concludes with reasonable certainty that

residues of pyriproxyfen (2-[1-methyl-2-

(4-phenoxyphenoxy)ethoxy]pyridine in

drinking water do not contribute

significantly to the aggregate chronic

human health risk at the present time

when considering the present uses and

uses proposed by this action. EPA

concludes that there is a reasonable

certainty that no harm will result to

infants and children from aggregate

exposure to pyriproxyfen (2-[1-methyl2-(4-phenoxyphenoxy)ethoxy]pyridine

residues.

4. Short- or intermediate-term risk.

Short-term and intermediate-term

dermal and inhalation risk assessments

for residential exposure are not required

due to the lack of significant

toxicological effects observed.

III. Other Considerations

A. Metabolism In Plants and Animals

EPA considers the nature of the

residue in cotton to be adequately

understood. Metabolism of pyriproxyfen

in cotton proceeds through

hydroxylation and cleavage of the

phenoxy ether linkage, with additional

metabolism by oxidation and

conjugation reactions. Much of the

metabolized pyriproxyfen is

reincorporated into natural products.

The HED Metabolism Committee

previously issued a tentative conclusion

(15-JUL-1996) that the residue of

concern in plants is pyriproxyfen per se.

A meeting of the Chemistry Science

Advisory Council (25-FEB-1998)

confirmed this conclusion for cotton

and determined that future food uses

involving pyriproxyfen should be

reviewed by the HED Metabolism

Committee. Metabolism of phenyl-14C

pyriproxyfen in poultry proceeds

through hydroxylation of the

phenoxyphenyl ring, sulfation of the 4′-

OH phenoxyphenyl moiety,

hydroxylation of the pyridyl ring, and

cleavage of the ether linkage.

Metabolism of pyridyl-14C pyriproxyfen

in poultry proceeds through

hydroxylation of the phenoxyphenyl

ring, sulfation of the 4′-OH

phenoxyphenyl moiety, hydroxylation

of the pyridyl ring, cleavage of the ether

linkage and oxidation of the side chain.

EPA concludes that the nature of the

residue in poultry is adequately

understood, and that tolerances are not

needed.

Metabolism of phenyl-14C

pyriproxyfen in goats proceeds through

hydroxylation of the phenoxyphenyl

and pyridyl rings, sulfation of the 4′-OH

phenoxyphenyl moiety, and cleavage of

the ether linkage. Metabolism of

pyridyl-14C pyriproxyfen in goats

proceeds through hydroxylation of the

phenoxyphenyl and pyridyl rings,

sulfation of the 4′-OH phenoxyphenyl

moiety, cleavage of the ether linkage

and oxidation of the side chain. EPA

concludes that the nature of the residue

in ruminants is adequately understood

for this present use and that tolerances

are not required.

B. Analytical Enforcement Methodology

Residue analytical method RM-33P-2

has undergone validation in EPA

laboratories and is suitable to gather

residue data and to enforce tolerances.

The multiresidue method will serve

as a confirmatory method for residues of

pyriproxyfen.

C. Magnitude of Residues

Based on the radioactive metabolic

studies and the calculated dietary

burden, EPA concludes that the

proposed uses on cotton fall under 40

CFR 180.6(a)(3) since there is no

reasonable expectation of finite residues

in meat, milk, poultry, and eggs and

thus tolerances are not required at this

time. If additional uses are sought that

could result in greater livestock dietary

exposure from feedstuffs, the need for

milk, meat, poultry and eggs tolerances

will be reassessed.

D. International Residue Limits

There are no CODEX, Canadian, or

Mexican tolerances for pyriproxyfen

residues on cottonseed or cotton gin

byproducts. Therefore, international

harmonization is not an issue at this

time. Pyriproxyfen is scheduled as a

new compound for JMPR review (both

toxicology and residue chemistry) in

1999.

E. Rotational Crop Restrictions

An acceptable confined accumulation

in rotational crops study with Ph-14C

and Py-14C pyriproxyfen was submitted

. The study showed no significant

uptake (<0.01 ppm) of radioactive

residues (pyriproxyfen) by lettuce,

radish, or wheat. The majority of the 14C

was found in the unextractable material

in the post extraction solids. These

findings indicated that the 14C has been

reincorporated in other, nonpyriproxyfen related compounds.

Therefore a plant back interval is not

necessary for cotton treated with

pyriproxyfen.

IV. Conclusion

Therefore, tolerances are established

for combined residues of pyriproxfen in

cotton seed and cotton gin byproducts at

0.05 and 2.0 ppm respectively.

V. Objections and Hearing Requests

The new FFDCA section 408(g)

provides essentially the same process

for persons to ‘‘object’’ to a tolerance

regulation issued by EPA under new

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

in the old section 408 and in section

409. However, the period for filing

objections is 60 days, rather than 30

days. EPA currently has procedural

regulations which govern the

submission of objections and hearing

requests. These regulations will require

some modification to reflect the new

law. However, until those modifications

can be made, EPA will continue to use

those procedural regulations with

appropriate adjustments to reflect the

new law.
36372 Federal Register / Vol. 63, No. 128 / Monday, July 6, 1998 /Rules and Regulations

Any person may, by September 4,

1998, file written objections to any

aspect of this regulation and may also

request a hearing on those objections.

Objections and hearing requests must be

filed with the Hearing Clerk, at the

address given above (40 CFR 178.20). A

copy of the objections and/or hearing

requests filed with the Hearing Clerk

should be submitted to the OPP docket

for this rulemaking. The objections

submitted must specify the provisions

of the regulation deemed objectionable

and the grounds for the objections (40

CFR 178.25). Each objection must be

accompanied by the fee prescribed by

40 CFR 180.33(i). If a hearing is

requested, the objections must include a

statement of the factual issues on which

a hearing is requested, the requestor’s

contentions on such issues, and a

summary of any evidence relied upon

by the requestor (40 CFR 178.27). A

request for a hearing will be granted if

the Administrator determines that the

material submitted shows the following:

There is genuine and substantial issue

of fact; there is a reasonable possibility

that available evidence identified by the

requestor would, if established, resolve

one or more of such issues in favor of

the requestor, taking into account

uncontested claims or facts to the

contrary; and resolution of the factual

issues in the manner sought by the

requestor would be adequate to justify

the action requested (40 CFR 178.32).

Information submitted in connection

with an objection or hearing request

may be claimed confidential by marking

any part or all of that information as

CBI. Information so marked will not be

disclosed except in accordance with

procedures set forth in 40 CFR part 2.

A copy of the information that does not

contain CBI must be submitted for

inclusion in the public record.

Information not marked confidential

may be disclosed publicly by EPA

without prior notice.

VI. Public Record and Electronic

Submissions

EPA has established a record for this

rulemaking under docket control

number [OPP–300666] (including any

comments and data submitted

electronically). A public version of this

record, including printed, paper

versions of electronic comments, which

does not include any information

claimed as CBI, is available for

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

Monday through Friday, excluding legal

holidays. The public record is located in

Room 119 of the Public Information and

Records Integrity Branch, Information

Resources and Services Division

(7502C), Office of Pesticide Programs,

Environmental Protection Agency,

Crystal Mall #2, 1921 Jefferson Davis

Hwy., Arlington, VA.

Electronic comments may be sent

directly to EPA at:

opp-docket@epamail.epa.gov.

Electronic comments must be

submitted as an ASCII file avoiding the

use of special characters and any form

of encryption.

The official record for this

rulemaking, as well as the public

version, as described above will be kept

in paper form. Accordingly, EPA will

transfer any copies of objections and

hearing requests received electronically

into printed, paper form as they are

received and will place the paper copies

in the official rulemaking record which

will also include all comments

submitted directly in writing. The

official rulemaking record is the paper

record maintained at the Virginia

address in ‘‘ADDRESSES’’ at the

beginning of this document.

VII. Regulatory Assessment

Requirements

This final rule establishes tolerances

under FFDCA section 408(d) in

response to a petition submitted to the

Agency. The Office of Management and

Budget (OMB) has exempted these types

of actions from review under Executive

Order 12866, entitled Regulatory

Planning and Review (58 FR 51735,

October 4, 1993). This final rule does

not contain any information collections

subject to OMB approval under the

Paperwork Reduction Act (PRA), 44

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

enforceable duty or contain any

unfunded mandate as described under

Title II of the Unfunded Mandates

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

104-4). Nor does it require any prior

consultation as specified by Executive

Order 12875, entitled Enhancing the

Intergovernmental Partnership (58 FR

58093, October 28, 1993), or special

considerations as required by Executive

Order 12898, entitled Federal Actions to

Address Environmental Justice in

Minority Populations and Low-Income

Populations (59 FR 7629, February 16,

1994), or require OMB review in

accordance with Executive Order 13045,

entitled Protection of Children from

Environmental Health Risks and Safety

Risks (62 FR 19885, April 23, 1997).

In addition, since these tolerances and

exemptions that are established on the

basis of a petition under FFDCA section

408(d), such as the tolerances in this

final rule, do not require the issuance of

a proposed rule, the requirements of the

Regulatory Flexibility Act (RFA) (5

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

Nevertheless, the Agency has previously

assessed whether establishing

tolerances, exemptions from tolerances,

raising tolerance levels or expanding

exemptions might adversely impact

small entities and concluded, as a

generic matter, that there is no adverse

economic impact. The factual basis for

the Agency’s generic certification for

tolerance actions published on May 4,

1981 (46 FR 24950) and was provided

to the Chief Counsel for Advocacy of the

Small Business Administration.

VIII. Submission to Congress and the

Comptroller General

The Congressional Review Act, 5

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

Business Regulatory Enforcement

Fairness Act of 1996, generally provides

that before a rule may take effect, the

agency promulgating the rule must

submit a rule report, which includes a

copy of the rule, to each House of the

Congress and to the Comptroller General

of the United States. EPA will submit a

report containing this rule and other

required information to the U.S. Senate,

the U.S. House of Representatives, and

the Comptroller General of the United

States prior to publication of the rule in

the Federal Register. This rule is not a

‘‘major rule’’ as defined by 5 U.S.C.

804(2).

List of Subjects in 40 CFR Part 180

Environmental protection,

Administrative practice and procedure,

Agricultural commodities, Pesticides

and pests, Reporting and recordkeeping

requirements.

Dated: June 18, 1998.

Stephen L. Johnson,

Acting Director, Office of Pesticide Programs.

Therefore, 40 CFR chapter I is

amended as follows:

PART 180— [AMENDED]

1. The authority citation for part 180

continues to read as follows:

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

2. Section 180.534 is added to subpart

C to read as follows:

§ 180.534 Pyriproxyfen; tolerances for

residues.

(a) General. Tolerances are

established for combined residues of the

insecticide pyriproxyfen in or on the

following agricultural commodities:

Commodity Parts per million

Cotton gin byproducts ... 2.0
Federal Register / Vol. 63, No. 128 / Monday, July 6, 1998 /Rules and Regulations 36373

1SCADA is an acronym for Supervisory Control

and Data Acquisition. SCADA systems utilize

computer technology to continuously gather data

(e.g., pressure, temperature, and delivery flow rates)

from remote locations on the pipeline. Dispatchers

use SCADA systems to assist in day-to-day

operating decisions on the pipeline. SCADA

systems can also provide input for real-time models

of the pipeline operation. Such models compare

current operating conditions with calculated data

values. A deviation may indicate the possibility of

a leak.

Commodity Parts per million

Cottonseed .................... 0.05

(b) Section 18 emergency exemptions.

[Reserved]

(c) Tolerances with regional

registrations. [Reserved]

(d) Indirect or inadvertent residues.

[Reserved]

[FR Doc. 98–17729 Filed 7-2-98; 8:45 am]

BILLING CODE 6560–50–F

DEPARTMENT OF TRANSPORTATION

Research and Special Programs

Administration

49 CFR Part 195

[Docket No. RSPA–97–2362; Amdt. 195–62]

RIN 2137—AD05

Pipeline Safety: Incorporation by

Reference of Industry Standard on

Leak Detection

AGENCY: Research and Special Programs

Administration (RSPA).

ACTION: Final rule.

SUMMARY: This rule adopts as a

referenced document an industry

publication for pipeline leak detection,

API 1130, ‘‘Computational Pipeline

Monitoring,’’ published by the

American Petroleum Institute (API).

This rule requires that an operator of a

hazardous liquid pipeline use API 1130

in conjunction with other information,

in designing, evaluating, operating,

maintaining, and testing its softwarebased leak detection system. The use of

this document will significantly

advance the acceptance of leak

detection technology on hazardous

liquid pipelines. However, this rule

does not require operators to install

such systems.

DATES: This final rule takes effect July 6,

1999.

FOR FURTHER INFORMATION CONTACT:

Lloyd W. Ulrich, telephone: (202) 366–

4556, FAX: (202) 366–4566, e-mail:

lloyd.ulrich@rspa.dot.gov regarding the

subject matter of this final rule, or

Dockets Unit, (202) 366–4453, for copies

of this final rule or other material in the

docket. Further information can be

obtained by accessing OPS’ Internet

Home Page at: ops.dot.gov.

SUPPLEMENTARY INFORMATION:

I. Background on Requiring Leak

Detection Equipment

A. Congressional Mandate To Issue

Regulations

Congress, in section 212 of the

Pipeline Safety Act of 1992 (codified at

49 U.S.C. 60102(j)), required the

Secretary of Transportation, by October

24, 1994, to survey and assess the

effectiveness of emergency flow

restricting devices (EFRDs) and other

procedures, systems, and equipment

used to detect and locate hazardous

liquid pipeline ruptures and minimize

product releases from hazardous liquid

pipeline facilities. Congress further

mandated that the Secretary issue

regulations two years after completing

the survey and assessment (no later than

October 24, 1996). These regulations

would prescribe the circumstances

under which hazardous liquid pipeline

operators would use EFRDs or other

procedures, systems, and equipment

used to detect and locate pipeline

ruptures and minimize product releases

from pipeline facilities. The Secretary

delegated this authority to the Research

and Special Programs Administration

(RSPA).

B. Advance Notice of Proposed

Rulemaking, Volpe Center Report and

Public Workshop

RSPA used several means to gather

information on EFRDs and leak

detection equipment. We issued an

advance notice of proposed rulemaking

(ANPRM) (59 FR 2802, Jan. 19, 1994) to

solicit information primarily from

hazardous liquid pipeline operators

about operational data and costs related

to EFRDs and about the performance of

leak detection systems to detect and

locate hazardous liquid pipeline

ruptures and minimize product release.

The ANPRM also sought information to

help determine which critical pipeline

locations should be protected from

product releases. Commenters provided

limited usable data and generally

opposed requiring leak detection

equipment and EFRDs.

We contracted with the Volpe

National Transportation Systems Center

(Volpe Center) to conduct a research

study on SCADA 1 systems, including

leak detection systems. Its report,

‘‘Remote Control Spill Reduction

Technology: A Survey and Analysis of

Applications for Liquid Pipeline

Systems’’ (September 29, 1996), found

that because of the pipeline industry’s

diversity, each system used for leak

detection must be custom configured for

a particular pipeline system, that

SCADA and leak detection systems were

dependent on the sophistication of the

host computer and how rapidly and

diverse remote field data can be

collected, and that operators have

invested in SCADA systems, but have

invested much less in software-based

leak detection systems.

RSPA also held a public workshop on

October 19, 1995, to obtain more data on

EFRDs and leak detection systems.

Participants confirmed the Volpe Center

report’s finding that each leak detection

system is unique to the pipeline on

which it is installed. Discussions

included operational and economic

problems with leak detection systems,

as well as their operational, economic

and environmental benefits.

Detailed discussion of the ANPRM,

Volpe Center report, and workshop can

be found at 62 FR 56141; October 29,

1997.

C. Development of API 1130

In 1994, the API formed a task force

to develop a document on

computational pipeline monitoring

(CPM). The task force produced API

1130, entitled ‘‘Computational Pipeline

Monitoring,’’ which addressed the use

of software-based leak detection

equipment. API 1130 defines

computational pipeline monitoring as

‘‘an algorithmic monitoring tool that

allows the pipeline controller to

respond to a pipeline operating anomaly

which may be indicative of a

commodity release.’’ The document’s

stated purpose is to assist the pipeline

operator in selecting, implementing,

testing, and operating a CPM system,

and to help to identify the complexities,

limitations, and other implications of

detecting anomalies on liquid pipelines

using CPM systems.

RSPA and the Volpe Center staff

monitored the task force’s work.

Minutes of the task force meetings, and

copies of final drafts of API 1130, are

available in Docket No. PS–133.

D. Definition of Areas Unusually

Sensitive to Environmental Damage

Congress required that in prescribing

standards, RSPA identify the

circumstances where EFRDs and other

equipment must be installed. RSPA’s

current policy is to base regulations on

risk assessment. We believe that a