19702 Federal Register / Vol. 60, No. 76 / Thursday, April 20, 1995 / Proposed Rules

2The South Coast Area retained its designation of

nonattainment and classified by operation of law

pursuant to sections 107(d) and 181(a) upon the

date of enactment of the CAA. See 55 FR 56694

(November 6, 1991).

3EPA adopted the completeness criteria on

February 16, 1990 (55 FR 5830) and, pursuant to

section 110(k)(1)(A) of the CAA, revised the criteria

on August 26, 1991 (56 FR 42216).

areas. The South Coast Area has been

designated as extreme 2; therefore, this

area was subject to the RACT fix-up

requirement and the May 15, 1991

deadline.

The State of California submitted

many revised RACT rules for

incorporation into its SIP on February

24, 1995, including the rule being acted

on in this document. This document

addresses EPA’s proposed action for

SCAQMD Rule 1164. SCAQMD adopted

Rule 1164 on January 13, 1995. This

submitted rule was found to be

complete on March 10, 1995 pursuant to

EPA’s completeness criteria that are set

forth in 40 CFR part 51 Appendix V 3

and are being proposed for approval

into the SIP.

SCAQMD Rule 1164 controls the VOC

emissions during the operations of

semiconductor manufacturing. VOCs

contribute to the production of groundlevel ozone and smog. This rule was

adopted as part of the SCAQMD’s efforts

to achieve the National Ambient Air

Quality Standard (NAAQS) for ozone

and in response to EPA’s SIP-Call and

the section 182(a)(2)(A) CAA

requirement. The following is EPA’s

evaluation and proposed action for this

rule.

EPA Evaluation and Proposed Action

In determining the approvability of a

VOC rule, EPA must evaluate the rule

for consistency with the requirements of

the CAA and EPA regulations, as found

in section 110 and part D of the CAA

and 40 CFR part 51 (Requirements for

Preparation, Adoption, and Submittal of

Implementation Plans). The EPA

interpretation of these requirements,

which forms the basis for today’s action,

appears in the various EPA policy

guidance documents listed in footnote

1. Among those provisions is the

requirement that a VOC rule must, at a

minimum, provide for the

implementation of RACT for stationary

sources of VOC emissions. This

requirement was carried forth from the

pre-amended Act.

For the purpose of assisting state and

local agencies in developing RACT

rules, EPA prepared a series of Control

Technique Guideline (CTG) documents.

The CTGs are based on the underlying

requirements of the Act and specify the

presumptive norms for what is RACT

for specific source categories. Under the

CAA, Congress ratified EPA’s use of

these documents, as well as other

Agency policy, for requiring States to

‘‘fix-up’’ their RACT rules. See section

182(a)(2)(A). EPA has not yet developed

a CTG to outline control requirements

for the semiconductor manufacturing

source category. Therefore,

interpretations of EPA policy are found

in the Blue Book, referred to in footnote

1, and the Region IX/CARB document

entitled, Guidance Document for

Correcting VOC Rule Deficiencies. In

general, these guidance documents have

been set forth to ensure that VOC rules

are fully enforceable and strengthen or

maintain the SIP.

SCAQMD Rule 1164—Semiconductor

Manufacturing includes the following

significant changes from the current SIP:

• Section (b)(1) includes an

appropriate definition for approved

emission control system which requires

the system to have an overall efficiency

of at least 90 percent.

• Section (b)(14) includes an equation

to determine VOC composite partial

pressure.

• Other definitions were added or

altered for clarity.

• Sections (e)(1) and (e)(2) list the test

methods for determining VOC content

of any VOC-containing materials or

vapors. These methods include EPA

Test Method 24, SCAQMD Method 303,

SCAQMD Method 304, SCAQMD

Method 308.

• Section (e)(3) includes test methods

for determining the efficiency of the

emission control systems. These

methods include the EPA method cited

in 55 Federal Register 26865, EPA Test

Methods 25, 25A, 18, ARB 422, or

SCAQMD Method 25.1.

• Section (e)(4) ensures that a

violation of any requirement of this rule

established by any one of the specified

test methods shall constitute a violation

of the rule when more than one test

method is specified for any testing.

EPA has evaluated the submitted rule

and has determined that it is consistent

with the CAA, EPA regulations, and

EPA policy. Therefore, SCAQMD Rule

1164 is being proposed for approval

under section 110(k)(3) of the CAA as

meeting the requirements of section

110(a) and Part D.

Nothing in this action should be

construed as permitting or allowing or

establishing a precedent for any future

request for revision to any state

implementation plan. Each request for

revision to the state implementation

plan shall be considered separately in

light of specific technical, economic,

and environmental factors and in

relation to relevant statutory and

regulatory requirements.

Regulatory Process

Under the Regulatory Flexibility Act,

5 U.S.C. 600 et seq., EPA must prepare

a regulatory flexibility analysis

assessing the impact of any proposed or

final rule on small entities. 5 U.S.C. 603

and 604. Alternatively, EPA may certify

that the rule will not have a significant

impact on a substantial number of small

entities. Small entities include small

businesses, small not-for-profit

enterprises and government entities

with jurisdiction over populations of

less than 50,000.

SIP approvals under sections 110 and

301 and subchapter I, part D of the CAA

do not create any new requirements, but

simply approve requirements that the

State is already imposing. Therefore,

because the Federal SIP-approval does

not impose any new requirements, it

does not have a significant impact on

any small entities affected. Moreover,

due to the nature of the Federal-state

relationship under the CAA, preparation

of a regulatory flexibility analysis would

constitute Federal inquiry into the

economic reasonableness of state action.

The CAA forbids EPA to base its actions

concerning SIPs on such grounds.

Union Electric Co. v. U.S. E.P.A., 427

U.S. 246, 256–66 (S.Ct. 1976); 42 U.S.C.

7410(a)(2).

The OMB has exempted this action

from review under Executive Order

12866.

List of Subjects in 40 CFR Part 52

Environmental protection, Air

pollution control, Hydrocarbons,

Intergovernmental relations, Ozone,

Reporting and recordkeeping

requirements, Volatile organic

compound.

Authority: 42 U.S.C. 7401–7671q.

Dated: April 11, 1995.

Felicia Marcus,

Regional Administrator.

[FR Doc. 95–9709 Filed 4–19–95; 8:45 am]

BILLING CODE 6560–50–W

40 CFR Part 372

[OPPTS–400092; FRL–4946–2]

Monosodium Methanearsonate and

Disodium Methanearsonate; Toxic

Chemical Release Reporting;

Community Right-to-Know

AGENCY: Environmental Protection

Agency (EPA).

ACTION: Denial of petition.
Federal Register / Vol. 60, No. 76 / Thursday, April 20, 1995 / Proposed Rules 19703

SUMMARY: EPA is denying a petition to

delist monosodium methanearsonate

(MSMA, CAS No. 2163–80–6) and

disodium methanearsonate (DSMA,

CAS No. 144–21–8) from the reporting

requirements under section 313 of the

Emergency Planning and Community

Right-to-Know Act of 1986 (EPCRA).

This action is based on EPA’s

conclusion that neither monosodium

methanearsonate or disodium

methanearsonate meet the deletion

criteria of EPCRA section 313(d)(3).

Specifically, EPA is denying this

petition because: (1) Monosodium

methanearsonate and disodium

methanearsonate are known to cause

toxic effects in experimental animals as

a result of chronic exposure to either of

these substances; and (2) monosodium

methanearsonate and disodium

methanearsonate can reasonably be

anticipated to cause cancer in humans.

FOR FURTHER INFORMATION CONTACT:

Maria J. Doa, Petitions Coordinator,

202–260–9592, for specific information

regarding this document. For further

information on EPCRA section 313,

contact the Emergency Planning and

Community Right-to-Know Information

Hotline, Environmental Protection

Agency, Mail Stop 5101, 401 M St., SW.,

Washington, DC 20460, Toll free: 800–

535–0202, Toll free TDD: 800–553–

7672.

SUPPLEMENTARY INFORMATION:

I. Introduction

A. Statutory Authority

This action is issued under sections

313(d) and (e)(1) of the Emergency

Planning and Community Right-toKnow Act of 1986 (EPCRA), 42 U.S.C.

11023. EPCRA is also referred to as Title

III of the Superfund Amendments and

Reauthorization Act (SARA) of 1986

(Pub. L. 99–499).

B. Background

Section 313 of EPCRA requires certain

facilities manufacturing, processing, or

otherwise using listed toxic chemicals

to report their environmental releases of

such chemicals annually. Beginning

with the 1991 reporting year, such

facilities also must report pollution

prevention and recycling data for such

chemicals, pursuant to section 6607 of

the Pollution Prevention Act of 1990

(PPA), 42 U.S.C. 13106. Section 313

established an initial list of toxic

chemicals that was comprised of more

than 300 chemicals and 20 chemical

categories. Section 313(d) authorizes

EPA to add or delete chemicals from the

list, and sets forth criteria for these

actions. EPA has added and deleted

chemicals from the original statutory

list. Under section 313(e), any person

may petition EPA to add chemicals to or

delete chemicals from the list. EPA must

respond to petitions within 180 days,

either by initiating a rulemaking or by

publishing an explanation of why the

petition is denied.

EPA issued a statement of petition

policy and guidance in the Federal

Register of February 4, 1987 (52 FR

3479), to provide guidance regarding the

recommended content and format for

submitting petitions. On May 23, 1991

(56 FR 23703), EPA issued guidance

regarding the recommended content of

petitions to delete individual members

of the section 313 metal compound

categories. EPA has also published a

statement clarifying its interpretation of

the section 313(d)(2) criteria for adding

and deleting chemical substances from

the section 313 list (59 FR 61439,

November 30, 1994).

II. Description of Petition and Relevant

Regulations

On October 18, 1994, EPA received a

petition from the ISK Biosciences

Corporation to remove monosodium

methanearsonate (MSMA) and disodium

methanearsonate (DSMA) from the list

of toxic chemicals subject to the

requirements of section 313 of the

Emergency Planning and Community

Right-to-Know Act of 1986 (EPCRA).

Specifically, the petition requests that

MSMA and DSMA be excluded from the

arsenic compounds category which is

subject to annual release reporting

requirements under EPCRA section 313.

The petitioner contends that MSMA and

DSMA should be deleted from the

EPCRA section 313 arsenic compounds

category because, in their opinion, the

available data show that neither of these

substances meet the criteria for

inclusion on the list of EPCRA section

313 chemicals. The petitioner did not

provide EPA with any of the studies

cited in the petition.

MSMA and DSMA are organic

arsenicals. EPA regulates arsenic and

certain arsenic compounds under the

Clean Air Act (CAA), Clean Water Act

(CWA), Comprehensive Environmental

Response, Compensation, and Liability

Act (CERCLA), Federal Insecticide,

Fungicide, and Rodenticide Act

(FIFRA), Resource Conservation and

Recovery Act (RCRA), Safe Drinking

Water Act (SDWA), and EPCRA. Arsenic

emissions from smelters and other

facilities are regulated under the CAA.

Under the CWA, guidelines have been

established controlling the

environmental release of arsenic

compounds for certain industrial

categories. Reportable quantities have

been established under CERCLA and

CWA for arsenic and certain arsenic

compounds. Under RCRA, EPA

regulates arsenic as a hazardous

constituent of waste. The SDWA limits

arsenic in drinking water to a maximum

level of 0.05 milligrams/liter (mg/L).

EPA and the National Toxicology

Program have classified inorganic

arsenicals, including arsenate, as known

human carcinogens.

III. EPA’s Technical Review of

Monosodium Methanearsonate (MSMA)

and Disodium Methanearsonate

(DSMA)

The technical review of the petition to

delete MSMA and DSMA included an

analysis of the chemistry, health,

ecological and environmental fate data

known for these substances and for

methanearsonic acid (MAA), the unionized form of MSMA and DSMA.

From a human health standpoint,

MSMA and DSMA will exist largely as

MAA (their un-ionized form) under

acidic conditions, such as those found

in the gastrointestinal tract. Also,

following absorption into the systemic

circulation, MSMA, DSMA, and MAA

will exist in an identical ionized form

at the physiological pH of 7.4, regardless

of their route of administration. EPA

and the ISK Biosciences Corporation (as

indicated in their petition) believe,

therefore, that mammalian toxicity data

on MAA should be suitable to assess the

toxicity of MSMA and DSMA in cases

where such data on the latter two

substances are not available.

A. Chemistry

Monosodium methanearsonate

(CH4AsO3.Na; CAS No. 2163–80–6), also

known as MSMA, and disodium

methanearsonate (CH3AsO3.2Na; CAS

No. 144–21–8), also known as DSMA,

are the monosodium and disodium

salts, respectively, of methanearsonic

acid (also known as MAA). MSMA,

DSMA, and MAA are often refered to as

organic arsenicals, because they each

contain a methyl (–CH3) group. Both

MSMA and DSMA are highly water

soluble crystalline solids, and are used

as herbicides for the postemergent

control of grassy weeds in cotton,

sugarcane, nonbearing orchards, citrus

groves, lawns, turf, and in noncrop

areas. The predominant use of MSMA

and DSMA is for postemergent control

of Johnsongrass and other grassy weeds

prior to planting cotton.

B. Toxicological Evaluation

Information on the health and

environmental effects of MSMA, DSMA,

and MAA were obtained from the

following sources: a 1993 Agency for

Toxic Substances and Disease Registry
19704 Federal Register / Vol. 60, No. 76 / Thursday, April 20, 1995 / Proposed Rules

document entitled Toxicological Profile

for Arsenic (Update) (Refs. 2, 15, and

30); a 1984 EPA document entitled

Health Assessment Document for

Arsenic (Ref. 7); a 1994 National

Toxicology Program document entitled

Seventh Annual Report on Carcinogens:

1994 Summary (Ref. 32); studies

obtained from EPA’s Office of Pesticide

Programs (Ref. 8, 10, 12–14, 16 and 19–

24); and studies found in the literature

(Refs. 1, 3–6, 9, 11, 17, 18, 25, 26, 28,

29, and 31). Specifically, toxicological

and related data on MSMA, DSMA, and

MAA (the un-ionized or free acid form

of MSMA and DSMA) were reviewed for

evidence indicating: (1) Bioavailability

and metabolism to inorganic arsenic; (2)

acute toxicity; (3) chronic toxicity; (4)

carcinogenicity; and (5) ecotoxicity.

1. Bioavailability and metabolism.

Shah and co-workers investigated the

absorption of MSMA and DSMA from

the skin of young and adult rats (Ref. 1).

Both substances were very poorly

absorbed through the skin of all animals

tested, particularly in the younger

animals. No human studies pertaining

to the dermal absorption of MSMA and

DSMA were found. However, human

and animal studies involving dermal

exposure to organic arsenicals closely

related to MSMA and DSMA indicate

that these substances are poorly

absorbed from the skin (Ref. 2).

Shariatpanahi and Anderson found

that MSMA is readily absorbed from the

gastrointestinal tract following oral

administration of the substance to sheep

and goats (Ref. 3). These investigators

observed that 90 percent of the arsenic

content of orally administered MSMA

was excreted in the urine of test animals

within 120 hours of administration.

Small amounts were excreted in the

feces. Arsenic accumulation in the

tissues was low. It is noteworthy to

point out that metabolism of MSMA to

other forms of arsenic (e.g., inorganic)

was not studied in this investigation,

and only total arsenic concentrations

were determined. Specific assays for

MSMA or other specific arsenicals were

not used. The results of this study were

consistent with the results of another

study, which investigated the

absorption, distribution and elimination

of MSMA in New Zealand white rabbits

following multiple oral doses of the

substance (Ref. 4).

A 1991 EPA study investigated the

absorption, distribution, and

elimination of radiolabeled MSMA

([14C-methyl]MSMA) in rats (Ref. 8).

Four groups of rats were used in this

study. Each group consisted of male and

female animals. One group received a

single oral dose of [14C-methyl]MSMA at

5 milligrams per kilogram (mg/kg),

while another group received a single

oral dose of 200 mg/kg. A third group

received a single oral dose of MSMA at

5 mg/kg every day for 14 consecutive

days, followed by a single oral dose of

[14C-methyl]MSMA. A fourth group

received a single oral dose of MSMA at

5 mg/kg every day for 14 consecutive

days, followed by a single intravenous

dose of [14C-methyl]MSMA at 5 mg/kg

or a single oral dose of [14Cmethyl]MSMA at 5 mg/kg. In each of the

test groups, the majority (79.7 to 97.4

percent) of administered [14Cmethyl]MSMA was excreted unchanged

in the urine and feces within 7 days

following dosing. Radiolabeled carbon

dioxide (14CO2) was detected in all

treated groups, and accounted for less

than 0.5 percent of administered [14Cmethyl]MSMA. An unidentified

metabolite, which accounted for 1.8 to

6.7 percent of administered [14Cmethyl]MSMA, was detected in the

urine and feces of all test groups except

the group receiving 200 mg/kg [14Cmethyl]MSMA orally. Another

unidentified metabolite, accounting for

0.7 percent of administered [14Cmethyl]MSMA was found in only one of

the test groups.

Buchet, et al., investigated the oral

absorption and metabolism of MSMA in

humans (Ref. 9). In this study four adult

males were administered MSMA in a

single oral dose equivalent to 500

micrograms of arsenic. The MSMA was

well absorbed, and nearly 70 percent of

the dose was excreted unchanged in the

urine within 24 hours, while a small

percentage was excreted in the urine as

cacodylic acid (dimethylarsonic acid).

Within 96 hours, 78.3 percent of the

MSMA dose was excreted in the urine

unchanged and approximately 13

percent was excreted in the urine as

cacodylic acid. No inorganic arsenic

metabolites were identified (Ref. 9).

Stevens and co-workers investigated

the toxicity of DSMA in rats and mice

exposed to the substance at aerosolized

doses of 6.1 mg/L (for the rats) and 6.9

mg/L (for the mice) for 2 hours (Ref. 5).

Total arsenic levels from body fluids or

tissues were not determined, but the

authors believed that some absorption of

DSMA occurred from the lung.

2. Acute toxicity. Several rat oral

median lethal dose (LD50) values for

MSMA and DSMA were found in the

literature. For DSMA, the rat oral LD50

values, in mg/kg, are (male, female):

2,005, 1,842 (Ref. 10); and 928, 821 (Ref.

11). For MSMA, the rat oral LD50 values

are 1,105 and 1,059 mg/kg for males and

females respectively (Ref. 11). These

data are consistent with rat median

lethal dose data provided by the

petitioner.

Neither DSMA or MSMA produced

significant toxicity in rabbits when

applied dermally at a dose of 2,000 mg/

kg for 24 hours (Refs. 12 and 13). In the

MSMA- treated group, however, there

was evidence of decreased muscle tone

noted in approximately 50 percent of

the animals on observation days 5

through 9 (Ref. 13). By observation day

10, muscle tone was normal in all

treated animals.

In a study investigating the acute

inhalation toxicology of DSMA, mice

and rats were placed in chambers and

were exposed for 2-hours to

experimental atmospheres containing

DSMA in concentrations of at least 8.6

mg/L (Ref. 5). The animals were

observed to have respiratory distress

during the 2–hour exposure period, but

recovered rapidly after removal from

exposure. Respiratory irritation was the

main toxicological effect observed. No

mortality occurred in either species.

These results are consistent with those

of a similar DSMA inhalation study

(Ref. 14). In the latter study, rats were

exposed to experimental atmospheres of

6.0 mg/L DSMA for 4 hours. No deaths

were noted during the 14-day postexposure observation period. Clinical

signs noted on the first day postexposure included body weight loss and

respiratory irritation. Lung discoloration

in 40 percent of the animals was also

noted (Ref. 14).

3. Chronic toxicity. Numerous studies

investigating the chronic toxicity of

inorganic arsenicals have been

conducted. Relatively few studies,

however, have investigated the potential

for chronic toxicity of organic arsenicals

such as MSMA, DSMA, and MAA. The

limited amount of published

mammalian toxicity data on these

substances have been summarized (Ref.

15). In addition, the petitioner

summarized unpublished chronic

toxicity data that are available from

EPA’s Office of Pesticide Programs.

Some of these studies will be briefly

discussed here.

In a study investigating the health

effects resulting from chronic

administration of MAA, four groups of

rats (each group consisting of 60 males

and 60 females) were fed diets

containing 0 (the control group), 50,

400, and 1,300 parts per million (ppm)

of MAA for 104 weeks (Ref. 16).

Mortality was significantly increased in

animals fed diets containing 1,300 ppm

MAA. Because of this increased

mortality, the 1,300 ppm concentration

was reduced to 1,000 ppm during week

53, and to 800 ppm at week 60. Animals

in this group had acute gastrointestinal

inflammation, ulceration and

perforation of the large intestines, and
Federal Register / Vol. 60, No. 76 / Thursday, April 20, 1995 / Proposed Rules 19705

evidence of acute or chronic peritonitis.

These observations were less evident in

animals receiving diets containing 400

ppm MAA. A reduction in the weight of

the thyroid glands was noted in female

rats receiving the 1,300 ppm and 400

ppm MAA diets, and in male rats

receiving 400 ppm MAA. Thickening of

the thyroid follicular epithelium was

noted in both sexes receiving the 1,300

and 400 ppm MAA diets. An increased

incidence of parathyroid adenomas may

have occurred in male rats receiving the

1,300 and 400 ppm MAA diets. This

observation is discussed in greater detail

in unit III.B.4 below.

Jaghabir and co-workers investigated

the health effects of low dose MSMA

exposure in white rabbits (Ref. 17).

Three groups of rabbits were used in

this study. The first group consisted of

four rabbits, which were administered

MSMA orally once a day for 40 days at

a dose of 5 mg/kg. The second group

consisted of two animals, which were

administered MSMA at a dose of 10 mg/

kg orally for 40 days. The third group

(also consisting of two animals) was

similarly administered MSMA at a dose

of 20 mg/kg. A control group of two

animals was also used. All animals were

euthanized and examined at the end of

the 40-day test period. Post-mortem

examination revealed distension and

hyperemia of the digestive tract,

intestinal wall fragility, enlargement of

the kidneys, and intense peripheral

hyperemia of the livers of all animals

administered MSMA. Histopathological

findings revealed hepatic cellular

degeneration, periportal inflammation,

renal tubular nephrosis, interstitial

nephritis and vascular hyperemia.

These observations are consistent with

the observations of similar

investigations cited in the study (Ref.

17), and indicate that low dose exposure

to MSMA can result in tissue damage.

Results from several studies suggest

that MSMA and DSMA may cause

developmental and reproductive

toxicity. In an investigation reported by

Prukop and Savage (Ref. 18) it was

observed that mice administered MSMA

at doses of either 11.9 or 119 mg/kg

orally three times a week for 10 weeks

had decreased reproductive capabilities

(males) and altered reproductive

behavior (females). In another study,

groups of beagle dogs were administered

MAA at 0 (control), 2.5, 8 or 40 mg/kg/

day for 1 week, followed by

administration of 0 (control animals), 2,

8, or 35 mg/kg/day for an additional 51

weeks (Ref. 19). Decreased body weight

gain occurred in male dogs that received

the 35 mg/kg/day dose, and in females

that received the 8 or 35 mg/kg/day

doses. The incidence of female animals

showing no corpora lutea were

increased in the 35 mg/kg/day animal

test group when compared to control

animals (Ref. 19).

In another study, groups of

inseminated New Zealand white rabbits

were administered MAA orally at doses

of 0 (control animals), 1, 3, 7, and 12

mg/kg/day during days 7 thru 19 of

gestation (Ref. 20). Maternal toxicity at

12 mg/kg/day was characterized by

abortion and decreases in mean absolute

body weight, body weight gain, and

food consumption. Decreases in body

weight gain and food consumption were

also noted in the 7 mg/kg/day test

group. An increased incidence of

skeletal variations was noted in the

offspring of animals administered MAA

at 12 mg/kg/day. These skeletal

variations consisited of increased

numbers of ribs and thoracic and

lumbar vertebrae (Ref. 20).

In a multigeneration toxicity study,

groups of male rats were fed MAA at

doses of 0 (control group), 5.8, 17.8, or

63.5 mg/kg/day, and groups of female

rats were fed 0 (control group), 7.5, 22.5,

and 77.6 mg/kg/day for 14 weeks.

Animals were mated, and mated females

continued to receive MAA throughout

gestation and lactation periods. Among

other toxic effects noted in the 63.5

(males) and 77.6 (females) mg/kg/day

dose groups, decreased pregnancy rates,

male fertility rates, and decreased

weights of the prostate and testes also

occurred for parenteral generations F0

and F1 (Ref. 21).

A study was conducted in which

MSMA was administered orally to

pregnant female rats at doses of 0, 10,

100, or 500 mg/kg once daily on

gestation days 6 through 15. No

developmental effects were noted in the

offspring of animals receiving 10 or 100

mg/kg MSMA. Decreased body weight

gain and food consumption were noted

in animals receiving 500 mg/kg MSMA.

The fetuses of this test group had lower

mean fetal body weights when

compared to control animals (Ref. 22).

Based on the results of the animal

studies discussed in the preceding

paragraphs, EPA has determined that

chronic exposure to either MSMA or

DSMA can reasonably be anticipated to

cause gastrointestinal toxicity,

thyrotoxicity, nephrotoxicity,

hepatotoxicity, and developmental and

reproductive toxicity in humans.

4. Carcinogenicity. Data regarding the

carcinogenic potential of MSMA,

DSMA, or MAA are extremely limited.

In a study involving chronic

administration of MAA, four groups of

rats, each group containing 60 males

and 60 females, were fed diets

containing 0 (the control group), 50,

400, and 1,300 ppm of MAA for 104

weeks (Ref. 16). Because of excessive

mortality, the 1,300 ppm concentration

was reduced to 1,000 ppm during week

53, and to 800 ppm at week 60. An

increased incidence of parathyroid

adenomas was observed in males

receiving the 1,300 ppm (4/45) and 400

ppm (4/53) MAA diets, and in females

(4/45) receiving the 1,300 ppm MAA

diets. Evidence of parathyroid adenoma

was also found in 1 of 52 male control

rats. The increased incidence of

parathyroid adenomas in the treated

groups was found to be statistically

significant relative to the control

animals.

As stated previously, cacodylic acid

(dimethylarsonic acid, CAS No. 75–60–

5) is a known human metabolite of

MSMA: Buchet and co-workers found

that in human volunteers approximately

13 percent of an orally-administered

dose of MSMA is converted into

cacodylic acid (Ref 9). EPA has recently

categorized cacodylic acid as a Group

B2 or probable human carcinogen (Ref.

23). EPA’s classification of cacodylic

acid as a Group B2 carcinogen was

based on the results of two studies. The

first was a 2-year dietary feeding study

in male and female rats receiving

cacodylic acid at doses of 0, 2, 10, 40,

and 100 ppm. An increase in urinary

transitional cell bladder tumors with

hyperplasia was noted in both sexes.

The second study was a two year

feeding study in which mice were fed

diets containing 0, 8, 40, 200, and 500

ppm cacodylic acid. An increase in

fibrosarcomas was noted in female mice

fed 500 ppm cacodylic acid (23).

EPA is unaware of any human

epidemiological studies pertaining to

MSMA, DSMA or MAA and cancer.

However, because MAA has been

associated with a possible increased

incidence of parathyroid adenomas in

experimental animals, and cacodylic

acid (a known human metabolite of

MSMA) is categorized by EPA as a

probable human (B2) carcinogen, EPA

believes that it is reasonable to assume

that MSMA, DSMA, and MAA may be

potential human carcinogens.

5. Ecotoxicity. EPA has calculated a

bobwhite quail oral LD50 of 425.2 mg

MSMA/kg (Ref. 24). This value was

based on 51 percent active ingredient

(MSMA) in the test material. EPA

concluded from this study that MSMA

is moderately toxic to bobwhite quail.

Based on the same study, the petitioner

gave an LD50 value of MSMA in

bobwhite quail as 834 mg/kg. This

value, however, was not adjusted to take

into account that the test product

contains only 51 percent MSMA.

Moffett, et al., have investigated the
19706 Federal Register / Vol. 60, No. 76 / Thursday, April 20, 1995 / Proposed Rules

toxicity of MSMA and DSMA in

honeybees (Refs. 25 and 26). In one of

the studies, MSMA was sprayed onto

honeybees at a rate of 4 lb/acre in a

carrier volume of 20 gallons/acre (Ref.

25). Mortalities were monitored for 14

days. Bee mortalities reached 50 percent

after only approximately 2 days.

Consequently, the investigators

concluded that MSMA is highly toxic to

honeybees (Ref. 25). In the other study

MSMA and DSMA were fed to newly

emerged honeybees in a 60 percent

sucrose syrup (Ref. 26). Half-lives (i.e.

the number of days for 50 percent

mortality to occur) for MSMA and

DSMA were 5.4 and 4.4 days at 100

parts per million by weight (ppmw)

concentrations, and 2.5 and 1.2 days at

1,000 ppmw, respectively. The

investigators concluded that both

chemicals are ‘‘extremely toxic’’ at 100

and 1,000 ppmw. Of the 14 herbicides

tested in this study, MSMA and DSMA

were found to be the most toxic to

honeybees (Ref. 26). EPA does not yet

have toxicity criteria for honeybees in

EPA’s Draft Hazard Assessment

Guidelines for Listing Chemicals on the

Toxic Release Inventory (Ref. 27). EPA

believes, however, that the results of the

studies described above strongly

indicate that MSMA and DSMA are

quite toxic to honeybees.

The petitioner stated that for MSMA

the acute median effective concentration

(EC50) producing lethality in the

freshwater alga Selenastrum

capricornutum is 7.6 mg/L. The

petitioner concluded (page 68 of the

petition) from this and other

information that MSMA and DSMA are

‘‘* * * .not particularly toxic to aquatic

life * * * .’’ However, based on the

draft criteria developed by EPA to assess

the hazard of chemical substances, EPA

considers MSMA to be moderately toxic

to aquatic life because the algal acute

EC50 value for MSMA is between 100

micrograms per liter (ug/L) and 10 mg/

L, the EC50 range considered by EPA to

be moderately toxic for aquatic biota

(Ref. 27). Other aquatic toxicity test data

mentioned in the petition also indicate

MSMA and DSMA are moderately

acutely toxic (i.e., have EC50 or LC50

[median lethal concentration] values

between 100 ug/L and 10 mg/L) to

aquatic biota. The 96-h LC50 of MSMA

in bluegill, for example, is 4.2 mg/L.

EPA obtained MSMA and DSMA

aquatic toxicity data not mentioned by

the petitioner (Ref. 28). The 28-day

daphnid LC0 (zero percent lethal

concentration) value for DSMA is 0.83

mg/L. The LC0 for DSMA in two species

of invertebrates (a snail and a stonefly)

and rainbow trout was found to be 0.97

mg/L (Ref. 28). A 28-day LC40 (40

percent lethal concentration) value of

0.97 mg/L DSMA was reported for a

gammarid amphipod invertebrate. In

bluegills, the 96-h LC50 for MSMA was

found to be 1.9 mg/L. These data

indicate that the toxicity of MSMA and

DSMA to aquatic species is greater than

that implied by the petitioner.

C. Environmental Fate

Anthropogenic input of arsenic into

the environment occurs through

smelting, coal burning, and the use of

arsenical herbicides (e.g., MSMA and

DSMA) (Refs. 29 and 30). Numerous

investigators have studied the

environmental fate of arsenic-containing

substances, including MSMA and

DSMA. Results from these studies have

been summarized (Refs. 29, 30, and 31).

Arsenic-containing substances such as

MSMA, DSMA, and MAA undergo

chemical and biochemical

transformations in the environment that

include oxidation, reduction, and

methylation. These transformations are

largely controlled by soil, sediment

absorption/desorption processes, and

affect the overall environmental

distribution of arsenic-containing

substances (Refs. 29, 30, and 31).

Following their release into the

environment, MAA, MSMA, and DSMA

bind reversibly to ferrous and aluminum

oxides contained on the surfaces of clay

particles of soils and sediments. The

bound form of these substances are

insoluble in water, and exist in

equilibrium with their unbound, soluble

forms in the water present in soils and

sediments. While unbound, MAA,

MSMA, and DSMA undergo a cascade

of biotic transformations that include

oxidation, reduction, methylation, and

demethylation (Ref. 31). Specifically,

MAA, MSMA, and DSMA undergo

oxidative demethylation to arsenate

(H2AsO4-), an inorganic form of arsenic,

and reductive methylation to cacodylic

acid. The arsenate can be methylated

back to MAA, and the two species will

exist in equilibrium. Cacodylic acid can

undergo further methylation to

dimethylarsine or trimethylarsine,

which will exist in equilibrium with

cacodylic acid. These alkylarsine

products volatilize from the soils and

waters in which they were formed and

enter the atmosphere. While in the

atmosphere the alkylarsines can be

transported to other locations, and the

transformation cascade is repeated: the

alkylarsines are oxidized back to

cacodylic acid, MAA, and arsenate

(Refs. 29–31). Thus, anthropogenic

releases of MSMA or DSMA may

indirectly lead to increased arsenic

concentrations in areas where direct

anthropogenic releases of these

substances do not occur (Refs. 29–31).

Terrestrial plants may accumulate

arsenic-containing substances by root

uptake from soils or by absorption of

airborne arsenic deposited on plant

leaves (Ref. 30).

The predominant form of arsenic in

surface waters (e.g., drinking waters, sea

waters, etc.) is usually arsenate

(H2AsO4-), an inorganic form of arsenic.

Arsenate in surface waters can result

from (or enter into) the transformation

cascade described in the preceding

paragraph. Above average exposure of

the general population to arsenic from

drinking waters is possible in areas of

high natural arsenic levels in ground

waters, or elevated arsenic levels in

drinking waters due to industrial

discharges, application of arseniccontaining pesticides, or leaching from

hazardous waste facilities (Ref. 30).

Individuals living in the vicinity of large

smelters and other industrial emitters of

arsenic substances may be exposed to

greater than average amounts of arsenate

as a result of environmental

transformation of organic (e.g., MSMA

or DSMA) or inorganic arsenic

substances to arsenate (Ref. 30).

Arsenate is an inorganic form of

arsenic. An association between skin

cancer and consumption of drinking

water containing inorganic arsenic has

been observed and confirmed (Ref. 32).

Epidemiologic studies in areas where

drinking waters containing inorganic

arsenic concentrations ranging from

0.35 to 1.14 mg/L indicate elevated risks

for cancers of the urinary bladder,

kidney, skin, liver, lung, and colon in

both men and women (Ref. 32).

Increased incidences of cancer in

individuals occupationally exposed to

inorganic forms of arsenic have also

been confirmed (Ref. 32). Because of

these findings and the findings from

other studies regarding human exposure

to inorganic forms of arsenic and

increased incidences of cancer, the

National Toxicology Program

categorizes arsenic and certain arsenic

compounds (e.g., arsenate) as known

human carcinogens (Ref. 32). EPA also

categorizes inorganic arsenicals,

including arsenate, as known human

(Group A) carcinogens. The

categorization by EPA of cacodylic acid

as a Group B2 (probable human)

carcinogen was discussed in unit III.B.4.

above. Thus, releases of MSMA or

DSMA into the environment will lead to

the formation of arsenate and cacodylic

acid, which have been categorized by

the National Toxicology Program and

EPA as carcinogens.
Federal Register / Vol. 60, No. 76 / Thursday, April 20, 1995 / Proposed Rules 19707

D. Technical Summary

MSMA and DSMA are highly water

soluble organic arsenicals that are used

as herbicides for the postemergent

control of grassy weeds. MSMA and

DSMA are poorly absorbed from the

skin and lung, and well absorbed from

the gastrointestinal tract. In the

gastrointestinal tract, both MSMA and

DSMA are expected to exist largely as

MAA. Based on human and animal

studies, MAA, MSMA, and DSMA are

expected to be completely absorbed and

widely distributed in humans following

oral administration. In humans, MSMA

is excreted largely unchanged in the

urine, and approximately 13 percent is

metabolized to cacodylic acid. MSMA

and DSMA are not believed to be

metabolized to inorganic arsenicals in

humans.

The mammalian LD50 values of

MSMA and DSMA following acute oral

exposure are quite high, indicating that

these substances have a low order of

acute lethality. Some animal studies

indicate, however, that chronic

exposure to lower doses of MSMA or

DSMA produce gastrointestinal toxicity,

thyrotoxicity, nephrotoxicity,

hepatotoxicity, developmental and

reproductive toxicity. Data regarding the

carcinogenic potential of MSMA,

DSMA, or MAA are extremely limited.

A suggestion of an increased incidence

of parathyroid adenomas was observed

in rats administered MAA in their diets.

Cacodylic acid, a known human

metabolite of MSMA, is categorized by

EPA as a Group B2 (probable human)

carcinogen. Because MSMA and,

presumably, DSMA are converted into

cacodylic acid, MSMA and DSMA may

also be carcinogenic in humans.

MSMA and DSMA are moderately

toxic to terrestrial and aquatic species

that include, among others, bobwhite

quail, honeybees, freshwater algae, fish,

and daphnids.

In the environment, MSMA, DSMA,

and MAA undergo a cascade of

chemical and biochemical

transformations that are controlled by

soil, sediment adsorption/desorption

processes. In this cascade, MSMA,

DSMA, and MAA are converted into

arsenate (inorganic arsenic), cacodylic

acid, dimethylarsine and

trimethylarsine. Inorganic arsenicals,

including arsenate, are categorized by

the National Toxicology Program and

EPA as known human carcinogens. In

addition, cacodylic acid is categorized

by EPA as a Group B2 or probable

human carcinogen.

IV. Rationale for Denial

EPA is denying the petition to delete

MSMA and DSMA from the section 313

list of toxic chemicals. This denial is

based on the Agency’s determination

that MSMA and DSMA: (1) May cause

chronic toxic effects in humans; and (2)

are potential carcinogens. In regard to

the latter point, EPA has determined

that because MSMA and, undoubtedly,

DSMA are metabolized in humans to

cacodylic acid (a probable human

carcinogen), it is reasonable to assume

that MSMA and DSMA are also

probable human carcinogens. In

addition, it has been demonstrated that

MSMA and DSMA are converted into

arsenate (an inorganic arsenic) and

cacodylic acid in soils and sediments.

Inorganic arsenics, including arsenate,

are categorized by the National

Toxicology Program and EPA as known

human carcinogens. EPA concludes that

MSMA and DSMA meet the EPCRA

section 313(d)(2)(B) criteria because

they can reasonably be anticipated to

cause cancer in humans as a result of

their metabolism to cacodylic acid or

their environmental conversion to

cacodylic acid and arsenate. Thus, in

accordance with EPCRA section

313(d)(2), EPA has determined that

MSMA and DSMA exhibit high chronic

toxicity and, therefore, should not be

deleted from the section 313 list of toxic

chemicals.

EPA’s denial of the petition to delist

MSMA and DSMA from the section 313

list of toxic chemicals is based, in part,

on the conversion of these substances to

substances that are regarded as being

either known or probable human

carcinogens, and is consistent with past

Agency decisions regarding section 313

delisting petitions. [See, e.g., Chromium

(III) Oxide (56 FR 58859, November 22,

1991)]

V. References

(1) Shah, P.V., Fisher, H.L., Sumler,

M.R., Monroe, R.J., Chernoff, N., Hall,

L.L. (1987) Comparison of the

Penetration of 14 Pesticides Through the

Skin of Young and Adult Rats. J.

Toxicol. Environ. Health. 21:353–366.

(2) Toxicological Profile For Arsenic

(Update). Agency for Toxic Substances

and Disease Registry (ATSDR) Report

No. ATSDR/TP-92/02; pp. 7–84.

(3) Shariatpanahi, M., Anderson, A.C.

(1984) Distribution and Toxicity of

Monosodium Methanearsonate

Following Oral Administration of the

Herbicide to Dairy Sheep and Goats. J.

Environ. Sci. Health B19(4 5):427–439.

(4) Jaghabir, M.D., Abdelghani, A.A.,

Anderson, A.C. (1991) Absorption,

Distribution, and Elimination of Arsenic

in New Zealand White Rabbits

(Oryctalagus cuniculus) Following

Multiple Oral Doses of Monosodium

Methane Arsonate. Environmental

Toxicology and Water Quality: An

International Journal 6:113–119.

(5) Stevens, J.T., DiPasquale, L.C.,

Farmer, J.D. (1979) The Acute Inhalation

Toxicology of the Technical Grade

Organoarsenical Herbicides, Cacodylic

Acid and Disodium Methanearsonic

Acid; A Route Comparison. Bull.

Environm. Contam. Toxicol. 21:304–

311.

(6) Goyer, R.A. (1991) Toxic Effects of

Metals. In: Amdur, M.O., Doull, J.

Klaassen, C.D. eds., Casarett and Doull’s

Toxicology, The Basic Science of

Poisons. Fourth Edition. Pergamon

Press: New York; pp. 631–632.

(7) U.S. Environmental Protection

Agency. (1984). Health Assessment

Document for Arsenic. Criteria and

Assessment Office, Research Triangle

Park, NC, Report No. EPA 600/8–83–

021F.

(8) U.S. Environmental Protection

Agency. (1991) Data Evaluation Report:

Metabolism Data on [14C-methyl]MSMA.

MRID No. 42010501 (Office of Pesticide

Programs).

(9) Buchet, J.P., Lauwerys, R., Roels,

H. (1981) Comparison of the Urinary

Excretion of Arsenic Metabolites After a

Single Oral Dose of Sodium Arsenite,

Monomethylarsonate, or

Dimethylarsinate in Man. Int. Arch.

Occup. Environ. Health 48:71–79.

(10) U.S. Environmental Protection

Agency. (1991) Data Evaluation Report:

Rat Acute Oral Toxicity of DSMA 81P

in the Rat. MRID No. 418920–04.

(11) Gaines, T.B., Linder, R.E. (1986)

Acute Toxicity of Pesticides in Adult

and Weanling Rats. Fundam. Appl.

Toxicol. 7:299–308.

(12) U.S. Environmental Protection

Agency. (1991) Data Evaluation Report:

Rabbit Acute Dermal Toxicity of DSMA.

MRID No. 418920–05.

(13) U.S. Environmental Protection

Agency. (1991) Data Evaluation Report:

Rabbit Acute Dermal Toxicity of MSMA.

MRID No. 418900–01.

(14) U.S. Environmental Protection

Agency. (1991) Data Evaluation Report:

Acute Inhalation Toxicity of DSMA 81P

in the Rat. MRID No. 418920–06.

(15) Toxicological Profile For Arsenic.

Agency for Toxic Substances and

Disease Registry (ATSDR) Report No.

ATSDR/TP-92/02; pp. 7–84.

(16) U.S. Environmental Protection

Agency. (1991) Data Evaluation Report:

Methanearsonic Acid Combined

Chronic Feeding and Oncogenicity

Study in the Rat. MRID No. 41669001.

(17) Jaghabir, M.T.W., Abdelghani,

A.A., Anderson, A.C. (1989)
19708 Federal Register / Vol. 60, No. 76 / Thursday, April 20, 1995 / Proposed Rules

Histopathological Effects of

Monosodium Methanearsonate (MSMA)

on New Zealand White Rabbits

(Oryctalagus cuniculus). Bull. Environ.

Contam. Toxicol. 42:289–293.

(18) Prukop, J.A., Savage, N.L. (1986)

Some Effects of Multiple, Sublethal

Doses of Monosodium Methanearsonate

(MSMA) Herbicide on Hematology,

Growth, and Reproduction of Laboratory

Mice. Bull. Environ. Contam. Toxicol.

36:337–341.

(19) U.S. Environmental Protection

Agency. (1989) Data Evaluation Report:

Methanearsonic Acid Fifty Two Week

Chronic Oral Toxicity Study in Beagle

Dogs. MRID No. 405461–01/412664–01.

(20) U.S. Environmental Protection

Agency. (1986) Data Evaluation Report:

Methanearsonic Acid Teratology Study

in the Rabbit. MRID No. 159390–01.

(21) U.S. Environmental Protection

Agency. (1994) Data Evaluation Report:

a Two Generation Reproduction Study

in Rats with Methanearsonic Acid

(MAA). MRID No. 431783–01.

(22) U.S. Environmental Protection

Agency. (1990) Data Evaluation Report:

a Teratology Study in Rats with

Methanearsonic Acid. MRID No.

419264–01.

(23) U.S. Environmental Protection

Agency. (1994) Carcinogenicity Peer

Review Document for Cacodylic Acid.

(24) U.S. Environmental Protection

Agency. (1991) Data Evaluation Report:

Monosodium Methane Arsonate

(MSMA); Avian Single Dose Oral LD50

Test (Bobwhite Quail). MRID No.

416100–02.

(25) Moffett, J.O., Morton, H.L.,

MacDonald, R.H. (1972) Toxicity of

Some Herbicidal Sprays to Honey Bees.

J. Econ. Entomol. 65:32–36.

(26) Morton, H.L., Moffett, J.O.,

MacDonald, R.H. (1972) Toxicity of

Herbicides to Newly Emerged Honey

Bees. Environ. Entomol. 1:102–104.

(27) Hazard Assessment Guidelines

for Listing Chemicals on the Toxic

Release Inventory. Revised Draft (May

26, 1992). Office of Pollution Prevention

and Toxics, U.S. Environmental

Protection Agency.

(28) Eisler, R. (1988) Arsenic Hazards

to Fish, Wildlife, and Invertebrates: A

Synoptic Review. Dept. of the Interior,

U.S. Fish Wildl. Serv. Biol. Rep.

85(1.12) .

(29) Menzer, R.E. (1991) Water and

Soil Pollutants. In: Amdur, M.O., Doull,

J. Klaassen, C.D. eds., Casarett and

Doull’s Toxicology, The Basic Science

of Poisons. Fourth Edition. Pergamon

Press: New York; pp. 891–893.

(30) Toxicological Profile For Arsenic.

Agency for Toxic Substances and

Disease Registry (ATSDR) Report No.

ATSDR/TP-92/02; pp. 99–108.

(31) Woolson, E.A. (1977) Fate of

Arsenicals in Different Environmental

Substrates. Environmental Health

Perspectives 19:73–81.

(32) Seventh Annual Report on

Carcinogens: 1994 Summary. United

States Department of Health and Human

Services, National Toxicology Program;

pp. 21–26.

VI. Administrative Record

The record supporting this decision is

contained in docket control number

OPPTS–400092. All documents,

including an index of the docket, are

available to the public in the TSCA

NonConfidential Information Center

(NCIC), also known as the Public Docket

Office, from noon to 4 p.m., Monday

through Friday, excluding legal

holidays. The TSCA NCIC is located at

EPA Headquarters, Rm. NE–B607, 401

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

List of Subjects in 40 CFR Part 372

Environmental protection, Chemicals,

Community right-to-know, Reporting

and recordkeeping requirements, and

Toxic chemicals.

Dated: April 14, 1995.

Lynn R. Goldman,

Assistant Administrator for Prevention,

Pesticides and Toxic Substances.

[FR Doc. 95–9782 Filed 4–17–95; 12:11 pm]

BILLING CODE 6560–50–F

GENERAL SERVICES

ADMINISTRATION

48 CFR Parts 501, 503, 505, 506, 507,

552, and 570

[GSAR Notice 5–399]

RIN–AF67

General Services Administration

Acquisition Regulation; Leasing Real

Property

AGENCY: Office of Acquisition Policy,

GSA.

ACTION: Proposed rule.

SUMMARY: The General Services

Administration (GSA) invites written

comments on a proposal to amend the

General Services Administration

Acquisition Regulation (GSAR) to

implement various provisions of the

Federal Acquisition Streamlining Act of

1994 as they apply to the acquisition of

leasehold interests in real property and

to implement recommendation of a GSA

process re-engineering team for

streamlining and/or improving the lease

acquisition process.

DATES: Comments on the proposed rule

should be submitted by June 19, 1995 to

be considered in the formulation of the

final rule.

ADDRESSES: Interested parties should

submit written comments to Ms.

Marjorie Ashby, General Services

Administration, Office of GSA

Acquisition Policy, 18th & F Streets,

NW, Washington, DC 20405.

FOR FURTHER INFORMATION CONTACT:

Tom Wiznowski, Office of GSA

Acquisition Policy, (202) 501–1224.

SUPPLEMENTARY INFORMATION:

A. Background

This proposed rule implements

several provisions of the Federal

Acquisition Streamlining Act (FASA),

Pub. L. 103–355, October 13, 1994 as it

applies to the acquisition of leasehold

interests in real property. Most of the

provisions of FASA which are

implemented in the Federal Acquisition

Regulation (FAR) will also apply to

leases of real property because the

GSAR incorporates provision of the FAR

that apply to leases of real property by

reference. Other provisions of FASA are

unique to leases of real property and are

addressed in Part 570 of the GSAR. The

most significant provisions of FASA

that are implemented through changes

in Part 570 are:

(1) Section 4402 of FASA amended

the Federal Property and Administrative

Services Act to authorize the

Administrator of General Services to

prescribe regulations that provide

special simplified procedures for

acquisitions of leasehold interests in

real property at rental rates that do not

exceed the simplified acquisition

threshold. For purposes of establishing

such procedures the rental rate or rates

under a multiyear lease do not exceed

the simplified acquisition threshold if

the average annual rent payable for the

period of the lease does not exceed the

simplified acquisition threshold

($100,000).

(2) Section 1061 of FASA amended

the Federal Property and Administrative

Services Act to provide for disclosure of

all significant evaluation factors and

subfactors and to provide for disclosure

to offerors whether all evaluation factors

other than cost or price, when

combined, are significantly more

important than cost or price;

approximately equal in importance to

cost or price; or significantly less

important than cost or price.

(3) Section 1063 of FASA amended

the Federal Property and Administrative

Services Act to provide for notification,

in writing or by electronic means, of

award to unsuccessful offerors within 3

days after the date of contract award.