61654 Federal Register / Vol. 58, No. 223 / Monday, November 22, 1993 / Proposed Rules

businesses. However, EPA expects to

receive few SNUNs for the substances.

Therefore. EPA believes that the number

of small businesses affected by this rule

would not be substantidl, even if all of

the SNUN submitters were small firms.

C. Paperwork Reduction Act.

The information collection

requirements contained in this rule have

been approved by OMB under the

provisions of the Paperwork Reduction

Act (44 U.S.C. 3501 et seq.), and have

been assigned OMB control number

2070-0012.

Public reporting burden for this

collection of information is estimated to

vary from 30 to 170 hours per response,

with an average of 100 hours per

response, including time for reviewing

instructions, searching existing data

sources, gathering and maintaining the

data needed, and completing and

reviewing the collection of information.

Send comments regarding the burden

estimate or any other aspect of this

collection of information, including

suggestions for reducing this burden, to

Chief, Information Policy Branch,

(2131), U.S. Environmental Protection

Agency, 401 M St., SW., Washington,

DC 20460; and to the Office of

Management and Budget, Paperwork

Reduction Project (2070-0012),

Washington, DC 20503.

List of Subjects in 40 CFR Part 721

Environmental protection, Chemicals,

Hazardous materials, Reporting and " recordkeeping requirements, Significant

new uses,

Dated: November 15, 1993.

Victor J. Kimm,

Acting Assistant Administrator for

Prevention, Pesticides and Toxic Substances.

Therefore, it is proposed that 40 CFR

part 721 be amended as follows:

PART 721--AMENDED]

1. The authority citation for part 721

would continue to read as follows:

Authority: 15 U.S.C. 2604, 2607, and

2625(c)

2. By adding new § 721.340 to subpart

E to read as follows:

§721.340 Acrylate esters.

(a) Chemical substances and

significant new uses subject to reporting.

(1) Chemical substances falling within

the acrylate ester category definition

and not on the TSCA Inventory as of

[Insert proposed date of this rule] are

subject to reporting under this section

for the significant new uses described in

paragraph (a)(2) of this section. The

acrylate ester category shall include any

ester of an acrylate, as defined in

paragraph (b)(3)(i) of this section

aving:

(i) A measured number-average

molecular weight of 1,000 amu (anu is

the unified atomic mass unit referenced

to the mass of Carbon 12) or less.

(ii) A measured number-average

molecular weight of over 1,000 amu and

containing more than 2 percent by

weight of any acrylate ester with a

molecular weight of 500 amu or less.

(2) The significant new uses are:

(i) Protection in the workplace.

Requirements as specified in

§ 721.63(a)(1), (a)(2)(i), (a)(2)(iii),

(a)(2)(iv), (a)(3). (a)(4), (a)(5)(xi). (a)(6)(i),

(a)(6)(ii). (a)(6)(iv). (b) (concentration set

at 0.1 percent), and (c). (ii) Hazard communication program.

Requirements as specified in

§ 721.72(a), (b), (c), (d), (e)

(concentration set at 0.1 percent), (0, (h)(1)(i}(A}, (h)(1)(i)(B), (h)(1)(i)(C),

(h)(1)(iii)(A}, (h)(1)(vi), (h)(2)(i)(B),

(h)(2)(i)(C), and (h)(2)(i)(D).

(iii) Industrial, commercial, and

consumer activities. Requirements as

specified in § 721.80(o). (b) Specific requirements. The

provisions of subpart A of this part

apply to this section except as modified

by this paragraph. (1) Recordkeeping requirements.

Recordkeeping requirements as

specified in § 721.125(a) through (i) are

applicable to manufacturers, importers,

and processors of these substances.

(2) Limitations or revocation of

certain notification requirements. The

provisions of § 721.185 apply to this

section.

(3) Definitions. (i) Acrylate means

those chemical substances (including

combinations of chemical substances

that are not mixtures) whose structures

contain one or more covalently bound

substructures which are described as

terminal or pendant acrylate groups.

Such chemical substances are

considered to contain a functional

acrylate moiety. The functional nature

of these chemical substances is

attributed to the conjugated carbon to

carbon double bond present in the

acrylate. Functional acrylate

substructures may be produced from

several types of reactions. Regardless of

the synthetic route, the unsaturated

bond of the acrylate group(s) remains

present and unreacted. Functional

acrylate substructures are typically but

not always produced from reactions

between mono- or polyhydric alcohols

and acrylic acid in which the -OH

radical(s) from the alcohol combines

with the -COOH radical of the acrylic

acid to form acrylate esters. This

reaction mechanism ensures that the

double bond remains intact. The

substructures produced from the

possible chemical reaction types are

diagramed below; the free valence is the

location of covalent linkage to the rest

of the molecule:

-0-(-C--O)CH=CH 2

Acrylate Group (2-Propenoate Group)

(ii) [Reserved]

[FR Doc. 93-28611 Filed 11-19-93; 8:45 am)

BILiNG CODE W60-"

40 CFR Part 799

[OPPTS-42150, FRL 4010-2]

RIN No. 2070-AS07

Acetophenone, Phenol, N,NDimethylaniline, Ethyl Acetate, and 2,6-

Dimethylphenol; Proposed Test Rule,

Notice of Opportunity to Initiate

Negotiations for TSCA Section 4

Testing Consent Agreements

AGENCY: Environmental Protection

Agency (EPA).

ACTION: Proposed rule.

SUMMARY: EPA is proposing a test rule

under section 4(a) of the Toxic

Substances Control Act (TSCA) that

would require manufacturers and

processors of five chemicals

(acetophenone, phenol, NNdimethylaniline, ethyl acetate, and 2,6-

dimethylphenol) to conduct testing for

certain chemical fate, health and

environmental effects. This rule would

require that testing be conducted to

develop data with respect to chemical

fate and health and environmental

effects for which there is an

insufficiency of data and experience and

which are relevant to a determination

that the manufacture, distribution in

commerce, processing, use, or disposal

of such chemicals, or that any

combination of such activities, does or

does not present an unreasonable risk of

injury to health or the environment. In

addition to the proposed test rule, EPA

has negotiated a testing consent

agreement development program under

TSCA section 4 to allow the Agency to

make greater use of enforceable consent

agreements (ECAs). Therefore, EPA is

soliciting interested parties for

participation in or monitoring of

consent agreement negotiations for the

chemicals that are proposed for testing

in this rulemaking. EPA is also inviting

manufacturers and/or processors of

chemical substances who wish to

participate in consent agreement

negotiations for the chemicals proposed

for testing to develop and submit testing

consent agreement proposals to EPA.
Federal Register / Vol. 58, No. 223 / Monday, November 22, 1993 / Proposed Rules

DATES: Written comments on the

proposed rule must be received by EPA

on or before January 21, 1994. If persons

request an opportunity to submit oral

comments by January 6, 1994, EPA will

hold a public meeting on this proposed

rule inWashington, DC. For further

information on arranging to speak at the

meeting see Unit VII of this preamble.

Written ECA testing proposals must be

received by January 21, 1994. Written

notice of interest in being designated an

"interested party" to the consent

agreement negotiations for the

chemicals proposed for testing in this

r-lemaking must be received by January

21, 1994. Those submitting written

testing proposals will be considered

"interested parties" and do not have to

submit separate written notice of

interest in being designated. EPA will

contact all "interested parties" and

advise them of meeting dates.

ADDRESSES: Submit written comments,

identified by the document control

number (OPPTS-42150) and the

chemical-specific docket number, in

triplicate to: TSCA Nonconfidential

Information Center (7407), Office of

Pollution Prevention and Toxics,

Environmental Protection Agency, East

Tower, Rm. G-99, 401 M St., SW.,

Washington, DC, 20460. A public

version of the administrative record

supporting this action, without

confidential business information (CBI),

is available for inspection at the above

address in Room G-102, from 8 a.m. to

12 noon, and I p.m. to 4 p.m., Monday

through Friday, except legal holidays.

FOR FURTHER INFORMATION CONTACT:

Susan B. Hazen, Director,

Environmental Assistance Division

(7408), Office of Pollution Prevention

and Toxics, Rm. E-543B, 401 M St.,

SW.,.Washington, DC 20460, (202) 554-

1404, TDD (202) 554-0551.

SUPPLEMENTARY INFORMATION: This

notice proposes a test rule under TSCA

section 4(a)(1)(A) and (B) to require

certain health, environmental, and

chemical fate tests for acetophenone

(CAS No. 98-86-2), phenol (CAS No.

108-95-2), N,N-dimethylanilne (CAS

No. 121-69-7), ethyl acetate (CAS No.

141-78-6), and 2,6-dimethylphenol

(CAS No. 576-26-1).

I. Introduction

A. ITC Recommendation

At the request of EPA, the ITC

reviewed a subset of chemicals included

on EPA's Integrated Risk Information

System (IRIS) data base for which theAgency believed there is inadequate

data. EPA brought these chemicals to

the ITC to foster interagency

coordination and cooperation on testing

needs. The ITC designated six chemicals

included in IRIS [acrylic acid

(addressed in a separate rulemaking at

57 FR 7656, March 4, 1992),

acetophenone, phenol, NNdimethylaniline, ethyl acetate, and 2,6-

dimethylphenol] for priority

consideration as candidates for

chemical fate, health effects and

environmental effects testing.

IRIS is an electronic database,

prepared and maintained by EPA,

containing both cancer and non-cancer

chronic health hazard information on

specific chemicals. IRIS provides hazard

identification and dose-response

assessment information. This

information, when combined with

specific exposure information, can be

used to help characterize the public

health risks posed by a chemical in a

particular situation (Ref. 7).

In addition, as other agencies brought

their testing needs and concerns for the

chemicals to bear on the ITC

deliberations, the ITC's testing

recommendations expanded to include

additional endpoints such as

mutagenicity and neurotoxicity testing.

Besides health effects data, the ITC

also recommended additional data to

better characterize the environmental

effects and chemical fate of two of these

chemicals. The reasons for these

particular testing recommendations by

the ITC are further discussed in the

Federal Register of March 6, 1991 (56

FR 9534), and in the chemical-specific

sections of this notice.

B. Test Rule Development Under TSCA

Under section 4(a) of TSCA, EPA

shall, by rule, require testing of a

chemical to develop appropriate test

data if the Administrator makes certain

findings as described in TSCA section

4(a)(1)(A) or (B). Discussions of the

statutory section 4 findings are provided

in EPA's first and second proposed test

rules, which were published in the

Federal Register of July 18, 1980 (45 FR

48510) and June 5, 1981 (46 FR 30300).

EPA also proposed its policy for making

findings under TSCA section 4(a)(l)(B)

in the Federal Register of July 15, 1991

(55 FR 32294) and finalized this policy

in the Federal Register of May 14, 1993

(58 FR 28736). This is referred to in this

test rule as the "B policy." For further

discussion of EPA's interpretation of its

authority under sections 4(a)(l)(A) and

(B) of TSCA, see Unit III of this

preamble.

In evaluating the ITC's testing

recommendations for these chemicals,

EPA considered the information

rovided by the ITC, the on-line IRIS

data base, and supplemental

information developed by EPA. In

developing the testing requirements for

this rule, EPA has also considered the

status of acetophenone and phenol

under the Clean Air Act Amendments of

1990 (Ref. 51). These considerations

have influenced the proposed testing

and routes of administration selected.

From this evaluation, EPA is proposing

health effects testing for five of these

chemicals, and chemical fate and

environmental effects testing for two of

these chemicals under TSCA section

4(a)(1)(A) and/or (B). Either finding

alone is sufficient to support a test rule.

EPA has entered into an enforceable

testing Consent Order for the sixth

chemical--acrylic acid.

EPA did not require reporting for

these chemicals under sections 8(a) or

8(d) of TSCA becausb production, use

and exposure information and toxicity

data for these chemical substances are

available in the general literature and

EPA expects that any unpublished

studies will be submitted in response to

the proposed rule. Where less is known

about the toxicity and exposures to the

chemical, section 8(a) and 8(d)

information is needed and routinely

required before EPA proposes a section

4 test rule.

This action constitutes EPA's

response to the ITC as required by TSCA

section 4(e)(1)(B).

H. Proposed Testing and Reporting

Requirements

A. Test Standards and Reporting

Requirements

EPA is proposing that health effects,

environmental effects, and/or chemical

fate testing be contlucted on

acetophenone, phenol, NNdimethylaniline, ethyl acetate, and 2,6-

dimethylphenol according to the

specific test guidelines set forth in

§ 799.4450.

Data developed under the final rule

must be reported in accordance with

TSCA Good Laboratory Practice (GLP)

Standards, 40 CFR part 792.

As required by section 4(b)(1) of

TSCA, EPA is proposing specific testing

and reporting requirements for each of

the proposed tests for the five IRIS

chemicals as specified in the following

Table 1:

61655
61656 Federal Register / Vol. 58, No. 223 / Monday, November 22, 1993 / Proposed Rules

TABLE 1.-TESTING AND REPORTING FOR FIVE IRIS CHEMICALS

Mini. Deadline for

mum Final Re- Chemical Name (CAS Test (Route of Administration) Guideline Per- Docket No.

No.) cent Purity (months)

Acetophenone (98-86-

2).

Phenol (108-95-2) ........

N,N-Dlmethylanline

(121-69-7).

Ethyl Acetate (141-78-

6).

Health effects testing:

Subchronic toxicity, Inhalation .................

Toxicokinetics2, Oral ................................

Toxicokinetics2, Inhalation ......................

Neurotoxicity, Acute and Subchronic, Inhalation.

Neurotoxicity, Subchronic, Inhalation ......

Reproductive toxicity, Gavage .................

Developmental toxicity, Inhalation ...........

Salmonella assay ....................................

In vitro gene mutation assay ...................

In vivo cytogenetics assay ......................

..... .............................................................

Health effects testing:

Subchronic toxicity. Inhalation .................

Toxicokinetics2, Oral ................................

Toxicokinetics2, Inhalation .......................

Neurotoxcity, Acute and Subchronic, Inhalation.

Neurotoxicity, Subchronic, Inhalation ......

Reproductive toxicity, Inhalation ..............

Developmental neurotoxicity, Gavage .....

Health effects testing:

Subchronlc toxicity, Inhalation .................

Toxlcokinetics2, Oral ................................

Toxicokinetics2, Inhalation .......................

Neurotoxclty, Acute and Subchronlc, Inhalation.

Neurotoxicity, Subchronic, Inhalation ......

Reproductive toxicity, Gavage .................

Developmental toxicity, Gavage ..............

In vivo cytogenetics assay ......................

Environmental Effects Testing:.

Algal test ..................................................

Daphnid acute test ..................................

Mysid shrimp acute test ..........................

Fathead minnow life stage test......

Sheepshead minnow life stage test ........

Daphnid chronic test ...........................

Mysid shrimp chronic test ........................

Chemical Fate Testing:.

Activated sludge testing ..........................

Anaerobic biodegradation testing ............

I Health effects testing:

§ 798.2450

OECD 417

OECD 417

§ 798.6050 and 798.6200

§ 798.6400

§ 798.4700

§ 798.4900

§ 798.5265

§ 798.5300

§ 798.5385 or 798.5395

§ 798.2450

OECD 417

OECD 417

§ 798.6050 and 798.6200

§ 798.6400

§ 798.4700

§ 795.250

§ 798.2450

OECD 417

OECD 417

§ 798.6050 and 798.6200

§ 798.6400

§ 798.4700

§ 798.4900

§ 798.5385 or 798.5395

§ 797.1050

§ 797.1300

§ 797.1930

§ 797.1600

§ 797.1600

§ 797.1330

§ 797.1950

§ 796.3340

§ 796.3140

.......... . . . . 142150/42151 ...... 

.................. .142150/42152

42150/42153

.......... 42150/42141A
Federal Register / Vol. 58, No. 223 / Monday, November 22, 1993 / Proposed Rules

TABLE 1.-TESTING AND REPORTING FOR FIVE IRIS CHEMICALS-Continued

mum Mini- Deadline FnaRefor

Chemical Name (CAS Test (Route of Administration) Guideline Per- Docket No. No.) Per- ~portl oke o No.) cent (months)

Purity

Reproductive toxicity, Gavage ................. § 798.4700 99.0 29

Developmental toxicity. Gavage .............. § 798.4900 99.0 12

In vitro gene mutation assay ................... § 798.5300 99.0 10

2,6-Dimethylphenol ................................................. ................ 42150/42154

(576-26-11.

Health effects testing:

Toxicokinetics2, Oral ................................ OECD 417 99.0 15

Toxicokinetics2, Inhalation ....................... OECD 417 99.0 15

Neurotoxicity, Acute and Subchronic, § 798.6050 and 798.6200 99.0 21

Gavage.

Neurotoxicity, Subchronic, Gavage ......... § 798.6400 99.0 21

Reproductive toxicity, Gavage ................. § 798.4700 99.0 29

Developmental toxicity, Gavage .............. § 798.4900 99.0 12

In vitro gene mutation assay ................... § 798.5300 99.0 10

In vivo cytogenetics assay ...................... § 798.5385 or 798.5395 99.0 14

Environmental Effects Testing:.

Algal test ................................................. § 797.1050 99.0 12

Fathead minnow life stage test ............... § 797.1600 99.0 12

Daphnid chronic test ................................ § 797.1330 99.0 18

Chemical Fate Testing:.

River die-away testing ............................. (incorporated by reference) 99.0 12

Anaerobic biodegradation testing ............ § 796.3140 99.0 12

Aqueous photolysis testing ...................... § 795.70 99.0 12

I Figure indicates the reporting deadline in months calculated from the effective date of the final rule or from the date of test sponsor notification by certified letter to initiate test where such notification is specified. 2 The toxicokinetics (pharmacokinetics and metabolism) guideline was developed by the European Organization for Economic Cooperation and

Development (OECD) and is proposed to be incorporated by reference in this rule.

All of the guidelines referenced in

Table I are intended to be used as

currently published in Title 40 of the

Code of Federal Regulations, except for

the neurotoxicity test guidelines, which

are modified in the codified section of

this rule. The neurotoxicity guideline

modifications specify the duration and

frequency of exposure and specify that

lower exposure levels shall show a

graded neurotoxic response or no

neurotoxicity. Exceptions also are the

toxicokinetics and biodegradation in

natural surface water guidelines, which

are proposed to be incorporated by

reference and are available in the docket

for this rule.

B. Interim Mutagenicity Testing Policy

The proposed health effects testing in

this rule reflects EPA's current thinking

in the area of mutagenicity testing, both

as an endpoint and as it leads to

oncogenicity testing. The science of

mutagenicity testing has undergone

considerable change since EPA first

required mutagenicity testing in a

section 4 test rule (50 FR 20662, May 17,

1985). This new information,

particularly data from EPA's Gene-tox

Program related to the ability of short

term tests to predict mutagenicity (Ref.

105), the National Toxicology Program's

study of the ability of short term tests to

predict carcinogenic potential (Ref. 90),

and expert meetings, such as the 1987

Williamsburg conference, has led EPA

to revise the TSCA section 4

mutagenicity testing scheme. This

includes how EPA requires additional

mutagenicity testing based on results

from lower-tier mutagenicity tests and

also how it requires oncogenicity testing

based on mutagenicity test results. EPA

believes the flexibility and opportunity

to apply professional scientific

judgment offered by the new approach

afford considerable advantages over the

prior scheme. EPA's rationale for these

changes is discussed in the technical

literature (Ref. 19) and will not be

discussedhere.

For purposes of this rule, in which

only Tier I testing is being proposed, the

changes are relatively minor. First, Tier

I is redefined as a battery of two in vitro

tests and one in vivo test. There is no

longer a distinction as to gene mutations

or chromosomal aberrations in Tier I,

and the previously utilized in vitro

cytogenetics test would be eliminated.

The purpose of Tier I testing, however,

continues to be to determine intrinsic

mutagenic potential.

Subsequent mutagenicity testing,

including Tier II testing, is not being

proposed at this time. The test

guidelines for several of the Tier II tests

are still undergoing refinement. Thus,

rather than delaying the Agency's

response to the ITC until all of the

details of the mutagenicity testing

scheme have been completed, EPA has

decided to propose only Tier I of the

new mutagenicity testing scheme at this

time. If appropriate, further

mutagenicity testing, including triggers

to oncogenicity testing, will be

61657
61658 Federal Register / Vol. 58, No. 223 / Monday, November 22, 1993 / Proposed Rules

addressed in a subsequent rulemaking after review of the Tier I results.

C. Persons Required to Test

Because of the findings in Unit IM of

this preamble, EPA is proposing that

persons who manufacture (including

import) or process, or who intend to

manufacture or process, acetophenone,

phenol. NN-dimethylaniline, ethyl

acetate, or 2,6-dimethylphenol, other

than as an impurity, at any time from

the effective date of the final test rule to

the end of the reimbursement period, be

subject to the testing requirements in

this rule. Byproduct manufacturers and

importers of acetophenone, phenol,

N,N-dimethylaniline, ethyl acetate, and/

or 2.6-dimethylphenol are considered

manufacturers under this rule. As

explained in 40 CFR 790.42,

manufacturers of these substances

would be required to submit letters of

intent to conduct testing or exemption

applications. However, small quantity

manufacturers, research and

development manufacturers and

processors would not be required to

submit letters of intent or exemption

applications unless directed to do so in

a subsequent notice as described in

§ 790.48(b).

EPA has specified relatively pure

substances for testing (99 percent, or

higher). EPA is not proposing to require

submission of equivalence data as a

condition for exemption from testing.

since EPA is interested in evaluating the

effects attributable to the substances

themselves.

III, Findings

EPA interprets TSCA section 4(a) to

mean that EPA's authority to require

testing under TSCA section 4(a)(1)(A)

and (B) is related to the "data

insufficiency" and "testing is

necessary" findings under TSCA section

4(a)(1)(A)(ii) and (iii) and (B)(ii) and

(iii). Thus, once the Administrator has

made a finding under TSCA section

4(a)(1)(A)(i) that a chemical may present

an unreasonable risk, or under TSCA

section 4(a)(1)(B)(i) that a chemical is or

will be produced in substantial

quantities and may either be released to

the environment in substantial

quantities or that there may be

substantial or significant human

exposure to the chemical, the

Administrator may require any type of

testing necessary to address unanswered

questions about the effects of the

chemical. EPA need not limit the scope

of testing required to the factual bases

for the section 4(a)(1)(A)(i) or (B)(i)

findings. For a more detailed discussion

of this interpretation, see EPA's final

"B-policy" rule (58 FR 28736, May 14,

1993).

The proposed chemical fate, health

and environmental effects testing is

based on the authority of section

4(a)(1)(A) and (B) of TSCA. EPA finds

that available data indicate that three of

the chemicals may present an

unreasonable risk of injury to human

health or the environment; all five of

these chemicals are produced in

substantial quantities; there is or may be

significant or substantial human

exposure to all five of these chemicals;

there is or may be substantial

environmental release of one of these

chemicals; there are insufficient data

and experience to determine or predict

the effects from manufacturing,

distribution, processing, use, and

disposal of all of these chemicals; and

testing is necessary to develop these

data.

As noted earlier, a general discussion

of the statutory section 4 findings is

provided in EPA's first and second

proposed test rules, which were

published in the Federal Register of

July 18, 1980 (45 FR 48510) and June 5,

1981 (46 FR 30300). in EPA's final "B"

policy, published in the Federal

Register of May 4, 1993 (58 FR 28736),

and in Unit II. C. of this preamble.

A. Acetophenone

EPA is proposing testing of

acetophenone under the authority of

section 4(a)1)(B) of TSCA.

1. Substantial quantities produced

finding. EPA believes that acetophenone

is or will be produced in substantial

quantities. According to records

available to EPA, acetophenone

production exceeds 1 million pounds

per year; actual production volumes are

CBI. EPA believes that production of 1

million pounds or greater constitutes

substantial production under TSCA

section 4(a)(1)(B)(i).

2. Substantial human exposure

finding. EPA believes that there is or

may be substantial human exposure to

acetophenone. This assessment is based

on a National Occupational Exposure

Survey (NOES) which indicates that

39,880 workers were potentially

exposed to acetophenone in various

industrial applications (Refs. 70 and

109). Of these workers, 97 percent were

potentially exposed during the use of

trade name products containing

acetophenone. As explained in EPA's

"B" policy, EPA believes that the

potential exposure of 39,880 workers to

acetophenone constitutes substantial

human exposure under section

4(a)(1)(B) of TSCA. Acetophenone is

used as a perfume base in the fragrance

industry, as a process solvent for gums,

resins, and dyestuffs, as an intermediate

for the synthesis of pharmaceuticals, in

corrosion inhibitors, in rubber

chemicals, in flavorings, as a

polymerization catalyst, and as a

photoinitiator (Refs. 14 and 81). The use

of acetophenone as a fragrance in soaps

and detergents also gives rise to

widespread consumer exposure. EPA

estimates an exposure of individual

persons up to 3,783 mg/yr from use of

hand soaps (Ref. 96).

EPA also believes that there is or may

be general population exposure to

acetophenone. Acetophenone has been

detected in U.S. drinking water

supplies. In a survey of 10 U.S. cities

between 1969 and 1972, acetophenone

was found in Philadelphia's drinking

water, on 7 different occasions, at a

concentration of approximately 1.0 pgg/

L (Refs. 54 and 89). This may result in

the exposure of millions of people. For

the reasons set forth in EPA's "B"

policy, EPA believes that the potential

exposure of 100,000 or more people in

the general population to acetophenone

constitutes substantial human exposure

under TSCA section 4(a)(1)(B)(i).

3. Insufficient data and experience

finding. EPA believes that there are

insufficient data and experience to

determine or predict the effects on

human health or the environment from

manufacturing, processing, distribution,

use, and/or disposal of acetophenone.

EPA believes that available studies are

insufficient and other data are lacking to

sufficiently evaluate the effects of

acetophenone.

Inhalation data to assess the

subchronic effects of exposure to

acetophenone do not adequately address

the concentration-response relationship

for the portal-of-entry effects via the

inhalation route. The primary study

cited as providing the baseline RfC (for

inhalation) indicated a no observed

effect level (NOEL) of 0.007 mg/m3 and

a lowest observed effect level (LOEL) of

0.07 mg/m3 based on congestion of

cardiac vessels, liver dystrophy and

changes in the ratios of blood proteins

and muscle chronaxie (Ref. 49). This

study exposed groups of 15 white male

rats continuously to acetophenone

vapor at 0, 0.007. or 0.07 Mg/ m3 for 70

days. While a NOEL and LOEL were

reported, this study is inadequate

because only one sex of animals was

examined, only five animals per group

were used to study cholinesterase

activity, and serum protein levels and

the number of animals which

underwent histopathological

examination were unreported (Ref. 51).

Another inhalation study reported a

specific pattern of degeneration of the

olfactory bulb in groups of four Wistar
Federal Register / Vol. 58, No. 223 / Monday, November 22, 1993 / Proposed Rules

rats continuously exposed to

acetophenone vapors from 1 week to 3

months (Ref. 78). However, other

parameters of toxicity were not

evaluated in this study.

EPA is also aware of two oral

subchronird.;tudies. These studies failed

to identify ddverse effects in groups of

five male and five female albino rats fed

diets containing acetophenone at levels

of 0.003, 0.05, 0.125, or 0.2 percent for

30 days (Ref. 85) or in groups of 10 male

and 10 female Osborne-Mendel rats fed

diets containing 1,000, 2,500, or 10,000

ppm acetophenone for 17 weeks (Ref.

40). These studies were judged adequate

to predict oral toxicity, but only

marginally so, because no LOAEL was

established (Ref. 51).

Developmental toxicity data on

acetophenone are limited to a study that

reported no effects on length of

gestation or postnatal development in

the offspring of rats exposed dermally at

0.48 mg/kg on days 10 - 15 of gestation

(Ref. 57). The data are insufficient

because key study parameters were not

reported, apparently only a single dose

was administered, and the critical

period of organogenesis may have been

missed.

Available mutagenicity data in

Salmonella (Ames testing) are

insufficient because only three strains of

the test organism were used, rather than

the usual four or five that EPA considers

necessary to establish a negative

response in this assay. EPA's

mutagenicity testing scheme (described

in more detail in Unit II.B. of this

preamble) also includes in vitro gene

mutation and in viva cytogenetics in the

lowest tier. As neither study is available

for acetophenone, additional

mutagenicity testing is necessary to

assess acetophenone's mutagenic

potential.

Available in vitro and in viva

pharmacokinetics and metabolism

studies are inadequate because

quantitative data on acetophenone's

rates of absorption, distribution, and

excretion are lacking in these studies

(Refs. 33, 58, 60, 91, 92, 84 and 55).

Finally, no data were found for

reproductive effects or neurotoxicity.

4. Testing is necessary to develop data

finding. EPA believes that testing of

acetophenone is necessary to develop

data for subchronic effects,

neurotoxicity, pharmacokinetics and

metabolism, reproductive effects,

developmental effects and mutagenic

effects. EPA believes that these testing

data are needed to determine if the

manufacturing, processing, distribution,

use, or disposal of acetophenone or any

combination of such activities does or

does not present an unreasonable risk of

injury to human health.

B. Phenol

EPA is proposing testing of phenol

under the authority of section 4(a)(1)(A)

and 4(a)(1)(B) of TSCA.

1. Unreasonble risk of injury to

human health or environment finding.

EPA believes that the manufacture,

processing, distribution in commerce,

use, or disposal, or any combination of

such activities for phenol may present

an unreasonable risk of injury to health

or the environment. This finding is

based on several studies that indicate

that phenol is neurotoxic. After 20

exposures by inhalation to 100-2.00 mg/

m3, hind limb paralysis was reported for

guinea pigs (Ref. 23). Continuous

exposure to phenol vapors at 100 mg/m3

for 15 days affected the performance of

rats in a test assessing central nervous

system (CNS) effects (Ref. 18). A

developmental toxicity screening test

with a single gavage dose of 100, 333,

667 or 1,000 mg/kg given to groups of

12-13 Sprague-Dawley rats on day 11 of

gestation (Ref. 53), produced a

syndrome of effects Involving the limbs,

tail, and urogenital system, which

provides evidence of developmental

neurotoxicity. The limb effects

consisted of paralysis andlor palsy.

Although the effect is not evident in

newborns, limb function matures

postnatally and requires a week to 10

days for effects to appear. This delayed

effect was seen in 21.4 percent and 27.3

percent of the litters at 667 and 1,000

mg/kg, respectively.

As discussed further below, over

320,000 workers may be exposed to

phenol in numerous industrial settings,

and the wide variety of uses of phenol

may result in more widespread worker

and consumer exposure. Furthermore,

phenol is produced and released into

the environment in substantial

quantities which may result in general

population exposures. Because of these

concerns, EPA believes that phenol may

present an unreasonable risk of injury to

health.

2., Substantial quantities produced

finding. EPA believes that phenol is or

will be produced in substantial

quantities. EPA records indicate that

phenol is produced in excess of I

million pounds per year. In 1989, 13

facilities were listed as manufacturing

this compound (Ref. 86). EPA estimates

the annual production for 1989 to be

3,512,000,000 pounds for 10

manufacturers at 11 sites. As explained

in the "B" policy, EPA believes that

production of I million pounds or

greater of phenol constitutes substantial

production under section 4(a)(1)(B)(i) of

TSCA.

3. Substantial human exposure

finding. EPA believes that here is or

will be substantial human exposure to

phenol. This assessment is based on

worker, general population and

consumer exposure to phenol. The

NOES conducted during 1981-1983 by

NJOSH estimated that 320,914 workers

were potentially exposed to phenol in

35 different industrial categories (Refs.

70 and 109). For the reasons set forth in

the "B" policy, EPA believes that the

potential exposure of 341,516 workers

to phenol is sufficient to qualify as

substantial human exposure under

section 4(a)(1)(B)(i) of TSCA.

Phenol is used in a variety of

commercial applications including

phenolic resins - 38 percent; synthesis

of bisphenol A - 23 percent; synthesis of

caprolactam - 17 percent; synthesis of

alkylphenols - 4 percent; synthesis of

aniline - 3 percent; miscellaneous uses

- 5 percent; exports - 6 percent (Ref. 16).

The miscellaneous uses of phenol

include: (1) The synthesis of adipic

acid, salicylic acid, phenolphthalein,

pentachlorophenol, acetophenetidine,

picric acid, and pharmaceuticals; (2) as

a selective solvent for refining

lubricating oils, germicidal paints,

laboratory reagent, dyes and indicators,

slimicide, biocide, and (3) as a general

disinfectant (Ref. 81). Many of these are

uses that can lead to worker and

consumer exposure.

In a compilation of air monitoring

data collected between 1970 and 1987,

the mean concentration of phenol in

suburban and urban areas was reported

as 0.015 and 6.883 ppb, respectively

(Ref. 83). The concentration of phenol in

the air of Portland, OR, during seven

rain events in 1984 was 56 to 105 ppt,

while the concentration of phenol in the

rain ranged from 75 to 1,200 ppt (Ref.

61). It has also been detected In U.S.

drinking water supplies (Refs. 29 and

69).

Phenol is used in numerous consumer

products indicating a potential for

exposure to consumers (Ref. 100).

4. Release to environment in

substantial quantities finding EPA

believes that phenol is released to the

environment in substantial quantities.

Over I million pounds of phenol is

released into the environment each year.

The Toxics Release Inventory (TRI) for

1987, indicates that 8,100,731 pounds of

phenol was released to the air, 402,579

pounds to water, and 1,098,624 pounds

to land (Ref, 93). For 1988, the TRI

indicates that 10,155,101 pounds was

released to air, 262,127 pounds to water,

and 2,162,250 pounds to land (Ref. 93).

As explained in EPA's "B" policy, EPA

. ..... . .... .. .... ... .. . . .. ... . . . . .. I I II!1 1 I I '[IIII Ill HIr[]lll I I

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61660 Federal Register / Vol. 58, No. 223 / Monday, November 22, 1993 / Proposed Rules

believes that 1 million pounds of release

to the environment each year is a

sufficiently large amount of release for

making a finding of substantial

environmental release under section

4(a)(1)(B) of TSCA.

Phenol was detected in 738 samples

obtained from 33 industries and

publicly owned treatment works

(POTWs) at a maximum concentration

range of 7.5 ppb to 530 ppm (Refl 82).

Data from the STORET database

indicate that phenol was found in 42.1

percent of industrial effluent samples

obtained from 1980-83, at a median

concentration of 10 ppb (Ref. 87). The

STORET database also indicates that

phenol was found in 13 percent of

ambient surface water samples, and 9

percent of sediment samples (Ref. 87),

and also in groundwater samples (Ref.

88). Phenol was detected in 4 percent of

86 samples obtained during the National

Urban Runoff Program of 1982, at

concentrations ranging from 3 to 10 ppb

(Ref. 17).

5. Insufficient data and experience

finding. EPA believes that there are

insufficient data and experience to

determine or predict the effects on

human health or the environment from

manufacturing, processing, distribution,

use, and/or disposal of phenol. EPA

believes that there are insufficient data

and experience to reasonably determine

or predict the potential subchronic

effects, neurotoxicity, pharmacokinetics

and metabolism, reproductive toxicity,

and developmental neurotoxicity from

the manufacturing, processing,

distribution, use, and/or disposal of

phenol. Although a number of studies

describe the metabolism and

pharmacokinetics of phenol (Refs. 13,

20, 22, 52, 62, 65, and 66), the

information is insufficient to make

comparisons and assumptions that

would allow full use of the existing

database for regulatory purposes. The

Chemical Manufacturers Association's

Phenol Panel is conducting

pharmacokinetic studies and has

consulted EPA on study design (Refs.

113, 114, and 115).

A number of subchronic and chronic

tests have been conducted with phenol

by the oral and inhalation routes (Refs.

6, 21, 23, 27, 67, and 80). None of these

studies are adequate to characterize

portal-of-entry effects via the inhalation

route. Several of the inhalation

subchronic studies did not use controls

and tested too few animals of

unspecified sex (Ref. 23). A one-doselevel study determined a NOEL of 19

mg/m3 (Ref. 80), but the design of this

study did not include establishing an

effect level for phenol. In addition, the

inforoation available shows phenol to

be more toxic by inhalation exposure

than by oral exposure, thereby

precluding a high degree of reliance on

conclusions based on route-to-route

extrapolation. For these reasons, EPA is

proposing to require testing to develop

data on the effects of phenol by the

inhalation route.

Anger and Johnson (1985),

summarizing known neurotoxic effects

of a number of chemicals, indicate

motor and mental disturbances for

phenol (Ref. 2). EPA has insufficient

information to evaluate these effects.

Deichmann et al. (1944) reported hindlimb paralysis in guinea pigs after 20

exposures by inhalation to 100-200 mg/

m3 phenol (Ref. 23). In addition, Dalin

and Kristoffersson (1974) found that

continuous exposure to phenol vapors

at 100 mg/m3 for 15 days adversely

affected the performance of rats in a test

assessing CNS effects (Ref. 18).

Furthermore, Kavlock (1990) noted

neurologically significant effects in the

pups of dams exposed to phenol in a

screening test for developmental effects

(Ref. 53). However, these studies did not

extend long enough to adequately

characterize these effects. Furthermore,

the Deichmann et al. study (Ref. 23) did

not include control animals, and the

Dalin and Kristoffersson study (Ref. 18)

did not establish a NOAEL for the

observed CNS effects.

The Kavlock study (Ref. 53) also

supports concern for developmental

neurotoxicity. When pregnant rats were

given a single gavage dose of phenol,

their offspring showed developmental

toxicity affecting the limbs, tail, and

urogenital systems. This study was a

screening test, designed to help identify

substances which may need additional

developmental toxicity testing, and was

not adequate to characterize these

effects, In order to address the

inadequacy of the data developed by

these studies, EPA proposes to require

both neurotoxicity and developmental

neurotoxicity testing for phenol.

No additional testing for

developmental effects is being proposed

because NTP studies (Refs. 71 and 112)

are adequate for this endpoint. Although

these studies were conducted by the

oral route, EPA expects that additional

reproductive effects testing, which will

be conducted by the inhalation route,

will be an adequate complement to the

existing database.

EPA believes a reproductive effects

study on phenol by Holler and Pursell

(1938) is inadequate for risk assessment

purposes because the experimental

methodology and test results reporting

are inadequate and unreliable (Ref. 44).

EPA is proposing to require

reproductive effects testing. The

inhalation route was selected because

information indicates that animals are

more sensitive to phenol when exposed

by the inhalation route.

6. Testing is necessary to develop data

findings. EPA believes that the testing of

phenol is necessary to develop data for

oral and inhalation pharmacokinetics

and metabolism, inhalation subchronic

effects, reproductive effects,

developmental neurotoxicity, and

neurotoxicity. EPA believes that these

testing data are needed to determine if

the manufacture, distribution in

commerce, processing, use, or disposal

of phenol, or any combination of such

activities, does or does not present an

unreasonable risk of injury to health or

the environment.

C. N,N-Dimethylaniline

EPA is proposing testing of N,Ndimethylaniline under the authority of

sections 4(a)(1)(A) and 4(a)(1)(B) of

TSCA.

1. Unreasonable risk of injury to

health or the environment finding EPA

believes that the manufacture,

processing, distribution in commerce,

use, or disposal, or any combination of

such activities for NN-dimethylaniline,

may present an unreasonable risk of

injury to health or the environment.

a. Evidence of potential for adverse

human health effects. The health

portion of this assessment is based on

N,N-dimethylaniline's toxicity in

subchronic (13-week), chronic,

oncogenicity, and mutagenicity studies.

A 2-year chronic toxicityoncogenicity gavage study in groups of

50 male and 50 female F344/N rats

treated with 3 or 30 mg/kg 5 days per

week and similarly sized groups of

B6C3F1 mice treated with 15 or 30 mg/

kg 5 days per week reported some

evidence of carcinogenicity in male rats

(sarcomas and osteosarcomas of the

spleen) and equivocal evidence of

carcinogenicity in female mice

(squamous cell papillomas of the

forestomach) (Ret 72). Mutagenicity

data were negative for reverse mutation

in four strains of Salmonella, but were

positive for forward mutation in mouse

lymphoma L5178Y cells and for sister

chromatid exchange and chromosomal

aberrations in Chinese hamster ovary

cells (Ref. 72).

A 13-week gavage study (that

included comprehensive

histopathological examination) in

groups of 10 malh and 10 female F344/

N rats and B6C3F1 mice treated with

31.25, 62,5, 125, 250, or 500 mg/kg for

5 days per week identified the

erythrocytes and the spleen as the most

sensitive targets in both species (Refs. I

and 72). Compound-related clinical
Federal Register / Vol. 58, No. 223 / Monday, November 22, 1993 / Proposed Rules

signs included lethargy in rats and mice

and cyanosis in rats. The National

Toxicology Program (NTP) study

identified the rat as more sensitive than

the mouse to the noncarcinogenic

effects of N,N-dimethylaniline on

erythrocytes and the spleen; these

effects were seen in rats even at the

lowest dose level tested, while an

NOAEL of 31.25 mg/kg was seen for the

mice (Ref. 72). An inhalation study

reported altered muscle chronaxie and

evidence of hemolytic anemia in the

high dose group of rats continuously

exposed for 100 days to 0.04 or 0.3 mg/ m3 (Ref. 64). Anger and Johnson (1985),

summarizing known neurotoxic effects

of NN-dimethylaniline, indicate vision

disturbances and central nervous system

depression (Ref. 2).

As discussed further elsewhere in this

preamble, over 28.000 workers maybe

exposed to NN-dimethylaniline in

various industrial settings and there is

also evidence of general population

exposure.

b. Evidence of potential

environmental toxicity. This assessment

is based on probabilistic dilution

modelling indicating that NNdimethylaniline is present in the

environment at levels within a factor of

100 of its known acute toxicity to

environmental organisms. EPA believes

that there may be an unreasonable risk

of injury to the environment from

chronic effects when acute toxicity is

observed at levels within a factor of 100

of predicted stream concentrations.

Specifically, EPA has determined a

concentration of concern of 300 ppb

(based on .N,N-dimethylaniline's

* predicted chronic toxicity to daphnids)

and has estimated that this

concentration is exceeded 144 to 198

days of the year in receiving streams

(Ref. 108).

Furthermore, NN-dimethylaniline,

which is produced in substantial

quantities, has been detected in soil and

water. According to the TRI, 147,692

pounds of NN-dimethylaniline were released to the environment in 1987

(Ref. 93). For 1988, the TRI indicates

that 119,122 pounds were released (Ref.

93). The TRI also indicates that some of

these releases would be to the marine or

estuarine environment (Ref. 116).

From these concerns. EPA believes

that NN-dimethylaniline may present

an unreasonable risk of injury to health

and the environment.

2. Substantial quantities produced

finding. EPA believes that NNdimethylaniline is or will be produced

in substantial quailtities. EPA records

indicate that domestic production of

NN-dimethylaniline in 1979 was 13.7

million pounds (Ref. 1021. Information

on current production volumes is CBI,

but production is substantial (1 million

pounds or greater). For the reasons set

forth above, EPA believes that

production of 1 million pounds or more

per year of N,N-dimethylaniline is

substantial production under section

4{a)(lJ)(Bi) of TSCA.

3. Substantial human exposure

finding. EPA believes that there is or

may be substantial human exposure to

N,N-dimethylaniline. This assessment is

based on an NOES survey which

estimated that 27,895 workers were

potentially exposed to NNdimethylaniline in 9 different industrial

classifications [Refs. 70 and 109). Of

these workers, 39 percent were

potentially exposed during the use of

trade name products containing this

compound. NN-Dimethylaniline is used

in dyes. as a synthetic intermediate for

vanillin, pharmaceuticals, and other

compounds, and as a sclvent, stabilizer.

and polymerization catalyst (Refs. 59, 81

and 99). For the reasons set forth in the

"B" policy, EPA believes that the

potential exposure of 28,048 workers to

N,N-dimethylaniline constitutes

substantial human exposure under

TSCA section 4(a)(1(B)(i).

Furthermore, there is or may be

general population exposure to NN

dimethylaniline. N,N-Dimethylaniline

was detected in 8 samples obtained

from three industries and POTWs at a

maximum concentration of 3.1 ppm

(Ref. 82). According to the TRL 129,829

pounds of N,N-dimethylaniline was

released to the air, 17,613 pounds to

water, and 250 pounds to land in 1987

(Ref. 93). For 1988, the TRI indicates

that 98,905 pounds was released to.air,

19,967 pounds to water, and 250

pounds to land (Ref. 93). NNDimethylaniline was detected in soil

samples obtained near the bank of the

Buffalo River, NY, at concentrations of

10 to 40 ppm (Ref. 68). NNDimethylaniline was reported as being

detected (no levels given) in water from

Lake Ontario (Ref. 39).

4. Insufficient data and experience

finding. EPA believes that there are

insufficient data and experience to

determine or predict the effects on human health or the environment from

manufacturing, processing, distribution,

use, and/or disposal of NNdimethylaniline. EPA believes that

available studies are insufficient and

other data are lacking to sufficiently

evaluate the effects of NNdimethylaniline.

Data assessing the potential

subchronic effects of inhalation

exposure to NNdimethylaniine were not found in the literature. Available

oral data are inadequate to estimate

inhalation risk because the dose levels

selected did not give a NOAEL (for rats)

and there are no data on comparative

pharmacokinetics or portal-of-entry

effects (Refs. 1 and 72). The only

inhalation study report available was a

brief abstract that indicated altered

muscle chronaxie and evidence of

hemolytic anemia in the high dose

group (0.3 mg/m3 of rats continuously

exposed for 100 days to 0.04 or 0.3 mg/ m3) (Ref. 64). This study cannot be used

for risk assessment because it was

reported in limited detail and

histopathologic effects were not

examined. Anger and Johnson (1985),

summarizing known neurotoxic effects

of a number of chemicals, cited visual

disturbances and CNS depression for

N,N-dimethylaniline (Ref. 2). EPA has

insufficient information to evaluate

these observations.

Developmental toxicity testing for

N,N-dimethylaniline is limited to a

screening study in 50 CD-i albino mice

treated with NN-dimethylaniline in

corn oil at 365 mg per kg per day on

gestation days 7 to 14; maternal

mortality, but no effects on body weight

or viability of the neonatal offspring,

was reported (Ref. 77). Although the test

results are negative, EPA considers this

test inadequate for risk assessment

purposes because the exposure period

did not cover the full period of major

organogenesis (days 6 to 15 for the

mouse), nor were sufficient dose groups

used (only one versus the three required

by EPA). EPA also specifies that two

animal species be tested for a definitive

developmental toxicity assessment.

Therefore, developmental toxicity by

gavage is proposed for two species, a rat

and a non-rodent.

The available (negative) Salmonellal

Ames data are adequate, as are the

(positive) data in mouse lymphoma

L51784 cells (Ref. 72). Available data

also include positive results for sister

chromatid exchange and chromosomal

aberrations in Chinese hamster ovary

cells (Ref. 72). Given these data, EPA

believes that gene mutation data are

adequate but that the chromosomal

toxicity of NN-dimethylaniline is

insufficiently characterized.

Although numerous metabolism

studies have been conducted for NNdimethylaniline, these are inadequate

because quantitative pharnacokinetics

data for absorption, distribution, or

excretion are lacking (Refs. 5, 10, 11. 25,

26, 28, 37, 38, 41,43, 45, 46. 47, 56, 73,

74, 75, 76, 79,95 and 106).

No reproductive effects data were

found for NN-dimethylaniline.

Environmental effects data for N,Ndimethylaniline are limited. Algal

toxicity data include a toxicity test in

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61662 Federal Register / Vol. 58, No. 223 / Monday, November 22, 1993 / Proposed Rules

bluegreen algae (Ref. 9) and a study on

energy metabolism enzymes in marine

algae (Ref. 4). The study by Batterton et

al. (Ref. 9) is inadequate because the

Agency needs data for a sensitive

species of green algae such as

Selenastrum capricornutum. Blue-green

algae are not an acceptable substitute for

green algae. The study by Armstrong et

al. (Ref. 4) is inadequate because a

rigorous measurement of growth

inhibition such as a 96-hour EC50 value

was not determined. The Agency

believes that the 96-hour EC50 Value for

growth will be a more sensitive measure

of effects on energy metabolism

enzymes and will have more relevance

in an environmental risk assessment.

Acute aquatic toxicity studies are

available for a ciliated protozoan and

several species of fish (Ref. 3). While the

acute toxicity studies for fish appear

adequate, no chronic toxicity data for

fish were found, nor were any relevant

data found for the acute or chronic

effects of NN-dimethylaniline on

aquatic invertebrates. The toxicity data

for the ciliated protozoan are of

unknown utility because little is known

about how representative protozoa are

as surrogate species for other aquatic

invertebrates.

EPA found no data to determine

anaerobic biodegradation or the

biodegradation of NN-dimethylaniline

in systems which simulate in situ

wastewater treatment.

5. Testing is necessary to develop data

finding. EPA believes that testing of

N,N-dimethylaniline is necessary to

develop data for subchronic effects,

neurotoxicity, pharmacokinetics and

metabolism, reproductive effects,

developmental effects, mutagenic

effects, algal toxicity, daphnid acute and

chronic toxicity, mysid shrimp acute

and chronic toxicity, fathead minnow

chronic toxicity, sheepshead minnow

chronic toxicity, anaerobic

biodegradation, and activated sludge

biodegradation. EPA believes that this

testing is needed to determine if the

manufacturing, processing, distribution,

use, or disposal of NN-dimethylaniline

or any combination of such activities

does or does not present an

unreasonable risk of injury to health or

the environment.

D. Ethyl Acetate

EPA is proposing testing of ethyl

acetate under the authority of sections

4(a)(1)(A) and 4(a)(1)(B) of TSCA.

1. Unreasonable risk of injury to

health or the environment. EPA believes

that the manufacture, processing,

distribution in commerce, use, or

disposal, or any combination of such

activities for ethyl acetate may present

an unreasonable risk of injury to health

or the environment.

a. Evidence of potential for adverse

human health effects. This finding is

based on ethyl acetate's neurotoxic

effects, as outlined and supported in

previous rule-making for the testing of

this chemical [cite final multi-substance

rule for the testing of neurotoxicity]. 1. Substantial quanitities produced

finding.. EPA believes that ethyl acetate

is or will be produced in substantial

quantities. In 1988, 254.2 million

pounds of ethyl acetate was produced in

the United States (Ref. 103). EPA

estimates the annual U.S. production for

1989 to be 292 million pounds for three

manufacturers at five production sites

(Ref.101). For the reasons set forth in the

"B" policy, EPA believes that

production of I million pounds or

greater of ethyl acetate constitutes

substantial production under section

4(a)(1)(B)(i) of TSCA.

2. Substantial human exposure

finding. EPA believes that there is or

will be substantial human exposure to

ethyl acetate. The NOES survey

estimated that 419,180 workers were

potentially exposed to ethyl acetate

(Refs. 70 and 109). Of these workers, 87

percent were potentially exposed during

the use of trade name products

containing this compound. Potential

exposure to ethyl acetate was associated

with 34 different industrial

classifications (Ref. 70). Ethyl acetate

has the following uses: coatings-41

percent; exports-36 percent; solvents13 percent; plastics-8 percent;

chemical synthesis-2 percent (Ref. 15).

In addition, ethyl acetate is used as a

solvent in numerous consumer

applications. For the reasons explained

in the "B" policy, EPA believes that the

potential exposure of 419,180 workers

to ethyl acetate is substantial human

exposure under TSCA section

4(a){1)(B)(i).

Ethyl acetate is found in numerous

consumer products including lacquers,

varnishes, coatings, detergents and

soaps. EPA estimates the highest

exposure levels occur by the dermal

(4,680 mg/yr from use of latex paints)

and inhalation (901 mg/yr from use of

lacquer thinner) routes (Ref. 98). There may also be widespread general

population exposure. Ethyl acetate was

detected in 66 samples obtained from 17

industries and POTWs at a maximum

concentration of 7.7 ppm (Ref. 82). In a

compilation of air monitoring data

collected between 1970 and 1987, the

median concentration of ethyl acetate in

urban sites was 0.733 ppb (Ref. 83).

Ethyl acetate was also detected in

industrialized and urban sites in

Virginia and West Virginia at

concentrations ranging from <0.012 to

1.9 ppb (Ref. 30). The STORET database

indicates that ethyl acetate has also been

detected in groundwater (Ref. 88).

3. Insufficient data and experience

finding. EPA believes that there are

insufficient data and experience to

determine or predict the effects on

human health or the environment from

manufacturing, processing, distribution.

use, and/or disposal of ethyl acetate.

Under section 4(a)(1)(B)(ii), EPA

believes that there are insufficient data

and experience to determine or predict

the potential reproductive toxicity,

developmental toxicity, and

mutagenicity from the manufacturing,

processing, distribution, use, and/or

disposal of ethyl acetate.

EPA is proposing to test ethyl acetate

for reproductive effects and

developmental toxicity. EPA found no

data for these effects.

EPA is also proposing mutagenicity

testing for ethyl acetate. Ethyl acetate

was negative for induction of reverse

mutation in Salmonella when tested

with and without metabolic activation

(Refs. 24 and 50). Positive results were

observed for mitotic aneuploidy but

negative results were observed for point

mutations and recombinations in yeast

(Ref. 107).

In mammalian test systems, a positive

response was reported for chromosomal

aberrations in Chinese hamster

fibroblasts in vitro (Ref. 50); however,

these results do not support a concern

or a finding for chromosomal effects

under TSCA section 4 (a)(1)(A) because,

in a more definitive in vivo test system,

a negative response was reported for

micronucleus formation in Chinese

hamsters (Ref. 8).

EPA considers the existing

Salmonella data (negative) on ethyl

acetate to be acceptable. However, these

data in bacteria alone are insufficient to

adequately characterize the gene

mutation effects of ethyl acetate, and

EPA is proposing an in vitro gene

mutation assay for ethyl acetate in

mammalian cells in culture.

4. Testing is necessary to develop data

finding. EPA believes that the testing of

ethyl acetate is necessary to develop

data for reproductive effects,

developmental toxicity, and

mutagenicity. EPA believes that this

testing is needed to determine if the

manufacture, distribution in commerce,

processing, use, or disposal of ethyl

acetate, or any combination of such

activities, does or does not present an

unreasonable risk of injury to health or

the environment.
Federal Register / Vol. 58, No. 223 / Monday, November 22, 1993 / Proposed Rules

E. 2,6-Dimethylphenol

EPA is proposing to test 2,6-

dimethylphenol under the authority of

sections 4(a){1)[A) and (B) of TSCA.

1. Unreasonable risk of injury to

human health and environment finding.

EPA believes that the manufacture,

processing, distribution in commerce,

use, or disposal, or any combination of

such activities for 2,6-dimethylphnol

may present an unreasonable risk of

injury to health or the environment.

a. Evidence of potential for adverse

human health effects. This assessment

is based on 2,6-dimethylphenol's

toxicity in an 8-month rat gavage study,

that showed histopathological changes

in the liver, spleen, and kidneys and

changes in body weight, blood pressure

and levels of protein sulfhydryl groups

in blood serum and internal organs in

53 male rats treated with 6 mg/kg/day

(Refs. 63 and 104). Effects were not seen

in rats dosed with 0.06 mg/kgfday. In

another study, increased relative liver

and spleen weights, decreased body.

weight gain and marked atrophy and

parenchymatous dystrophy of liver cells

were observed in 10 male albino rats

treated by gavage with 29.5 mg/kglday

for 10 weeks (Ref. 63).

b. Evidence of potential for

environmental toxicity. This assessment

is based on probabilistic dilution

modelling indicating that 2,6-

dimethylphenol is present in the

environment at levels within a factor of

100 of its known acute toxicity to

environmental organisms (Ref. 106).

EPA believes that there may be an

unreasonable risk of injury to the

environment from chronic effects when

acute toxicity is observed at levels

within a factor of 100 of predicted

stream concentrations. Specifically, EPA

has preliminarily determined a

concentration of concern of 100 ppb

(based on 2,6-dimethylphenol's

predicted chronic toxicity to daphnids)

and has estimated that this

concentration is exceeded 260. days of

the year in receiving streams (Ref. 108).

As discussed further below, over

1,900 workers may be exposed to 2,6-

dimethyiphenol in a variety of

commercial applications. Furthermore,

2,6-dimethylphenol. which is produced

in substantial quantities, has been

detected in air, rain, wastewater, and

groundwater samples, which may

indicate general population and

environmental exposures (Refs. 34, 36,

42,61. 81 and 83). Because of these

concerns, EPA believes that 2,6-

dimethylphenol may present an

unreasonable risk of injury to health and

the environment.

2. Suhstantial quantities produced

finding. EPA believes that 2,6-

dimethylphenol is or will be produced

in substantial quantities. Information

available to EPA indicates that in 1977,

from 2 to 20 million pounds of 2,6-

dimethyiphenol was produced at six

different facilities in the United States

(Ref. 94). There were two facilities that

manufactured 2,6-dimethylphenol in

the United States in 1989 (Ref. 86). EPA

estimates production in 1989 to have

been 130 million pounds (Ref. 101). For

the reasons set forth in the "B" policy,

EPA believes that production of 1

million pounds or greater of 2,6-

dimethylphenol constitutes substantial

production under section 4(a)(1)(B)(i) of

TSCA.

3. Substantial human exposure

finding. EPA believes that there is or

may be substantial human exposure to

2,6-dimethylphenol. EPA finds that 2,6-

dimethylphenol is used in a variety of

commercial applications, many of

which can lead to worker exposure. The

NOES survey estimated that 1.941

workers were potentially exposed to 2,6-

dimethylphenol (Refs. 70 and 109). Of

these workers, 95 percent were

potentially exposed during the use of

trade name products containing this

chemical. 2,6-Dimethylphenol is used

primarily in the production of

poly(phenylene oxide) resins (Ref. 31).

2,6-Dimethylphenol is also used in the

manufacture of tetramethylbisphenol A,

2,6-dimethylaniline, bis(4-hydroxy-2,5-.

dimethylphenyl)methane, dyes,

pharmaceuticals and fragrances, and as

a mixture with other xylenols, in

disinfectants, solvents, pharmaceuticals,

insecticides, fungicides, plasticizers,

rubber chemicals, lubricant and gasoline

additives, and wetting agents (Ref. 81).

As explained in the "B" policy, EPA

believes that the potential exposure of

1,941 workers to 2,6-dimethylphenol is

substantial human exposure under

section 4(a)(1)(B)(i) of TSCA.

Furthermore, general population

exposure to 2,6-dimethylphenol is also

indicated. 2,6-Dimethylphenol was

detected in 64 samples obtained from 33

industries and POTWs at a maximum

concentration of 2,895 ppm (Ref. 81).

Monitoring data indicate trace

quantities of 2,6-dimothylphenol in air

and rain (Refs. 61 and 83). 2,6-

Dimethylphanol was detected in shale

oil wastewater in the range 0.75 to 1.7

tig/L (Ref. 42) and at 12 mgfL in the

wastewater from the gasification of coal

(Ref. 34). In addition' it was detected in

groundwater samples from a wood

preserving facility in Florida at a

concentration of 0.90 mg/L, while the

concentration of 2,6-dimethylphenol in

groundwater 330 meters from the site

was 0.29 mg/L (Ref. 36).

4. Insufficient data and experience

finding. EPA believes that there are

insufficient data and experience to

determine or predict the effects on

human health or the environment from

manufacturing, processing, distribution,

use, and/or disposal of 2,6-

dimethylphenol. This assessment is

based on the following information.

EPA has adequate negative data

evaluating the gbne mutation effects of

2,6-dimethylphenol in Salmonella (Refs.

24 and 32). However, EPA has no data

evaluating this chemical's potential as a

gene toxicant in mammalian cells or as

a chromosomal toxin. EPA found no

data for neurotoxicity, pharmacokinetics

and metabolism, reproductive effects, or

developmental toxicity.

For environmental effects, acute

aquatic toxicity studies are available for

green algae, duckweed, daphnids, sea

urchins, fathead minnows and Atlantic

cod (Ref. 3). The study for green algae

is inadequate because It lacks a rigorous

measurement of growth inhibition as a

96-hour EC50 value. The effect

measured was inhibition of chlorophyll

synthesis and the lowest-observed-effect

concentration (LOEC was the only

effective concentration reported. The

Agency believes that the 96-hour EC5O

value for growth will be a more

sensitive effect than inhibition of

chlorophyll synthesis and will be more

relevant in an environmental risk

assessment. While fish and invertebrate

acute toxicity data are adequate, EPA

found no available data for aquatic

invertebrate chronic toxicity. An

available 8-day study on fathead

minnows for 2,-dimethylphenol is of

too short duration to be considered a

chronic effects study, nor did it evaluate

sensitive life stages, and, thus, this

study is inadequate (Ref. 3).

Available chemical fate screening data

for 2,6-dimethylphanol indicate that it

may undergo substantial degradation

under aerobic conditions; however, EPA

found no available data to determine or

reliably predict the half-life for the

removal of 2,6-dimethylphenol by this

process (Ref. 12).,Data on the anaerobic

degradation of 2,6-dimethylphenol are

likewise limited. One screening study

indicates that 2i6-dimethylphenol may

not degrade under anaerobic conditions;

another study indicated that this

chemical undergoes anaerobic

biodegradation in ground water and

laboratory digestors (Refs. 12 and 35).

These (contradictory) data ere

insufficient to adequately characterize

this removal process. EPA also believes

that the aqueous photolysis of 2,6-

dimethylphenol is inadequately

61663
61664 Federal Register / Vol. 58, No. 223 / Monday, November 22, 1993 / Proposed Rules

characterized, with no data available

which simulates this process under

natural conditions (Ref. 12).

5. Testing necessary to develp data

finding. EPA believes that testing of 26-

dimethylphenol is necessary to develop

data for neurotoxicity, pharmacokinetics

and metabolism, reproductive effects,

developmental effects, mutagenic

effects, algal toxicity, fathead minnow

chronic toxicity, daphnid chronic

toxicity, aerobic biodegradation,

anaerobic biodegradation, and aqueous.

photolysis. EPA believes that these

testing data are needed to determine if

the manufacturing, processing.

distribution, use, or disposal of 2,6-

dimethylphenol or any combination of

such activities, does or does not present

an unreasonable risk of injury to health

or the environment.

IV. Issues for Comment

In addition to any relevant, general

comments on the chemicals and

,proposed testing in this rulemaking,

EPA would appreciate comments on the

following specific issues:

1. EPA is proposing subchronic

testing of acetophenone by the

inhalation route of exposure. EPA is

soliciting comment on the feasibility of

inhalation testing given acetophenone's

known irritant properties. If inhalation

testing is not feasible, should EPA

require subchronic testing by the oral

route given the, at best, marginally

acceptable nature of the existing oral

studies?

2. In this rule, EPA is only proposing

to require first tier mutagenicity testing

at this time. For purposes of this

rulemaking, EPA solicits comments on

the appropriateness of these tests and its

decision to defer higher tier

mutagenicity testing and oncogenicity

testing pending the receipt of first tier

results.

a. EPA is also soliciting comments on

the proposed toxicokinetics and

biodegradation in natural surface water

guidelines, which are proposed to be

incorporated by reference.

V. Economic Analysis of the Proposed

Rule

EPA has prepared an economic

analysis that evaluates the potential for

significant economic impacts as a result

of the testing proposed in this notice

(Ref. 101). Total costs of testing,

including both laboratory costs and

administrative costs, are as follows:

acetophnone--$1.3 to 2.0 million;

phenol-$1.5 to 2.4 million; NNdimethylaniline-$1.4 to 2.2 million;

ethyl acetate-$0.8 to 1.2 million; and

2,6-dimethylphenol--$1.2 to 1.7

million.

Total costs of testing for each

chemical have been annualized and

compared with annual revenues as an

indication of potential economic

impact. Annualized costs, calculated

over 15 years using a 7 percent discount

rate, represent the equivalent constant

costs which would have to be recouped

each year of the payback period to

finance the testing expenditure in the

first year.

On the basis of these calculations,

EPA believes that for phenol, ethyl

acetate and 2,6-dimethylphenol there is

no potential for adverse economic

impact. Because these three chemicals

have relatively large production

volumes, the annualized costs of testing,

expressed as a percentage of annual

revenue, are very small-ranging from

0.2- to 0.13 percent. Costs of testing are

therefore found to be insignificant

relative to revenues for these three

chemicals.

For the remaining two chemicalsacetophenone and NNdimethylaniline-there may be some

potential for adverse economic impacts

due to the proposed testing. Because

these two chemicals are produced in

smaller quantities than the other three

chemicals subject to this proposed rule,

costs of testing as a percentage of

revenues are higher-ranging from

approximately 2- to 4 percent. Costs of

testing may therefore be significant

relative to revenues for acetophenone

and NN-dimethylaniline.

VI. Availability of Test Facilities and

Personnel

EPA believes that test facilities and

personnel are available to perform the

testing specified in this proposed rule.

(Ref. 111).

VII. Public Meeting

If requested, EPA will hold a public

meeting in Washington, DC after the

close of the public comment period.

Persons who wish to attend or to

present comments at the meeting should

contact Mary Louise Hewlett, Chemical

Testing Branch (202) 260-8162 by

January 6, 1994. The meeting will be

open to the public, but active

participation will be limited to those

who requested to comment and EPA

representatives. Participants are

requested to submit copies of their

statements by the meeting date. These

statements and a transcript of the

meeting will become part of EPA's

rulemaking record.

VIII. Comments Containing

Confidential Business Information

All comments will be placed in the

public file unless they are clearly

labeled as Confidential Business

Information (CBI) when they are

submitted. While a partof the record,

CBI comments will be treated in

accordance with 40 CFR part 2. A

sanitized version of all CBI comments

must be submitted to EPA for inclusion

in the public file.

It is the responsibility of the

commenter to comply with 40 CFR part.

2 in order that all materials claimed as

confidential may be properly protected.

This includes, but is not limited to,

clearly indicating on the face of the

comment (as well as on any associated

correspondence) that information

claimed as CBI is included, and m arking

"CONFIDENTIAL", "TSCA CBI" or

similar designation on the face of each

document or attachment in the

comment which contains information

claimed as CBI. Should information be

put into the public file because of

failure to clearly designate its

confidential status on the face of the

comment, EPA will presume any such

information which has been in the

public file for more than 30 days to be

in the public domain.

IX. Rulemaking Record

EPA has established a record for this

rulemaking (docket number OPPTS42150). This record contains the basic

information considered by EPA in

developing this proposal and

appropriate Federal Register notices.

EPA will supplement this record as

necessary.

A public version of the record, from

which all information claimed as CBI

has been deleted, is available for

inspection in the TSCA Noncynfidential

Information Center, also known as the

TSCA Public Docket Office, East Tower,

Rm. G-102,401 M St., SW.,

Washington, DC. 20460, from 8 a.m. to

noon, and I p.m. to 4 p.m., Monday

through Friday, except legal holidays. The record includes the following information:

A. Supporting Documentation

(1) Notice containing the ITC

designation. (2) Federal Register notices pertaining

to this rule consisting of:

(a) "Twenty-seventh Report of the

Interagency Testing Committee to the

Administrator; receipt of report and

request for comments regarding priority

list of chemicals." (March 6, 1991, 56

FR 9534).

(b) Notice of final rule on EPA's TSCA

Good Laboratory Practice Standards (54

FR 34034, August 17, 1989).

(c) Notice of final rule on data

reimbursement policy and procedures

(48 FR 31786, July 11, 1983).
Federal Register / Vol. 58, No. 223 / Monday, November 22, 1993 / Proposed Rules

(d) Notice of proposed test rule on

chloromethane and chlorinated

benzenes (45 FR 48524, July 18, 1980).

(e) Notice of proposed test rule on

dichloromethane, nitrobenzene and

1,1,1 trichloroethane (46 FR 30300, June

5, 1981).

(f) Notice of final test rule on the C9

aromatic hydrocarbon fraction (50 FR

20662, May 17, 1985).

(g) Notice of proposed TSCA section

4(a)(1)(B) statement of policy (56 FR

32294, July 15, 1991).

(h) Notice of final TSCA section

4(a)(1)(B) statement of policy (58 FR

28736, May 14, 1993).

(i) Notice of proposed test rule on

glycidol and its derivatives category (56

FR 57144, November 7, 1991). (j) Notice of testing consent order for

acrylic acid (57 FR 7656, March 4,

1992).

(3) TSCA test guidelines cited as test

standards for this rule.

(4) Communications consisting of:

(a) Written letters.

(b) Contact reports of telephone

conversations

(c) Meeting summaries.

B. References

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"Subchronic toxicity of NN-dimethylaniline

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(2) Anger, W.K., and Johnson, B.L.

"Chemicals Affecting Behavior."

Neurotoxicity of Industrial and Commercial

Chemicals. J.L. O'Donoghue, ed. Boca Raton,

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(3) AQUIRE. Aquatic Toxicity Information

Retrieval Data Base. Duluth, MN: U.S.

Environmental Protection Agency,

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(4) Armstrong, J.E., Fehler, S.W., and

Calder, J.A. "Effects of petroleum

hydrocarbons on the growth and energetics of

marine microalgae." Biological Monitoring of

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(5) Arrhenius, E. "Effects on hepatic

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"The skin resorptive action of

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Gig. Prof. Sabol. Air Pollution and Industrial

Hygiene. 5: 90-94 (1969)

(58) Lande, S.S., Durkln, P.R.. Christopher.

D.H.. Howard, P.H., and Saxena, J.

"Investigation of selected potential

environmental contaminants: ketonic

solvents." EPA-,60/2-76--003. Washington,

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(1976).

(59) Lawrence. F.R., and Marshall, W.J.

"Aniline" In: Ullmann's Encyclopedia of

Industrial Chemistry. 5th edition. Vol. A2.

Gerhartz, W., ad. Weinheim, Germany: VCH

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. (60) Leibman, K.C. "Reduction of ketones

in liver cytosol." Xenobiotica, 1(1)7 97-104

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(61) Leuenberger, C., Ligocki, M.P., and

Pankow, J.F. "Trace organic compounds in

rain. 4. Identities, concentrations, and

scavenging mechanisms for phenols in urban

air and rain." Environmental Science and

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(62) Liao, T.F., and Oehme, F.W. "Tissue

distribution and plasma protein binding of

[14Clphenol in rats." Toxicology and Applied

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(63) Maazik, I.K. "Standards for

dimethylphenol isomers in water bodies."

Gigiena I Sanitaria. (Hygiene and Sanitation).

11: 28-35 (1968).

(64) Markosyan, T.M. "Comparative

toxicity of monomethylaniline and

dimethylaniline in chronic experimental

exposure." Chemical Abstracts. 71: 11369u

(1969).

(65) Mehta, R., Hirom, P.C., and Millburn,

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445-452 (1978).

(66) Miller, J.J., Powell, G.M., Olavesen,

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dimethoxyphenol and related compounds in

the cat." Toxicology and Applied

Pharmacology. 38:47-57 (1976).

(67) NCI (National Cancer Institute),

Bioassasy of phenol for possible

carcinogenicity in F344 rats and B6C3P1

mice. NIH Publication No. 80-1759 (1980).

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"Aromatic amines in and near the Buffalo

River." Environmental Science and

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(69) Nicola, R.M., Branchflower, R., and

Douglas, P. "Chemical contaminants in

bottomfish," Journal of Environmental

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(70) NIOSH (National Institute for

Occupational Safety and Health). National

Occupational Exposure Survey (NOES)

(1990).

(71) NTP (National Toxicology program).

Teratologic evaluation of phenol in CD rats.

Prepared by Research Triangle Institute,

Research Triangle Park, NC. NTIS PB83-

247726. (uly 29, 1983).

(72) NTP (National Toxicology Program).

Toxicology and carcinogenesis studies of

N,N-dimethylaniline in F344/N rats and

B6C3F1 mice. NTP Technical Report No. 350.

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Services, Public Health Service, National

Institute of Health, Research Triangle Park,

NC. (1989).

(73) Odenbro, A., and Arrhentus, E. "Effect

of triethyl lead chloride on hepatic

microsomal N-oxygenation and Coxygenation

of NN-dimethylaniline in rats." Toxicology

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(1984).

(74) Ohmiya, Y., and Mehendale, H.M. "N

Oxidation of NN-dimethylaniline in the

rabbit and rat lung." Biochemical

Pharmacology. 32(7): 1281-1285 (1983).

(75) Olsson, U., Belje, B., Wachtmeister,

C.A., and Arrhenius, E. "Effects of

dimethylnitrosoamine on metabolism of Ndimethylaniline by rat liver microsomes. A

comparative study of treatment in vivc in

isolated liver perfusion and in the

microsomal system." Chemico-Biological

Interactions. 45(2): 191-201 (1983).

(76) Olsson, U., Onflet, A., and Beije B.

"Dietary selenium deficiency causes

decreased N-oxygenation of NNdimethylanihne and increased mutagenicily

of dimethylnitrosoamine in the isolaied rat

liver/cell culture system." Mutation

Research. 126(1): 73-80 (1984). (77) Piccirillo, V.J., McCall, D.L., Luntebhick,

C., Plankenhom, L.J., and Sexsmith. C.

Screening of priority chemicals for

reproductive hazards. NTIS PB 83-2576000.

p. 108 (1983).

(78) Pinching, A.J., and Doving, K.B.

"Selective degeneration in the rat olfactory

bulb following exposure to different odors."

Brain Research. 82(2): 195-204 (1974).

(79) Rane, A. "N-Oxidation of a tertiary

amine (N,N-dimethylaniline) by human feta!

liver microsomes." Clinical Pharmacology

and Therapeutics. 15(1): 32-38 (1974).

(80) Sandage, C "Tolerance criteria for

continuous inhalation exposure to toxic

material." ASD Technical Report 61519 I).

Kansas City, MO: Midwest Research Institute

pp. 1-29 (1961).

(81) Sax, N.I., and l4wis, R.J. Haweley's

Condensed Chemical Dictionary. 11th

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Reinhold Company. pp. 9-10, 411, 421, 896-

897, 1244 (1987).

(82) Shackelford, W.M., Cline, D.M., Fass,

L., and Kurth, G. "An evaluation of

automated spectrum matching for survey

identification of wastewater components by

gas chromatography mass spectrometry."

Analytica Chemica Acta. 146: 15-27

[supplemental data) (1983).

(83) Shah, J.J., and Heyerdahl, E.K.

National ambient volatile organic compGunds

(VOCS) database update. EPA/600-3-88 010

p. 48 (1988).

(84) Smith, J.N., Smithies, R.H., and

Williams, R.T. "Studies in detoxication 5b.

The metabolism of alkylbenzenes.

Stereochemical aspects of the biological

hydroxylation of ethylbenzene to

methylphenylcarbinol." Biochemical Jourrma

56: 320-324 (1954).

(85) Smyth, H.F. "Acute and sub-acute

toxicity of acetophenone." Report 9-42.

Mellon Institute of Ind. Res. (1946).

(86) SRI (SRI International). Directory of

Chemical Producers. Menlo Park, CA: SRI

International. pp. 844-845, 1063 (1989).

(87) Staples, C., Wener, A., and Hoogheem•

T. "Assessment of priority pollutant

concentrations in the United States usiy

STORET database." Environmental

Toxicology and Chemistry. 4: 131-142

(1985).

(88) STORET. STORET Date Base retrieval

3/19/90. Washington, DC: U.S. EPA. (1990).

61666 Federal Register / Vol. 58, No. 223 / Monday, November 22, 1,993 / Proposed Rules
Federal Register / Vol. 58, No. 223 / Monday, November 22, 1993 / Proposed Rules

(89) Suffet, I.H, Brenner, L., and Cairo, P.R.

"Gas chromatography-mass spectrometry

identification of trace organics in

Philadelphia, Pennsylvania, USA drinking

waters during a two year period." Water

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(90) Tennant, R.W., Margolin, B.H., Shelby,

M.D., Zeiger, E., Haseman, J.K., Spalding, J.,

Caspary, W., Resnick, M., Stasiewicz, S.,

Anderson, B.. and Minor, R. "Prediction of

chemical carcinogenicity in rodents from in

vitro genetic toxicity assays." Science. 236:

933-941. (1987).

(91) Thierfelder, K., and Daiber, K. "Zur

kenntis des Verhaltens fettaromatischer

Ketone in Tierk6rper." Hoppe Seyler's

Zeitschrift fur Physiologie Chemie. 130: 380-

396 (1923).

(92) Thierfelder, K., and Klenk, E. "Zur

kenntis des Verhaltens des Acetophenons

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Zeitschrift fir Physiologie Chemie. 141: 29-

32 (1924).

(93) TRI (Toxics Release Inventory).

Database retrieval 3/16/90. U.S. EPA. (1990).

(94) TSCAPP. Computer printout of non- confidential production data from TSCA

inventory. Washington, DC: OTS, CID, U.S.

EPA. Online 3/15/90 (1990).

(95) Uehleke, H., Reiner, 0., and Hellmer,

K.H. "Perinatal development of tertiary

amine N-oxidation and NADPH cytochrome

c reduction in rat liver microsomes."

Research Communications in Chemical

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(1971).

(96) USEPA. U.S. Enviromental Protection

Agency. "27th ITC list exposure report - acetophenone." Washington, DC, Office of

Toxic Substances, USEPA (October 23, 1991).

(97) USEPA. U.S. Enviromental Protection

Agency. "27th ITC list exposure report - 2,6-

dimethylphenol." Washington, DC, Office of

Toxic Substances, USEPA (November 7,

1991).

(98) USEPA. U.S. Enviromental Protection

Agency. "27th ITC list exposure report - ethyl

acetate." Washington, DC, Office of Toxic

Substances, USEPA (October 23, 1991).

(99) USEPA. U.S. Enviromental Protection

Agency. "27th ITC list exposure report - NNdimethylaniline." Washington, DC, Office of

Toxic Substances, USEPA (November 7,

1991).

(100) USEPA. U.S. Enviromental Protection

Agency. "27th ITC list exposure report -

phenol." Washington, DC, Office of Toxic

Substances, USEPA (October 23, 1991).

(101) USEPA. U.S. Environmental

Protection Agency. Economic impact

evaluation of proposed test rule for IRIS

chemicals (group I). Prepared by Dan

Axelrad, Regulatory Impacts Branch,

Economics and Technology Division, USEPA

(March, 1992).

(102) U.S. ITC (U.S. International Trade

Commission). Synthetic Organic Chemicals..

U.S. Production and Sales, 1979.

Washington, DC: U.S. Goverment Printing

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(103) U.S. ITC (U.S. International Trade

Commission). Synthetic Organic Chemicals.

U.S. Production and Sales 1988. Washington,

DC. U.S. Government Printing Office.

Publication No. 2219. pp. 3-12, 15-4, and

15--6 (1989).

(104) Veldre, I.A., and Janes, H.J.

"Toxicological studies of shale oils, some of

their components and commercial products."

Environmental Health Perspectives. 30: 141-

146 (1979).

(105) Waters, M.D., and Auletta, A. "The

gene-tox program: genetic activity

evaluation." ,. Chem: Inf. Comput. Sci. 21:

35-38 (1981).

(106) Ziegler, D.M., and Gold, M.S.

"Oxidative metabolism of tertiary amine

drugs by human and liver tissue."

Xenobiotica. 1: 325-326 (1971).

(107) Zimmermann, F.K., Mayer, V.W.,

Sqheel, I., and Resnik, M.A. "Acetone,

methyl ethyl ketone, ethyl acetate,

acetonitrile and other polar aprotic solvents are strong inducers of aneuploidy in

Saccharomyces cerevisiae." Mutation

Research. 149: 339-351 (1985).

(108) USEPA. U.S. Environmental

Protection Agency. "PDM estimates for NNdimethylaniline and 2,6-dimethylphenol."

Memorandum from Sidney Abel to John

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Pollution Prevention and Toxics, USEPA

(October 8, 1991).

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Occupational Exposure Survey Field

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of Toxic Substances. USEPA. (1977).

(111) Booz, Allen, Hamilton., Inc.,

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toxicological testing industry." Prepared for

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Washington, DC (June 1990).

(112) NTP (National Toxicology Program).

Teratologic evaluation of phenol in CD mice.

Prepared by Research Triangle Institute,

Research Triangle Park, NC. NTIS PB85-

104461 (July 29, 1983).

(113) USEPA. Memorandum from Andrea

Blaschka and John Schaeffer to the

Workgroup scheduling a meeting with the

Phenol Panel to discuss pharmacokinetic

testing for phenol. CMA's Phenol Panel

comments to the ITC Report and a protocol

for pharmacokinetic testing for phenol are attached. Washington, DC, Office of Pollution

Prevention and Toxics, USEPA (April 24,

1991).

(114) USEPA. Memorandum from Andrea

Blaschka and John Schaeffer to the

Workgroup summarizing the results of the

meeting with the Phenol Panel on 4/24/91

and a request for comments on pharmacokinetic protocols. Washington, DC,

Office of Pollution Prevention and Toxics,

USEPA (May 9, 1991).

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Blaschka to the Workgroup summarizing the

meeting held on 11/7/91 and requesting

comments on further testing. Washington,

DC, Office of Pollution Prevention and

Toxics, USEPA (November 22, 1991).

(116) USEPA. Discharge of NN,-

dimethylaniline and 2,6-dimethylphenol to

saline surface waters. Memorandum from Sid

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Schaeffer, Chemical Testing Branch.

Washington, DC, Office of Toxic Substances,

USEPA (April 15, 1992).

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typhimurium: New structure-activity

relationships." Mutation Research. 135:77-

86 (1984).

X. Regulatory Assessment

Requirements

A. Executive Order 12291

Under Executive Order 12291, EPA

must judge whether a rule is "major"

and therefore subject-to the requirement

of a Regulatory Impact Analysis. EPA

has determined that this proposed test

rule would not be major because it does

not meet any of the criteria set forth in

section 1(b) of the Order; i.e., it would

not have an annual effect on the

economy of at least $100 million, would

not cause a major increase in prices, and

would not have a significant adverse

effect on competition or the ability of U.

S. enterprises to compete with foreign

enterprises.

This proposed rule was submitted to

the Office of Management and Budget

(OMB) for review as required by

Executive Order 12291. Any written

comments from OMB to EPA, and any

EPA response to those comments, are

included in the rulemaking record.

B. Regulatory Flexibility Act

Under the Regulatory Flexibility Act

(5 U.S.C. 601 et seq.) EPA is certifying

that this test rule, if promulgated, would

not have a significant impact on a

substantial number of small businesses

because: (1) They would not be

expected to perform testing themselves,

or to participate in the organization of

the testing effort; (2) they would

experience only very minor costs, if any,

in securing exemption from testing

requirements; and (3) they are unlikely

to be affected by reimbursement.

requirements.

C. Paperwork Reduction Act

OMB has approved the information

collection requirements contained in

this rule under the provisions of the

Paperwork Reduction Act of 1980, 44

U.S.C. 3501 et seq., and has assigned

OMB Control number 2070-0033.

Public reporting burden for this

collection of information is estimated to

average 10,100 hours per response,

including time for reviewing

instructions, searching existing data

sources, gathering and maintaining the

data needed, and completing and

reviewing the collection of information.

The total public reporting burden is

estimated to be 222,000 hours for all

responses. Send comments regarding

the burden estimate or any other aspect

of this collection of information,

61667
61668 Federal Register / Vol. 58, No. 223 / Monday, November 22, 1993 / Proposed Rules

including suggestions for reducing this

burden, to Chief, Information Policy

Branch, 2131, U.S. Environmental

Protection Agency, 401 M St., SW..

Washington, DC 20460; and to the

Office of Management and Budget,

Paperwork Reduction Project (2070-

0033), Washington DC 20503. The final

rule will respond to any 0MB or public

comments on the information collection

requirements contained in this proposal

List of Subjects in 40 CFR Part 799

Environmental protection, Chemicals,

Hazardous substances, Reporting and

recordkeeping requirements, Testing,

Incorporation by reference.

Dated: November 15, 1993.

Victor J. Kimm,

Acting Assistant Administrator for

Prevention, Pesticides and Toxic Substances.

Therefore, it is proposed that 40 CFR,

chapter I, subchapter R, part 799 be

amended as follows:

PART 799--[AMENDED]

a. The authority citation for part 799

would continue to read as follows:

Authority: 15 U.S.C. 2601, 2603, 2611,

2625.

b. By adding § 799.4450 to subpart B

to readas follows:

§799.4450 Designated IRIS chemicals.

(a) Identification of test substances.

(1) The IRIS chemicals subject to this

test guideline were designated in the

Twenty-Seventh ITC report. These

chemicals include acetophenone (CAS

No. 98-86-2), phenol (CAS No. 108-95-

2), NN-dimethylaniline (CAS No. 121-

69-7), ethyl acetate (CAS No. 141-78-

6), and 2,6-dimethylphenol (CAS No.

576-26-1).

(2) Acetophenone, phenol, NNdimethylaniline, ethyl acetate, and 2,6-

dimethylphenol of at least 99 percent

purity shall be used as the test

substance.

(b) Persons required to submit study

plans, conduct tests and submit data.

All persons who manufacture (includin

import) or process or intend to

manufacture or process acetophenone,

phenol, NN-dimethylaniline, ethyl

acetate, and 2,6-dimethylphenol other

than as an impurity, after January 5,

1994, to the end of the reimbursement

period shall submit letters of intent to

conduct testing, submit study plans,

conduct tests, and submit data, or

submit exemption applications as

specified in this section, subpart A of

this part and parts 790 and 792 of this

chapter for single-phase rulemaking, for

the substances they manufacture subjec

* to exclusions contained in

§ 790.42(a)(2), (a)(4) and (a)(5). These

sections provide that processors,

persons who manufacture less than 500

g(1,100 lbs) annually, or persons who

manufacture small quantities of the

chemical solely for research and

development as defined in § 790.42(a)(5)

shall not be required to submit study

plans, conduct tests and submit data, or

submit exemption applications as

specified in this section unless directed

to do so in a subsequent notice as set

forth in § 790.48(b).

(c) Health effects -41) Subchronic

toxicity - (i) Required testing.

Subchronic toxicity testing shall be

conducted by inhalation with

acetophenone, phenol, and NNdimethylaniline in accordance with

§ 798.2450 of this chapter.

(ii) Reporting requirements. (A) The

required subchronic toxicity test shall

be completed and the final reports

submitted to EPA within 18 months of

the effective date in paragraph (f) of this

section.

(B) Progress reports shall be submitted

to EPA every 6 months beginning 6

months after the effective date in

Raragraph (f) of this section until the

nal report is submitted.

(2) Pharmacokinetics and

metabolism-(i) Required testing. (A)

Pharmacokinetics and metabolism

studies shall be conducted with

acetophenone, phenol, NNdimethylaniline, and 2,6-

dimethylphenol by the oral route of

administration in accordance with

OECD test guideline 417

"Toxicokinetics", which is incorporated - by reference. Copies of this guideline

are available in the TSCA

Nonconfidential Information Center,

East Tower, Rm. G-102, 401 M St., SW.,

Washington, DC 20460. This guideline

is also available for public inspection at

the Office of the Federal Register, 800

North Capital St., Suite 700,

Washington, DC. This incorporation by

reference was approved bythe Director

of the Federal Register in accordance

with 5 U.S.C. 552(a) and 1 CFR part 51.

g This guideline is incorporated as it

exists on the date of approval and a

notice of any changes to the guideline

will be published in the Federal

Register.

(B) Pharmacokinetics and metabolism

studies shall be conducted with

acetophenone, phenol, NNdimethylaniline, and 2,6-

dimethylphenol by the inhalation route

of administration In accordance with

OECD test guideline 417

"Toxicokinetics", which is incorporated

by reference. Copies of this guideline

t are available in the TSCA

Nonconfidential Information Center,

East Tower, Rm. G-102,401 M St., SW.,

Washington, DC 20460. This guideline

is available for public inspection at the

Office of the Federal Register, 800 North

Capital St., Suite 700, Washington, DC.

This incorporation by reference was

approved by the Director of the Federal

Register in accordance with 5 U.S.C.

552(a) and 1 CFR part 51. This guideline

is incorporated as it exists on the date

of approval and a notice of any changes

to the guideline'will be published in the

Federal Register.

(ii) Reporting requirements. (A) The

required pharmacokinetics and

metabolism studies shall be completed

and the final reports submitted to EPA

within 15 months aftefthe effective date

in paragraph (f) of this section.

(B) Progress reports shall be submitted

to EPA every 6 months beginning 6

months after the effective date in

paragraph (f) of this section until the

final report is submitted.

(3) Neurotoxicity (Inhalation)-i)

Required testing-(A) Functional

observational battery. (1) Functional

observational battery tests shall be

conducted with acetophenone, phenol,

and N,N-dimethylaniline in accordance

with § 798.6050 of this chapter except

for the provisions in paragraphs

(d)(4)(ii), (d)(5), and (d)(6) of § 798.6050.

(2) For the purpose of paragraph

(c)(3)(i)(A) of this section, the following

provisions also apply:

(i) Lower doses. Either the data from

the lower doses shall show graded dosedependent effects or there shall be no

neurotoxic (behavioral) effects at any

dose tested.

(ii) Duration and frequency of

exposure. For the acute testing, animals

shall be exposed for 6 hours per day for

I day. For the subchronic testing,

animals shall be exposed for 6 hours per

day 5 consecutive days per week for a

90-day period.

(iii) Route of exposure. Animals shall

be exposed to acetophenone, phenol,

and NN-dimethylaniline by inhalation

administration.

(B) Motor activity. (1) Motor activity

testing shall be conducted with

acetophenone, phenol, and NNdimethylaniline in accordance with

§ 798.6200 of this chapter except for the

rovisions in paragraphs (d)(4)(ii),

d)(5), and (d)(6) of § 798.6200.

(2) For the purpose of paragraph

(c)(3)(i)(B) of this section, the following

provisions also apply:

I) Lower doses. Either the data from

the lower doses shall show graded dosedependent effects or there shall be no

neurotoxic (behavioral) effects at any

dose tested.
Federal Register / Vol. 58, No. 223 / Monday, November 22, 1993 / Proposed Rules

(i) Duration and frequency of

exposure. For the acute testing, animals

shall be treated for 6 hours per day for

I day. For the subchronic testing,

animals shall be exposed 6 hours per

day 5 consecutive days per week for a

90-day period.

(iii) Route of exposure. Animals shall

be exposed to acetophenone, phenol,

and NN-dimethylaniline by inhalation

administration.

(C) Neuropathology. (1)

Neuropathology testing shall be

conducted with acetophenone, phenol,

and NN-dimethylaniline in accordance

with § 798.6400 of this chapter except

for the provisions in paragraphs

(d)(4}(ii), (d)(5), (d)(6) and (d)(8)(iv)(C)

of § 798.6400.

(2) For the purpose of paragraph

(c)(3)(i)(C) of this section, the following

provisions also apply:

(i) Lower doses. Either the data from

the lower doses shall show graded dosedependent effects or there shall be no

neurotoxic (behavioral) effects at any

dose tested.

(i) Duration and frequency of

exposure. For the acute testing, animals

shall be exposed for 6 hours per day for

1 day. For the subchronic testing,

animals shall be exposed for 6 hours per

day 5 consecutive days per week for a

90-day period.

(iii) Route of exposure. Animals shall

be exposed to acetophenone, phenol,

and NN-dimethylaniline by inhalation

administration.

(iv) Clearing and embedding. After

dehydration, tissue specimens shall be

cleared with xylene and embedded in

wax or plastic medium, except for the

sural nerve, which should be embedded

in plastic. Multiple tissue specimens

(e.g. brain, cord, ganglia) may be

embedded together in one single block

for sectioning. All tissue blocks shall be

labelled to provide unequivocal

identification. Plastic embedding should

follow the method described by

Spencer, et al., in § 798.6400(f) of this

chapter, or an equivalent method.

(ii) Reporting requirements. (A) The

functional observational battery, motor

activity, and neuropathology testing

with acetophenone, phenol, and N,Ndimethylaniline shall be completed and

the final reports submitted to EPA

within 21 months of the effective date

in paragraph (f) of this section.

B Progress reports shall be submitted

every 6 months beginning 6 months

after the effective date in paragraph (f)

of this section until the final report is

submitted.

(4) Neurotoxicity (Gavage)-(i)

Required testing-(A) Functional

observational battery. (1) A functional

observational battery test shall be

conducted with 2,6-dimethylphenol in

accordance with S 798.6050 of this

chapter except for the provisions in

paragraphs (d)(4)(ii), (d)(5), and (d)(6) of

§ 798.6050.

(2) For the purpose of paragraph

(c)(4)(i)(A) of this section the following

provisions also apply:

(i) Lower doses. Either the data from

the lower doses shall show graded dosedependent effects or there shall be no

neurotoxic (behavioral) effects at any

dose tested.

(iij Duration and frequency of

exposure. For the acute testing, animals

shall be treated once. For the subchronic

testing, animals shall be treated 5

consecutive days per week for a 90-day

period.

(iii) Route of exposure. Animals shall

be exposed to 2,6-dimethylphenol by

gavage administration.

(B) Motor activity. (1) Motor activity

testing shall be conducted with 2,6-

dimethylphenol in accordance with

§ 798.6200 of this chapter except for the

provisions in paragraphs (d)(4)(ii),

(d)(5), and (d)[6) of § 798.6200.

(2) For the purpose of paragraph

(c)(4)(i)(B) of this section, the following

provisions also apply:

01) Lower doses. Either the data from

the lower doses shall show graded dosedependent effects or there shall be no

neurotoxic (behavioral) effects at any

dose tested.

(ii) Duration and frequency of

exposure. For the acute testing, animals

shall be treated once. For the subchronic

testing, animals shall be treated 5

consecutive days per week for a 90-day

period.

(iiN) Route of exposure. Animals shall

be exposed to 2,6-dimethylphenol by

gavage administration.

(C) Neuropathology. (1)

Neuropathology testing shall be

conducted with 2,6-dimethylphenol in

accordance with § 798.6400 of this

chapter except for the provisions in

paragraphs (d)(4)(ii), (d)(5), (d)(6) and

(d)(8)(iv)(C) of § 798.6400.

(2) For the purpose of paragraph

(c)(4)(i)(C) of this section, the following

provisions also apply: (i) Lower doses. Either the data from

the lower doses shall show graded dosedependent effects or there shall be no

neurotoxic (behavioral) effects at any

dose tested.

(iij Duration and frequency of

exposure. For the acute testing, animals

shall be treated once. For the subchronic

testing animals shall be treated 5

consecutive days per week for a 90-day

period.

(iii) Route of exposure. Animals shall

be exposed to 2,6-dimethylphenol by

gavage administration.

(iv) Clearing and embedding. After

dehydration, tissue specimens shall be

cleared with xylene and embedded in

wax or plastic medium, except for the

sural nerve, which should be embedded

in plastic. Multiple tissue specimens

(e.g. brain, cord, ganglia) may be

embedded together in one single block

for sectioning. All tissue blocks shall be

labelled to provide unequivocal

identification. Plastic embedding should

follow the method described by

Spencer, et al., in paragraph (0 of

§ 798.6400 of this chapter, or an

equivalent method.

(ii) Reporting requirements. (A) The

functional observational battery, motor

activity, and neuropathology testing

with 2,6-dimethylphenol shall be

completed and the final reports

submitted to EPA within 21 months of

the effective date in paragraph (f) of this

section.

(B) Progress reports shall be submitted

every 6 months beginning 6 months

after the effective date in paragraph (f)

of this section until the final report is

submitted,

(5) Reproductive toxicity-(i)

Required testing. Reproductive toxicity

testing shall be conducted with

acetophenone, NN-dimethylaniline,

ethyl acetate, and 2,6-dimethylphenol

by gavage, and phenol by inhalation in

accordance with § 798.4700 of this

chapter.

(ii) Reporting requirements. (A) The

reproductive toxicity tests shall be

completed and the final reports

submitted to EPA within 29 months of

the effective date in paragraph (0 of this

section.

(B) Progress reports shall be submitted

to EPA every 6 months beginning 6

months after the effective date in

paragraph (f0 of this section.

(6) Developmental toxicity--(i)

Required testing. Developmental

toxicity testing in two species, a rat and

a non-rodent, shall be conducted with

acetophenone by inhalation, and NNdimethylaniline, ethyl acetate, and 2,6-

dimethylphenol by gavage in

accordance with § 798.4900 of this

chapter. (ii) Reporting requirements. (A) The

developmental toxicity testing shall be

completed and the final reports

submitted to EPA within 12 months of

the effective date in paragraph (f) of this

section.

(B) Progress reports shall be submitted

to EPA every 6 months beginning 6

months after the effective date in

paragraph (f) of this section until the

final report is submitted.

(7) Developmental neurotoxicity-(i)

Required testing. Developmental neurotoxicity testing in the rat shall be

61669
61670 Federal Register / Vol. 58, No. 223 / Monday, November 22, 1993 / Proposed Rules

conducted with phenol by gavage

administration in accordance with

§ 795.250 of this chapter.

(ii) Reporting requirements. (A) The

developmental toxicity testing shall be

completed and the final report

submitted to EPA within 21 months of

the effective date in paragraph (f) of this

section.

(B) Progress reports shall be submitted

to EPA every 6 months beginning 6

months after the effective date in

paragraph (f) of this section until the

final report is submitted.

(8) Mutagenic effects-gene

mutation--(i) Required testing. (A) Gene

mutation assays in the Salmonella

typhimurium histidine reversion system

shall be conducted with acetophenone

in accordance with § 798.5265 of this

chapter. (B) Gene mutation assays in somatic

cells in culture shall be conducted with

acetophenone, ethyl acetate, and 2,6-

dimethylphenol in accordance with

§ 798.5300 of this chapter.

(ii) Reporting requirements.

Mutagenic effects-gene mutation tests

shall be conducted and the final reports

submitted to EPA as follows:

(A] Gene mutation in Salmonella, 9

months after the effective date in

paragraph (f) of this section.

(B) Gene mutation in somatic cells in

culture, 10 months after the effective

date in paragraph (f) of this section.

(9) Mutagenic effects-chromosomal

aberrations - (i) Required testing. In

viva cytogenetic assays shall be

conducted by gavage with

acetophenone, NN-dimethylaniline,

and 2,6-dimethylphenol in accordance

with § § 798.5385 or 798.5395 of this

chapter. (ii) Reporting requirements. (A)

Mutagenic effects - In vivo cytogenetics

testing shall be completed and the final

reports submitted to EPA within 14

months after the effective date in

paragraph (f) of this section.

(B} Progress reports shall be submitted

to EPA every 6 months beginning 6

months after the effective date in

paragraph (f) of this section.

(d) Environmental effects -(1) Algal

toxicity testing - (i) Required testing.

Algal toxicity testing shall be conducted

with NN-dimethylaniline and 2,6-

dimethylphenol in accordance with

§ 797.1050 of this chapter.

(ii) Reporting requirements. (A) The

algal toxicity test for NNdimethylaniline and 2,6-

dimethylphenol shall be completed and

the final reports submitted to EPA

within 12 months of the effective date

in paragraph (f) of this section.

(B) Progress reports shall be submitted

to EPA every 6 months beginning 6

months after the effective date in

paragraph (f) of this section until the

final report is submitted.

(2) Invertebrate acute toxicity - (i)

Required testing. (A) Daphnid acute

toxicity tests shall be conducted with

N,N-dimethyaniline and 2,6-

dimethylphenol in accordance with

§ 797.1300 of this chapter. (B) Mysid shrimp acute toxicity tests

shall be conducted with NNdimethylaniline in accordance with

§ 797.1930 of this chapter.

(ii) Reporting requirements. (A)

Invertebrate acute toxicity testing shall

be conducted and the final reports

submitted to EPA within 12 months

after the effective date in paragraph (f)

of this section.

(B) Progress-reports shall be submitted

to EPA every 6 months beginning 6

months after the effective date in

paragraph (f) of this section until the

final report Is submitted.

(3) Invertebrate chronic toxicity

testing -(i) Required testing. (A)

Daphnid chronic toxicity tests shall be

conducted with N,N-dimethylaniline

and 2,6-dimethylphenol in accordance

with § 797.1330 of this chapter.

(B) Mysid shrimp chronic toxicity

tests shall be conducted with NNdimethylaniline in accordance with

§ 797.1950 of this chapter.

(ii) Reporting requirements. (A)

-Invertebrate chronic toxicity testing

shall be conducted and the final reports

submitted to EPA within 24 months

after the effective date in paragraph (f)

of this section. . (B) Progress reports shall be submitted

to EPA every 6 months beginning 6 -

months after the effective date in

paragraph (f) of this section until the

final report is submitted.

(4) Fish chronic toxicity -(i) Required

testing. Fish early life stage toxicity tests

shall be conducted with fathead

minnows with NN-dimethylaniline and

2,6-dimethylphenol, and sheepshead

minnows with NN-dimethylaniline, in

accordance with § 797.1600 of this

chapter. (ii) Reporting requirements. (A) Fish

early life stage toxicity tests shall be

completed and the final reports

submitted to EPA within 12 months of

the effective date in paragraph () of this

section.

(B) Progress reports shall be submitted

to EPA every 6 months beginning 6

months after the effective date in

paragraph (f) of this section until the

final report is submitted.

(e) Chemical fate-(I) Biodegradation

in natural surface waters -(i) Required

testing. (A) Biodegradation testing in

natural surface waters shall be

conducted with 2,6-dimethylphenol.

(B) The testing shall be conducted in

accordance with the test procedure

specified in the American Society for

Testing and Materials (ASTM) test

method, entitled "Standard Test Method

for Biodegradation By a Shake-Flask

DieAway Method, Designation: E 1279-

89," published in the Annual Book of

ASTM Standards, March 1989,

Philadelphia, Pa., which is incorporated

by reference. Copies of this test method

are available in the TSCA

Nonconfidential Information Center,

East Tower, Rm. G-102, 401 M St., SW.,

Washington, DC 20460. This test

method is also available for inspection

at the Office of the Federal Register, 800

North Capital St., Suite 700,

Washington, DC. This incorporation by

reference was approved by the Director

of the Federal Register in accordance

with 5 U.S.C. 552(a) and 1 CFR part 51.

This method is incorporated as it exists

on the date of approval and a notice of

any changes to the method will be

published in the Federal Register.

(ii) Reporting requirements. (A) The

biodegradation test in natural surface

waters shall be completed and the final

reports submitted to EPA within 12

months of the effective date in -paragraph (f) of this section.

(B Progress reports shall be submitted

to EPA every 6 months beginning 6

months after the effective date in

paragraph (f) of this section until the

final report is submitted.

(2) Biodegradation in activated sludge

- (i) Required testing. Biodegradation

testing in activated sludge shall be

conducted with N,N-dimethylaniline in

accordance with § 796.3340 of this

chapter. (ii) Reporting requirements. (A) The

biodegradation test in activated sludge

shall be completed and the final report

submitted to EPA within 12 months of

the effective date in paragraph (f) of this

section.

(B) Progress reports shall be submitted

to EPA every 6 months beginning 6

months after the effective date in

paragraph (f) of this section until the

final report is submitted.

(3) Anaerobic biodegradation - (i)

Required testing. Anaerobic

biodegradation testing shall be

conducted with NN-dimethylaniline

and 2,6-dimethylphenol in accordance

with § 796.3140 of this chapter.

(ii) Reporting requirements. (A) The

required anaerobic biodegradation

testing shall be completed and the final

report submitted to EPA within 12

months of the effective date in

paragraph () of this section.

(B) Progress reports shall be submitted

to EPA every 6 months beginning 6

months after the effective date in
Federal Register / Vol. 58, No. 223 / Monday, November 22, 1993 / Proposed Rules

paragraph (f) of this section until the

final report is submitted,

(4) Photolysis-(i) Required testing.

Aqueous photolysis testing shall be

conducted on 2,6-dimethylphenol in

accordance with § 795.70 of this

chapter.

(ii) Reporting requirements. (A) The

required aqueous photolysis testing

shall be completed and the final report

submitted to EPA within 12 months of

the effective date in paragraph (f) of this

section.

(B) Progress reports shall be submitted

to EPA every 6 months beginning 6

months after the effective date in

paragraph (0 of this section until the

final report is submitted.

(f) Effective date. This test guideline

is effective (44 days after publication of

the final rule in the Federal Register).

[FR Doc. 93-28614 Filed 11-19-.3; 8:45 am]

BILLNG CODE 6560-0-F

FEDERAL COMMUNICATIONS

COMMISSION

47 CFR Part 73

[MM Docket No. 93-279, RM-8368]

Radio Broadcasting Services; Cal-NevAr], NV

AGENCY: Federal Communications

Commission.

ACTION: Proposed rule.

SUMMARY: The Commission requests

comments on a petition filed by Richard

W. Myers seeking the allotment of

Channel 285A to Cal-Nev-Ari, Nevada,

as its first local aural transmission

service. Channel 285A can be allotted to

Cal-Nev-Ari in compliance with the

Commission's minimum distance

separation requirements with a site

restriction of 2.6 kilometers (1.6 miles)

southeast, at coordinates North Latitude

35-17-12 and West Longitude 114-51-

57, to avoid a short-spacing to Station

KJUL, Channel 282C, North Las Vegas,

Nevada. The petitioner is requested to

provide further information to

demonstrate that Cal-Nev-Ari is a

community for allotment purposes.

Concurrence by the Mexican

Government is required because CalNev-Ari is located within 320

kilometers (199 miles) of the U.S.-

Mexican border.

DATES: Comments must be filed on or

before January 3, 1994, and reply

comments on or before January 18.

1994.

ADDRESSES: Federal Communications

Commission, Washington, DC 20554. In

addition to filing comments with the

FCC, interested parties should serve the

petitioner, or its counsel or consultant,

as follows: Peter Tannenwald, Esq.,

Kathleen L. Franco, Esq., Arent Fox

Kintner Plotkin & Kahn, 1050

Connecticut Avenue NW., Washington, DC 20036-5339 (Counsel to petitioner).

FOR FURTHER INFORMATION CONTACT:

Leslie K. Shapiro, Mass Media Bureau,

(202) 634-6530.

SUPPLEMENTARY INFORMATION: This is a

synopsis of the Commission's Notice of

Proposed Rule Making, MM Docket No.

93-279, adopted October 20, 1993, and

released November 12, 1993. The full

text of this Commission decision is

available for inspection and copying during normal business hours in the

FCC Reference Center (room 239), 1919

M Street NW., Washington, DC. The

complete text of this decision may also

be purchased from the Commission's

copy contractor, International

Transcription Services, Inc., (202) 857-

3800, 2100 M Street NW., suite 140,

Washington, DC 20037.

Provisions of the Regulatory

Flexibility Act of 1980 do not apply to

this proceeding.

Members of the public should note

that from the time a Notice of Proposed Rule Making is issued until the matter

is no longer subject to Commission

consideration or court review, all ex

parte contacts are prohibited in

Commission proceedings, such as this

one, which involve channel allotments.

See 47 CFR 1.1204(b) for rules

governing permissible ex parte contacts.

For information regarding proper

filing procedures for comments, see 47

CFR 1.415 and 1.420.

List of Subjects in 47 CFR Part 73

Radio broadcasting.

-Federal Communications Commission.

Victoria M. McCauley,

Assistant Chief, Allocations Branch, Policy

and Rules Division, Mass Media Bureau.

[FR Doc. 93-28546 Filed 11-19-93; 8:45 am]

BILLING CODE 6712-01-M

DEPARTMENT OF COMMERCE

National Oceanic and Atmospheric

Administration

50 CFR Part 651

[Docket No. 931076-3276; I.D. 100193A]

RIN 0648-AD33

Northeast Multlspecles Fishery;

Correction

AGENCY: National Marine Fisheries

Service (NMFS), National Oceanic and

Atmospheric Administration .(NOAA),

Commerce.

ACTION: Proposed rule; request for

comments; correction.

SUMMARY: This document corrects a

proposed rule published on October 27,

1993 (58 FR 57774), which is related to

Amendment 5 to the Fishery

Management Plan for the Northeast

Multispecies Fishery (FMP). This

document corrects Figure 2 of the

proposed rule to depict Closed Areas

properly.

EFFECTIVE DATES: November 22, 1993.

FOR FURTHER INFORMATION CONTACT:

John G. Terrill, Fishery Policy Analyst,

Northeast Regional Office, 508-281-

9252.

. The publication on October 27, 1993,

of the proposed rule, which was the

subject of FR Doc. 93-26251, is

corrected as follows:

On page 57801, inFigure 2: Closed

Areas, "Closed Area I" should read

"Closed Area II". and "Closed Area II"

should read "Closed Area I". A

corrected Figure 2 appears below.

Dated: November 16, 1993.

Samuel W. McKeen,

Acting Assistant Administrator for Fisheries,

National Marine Fisheries Service.

BIUNG CODE 3510-22-4

61671