Addition of Certain Chemicals; Toxic Chemical Release Reporting; Community Right-to-Know; Final Rule

ENVIRONMENTAL PROTECTION AGENCY

40 CFR Part 372

[OPPTS-400082B; FRL-4922-2]

RIN 2070-AC47

Addition of Certain Chemicals; Toxic Chemical Release Reporting;

Community Right-to-Know

AGENCY: Environmental Protection Agency (EPA).

ACTION: Final rule.

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SUMMARY: EPA is adding 286 chemicals and chemical categories, which

include 39 chemicals as part of two delineated categories, to the list

of toxic chemicals subject to reporting under section 313 of the

Emergency Planning and Community Right-to-Know Act of 1986 (EPCRA) and

section 6607 of the Pollution Prevention Act of 1990 (PPA). The

additions of these chemicals and chemical categories are based on their

acute human health effects, carcinogenicity or other chronic human

health effects, and/or their adverse effects on the environment. EPA is

taking this action pursuant to its authority to add to the list those

chemicals and chemical categories that meet the EPCRA section 313(d)(2)

criteria for addition to the list of toxic chemicals. EPCRA section 313

reporting for the newly listed chemicals and chemical categories will

be required beginning with the 1995 calendar year. As such, the first

reports for the added chemicals and chemical categories must be

submitted to EPA and States by July 1, 1996.

EFFECTIVE DATE: This rule is effective November 22, 1994.

FOR FURTHER INFORMATION CONTACT: Maria J. Doa, Project Manager, 202-

260-9592, for specific information regarding this final rule. For

further information on EPCRA section 313, contact the Emergency

Planning and Community Right-to-Know Information Hotline, Environmental

Protection Agency, Mail Stop 5101, 401 M St., SW., Washington, DC

20460, Toll free: 800-535-0202, TDD: 800-553-7672.

SUPPLEMENTARY INFORMATION:

I. Introduction

A. Statutory Authority

This rule is issued under section 313(d) of the Emergency Planning

and Community Right-to-Know Act of 1986 (EPCRA), 42 U.S.C. 11001 et

seq.. EPCRA is also referred to as Title III of the Superfund

Amendments and Reauthorization Act of 1986.

B. Background

Section 313 of EPCRA requires certain facilities manufacturing,

processing, or otherwise using listed toxic chemicals to report their

environmental releases of such chemicals annually. Beginning with the

1991 reporting year, such facilities also must report pollution

prevention and recycling data for such chemicals, pursuant to section

6607 of the Pollution Prevention Act, 42 U.S.C. 13106. Section 313

established an initial list of toxic chemicals that was composed of

more than 300 chemicals and 20 chemical categories. Section 313(d)

authorizes EPA to add or delete chemicals from the list, and sets forth

criteria for these actions. Under section 313(e), any person may

petition EPA to add chemicals to or delete chemicals from the list. EPA

issued a statement of petition policy and guidance in the Federal

Register of February 4, 1987 (52 FR 3479), to provide guidance

regarding the recommended content and format for petitions. On May 23,

1991 (56 FR 23703), EPA issued guidance regarding the recommended

content of petitions to delete individual members of the section 313

metal compound categories.

II. Background

On January 12, 1994 (59 FR 1788), EPA issued a proposal in the

Federal Register to add 313 chemicals and chemical categories to the

list of toxic chemicals under EPCRA section 313 based on their acute

human health effects, carcinogenicity or other chronic human health

effects, and/or their environmental effects. EPA's decision to add the

chemicals and chemical categories in today's rule to the section 313

list is based on a further assessment, in light of public comments of

both the relative toxicity of the chemicals--the potency of the

chemical's inherent toxicity--and a careful consideration of the type

of adverse effect the chemical causes or can reasonably be anticipated

to cause. Under section 313(d)(2)(A) (acute human toxicity), the effect

must be ``significant.'' Under section 313(d)(2)(B) the effect must

either be cancer or teratogenicity, or some other ``serious or

irreversible'' chronic health effect. Under section 313(d)(2)(C)

(environmental toxicity) the effect must be ``significant'' and ``of

sufficient seriousness in the judgment of the Administrator'' to

warrant reporting.

The statute does not specify how serious or significant an effect

must be in order for a chemical to be listed under any of the criteria.

This determination is left to the EPA's discretion and scientific

judgment. The Agency recognizes that not every adverse effect is

sufficiently significant or serious to satisfy the criteria. For

chemicals with effects that satisfy the criteria, Congress made it

clear in section 313 that communities have a right to know about

releases of such chemicals. The Agency's goal in implementing section

313 is to ensure that the communities are provided with that release

information to allow them to further educate themselves and, if

appropriate, take or recommend action.

A brief description of the selection process follows, however, a

detailed description of EPA's methodology and rationale for the

proposed addition of these chemicals and chemical categories can be

found in the proposed rule.

1. Development of the chemical addition list. As a starting point

for screening candidates for addition to the toxic chemical list under

EPCRA section 313, EPA chose to examine the lists of chemicals

regulated or identified, as of concern, under various environmental

statutes including: Section 112(b) of the Clean Air Act (CAA) as

amended in 1990 (Hazardous Air Pollutants); (2) section 602(b) of the

CAA (Class II ozone depleting substances); (3) section 307(a) of the

Clean Water Act (CWA) (Priority Pollutant List); (4) Federal

Insecticide, Fungicide, and Rodenticide Act (FIFRA) Active Ingredients,

including Special Review, Canceled/Denied or Suspended, and Restricted

Use Pesticides; (5) section 302 of EPCRA (Extremely Hazardous

Substances); (6) section 102 of the Comprehensive Environmental

Response, Compensation, and Liability Act (CERCLA); (7) section 3001 of

the Resource Conservation and Recovery Act (RCRA) and chemicals listed

at 40 CFR 261.33(e) and Appendix VIII; (8) section 1412 of the Safe

Drinking Water Act as amended; (9) certain chemicals subject to the

Toxics Substance Control Act (Existing Chemicals); and (10) the State

of California Safe Drinking Water and Toxic Enforcement Act of 1986

(Proposition 65) (List of Chemicals Known to the State to Cause

Reproductive Toxicity); and/or those chemicals designated as possible,

probable, or known carcinogens in the Monographs of the International

Agency for Research on Cancer (IARC) and the 6th Annual Report on

Carcinogens of the National Toxicology Program (NTP), U.S. Department

of Health and Human Services (DHHS).

2. Screening of chemicals. To prioritize chemicals for possible

addition to EPCRA section 313, EPA applied a human health and

ecotoxicity screen and a production volume screen, which are described

below.

a. Toxicity screen. A toxicity screen is a limited review of

readily available toxicity data that is used for a preliminary

categorization of a chemical during the process of selecting candidates

for possible listing under EPCRA section 313. The toxicity screen is

used to identify chemicals for further consideration and does not

reflect a final determination for listing a chemical under EPCRA

section 313. Such a determination can only be made after a hazard

assessment is conducted (See Unit II.3. of this preamble). The

chemicals identified above were screened for four general effect

categories: Acute human health effects, cancer, other chronic human

health effects, and ecological effects.

The screening criteria associated with each of the effect areas

used in the toxicity screen are discussed in detail in the Revised

Draft Hazard Assessment Guidelines for Listing Chemicals on the Toxic

Release Inventory (Draft Hazard Assessment Guidelines), (Ref. 11).

Based on the results of this screen, the chemicals were preliminarily

placed in one of three screening categories defined in the Draft Hazard

Assessment Guidelines: ``high priority;'' ``medium priority;'' or ``low

priority.''

Chemicals that were categorized as ``low priority'' during the

screening process were not considered further as candidates for

addition to the EPCRA section 313 list in this rulemaking.

b. Production volume screen. EPCRA section 313(f) establishes

reporting thresholds of either 25,000 or 10,000 pounds per facility per

year related to the amount of a chemical that is manufactured,

processed, or otherwise used. EPA anticipates that the addition of

chemicals manufactured, imported, processed, or used in quantities less

than the EPCRA section 313 activity thresholds would not result in the

submission of Toxic Release Inventory (TRI) reports. Thus, EPA elected

to focus its attention on chemicals likely to yield reports and also

screened potential candidates for the likelihood of meeting the EPCRA

section 313 volume thresholds. Chemicals for which there were no data

to indicate that the chemical is likely to meet or exceed the EPCRA

section 313 volume thresholds were not considered further as possible

candidates for addition to the section 313 list at this time.

3. Hazard evaluation. After completing the screening phase, EPA

conducted a thorough hazard assessment for each of the addition

candidates that resulted from the above analyses and determined based

on the weight-of-the evidence if there was sufficient evidence to

establish that the candidate chemical met the statutory criteria for

addition to EPCRA section 313. To make this determination, EPA senior

scientists reviewed readily available toxicity information on each

chemical for each of the following effect areas: acute human health

effects; cancer; other chronic human effects; and environmental

effects. In addition, EPA reviewed, where appropriate, information on

the environmental fate of the chemical.

The hazard assessment was conducted in accordance with relevant EPA

guidelines for each adverse human health or environmental effect (e.g.,

the appropriate guidelines for hazard evaluation of chemical

carcinogens and for the type of evidence required to substantiate a

determination of carcinogenicity are the Assessment Guidelines for

Carcinogen Risk (Ref. 4)). During this assessment the number, severity,

and significance of the effects induced by the chemical, the dose level

causing the effect, and the quality and quantity of the available data,

including the nature of the data (e.g., human epidemiological,

laboratory animal, field or workplace studies) and confidence level in

the existing data base, were all considered. Where a careful review of

the scientific data for a particular chemical results in a high level

of confidence that the chemical causes an adverse effect at relatively

low dose levels, EPA believes that this evidence is sufficient for

listing the chemical under section 313. EPA also believes that where a

review of the scientific data indicates that the chemical will cause

various adverse effects at moderate dose levels, the total weight-of-

the-evidence indicates that there is sufficient evidence for listing

the chemical under EPCRA section 313. EPA believes that both types of

chemicals described above exhibit moderately high to high toxicity

based on a hazard assessment.

EPA also conducted an analysis of exposure for each chemical or

chemical category proposed for listing under EPCRA section 313(d)(2)(A)

(i.e., based on adverse acute human health effects), and, where

appropriate, under section 313(d)(2)(C) (i.e., based on adverse

ecological effects). For chemicals listed under EPCRA section

313(d)(2)(A), this analysis included estimated concentrations of the

chemical at or beyond the facility site boundary through the use of

estimated releases and modelling techniques. EPA did not conduct an

analysis of exposure for the chemicals proposed for listing under

section 313(d)(2)(B) because these chemicals exhibit moderately high to

high toxicity based on a hazard assessment (see Unit IV.B. for a

discussion of the use of exposure). As discussed more thoroughly in

Unit IV.B. of this preamble, EPA does not believe that it is

appropriate to factor exposure into the listing decisions for the

chemicals being listed pursuant to section 313(d)(2)(B) in this

rulemaking.

Following a review and analysis of the information available about

each chemical in this final rule (including information provided

through public comment) by senior Agency scientists, the Agency

concludes that for each of the chemicals listed one or more of the

EPCRA section 313 listing criteria are met. Moreover, the adverse

effects associated with each of the chemicals being listed today are

serious and significant. In some cases the effects are extreme, such as

cancer or death. In others, the effects are serious and lasting,

including, for example, impairment of a fetus' or an offspring's

physical development, neurological effects inhibiting motor abilities

or mental processes or impairing the ability to reproduce, or the

sustainability of a fragile ecosystem such as an estuary. For a number

of chemicals in the final rule, there is more than one adverse effect.

It is important to understand that although an adverse effect is

known or can be reasonably anticipated to be caused by a chemical on

the section 313 list, a release of a chemical into a community does not

necessarily mean that the effect will occur. Exposure and dose are also

important factors in determining whether an adverse effect occurs and

how serious the manifestation will be. The listing of a chemical on the

section 313 list does not mean that a particular community will

experience these adverse effects. Instead the purpose for listing a

chemical is to ensure that the public gets information about releases

of such chemicals. Thus, EPA believes that for chemicals that typically

do not affect solely one or two species but rather affect changes

across a whole ecosystem and for which there is well-documented

evidence supporting the adverse effects, that their addition to the

EPCRA section 313 list is warranted even though the severity of the

adverse effects that they induce will be dependent upon site-specific

characteristics. Once EPA makes release data available through TRI, the

community may then make its own determination on the importance of

these releases (and their potential adverse effects).

The expansion of the EPCRA section 313 toxic chemical list is the

first phase of the expansion of the TRI program. EPA plans to issue a

proposed rule in early 1995 expanding the scope of industry sectors

that would be subject to EPCRA section 313. EPA's initial analysis for

this effort is focused on industrial sectors which have activities

related to manufacturing that result in significant releases of

chemicals listed on EPCRA section 313. EPA is also considering further

expanding right-to-know by investigating the feasibility of adding data

on exposure to and use of chemicals at TRI facilities. The Agency

believes that the collection of this type of data would provide a

greater understanding of risk reduction and pollution prevention

opportunities.

In conjunction with these expansion activities, the Agency is also

considering situations where data of lesser value can be removed from

the TRI system. Elsewhere in this issue of the Federal Register, EPA is

promulgating a rule establishing an alternate threshold for facilities

with low annual reportable amounts of listed toxic chemicals. This

alternate threshold will provide considerable relief for facilities

which generate ``small'' amounts of EPCRA section 313 chemicals in

reportable amounts. This relief will offset the increased burden that

this expansion rule may impose. The alternate threshold for

manufacture, or process, or otherwise use for each of the chemicals

meeting the facility category will be an amount greater than one

million pounds per year. If a facility meets the alternate threshold

criteria, that facility will not be required to file a complete TRI

report (Form R), but will be required to submit an annual certification

statement for each chemical meeting these conditions for the reporting

year for which these conditions were met and maintain records

supporting calculations made to determine these conditions. EPA

estimates that this alternate threshold provides the option to convert

approximately 20,100 Form R reports to certification statements.

III. Summary of Final Rule

In this action, EPA is adding 286 chemicals and chemical

categories, which includes 39 chemicals as part of two delineated

categories, to the EPCRA section 313 list. EPA finds that each of these

chemicals and chemical categories meets one or more of the EPCRA

section 313(d)(2) criteria. Additionally, EPA believes that each of

these chemicals can reasonably be anticipated to be manufactured or

imported in quantities of at least 10,000 pounds (the EPCRA section 313

otherwise use reporting threshold) by at least one facility. Therefore,

the Agency believes that the listing of these chemicals can reasonably

be anticipated to generate EPCRA section 313 reports and that adding

these chemicals to the toxic chemical list is appropriate.

The proposed rule and record supporting the rulemaking contain

information on EPA's review of these chemicals, including the toxicity

evaluation. This background information will not be repeated here in

the final rule. However, to the extent that comments were received on

these issues, those comments are addressed in this document. In

addition to general comment and comment addressing a broad number of

chemicals, EPA received specific technical comments on 110 of the

chemicals and chemical categories. Detailed responses to comments are

contained in Response to Comments Received on the January 12, 1994

Proposed Rule to Expand the EPCRA Section 313 List (Response to Comment

Document, Ref. 14). Summaries of responses to comments on selected

chemicals appear in units IV.F. and IV.G. of this preamble. Table 1

lists the chemicals that EPA has determined meet the statutory criteria

of EPCRA section 313(d)(2) and are therefore being added to the toxic

chemical list. Each of the chemicals and chemical categories listed

below were found to meet the statutory criteria described in EPCRA

section 313(d)(2)(A)-(C). This means that the Agency has made a finding

that the chemical is known to cause an effect, or is reasonably

anticipated to do so. It does not necessarily mean that the chemical is

known to cause a given effect. The specific criterion or criteria that

the chemical meets are also listed in Table 1 below.

Table 1.--Chemicals Being Added to the EPCRA Section 313 List

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Section Section Section

Chemical Name CAS No. 313(d)(2)(A) 313(d)(2)(B) 313(d)(2)(C)

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Abamectin (Avermectin B1) 071751-41-2 X X

Acephate (Acetylphosphoramidothioic 030560-19-1 X

acid O,S-dimethyl ester)

Acifluorfen sodium salt (5-(2-Chloro-4- 062476-59-9 X

(triflouromethyl)phenoxy)-2-nitro-

benzoic acid, sodium salt)

Alachlor 015972-60-8 X

Aldicarb 000116-06-3 X

d-trans-Allethrin [d-trans- 028057-48-9 X

Chrysanthemic acid of d-allethrone]

Allylamine 000107-11-9 X

Aluminum phosphide 020859-73-8 X

Ametryn (N-Ethyl-N'-(1-methylethyl)-6- 000834-12-8 X X

(methylthio)-1,3,5,-triazine- 2,4

diamine)

Amitraz 033089-61-1 X

Anilazine (4,6-Dichloro-N-(2- 000101-05-3 X X

chlorophenyl)-1,3,5-triazin-2-amine)

Atrazine (6-Chloro-N-ethyl-N'-(1- 001912-24-9 X

methylethyl)-1,3,5,-triazine-2,4-

diamine)

Bendiocarb (2,2-Dimethyl-1,3- 022781-23-3 X X

benzodioxol-4-ol methylcarbamate)

Benfluralin (N-Butyl-N-ethyl-2,6- 001861-40-1 X

dinitro-4-(trifluoromethyl)

benzenamine)

Benomyl 017804-35-2 X

Bifenthrin 082657-04-3 X X

Bis(tributyltin) oxide 000056-35-9 X X

Boron trichloride 010294-34-5 X

Boron trifluoride 007637-07-2 X

Bromacil (5-Bromo-6-methyl-3-(1- 000314-40-9 X

methylpropyl)-2,4(1H,3H)-

pyrimidinedione)

Bromacil lithium salt (2,4(1H,3H)- 053404-19-6 X

Pyrimidinedione, 5-bromo-6-methyl-3 (1-

methylpropyl), lithium salt)

Bromine 007726-95-6 X

1-Bromo-1-(bromomethyl)-1,3- 035691-65-7 X

propanedicarbonitrile

2-Bromo-2-nitropropane-1,3-diol 000052-51-7 X

(Bronopol)

Bromoxynil (3,5-Dibromo-4- 001689-84-5 X

hydroxybenzonitrile)

Bromoxynil octanoate (Octanoic acid, 001689-99-2 X

2,6-dibromo-4-cyanophenyl ester)

Brucine 000357-57-3 X

C.I. Acid Red 114 006459-94-5 X

C.I. Direct Blue 218 028407-37-6 X

Carbofuran 001563-66-2 X

Carboxin (5,6-Dihydro-2-methyl-N-phenyl- 005234-68-4 X

1,4-oxathiin-3-carboxamide)

Chinomethionat (6-Methyl-1,3- 002439-01-2 X

dithiolo[4,5-b]quinoxalin-2-one)

Chlorendic acid 000115-28-6 X

Chlorimuron ethyl (Ethyl-2-[[[(4-chloro- 090982-32-4 X

6-methoxyprimidin-2-yl)-carbonyl]-

amino]sulfonyl]benzoate)

1-(3-Chloroallyl)-3,5,7-triaza-1- 004080-31-3 X

azoniaadamantane chloride

p-Chloroaniline 000106-47-8 X

3-Chloro-2-methyl-1-propene 000563-47-3 X

p-Chlorophenyl isocyanate 000104-12-1 X

Chloropicrin 000076-06-2 X

3-Chloropropionitrile 000542-76-7 X

p-Chloro-o-toluidine 000095-69-2 X

2-Chloro-1,1,1-trifluoroethane (HCFC- 000075-88-7 X X

133a)

Chlorotrifluoromethane (CFC-13) 000075-72-9 X X

3-Chloro-1,1,1-trifluoropropane(HCFC- 000460-35-5 X X

253fb)

Chlorpyrifos methyl (O,O-Dimethyl-O- 005598-13-0 X X

(3,5,6-trichloro-2-

pyridyl)phosphorothioate)

Chlorsulfuron (2-Chloro-N-[[(4-methoxy- 064902-72-3 X

6-methyl-1,3,5-triazin-2-yl)

amino]carbonyl]benzenesulfonamide)

Crotonaldehyde 004170-30-3 X

Cyanazine 021725-46-2 X

Cycloate 001134-23-2 X

Cyclohexanol 000108-93-0 X

Cyfluthrin (3-(2,2-Dichloroethenyl)-2,2- 068359-37-5 X X

dimethylcyclopropanecarboxylic acid,

cyano(4-fluoro-3-

phenoxyphenyl)methylester)

Cyhalothrin (3-(2-Chloro-3,3,3- 068085-85-8 X

trifluoro-1-propenyl)-2,2-

Dimethylcyclopropanecarboxylic acid

cyano(3-phenoxyphenyl)methyl ester)

Dazomet (Tetrahydro-3,5-dimethyl-2H- 000533-74-4 X

1,3,5-thiadiazine-2-thione)

Dazomet sodium salt (2H-1,3,5- 053404-60-7 X

Thiadiazine-2-thione, tetrahydro-3,5-

dimethyl-, ion(1-), sodium)

2,4-DB 000094-82-6 X

2,4-D butoxyethyl ester 001929-73-3 X

2,4-D butyl ester 000094-80-4 X

2,4-D chlorocrotyl ester 002971-38-2 X

Desmedipham 013684-56-5 X

2,4-D 2-ethylhexyl ester 001928-43-4 X

2,4-D 2-ethyl-4-methylpentyl ester 053404-37-8 X

Diazinon 000333-41-5 X X

2,2-Dibromo-3-nitrilopropionamide 010222-01-2 X

Dicamba (3,6-Dichloro-2-methyoxybenzoic 001918-00-9 X

acid)

Dichloran (2,6-Dichloro-4-nitroaniline) 000099-30-9 X

3,3'-Dichlorobenzidine dihydrochloride 000612-83-9 X

3,3'-Dichlorobenzidine sulfate 064969-34-2 X

trans-1,4-Dichloro-2-butene 000110-57-6 X

1,2-Dichloro-1,1-difluoroethane (HCFC- 001649-08-7 X X

132b)

Dichlorofluoromethane (HCFC-21) 000075-43-4 X X

Dichloropentafluoropropane 127564-92-5 X X

1,3-Dichloro-1,1,2,3,3- 136013-79-1 X X

pentafluoropropane (HCFC-225ea)

2,2-Dichloro-1,1,1,3,3- 128903-21-9 X X

pentafluoropropane (HCFC-225aa)

1,1-Dichloro-1,2,3,3,3- 111512-56-2 X X

pentafluoropropane (HCFC-225eb)

1,1-Dichloro-1,2,2,3,3- 013474-88-9 X X

pentafluoropropane (HCFC-225cc)

1,3-Dichloro-1,1,2,2,3- 000507-55-1 X X

pentafluoropropane (HCFC-225cb)

1,2-Dichloro-1,1,3,3,3- 000431-86-7 X X

pentafluoropropane (HCFC-225da)

3,3-Dichloro-1,1,1,2,2- 000422-56-0 X X

pentafluoropropane (HCFC-225ca)

2,3-Dichloro-1,1,1,2,3- 000422-48-0 X X

pentafluoropropane (HCFC-225ba)

1,2-Dichloro-1,1,2,3,3- 000422-44-6 X X

pentafluoropropane (HCFC-225bb)

Dichlorophene (2,2'-Methylenebis(4- 000097-23-4 X X

chlorophenol)

trans-1,3-Dichloropropene 010061-02-6 X

Diclofop methyl (2-[4-(2,4- 051338-27-3 X

Dichlorophenoxy)

phenoxy]propanoicacid, methyl ester)

Dicyclopentadiene 000077-73-6 X

Diethatyl ethyl 038727-55-8 X

Diflubenzuron 035367-38-5 X X

Diglycidyl resorcinol ether 000101-90-6 X

Diisocyanates, consisting of: NA X

1,3-Bis(methylisocyanate) cyclohexane 038661-72-2

1,4-Bis(methylisocyanate) cyclohexane 010347-54-3

1,4-Cyclohexane diisocyanate 002556-36-7

Diethyldiisocyanatobenzene 134190-37-7

4,4'-Diisocyanatodiphenyl ether 004128-73-8

2,4'-Diisocyanatodiphenyl sulfide 075790-87-3

3,3'-Dimethoxybenzidine-4,4'- 000091-93-0

diisocyanate

3,3'-Dimethyl-4,4'-diphenylene 000091-97-4

diisocyanate

3,3'-Dimethyl diphenylmethane-4,4'- 000139-25-3

diisocyanate

Hexamethylene-1,6-diisocyanate 000822-06-0

Isophorone diisocyanate 004098-71-0

Methylenebis(phenyl isocyanate) 000101-68-8

4-Methyldiphenylmethane-3,4- 075790-84-0

diisocyanate

1,1-Methylene bis(4- 005124-30-1

isocyanatocyclohexane)

1,5-Naphthalene diisocyanate 003173-72-6

1,3-Phenylene diisocyanate 000123-61-5

1,4-Phenylene diisocyanate 000104-49-4

Polymeric diphenylmethane 009016-87-9

diisocyanate

2,2,4-Trimethylhexamethylene 016938-22-0

diisocyanate

2,4,4-Trimethylhexamethylene

diisocyanate 015646-96-5

Dimethipin (2,3,-Dihydro-5,6-dimethyl- 055290-64-7 X

1,4-dithiin 1,1,4,4-tetraoxide)

Dimethoate 000060-51-5 X

3,3'-Dimethoxybenzidine dihydrochloride 020325-40-0 X

(o-Dianisidine dihydrochloride)

3,3'-Dimethoxybenzidine hydrochloride 111984-09-9 X

(o-Dianisidine hydrochloride)

Dimethylamine 000124-40-3 X

Dimethylamine dicamba 002300-66-5 X

3,3'-Dimethylbenzidine dihydrochloride 000612-82-8 X

(o-Tolidine dihydrochloride)

3,3'-Dimethylbenzidine dihydrofluoride 041766-75-0 X

(o-Tolidine dihydrofluoride)

Dimethyl chlorothiophosphate 002524-03-0 X

Dimethyldichlorosilane 000075-78-5 X

N,N-Dimethylformamide 000068-12-2 X

2,6-Dimethylphenol 000576-26-1 X

Dinitrobutyl phenol (Dinoseb) 000088-85-7 X X

Dinocap 039300-45-3 X X

Diphenamid 000957-51-7 X

Diphenylamine 000122-39-4 X

Dipotassium endothall (7- 002164-07-0 X

Oxabicyclo(2.2.1)heptane-2,3-

dicarboxylic acid, dipotassium salt)

Dipropyl isocinchomeronate 000136-45-8 X

Disodium cyanodithioimidocarbonate 000138-93-2 X

2,4-D isopropyl ester 000094-11-1 X

2,4-Dithiobiuret 000541-53-7 X

Diuron 000330-54-1 X X

Dodine (Dodecylguanidine monoacetate) 002439-10-3 X

2,4-DP (Dichlorprop) 000120-36-5 X

2,4-D propylene glycol butyl ether 001320-18-9 X

ester

2,4-D sodium salt 002702-72-9 X

Ethoprop (Phosphorodithioic acid O- 013194-48-4 X X

ethyl S,S-dipropyl ester)

Ethyl dipropylthiocarbamate (EPTC) 000759-94-4 X X

Famphur 000052-85-7 X X

Fenarimol (.alpha.-(2-Chlorophenyl)- 060168-88-9 X

.alpha.-4-chlorophenyl)-5-

pyrimidinemethanol)

Fenbutatin oxide (hexakis(2-methyl-2- 013356-08-6 X X

phenylpropyl)distannoxane)

Fenoxaprop ethyl (2-(4-((6-Chloro-2- 066441-23-4 X X

benzoxazolylen)oxy)phenoxy)propanoic

acid,ethyl ester)

Fenoxycarb (2-(4- 072490-01-8 X

Phenoxyphenoxy)ethyl]carbamic acid

ethyl ester)

Fenpropathrin (2,2,3,3- 039515-41-8 X X

Tetramethylcyclopropane carboxylic

acid cyano(3-phenoxyphenyl)methyl

ester)

Fenthion (O,O-Dimethyl O-[3-methyl-4- 000055-38-9 X X

(methylthio) phenyl] ester,

phosphorothioic acid)

Fenvalerate (4-Chloro-alpha-(1- 051630-58-1 X X

methylethyl)benzeneacetic acid cyano(3-

phenoxyphenyl)methyl ester)

Ferbam (Tris(dimethylcarbamodithioato- 014484-64-1 X X

S,S')iron)

Fluazifop butyl (2-[4-[[5- 069806-50-4 X

(Trifluoromethyl)-2-pyridinyl]oxy]-

phenoxy]propanoic acid, butyl ester)

Fluorine 007782-41-4 X

Fluorouracil (5-Fluorouracil) 000051-21-8 X

Fluvalinate (N-[2-Chloro-4- 069409-94-5 X X

(trifluoromethyl)phenyl]-DL-valine(+)-

cyano (3-phenoxyphenyl)methyl ester)

Folpet 000133-07-3 X X

Fomesafen (5-(2-Chloro-4- 072178-02-0 X

(trifluoromethyl)phenoxy)-N

methylsulfonyl)-2-nitrobenzamide)

alpha-Hexachlorocyclohexane 000319-84-6 X X

n-Hexane 000110-54-3 X

Hexazinone 051235-04-2 X X

Hydramethylnon (Tetrahydro-5,5-di- 067485-29-4 X X

methyl-2(1H)- pyrimidinone[3-[4-

(trifluoromethyl)phenyl]-1-[2-[4-

(trifluoromethyl) phenyl]ethenyl]-

2propenylidene]hydrazone)

Imazalil (1-[2-(2,4-Dichlorophenyl)-2- 035554-44-0 X

(2-propenyloxy)ethyl]-1H-imidazole)

3-Iodo-2-propynyl butylcarbamate 055406-53-6 X

Iron pentacarbonyl 013463-40-6 X

Isodrin 000465-73-6 X

Isofenphos (2-[[Ethoxyl[(1- 025311-71-1 X X

methylethyl)amino]phosphinothioyl]oxy]

benzoic acid 1-methylethyl ester)

Lactofen (5-(2-Chloro-4- 077501-63-4 X

(trifluoromethyl)phenoxy)-2-nitro-2-

ethoxy-1-methyl-2-oxoethyl ester)

Linuron 000330-55-2 X

Lithium carbonate 000554-13-2 X

Malathion 000121-75-5 X X

Mecoprop 000093-65-2 X

2-Mercaptobenzothiazole (MBT) 000149-30-4 X

Merphos 000150-50-5 X

Metham sodium (Sodium 000137-42-8 X

methyldithiocarbamate)

Methazole (2-(3,4-Dichlorophenyl)-4- 020354-26-1 X

methyl-1,2,4-oxadiazolidine-3,5-dione)

Methiocarb 002032-65-7 X

Methoxone ((4-Chloro-2-methylphenoxy) 000094-74-6 X

acetic acid) (MCPA)

Methoxone sodium salt ((4-Chloro-2- 003653-48-3 X

methylphenoxy) acetate sodium salt)

Methyl isothiocyanate 00556-61-6 X

2-Methyllactonitrile 000075-86-5 X

N-Methylolacrylamide 000924-42-5 X

Methyl parathion 000298-00-0 X X

N-Methyl-2-pyrrolidone 000872-50-4 X

Methyltrichlorosilane 000075-79-6 X

Metiram 009006-42-2 X

Metribuzin 021087-64-5 X

Mevinphos 007786-34-7 X

Molinate (1H-Azepine-1 carbothioic 002212-67-1 X

acid, hexahydro-S-ethyl ester)

Monuron 000150-68-5 X

Myclobutanil (.alpha.-Butyl-.alpha.-(4- 088671-89-0 X

chlorophenyl)-1H-1,2,4-triazole-1-

propanenitrile)

Nabam 000142-59-6 X

Naled 000300-76-5 X X

Nicotine and salts NA X

Nitrapyrin (2-Chloro-6- 001929-82-4 X

(trichloromethyl)pyridine)

Nitrate compounds (water dissociable) NA X

p-Nitroaniline 000100-01-6 X

Norflurazon (4-Chloro-5-(methylamino)-2- 027314-13-2 X

[3-(trifluoromethyl)phenyl]-3(2H)-

pyridazinone)

Oryzalin (4-(Dipropylamino)-3,5- 019044-88-3 X

dinitrobenzenesulfonamide)

Oxydemeton methyl (S-(2- 000301-12-2 X

(Ethylsulfinyl)ethyl) O,O-dimethyl

ester phosphorothioic acid)

Oxydiazon (3-[2,4-Dichloro-5-(1- 019666-30-9 X

methylethoxy)phenyl]-5-(1,1-

dimethylethyl)-1,3,4-oxadiazol-2(3H)-

one)

Oxyfluorfen 042874-03-3 X X

Ozone 010028-15-6 X X

Paraquat dichloride 001910-42-5 X

Pebulate (Butylethylcarbamothioic acid 001114-71-2 X

S-propyl ester)

Pendimethalin (N-(1-Ethylpropyl)-3,4- 040487-42-1 X

dimethyl-2,6-dinitrobenzenamine)

Pentobarbital sodium 000057-33-0 X

Perchloromethyl mercaptan 000594-42-3 X

Permethrin (3-(2,2-Dichloroethenyl)-2,2- 052645-53-1 X X

dimethylcyclopropanecarboxylic acid,

(3-phenoxyphenyl)methyl ester)

Phenanthrene 000085-01-8 X

Phenothrin (2,2-Dimethyl-3-(2-methyl-1- 026002-80-2 X X

propenyl) cyclopropanecarboxylic acid

(3-phenoxyphenyl)methyl ester)

1,2-Phenylenediamine 000095-54-5 X

1,3-Phenylenediamine 000108-45-2 X

1,2-Phenylenediamine dihydrochloride 000615-28-1 X

1,4-Phenylenediamine dihydrochloride 000624-18-0 X

Phenytoin 000057-41-0 X

Phosphine 007803-51-2 X

Picloram 001918-02-1 X

Piperonyl butoxide 000051-03-6 X

Pirimiphos methyl (O-(2-(Diethylamino)- 029232-93-7 X

6-methyl-4- pyrimidinyl)-O,O-dimethyl

phosphorothioate)

Polychlorinated alkanes NA X X

Polycyclic aromatic compounds (PACs) NA X

consisting of:

Benz(a)anthracene 000056-55-3

Benzo(a)phenanthrene 000218-01-9

Benzo(a)pyrene 000050-32-8

Benzo(b)fluoranthene 000205-99-2

Benzo(j)fluoranthene 000205-82-3

Benzo(k)fluoranthene 000207-08-9

Benzo(rst)pentaphene 000189-55-9

Dibenz(a,h)acridine 000226-36-8

Dibenz(a,j)acridine 000224-42-0

Dibenzo(a,h)anthracene 000053-70-3

Dibenzo(a,e)fluoranthene 005385-75-1

Dibenzo(a,e)pyrene 000192-65-4

Dibenzo(a,h)pyrene 000189-64-0

Dibenzo(a,l)pyrene 000191-30-0

7H-Dibenzo(c,g)carbazole 00194-59-2

7,12-Dimethyl benz(a)anthracene 000057-97-6

Indeno[1,2,3-cd]pyrene 000193-39-5

5-Methylchrysene 003697-24-3

1-Nitropyrene 005522-43-0

Potassium bromate 007758-01-2 X

Potassium dimethyldithiocarbamate 000128-03-0 X

Potassium N-methyldithiocarbamate 000137-41-7 X

Profenofos (O-(4-Bromo-2-chlorophenyl)- 041198-08-7 X

O-ethyl-S-propyl phosphorothioate)

Prometryn (N,N'-Bis(1-methylethyl)-6- 007287-19-6 X

methylthio-1,3,5-triazine-2,4-diamine)

Propachlor (2-Chloro-N-(1-methylethyl)- 001918-16-7 X

N-phenylacetamide)

Propanil (N-(3,4- 000709-98-8 X

Dichlorophenyl)propanamide)

Propargite 002312-35-8 X X

Propargyl alcohol 000107-19-7 X

Propetamphos (3- 031218-83-4 X

[(Ethylamino)methoxyphosphinothioyl]ox

y]-2-butenoic acid, 1-methylethyl

ester)

Propiconazole (1-[2-(2,4- 060207-90-1 X

Dichlorophenyl)-4-propyl-1,3-dioxolan-

2-yl]-methyl-1H-1,2,4,-triazole)

Quizalofop-ethyl (2-[4-[(6-Chloro-2- 076578-14-8 X

quinoxalinyl)oxy]phenoxy] propanoic

acid ethyl ester)

Resmethrin ([5-(Phenylmethyl)-3- 010453-86-8 X X

furanyl]methyl 2,2-dimethyl-3-(2-

methyl-1-

propenyl)cyclopropanecarboxylate])

Sethoxydim (2-[1-(Ethoxyimino)butyl]-5- 074051-80-2 X

[2-(ethylthio)propyl]-3-hydroxyl-2-

cyclohexen-1-one)

Simazine 000122-34-9 X

Sodium azide 026628-22-8 X

Sodium dicamba (3,6-Dichloro-2- 001982-69-0 X

methoxybenzoic acid, sodium salt)

Sodium dimethyldithiocarbamate 000128-04-1 X

Sodium fluoroacetate 000062-74-8 X X

Sodium nitrite 007632-00-0 X

Sodium pentachlorophenate 000131-52-2 X X

Sodium o-phenylphenoxide 000132-27-4 X

Strychnine and salts NA X

Sulfuryl fluoride (Vikane) 002699-79-8 X

Sulprofos (O-Ethyl O-[4- 035400-43-2 X X

(methylthio)phenyl]phosphorodithioic

acid S propyl ester)

Tebuthiuron (N-[5-(1,1-Dimethylethyl)- 034014-18-1 X

1,3,4-thiadiazol-2-yl)- N,N'-

dimethylurea)

Temephos 003383-96-8 X

Terbacil (5-Chloro-3-(1,1- 005902-51-2 X

dimethylethyl)-6-methyl- 2,4 (1H,3H)-

pyrimidinedione)

1,1,1,2-Tetrachloro-2-fluoroethane 000354-11-0 X X

(HCFC-121a)

1,1,2,2-Tetrachloro-1-fluoroethane 000354-14-3 X X

(HCFC-121)

Tetracycline hydrochloride 000064-75-5 X

Tetramethrin (2,2-Dimethyl-3-(2-methyl- 007696-12-0 X X

1-propenyl) cyclopropanecarboxylic

acid (1,3,4,5,6,7-hexahydro-1,3-dioxo-

2H-isoindol-2-yl)methyl ester)

Thiabendazole (2-(4-Thiazolyl)-1H- 000148-79-8 X X

benzimidazole)

Thiobencarb (Carbamic acid, diethylthio- 028249-77-6 X

, S-(p-chlorobenzyl))

Thiodicarb 059669-26-0 X X

Thiophanate ethyl ([1,2- 023564-06-9 X

Phenylenebis(iminocarbonothioyl)]

biscarbamic acid diethyl ester)

Thiophanate-methyl 023564-05-8 X

Thiosemicarbazide 000079-19-6 X

Triadimefon (1-(4-Chlorophenoxy)-3,3- 043121-43-3 X

dimethyl-1-(1H-1,2,4-triazol-1-yl)-2-

butanone)

Triallate 002303-17-5 X

Tribenuron methyl (2-(4-Methoxy-6- 101200-48-0 X

methyl-1,3,5-triazin-2-yl)-

methylamino)carbonyl)amino)sulfonyl)-,

methyl ester)

Tributyltin fluoride 001983-10-4 X

Tributyltin methacrylate 002155-70-6 X

S,S,S-Tributyltrithiophosphate (DEF) 000078-48-8 X X

Trichloroacetyl chloride 000076-02-8 X

1,2,3-Trichloropropane 000096-18-4 X

Triclopyr triethylammonium salt 057213-69-1 X

Triethylamine 000121-44-8 X

Triforine (N,N'-[1,4-Piperazinediylbis- 026644-46-2 X

2,2,2-trichloroethylidene)]

bisformamide)

Trimethylchlorosilane 000075-77-4 X

2,3,5-Trimethylphenyl methylcarbamate 002655-15-4 X

Triphenyltin chloride 000639-58-7 X X

Triphenyltin hydroxide 000076-87-9 X X

Vinclozolin (3-(3,5-Dichlorophenyl)-5- 050471-44-8 X

ethenyl-5-methyl-2,4-oxazolidinedione)

----------------------------------------------------------------------------------------------------------------

EPA is deferring final action on 40 chemicals and one chemical

category until a later date. These chemicals and the comments received

on them raised particularly difficult technical or policy issues which

will require additional time to address. The Agency does not believe

that it would be in the spirit of community right-to-know to delay

final action on the remaining 286 chemicals and chemical categories,

pending completion of work on the more limited group. In a future

rulemaking, EPA will make a final determination as to whether these

chemicals should be added to EPCRA section 313. The public comment that

has been received specific to these deferred chemicals will be

addressed as part of the future rulemaking discussed above. These

chemicals follow:

o-benzyl-p-chlorophenol

butylate

butylated hydroxyanisole (BHA)

calcium hypochlorite

caprolactam

carbon monoxide

cyromazine

dichloromethylphenylsilane

dithiopyr

2,4-D 2-octyl ester

flumetralin

iprodione

isophorone

man made mineral fibers

methylene bis(thiocyanate)

nitric oxide

nitrogen dioxide

nine polycyclic aromatic compounds, specifically:

carbazole

cyclopenta(cd)pyrene

dibenz(a,c)anthracene

dibenz(a,j)anthracene

2-methylchrysene

3-methylchrysene

4-methylchrysene

6-methylchrysene

2-methylfluoranthene

phosphorus oxychloride

phosphorus pentachloride

phosphorus pentasulfide

phosphorus pentoxide

primsulfuron

sodium chlorite

sodium hypochlorite

sodium 2-pyridinethiol-1-oxide

sulfur dioxide

sulfur trioxide

tefluthrin

thiabendazole, hypophosphite salt

trichloroethylsilane

trichlorophenylsilane

vanadium pentoxide

Based on an evaluation of the public comments received and a

reanalysis of the available data cited in the proposed rule, EPA has

determined that three chemicals, clomazone, 5-chloro-2-(2,4-

dichlorophenoxy)phenol, and tetrasodium ethylenediaminetetraacetate,

that were proposed for listing do not have sufficient evidence of

toxicity at this time to meet the statutory criteria of EPCRA

section313(d)(2) and thus are not listed in this final rule. Summaries

of responses to chemical-specific comments for these chemicals appear

in unit IV.G. of this preamble.

IV. Summary of Public Comment

The public comment period for the proposed rule closed April 12,

1994. On March 9, 1994, EPA held a public meeting on the proposed

addition of chemicals and chemical categories. Two hundred and sixty-

six comments were received, including 136 from industry, 60 from trade

associations, 32 from environmental groups, 15 from private citizens, 3

from Federal agencies, 7 from State agencies and 13 from other public

interest groups, labor groups, universities, and associations. In

addition to general comment and comment addressing a broad number of

chemicals, EPA received specific technical comments on 110 of the

chemicals and chemical categories. Detailed responses to all comments,

except those comments specific to chemicals for which final action is

being deferred, are contained in the Response to Comment Document (Ref.

14).

In addition to a number of comments supporting the concept of

chemical expansion, EPA received comments in the following major areas:

EPA's screening process used to identify potential candidates and the

Agency's use of the Draft Hazard Assessment Guidelines (Ref. 11); the

use of exposure in determining if a chemical meets the statutory

criteria of EPCRA section 313; listing of categories; the addition of

chemicals that are regulated by the Food and Drug Administration (FDA);

the addition of chemicals that are regulated under FIFRA; duplicative

reporting; general technical comments; and chemical-specific comments.

A. Comments on EPA's Screening Process Used to Identify Potential

Candidates for Addition to EPCRA Section 313 and on EPA's Use of the

Draft Hazard Assessment Guidelines

1. Screening based on toxicity. Monsanto, Zeneca Incorporated, and

the National Oilseed Processors Association contend that the use of

minimum effective doses (MEDs) to screen chemicals as potential

candidates for addition to the EPCRA section 313 list was unrealistic

and overly broad as a screening tool. One of these commenters also

contended that EPA based its proposed addition on toxicity screening

only.

EPA believes that the commenter may have misunderstood the use of

the MED screening criteria. The MED screen is not intended, and is not

used by EPA, as a surrogate for the actual statutory listing criteria.

The MED was used as a screening tool during the preliminary review of

several thousand candidate chemicals, because MED values were available

and they are based on experimental values. MEDs are not equivalent to

lowest-observed-adverse-effect levels (LOAELs). MEDs are generally

derived from LOAELs from chronic toxicity studies using a log

transformation and as such a MED is a single value based upon the best

available study. Satisfying the MED screening criteria, however, does

not mean that a chemical will necessarily be added to the list. In

every case, the Agency determines that at least one of the section

313(d)(2) criteria is met before a chemical is listed. For example,

isoprene, 1,3-dichloropropane, and dichlorodimethylmethane passed the

toxicity screen, but upon a more detailed review, were determined not

to meet the criteria of EPCRA section 313(d)(2) and thus were not

proposed for addition.

EPA believes that MEDs are useful as a screening tool and that the

methodology has been adequately reviewed both internal and external to

the Agency. The MED system was first presented in a peer reviewed

article by DeRosa, et. al (Ref. 2). The MED methodology has been used

by EPA in programs other than EPCRA section 313. For example, the MED

methodology is integral to the reportable quantity (RQ) scoring system

as utilized by EPA in CERCLA section 102. The RQ scoring system scheme

is described in several Federal Register documents (April 4, 1985, 50

FR 13456; September 29, 1986, 51 FR 34535; and March 16, 1987, 52 FR

8140). Further, the Superfund Amendments and Reauthorization Act of

1986 (SARA) required EPA and the Agency for Toxic Substances and

Disease Registry (ATSDR) to develop a list of 275 hazardous substances

most commonly found at facilities on the National Priorities List (NPL)

and considered to present the most significant threat to human health

at those sites or at other facilities where releases may occur. During

development of criteria to select the first list of 100, the RQ

methodology (as discussed in the Draft Hazard Assessment Guidelines,

Ref. 11) was selected as one of the evaluation tools used to develop

the initial list, and the annual updates. When the initial list was

published (April 17, 1987, 52 FR 12866) a summary of the methodology

used to develop the list was provided.

Monsanto believes that the use of an MED of 500 mg/kg/day as the

upper limit of the ``may be sufficient'' category of the screening

criteria required an unrealistically high dose to have been used for

toxicity testing.

EPA agrees that the upper bound for the medium priority category

may warrant reconsideration. EPA will address this issue and other

comments received on the Draft Hazard Assessment Guidelines (Ref. 11),

when the Agency finalizes that document. However, none of the chemicals

proposed for listing in the proposed rule had MEDs that approached this

upper bound. Of the chemicals proposed for addition pursuant to EPCRA

section 313(d)(2)(B), greater than 93 percent had MED values that were

in the range for the high priority category; the remaining chemicals

(less than 7 percent) had MEDs in the lowest fifth of the medium

priority category range, i.e., MEDs only slightly greater than the high

priority category range. EPA reiterates that the MED screen is not

intended, and is not used by EPA, as a surrogate for the actual

statutory listing criteria. Additions to EPCRA section 313 are based on

a hazard assessment, and, where appropriate, an analysis of exposure,

to determine whether the chemical meets one or more of the EPCRA

section 313(d)(2) listing criteria.

The Natural Resources Defense Council supports the health and

environmental effects screening criteria used by EPA as a reasonable

basis to screen chemicals as candidates for possible addition to EPCRA

section 313.

The Agency agrees with this commenter in its support of the use of

the screening criteria and believes that the screening criteria provide

a reasonable basis to make a preliminary evaluation of chemicals for

possible addition to the EPCRA section 313 list. EPA also agrees with

the commenter's statement that the specific screening values are

consistent with established risk assessment procedures applied in other

EPA programs.

2. Screening based on production volume. Eastman Chemical Company

states that, in addition to the use of a production volume screen, the

Agency should consider the number of TRI Form Rs that would likely be

submitted subsequent to listing. If the number is considered to be

minimal (perhaps 5, 10, 15 or more reports), then EPA should balance

the public's right-to-know with the economic burden placed on an

industry.

EPA adopted a production volume screen for the development of the

proposed rule to screen out those chemicals for which no reports are

expected to be submitted. The Agency believes that it has the

discretion to not include such chemicals at this time. If chemicals

that did not meet the production volume screen were listed, there would

be an economic burden for firms that would have to determine that they

did not exceed the reporting threshold, without providing any

information to the public.

While the Agency has determined to not list chemicals for which no

reports would be submitted, EPA believes that it is appropriate to add

chemicals to EPCRA section 313 for which even a small number of reports

are likely to be submitted nationally. In such cases, the reporting

facilities will still provide important information to the surrounding

communities. Even though a particular chemical may only be

manufactured, processed, or otherwise used at a relatively small number

of facilities, the data provided in the TRI Form R reports by these

facilities could represent significant information in the communities

in which the facilities are located. The Agency believes that it would

be inconsistent with the public's right-to-know not to list chemicals

even if only a low number of reports is expected.

3. Use of the Draft Hazard Assessment Guidelines. Six industry

trade organizations and three companies contend that EPA's use of the

Draft Hazard Assessment Guidelines (Ref. 11) was inappropriate. The

commenters state that the use of the term ``draft guidelines''

indicates that the document requires additional review. Therefore, they

believe that EPA should refrain from using the document to support this

rulemaking.

It is appropriate for EPA to use the Draft Hazard Assessment

Guidelines (Ref. 11), as it did in this rule, in considering whether to

list a chemical on the section 313 list. The Draft Hazard Assessment

Guidelines are an embodiment of internal EPA practices that have been

used in listing determinations that have evolved since the inception of

the TRI program. The Draft Hazard Assessment Guidelines do not

constitute a set of rules for adding or deleting chemicals to or from

the list: the Draft Hazard Assessment Guidelines are an explanation of

the process and general standards for evaluating chemicals against the

EPCRA section 313 listing criteria. These Draft Hazard Assessment

Guidelines notwithstanding, EPA has evaluated every chemical proposed

for addition directly against the EPCRA section 313 statutory criteria,

and has taken into consideration comments submitted by the public

specific to those chemicals (responses to those chemical-specific

comments are found in the Response to Comment Document, (Ref. 14);

summaries of most significant chemical-specific comments are found in

units IV.F. and IV.G. of this preamble).

B. Use of Exposure Assessments

One of the most significant issues raised by commenters relates to

the Agency's consideration of hazard, exposure, and risk in

interpreting the section 313(d)(2) criteria. Specifically, a number of

commenters believe that EPA's interpretation of the EPCRA section

313(d)(2)(B) criterion, chronic human health effects, and the section

313(d)(2)(C) criterion, ecological effects, has been overly

restrictive. The commenters contend that EPA should conduct risk

assessments and make a formal determination that a chemical poses a

risk (i.e., a combination of exposure and hazard) before adding it to

the EPCRA section 313 list. The commenters argue that the following

factors support their contention: (1) The statutory criteria include an

implicit exposure and thus risk component; (2) the legislative history

illustrates Congress' intent that exposure considerations were to be an

integral part of determining whether a chemical should be listed on the

EPCRA section 313 list; and (3) EPA should consider exposure in

conjunction with section 313(d)(2)(B), chronic human health effects,

and for all listings pursuant to section 313(d)(2)(C), ecological

effects, because there is precedent for the use of exposure in previous

listing and delisting actions.

In light of the many comments received on this issue, EPA has

reviewed its positions in this area, and agrees with many of the

commenters that there are limited circumstances under which it is

appropriate for EPA to consider exposure factors for listing decisions

under section 313(d)(2). The Agency believes that exposure

considerations are appropriate in making determinations (1) under

section 313(d)(2)(A), (2) under section 313(d)(2)(B) for chemicals that

exhibit low to moderately low toxicity based on a hazard assessment

(i.e., those chemicals for which the value of listing on the EPCRA

section 313 list on hazard alone is marginal), and (3) under section

313(d)(2)(C) for chemicals that are low or moderately ecotoxic but do

not induce well-documented serious adverse effects as described below.

The Agency believes that exposure considerations are not appropriate in

making determinations (1) under section 313(d)(2)(B) for chemicals that

exhibit moderately high to high human toxicity (These terms, which do

not directly correlate to the numerical screening values reflected in

the Draft Hazard Assessment Guidelines, are defined in unit II.) based

on a hazard assessment, and (2) under section 313(d)(2)(C) for

chemicals that are highly ecotoxic or induce well-established adverse

environmental effects. For chemicals which induce well-established

serious adverse effects, e.g., chlorofluorocarbons, which cause

stratospheric ozone depletion, EPA believes that an exposure assessment

is unnecessary. EPA believes that these chemicals typically do not

affect solely one or two species but rather cause changes across a

whole ecosystem. EPA believes that these effects are sufficiently

serious because of the scope of their impact and the well-documented

evidence supporting the adverse effects.

EPA, however, disagrees with those commenters who suggest that EPA

must include a risk assessment component to EPCRA section 313

determinations. Specifically, EPA does not agree with the commenters

about the extent to which exposure must be considered in making

determinations under sections 313(d)(2)(B) and (C). This is primarily

because EPA does not agree with the commenters' understanding of EPCRA

section 313. Risk assessment may be pertinent and appropriate for use

under statutes that control the manufacture, use, and/or disposal of a

chemical, such as the Clean Air Act or the Toxic Substances Control

Act. However, EPCRA section 313 is an information collection provision

that is fundamentally different from other environmental statutes that

control or restrict chemical activities.

EPCRA section 313 charges EPA with collecting and disseminating

information on releases, among other waste management data, so that

communities can estimate local exposure and local risks; risks which

can be significantly different than those which would be assessed using

generic exposure considerations. The intent of EPCRA section 313 is to

move the determination of what risks are acceptable from EPA to the

communities in which the releases occur. This basic local empowerment

is a cornerstone of the right-to-know program.

EPCRA section 313 establishes an information collection and

dissemination program, the burden it imposes is significantly less than

the burden imposed by a statute which controls the manufacture, use,

and/or disposal of a chemical. EPCRA section 313 requires that a

facility use the best available information to prepare each chemical-

specific TRI report. However, the statute does not require that the

facility conduct monitoring or emissions measurements to determine

these quantities. A facility must only estimate, to the best of its

ability, the quantitative information it reports. This is in contrast

to other environmental statutes that may require a facility to monitor

releases, change its manufacturing process, install specific waste

treatment technology, or dispose of wastes in a certain manner. As

such, the Agency believes that the standard that must be met to require

information submission under EPCRA section 313 is less than that to

regulate a chemical under a statute such as the Clean Air Act.

EPA believes that its position regarding the use of hazard,

exposure, and risk in listing decisions is consistent with the purpose

and legislative history of EPCRA section 313, as illustrated in the

following passage from the Conference report:

The Administrator, in determining to list a chemical under any

of the above criteria, may, but is not required to conduct new

studies or risk assessments or perform site-specific analyses to

establish actual ambient concentrations or to document adverse

effects at any particular location. (H. Rep. 99-962, 99th Cong., 2nd

Sess., p. 295 (Oct. 3, 1986) ).

This passage indicates Congress did not intend to require EPA to

conduct new studies, such as exposure studies, or perform risk

assessments, and therefore did not consider these activities to be

mandatory components of all section 313 decisions. EPA believes that

this statement combined with the plain language of the statutory

criteria clearly indicate that Congress intended that the decision of

whether and how to consider exposure under EPCRA section 313(d)(2)(B)

and (C) should be left to the Agency's discretion. EPA has carefully

considered when and how to use exposure to fully implement the right-

to-know provisions of EPCRA. The Agency believes that in this final

rule, EPA has appropriately used the discretion provided to it to

assure the addition of chemicals that meet the right-to-know objectives

of EPCRA section 313 while not unduly burdening the regulated

community.

EPCRA section 313 specifically requires that exposure be considered

for listing a chemical pursuant to section 313(d)(2)(A). The statute

mandates that EPA consider whether ``a chemical is known to cause or

can reasonably be anticipated to cause significant adverse acute human

health effects at concentration levels that are reasonably likely to

exist beyond facility site boundaries.'' EPA has, and will continue to

look at exposures reasonably likely to exist beyond facility site

boundaries when making a listing determination pursuant to EPCRA

section 313(d)(2)(A).

The statute is silent on the issue of exposure considerations for

the section 313(d)(2)(B) and (C) criteria. The language of section 313

does not prohibit EPA from considering exposure factors when making a

finding under either section 313(d)(2)(B) or section 313(d)(2)(C).

However, the language of sections 313(d)(2)(B) and (C) does not require

the type of exposure assessment and/or risk assessment argued by the

commenters. EPA believes that it has the discretion under both section

313(d)(2)(B) and section 313(d)(2)(C) to consider, where appropriate,

those exposure factors that may call into question the validity of

listing of any specific chemical on TRI. In exercising this discretion,

EPA considers it appropriate to employ exposure considerations to a

limited extent in making determinations under EPCRA section

313(d)(2)(C) because this criterion requires the Agency to find a

``significant adverse effect on the environment of sufficient

seriousness, in the judgment of the Administrator to warrant

reporting'' under EPCRA section 313. This language recognizes the

possibility that under certain circumstances, a chemical that could

theoretically cause an adverse effect on the environment is unlikely to

cause one of a magnitude sufficient to warrant listing. Moreover,

because of the limitation on the number of chemicals listed pursuant to

only section 313(d)(2)(C) that may be listed, EPA believes that it is

appropriate to use both hazard and exposure factors as prioritizing

considerations in these listing decisions. Therefore, to meet its

obligation under section 313(d)(2)(C), in cases where a chemical is low

or moderately ecotoxic, EPA may look at certain exposure factors

(including pollution controls, the volume and pattern of production,

use, and release, environmental fate, as well as other chemical

specific factors, and the use of estimated releases and modeling

techniques) to determine if listing is reasonable, i.e., could the

chemical ever be present at high enough concentrations to cause a

significant adverse effect upon the environment to warrant listing

under section 313(d)(2)(C). Of the chemicals being added in today's

action pursuant to section 313(d)(2)(C), all but one are highly

ecotoxic. These highly ecotoxic chemicals are being added to the EPCRA

section 313 list pursuant to section 313(d)(2)(C) based on their

hazard. The other chemical, which is moderately ecotoxic, is being

added to the EPCRA section 313 list pursuant to section 313(d)(2)(C)

based on both its hazard and an exposure assessment for this chemical.

For listing determinations made pursuant to EPCRA section

313(d)(2)(B), in instances where the hazard assessment indicates that

the value of listing on EPCRA section 313 on hazard alone is marginal

(i.e., a chemical is of low toxicity and unrealistic exposures would be

necessary for it to pose a risk to communities), EPA may use exposure

considerations in its listing decisions. Only chemicals for which the

hazard assessments indicate moderately high to high toxicity are being

added in today's action to the EPCRA section 313 list pursuant to

section 313(d)(2)(B). None of these chemicals are chemicals for which

the consideration of exposure factors would be appropriate.

Through this rulemaking, EPA is clarifying its position regarding

the use of hazard, exposure, and risk in listing decisions under EPCRA

section 313. EPA will consider exposure factors when making

determinations under section 313(d)(2)(A) (acute human toxicity). In

addition, EPA has discretion to consider exposure factors where

appropriate for determinations under sections 313(d)(2)(B) (chronic

human toxicity) and (C) (environmental toxicity), and that there is a

broader range of circumstances in which exposure will be considered

under section 313(d)(2)(C) than under (B).

EPA has reviewed its past listing decisions in light of this

clarification, and believes that its prior listing determinations have

been consistent in the consideration of exposure in 31 of the 32

listing/delisting determinations previous to this action, including a

number of deletions of low toxicity chemicals that Congress placed on

the initial EPCRA section 313 list. EPA is currently reviewing the one

exception, inorganic fluorides, to determine if additional action is

warranted. EPA will continue to evaluate petitions according to this

clarification and will delete chemicals that do not meet the statutory

criteria.

C. Addition of Categories

Six industry trade organizations, 7 companies, and the Department

of Energy contend that section 313 does not provide EPA the statutory

authority to list chemical categories. Some of the commenters contend

that the intent of Congress was for EPA to review individual chemicals.

Therefore, the commenters believe that EPA should list all chemicals

individually. General Electric, American Iron and Steel Institute, and

Eastman Chemical Company further contend that, based on legal precedent

(citing AFL-CIO vs. OSHA, 965 F.2d 9262 (11th Cir. 1992)), EPA does not

have the authority to list chemical categories or specific groups of

chemicals.

EPA believes that the statutory authority to add ``a chemical'' to

the list may be reasonably interpreted to include the authority to list

groups or categories of chemicals. Indeed, this interpretation is

supported by the initial list of chemicals and chemical categories

adopted by Congress in section 313(c). In that initial list, Congress

included 20 chemical categories, mainly metal compounds, but also

categories of organic chemicals such as chlorophenols. Nothing in

section 313 or its legislative history indicates or even suggests that

Congress intended to preclude EPA from adding chemical categories to

the list where the appropriate findings can be made.

Where, as with the categories being added in this final rule, EPA

determines that the primary purpose of TRI--providing information to

the community about the release of chemicals--is most appropriately

served by listing a category of chemicals, EPA has the discretion to

list a category rather than individual chemicals. Of course, in adding

a category to the list, EPA must comply with the statutory criteria.

The Agency believes it satisfies the statutory criteria to add a

category to the list by identifying the toxic effect of concern for at

least one member of the category and then showing why that effect may

reasonably be expected to be caused by all other members of the

category. A specific justification for each of the categories included

in the final rule has been provided in the preamble of the January 12,

1994 proposed rule, in the docket supporting this rulemaking, and in

the Response to Comment Document (Ref. 14).

Several commenters raised policy concerns and suggested that there

would be regulatory difficulties associated with adding chemical

categories. These are addressed below.

One commenter suggested that the regulated community would face

uncertainty in deciding which chemicals belong in the category. In this

final rule, EPA has described the categories in sufficient detail to

alleviate uncertainty regarding their membership. Of course, the Agency

will work with the public and the regulated community to develop, as

appropriate, any interpretations and guidance the Agency determines are

necessary to facilitate accurate reporting for these categories.

One commenter questions how to properly report a chemical which

could be considered part of a category and which is also specifically,

individually listed. Threshold determinations should be made for the

individually-listed chemical rather than for the category. The current

EPCRA section 313 list contains some individually-listed chemicals that

also meet the definition of an EPCRA section 313 listed category. For

example, pentachlorophenol is listed individually on EPCRA section 313

but also meets the definition of the chlorophenol category. In these

situations, threshold determinations should be made for the chemical as

an individual entity rather than as a member of the category. A

facility would not count the quantities manufactured, processed, or

otherwise used toward threshold determinations for both the individual

listing and the category listing, but rather only toward the individual

chemical threshold.

One commenter contends that categories will lead to inadvertent

non-compliance with reporting requirements. EPA does not believe that

this is a significant concern. Because the categories being added to

the EPCRA section 313 list today each consist of chemicals that are

similar chemically and in effect, EPA believes that these categories

will not be difficult for the public or industry to understand or for

the Agency to administer. In addition, there are already categories on

the current list, and EPA has not experienced a significant problem of

the sort suggested by the commenter. The Congressional objective of

providing information is outweighed by any possible problems that some

facilities might have with inadvertent noncompliance.

One commenter states that the use of categories will artificially

lower the thresholds for reporting chemicals within the category. The

Agency believes that calculating the thresholds based on the category

(i.e., a sum of the activities for each individual category member) is

appropriate and not ``artificially lower.'' As described above,

categories are placed on the EPCRA section 313 list where each of the

members can be expected to cause similar effects because all members of

the category have a similar functional group or exhibit a similar

characteristic. For each of the categories added in today's rule, EPA

believes that because each member of the category has this similar

functional group or exhibits a similar characteristic, each member of

the category can be reasonably anticipated to cause similar adverse

effects. The members of the category are not randomly selected, but are

closely related and warrant being reported as a category. These

chemicals in aggregate can reasonably be anticipated to cause an

aggregate impact of the adverse effect associated with each member of

the category. Thus, it is appropriate to apply the reporting thresholds

to the category regardless of whether the threshold amount is

attributable to one member of the category or to individual members in

aggregate.

One commenter believes that listing broad categories where the

individual members have diverse properties and cause diverse effects

does not constitute ``good science.'' The Agency agrees that a category

must be rationally constructed both in terms of similarity in the

properties of the individual members and in terms of their effects.

There is, of course, no requirement that the properties across category

members be absolutely identical. EPA agrees that the members of a

category be reasonably expected to elicit the same type of effect or

related effects in order for a category to satisfy the statutory

listing criteria. Furthermore, EPA agrees that determinations to list a

category, as with listing an individual chemical are to be based on

``good science.'' EPA has applied these principles to the categories

being added in the final rule.

D. Policy Issues

There are several policy issues which were consistently raised in

comments on specific chemicals and general comment on the entire

proposed rule. For purposes of this final rule, EPA addresses these

issues in this unit of the preamble and not in unit IV.F. of the

preamble in the responses to chemical-specific comments. Detailed

responses to comments on specific individual chemicals are available in

the Response to Comments Document (Ref. 14).

1. The addition of chemicals that may be released in small

quantities. Many commenters object to the addition of many of the

chemicals to the EPCRA section 313 list because they do not believe

that there will be significant releases of these chemicals. Therefore,

they contend there will not be significant exposure to these chemicals

and the associated risks will be low.

EPA believes that the chemicals added today meet the EPCRA section

313(d)(2) criteria and should be included on the EPCRA section 313

list. The quantity of a chemical released is not part of the statutory

criteria. The purpose of EPCRA section 313 is to collect data on the

quantity released so that local communities can make their own

determinations about exposure.

Congress intended EPCRA section 313 to address the lack of

information on toxic chemicals in communities by providing information

on releases of toxic chemicals. The public can then use this release

information with site-specific information and the appropriate

attributes of a chemical to evaluate exposure. EPA considers it

inappropriate under the right-to-know program to supplant the public's

power to make risk determinations on a community level by the Agency's

use of specified levels of potential releases, exposure, or risk as

screening criteria to exclude chemicals from the EPCRA section 313

list. By listing chemicals that present a hazard and providing TRI data

on these chemicals to the public, EPA allows the public to make the

determination as to whether there is a risk in their community.

Furthermore, any exposure assessment conducted by EPA would be

conducted from a national perspective and may not truly represent the

risks to a specific community. (For a more detailed discussion on the

Agency's use of exposure see Unit IV.B. of this preamble).

2. The addition of chemicals that are regulated by FDA. Eli Lily

and Company, National Agricultural Chemical Association, Pharmeceutical

Manufacturers Association, and Hoffman-La Roche state that chemicals

which are regulated by the FDA should not be added to EPCRA section

313. The commenters argue that the FDA approves a drug only after

extensive testing and a determination that the benefits to the patients

outweigh the risks. The commenters further state that access to these

drugs is controlled because they can only be obtained through a medical

doctor.

EPA agrees that the drug testing and approval process conducted by

the FDA is extensive and necessary to protect the public health and

well-being. However, as discussed above, the purpose of listing these

chemicals under EPCRA section 313 is to provide information on the

release, transfer, and waste management activities occurring in the

community. This is a different function that addresses different issues

than those addressed by FDA. Furthermore, while the main use of these

chemicals is pharmaceutical in nature, that does not mean that they are

not a hazard in other contexts. EPA agrees that in controlled

situations (e.g., a doctor's prescription) ingestion of a drug is

likely to have certain intended benefits. However, outside of this

controlled situation, any adverse effects are not balanced by the

benefits received from the use of the drug. Further, EPCRA section 313

will collect information on the release and disposal of these

chemicals, which is not covered by the regulation of the use of a

chemical as a drug.

3. Chemicals regulated under FIFRA. Several commenters do not

support the addition of chemicals regulated under FIFRA to the EPCRA

section 313 list of toxic chemicals because, they contend, the major

route of exposure, agricultural field use, has been addressed through

FIFRA regulation which establishes safety factors and use directions

allowing for safe use. They further contend that the use of these

chemicals has been determined not to present an unreasonable risk and

therefore, listing pesticides under EPCRA section 313 is unnecessary.

FIFRA regulations require that the Agency determine that pesticidal

uses of a chemical do not cause ``unreasonable adverse effects on the

environment'' which is defined in FIFRA section 2(bb) as ``any

unreasonable risk to man or the environment taking into account the

economic, social, and environmental costs and benefits of the use of

pesticides'' (7 U.S.C. section 136(bb)). FIFRA is a regulatory statute,

and the impacts of regulation can be immediate and direct (e.g.,

banning of a chemical), and as such EPA examines not only the hazards

presented by the chemical, but also the specific exposure scenarios,

and weighs the risks against the benefits of the chemical. The

``unreasonable adverse effects'' determination under FIFRA is specific

to the intentional use of the chemical as a pesticide and does not

address other uses or releases of the chemical that may result from

manufacture, processing, or other use. Furthermore, a determination

under FIFRA that the use of a chemical will not result in an

``unreasonable adverse effect'' is not a determination that the

chemical is not hazardous or that the use of the chemical is without

risk. Finally, EPCRA section 313 was not enacted to serve the same

purpose as FIFRA. Listing on EPCRA section 313 provides communities

with some of the information required to determine what risks may

result from the manufacture, processing and non-pesticidal use of a

chemical, information not generally provided through FIFRA.

4. Duplicative reporting. Many commenters believe that listing some

of the chemicals proposed will result in duplicative regulation that

will be unduly burdensome and of little benefit. One other commenter,

Westinghouse Electric Corporation, states that EPA should utilize

existing sources of information to avoid duplicative reporting.

Congress did not intend that the chemicals listed under EPCRA

section 313 be limited to those that are not regulated under other

environmental statutes and for which no information is collected

pursuant to other requirements. The initial list of chemicals that

Congress included in section 313 consisted of substances regulated

under RCRA, CWA, SDWA, CERCLA, FIFRA, and CAA. Further, as

Representative Edgar stated in the House of Representatives debate on

the Conference bill:

With respect to the contents of the toxic release form,

estimates of releases into each environmental medium must be

provided. This shall include any releases into the air, water, and

land, as well as releases from waste treatment and storage

facilities. This shall include all releases of toxic chemicals into

surface waters whether or not such releases are pursuant to the

Clean Water Act permits. (132 Cong. Rec. H9561, October 8, 1986)

EPA believes that the chemicals being added today meet the toxicity

criteria of EPCRA section 313(d)(2) and, therefore, should be added to

the EPCRA section 313 list. EPA further believes that the EPCRA section

313 requirements do not duplicate other regulatory program

requirements. EPCRA was not enacted to serve the same purpose as other

regulatory programs but to collect and disseminate information to the

public. Nor is EPCRA section 313 intended to regulate how a chemical

may be used, the amount of chemical a facility manufactures, processes,

otherwise uses, and releases, what media the chemical is released to,

or how the chemical is disposed. Therefore, TRI, as an information

collection and dissemination program, is not designed to directly

impose controls for the protection of human health or the environment

in the same manner as other regulatory programs. The benefit of TRI is

that it empowers the public, through access to release, transfer, and

waste management data on toxic chemicals, to make determinations about

risks in their communities based on TRI data, site-specific

information, and the properties of the chemicals.

E. General Technical Comments

1. Maternal toxicity. A number of commenters argued that for

certain chemicals in animal tests, the only evidence for developmental

toxicity occurred at maternally toxic doses (that is, doses that were

high enough to induce toxicity in the mother), and, therefore,

developmental toxicity cannot be used as a basis for listing these

chemicals under EPCRA section 313. EPA disagrees that fetal effects

only in the presence of maternal toxicity demonstrate that a given

substance does not present a developmental hazard. Although the

developmental effects may have been seen in the presence of reversible

maternal effects, the developmental effects may be more permanent and

cannot be treated as only secondary to reversible maternal toxicity.

With regard to adverse effects in the presence of maternal toxicity,

EPA believes that developmental effects at maternal toxicity are ``. .

.toxic manifestations and as such are generally considered a reasonable

basis for Agency regulation and/or risk assessment'' (Ref 6). This

approach has particular relevance in situations where reversible

maternal toxicity may occur in the presence of irreversible adverse

fetal effects. The Agency does not distinguish between fetal effects

observed in the presence of maternal toxicity or those observed without

concomitant maternal toxicity. Both maternal and fetal toxicity are of

concern to the Agency, and are within the criteria of EPCRA section

313(d)(2). Thus, EPA will use the effect, maternal or fetal, which is

most sensitive to set LOAELs and no-observed-adverse-effect levels

(NOAELs). If both occur at the same level, the LOAELs and NOAELs for

both are the same. When the LOAEL is the same for the adult and

developing organisms, it may simply indicate that both are sensitive to

that dose level, rather than that the developmental effects result only

from maternal toxicity. Moreover, whether developmental effects are

secondary to maternal toxicity or not, the maternal effects may be

reversible while effects on offspring may be permanent. There are

several agents known to produce adverse developmental effects at

minimally toxic doses in adult humans (e.g., tobacco smoking, alcohol,

isotretinoin).

2. Use of IRIS and other secondary sources. Several commenters

object to EPA's use of the Agency's Integrated Risk Information System

(IRIS) data base, the Agency's Office of Pesticide Programs' 1988 TOX-

One-Liners data base, Registry of Toxic Effects of Chemical Substances

(RTECS) data base, and the Aquatic Information Retrieval (AQUIRE) data

base. The commenters contend that in relying on these sources the

Agency ignores other pertinent data that may be in its possession. They

contend that EPA should have examined the primary sources, rather than

relying on data bases which are summaries of studies. Specifically,

some commenters claim that there are many studies in EPA's possession,

but not included in the 1988 TOX-One-Liner data base, that appear not

to have been considered in the review process, because they have not

yet been reviewed by EPA's Office of Pesticide Programs. The commenters

contend that reliance on IRIS or the 1988 TOX-One-Liner data base does

not constitute a detailed analysis and careful examination of the

available data on a chemical.

EPA disagrees with the commenters. EPA's use of the Agency's IRIS

data base for EPCRA section 313 purposes does constitute a hazard

evaluation. That data base generally provides information against which

EPA can evaluate the section 313(d)(2) criteria. The information

contained in the IRIS data base represents the Agency's weight-of-

evidence hazard assessment for chemicals contained in the data base.

The information was developed after the Agency's thorough scientific

review of the available data. Therefore, by relying on information in

the IRIS data base in the review of chemicals for listing on EPCRA

section 313, EPA made statutory determinations based on hazard

assessments conducted by the Agency.

Although the 1988 TOX-One-Liners were used as part of the Agency's

evaluation of the toxicity of a candidate chemical, a number of other

sources were also used. These include decision documents from a number

of Agency and EPA internal peer review groups, deliberations of the

FIFRA Scientific Advisory Panel, and reference to data evaluation

records for studies used in support of listing. Therefore, evaluations

of the toxicity of individual chemicals has been made on the entire

data base and did not rely only on the 1988 TOX-One-Liners data base.

Furthermore, inclusion of all of the detailed studies in the docket was

not possible, because of the proprietary nature of some of the

information. However, in cases where relevant information was used in

support of the listing decision, but was not included in the 1988 TOX

One-Liners data base (which is the most recent sanitized version of the

data base), sanitized versions of the additional sources were included

in the docket. In those cases where only the 1988 TOX-One-Liners data

base or other similar sources were cited, no additional data not

described in the 1988 TOX-One-Liners, RTECS, or the AQUIRE data bases

was considered to be relevant to this listing. For a few chemicals it

has become apparent based on comments received that EPA's analysis did

not include studies which are in EPA's possession but which EPA has not

reviewed. The Agency is deferring the final action on these chemicals

until such studies can be reviewed.

3. Testing at toxic doses. A number of commenters stated that

pesticides which are registered under FIFRA should not be listed under

EPCRA section 313 because the testing conducted to obtain a pesticide

registration under the FIFRA review process requires testing at dose

levels ``virtually guaranteed to produce a toxicological effect.''

It is not EPA's position that chemicals registered as pesticides

under FIFRA should be precluded from listing simply because these

chemicals were tested at doses which are designed to produce toxic

effects. The commenters are correct that the FIFRA standard study

design attempts to set the doses at levels which bracket the minimal

toxic dose, and, therefore, the high dose(s) by design produces an

effect. The purpose of this study design under FIFRA is to determine

the potential for toxicity of the chemical, whether the responses are

dose-related and, depending on the effects produced, the degree of

toxicity. Because virtually any chemical substance can elicit a

toxicological response at some dose level, the mere presence of the

toxic response is not used in isolation in listing decisions under

EPCRA section 313. Rather, it is the relative severity of the effect,

the presence of a dose/response relationship, and whether the effect is

manifested at relatively low doses which are considered in determining

the hazard of the chemical, and in making listing determinations under

EPCRA section 313.

4. Precursor chemicals. CRF AG Products Company, Monsanto, FMC

Corporation, Eastman Chemical Company, and the Chemical Manufacturers

Association question EPA's authority to list precursor chemicals (i.e.,

a chemical that reacts in vivo or in the environment to generate

another chemical that produces the toxic effect supporting the listing)

on the EPCRA section 313 list. The commenters believe that a chemical

should only be added to the list based on the toxicity of the chemical

itself. Further they contend that nowhere in the legislative history is

there any indication that post-release transformation products,

degradation products, or products of chemical reactions are legitimate

bases for adding chemicals to the EPCRA section 313 list.

The EPCRA section 313(d)(2) listing criteria each state that EPA

may list a chemical that it determines ``causes or may reasonably be

anticipated to cause'' the relevant adverse human health or

environmental effects. EPA believes that this language allows EPA to

consider the effects caused by the degradation products of a listed

chemical. Where it may reasonably be anticipated, based on available

data, that the listed chemical would readily degrade into another

chemical that would cause the adverse effect, EPA is acting reasonably

and within its grant of authority in listing the precursor to the toxic

degradation product.

Furthermore, one could also view the effects caused by the

degradation product as effects indirectly caused by the listed

chemical. EPA believes it is within its authority to consider both the

direct and indirect adverse human health and environmental effects of a

chemical in making a listing determination. Based on the statutory

language and legislative history, EPA interprets EPCRA section

313(d)(2) to include toxic effects indirectly caused by a listed

chemical. The statute and the legislative history do not specifically

preclude EPA from considering indirect effects in deciding whether a

chemical meets the toxicity criteria under section 313. In the absence

of specific congressional intent on the issue, it is reasonable for EPA

to consider indirect effects in light of the broad statutory purpose to

inform the public about releases of toxic chemicals to the environment.

Were EPA to exclude indirect effects from consideration it would ill-

serve the purpose of the statute by precluding public access to

information about chemicals that, albeit, indirectly cause a wide range

of adverse health and environmental effects.

There is precedent for the Agency to consider the ``indirect''

toxicity of a chemical being considered for listing. Indirect toxicity

was the basis for the granting of two petitions, one to add seven

chlorofluorocarbons and halons (August 30, 1990, 55 FR 31594) and a

second to add hydrochlorofluorocarbons to the EPCRA section 313 list

(December 1, 1993, 58 FR 64936). EPA also used indirect toxicity in

support of its denial of petitions to delete certain volatile organic

chemicals from the section 313 list, specifically, the ethylene and

propylene petition (January 27, 1989, 54 FR 4072) and the cyclohexane

petition (March 15, 1989, 54 FR 10668).

5. Use of studies conducted by routes other than oral, inhalation,

or dermal. Several commenters maintain that intraperitoneal,

intravenous, or subcutaneous injection (injection into the abdomen, a

vein, or under the skin, respectively) has minimal relevance for

evaluating potential human exposure from industrial situations and

should not be used to support an EPCRA section 313 listing decision.

One commenter contends that, if considered at all, intraperitoneal

injection is a form of exposure that should be considered in

establishing a section 313(d)(2)(A) finding of acute effects, not a

section 313(d)(2)(B) finding of chronic effects.

EPA disagrees with the commenters. In making section 313 listing

decisions, the Agency cannot ignore the possible significance of any

existing data, including data from intraperitoneal, intravenous, or

subcutaneous injection studies. Although it is preferable to have

toxicity data from the common routes of human exposure, EPA believes

that for hazard assessment under EPCRA section 313, the Agency should

use all available information to identify the hazard associated with a

chemical. This comment relates to five chemicals (bromacil lithium

salt, fluorouracil, pentobarbital sodium, tetracycline hydrochloride,

and sodium nitrite) that are being added to the section 313 list today.

For three of these chemicals, bromacil lithium salt, fluorouracil, and

sodium nitrite, any data from intraperitoneal or other injection routes

of exposure are supplemented by data from other, non-injection exposure

routes. For example, in addition to chronic dog and rat injection

studies to support the chronic hematological concerns of sodium

nitrite, there are human oral data. For bromacil lithium salt,

intraperitoneal injection studies in rats are supplemented by gavage

studies in mice to support the developmental concerns for this

chemical. In addition to the developmental effects observed in the

offspring of women receiving fluorouracil intravenously, developmental

abnormalities in mice, rats and hamsters receiving fluorouracil orally

were used to support the developmental toxicity finding. For both

pentobarbital sodium and tetracycline hydrochloride, the studies cited

in the proposed rule in support of the developmental effects of these

chemicals are either studies in which the chemical was administered via

injection or studies in which the chemical was administered via another

route. However, because both of these chemicals are commonly

administered orally, and are efficacious by this route (orally), there

is reason to extrapolate the effects observed in injection studies to

effects by other routes. The proposed rule and the Response to Comment

Document (Ref. 14) contain information on EPA's review of these

chemicals, including the toxicity evaluation. This background

information will not be repeated here in the final rule. Based on EPA's

reanalysis of the available information in the proposed rule for these

five chemicals, EPA has sufficient evidence to determine that bromacil

lithium salt, fluorouracil, pentobarbital sodium, tetracycline

hydrochloride, and sodium nitrite have sufficient evidence to meet the

statutory listing criteria under EPCRA section 313(d)(2)(B).

6. Use of acute studies to support a chronic finding. Several

commenters object to the use of data from acute studies to support a

finding of chronic toxicity. The commenters contend that there is no

correlation between transient acute impact and chronic toxicity that is

appropriate to industrial chemicals as a whole. The commenters contend

that, if a chemical exhibits transient acute but not chronic effects,

it should not be listed based on chronic toxicity, unless additional

data on chronic effects are also used in the determination to list the

chemical.

EPA agrees with the commenter that if a chemical exhibits acute

toxic effects, it should be listed based on acute effects unless

additional data on adverse effects after long-term exposure are

available. This comment relates to three of the chemicals (bromine, 2-

bromo-2-nitropropane-1,3-diol, and sodium nitrite) that are being added

to the section 313 list today. For these chemicals, any data from acute

studies are supplemented by chronic toxicity information. In chronic

toxicity studies, bromine produced upper respiratory irritation and

neurological symptoms. In chronic toxicity studies, 2-bromo-2-

nitropropane-1,3-diol produced various effects including lesions of the

stomach mucosa, ulceration, raised areas and excrescences,

inflammation, epithelial hyperplasia and hyperkeratosis, and congested

vessels of the mucosa of the gastrointestinal (G.I.) tract. Sodium

nitrite induced, in a chronic study in mice, reduced motor activity and

major electroencephalogram (EEG) changes in treated animals. The

proposed rule and the Response to Comment Document (Ref. 14) contain

information on EPA's review of these chemicals, including the toxicity

evaluation. This background information will not be repeated here in

the final rule. A summary of the response to comments for these

chemicals is provided in Unit IV.F. of this preamble.

7. Use of cholinesterase inhibition as a measure of neurotoxicity.

Several commenters expressed concern that the Agency has used a

chemical's effect of inhibiting plasma, red blood cell (RBC) or brain

cholinesterase activity as a basis for listing chemicals on the EPCRA

section 313 list. These commenters feel that this effect is not an

adequate indicator of neurotoxicity.

The Agency believes that inhibition of plasma, RBC, or brain

cholinesterase activity is an appropriate indicator to assess the

toxicity of potential neurotoxicants (Ref. 7). In order for the normal

activity of the nervous system to be altered by a toxic chemical, the

chemical must enter the body, reach the tissue target site(s), and be

maintained at a sufficient concentration for a period of time in order

for an adverse effect to occur. Biochemical changes precede the more

overt, physiological changes associated with neurotoxicity, and are

more easily detectable. Acetylcholinesterase (AChE) is the enzyme that

inactivates or terminates the effect of the neurotransmitter

(acetylcholine) on its target. When this enzyme is inhibited,

acetylcholine is built up in the body, and may result in loss of

appetite, anxiety, muscle twitching, paralysis, or other neurotoxic

effects. Thus, one can assess the signs and symptoms of systemic

poisoning by many neurotoxins from their biochemical mechanism of

action, such as the inhibition of AChE. Because of the severity of

these effects, EPA takes a cautious approach by using a measure of

cholinesterase activity as an indicator of neurotoxicity.

The comments concerning cholinesterase inhibition relate to six of

the chemicals that are being added to the section 313 list today. The

proposed rule and the Response to Comment Document (Ref. 14) contain

information on EPA's review of these chemicals, including the toxicity

evaluation. This background information will not be repeated here.

Based on comments received and EPA's reanalysis of the available

information in the proposed rule for these six chemicals, EPA has

sufficient evidence to determine that acephate, cycloate, diazinon,

ethyl dipropylthiocarbamate, pirimphos methyl, and profenofos meet the

statutory listing criteria under EPCRA section 313(d)(2)(B) based on

available neurotoxicity data for these chemicals.

8. Use of certain studies for hazard assessment. Several commenters

argue that EPA should not use studies in support of listing a chemical

on the EPCRA section 313 list, if these studies have been determined to

be insufficient for use in risk assessments under FIFRA or TSCA. For

example, the commenters point to studies EPA considered in this

rulemaking in conducting hazard assessments even though the studies

when submitted for use under FIFRA or TSCA were determined by EPA to be

of ``low confidence.'' EPA believes its use of these studies for

section 313 purposes is appropriate. The ``low confidence''

determination under FIFRA or TSCA applies to the use of the studies for

purposes of risk assessment associated with regulations that impose

controls. The data base for a chemical may be rated low confidence

because of shortcomings such as lack of experimental detail. Although

these studies may be of limited value for purposes of risk assessment

in support of regulatory controls, when considered together, they

present a sufficient weight-of-evidence as to the hazard associated

with the chemical. As additions to EPCRA section 313 made pursuant to

EPCRA section 313(d)(2)(B) are not based on the kind of risk assessment

needed for regulatory controls, EPA believes that such studies can be

used to support listing.

9. Docket was incomplete for certain chemicals. Several commenters

contend that the docket information supporting the listing of certain

chemicals is incomplete. Other commenters contend that, overall, the

docket is too general and limited. Responses to comments about the

evidence provided in the docket for specific chemicals are provided in

the Response to Comment Document (Ref. 14).

In the public docket supporting this rulemaking, EPA included

copies of EPA's support documents (Refs. 9, 12, and 13) for the

proposed rule and copies of the main references cited in those

documents. The primary references that are cited in these main

reference documents were not themselves included. However, these

reference documents are published material, readily accessible, and are

in the public domain. EPA believes that the docket material for both

the proposed and final rules contains the appropriate information to

support the addition of these chemicals to the EPCRA section 313 list

and to have provided the public an adequate basis on which to comment

on the proposed rule.

F. Chemical-Specific Comments for Chemicals that Are Being Finalized in

Today's Action

The Agency received comments on 110 of the 313 specific chemicals

included in the proposed rule. This unit of the preamble summarizes the

most significant of those comments and the Agency's responses. More

detailed responses are included in the Response to Comment Document

(Ref. 14). Neither this unit of the preamble nor the Response to

Comment Document addresses comments specific to chemicals that have

been deferred for final action. These comments will be addressed in a

separate rulemaking specific to those chemicals.

1. Abamectin. One commenter, Merck, states that primates are less

sensitive to the acute effects of abamectin and its analog, ivermectin,

than rodents. The commenter implies that because humans are primates,

abamectin should be less toxic in humans than in rodents. The commenter

further contends that ivermectin and abamectin have been used safely in

animals and humans.

Abamectin interferes with gamma-aminobutyric acid (GABA)

transmission and, as such, produces neurotoxic clinical signs such as

tremors, ataxia, convulsions, or coma that are more severe in rodents

and dogs than primates. EPA agrees that the available studies indicate

that the sensitivity as well as doses required to produce neurotoxic

effects vary from rodents to primates by a 20-fold factor. However,

abamectin was proposed for addition to the EPCRA section 313 list based

on developmental effects rather than neurotoxicity. There are no

developmental studies with abamectin in primates. Therefore, EPA

believes that the rodent studies cited in the proposed rule provide

sufficient evidence that abamectin can reasonably be anticipated to

cause developmental toxicity in humans.

When administered in therapeutic doses, the Agency does not dispute

the animal and human safety and efficacy of ivermectin and abamectin,

but the safety of a 0.2 to 0.3 mg/kg single therapeutic dose does not

diminish the findings of the developmental, reproductive, neurotoxic,

chronic, and carcinogenic animal studies with abamectin which in some

cases demonstrate serious compound-related effects at higher than

therapeutic doses in all species tested.

The same commenter states that although the aquatic toxicity data

cited for the proposed listing of abamectin under EPCRA section 313 are

accurate and valid, it may be inappropriate to list abamectin under

EPCRA section 313 based on the environmental fate of this chemical,

because of environmental fate factors which were not presented by EPA

in the proposed rule.

EPA agrees with the commenter that the aquatic toxicity values

presented in the proposed rule are accurate and valid. EPA disagrees

that the environmental fate of abamectin will negate the chemical's

ecological toxicity. EPA believes that the environmental fate factors

presented by the commenter may reduce, but do not eliminate, the

potential for adverse effects on aquatic organisms because the chemical

is extremely acutely toxic to aquatic organisms.

EPA reaffirms that there is sufficient evidence for listing

abamectin on the EPCRA section 313 list pursuant to EPCRA section

313(d)(2)(B) based on the available developmental toxicity data and

pursuant to EPCRA section 313(d)(2)(C) based on the available

ecotoxicity data. Therefore, EPA is finalizing the addition of

abamectin on the EPCRA section 313 list.

2. Alachlor. Monsanto states that at the highest dose tested in the

chronic mouse study cited in the proposed rule, EPA concluded there was

an increase in lung tumors in females. Monsanto believes that other

regulatory agencies have disagreed with this conclusion. The commenter

contends that these tumors occur spontaneously in mice with a fairly

high and variable frequency and a possible slight increase in a common

rodent tumor at the highest dose tested does not represent a risk to

humans receiving, at most, trace level exposure.

The Agency has concluded that there was statistically significant

increase (the increase was greater than that which would be expected to

occur spontaneously) in lung tumors in female CD-1 mice at 2 dose

levels which were relevant to potential carcinogenicity to humans. The

commenter provides no specifics to support its contention that ``other

regulatory agencies have disagreed with this conclusion'' nor is the

Agency aware of any.

The commenter further states that the Support Document for the

Health and Ecological Toxicity Review of TRI Expansion Chemicals (Ref.

13) also incorrectly listed the dose levels (``[greater than] 42 mg/kg/

day'') producing tumors in rats in the 2-year rat feeding study cited

in the proposed rule. The commenter argues that significant increases

in thyroid and stomach tumors were observed only at 126 mg/kg/day, the

highest dose tested; this dose level also produced severe, excessive

toxicity. Thus, the commenter concludes that the dose-response curves

for the stomach and thyroid tumors are exceptionally steep, with

increased incidences observed only at a dose which exceeded the Maximum

Tolerated Dose (MTD).

EPA believes that the Support Document for the Health and

Ecological Toxicity Review of TRI Expansion Chemicals (Ref. 13)

correctly states the toxic dose levels in the 2-year rat feeding study

as being greater than or equal to 42 mg/kg/day. In this study, nasal

tumors were significantly increased at 42 mg/kg/day and above and the

stomach and thyroid follicular cell tumors at 126 mg/kg/day. The Agency

agrees that the 126 mg/kg/day dose level probably exceeded the MTD;

however, upon reconsideration of the carcinogenicity data, the Agency

determined that the MTD is between 42 mg/kg/day and 126 mg/kg/day.

Although the MTD was exceeded by the highest dose (126 mg/kg/day),

significant effects were seen at 42 mg/kg/day, which does not exceed

the MTD. Therefore, EPA believes that the 2-year chronic dog study

cited in the proposed rule is a valid measure of the oncogenic

potential of alachlor.

The commenter cites a chronic rat feeding study, not cited by EPA

in the proposed rule, in which 5 to 6 months of alachlor administration

followed by 19 months on control diet did not produce a significant

increase in stomach or thyroid tumors in rats. The commenter believes

that this information is consistent with the results of a study, not

cited by EPA in the proposed rule, in which a close structural

chloroacetanilide analog of alachlor has been shown to be a promoter

but not an initiator of stomach tumors. The commenter did not further

identify this study.

Although in the chronic rat feeding study referred to by Monsanto,

the specific group which received alachlor in the diet for 5 to 6

months in this study, and then control diet as a recovery period did

not develop stomach or thyroid tumors, the other groups on study which

continued to receive alachlor in the diet developed both stomach and

thyroid tumors as well as nasal turbinate tumors. Therefore, the

failure to develop stomach tumors after 5 to 6 months treatment

reflects the time frame required for tumor development rather than

indicating a lack of carcinogenic response.

The commenter also discusses the mechanism of carcinogenicity for

alachlor. The commenter states that the mechanism is nongenotoxic and

hormonally mediated. The commenter argues that the mechanism exhibits a

threshold and that nasal turbinate tumors in particular are not

relevant to humans.

The Agency acknowledges the mechanism of carcinogenicity may be

hormonally mediated. However, the mechanism does not alter the fact

that the tumors are relevant to potential carcinogenesis in man.

Mechanism of tumor development relates to the appropriate model by

which cancer risk is calculated. However, mechanism has no impact on

the determination of carcinogenicity hazard. In determining cancer

classification, EPA does not assume that the specific types of tumors

seen in animals will develop in humans. However, EPA believes that the

development of tumors, such as nasal turbinates, in animals

demonstrates the potential for tumor development in humans.

The same commenter states that two epidemiology studies, not cited

by EPA in the proposed rule, have been conducted on alachlor

manufacturing workers. The commenter contends that neither study

indicates an increase in tumors in humans due to exposure to alachlor.

The commenter believes that these studies provide important additional

evidence indicating that the tumors produced in rats by alachlor are

not produced in humans and should have been considered by the Agency.

Epidemiological studies are used by the Agency in the overall

evaluation of the carcinogenic potential of a chemical, along with

other evidence. However, the studies cited by the commenter are based

on a small sample size. Studies of this type cannot verify the levels

and duration of exposure and represent results from a heterogeneous

population. In addition, one of the two studies apparently only focused

on tumors resulting in death of the study subjects and may reflect an

under estimation of tumor incidence. Therefore, in the face of evidence

of carcinogenicity in two adequately performed bioassays in two

species, the epidemiology data, although pertinent, do not negate the

importance of the animal data in the studies relied upon in the

proposed rule.

EPA reaffirms that there is sufficient evidence for listing

alachlor on the EPCRA section 313 list pursuant to EPCRA section

313(d)(2)(B) based on the available carcinogenicity data for this

chemical. Therefore, EPA is finalizing the addition of alachlor on the

EPCRA section 313 list.

3. Ametryn. Ciba-Geigy Corporation objects to listing ametryn under

EPCRA section 313 on the basis of liver effects, stating that

hepatotoxicity was observed only at high dose levels (100 and 500 mg/

kg/day) in subchronic studies.

The Agency believes that the LOEL of 100 mg/kg/day is sufficiently

low given the seriousness of the effect (hepatic toxicity) to justify

listing on the EPCRA section 313 list. Thus, EPA reaffirms that there

is sufficient evidence for listing ametryn on the EPCRA section 313

list pursuant to EPCRA section 313(d)(2)(B) based on the available

hepatotoxicity data for this chemical, and pursuant to EPCRA section

313(d)(2)(C) based on the available environmental toxicity data.

Therefore, EPA is finalizing the addition of ametryn on the EPCRA

section 313 list.

4. Amitraz. Nor-Am Chemical Company states that in the 2-year

beagle dog feeding study cited in the proposed rule, contrary to EPA's

conclusions, the only effects seen in the high dose (1.0 mg/kg/day)

group were a small but insignificant increase in blood glucose and in

one animal slight hypothermia during weeks 52 and 79.

EPA disagrees with the commenter. EPA has re-evaluated this study,

and determined that in this study amitraz induced significant changes

in blood chemistry (increased blood glucose). Hypothermia occurred not

only at the times noted by the commenter, but also on days 1 and 2, and

in one dog 3 hours after dosing, which returned to normal within 24

hours, at the 1.0 mg/kg/day level, the LOEL. As noted in the proposed

rule, these findings were supported by similar results obtained in a

90-day feeding study in dogs cited in the proposed rule.

Nor-Am disagrees with the Agency's conclusion that the NOAEL for

fetotoxicity was 5 mg/kg/day in the 3-generation rat reproduction study

cited in the proposed rule. The commenter believes that while there was

a slight decrease in the mean litter size at birth in the 20 mg/kg/day

dose group and decreased pup viability in the 5 and 20 mg/kg/day dose

groups post partum, there was no direct evidence of fetotoxicity. Nor-

Am states that the effect on litter size was only significant in the

third generation animals at 5 mg/kg/day, and may have been due to an

effect on lactation.

EPA's reanalysis of this data indicates that there was a decrease

in litter size and pup survival at 5 mg/kg/day in all 3 generations and

a slight reduction in pup weight in the F1 and F2

generations. Thus, there was direct evidence of fetotoxicity.

The commenter contends that the rabbit teratology study reported by

the Agency in the proposed rule was considered by EPA to be invalid

(i.e., significantly flawed) due to high abortion rates in all groups,

inadequately small group sizes, and lack of assessment of fetuses. The

commenter argues that the low incidence of anomalies upon which the

NOAEL of 1 mg/kg/day was based were within historical control ranges

and failed to show any clear dose-related effect. The commenter claims

that a subsequent study, not cited by EPA in the proposed rule,

revealed no effects on fetal morphology at doses up to 12 mg/kg/day

while maternal toxicity was found at 3 mg/kg/day and above; no NOEL

could be established. The commenter claims that this subsequent study,

not cited by EPA in the proposed rule, should have been considered by

EPA.

EPA disagrees. The rabbit teratology study cited by EPA in the

proposed rule was never declared by EPA to be invalid (i.e., seriously

flawed). Upon reanalysis of the rabbit teratology study, EPA determined

that although this study does not fully satisfy the guidelines for

study conduct under FIFRA, it is sufficient for the purposes of hazard

assessment, with a NOEL and LOEL for maternal and developmental

toxicity of 5 and 25 mg/kg/day, respectively. As described in the

proposed rule, at 25 mg/kg/day, the following effects were seen:

Decreased litter size and increased pre and post-implantation losses,

decreased maternal body weight gain, and increased abortions. The high

abortion rate is indicative of maternal toxicity. Although the abortion

rates were higher than the control, enough animals remained at

sacrifice to evaluate the toxicity potential of this chemical, and to

support the finding that amitraz can reasonably be anticipated to cause

developmental toxicity.

The subsequent study cited by the commenter was also considered by

EPA. This study also does not fully satisfy the guidelines for study

conduct under FIFRA. Although the fetotoxic effects observed in the

initial study (cited in the proposed rule) were not reproduced in the

subsequent study referred to by the commenter and not cited in the

proposed rule, this does not invalidate the results obtained in the

initial study. Both studies were considered by EPA in determining the

developmental toxicity of amitraz.

EPA reaffirms that there is sufficient evidence for listing amitraz

on the EPCRA section 313 list pursuant to EPCRA section 313(d)(2)(B)

based on the chronic toxicity and developmental toxicity data for this

chemical. Therefore, EPA is finalizing the addition of amitraz on the

EPCRA section 313 list.

5. Atrazine. Ciba-Geigy Corporation objects to the listing of

atrazine under EPCRA section 313 based on increased incidence of

mammary tumors in female Sprague-Dawley rats because the commenter

contends that this tumor type is not indicative of potential

carcinogenicity in humans. The commenter states that the effect is

species (rat) and strain (Sprague-Dawley) specific. Further, the

commenter states epidemiology data from Ciba-Geigy manufacturing and

use indicate no evidence of carcinogenicity in a human population

exposed for up to 30 years. Ciba-Geigy did not provide EPA with a copy

of this study but did discuss the results in their comments.

While epidemiology data are considered in the weight of the

evidence for carcinogenicity, the current classification is based upon

a positive finding in a well conducted animal study as described in the

Risk Assessment Guidelines of 1986 (Ref. 5). Atrazine has been

classified as a category C chemical by EPA's OPP Carcinogenicity Peer

Review Committee and the Scientific Advisory Panel (EPA, 1988). The use

of mammary tumor data for hazard assessment purposes, even when only

one strain of test animal has been demonstrated to be positive, is

consistent with current Agency policy. The Agency considers the cancer

classification to be sufficient basis for listing of atrazine.

EPA reaffirms that there is sufficient evidence for listing

atrazine on the EPCRA section 313 list pursuant to EPCRA section

313(d)(2)(B) based on the available carcinogenicity data. Therefore,

EPA is finalizing the addition of atrazine on the EPCRA section 313

list.

6. Bendiocarb. Nor-Am Chemical Company states that bendiocarb does

not meet the criteria of EPCRA section 313(d)(2)(C) due to its

environmental fate. The commenter alleges that it has been shown not to

accumulate in soil, water, or plants and has a relatively short half-

life (a few days). Nor-Am Chemical Company also contends that

bendiocarb is rapidly broken down by hydrolysis to a biologically

inactive product. As a result, the commenter states that there is no

clear evidence of adverse effects on the environment associated with

bendiocarb.

EPA disagrees that the environmental fate of bendiocarb will negate

the chemical's ecological toxicity. EPA believes that the environmental

fate factors presented by the commenter may reduce but do not eliminate

the potential for adverse effects on aquatic organisms and birds

because the chemical induces environmental toxicity at low dose levels.

Thus, EPA believes that the chemical can reasonably be anticipated to

cause a significant adverse effect on the environment.

EPA reaffirms that there is sufficient evidence for listing

bendiocarb on the EPCRA section 313 list pursuant to EPCRA section

313(d)(2)(B) based on neurological toxicity data for this chemical, and

pursuant to EPCRA section 313(d)(2)(C) based on the available

environmental toxicity data. Therefore, EPA is finalizing the addition

of bendiocarb on the EPCRA section 313 list.

7. Bifenthrin. FMC Corporation does not support the addition of

bifenthrin under EPCRA section 313 because ``EPA overstates the

neurological and [developmental effects] of bifenthrin. The

neurological effects to which EPA referred were tremors or twitching,

neurological signs that did not persist for the entire duration of the

studies.'' EPA agrees with the commenter regarding the developmental

toxicity potential or lack thereof, but disagrees with the commenter

regarding the neurological hazards. In addition to the tremors or

twitching effects cited by the commenter, more severe symptoms,

including clonic convulsions and death, occur in the studies referred

to by the commenters that are cited in the proposed rule, at dose

levels only slightly higher than those causing slight or occasional

tremors and/or twitching. In a rat developmental toxicity study by

gavage, cited in the proposed rule, the maternal LOEL based on tremors

was 2 mg/kg/day; the NOEL was 1 mg/kg/day. The MTD of 2 mg/kg/day was

established on the basis of findings in a rat pilot study (included as

part of the chronic rat study cited in the proposed rule) in which

there were 3 deaths out of 10 animals at 2.5 mg/kg/day. With regard to

the comment concerning the transitory nature of the effects, although

they may be transitory in nature, this does not diminish the

significance of the adverse effects. In particular, neurotoxic effects

leading to convulsion may result in more permanent, underlying damage

which is not reversible upon cessation of immediate signs and symptoms.

Therefore, the Agency concludes that the neurological effects due to

bifenthrin are of sufficient seriousness to warrant listing.

EPA reaffirms that there is sufficient evidence for listing

bifenthrin on the EPCRA section 313 list pursuant to EPCRA section

313(d)(2)(B) based on the available neurological toxicity data, and

pursuant to EPCRA section 313(d)(2)(C) based on the available

environmental toxicity data. Therefore, EPA is finalizing the addition

of bifenthrin on the EPCRA section 313 list.

8. Bromine. Great Lakes Chemical Corporation and Albemarle

Corporation believe that bromine does not meet the listing criteria of

EPCRA section 313. They contend that the Agency has failed to show that

chronic exposure to bromine causes serious or irreversible effects.

They also contend that the time-weighted average (TWA) of 0.1 part per

million (ppm) established by the National Institute of Occupational

Safety and Health (NIOSH) will protect against the acute effects of

exposure. They believe, therefore, that the addition of bromine to the

EPCRA section 313 list should not be finalized.

NIOSH established the TWA for bromine for acute effects. However,

the Agency is not listing bromine on the EPCRA section 313 list on the

basis of its acute effects but on the basis of the adverse effects it

induces after chronic exposure. These effects include functional

neurologic effects and abnormalities in respiratory and endocrine

systems. In humans, chronic exposure to bromine can cause severe

irritation of the skin, mucous membranes and respiratory tract,

gastroenteritis, and death. This severe irritation which can lead to

death through either, or both, respiratory or gastroenteric irritation

is the primary endpoint of concern although neurologic signs and

symptoms which include dizziness, headache, and ``feelings of

oppression'' along with other functional disturbances of the central

nervous system (CNS) may also occur after exposure to bromine.

EPA reaffirms that there is sufficient evidence for listing bromine

on the EPCRA section 313 list pursuant to EPCRA section 313(d)(2)(B)

based on the available chronic toxicity data for this chemical.

Therefore, EPA is finalizing the addition of bromine on the EPCRA

section 313 list.

9. 2-Bromo-2-nitropropane-1,3-diol (Bronopol). Boots Microcheck

contends that 2-bromo-2-nitropropane-1,3-diol presents only a moderate

acute hazard, but does not present a chronic hazard. Therefore, the

commenter concludes that the compound should not be listed under EPCRA

section 313 pursuant to EPCRA section 313(d)(2)(B).

Although the Agency agrees with the commenter that 2-bromo-2-

nitropropane-1,3-diol presents a moderate acute hazard, EPA does not

agree that the chemical is not a chronic toxicant. The effects noted in

both acute and chronic studies, cited in the proposed rule, indicate

irritation due to exposure to the compound. However, differing

expressions of irritation are obtained depending upon the level of

material to which the test animals were exposed and the duration of

exposure. In the acute studies cited in the proposed rule, the acute

gastric effects were seen at relatively high doses. In the chronic

studies, cited in the proposed rule, the effects, described below, were

noted following repeated oral exposure to lower doses of 2-bromo-2-

nitropropane-1,3-diol. The NOEL for chronic oral exposure in rats was

10 mg/kg/day, with effects including lesions of the stomach mucosa,

ulceration, raised areas and excrescences. In a 13-week study in rats

cited in the proposed rule, effects included inflammation, epithelial

hyperplasia and hyperkeratosis, and congested vessels of the mucosa of

the G.I. tract. The chronic studies cited in the proposed rule show

that irritation was caused by a repeated number of low doses. In these

chronic studies multiple doses were required before irritation

occurred. Further, the type of irritation caused by acute and chronic

exposure are different. Therefore, the irritation due to chronic

exposure to 2-bromo-2-nitropropane-1,3-diol is distinguishable from

that caused by acute exposure. EPA believes that the effects observed

in the longer term studies are serious and potentially irreversible.

EPA reaffirms that there is sufficient evidence for listing 2-

bromo-2-nitropropane-1,3-diol on the EPCRA section 313 list pursuant to

EPCRA section 313(d)(2)(B) based on the available chronic toxicity data

for this chemical. Therefore, EPA is finalizing the listing of 2-bromo-

2-nitropropane-1,3-diol on the EPCRA section 313 list.

10. Carboxin. Zeneca Incorporated and Uniroyal Chemical oppose the

listing of carboxin. The commenters claim that the effect of renal

toxicity noted by EPA in the proposed rule was seen only in rat feeding

studies and not in a chronic dog feeding study. Thus, they claim it

appears to be a species-specific effect that may not be relevant to

man.

EPA disagrees with the conclusions of the commenters. Because

direct human testing is generally unavailable, animals are commonly

accepted as surrogates for toxicity testing to predict potential

hazard(s) to humans. Exceptions occur only in a few rare cases where

effects have been determined to be species-specific (e.g.,

2-globulin). It should be noted that the actual

number of species tested with carboxin is limited and, therefore, it is

premature to state that the renal toxicity of carboxin is species-

specific. Significantly, the commenters did not provide any additional

evidence to support their contention that the renal toxicity is

species-specific. EPA uses information from the most sensitive species

to evaluate potential human hazard(s), as a conservative assumption.

EPA reaffirms that there is sufficient evidence for adding carboxin

on the EPCRA section 313 list pursuant to EPCRA section 313(d)(2)(B)

based on the available renal toxicity data for this chemical.

Therefore, EPA is finalizing the listing of carboxin on the EPCRA

section 313 list.

11. 1-(3-Chloroallyl)-3,5,7-triaza-1-azoniaadamantane chloride. Dow

Chemical Company notes that, in the dog study cited in the proposed

rule, the test material was administered in gelatin capsules due to

problems with palatability. They argue that this mode of administration

is unusual and introduces the confounding factor of what is in essence

a bolus administration (given all at one time) of the chemical, and

results in an artificially lowered NOEL.

The Agency does not agree that this mode of administration is

unusual. EPA frequently reviews dog studies in which the test material

is administered by capsule. In addition, dog studies rarely permit ad

libitum feeding as used in rat studies, even when dietary incorporation

is the means of dose administration. Dogs generally receive a measured

amount of food that they rapidly consume. Therefore, bolus

administration closely approximates actual behavior in dogs. The

concern that capsule administration produces an apparently altered

response is not a confounding factor in the study cited in the proposed

rule, and therefore the reported NOEL does not need to be raised as

suggested by the commenter.

The same commenter contends that the effects used as a basis for

listing occurred only in dogs and only in a single study, and,

therefore, are not relevant to humans.

Because direct human testing is generally unavailable, animals are

commonly accepted in the scientific and regulatory communities as

surrogates for toxicity testing to predict potential hazard to humans,

except in a few rare cases where effects have been determined to be

species-specific (e.g., 2-globulin). In the interest

of being protective, EPA uses information from the most sensitive

species to evaluate potential human hazard. In addition, results

demonstrated in a single well-conducted study are sufficient and can

serve as a basis for listing on the section 313 list.

The same commenter states that the LOEL in the study was based upon

a slight, reversible effect in the liver of a single animal. The study,

the commenter argues, should have been considered in toto rather than

relying on a single effect. The commenter implies that EPA should have

set the LOEL at a higher dose.

The commenter is incorrect. The LOEL of 15 mg/kg/day is correct.

This LOEL was based upon obliterative vasculitis and perivasculitis in

one animal. However, these effects are not commonly seen in dogs, yet

in the study cited in the proposed rule, they occurred in seven of

eight dogs at 30 mg/kg/day, the dose next highest to the LOEL. EPA

considers the effects seen in this study to be serious effects.

EPA reaffirms that there is sufficient evidence for listing 1-(3-

chloroallyl)-3,5,7-triaza-1-azoniaadamantane chloride on the EPCRA

section 313 list pursuant to EPCRA section 313(d)(2)(B) based on the

available chronic toxicity data for this chemical. Therefore, EPA is

finalizing the addition of 1-(3-chloroallyl)-3,5,7-triaza-1-

azoniaadamantane chloride on the EPCRA section 313 list.

12. Chlorosilanes. Silicones Environmental Health and Safety

Council and General Electric oppose the listing of the six

chlorosilanes that were proposed for addition

(dichloromethylphenylsilane, dimethyldichlorosilane,

methyltrichlorosilane, trichloroethylsilane, trichlorophenylsilane, and

trimethylchlorosilane) arguing that they undergo rapid hydrolysis and

are not expected to be found in the atmosphere in appreciable

concentrations. The commenters further state that EPA estimated

conditions in its exposure assessment that greatly exceed actual

conditions.

Based on these comments, EPA conducted revised exposure assessments

for each of the chlorosilanes. These revisions support EPA's initial

finding that dimethyldichlorosilane, methyltrichlorosilane, and

trimethylchlorosilane can reasonably be anticipated to be present at

facility boundaries in concentration levels that would cause a

significant adverse effect. EPA believes that the exposure assessments

were based on reasonable release estimates and reasonable worst-case

concentration modeling. Details of this analysis are provided in the

Response to Comment Document (Ref. 14). Thus EPA reaffirms that there

is sufficient evidence to list dimethyldichlorosilane,

methyltrichlorosilane, and trimethylchlorosilane on the EPCRA section

313 list pursuant to EPCRAsection 313(d)(2)(A). Therefore, EPA is

finalizing the listings for dimethyldichlorosilane,

methyltrichlorosilane, and trimethylchlorosilane on the EPCRA section

313 list.

The revised exposure assessments for dichloromethylphenylsilane,

trichloroethylsilane, and trichlorophenylsilane, however, indicate that

these chemicals are not individually present at facility boundaries in

concentration levels that would cause a significant adverse effect.

However, two or more of these chemicals are usually produced together

and as a category are reasonably anticipated to be present at facility

boundaries in concentration levels that would cause a significant

adverse effect. Therefore, EPA is deferring the individual listings of

these three chemicals for consideration as a category possibly to be

added at a later date.

13. Crotonaldehyde. Eastman Chemical and Monsanto believe that

crotonaldehyde should not be added to the EPCRA section 313 list

because of inadequate data on human health. Furthermore, they contend

that crotonaldehyde does not meet the criteria for listing as a

carcinogen as put forth in the Risk Assessment Guidelines for

Carcinogen Risk (Ref. 4) because it was tested in a single sex, single

species experiment. The commenters further believe that EPA's statement

that crotonaldehyde did not induce tumors at the high dose, because at

that high dose crotonaldehyde is cytotoxic, is a contention which is

not supported by scientific evidence. They believe that overall the

weight of evidence for carcinogenicity, including reactivity and

mutagenicity, is insufficient to support listing.

EPA agrees that the human carcinogenicity data are inadequate but

feels that the available animal data are adequate to support a concern

for carcinogenicity. The Agency accepts the single-sex, single species

testing of crotonaldehyde as being sufficient for listing because these

data are supported by strong evidence of mutagenicity in Salmonella

typhimurium; a statistically significant increase in the number of both

benign and malignant tumors in low dose animals and induced altered

liver foci but not tumor formation in the high dose group.

Crotonaldehyde is known to be severely cytotoxic with the capacity to

induce cell death and alter cellular macromolecules. It caused gross

degeneration, chromosome breakage and reciprocal translocations in

Drosophila melanogaster and gross degeneration and polyploidy in all

stages of spermatogenesis in mouse seminiferous tubules thus showing

that is has ample ability to interact with cellular DNA and cause

severe disruption in chromosome structure and cellular integrity. It is

logical to assume that if crotonaldehyde is capable of such damage in

the mammalian testis which is protected by the blood/testis barrier, it

can also cause severe toxicity and cell death in the liver which has no

such protection from toxic agents. Absent evidence to the contrary,

which the commenter did not provide, EPA continues to believe that

failure to observe tumor formation is due to cell death before tumors

could develop. Based on these findings, the Agency believes that the

weight of evidence for crotonaldehyde is sufficient for listing. EPA

reaffirms that there is sufficient evidence for listing crotonaldehyde

on the EPCRA section 313 list pursuant to EPCRA section 313(d)(2)(B)

based on available carcinogenicity and mutagenicity data for this

chemical. Therefore, EPA is finalizing the addition of crotonaldehyde

on the EPCRA section 313 list.

14. Cycloate. Zeneca Incorporated contends that in the 3-generation

rat feeding study, cited in the proposed rule as being of unknown

duration, the distended myelin sheath demyelination and nerve fiber

loss at the LOEL of 3.0 mg/kg/day occurred only after extensive

exposure and as such would not be relevant to a toxic release type of

short exposure.

The effects described in this study are considered to be both

serious and irreversible. Adverse effects that are induced by a

chemical after repeated long-term exposures and are a valid basis for

listing under EPCRA section 313.

The same commenter states that the 3-generation rat reproduction

study cited in the proposed rule was replaced by a more recent (1990)

2-generation rat reproduction study, also cited in the proposed rule,

in which the toxic effects on pup survival (LOEL of 50 mg/kg/day) and

pup body weight (LOEL of 20 mg/kg/day) occurred at doses which were

maternally toxic as well.

EPA considered both studies in its evaluation of cycloate. As

described in unit IV.E. of this preamble, developmental effects seen in

developing organisms are considered to be adverse whether or not they

occur at doses that are also maternally toxic.

EPA reaffirms that there is sufficient evidence for listing

cycloate on the EPCRA section 313 list pursuant to EPCRA section

313(d)(2)(B) based on the available neurological and developmental

toxicity data. Therefore, EPA is finalizing the addition of cycloate on

the EPCRA section 313 list.

15. Cyclohexanol. Monsanto opposes the listing of cyclohexanol

because concentrations that led to tremors, central nervous system

depression, lethargy, or hypothermia in rabbits, as cited in the

proposed rule, are above the level of MED that EPA identified in the

Draft Hazard Assessment Guidelines (Ref. 11) as high priority or

moderate priority. Furthermore, the concentrations that led to

reproductive impacts in rats were above the MED level of high priority.

In addition, Monsanto states that the Industrial Health Foundation

submitted to EPA's TSCA office the results of a 2-generation

reproduction study demonstrating a NOEL of 500 ppm in air which should

have been considered. The commenter claims that EPA has also not

demonstrated that the effects mentioned, or concentrations at which

they occurred, were serious or irreversible.

EPA agrees that the concentrations that led to tremors, central

nervous system depression, lethargy, or hypothermia in rabbits are

above the level of MED that EPA identifies in the Draft Hazard

Assessment Guidelines (Ref. 11) as high priority for listing. However,

while the 2,500 mg/kg/day dermal exposure is above the moderate

priority MED guideline, the 997 ppm (438 mg/kg/day) is within this

category. In addition to the neurotoxicity effects, as cited in the

proposed rule, cyclohexanol also induces renal, hepatic, and myocardial

effects at moderate dose levels (for example, inhalation of 0.59 mg/L

of cyclohexanol induced degenerative changes in the livers and kidneys

of rabbits). EPA considers these effects to be serious. In this case,

based on a weight-of-evidence approach, EPA believes that cyclohexanol

presents a sufficient hazard to warrant listing under EPCRA section 313

even though the reported values for neurotoxicity effects are in excess

of the MEDs placing a chemical in the high priority grouping.

EPA disagrees that the concentrations that led to reproductive

impacts in rats and gerbils (15 mg/kg) as described in the proposed

rule are above the MED range for high priority listing. EPA reiterates

the overall reproductive toxicity of this chemical, based on a weight-

of-evidence, supports the addition of cyclohexanol to the EPCRA section

313 list.

The chemical tested in the 2-generation reproduction study

submitted to the Agency by the Industrial Health Foundation, cited by

the commenter, was cyclohexanone not cyclohexanol as claimed by the

commenter.

EPA reaffirms that there is sufficient evidence for listing

cyclohexanol pursuant to EPCRA section 313 pursuant to EPCRA section

313(d)(2)(B) based on the available chronic neurological, hepatic,

renal, myocardial, and reproductive toxicity data for this chemical.

Therefore, EPA is finalizing the addition of cyclohexanol on the EPCRA

section 313 list.

16. Cyhalothrin. Zeneca Incorporated contends that the

neurotoxicity signs observed in the 6-month and 1-year dog studies

cited in the proposed rule occurred at doses that were ``otherwise

toxic as well'' and do not provide any evidence of a specific

neurotoxicity. Zeneca Incorporated implies that the presence of

``otherwise toxic'' signs reduces the significance of the neurotoxicity

observed in the cited study.

The phrase ``otherwise toxic as well'' was not defined by the

commenter. The clinical signs of neurotoxicity observed in the dogs at

3.5 mg/kg/day (ataxia, muscle tremors, and convulsions in the 1-year

study cited in the proposed rule) and at 10 mg/kg/day (unsteadiness and

trembling in the 6-month study cited in the proposed rule) are

considered by EPA to be evidence of physiological neurotoxicity.

Although there were no pathologic changes in the nervous tissue, EPA

considers these effects to be serious because they often precede

pathologic neurotoxicity. With the exception of liquid feces, there

were no reported toxic findings other than those related to

neurotoxicity.

EPA reaffirms that there is sufficient evidence for listing

cyhalothrin on the EPCRA section 313 list pursuant to EPCRA section

313(d)(2)(B) based on the available neurological toxicity data.

Therefore, EPA is finalizing the addition of cyhalothrin on the EPCRA

section 313 list.

17. Desmedipham. Nor-Am Chemical states that methemoglobin

formation, which is cited by EPA as the basis for listing, is an

entirely reversible effect which occurs only after prolonged and

consistent exposure. Therefore, the commenter concludes that this

finding, by itself, should not be used.

Based on the 90-day dog study, cited in the proposed rule, EPA

considers 150 ppm to be a NOAEL. Methemoglobin values were only

minimally higher than control levels and were not associated with an

increase in Heinz bodies. In the 1-year dog feeding study, after 13

weeks treatment at 300 ppm, methemoglobin was seen associated with

histopathological changes (hemosiderin and hemopoiesis). While

methemoglobinemia may be a reversible effect, it is nevertheless a

serious effect, and in some cases irreversible damage may occur as a

result of methemoglobinemia. Methemoglobinemia interfers with the

oxygenating capacity of blood resulting in an undersupply of oxygen to

the tissues. Therefore, methemoglobinemia is a toxic effect and not

simply an indicator of exposure to desmedipham as concluded by the

commenter.

Therefore, EPA reaffirms that there is sufficient evidence for

listing desmedipham on the EPCRA section 313 list pursuant to EPCRA

section 313(d)(2)(B) based on the available hematological toxicity

data. Therefore, EPA is finalizing the addition of desmedipham on the

EPCRA section 313 list.

18. 2,2-Dibromo-3-nitrilopropionamide. Dow Chemical Company and

Rohm Haas state that the corrosivity and irritancy of the 2,2-dibromo-

3-nitrilopropionamide (DBNPA) solutions to the esophagus, pharynx,

trachea, and lungs led to development of dyspnea in rats. The

commenters imply that the dyspnea in rats should be discounted because

it was caused by the method of administration rather than the toxicity

of the chemical.

The Agency agrees that the dyspnea observed in the 4-week and 13-

week rat gavage studies cited in the proposed rule may have been due to

severe irritation of the trachea and lungs from accidental or

incidental delivery of small amounts of the DBNPA dosing solutions into

the larynx, pharynx, trachea, and/or lungs during the procedure.

However, this suggestion of possible cause can be neither refuted nor

confirmed based upon the available data. Dyspnea is the basis for the

LOEL in the study. One of the commenters agrees that DBNPA is

corrosive, particularly to the eyes and, at the least, is severely

irritating to the respiratory tract. This is consistent with the

effects observed in the two subject studies. The Agency considers the

finding of dyspnea in the 4- and 13-week studies to be of sufficient

seriousness to warrant listing on the EPCRA section 313 list.

EPA reaffirms that there is sufficient evidence for listing 2,2-

dibromo-3-nitrilopropionamide on the EPCRA section 313 list pursuant to

EPCRA section 313(d)(2)(B) based on the available chronic respiratory

toxicity data. Therefore, EPA is finalizing the addition of 2,2-

dibromo-3-nitriloproprionamide on the EPCRA section 313 list.

19. Diclofop-methyl. Nor-Am Chemical and Hoechst-Celanese contend

that EPA interpreted the doses administered by gavage as diet

concentrations (ppm) in the rat teratology study cited in the proposed

rule. One commenter states the Agency should provide clarifications

concerning ``mortality'' of the pups and the calculation of the actual

test substance intake at different stages during the in-life phases

during development in the 3-generation rat reproduction study.

The commenter is correct in stating that the Agency erred in

interpreting gavage doses as ppm in the rat teratology study. However,

EPA still believes that the doses at which adverse effects occur are

sufficiently low and the adverse effects reported are of sufficient

seriousness to warrant listing. The developmental NOEL is 10 mg/kg/day

and the LOEL is 32 mg/kg/day based on an increased incidence of a

number of variations and malformations, as described in the proposed

rule. While the maternal effects on body weight and food consumption at

32 mg/kg/day are transient and reversible, some of the developmental

effects at this dose are irreversible. In the 3-generation rat

reproduction study cited in the proposed rule, a decrease in pups born

alive in the F1a, reduced pup weights (F1a and 2a) and

general retardation of physical development (F1a and 2a) was

noted in offspring at 100 ppm (5 mg/kg/day). The commenter considers

the LOEL for this study to be 6.7 mg/kg/day. This dose resulted in

decreased parental food consumption and body weight and there were no

post partum pup mortalities. Additionally, there were no effects on

fertility at the LOEL at any time during the three generations.

The commenters further stated that EPA should ``consider the

validity'' of the 30-day rat study cited in the proposed rule because

heart, kidney, and adrenal weights were increased only at doses with no

histopathological correlates and were due to the pharmacodynamic lipid

metabolism of the test material by the liver.

The increased relative heart, liver, and kidney weights at 80 ppm

(4 mg/kg/day) in the 30-day rat feeding study is further substantiated

by a recent 90-day rat feeding study cited in the proposed rule with a

LOEL of 80 ppm and a NOEL of 20 ppm (1 mg/kg/day). In the recent 90-day

study cited in the proposed rule, absolute and relative liver and

kidney weight was increased in males and relative liver and kidney

weight was increased in females at 80 ppm. These increased organ

weights are evidence of a compound-related effect. The Agency

interprets Hoechst-Celanese's own statements regarding the 30-day rat

feeding study that ``increased liver weights and centrilobular

enlargement of hepatic cells at dietary concentrations of 80 ppm and

higher'' as evidence of toxicity.

Hoechst-Celanese also contends that the effects in the renal cortex

observed in the 90-day dog study cited in the proposed rule at 250 ppm

(15 and 13.4 mg/kg/day in males and females, respectively) did not

occur at the highest concentration tested in the 1-year dog study (80

ppm, 4-5mg/kg/day) indicating that the finding in the 90-day study was

not test substance related.

EPA believes that the effects occurring in the renal cortex in the

90-day dog study at 13 to 15 mg/kg/day may not have appeared in the 1-

year dog study, since the highest dose tested was 4-5 mg/kg/day. If

higher doses were employed in the 1-year study, then renal effects

could possibly have occurred. However, the results of the 1-year study

do not negate the 90-day results, since the dose levels used in the 90-

day study were so much higher.

Hoechst-Celanese also states that the Agency used an invalid

(flawed) reproductive toxicity study to support the listing. The

commenter indicates that the study was compromised by infection of the

rat colony with RCV/SDA virus. They further state that another

reproductive toxicity study, which EPA did not cite in the proposed

rule, should have been evaluated in which the fetotoxic NOEL was 30 mg/

kg/day instead of greater than 5 mg/kg/day as in the original study.

The Agency does not find the original study to be invalid. The data

were considered to be valid for regulatory purposes. In addition, the

Agency found the fetotoxic NOEL in the study referred to by the

commenter, not cited by EPA in the proposed rule, to be 5 mg/kg/day,

not 30 mg/kg/day as stated by the commenter.

EPA reaffirms that there is sufficient evidence for listing

diclofop-methyl on the EPCRA section 313 list pursuant to EPCRA section

313(d)(2)(B) based on the available developmental, hepatic, and renal

toxicity data. Therefore, EPA is finalizing the addition of diclofop-

methyl on the EPCRA section 313 list.

20. Diisocyanates. EPA originally proposed to list three

diisocyanates (hexamethylene-1,6-diisocyanate, isophorone diisocyanate,

and 1,1-methylene bis(4-isocyanatocyclohexane) on the basis of acute

toxicity pursuant to EPCRA section 313(d)(2)(A). As an alternative, EPA

proposed to create a delimited diisocyanates category containing these

3 diisocyanates and 17 other diisocyanates based on chronic pulmonary

irritation pursuant to EPCRA section 313(d)(2)(B). EPA is finalizing

addition of the delimited diisocyanate category based on chronic

pulmonary toxicity and therefore has not addressed comments concerning

the acute toxicity of any of the diisocyanates. EPA believes that

diisocyanates are best added as a category because the members of this

category are structurally similar (i.e., each contains the diisocyanate

functionality), they induce a similar toxic effect (chronic pulmonary

irritation), and their toxicity is due to the diisocyanate portion of

the molecule common to all members.

Chemical Manufacturers Association Hexamethylene-1,6-Diisocyanate

Panel, Dow Chemical Company, Monsanto, Olin Chemicals, Sealed Air

Corporation, Huls America Incorporated, and the Diisocyanates Panel of

the Chemical Manufacturers Association oppose EPA's alternative

proposal to create a diisocyanate category and believe that individual

diisocyanates should be evaluated and included on the EPCRA section 313

list only if the diisocyanate independently satisfies the statutory

listing criteria. The commenters state that in adding a broad category

of diisocyanates, EPA ignores its statutory mandate to evaluate the

individual toxicity of each chemical and to evaluate the exposure

potential to the EPCRA community by each individual chemical. The

commenters contend that the category would mislead the public as to the

amount and type of toxic chemicals to which communities may be exposed.

The commenters contend that data collected in aggregate is confusing

and difficult to use or interpret. Commenters state that adding a

category of diisocyanates based upon the isocyanate functionality is

based on the chronic effects associated with exposures to a limited

number of diisocyanates and that this method unjustifiably equates

toxicity across an entire class of chemicals that have different

properties and effects. Commenters state that diisocyanates encompass a

diverse group of chemicals which vary significantly in physical and

chemical properties and in potential toxicity. Commenters state that

the available evidence on the pulmonary effects or toxicity of

individual diisocyanates (toluene diisocyanate,

methylenebis(phenylisocyanate), and isophorone diisocyanate) does not

support the addition of a diisocyanates category. The commenters also

state that EPA has not cited any data to support the assertions that

diisocyanates cause these effects. Commenters state that individual

diisocyanates have been shown to respond differently in mutagenicity

studies and that other toxicological differences would be expected

among individual diisocyanates, because of differences in their ability

to penetrate membranes, the capacity of organisms to metabolize them,

the specific reactivity of the diis

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