[Federal Register: November 30, 1994]

_______________________________________________________________________

Part V

Environmental Protection Agency

_______________________________________________________________________

40 CFR Part 372

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.

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

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-ofthe-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 

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

 Section Section Section 

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

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

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-nitrobenzoic 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-dioxolan2-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-dioxo2H-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 sixtysix 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 chemicalspecific 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 rightto-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 TOXOne-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-ofevidence 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 illserve 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. NorAm 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 F<INF>1 and F<INF>2 

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-bromo2-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., 

<greek-a>2<greek-m>-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 speciesspecific. 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., <greek-a>2<greek-m>-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 weightof-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-dibromo3-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 F<INF>1a, reduced pup weights (F<INF>1a and <INF>2a) and 

general retardation of physical development (F<INF>1a and <INF>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 diclofopmethyl 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 diisocyanate groups, etc. Commenters 

state that in the proposed rule EPA recognized these differences by 

stating that some diisocyanates are classified as probable carcinogens 

and others are not. The Wisconsin Department of Natural Resources 

supports EPA's alternative proposal to create a diisocyanate category 

and would prefer this manner of listing to listing each diisocyanate 

separately.

 As discussed in unit IV.C. of the preamble, EPA believes that it is 

acting reasonably within its discretion in listing a category of 

chemicals by showing that at least one member of the category meets the 

listing criteria of EPCRA section 313 and that the other members can 

reasonably be expected to exhibit the same or similar toxic effect. EPA 

believes that the available data on the chronic pulmonary toxicity for 

several members of the diisocyanates category are sufficient for 

listing under EPCRA section 313(d)(2)(B). EPA also believes that the 

diisocyanate moiety, common to all members of the category, is 

responsible for the observed chronic pulmonary toxicity. Therefore, EPA 

believes that it is reasonable to anticipate that all members of the 

diisocyanate category will exhibit chronic pulmonary toxicity and that 

creating a category of diisocyanates is the most appropriate way to 

list this class of chemicals. As stated in Unit IV.B. of the preamble, 

EPA does not believe that it is required to consider exposure for 

chemicals that are moderately high to highly toxic based on a hazard 

assessment when determining if a chemical can be added for chronic 

effects pursuant to EPCRA section 313(d)(2)(B); therefore, EPA is not 

required to evaluate the exposure potential for the members of the 

diisocyanates category. EPA believes that, because each member of the 

diisocyanates category has the same functional groups and can 

reasonably be anticipated to cause similar toxic effects, the 

diisocyanates category will not mislead the public as to the amounts 

and type of chemicals released and will not be confusing to use or 

interpret.
 EPA agrees that the diisocyanates are a diverse group of chemicals 

which vary in physical and chemical properties. However, EPA also 

believes that the reactive portion of diisocyanate chemicals is the 

diisocyanate moiety itself and that the rest of the molecule does not 

affect the reactivity of this portion of the molecule. EPA stands by 

its interpretation of the literature, as cited in the proposed rule and 

background material, on the adverse pulmonary effects of diisocyanates 

and believes that this information supports the addition of a 

diisocyanates category. The Agency agrees that structural differences 

among individual diisocyanates may indeed affect their absorption and 

metabolism. However, since absorption and metabolism are not necessary 

for chronic pulmonary irritation to occur, the effect of structural 

differences upon either absorption or metabolism is not an issue in 

this case. The Agency agrees with the commenter that there are 

differences in the carcinogenicity/mutagenicity of toluene 

diisocyanate, methylenebis(phenylisocyanate), and isophorone 

diisocyanate and that these differences are most likely the result of 

the differences in absorption and metabolism. However, since neither of 

these endpoints is the basis for listing diisocyanates as a category 

and since chronic pulmonary irritation can occur without absorption and 

metabolism taking place, these issues do not affect the Agency's 

overall concern for diisocyanates or its decision to list them as a 

category on the EPCRA section 313.

 As EPA discussed in the proposed rule, there currently are four 

other diisocyanates listed on the EPCRA section 313 list, these are:

 Toluene-2,4-diisocyanate (000584-84-9)

 Toluene-2,6-diisocyanate (000091-08-7)

 Toluene diisocyanate (mixed isomers) (026471-62-5)

 Methylenebis(phenylisocyanate) (000101-68-8)

 EPA is leaving the toluene diisocyanate compounds listed 

individually. In addition to the effects discussed above, these 

compounds have been shown to be carcinogenic. EPA believes it is 

appropriate to continue to individually list carcinogenic diisocyanates 

because they exhibit a different toxic endpoint than other members of 

the category. Methylenebis(phenylisocyanate) has not been shown to be a 

carcinogen and as EPA discussed in the proposed rule it is being moved 

into the diisocyanate category.

 EPA reaffirms its determination that diisocyanates meet the 

criteria of EPCRA section 313(d)(2)(B). Therefore, EPA is finalizing 

the addition of the diisocyanates category that consists of the 

following chemicals:

 1,3-Bis(methylisocyanate)cyclohexane (CAS No. 038661-72-2)
 1,4-Bis(methylisocyanate)cyclohexane (CAS No. 010347-54-3)

 1,4-Cyclohexane diisocyanate (CAS No. 002556-36-7)

 Diethyldiisocyanatobenzene (CAS No. 134190-37-7)

 4,4'-Diisocyanatodiphenyl ether (CAS No. 004128-73-8)

 2,4'-Diisocyanatodiphenyl sulfide (CAS No. 075790-87-3)

 3,3'-Dimethoxybenzidine-4,4'-diisocyanate (CAS No. 000091-93-0)

 3,3'-Dimethyl-4,4'-diphenylene diisocyanate (CAS No. 000091-97-4)

 3,3'-Dimethyldiphenylmethane-4,4'-diisocyanate (CAS No. 000139-25-

3)

 Hexamethylene-1,6-diisocyanate (CAS No. 000822-06-0)

 Isophorone diisocyanate (CAS No. 004098-71-0)

 Methylenebis(phenylisocyanate) (CAS No. 000101-68-8)

 4-Methyldiphenylmethane-3,4-diisocyanate (CAS No. 075790-84-0)

 1,1-Methylene bis(4-isocyanatocyclohexane) (CAS No. 005124-30-1)

 1,5-Naphthalene diisocyanate (CAS No. 003173-72-6)

 1,3-Phenylene diisocyanate (CAS No. 000123-61-5)

 1,4-Phenylene diisocyanate (CAS No. 000104-49-4)

 Polymeric diphenylmethane diisocyanate (CAS No. 009016-87-9)

 2,2,4-Trimethylhexamethylene diisocyanate (CAS No. 016938-22-0)

 2,4,4-Trimethylhexamethylene diisocyanate (CAS No. 015646-96-5)

 In reassessing the Agency's proposal in light of comments received 

and other information, it has become clear to EPA that the effect of 

concern (chronic pulmonary toxicity) is related to the diisocyanate 

moiety and therefore common to all diisocyanate compounds not just 

those included in the delimited category finalized in this rule. EPA 

believes that many other diisocyanates not covered by the category may 

meet the EPCRA section 313 criteria. Therefore, EPA believes that it 

may be more appropriate to create a diisocyanates category based on a 

molecular formula description rather than a more limited category 

comprised of certain named diisocyanates. However, EPA did not include 

a molecular formula category option in its proposal and therefore has 

not given the public an opportunity to comment on such a category. 

Accordingly, in this action EPA is finalizing the addition of a 

delimited category consisting of the 20 diisocyanates on which the 

Agency has received comment and for which the Agency has made a final 

determination that the chemicals meet the EPCRA section 313 criteria 

for listing. EPA believes that the chemicals covered by this category 

represent the majority of diisocyanates in production and that listing 

the delimited category will provide meaningful data to the public. At a 

later date, EPA will consider whether a more broad diisocyanates 

category is warranted and appropriate.
 21. Dimethylamine. Olin Chemicals does not believe that the data 

cited by EPA are sufficient to prove that dimethylamine causes ``. . . 

significant adverse acute human health effects at concentration levels 

that are reasonably likely to exist beyond facility site boundaries. . 

. .'' The commenter did not substantiate this contention. The commenter 

requests a more rigorous review of the available data before adding 

dimethylamine to the EPCRA section 313 list.

 The Agency is not proposing to list dimethylamine pursuant to 

section 313(d)(2)(A), therefore the Agency does not have to show that 

the chemical causes ``. . .significant adverse acute human health 

effects at concentration levels that are reasonably likely to exist 

beyond facility site boundaries. . . .'' EPA disagrees that the data 

cited are insufficient to prove that dimethylamine is likely to cause 

significant human health effects. As articulated in the proposed rule, 

dimethylamine is corrosive to mucous membranes, the eyes and 

respiratory tract. Chronic exposure results in dose-related lesions in 

the respiratory and olfactory epithelium and is associated with 

centrilobular fatty degeneration and necrosis of parenchymal cells 

after inhalation exposure for 18 to 20 weeks. Rats exposed to oral 

doses as low as 0.035 mg/kg for 8 months showed neurological effects 

including changes in conditioned reflexes while single doses of 240 to 

260 mg/kg caused excitement and muscle weakness in mice, rats, guinea 

pigs, and rabbits. Dimethylamine is corrosive to the respiratory tract, 

exhibits hepatotoxicity and is neurotoxic. EPA reaffirms that there is 

sufficient evidence to list dimethylamine on the EPCRA section 313 list 

pursuant to EPCRA section 313(d)(2)(B) based on the available chronic 

respiratory, hepatic, and neurological toxicity data for this chemical. 

Therefore, EPA is finalizing the addition of dimethylamine on the EPCRA 

section 313 list.

 22. 2,6-Dimethylphenol. One commenter, General Electric, states 

that the proposed addition of 2,6-dimethylphenol to EPCRA section 313 

is based upon a ``low confidence'' study and a 10-week subchronic study 

which the ITC found insufficient to evaluate.

 The commenter is concerned that EPA is using the same data set in 

two rule makings; TSCA section 4 and the decision to list on the EPCRA 

section 313 list. The commenter quotes the ITC finding that the studies 

are of ``low confidence.'' The Agency used these data to derive an oral 

RfD of 0.0006 mg/kg/day. IRIS confidence in the studies is low because 

of lack of experimental detail. EPA also concedes that the ITC had low 

confidence in these studies for its purposes which are risk assessment. 

However, EPA believes that these data are sufficient for the purposes 

of hazard assessment and concludes that these studies when considered 
together present a sufficient weight of the evidence determination for 

listing 2,6-dimethylphenol on EPCRA section 313 because 2,6-

dimethylphenol causes hepatotoxicity and nephrotoxicity at relatively 

low dose levels. EPA reaffirms that there is sufficient evidence to 

list 2,6-dimethylphenol on the EPCRA section 313 list pursuant to EPCRA 

section 313(d)(2)(B) based on the available hepatotoxicity and 

nephrotoxicity data for this chemical. Therefore, EPA is finalizing the 

addition of 2,6-dimethylphenol on the EPCRA section 313 list.

 23. Dinoseb. Uniroyal Chemical Company objects to the listing of 

dinoseb (dinoseb is the trade name for dinitrobutyl phenol) because the 

sale of dinoseb as a herbicide or insecticide is prohibited and 

remaining inventories have been used up or disposed. However, the 

commenter notes that dinitrobutyl phenol continues to be produced and 

sold for uses not subject to FIFRA (e.g. as an inhibitor in the polymer 

industry).

 EPA believes that the chemical is more properly listed by its 

common chemical name, dinitrobutyl phenol, rather than its trade name. 

However, EPA also recognizes that this chemical is well known as 

dinoseb. Therefore, EPA is finalizing the addition of this chemical as 

dinitrobutyl phenol (dinoseb).

 24. Disodium cyanodithiomidocarbamate. Buckman Laboratories 

International, Incorporated contends that the compound was not 

teratogenic in either the rat or rabbit studies cited in the proposed 

rule. Specifically, they contend that skeletal variations and increased 

resorptions should be considered an artifact (i.e., occurring by chance 

rather than as a result of treatment), and should not be considered as 

evidence of developmental toxicity.

 EPA disagrees with the commenter. In both the rabbit and rat 

teratology studies cited in the proposed rule, developmental effects 

were observed at levels that were above the maternally toxic level 

(greater than 3 mg/kg for rabbits and greater than 6 mg/kg for rats). 

Furthermore, the effects observed cannot be considered an artifact, 

because in rabbits receiving 30 mg/kg, there is a continuation of the 

effects observed at 10 mg/kg, with an accompanying increase in the 

severity of the developmental findings. This shows that the effects are 

related to the dose received and do not occur by chance.

 EPA reaffirms that there is sufficient evidence for listing 

disodium cyanodithioimidocarbonate on the EPCRA section 313 list 

pursuant to EPCRA section 313(d)(2)(B) based on the available 

developmental toxicity data. Therefore, EPA is finalizing the listing 

of disodium cyanodithiomidocarbamate on the EPCRA section 313 list.

 25. Ethyl dipropylthiocarbamate (EPTC). Zeneca Incorporated states 
that in the study cited by EPA in the proposed rule in which rats were 

orally administered the test compound for 2 years, brain cholinesterase 

reductions were slight and only occurred at 120 mg/kg/day, not 15 mg/

kg/day. The commenter claims that neuromuscular changes occurred only 

after extended exposure, and are not relevant to listing on the EPCRA 

section 313 list.

 The commenter is referring to two studies cited in the proposed 

rule. A 2-year rat feeding study established a NOEL of 5 mg/kg/day and 

a systemic LOEL of 25 mg/kg/day with neuromuscular atrophy/degeneration 

and decreased body weight gains as the findings. At 125 mg/kg/day, the 

effects included chronic myocarditis, cataracts, increased SGOT and 

decreased RBC cholinesterase (ChE) activity. The neuromuscular and 

cardiac changes are serious and potentially irreversible effects. The 

second study is a 3-month feeding study in Sprague-Dawley rats. 

Although this study was not identified in the proposed rule, the 

results of the study were described. The systemic NOEL in this study 

was 3 mg/kg/day, and the LOEL was 15 mg/kg/day. The effects seen 

included increase in cardiomyopathy and decreased weight gain and food 

consumption. As noted by the commenter, brain ChE depression in this 

study in females was slight and occurred at 120 mg/kg/day and, taken by 

itself, is not sufficient for listing, however, when considered with 

other effects in a weight-of-evidence approach, this endpoint is 

supportive of listing. The commenter further states that the 2-year 

dietary rat study is old and has been superseded by another study (Ref. 

8), in which the NOEL was 25 mg/kg/day.

 The Agency agrees with the commenter's comment regarding the 

replacement of the older study with a newer study, but disagrees with 

the commenter's NOEL. The Agency's NOEL for this study is 5 mg/kg/day 

and not 25 mg/kg/day. However, the results of the older study 

demonstrate that heart effects of EPTC are seen in more than one study.

 The commenter further states that in the 2-generation rat 

reproduction study, cardiomyopathy was observed only in the F<SUP>1A 

females and was incidental to treatment. EPA disagrees with this 

contention. The investigators did not look for this effect in other 

generations. Thus, there is no reason to conclude that this effect was 

not manifested in other generations. In addition, this type of adverse 

effect has been seen in other studies, such as the 2-year rat study and 

the 3-month rat study discussed above and cited in the proposed rule.

 The Agency believes that the cardiopathic finding at 10 mg/kg/day, 

degenerative cardiomyopathy, is the pivotal finding of toxicological 

significance for EPTC. EPA believes that this is a serious effect. 

Therefore, this effect cannot be considered incidental to treatment.
 The commenter further states that the neurological effects seen in 

the study are not relevant to the EPCRA section 313 due to prolonged 

exposure and the cardiovascular observations occurred at the highest 

dose tested in the studies cited.

 The cardiovascular effects occur after relatively short exposures 

at doses of 9 mg/kg/day in male rats and 18 mg/kg/day in female rats. 

These dose levels are sufficiently low and the adverse effects are 

serious and potentially irreversible. The Agency considers the 

neurotoxicity due to prolonged exposure to be relevant for purposes of 

listing on the EPCRA section 313 list. Releases of chemicals that 

induce adverse effects after prolonged exposure is among the type of 

information that Congress intended TRI to include.

 EPA reaffirms that there is sufficient evidence for listing EPTC on 

the EPCRA section 313 list pursuant to EPCRA section 313(d)(2)(B) based 

on the available neurological, cardiovascular, and reproductive 

toxicity data for this chemical. Therefore, EPA is finalizing the 

addition of EPTC on the EPCRA section 313 list.

 26. Fenoxaprop-ethyl. Hoechst-Celanese and Nor-Am Chemical indicate 

that the chronic interstitial nephritis reported at 80 ppm in the 3-

month dog study cited in the proposed rule ``was [a] non substancerelated, incidental finding since 12/24-months chronic treatment 

produced no comparable pathogenesis'' and that ``liver and kidney were 

not the target organs in dogs; effects were confined to reduced body 

weight gains at the highest concentration (75 ppm).''

 EPA disagrees with the commenters. The dietary levels of 

fenoxaprop-ethyl in the studies compared by the commenter were 0, 16, 

80, and 400 ppm and 0, 3, 15, and 75 ppm for the 3-month and 24-month 

studies, respectively; both studies are cited in the proposed rule. The 

microscopic findings in the 3-month study indicated that there was a 

dose response for chronic interstitial nephritis with inflammatory 

changes in the medulla and inner cortex. One half of the dogs were 

affected at 400 ppm, which is much higher than the highest dietary 

level in the 24-month study (75 ppm). Therefore, the inflammatory 

changes in the kidneys of treated dogs at 80 and 400 ppm in the 3-month 

study appear to be related to the ingestion of fenoxaprop-ethyl and, 

therefore, the kidney appears to be a target organ. The Agency did not 

cite liver effects in dogs as a basis for listing.

 EPA reaffirms that there is sufficient evidence for listing 

fenoxaprop-ethyl on the EPCRA section 313 list pursuant to EPCRA 

section 313(d)(2)(B) based on the available renal and developmental 

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 fenoxaprop-ethyl on the 

EPCRA section 313 list.

 27. Fenoxycarb. Ciba-Geigy Corporation and Miles Incorporated 

disagree with the listing of fenoxycarb on the EPCRA section 313 list 

because they believe that the adverse hepatic effects observed in mice 

and rats (3-month dietary study and 2-year oncogenicity study, both 

cited in the proposed rule) are not sufficiently serious to support 

listing. They note that no evidence of neoplastic lesions was reported 

in the chronic studies. They further state that delayed pinna unfolding 

in the reproductive toxicity study in rats cited in the proposed rule 

is a reflection of slower growth only, and therefore should not be used 

to support listing.

 The Agency disagrees that the evidence does not support a finding 

that section 313(d)(2)(B) are satisfied. The effects in the chronic 

studies include focal necrosis, changes which are considered by the 

Agency to be serious and potentially irreversible in nature. The liver 

effects in the subchronic study demonstrate the progression of changes 

leading to necrosis in the chronic study. The Agency considers these to 

be serious adverse effects.

 The developmental effects (slight delays in pinna unfolding) were 

said by the commenter not to reflect developmental effects since 

development was complete and function apparently unaffected, and that 

these effects were considered a reflection of slower growth (reduced 

body weights) as were the differences in relative organ weights. The 

Agency considers reduced rat pup body weight and slower growth with 

resulting differences in organ weight to be effects that are indicators 

of potential hazard. The Agency's Developmental Risk Assessment 

Guidelines (Ref. 6) state ``A change in offspring body weight is a 

sensitive indicator of developmental toxicity, in part because it is a 

continuous variable. In some cases, offspring weight reduction may be 

the only indicator of developmental toxicity. While there is always a 

question as to whether weight reduction is a permanent or transitory 

effect, little is known about the long-term consequences of short-term 

fetal or neonatal weight changes. Therefore, when significant weight 

reduction effects are noted, they are used as a basis to establish the 

NOAEL.'' EPA, therefore, considers evidence of delayed development, 

including delayed pinna unfolding and reduced body weight gain, to be 

significant signs of developmental toxicity.

 EPA reaffirms that there is sufficient evidence for listing 

fenoxycarb on the EPCRA section 313 list pursuant to EPCRA section 

313(d)(2)(B) based on the available hepatic and developmental toxicity 

data for this chemical. Therefore, EPA is finalizing the addition of 
fenoxycarb on the EPCRA section 313 list.

 28. Fomesafen. Zeneca Incorporated states that clear species 

differences are evident which would suggest that peroxisome 

proliferation and consequential liver toxicity is not relevant to man.

 Zeneca Incorporated did not provide any new evidence which supports 

the lack of relevance of these effects to man. In the absence of 

evidence to the contrary, the Agency believes that liver toxicity, 

which is associated with peroxisome proliferation is relevant to the 

assessment of potential human health effects. As there is evidence of 

hepatic toxicity in three different rat studies at varying dosages and 

durations and one dog study, EPA reaffirms that there is sufficient 

evidence for listing fomesafen on the EPCRA section 313 list pursuant 

to EPCRA section 313(d)(2)(B) based on the available hepatic toxicity 

data for this chemical. Therefore, EPA is finalizing the addition of 

fomesafen on the EPCRA section 313 list.

 29. n-Hexane. The National Oilseed Processors Association and The 

National Cotton Council of America contend that EPA failed to perform a 

detailed hazard evaluation that culminated in a weight-of-evidence 

determination regarding the toxicity of n-hexane as required under the 

Agency's Draft Hazard Assessment Guidelines (Ref. 11). Commenters state 

that portions of EPA's support document were taken almost verbatim from 

the Agency's IRIS data base and that the Agency appears to have relied 

extensively on the IRIS summary previously prepared for n-hexane. 

Commenters state that EPA should have evaluated the merits and 

conclusions of each study separately.

 The IRIS data base that EPA cited in support of the listing of nhexane represents the Agency's weight-of-evidence hazard determination 

for chemicals contained in the data base. The information contained in 

the IRIS data base was developed after the Agency's thorough review of 

the available data on n-hexane. Therefore, by relying on the IRIS data 

base EPA did not fail to perform a detailed hazard evaluation of nhexane as required by the Draft Hazard Assessment Guidelines (Ref. 11).

 The same commenters state that based on EPA's screening criteria 

included in the Draft Hazard Assessment Guidelines (Ref. 11) if a 

substance produces neurotoxic effects at doses that are greater than 

500 mg/kg/day (i.e., if the lowest observable adverse effect level is 

500 mg/kg/day), then the substance would be placed in the 

``insufficient for listing'' category. Commenters went on to state that 

most of the studies that EPA-cited in support of the listing of nhexane indicated that n-hexane produces neurotoxic effects only at very 

high dose levels and in many cases significant effects are only seen at 

doses that exceed 500 mg/kg/day.
 EPA believes that the commenters have misinterpreted the screening 

criteria contained in the Draft Hazard Assessment Guidelines (Ref. 11). 

The criteria are based on the MED levels which are not LOAELs. These 

MED values are derived from the LOAELs and, therefore, the direct

comparison of the screening criteria with LOAELs is inappropriate. 

However, EPA notes that significant effects from n-hexane are seen in 

quantities significantly less than 500 mg/kg/day, for example, a LOAEL 

of 204 mg/m<SUP>3 (58 ppm, LOAEL(ADJ) of 73 mg/m<SUP>3) was established 

for certain electrophysiological alterations in humans.

 These commenters made numerous specific comments concerning the 

adequacy of the studies summarized in IRIS used to support a chronic 

neurotoxicity finding for n-hexane. Commenters state that n-hexane is 

only toxic at very high levels if at all and that the data are not 

sufficient to support listing under EPCRA section 313. The commenters 

state that EPA failed to show how the data contained in the Support 

Document for the Addition of Chemicals from Section 112(b) of the Clean 

Air Act Amendments and Chlorinated Paraffins to EPCRA Section 313 (Ref. 

12) and the IRIS data base compare with the criteria for adding 

substances to the EPCRA section 313 list and how the Agency evaluated 

these studies in light of such criteria.

 In the Response to Comment Document (Ref. 14), EPA has addressed 

the specific comments concerning the adequacy of the studies used to 

support a chronic neurotoxicity finding for n-hexane. EPA agrees with 

the commenters that some of the studies included in the data base for 

n-hexane have limitations. However, the review of the comments and data 

have not changed EPA's position that the weight-of-evidence supports a 

finding of chronic neurotoxicity for n-hexane. The weight-of-evidence 

determination contained in the Agency's IRIS data base is the basis for 

determining that n-hexane can reasonably be anticipated to cause 

neurotoxicity in humans. EPA reaffirms that there is sufficient 

evidence for listing n-hexane on the EPCRA section 313 list pursuant to 

EPCRA section 313(d)(2)(B) based on the available neurotoxicity data 

for this chemical. Therefore, EPA reaffirms its determination that nhexane meets the listing requirements of EPCRA section 313.

 DuPont states that if EPA adds n-hexane (CAS No. 110-54-3) to the 

EPCRA section 313 list the Agency should clarify that isomers of nhexane are not included in the addition of n-hexane.

 EPA notes that the listing of n-hexane is for the straight chain 

(i.e., ``n'') isomer of hexane only as the chemical name and CAS number 

indicate. EPA does not believe that any special qualifier is needed to 

make the distinction between n-hexane and other isomers of hexane that 

are not included in this listing.
 30. 3-Iodo-2-propynyl butylcarbamate. Troy Corporation disagrees 

with the Agency's conclusion that no NOEL was achieved in the rat 

chronic toxicity/carcinogenicity study cited in the proposed rule. The 

commenter states that the non-neoplastic changes observed at the 40 mg/

kg/day and 80 mg/kg/day dose levels, while also present at the 20 mg/

kg/day dose level (lowest dose tested), were not statistically 

significant and therefore a NOEL was clearly established at this dose. 

The commenter also contends that non-neoplastic lesions of the stomach 

in rats are not relevant to humans.

 The Agency agrees with the commenter that the increases in 

nonneoplastic changes reported at 20 mg/kg/day were not statistically 

significant. However, the lack of a study NOEL was based upon decreased 

body-weight gain in males at 20 mg/kg/day (the lowest dose tested), not 

the nonneoplastic lesions. The non-neoplastic lesions reported at 40 

and 80 mg/kg/day are still considered serious enough to support a 

listing on the EPCRA section 313 list.

 The same commenter states that the simple findings of increased 

liver-to-body weight ratio found in the subchronic oral toxicity study 

in rats cited in the proposed rule as well as the incidence of nonneoplastic stomach irritation found in the chronic toxicity/

carcinogenicity study cited in the proposed rule in rats is not of 

sufficient seriousness to warrant EPCRA section 313 listing. The 

commenter claims that neither study cited demonstrates a sufficiently 

known or reasonably anticipated adverse health effect in humans to 

warrant section 313 listing.

 EPA disagrees. The commenter provides no basis for the contention 

that the nonneoplastic lesions of the stomach in rats are not relevant 

to humans. The incidence of these lesions was dose dependent, and was 

apparent at both sacrifices. Moreover, incidence increased with 

duration of treatment. The Agency considers this effect to be serious 

in nature and not readily reversible, and therefore the chemical 

warrants listing. The liver-to-body weight ratio from the subchronic 

study is not in itself sufficient to warrant listing on the EPCRA 

section 313 list but is provided as corroborating information.

 EPA reaffirms that there is sufficient evidence for listing 3-iodo2-propynyl butylcarbamate 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 3-iodo2-propynyl butylcarbamate on the EPCRA section 313 list.

 31. Iron pentacarbonyl. International Specialty Products contends 

that iron pentacarbonyl cannot reasonably be anticipated to cause

significant adverse human health effects at concentration levels that 
are likely to exist beyond facility site boundaries because it rapidly 

decomposes.

 EPA disagrees. The Agency considered the instability of iron 

pentacarbonyl under certain conditions, such as high temparature and/or 

prolonged exposure to direct sunlight, in its original modeling of 

exposure to iron pentacarbonyl cited in the proposed rule. EPA believes 

that its modeling was based on reasonable reactivity data. EPA 

reiterates that its exposure assessment indicates that iron 

pentacarbonyl can reasonably be anticipated to be present at facility 

boundaries at concentration levels that would cause an adverse effect. 

EPA reaffirms that iron pentacarbonyl is sufficient for listing on the 

EPCRA section 313 list pursuant to EPCRA section 313(d)(2)(A) based on 

available acute toxicity and exposure data for this chemical. 

Therefore, EPA is finalizing the addition of iron pentacarbonyl on the 

EPCRA section 313 list.

 32. Lithium carbonate. FMC Corporation contends that although 

lithium is toxic at therapeutic levels, naturally occurring levels are 

below the toxic range and therefore, lithium carbonate poses no threat

to the general population. The commenter also contends that there is no 

evidence that lithium carbonate 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 as a result of continuous, or frequently 

recurring, releases.'' Thus, the commenter feels that there is no basis 

for the listing of lithium carbonate on the EPCRA section 313 list.

 The Agency is not proposing to list lithium carbonate on the basis 

of acute effects but on the basis of developmental effects. Therefore, 

the Agency does not need to determine that lithium carbonate 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 as a result of 

continuous, or frequently recurring, releases,'' but rather must 

satisfy the section 313(d)(2)(B) criteria.

 As the commenter noted, lithium carbonate is a well-known 

developmental toxicant in both animals and humans at therapeutic levels 

and can cause life-threatening cardiac abnormalities in the developing 

human fetus. The commenter argues that lithium is toxic at therapeutic 

levels but not at naturally ``occurring levels.'' The Agency agrees 

that lithium may be toxic at therapeutic levels but also recognizes 

that use of lithium in a therapeutic setting is carefully controlled. 

Levels observed in a therapeutic setting may have little or no 

relationship to levels seen in an uncontrolled release setting. 
Furthermore, both the efficacy of lithium and its associated toxicity 

in humans is dependent upon individual sensitivity and can vary widely 

from individual to individual making uncontrolled release even more 

problematic. EPA reaffirms that there is sufficient evidence to list 

lithium carbonate under EPCRA section 313 pursuant to EPCRA section 

313(d)(2)(B) based on the available developmental toxicity data for 

this chemical. Therefore, EPA is finalizing the addition of lithium 

carbonate on the EPCRA section 313 list.

 33. Metam sodium. Buckman Laboratories International, Incorporated 

and Zeneca Incorporated state that the developmental toxicity studies 

cited in support of listing for metam sodium were rejected by the 

Agency to support the registration of a pesticide under FIFRA, and 

therefore should not be used. Further, they state that these data have 

been superseded by two new studies that have been accepted by the 

Agency, and that only the new studies should be considered for listing 

of metam sodium.

 The two earlier studies referred to by the commenters and cited in 

the proposed rule were submitted to the Agency under FIFRA. EPA's 

evaluation of those studies for purposes of FIFRA indicated that they 

did not fully satisfy the guidelines for developmental toxicity studies 

(Ref. 6); however, EPA did not reject these studies. EPA considers them 

sufficient as part of a weight-of-evidence evaluation, in determining 

the developmental toxicity of this chemical. The two new studies cited 

by the commenter have been reviewed by the Agency. The Agency found 

these studies to fully satisfy the guidelines (Ref. 6). However, these 

new studies do not supersede the previous studies nor did the Agency 

ignore them. Rather, all four studies were used together as part of the 

Agency's weight-of-evidence to evaluate the chemical. EPA does not 

ignore indications of potential toxicity simply because of study design 

flaws. A full discussion of these studies is contained in the Response 

to Comment Document (Ref. 14).

 Zeneca Incorporated further stated that the rat teratology study 

was a gavage study and not a dietary study. The commenter claims that 

this is an unrealistic route of human exposure.

 The commenter is correct in stating that the rat teratology study 

was a gavage study and not a dietary study. This does not diminish its 

appropriateness for consideration in the hazard assessment for listing. 

In fact, EPA requests that developmental toxicity studies be conducted 

by gavage, because this route allows for a more accurate assessment of 

the dose the animal actually receives.

 EPA reaffirms that there is sufficient evidence for listing metam 

sodium on the EPCRA section 313 list pursuant to EPCRA section 
313(d)(2)(B) based on the available developmental toxicity data for 

this chemical and its metabolite, carbon disulfide. Therefore, EPA is 

finalizing the addition of metam sodium on the EPCRA section 313 list.

 34. N-Methyl-2-pyrrolidone. IBM, American Automobile Manufacturers 

Association, and N-Methylpyrrolidone Producers Group object to the 

listing of N-methyl-2-pyrrolidone (NMP) on the EPCRA section 313 list. 

NMP Producers Group contends that the 2-generation reproductive study 

and the rabbit gavage developmental study cited in the proposed rule 

are flawed. NMP Producers Group further contends that the author of the 

2-generation rat reproductive study and an independent reviewer have 

reached similar conclusions.

 In reviewing the material submitted by the commenter, EPA failed to 

find a statement from the author that the study was flawed. The review 

of the 2-generation rat reproductive study by an independent reviewer 

did not find fault with the entire study but stated that it should not 

be used for risk assessment purposes. EPA agrees with this judgement 

but is not using this study for risk assessment purposes but rather as 

an indication of human health hazard. The Agency believes that the 

adverse effects seen in these studies are of sufficient seriousness to 

warrant listing under EPCRA section 313(d)(2)(B).

 NMP Producers Group also states that when the 2-generation 

reproductive study is evaluated taking into account the genetic 

fertility problem in the strain of male rats, the study establishes a 

NOAEL of 160 mg/kg rather than the NOAEL of 50 mg/kg cited in the 

proposed rule. The commenters also believe the study should not be 

considered because the variability in male fertility was not dosedependent.

 EPA does not agree that the NOAEL should be adjusted for the 

fertility problem of the strain of male rats used in the study. During

the first mating on which EPA based its concern level (F<INF>2a) the 

high-dose male group exhibited a 24 percent reduction in the mating 

index. In addition, there was a statistically significant, dose-related 

reduction in the male fertility index; thus, the index was 93.1, 72.4, 

72.4, and 46.7 in the control, low-, mid-, and high-dose groups, 

respectively. The control value in this study is 93.1 percent, well 

within acceptable limits for any reproductive effects study and as seen 

the reduction in mating index is dose-related being 72.4 percent in the 

low- and mid-dose groups and 46.7 percent in the high-dose group. With 

a control value of 93.1 percent and using the concurrent controls as an 

index of mating performance for the males in this study, the Agency 

feels that there is no reason to adjust the NOAEL of 50 mg/kg to 

account for reduced fertility in the test animals. During the second 
mating (F<INF>2b), the male high-dose group exhibited a 31 percent 

reduction in the mating index, and again, there was a statistically 

significant, dose-related reduction in the male fertility index (83.3, 

69.0, 60.0, and 34.5 in the control, low-, mid-, and high-dose groups, 

respectively). The female high-dose group exhibited a 28 percent 

reduction in the fertility index, and again, there was a statistically 

significant, dose-related reduction in the fecundity index (92.6, 74.1, 

64.3, and 50.0 in the control, low-, mid-, and high-dose groups, 

respectively). Again, the Agency does not feel that a control value of 

83.3 percent fertility index in the control animals is abnormal and is 

more concerned with the dose-related decrease in fertility as an 

indication that NMP is a reproductive toxicant. EPA is also concerned 

with the decrease in fecundity index in the females and does not feel 

that the control value of 92.6 percent warrants any adjustment of NOAEL 

for reduced fertility or mating ability among males in the study.

 The Agency also disagrees with NMP Producers Group's contention 

that decreases in male fertility observed are not dose dependent. The 

data presented above clearly show a correlation between dose and 

decreased fertility.

 NMP Producers Group claims that the effects of NMP administration 

manifested only in the second generation of animals.

 EPA disagrees and believes that effects were manifested in the 

first generation. There was a reduction in fertility in the F1 

generation, histological evidence of reproductive effects including 

hypospermia and significant systemic toxicity in the F1 generation. In 

addition, EPA does not believe that it is unusual to see increased 

severity in the second generation since animals have either been 

treated for 2 generations or are the offspring of treated animals and 

cumulative effects or effects on the reproductive system of the first 

generation animals may manifest in the second generation.

 NMP Producers Group further believes that NMP is not a 

developmental hazard because EPA's conclusion is based on observations 

from what the commenter claims is a flawed reproductive study. The 

commenter adds that a considerable body of evidence supports the 

conclusion that NMP is not uniquely toxic to a developing fetus.

 EPA's conclusions about the developmental toxicity of NMP are based 

upon a rabbit gavage study and the developmental portion of the 2-

generation reproductive study referred to above and cited in the 

proposed rule. The rabbit gavage study showed a significant increase in 

resorptions and malformations (misshapen skull bone and cardiovascular 

malformations). The LOAEL for developmental toxicity in this study was 

540 mg/kg and the NOAEL was 175 mg/kg. The developmental portion of the 
2-generation reproductive effects study showed evidence of 

developmental toxicity in both generations after exposure to 500 mg/kg 

as demonstrated by reduced litter size, reduced postnatal survival, and 

reduced pup body weight. The Agency believes that despite the flaws in 

the study, the data described above clearly show evidence of 

developmental toxicity. In addition, EPA believes that the body of 

evidence supports the finding that NMP is uniquely toxic to the 

developing fetus and the information available to the Agency both from 

the rat developmental study and rabbit gavage study is sufficient to 

list NMP on the EPCRA section 313 list.

 EPA reaffirms that there is sufficient evidence to list N-methyl-2-

pyrrolidone under EPCRA section 313 pursuant to EPCRA section 

313(d)(2)(B) based on available developmental and reproductive toxicity 

data for this chemical. Therefore, EPA is finalizing the addition of Nmethyl-2-pyrrolidone on the EPCRA section 313 list.

 35. Molinate. Zeneca Incorporated contends that the observations 

attributed to the 35 mg/kg/day dose level in the rat developmental 

toxicity study ``in fact occurred at 140 mg/kg/day, the highest dose 

tested and were thus a consequence of maternal toxicity.'' The 

commenter states that the NOEL for that study was 35 mg/kg/day.

 The Agency does not agree that the NOEL for this study was 35 mg/

kg/day. The NOEL for developmental toxicity was 2.2 mg/kg/day based on 

an increase in runting at the next highest doses, 35 and 140 mg/kg/day. 

The other adverse effects listed in the comments for this study 

occurred only at the highest dose tested (140 mg/kg/day). The NOEL for 

maternal toxicity was 35 mg/kg/day and that the effects on the pups 

(runting) occurred at a dose level lower than the dose level found to 

be maternally toxic.

 The same commenter stated that the issue of whether molinate is a 

reproductive toxin on the basis of its adverse effect on fertility in 

rodents has been very extensively investigated with studies in rabbits, 

dogs, monkeys, and man, and these studies have shown ``conclusively 

that the effects seen in rodents is [sic] not relevant to man.''

 While EPA agrees that there has been extensive testing of molinate 

with respect to fertility, the data on the rabbit and dog do not 

support the commenter's contention that the effects seen in rodents are 

specific only to rodents. For example, in each of the fertility studies 

in rabbits, both an increase in pre-implantation loss and abnormal 

sperm were observed. These two consistent [reproducible] observations 

are suggestive of fertility effects, are two of the same observations 

found in rats and, although not as dramatic as observed in rats, cannot 

be negated. In the chronic dog study, lesions in male reproduction 
organs and effects on sperm were observed, which demonstrate that, at 

least in the males, the gonads are target organs for molinate. The lack 

of any effect on the limited parameters assessed in the male monkey 

studies lends little credence to the argument since only male monkeys 

were exposed to molinate, and no reproduction studies have been 

performed to assess reproductive performance. Since molinate is 

reaching the gonads in all species, not only in rodents as the 

commenter claims, molinate can reasonably be anticipated to cause 

fertility/reproductive effects in humans. Further, animals are accepted 

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., <greek-a>2<greek-m>-globulin].

 The same commenter further contends that a NOEL of 2 mg/kg/day was 

established in the rat 2-year study, and that this study should not be 

used to evaluate the neurotoxicity of molinate because the study was 

not designed to evaluate that effect. Rather, the commenter contends 

that the ``definitive position on neurotoxicity has been determined by 

specific [neurotoxicity] studies.'' Zeneca Incorporated did not provide 

a reference for these ``specific studies.''

 EPA agrees that the NOEL for effects other than neurotoxic effects 

is 2 mg/kg/day in the chronic rat study. No NOEL for neurotoxic effects 

was established in that study. The LOEL for neurotoxicity in this study 

is 0.35 mg/kg/day. Although this study was not specifically designed to 

evaluate the neurotoxic effects of molinate, adverse neurological 

effects were reported. Further, they were substantiated by the findings 

from a 1-year study in dogs.

 The same commenter stated that the effects observed in the dog 

study were found at the highest dose administered for 1-year and were 

``largely a consequence of extended exposure'' and as such should not 

form a part of the EPCRA listing. The commenter implies that because 

this is a chronic adverse effect, the effect is not relevant to the 

EPCRA section 313 criteria.

 As specified in section 313(d)(2)(B), a chemical may be listed if 

it causes chronic toxicity. Thus, the comment is not relevant.

 EPA reaffirms that there is sufficient evidence for listing 

molinate on the EPCRA section 313 list pursuant to EPCRA section 

313(d)(2)(B) based on the available developmental, reproductive, and 

neurological toxicity data for this chemical. Therefore, EPA is 

finalizing the addition of molinate on the EPCRA section 313 list.

 36. Nitrate compounds (proposed as nitrate ion). American 

Automobile Manufacturers Association, Merck, and the Department of 

Energy disagree with EPA's proposal to list nitrate ion because an ion 
is not a chemical. Merck further states that nitrate ion ``exists only 

in aqueous media.'' The Chevron Companies, the Department of Energy, 

Chemical Manufacturers Association, and Air Products and Chemicals, 

Incorporated contend that in proposing to add nitrate ion to EPCRA 

section 313 the Agency actually proposed to add a category of chemicals 

that dissociate to generate nitrate ion. EPA agrees with the commenters 

that an ion does not meet the definition of a chemical for purposes of 

listing on the EPCRA section 313 list and that by proposing nitrate ion 

the Agency had, in effect, proposed the addition of a category of 

nitrate compounds that dissociate in water that are reportable only 

when in aqueous solution. Thus based on the comments provided by the 

commenters, the Agency is finalizing the addition of the following 

category: water dissociable nitrate compounds (reportable only when in 

aqueous solution). Qualifiers of this sort have been used to define the 

form of a chemical for which reports should be submitted, e.g., zinc 

(fume or dust). The qualifier following this listing indicates that 

only water dissociable nitrate compounds that are manufactured, 

processed, or otherwise used as an aqueous solution at a facility are 

subject to reporting. As with all other aspects of EPCRA section 313 

reporting, only the weight of the listed chemical is subject to 

threshold determinations. That determination does not include, for 

example the weight of the water or any other constituent in the 

solution other than the nitrate compound. Beyond the threshold 

determination, the amounts reportable on Form R should only include the 

mass of the nitrate portion of the compound in solution. This approach 

is consistent with guidance given for determining threshold and release 

amounts for metal compounds. EPA recognizes that most monitoring data 

available measure only the dissociated nitrate ion released and not the 

amount of total nitrate compounds from which the nitrate ion 

dissociated. Reporting of the amount of the total water dissociable 

nitrate compound in wastes would be complicated when more than one 

substance contributes to the nitrate ion content of the waste and when 

the nitrate compound is converted to a different substance due to waste 

treatment or other processes. It is therefore reasonable to require 

reporting of only the nitrate ion released in order to avoid confusion 

over the meaning of total compound released.

 EPCRA section 313 requires threshold determinations for chemical 

categories to be based on the total of all chemicals in the category 

manufactured, processed, or otherwise used. For example, a facility 

that manufactures three members of a chemical category would count the 

total amount of all three chemicals manufactured towards the 

manufacturing threshold for that category. One report is filed for the 
category and all releases are reported on this form.

 In the proposed rule, EPA discussed both the human health and 

environmental adverse effects attributable to nitrates. EPA continues 

to be concerned about the potential environmental impacts of nitrates. 

In today's action, EPA is adding nitrate compounds based on the adverse 

human health effects that the nitrate moiety causes. Nitrate causes 

methemoglobinemia. Methemoglobinemia, like carbon monoxide, interferes 

with the oxygenating capacity of the blood resulting in an under supply 

of oxygen to the tissues. In adults, cyanosis to lips and mucous 

membranes occurs at a level of 1.5 g/dL (10 percent saturation in an 

adult with normal hemoglobin levels). Levels between 30 percent and 50 

percent saturation in adults produce depression of the cardiovascular 

and central nervous systems; levels between 50 percent and 70 percent 

cause stupor, convulsions and respiratory depression and levels above 

70 percent are usually fatal. Because of increased requirement for 

oxygen in growing tissue and because of decreased blood volume in 

infants, they are much more sensitive to nitrate ion toxicity than 

adults. Infants have a lower activity of methemoglobin reductase and 

thus are more susceptible. Consequently adverse effects are seen at 

much lower levels in infants than in adults. Irreversible damage to 

organs such as the heart or brain, and the development of coronary 

artery disease or pulmonary disease are more likely to develop in 

infants because the anoxia caused by methemoglobinemia can occur more 

rapidly and have more devastating effects in growing tissue than in the 

``static'' tissue of the adult body. EPA believes that these are 

serious adverse effects that satisfy the criteria of EPCRA section 

313(d)(2)(B).

 37. Ozone. Many commenters opposed the addition of the CAA criteria 

pollutants (sulfur dioxide, sulfur trioxide (SO<INF>x), nitric oxide 

and nitrogen dioxide (NO<INF>x), carbon monoxide (CO), and ozone) to 

the EPCRA section 313 list since extensive data on these chemicals is 

already collected under the CAA.

 EPA agrees with the commenters that there are many complex issues 

associated with the extensive collection of data on these chemicals 

under the Clean Air Act. Therefore, EPA is deferring the listing of 

these chemicals for possible addition at a later time to address some 

of the issues involving the availability of data collected under the 

CAA. The Agency does not believe, however, that the listing of ozone 

should also be deferred. Emissions of ozone, also a criteria pollutant, 

are not captured under the CAA. The CAA mandates the collection of data 

on the releases of VOCs (VOCs react in the troposphere to generate 

ozone and other air pollutants), which are regulated to maintain the 
ambient air quality standard for ozone. EPA believes there are many 

other significant uses of ozone (e.g., wastewater treatment, bottled 

water purification, and chemical intermediate) that would be captured 

by EPCRA section 313 reporting. Accordingly, EPA does not believe that 

the finalization of ozone should be deferred. EPA reaffirms that ozone 

meets the EPCRA section 313(d)(2) criteria pursuant to EPCRA section 

313(d)(2)(B) and 313(d)(2)(C) based on the available toxicity data for 

this chemical. Therefore, EPA is finalizing the addition of ozone on 

the EPCRA section 313 list.

 38. Pebulate. Zeneca Incorporated comments that the neurological 

effects noted in the 1-year feeding study in dogs cited in the proposed 

rule occurred at the highest dose level (100 mg/kg/day), which was, by 

design, a toxic dose. Thus, the commenter claims that there is no 

reasonable hazard.

 The Agency disagrees. Although the highest dose tested is designed 

to elicit toxicity in the dogs, the presence of Wallerian type 

degeneration of the white matter of the spinal cord at the 100 mg/kg/

day dose level in dogs of both sexes is of considerable seriousness and 

cannot be dismissed only because it occurred at the highest dose 

tested. Although the dose eliciting degeneration of the spinal cord was 

the highest dose tested, 100 mg/kg/day, these adverse effects are of 

sufficient seriousness to warrant listing based upon the potential for 

similar effects in humans.

 In this study, the NOEL for the Wallerian type neurological lesions 

is 50 mg/kg/day. However, the NOEL in males is less than 5 mg/kg/day 

(LOEL based on findings of abnormal behavior, ataxia, severe 

convulsions, and congestion in both kidneys in one dog). In females, 

the NOEL was 5 mg/kg/day and the LOEL was 25 mg/kg/day with occurrence 

of blood in feces, increased absolute and relative liver weight, 

increase in severity of lipofuscin deposition in kidneys, and 

hemosiderin deposition in liver and spleen.

 EPA reaffirms that there is sufficient evidence for listing 

pebulate on the EPCRA section 313 list pursuant to EPCRA section 

313(d)(2)(B) based on the available neurological toxicity data for this 

chemical. Therefore, EPA is finalizing the addition of pebulate on the 

EPCRA section 313 list.

 39. Permethrin. Zeneca Incorporated states that the hepatic effects 

noted in the liver of rats and dogs are adaptive rather than toxic 

responses to the pyrethroid. The commenter further claims that there 

were no changes in liver weight relative to body weight.

 EPA does not agree that the incidence of liver weight increase is 

not a significant effect, or that there were no changes in liver weight 
relative to body weight. The liver weights, relative to bodyweight, 

were increased in all treated groups in the 2-year rat study. EPA 

believes that the hepatic changes noted in these studies represent a 

significant adverse effect.

 The same commenter contends that in the 2-year rat study cited in 

the proposed rule, ``the NOEL is also incorrectly stated as 5 mg/kg/

day, where EPA states a LOEL of 100 mg/kg/day.''

 The Agency disagrees with the commenter. The NOEL and LOEL should 

be 5 and 100 mg/kg/day, respectively. At 100 mg/kg/day there was an 

increase in alkaline phosphatase, liver weight and cellular swelling of 

the liver (indicative of typical smooth endoplasmic reticulum 

proliferation), and one male in the low dose group was affected, focal 

inflammation with degenerative change in the zona fasciculate and 

swelling and vacuolation ofcells in the zona reticularis of the 

adrenals and reduced body weight in females. EPA considers these to be 

serious adverse effects.

 EPA reaffirms that there is sufficient evidence for listing 

permethrin on the EPCRA section 313 list pursuant to EPCRA section 

313(d)(2)(B) based on the available hepatic 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 permethrin on the EPCRA section 313 list.

 40. Phosphine. Coors Brewing Company states that only liquid 

phosphine can cause the health effects necessary to support a listing 

on the EPCRA section 313 list.

 Phosphine is a gas (the boiling point is negative 87.4 deg.C); it 

only occurs as a liquid when placed under reduced temperature and/or 

pressure. The acute toxicity data used to support the listing of 

phosphine is based on exposure to phosphine in the air (i.e., phosphine 

gas). Thus, EPA does not agree that only liquid phosphine could cause 

the health effects necessary to support listing under EPCRA section 

313. EPA reaffirms that there is sufficient evidence for listing 

phosphine on the EPCRA section 313 list pursuant to EPCRA section 

313(d)(2)(A). Therefore, EPA is finalizing the addition of phosphine on 

the EPCRA section 313 list.

 41. Polychlorinated alkanes (proposed as chlorinated paraffins). 

EPA proposed the addition of clorinated paraffins that consisted of 

polychlorinated alkanes. Occidental Chemical Corporation and the 

Chlorinated Paraffins Industry Association state that the proposed 

chlorinated paraffins category is really a category of chlorinated 

hydrocarbons since it covers a broad range of chlorinated hydrocarbons 

including chlorinated paraffins and chlorinated <greek-a>-olefins.
 EPA believes that there may be confusion over what is covered by 

the chlorinated paraffins category, as named, because the name 

chlorinated paraffins identifies a particular feedstock used to make 

this class of compounds. However, as discussed below, EPA believes that 

the chlorination of paraffins and <greek-a>-olefins results in products 

that do not differ significantly structurally, physically, or 

toxicologically. EPA believes that, rather than name the category based 

on one of the feedstocks used to make these compounds, a more 

appropriate name for the category is one that describes the actual 

members of the category. Therefore, because the members of this 

category are alkanes containing three or more chlorines, EPA is 

renaming this category polychlorinated alkanes. The new category name 

will not expand the scope of the category. EPA believes that the 

toxicity data for chlorinated paraffins is sufficient for all 

polychlorinated alkanes that fall within the same carbon number and 

chlorine content regardless of what materials where used to manufacture 

them.

 Courtlands Aerospace, ELF Lubricants North America, Incorporated, 

Tower Oil & Technology Company, National Oil Products, Incorporated, 

OxyChem, the American Automobile Manufacturers Association, the 

Association of International Automobile Manufacturers, Incorporated, 

the Specialty Steel Industry of the United States, the Independent 

Lubricant Manufacturers Association, Engineered Lubricants, Sealed Air 

Corporation, American Federation of Labor and Congress of Industrial 

Organizations, Chlorinated Paraffins Industry Association, and Far West 

Oil Company, Incorporated contend that the available toxicity data is 

insufficient to support the addition of chlorinated paraffins to EPCRA 

section 313. Some of these commenters state that they do not believe 

that EPA should create chemical categories such as that proposed for 

chlorinated paraffins on the EPCRA section 313 list. Some of these 

commenters state that the long-chain chlorinated paraffins have not 

been classified as ``probable human carcinogens'' by NTP or IARC. Some 

of these commenters made numerous specific comments concerning the 

adequacy of the studies used to support EPA's listing of chlorinated 

paraffins and pointed out flaws in the data for both long and shortchain chlorinated paraffins. Some of the flaws that the commenters 

allege concern the studies used to support the listing of the shortchain species and included: (1) Kidney tumors in male rats may be due 

to binding to <greek-a>2<greek-m>-globin, a male rat-specific protein; 

(2) route of administration (forced gavage feeding); (3) corn oil as a 

vehicle; (4) use of the B6C3F1 mouse; (5) short-chain chlorinated 

paraffins are non-genotoxic in a variety of short-term assays; (6) 
peroxisome proliferation, liver growth in male and female rats and mice 

and stimulation of replicative DNA in rodents have not been shown to 

occur in guinea pigs indicating that they are mouse and rat specific 

and have no relation to tumor formation in humans; and (7) thyroid 

tumors may be a consequence of a perturbation in the metabolism of 

thyroxine. Some of the commenters contend that only the data on shortchain chlorinated paraffins are sufficient to justify a listing on the 

EPCRA section 313 list and that EPA should limit the category to just 

the short-chain species.

 a. Long-chain chlorinated paraffins. IARC has not classified the 

long-chain chlorinated paraffins because there is insufficient evidence 

that they cause cancer in treated animals. The NTP found no evidence of 

cancer in male rats treated with 1,875 or 3,750 mg/kg/day for 24 months 

with long-chain chlorinated paraffins. Female rats treated with 900 mg/

kg/day showed marginal increases in adrenal gland tumors; female rats 

treated with 5,000 mg/kg/day had marginal increases in liver tumors. 

The only significant increase in tumor formation occurred in male mice 

which had a significant increase in malignant lymphomas. After further 

evaluation of the available data and considering the available 

statistics, the high background rate of lymphoma in the strain of mice 

used in the NTP bioassay and the statements made by the NTP Working 

Group and the Quality Assessment Narrative, which was submitted by the 

commenters, EPA agrees that there is insufficient evidence to conclude 

that the malignant lymphomas observed in male mice were treatment 

related and that long-chain chlorinated paraffins should not be 

classified as potential carcinogens. Therefore, the Agency concludes 

that there is insufficient evidence to list long-chain chlorinated 

paraffins on the EPCRA section 313 list.

 b. Short-chain chlorinated paraffins. IARC has classified the 

short-chain chlorinated paraffins as Group 2B, i.e., sufficient 

evidence for carcinogenicity in animals and probably carcinogenic in 

humans. Detailed responses to all of the comments concerning the 

toxicity of the short-chain species are contained in the Response to 

Comment Document (Ref. 14). Summaries of the responses to the most 

significant comments concerning flaws in the studies used to support 

the listing of the short-chain species are provided below.

 (1) The Agency agrees that the kidney tumors observed in rats are 

most likely not relevant to tumor formation in man because the male rat 

kidney possess a unique protein, <greek-a>2<greek-m>-globulin which has 

been shown to be responsible for the development of rat liver kidney 

tumors, not only after administration of short-chain chlorinated 

paraffins but after administration of many other chemicals also. 
However, to state that chlorinated paraffins bind to a protein which is 

similar to <greek-a>2<greek-m>-globulin and that this binding is not 

seen in guinea pigs as evidence that kidney tumor formation is not 

relevant to human tumor formation in this instance is not a convincing 

argument.

 (2) The Agency agrees that forced gavage feeding may not be a 

relevant route of administration when one is using the data for human 

risk assessment. In this instance, the data are being used as an 

indication of potential human hazard and EPA accepts the data as being 

indicative of such potential.

 (3) EPA believes that corn oil is an accepted vehicle of 

administration for many in vivo studies because it is relatively inert 

and has not been shown to interact with test agents.

 (4) The B6C3F1 mouse is the accepted test species of the NTP and 

EPA has no reason to question the NTPs choice of test species nor to 

discount results of cancer bioassays using this species.

 (5) EPA does not believe that non-genotoxicity is a sufficient 

reason to dismiss the relevance to man of tumor formation by the shortchain chlorinated paraffins. Non-genotoxicity may be a factor in 

selecting a model to use for dose response estimation, once tumor 

formation has been established, but it is not a reason to disregard the 

significance of tumors which are formed by agents which are nongenotoxic in short-term tests.

 (6) The Agency is not convinced that failure to observe liver 

growth, peroxisome proliferation in hepatocytes and stimulation of 

replicative DNA in guinea pigs is proof that these effects are specific 

to rats and mice and have no bearing on tumor formation in humans.

 (7) The Agency agrees that there was a perturbation of thyroxine 

levels in treated animals but does not agree that the observed tumors 

are therefore irrelevant.

 Therefore, the Agency finds that there is sufficient evidence for 

listing short-chain chlorinated paraffins on the EPCRA section 313 list 

pursuant to EPCRA section 313(d)(2)(B) based on the available 

carcinogenicity data for these chemicals.

 i. Ecotoxicity data. Courtaulds Aerospace, Occidental Chemical 

Corporation, and the American Automobile Manufactures Association 

contend that ecotoxicity data are only available for the short-chain 

(10 to 13 carbons, 59 percent chlorine) chlorinated paraffins. The 

commenters object to EPA assuming the same ecotoxicity for all members 

of the chlorinated paraffin category because of the potential 

difference in effects related to chain length and chlorine content.

 Although it was stated as such in the proposed rule, EPA did not 
intend to equate the ecotoxicity of the short-chain chlorinated 

paraffins with the ecotoxicity of other members of the category. The 

ecotoxicity data on the short-chain chemicals was provided as further 

support for the listing of the short-chain chemicals. However, as EPA 

is not finalizing the addition of the long-chained species, this issue 

is no longer relevant.

 ii. Chlorinated paraffins versus chlorinated <greek-a>-olefins. 

OxyChem, the American Automobile Manufacturers Association, the 

Association of International Automobile Manufacturers, the Independent 

Lubricant Manufacturers Association, and the Chlorinated Paraffins

Industry Association correctly state that EPA's proposed definition of 

chlorinated paraffins does not exclude chlorinated <greek-a>-olefins. 

The commenters further contend that chlorinated paraffins and 

chlorinated <greek-a>-olefins are distinctly different chemicals with 

different physical, chemical, and biological properties.

 The information provided by the commenters does not substantiate 

their claim that chlorinated paraffins and chlorinated <greek-a>-

olefins are distinctly different chemicals with different physical/

chemical properties. The main difference between chlorinated paraffins 

and chlorinated <greek-a>-olefins that EPA is aware of is that 

chlorinated paraffins, typically manufactured from paraffin mixtures, 

are also mixtures whereas individual chlorinated <greek-a>-olefins can 

be manufactured in moderate to high purity. The issue is whether a pure 

chlorinated <greek-a>-olefin falls within the range of structural 

characteristics that vary in a chlorinated paraffin mixture. In this 

case, EPA believes that there are no significant structural differences 

between chlorinated paraffins and chlorinated <greek-a>-olefins. Both 

are primarily linear hydrochlorocarbons, and the degree of chlorination 

of both groups of substances can be controlled. Sixty percent 

chlorination of 1-dodecene, for example, would yield a product with the 

formula C<INF>12H<INF>19Cl<INF>7 and a molecular weight of 

approximately 411. Sixty percent chlorination of the short-chain grade 

paraffin mixture would yield a mixture of products with an average 

formula of C<INF>12H<INF>19Cl<INF>7 and an average molecular weight of 

approximately 411.

 The commenters claim that the chlorine positions in chlorinated 

<greek-a>-olefins differ significantly compared to the chlorine 

positions in chlorinated paraffins. EPA does not believe that 

chlorination at carbons 1 and 2 of the <greek-a>-olefins makes a 

significant difference in the majority of the isomers formed by both 

reactions and even if it did, there are no data that indicate that 

having two of the chlorines at carbons 1 and 2 is significant from a 
toxicity standpoint. The commenters do not substantiate their claim 

(mass spectral data submitted by one commenter is inconclusive and 

cannot be used in support, for or against, the commenter's position); 

EPA is not aware of experimental evidence that suggests that the 

possible variations in chlorine positions between the chlorinated 

paraffins and the chlorinated <greek-a>-olefins differ significantly 

from the variations possible within these two groups of substances. 

Since for the <greek-a>-olefins the first two chlorines are added at 

carbons 1 and 2, the relative amounts rather than type of each isomer 

formed may differ between the chlorination of paraffins and <greek-a>-

olefins, especially as the degree of chlorination decreases.

 The commenters' claim that chlorinated <greek-a>-olefins are 

distinctly different from chlorinated paraffins because their physical 

properties are very different is unjustifiable. As discussed in detail 

in the Response to Comment Document (Ref. 14), the physical properties 

of discreet chemicals cannot be compared to those of chemical mixtures. 

The commenters do not discuss specific differences between chlorinated 

paraffins and chlorinated <greek-a>-olefins and therefore do not 

substantiate their claim. They do, however, elaborate on the 

differences between structures within the chlorinated paraffins group, 

particularly those structures that represent the extremes in the 

C<INF>10 to C<INF>30 range. This discussion is therefore more relevant 

to the issue of listing categories versus individual chemicals 

discussed subsequently and does not address the issue of differences in 

the physical properties between chlorinated paraffins and chlorinated 

<greek-a>-olefins, discussed previously. Furthermore, EPA believes that 

the specific differences between structural extremes within the 

chlorinated paraffins group that the commenters elaborate on are trends 

that are also observed between structural extremes within the 

chlorinated <greek-a>-olefins group.

 A valid comparison of physical property data can only be made 

between two discreet substances of known purity or, in some cases, 

between two mixtures of chemicals with well defined compositions. EPA 

believes that an <greek-a>-olefin and a paraffin, both with the same 

chain length and both with the same degree of chlorination, are 

essentially identical structurally (especially if the degree of 

chlorination is high); the same isomers can be predicted for the 

chlorination of an <greek-a>-olefin and a paraffin of the same chain 

length. The physical properties of chlorinated <greek-a>-olefins and 

the corresponding chlorinated paraffins are therefore expected to be 

very similar. The differences in the chemical and physical properties 

that the commenters refer to are largely or completely due to the fact 
that the chlorinated paraffins are mixtures of different chain lengths 

while the chlorinated <greek-a>-olefins typically are composed of a 

single chain length.

 iii. Category definition. Since EPA has determined that only the 

short-chain species meet the listing requirements of EPCRA section 313, 

the polychlorinated alkanes category will be defined by the following 

formula and description: C<INF>xH<INF>2x-yCl<INF>y; where x = 10 to 13 

and y = 3 to 12 and where the average chlorine content ranges from 40 

to 70 percent with the limiting molecular formulas set at 

C<INF>10H<INF>19Cl<INF>3 and C<INF>13H<INF>16Cl<INF>12.

 EPCRA section 313 requires threshold determinations for chemical 

categories to be based on the total of all chemicals in the category 

manufactured, processed, or otherwise used. For example, a facility 

that manufactures three members of a chemical category would count the 

total amount of all three chemicals manufactured towards the 

manufacturing threshold for that category. One report is filed for the 

category and all releases are reported on this form.

 42. Polycyclic aromatic compounds. In the proposed rule, EPA 

proposed the addition of a delineated polycyclic aromatic compounds 

(PAC) category that consisted of 28 polycyclic aromatic compounds. 

Alternatively, EPA proposed the addition of a PAC category based on the 

following broad definition: ``includes all chemical species from the 

polycyclic aromatic hydrocarbon, aza-polycyclic, thio-polycyclic, or 

nitroarene families where polycyclic means three or more fused rings. 

More specifically, it means any combination of three or more fused six 

or five membered hydrocarbon rings with at least two or more rings 

being aromatic. The structure may contain fused non-aromatic 5-membered 

rings, a ring nitrogen, a ring sulfur, one or more attached nitro 

groups, or one or more attached alkyl groups'' (January 12, 1994, 59 FR 

1832).

 Monsanto, The Chevron Companies, Amoco Corporation, Armco Steel 

Company, Mobil Oil Corporation, UNOCAL, Pennzoil, Phillips Petroleum 

Company, American Petroleum Institute, and the Department of Energy 

object to listing polycyclic aromatic compounds as a category and 

recommend that EPA list them separately as individual chemicals. 

American Coke and Coal Chemicals Institute and Mobil Oil Corporation 

state that if the chemicals are not individually listed then the 

proposed delineated category should be used. Koch Industries 

Incorporated, Texaco Incorporated, and the Wisconsin Department of 

Natural Resources object to the alternative proposal for a PAC category 

with the broad definition and recommend that EPA implement the 

delineated category approach. The Natural Resources Defense Council 
recommends that EPA use the broad category definition.

 EPA believes that polycyclic aromatic compounds should be listed as 

a delineated category rather than listed individually or defined under 

the broad category definition. Most if not all of the polycyclic 

aromatic compounds included in the category are not intentionally 

manufactured, they are byproducts and impurities from various 

industrial processes. As such, they occur as complex mixtures that are 

typically released or transferred together. EPA believes that for this 

class of compounds a category listing is the most appropriate way to 

track releases and transfers under EPCRA section 313 because members of 

this category are structurally similar and induce a similar toxic 

effect.

 The American Petroleum Institute, Mobil Oil Corporation, American 

Coke and Coal Chemicals Institute, Koch Industries Incorporated, 

Monsanto, The Chevron Companies, and Amoco Corporation state that 

analytical methodologies do exist to identify specific chemicals such 

as those proposed for the delimited PAC category; however, these 

analytical methodologies require a chemical-by-chemical analysis. They 

add that since a chemical-by-chemical analysis is required, there would 

be no reduction in the reporting burden for either a category based on 

the broad definition or for the proposed delimited category.

 EPA proposed the broad category definition approach as a possible 

way to reduce the reporting burden for a PAC category. However, the 

majority of the industries that would have to report do not agree that 

this will result in a reduction of their reporting burden, they believe 

that it will cause confusion over what chemicals are covered by this 

category, and do not believe that analytical methodologies exist to 

identify all of the thousands of chemicals that would be covered by a 

PAC category based on the alternative broad definition. EPA is 

therefore not finalizing the alternative proposal to create a PAC 

category based on the broad definition but is finalizing the proposed 

delimited PAC category as explained above.

 EPA believes that although it may be necessary to perform a 

chemical- by-chemical analysis for members of this delimited category, 

the most appropriate way to track releases and transfers under EPCRA 

section 313 is by creating this category as explained above.

 The Chevron Companies, Amoco Corporation, Mobil Oil, UNOCAL, 

Pennzoil, and the American Petroleum Institute state that polycyclic 

aromatic compounds share some physical and chemical properties but that 

this does not necessarily imply similar toxicities. These commenters 

state that the toxicity potentials vary widely among the polycyclic 

aromatic compounds but that the public tends to associate all members 
of a category with the most toxic chemical in the category.

 EPA recognizes that similarities in physical and chemical 

properties do not necessarily indicate that the ability to induce 

carcinogenic effect among the members of the polycyclic aromatic 

compounds category are identical. However, these compounds are 

chemically similar, induce the same toxicological effect 

(carcinogenicity), and typically are produced, released, and 

transferred as complex mixtures rather than individual chemicals. EPA 

therefore believes that it is appropriate to consider these compounds 

as a category.

 Mobil Oil Corporation contends that 11 of the PACs proposed for 

listing have been reviewed by IARC and found to have insufficient data 

in animals and no data in humans making the overall evaluation IARC-3 

or inadequate evidence of carcinogenicity.

 The 11 chemicals the commenter cites as being classified by IARC as 

a group 3 chemical, i.e., the chemical is not classifiable as to its 

carcinogenicity, are: carbazole (CAS No. 86-74-8); cyclopenta(cd)pyrene 

(CAS No. 27208-37-3); dibenz(a,c)anthracene (CAS No. 215-58-7); 

dibenz(a,j)anthracene (CAS No. 224-41-9); dibenzo(a,e)fluoranthene (CAS 

No. 5385-75-1); 2-methylchrysene (CAS No. 3351-32-4); 3-methylchrysene 

(CAS No. 3351-31-3); 4-methylchrysene (CAS No. 3351-30-2); 6-

methylchrysene (CAS No. 1705-85-7); 2-methylfluoranthene (CAS No. 

33543-31-6); and 1-nitropyrene (CAS No. 5522-43-0). The commenter is 

correct in that 10 of these 11 compounds have been classified as IARC 

group 3 chemicals. The 11th compound, 1-nitropyrene (CAS No. 5522-43-

0), was classified by IARC as a Group 2B chemical, i.e., a possible 

human carcinogen. The IARC classification and a review of the data 

indicate that the data is sufficient to support the listing of this 

chemical on the EPCRA section 313 list pursuant to EPCRA section 

313(d)(2)(B). A second compound, dibenzo(a,e)fluoranthene (CAS No. 

5385-75-1) was classified by EPA as a B2 category chemical, the 

chemical is a probable human carcinogen, which justifies its addition 

to EPCRA section 313 pursuant to EPCRA section 313(d)(2)(B). Upon 

further review of the other 9 IARC group C chemicals, the Agency 

believes that a more detailed review of their relationship to the 19 

PACs for which cancer data is available and is sufficient is necessary 

before they can be placed on the list on the basis of structure alone. 

Therefore, EPA will not add these 9 chemicals to the EPCRA section 313 

list at this time and the delineated category will consist of the other 

19 chemicals proposed for this category.

 EPCRA section 313 requires threshold determinations for chemical 

categories to be based on the total of all chemicals in the category 
manufactured, processed, or otherwise used. For example, a facility 

that manufactures three members of a chemical category would count the 

total amount of all three chemicals manufactured towards the 

manufacturing threshold for that category. One report is filed for the 

category and all releases are reported on this form.

 43. Potassium dimethyldithiocarbamate. Buckman Laboratories 

International, Incorporated states that the proposed listing of the 

chemical was based on the results of the rat and rabbit teratology 

studies, cited in the proposed rule, although neither study 

demonstrates evidence of developmental toxicity. They contend that the 

findings in the developmental studies should be considered an artifact.

 The findings in rabbits cannot be considered artifacts because 

there is a dose-related increase in the severity of developmental 

effects at 38 and 77 mg/kg. At 38 mg/kg, developmental toxicity was 

characterized by increased post implantation loss, malformations, and 

sternebral malalignments. At 77 mg/kg, there were reports of severe 

fetal and embryo lethality. EPA did not cite a rat study in the 

proposed rule as the commenter claims.

 EPA reaffirms that there is sufficient evidence for listing 

potassium dimethyldithiocarbamate on the EPCRA section 313 list 

pursuant to EPCRA section 313(d)(2)(B) based on the available 

neurological toxicity data for this chemical. Therefore, EPA is 

finalizing the addition of potassium dimethyldithiocarbamate on the 

EPCRA section 313 list.

 44. Prometryn. Ciba-Geigy Corporation states that marked renal and 

hepatic degenerative changes were noted in the high-dose dogs only in 

the 2-year dog study cited in the proposed rule. The commenter further 

claims that although minor liver effects were seen in rats in the 28-

day study cited in the proposed rule, there were no liver effects in 

rats after 90 days at dose levels up to 5,000 ppm. This 90-day study 

that the commenter cited was not cited by EPA in the proposed rule. 

Thus, the commenter does not believe that the data support the addition 

of this chemical to the EPCRA section 313 list.

 EPA disagrees with the commenter. In the 2-year dog feeding study, 

prometryn induced degenerative changes in liver and kidney and bone 

marrow atrophy at 37.5 mg/kg/day (LOEL, the NOEL is 3.75 mg/kg/day). 

Although the dose eliciting degenerative changes in liver and kidney 

and bone marrow atrophy was the highest dose tested, these adverse 

effects are of sufficient seriousness to warrant listing based upon the 

potential for similar effects in humans. Further, the findings of the 

2-year dog study and the 28-day rat study, cannot be discounted based 

solely on of the results of the 90-day study referred to by the 
commenter. Rather EPA has considered all of the data in concluding that 

prometryn meets the criteria for addition to the EPCRA section 313 

list.

 The commenter questions the use of the rabbit developmental 

toxicity study because only a slight effect (if real) was noted at the 

highest dose tested, and was not statistically significant. Although 

the use of the rabbit developmental toxicity study may not be 

justified, and the potential for developmental effects therefore not 

supported, EPA reaffirms that there is sufficient evidence for listing 

prometryn on the EPCRA section 313 list pursuant to EPCRA section 

313(d)(2)(B) based on available hepatic, renal, and bone marrow 

toxicity data. Therefore, EPA is finalizing the addition of prometryn 

on the EPCRA section 313 list.

 45. Propachlor. Monsanto contends that the developmental toxicity 

study in rabbits cited in the proposed rule was a study that was 

rejected by the Agency. Monsanto further stated that in this study ``a

slight decrease in viable fetuses, slight increase in post-implantation 

loss, and slight decrease in mean fetal weight was noted at the highest 

dose tested (116.7 mg/kg/day) which caused severe treatment-related 

maternal toxicity including death. An equivocal increase in postimplantation loss on a percent basis was noted in the mid-dose (58.3 

mg/kg/day) level. Marginal developmental effects that were seen were 

not statistically significant and were within the historical control 

limits. Propachlor does not produce any observable maternal or fetal 

toxicity at 5.8 or 58.3 mg/kg/day. In addition, propachlor does not 

cause developmental toxicity in rats.'' Monsanto concluded that, based 

on the ``weight of evidence from the rat and rabbit studies, there does 

not appear to be any developmental risk to humans.''

 The Agency does not concur with the commenter's statement that 

``propachlor does not produce any observable maternal or fetal toxicity 

at 5.8 or 58.3 mg/kg/day dose levels,'' nor with the statement that 

``the marginal developmental effects that were seen were .... within 

the historical control limits.'' The Agency's rationale for the 

disagreements are as follows:

 In a developmental toxicity study in rabbits, oral administration 

of propachlor at 116.7 mg/kg/day caused maternal toxicity as evidenced 

by death, clinical signs [salivation and reduced defecation], decreased 

body weight gain and food consumption, and gross pathological lesions 

of the stomach. Developmental toxicity at 58.3 and 116.7 mg/kg/day 

included dose-related increases in the total number of resorptions/

litter and post-implantation losses compared to concurrent and/or 

historical controls.
 Based on these findings, it is apparent that the developmental 

effects seen at 58.3 and 116.7 mg/kg/day levels are attributable to 

propachlor; the NOEL was 5.8 mg/kg/day.

 EPA reaffirms that there is sufficient evidence for listing 

propachlor on the EPCRA section 313 list pursuant to EPCRA section 

313(d)(2)(B) based on the available developmental toxicity data for 

this chemical. Therefore, EPA is finalizing the addition of propachlor 

on the EPCRA section 313 list.

 46. Propargyl alcohol. International Specialty Products is opposed 

to the listing of propargyl alcohol apparently because an uncertainty 

factor of 3,000 was used by EPA in setting the RfD. The commenter feels 

that an uncertainty factor of 100 would have been more appropriate and 

cites instances where such an uncertainty factor has been used by IRIS 

in setting reference doses. The commenter does not question the renal 

or hepatotoxicity cited in IRIS as a basis of its concern.

 The commenter is correct in stating that EPA has used uncertainty 

factors of 100 for other chemicals. However, that was not deemed 

appropriate in this instance for reasons which are set out by EPA in 

the IRIS data base. EPA continues to support the listing of propargyl 

alcohol under EPCRA section 313 on the basis of chronic toxicity which 

may pose a significant health hazard as manifested by renal and hepatic 

effects. The uncertainty factor plays no part in this decision. EPA 

reaffirms that there is sufficient evidence for listing propargyl 

alcohol on the EPCRA section 313 list pursuant to EPCRA section 

313(d)(2)(B) based on the available hepatotoxicity and nephrotoxicity 

data for this chemical. Therefore, EPA is finalizing the addition of 

propargyl alcohol on the EPCRA section 313 list.

 47. Propiconazole. Ciba-Geigy Corporation states that the increased 

incidence of liver tumors in the oncogenicity study on propiconazole 

was noted only in male mice in the high dose (2,500 ppm), which 

exceeded the MTD, based on decreased survival and body weight gain.

 EPA believes that the study high dose (2,500 ppm, equivalent to 325 

mg/kg/day) was excessively toxic; however, the Agency also determined 

that the mid dose (500 ppm, equivalent to 65 mg/kg/day) was not 

considered sufficiently high to evaluate the carcinogenic potential of 

propiconazole. The Agency believes that a supplementary study should be 

conducted in male mice at doses selected to sufficiently evaluate 

carcinogenic potential without excessive toxicity. At this time 

however, based on the currently available evidence, propiconazole 

remains classified as a Group C, possible human carcinogen, with the 

RfD approach recommended for quantification of human risk.

 The commenter further states that relatively minor gastrointestinal 
effects were noted in dogs at the high dose only (250 ppm).

 EPA believes that the data in both the 3-month and 1-year dog 

studies demonstrate gastrointestinal effects at the high-dose (250 ppm, 

equivalent to 6.25 mg/kg/day). These effects are considered severe, 

and, therefore, are of sufficient seriousness to warrant listing 

propiconazole on the EPCRA section 313 list.

 EPA reaffirms that there is sufficient evidence for listing 

propiconazole on the EPCRA section 313 list pursuant to EPCRA section 

313(d)(2)(B) based on the available hepatic and gastrointestinal 

toxicity data for this chemical. Therefore, EPA is finalizing the 

addition of propiconazole on the EPCRA section 313 list.

 48. Simazine. Ciba-Geigy Corporation objects to the listing of 

simazine under EPCRA section 313 based on reports of liver, kidney, 

testicular and neural pathology in sheep and increases in liver enzymes 

in a dog 2-year study. The commenter maintains that the sheep study was 

conducted to investigate the possible effects that would result if 

large amounts of simazine were ingested by this species. The commenter 

also states that in a 1-year study there were some indications of 

effects on the hematopoietic system but not the hepatic system at the 

high dose of 1,500 ppm.

 In a 1-year study, NOEL and LOELs of 0.68 and 3.41 mg/kg/day, 

respectively, were established based on decreased body weight gain, and 

decreased RBC, HGB, HCT in females. Although the sheep study was 

conducted for a purpose other than to investigate the overall toxicity 

of simazine, this does not negate the relevance of its results. EPA 

reaffirms that there is sufficient evidence for listing simazine on the 

EPCRA section 313 list pursuant to EPCRA section 313(d)(2)(B) based on 

the available hepatic, renal, neurological, and reproductive toxicity 

data for this chemical. Therefore, EPA is finalizing the addition of 

simazine on the EPCRA section 313 list.

 49. Sodium nitrite. American Automobile Manufacturers Association 

contends that EPA has proposed listing on the basis of chronic toxicity 

but the support document cites studies based on high dose, acute 

exposures. High dose gestational studies in rats and mice were also 

cited as the basis for developmental (fetal) toxicity.

 EPA agrees that the human studies cited in the proposed rule are 

acute studies. However, these studies in conjunction with the chronic 

study in mice, which showed reduced motor activity and major EEG 

changes in treated animals, support the basis for concern for chronic 

neurological effects. EPA thus considers sufficient indication of a 

potential chronic neurologic hazard to list this chemical on the EPCRA 

section 313.
 There were two developmental studies in mice and one reproductive 

study in rats cited in the proposed rule which showed effects on the 

fetal development whether sodium nitrite was administered during 

gestation or lactation. The doses used in the studies with mice, 30 and 

80 mg/kg/day, respectively, are not abnormally high for this type of 

study; the dose range reported for the rat reproductive study, 26 to 

256 mg/kg/day is also not abnormally high. The results from all three 

studies indicate that sodium nitrite induces developmental effects in 

animals and are sufficient to make a determination that the chemical is 

a potential health hazard in man.

 EPA reaffirms that there is sufficient evidence for listing sodium 

nitrite on the EPCRA section 313 list pursuant to section 313(d)(2)(B) 

based on the chronic hematological and developmental toxicity data for 

this chemical. Therefore, EPA is finalizing the addition of sodium 

nitrite on the EPCRA section 313 list.

 50. Triallate. Monsanto contends that the hepatic health effects 

listed in the proposed rule for triallate are trivial effects that do 

not provide sufficient evidence that triallate causes hepatic toxicity. 

In addition, Monsanto claims that pregnant rats exhibited abnormal 

behavioral signs at 90 but not at 30 mg/kg/day.

 Although the Agency agrees that there is not sufficient evidence 

for hepatotoxic potential of triallate, the Agency does not concur with 

the commenter that ``pregnant rats exhibited abnormal behavioral signs 

at 90 but not at 30 mg/kg/day.'' Head bobbing and circling, clear signs 

of neurotoxicity, were observed in pregnant females at 30 mg/kg/day. 

Males and non-pregnant females did not exhibit these clinical signs. 

These data suggest that pregnant rats are more susceptible to the 

neurologic potential of triallate than the general population.

 The commenter noted the existence of a subchronic neurotoxicity 

study in rats and indicated that this study provides a better 

estimation of the neurotoxic potential of triallate than the 2-

generation reproduction study.

 The Agency agrees that the subchronic neurotoxicity study in rats 

(Ref. 10) provides a clearer picture of the neurotoxic potential of 

triallate. The Agency has reviewed this study and concludes that the 

results indicate the neurotoxic potential of triallate and further 

corroborates the findings cited by EPA in the proposed rule.

 Thus, the Agency reaffirms that there is sufficient evidence for 

listing triallate on the EPCRA section 313 list pursuant to EPCRA 

section 313(d)(2)(B) based on the available chronic neurotoxicity data 

for this chemical. Therefore, EPA is finalizing the addition of 

triallate on the EPCRA section 313 list.
G. Chemicals Not Being Added to EPCRA Section 313

 1. 5-Chloro-2-(2,4-dichlorophenoxy)phenol. Ciba-Geigy Corporation 

and The Dial Corporation contend that insufficient evidence is 

available to support the conclusion that 5-chloro-2-(2,4-

dichlorophenoxy)phenol poses a risk of hematological toxicity to humans 

based on handling and uses of the product.

 Based on these comments and EPA's reanalysis of the data, the 

Agency has concluded that the information presented in the proposed 

rule is not sufficient to justify adding 5-chloro-2-(2,4-

dichlorophenoxy)phenol to the EPCRA section 313 list based upon 

potential human hazard. Therefore, EPA is not finalizing the addition 

of this chemical on the EPCRA section 313 list.

 2. Clomazone. FMC Corporation claims that clomazone induces adverse 

effects only at high dose levels.

 The Agency agrees with the commenter. Based on these comments and 

EPA's reanalysis of the data, the Agency has concluded that the 

information presented in the proposed rule is not sufficient to justify 

adding clomazone to the EPCRA section 313 list based upon potential 

human hazard. Therefore, EPA is not finalizing the addition of this 

chemical to EPCRA section 313.

 3. Tetrasodium ethylenediaminetetraacetate. Eight commenters 

contend that the proposed listing for this chemical was based solely on 

a single, unreliable developmental toxicity study which used a mixture 

that contained tetrasodium ethylenediaminetetraacetate along with 

several other chemicals.

 EPA concedes that the effects cannot be attributed solely to 

tetrasodium ethylenediaminetetraacetate. Therefore, the Agency is not 

finalizing the addition of tetrasodium ethylenediaminetetraacetate on 

the EPCRA section 313 list.

H. Miscellaneous Comments

 1. Year-to-year comparisons of the TRI data. BP America, Texaco, 

and American Automobile Manufacturers Association contend that the 

proposed expansion of the EPCRA section 313 list will eliminate any 

consistency with earlier TRI data and make tracking environmental 

progress impossible. American Automobile Manufacturers Association 

further states that EPA needs to ensure that the ``total TRI releases 

and transfers'' measurement system allows accurate interpretation of 

the data, allowing the public to realistically assess progress in 
pollution prevention. Also, the commenters add that considerable 

confusion results in trying to explain the different data sets to the 

public. Mobil Oil Corporation states that EPA should divide the list 

into three sub-groups so that a facility's history can be tracked on a 

more common basis.

 EPA recognizes that changes in the EPCRA section 313 list and in 

the reporting requirements have an effect on the characterization of 

the TRI data. In fact, some change has occurred for every reporting 

year. In an attempt to provide useful year-to-year comparisons, EPA has 

presented the TRI data annually on a normalized list of chemicals, 

i.e., the list of chemicals used for year-to-year comparisons is the 

same for every year in the comparison. EPA further recognizes the 

effect that expansion of the EPCRA section 313 list will have on the 

TRI data and will continue to work to find ways to make the data 

useable for cross-year comparisons. EPA will use the 1995 reporting 

year as the base year for comparisons that include the chemicals added 

today. Facilities should still be able to track pollution prevention 

progress for those chemicals previously listed (using 1988 as the base 

year) and have a new base year for the additional chemicals which can 

be used to track future pollution prevention progress.

 2. Public perceptions. Roussell Uclaf Corporation, National Paint 

and Coatings Association, Association of International Automobile 

Manufacturers, and American Frozen Food Institute oppose the listing of 

these chemicals under EPCRA section 313 because of the public's 

misperception of the associated dangers. American Automobile 

Manufacturers Association (AAMA) states that since the public considers 

all chemicals on the EPCRA section 313 list to be toxic, any chemical 

on the list is subject to adverse scrutiny, regardless of the actual 

risks associated with the chemical. While recognizing past efforts by 

EPA towards public education, AAMA believes that misunderstanding and 

misinterpretation of the data still exists which makes it more critical 

that EPA not expand the list with low risk chemicals. Texaco and AAMA 

believe that before the Agency expands the EPCRA section 313 list, 

resources should be committed to provide public education on actual 

risks portrayed by the data and educate the public on viable means of 

chemical risk reduction and chemical management.

 The chemicals that are listed under EPCRA section 313 exhibit a 

wide range of effects at various dose levels. While EPA attempts to 

communicate the TRI data in the most accurate manner, the Agency 

recognizes that there exists the perception that the TRI data may 

sometimes be mischaracterized, but that does not justify not adding a 

chemical for which the statutory criteria are clearly met. EPA agrees 
that the better approach to such a problem is improving public 

information on the chemical, which, combined with the release, 

transfer, and waste management data will enable the public to 

participate in informed environmental decision-making. EPA continues to 

attempt to provide the public with means for interpreting the TRI data.

 3. Persistent bioaccumulative chemicals. In the proposed rule, EPA 

requested comment on whether chemicals that are manufactured in trace 

amounts in waste streams, are highly toxic at very low dose levels and 

have physical, chemical, or biological properties that make the 

chemicals persist for extended periods in the environment, and 

bioaccumulate through the food chain should be listed on the EPCRA 

section 313 list (January 12, 1994, 59 FR 1791). EPA noted that 

persistent bioaccumulative toxic chemicals, such as dioxins, are of 

particular concern in ecosystems such as the Great Lakes Basin due to 

the long retention time of the individual lakes and the cycling of the 

chemical from one component of the ecosystem to another. EPA also 

requested comment on the following: If EPA were to add this type of 

chemical to EPCRA section 313, what modifications to EPCRA section 313, 

such as lowering the reporting thresholds and modifying the de minimis 

in mixture exemption (40 CFR 372.38), would be required to ensure that 

release and transfer information would be collected? In addition to two 

comments opposed to the addition of this type of chemical, EPA received 

35 comments supporting the addition of toxic persistent bioaccumulative 

chemicals. The majority of these commenters also supported lowering the 

reporting thresholds for this type of chemical.

 Monsanto and Dow Chemical Company object to the addition of 

persistent bioaccumulative chemicals that are produced in quantities 

less than the EPCRA section 313 reporting thresholds. The commenters 

state that many of the persistent, bioaccumulative toxic compounds 

which are of concern are no longer manufactured in the United States, 

and are merely present in the environment due to historical activities 

and not current activities.

 EPA disagrees with this contention. EPA's request for comment 

focused on chemicals that are generated in small quantities. This is 

not limited to chemicals produced as a product, but includes chemicals 

that are generated in waste streams. Many persistent, bioaccumulative 

toxic chemicals are produced in waste streams. Further, EPCRA section 

313 requires the reporting of chemicals manufactured in waste streams 

if the quantity produced exceeds the appropriate reporting threshold.

 Monsanto further claims that ``the amounts of these particularly 

dangerous substances coming from industrial facilities are so small 

that they can have no measurable impact on health or the environment.''
 EPA disagrees that releases of these chemicals are so low that they 

will not have an adverse effect upon human health or the environment. 

The persistent bioaccumulative aspects of these toxic chemicals are 

such that even very small quantities released can reasonably be 

anticipated to cause adverse effects upon human health and the 

environment.

 Monsanto also states that the concept of different reporting 

thresholds suggests that this threshold would be proportional to the 

relative hazard. Thresholds for practically non-toxic chemicals may be 

very high using this concept.

 EPA requested comment on lowering the thresholds for these 

chemicals not so that the reporting thresholds for chemicals listed on 

the EPCRA section 313 list would be proportional to the relative hazard 

of the chemicals. Rather, EPA requested comment on lowering the 

threshold for persistent bioaccumulative chemicals because even minimal 

releases of these chemicals may result in elevated concentrations in 

the environment or in an organism that can reasonably be anticipated to 

result in significant adverse effects. This reflects the increased 

likelihood that there will be exposure to a chemical that persists due 

to its longer residence time in the environment. Repeated minimal 

releases of a persistent chemical may result in elevated concentrations 

in the environment. For a chemical that bioaccumulates, even low levels 

of the chemical in the environment may result in increased 

concentrations in an organism. Thus, lower thresholds for these 

substances would be considered due to the persistent and 

bioaccumulative nature of the substances, rather than the direct 

hazard.

 In its next action to add chemicals to the EPCRA section 313 list, 

the Agency intends to consider the addition of chemicals that are 

persistent and bioaccumulate. EPA also intends to consider lowering the 

reporting thresholds for these additional chemicals and those chemicals 

that are persistent and bioaccumulate that are now on the EPCRA section 

313 list. Accordingly, comments received in response to EPA's request 

for comment on the potential addition of persistent bioaccumulators 

will be addressed in the future rulemaking if these chemicals are 

proposed for addition.

 4. Additional chemicals. The Wisconsin Department of Natural 

Resources states that the EPCRA section 313 chemical list should be 

expanded to include the six chemicals listed in section 112(b) of the 

CAA not currently included on the EPCRA section 313 list or as part of 

the January 12, 1994 proposal.

 EPA has reviewed all of the chemicals listed under section 112(b) 
of the CAA not currently on the EPCRA section 313 list and has 

determined that the remaining chemicals either do not meet the current 

listing criteria or no reports would be received since their production 

volumes are below reporting thresholds.

 5. Hormone mimics. The National Wildlife Federation recommends that 

EPA add to the section 313 list all chemicals with estrogenic or other 

hormone-mimicking qualities, and the reporting thresholds and de 

minimis exemption for mixtures eliminated for these chemicals.

 EPA agrees that the deleterious effects of hormone mimicking 

chemicals may warrant their future review for listing on the EPCRA 

section 313 list. Although the effects of these chemicals are difficult 

to predict, and it is often impossible to establish a clear cause/

effect relationship, still it is clear from the available evidence that 

these chemicals warrant consideration. Wide scale changes in wildlife 

and human populations have been noted by some researchers. Population 

decreases and reproductive effects have been linked to these chemicals 

in a number of wildlife species, including but not limited to bears, 

Florida panthers, songbirds, and bald eagles, to list just a few. 

Possibly of greater concern are the effects of these chemicals in 

humans. In addition to the carcinogenic potential of many of these 

chemicals, effects on fertility, immune system damages, and many 

childhood problems have been attributed to hormone-mimics. A number of 

the chemicals with widespread distribution in the environment reported 

to have reproductive and endocrine-disrupting effects (Ref. 1) are 

either already on the EPCRA section 313 list, or are being added as a 

result of this action. EPA may consider reviewing the remaining 

chemicals on this list as part of a future action.

 As to removing the reporting thresholds and de minimis exemption 

for the hormone-mimicking chemicals already on the section 313 list, 

these possibilities will be examined at the time that modifying the 

reporting thresholds and de minimis exemption for persistent and 

bioaccumulative chemicals is addressed. As many of the hormone 

mimicking chemicals are also either persistent or bioaccumulative they 

could be included as part of such a review.

I. Comment on EPA's Regulatory Impact Assessment

 Comments that are specific to individual chemicals or chemical 

categories are addressed in the Response to Comments Document (Ref. 

14).

 Many commenters state that EPA's Regulatory Impact Analysis (RIA) 

failed to meet the requirements of Executive Order 12866, which 
mandates regulatory planning and review. The commenters state that: (1) 

The RIA for the proposed rule did not analyze any alternatives other 

than adding the 313 chemicals and chemical categories to the EPCRA 

section 313 list, (2) that it excluded the economic effects due to 

complying with state, local and other federal requirements that are 

triggered when a chemical is listed under EPCRA section 313, and (3) 

that it did not analyze the benefits of the rule. Many commenters also 

contend that small business impacts were understated in the RIA, and 

that the time required for compliance is higher than estimated in the 

RIA. These comments and the Agency's responses are discussed below.

 1. Alternatives. The commenters believe that the RIA should have 

included alternatives to adding all of the proposed chemicals and 

chemical categories to the EPCRA section 313 list. In response to these 

comments, EPA has revised the RIA to include a variety of alternatives, 

such as adding the CAA criteria air pollutants, not adding chemicals 

regulated under FIFRA, not adding the water dissociable nitrate 

compounds category, and adding the proposed chemicals in conjunction 

with an alternate reporting threshold for facilities with low-levels of 

TRI chemicals in wastes. The commenters requested that EPA present the 

costs for adding each individual chemical. EPA cannot provide the costs 

on an individual chemical basis because the estimates for most of the 

chemicals were derived from confidential business information. 

Displaying the costs for each chemical could disclose this confidential 

information.

 2. Linked requirements. Numerous commenters state that the RIA 

excludes the costs of compliance with state, local and other federal 

requirements that are triggered when a chemical is listed under EPCRA 

section 313. The linked requirements that the commenters raise include 

state taxes and fees, state pollution prevention planning requirements, 

special requirements for certain National Pollutant Discharge 

Elimination System (NPDES) storm water permits, and requirements for 

federal facilities under Executive Order 12856. EPA has revised the RIA 

to discuss state and federal requirements that are linked to reporting 

under EPCRA section 313. However, EPA has not quantified the costs of 

such requirements. In some cases, this is because there is insufficient 

data to make a reasonable estimate. In other cases, EPA does not 

believe that the requirements represent a social cost. The requirements 

that may be linked to listing under EPCRA section 313 are discussed 

below.

 a. State fees. Thirteen states place a tax or fee on facilities 

filing TRI Form R reports. These states are Colorado, Florida, Iowa, 

Kansas, Maine, Massachusetts, Minnesota, Mississippi, Nevada, Ohio, 
Pennsylvania, South Dakota, and Texas. Many commenters estimate that 

the costs resulting from state fees and taxes linked to EPCRA section 

313 reporting are up to 50 percent of the direct cost of filing the 

forms, and state that any tax is likely to induce a reduction in 

economic welfare. EPA has revised the RIA to discuss state fees and 

taxes that are linked to reporting under EPCRA section 313. However, 

the taxes and fees are not direct social costs, and EPA does not 

believe that there is sufficient information to estimate the net social 

costs or benefits of these requirements.

 The commenters treat state taxes and fees on the EPCRA section 313 

reports as costs, but these are transfer payments and not economic 

costs to society. Specifically, the standard definition of a cost in 

economics is the consumption of a resource (e.g., labor, equipment, 

natural resources, etc.). A tax or fee is a transfer payment from one 

party to another. While the fee is a cost to the firm (and/or its 

customers), it is income to the state. No resources are consumed, 

except for transaction costs, so the amount of the fee is not a cost to 

society.

 EPA disagrees with the commenters' contention that any tax or fee 

is likely to induce a reduction in economic welfare. EPA believes that 

taxes or fees on toxic chemicals may resolve a market failure and 

increase social welfare. The use of toxic chemicals often creates a 

negative externality. For instance, releases of a chemical may cause 

health and environmental effects in the surrounding community. In such 

cases, it is likely that private costs are below true social costs, 

because private markets do not provide an adequate incentive for firms 

to internalize these externalities. In such cases, taxes may be the 

optimal method to correct the market failure. EPA believes that if the 

commenters feel that the fees are not set at the level that optimizes 

social welfare, their remedy lies with the appropriate state agency, 

and not EPA.

 EPA does not feel that it is feasible to estimate the size of the 

transfer payment resulting from state fees and taxes linked to EPCRA 

section 313, or the net social costs or benefits of these payments. The 

commenters made their estimates by applying the maximum state fees to 

all facilities nation-wide. EPA does not feel that such a calculation 

is appropriate. Most states have no fees or taxes linked to EPCRA 

section 313 reporting, and the level of the fees or taxes (and how they 

are assessed) is different in each of the rest of the states, varying 

from $25 to $50,000. Many of the state requirements are not flat fees, 

but are graduated depending on the level of releases that a facility 

reports. An accurate representation of the size of the transfer 
payments would require estimating the geographic distribution of new 

reports, and the level of releases and transfers for each report. EPA 

feels that it is not possible to predict with a reasonable degree of 

accuracy the location and level of releases for facilities that will 

report on the chemicals being added to the EPCRA section 313 list.

 Nor is it feasible to accurately estimate the net social costs or 

benefits of the state fees and taxes. To do so would require knowing 

not only the size of the transfer payments, but the damages caused by 

the use and release of the chemicals, and the change in behavior that 

would result from the fees and taxes. EPA does not have adequate 

information on the facilities that would be affected by the rule to 

make such estimates. As a result, the RIA has been revised to 

qualitatively discuss state fees and taxes linked to EPCRA section 313 

reporting, but does not estimate the size of the resulting transfer 

payments, or the net social costs or benefits.

 b. State pollution prevention programs. Seven states (Arizona, 

Maine, Massachusetts, Minnesota, Mississippi, New Jersey, and Texas) 

mandate pollution prevention plans from facilities reporting under 

EPCRA section 313. Facilities in these states that are reporting to TRI 

for the first time because of the additions to the chemical list will 

have to prepare pollution prevention plans. Although the development of 

pollution prevention plans imposes a cost on facilities, the RIA did 

not analyze the costs of these requirements. Many commenters contend 

that there are significant costs for preparing such plans, and that the 

RIA should have included these costs.

 Quantifying the impacts of state pollution prevention requirements 

would require predicting which facilities reporting for the additional 

chemicals would be located in these seven states. As stated above, it 

is not possible to accurately predict the geographic location of new 

reporters. Thus, no costs are estimated for state pollution prevention 

plans in the RIA.

 Nor does the RIA quantify the benefits derived from these pollution 

prevention planning requirements. None of the commenters submitted any 

evidence comparing the social benefits of such requirements to the 

costs. Therefore, EPA has no information from which to conclude that

the linked requirements for state pollution prevention plans would 

reduce the net social benefits of adding chemicals to EPCRA section 

313.

 EPA has not quantitatively estimated either the costs of state 

pollution prevention planning requirements or the benefits of such 

programs in the RIA. However, the RIA has been revised to qualitatively 

discuss requirements that are linked to EPCRA section 313 reporting, 
including pollution prevention plan preparation.

 c. NPDES storm water permits. EPA issued National Pollutant 

Discharge Elimination System (NPDES) ``baseline'' general permits for 

storm water discharges associated with industrial activity on September 

9, 1992 (57 FR 41236). EPA subsequently proposed a multi-sector storm 

water industrial permit covering 29 industrial sectors (November 19, 

1993, 58 FR 61147). The ``baseline'' general and multi-sector general 

permits have special pollution prevention requirements for certain 

EPCRA section 313 facilities, and the ``baseline'' permits also contain 

special monitoring requirements. Many commenters assert that the RIA 

underestimates the costs of the rule by a factor of up to 5.6 by not 

including the costs of NPDES storm water permit requirements that are 

triggered by adding chemicals to the EPCRA section 313 list.

 EPA believes that the commenters' estimates are based on a cost 

scenario that is not applicable to the typical facility affected by the 

proposal to add chemicals under EPCRA section 313. There are four 

reasons that the commenters' estimates are not generally appropriate. 

Any of these reasons alone demonstrate that the commenters have 

overestimated the number of facilities that are affected and the the 

size of the impact. Because there may also be a significant overlap 

among the four, the commenters' estimates are likely to apply to few, 

if any, facilities. The commenters' estimates would not apply to all 

facilities affected by the rule, as the commenters contend.

 First, only a fraction of the facilities that would report under 

EPCRA section 313 for the additional chemicals would be affected by the 

NPDES storm water permits. A facility that submits TRI Form R is only 

subject to storm water permitting requirements if industrial materials 

or activities are exposed to storm water, and if the facility is 

reporting to TRI for one of the section 313 water priority chemicals. 

Only about two dozen of the chemicals being added to the EPCRA section 

313 list qualify as section 313 water priority chemicals, and thus 

would be covered by the NPDES requirements. About half of these are 

pesticides, which would not be manufactured or processed at many 

facilities.

 Second, EPA expects the majority of facilities to have existing 

containment systems that meet most of the requirements of the NPDES 

permits. Third, many of the costs for the storm water requirements are 

likely to apply at the facility level. In such cases, facilities that 

installed systems for the current EPCRA section 313 chemicals will not 

face incremental costs for the additional chemicals. Fourth, the 

special requirements of the NPDES storm water permits are based on the 

coverage of EPCRA section 313 at the time the permits were issued. The 
NPDES requirements do not apply to chemicals that are added to the 

EPCRA section 313 list until the time of permit renewal (which occurs 

every 5 years), and may not apply in subsequent permits, depending on 

the Agency's decisions at the time those permits are issued.

 In addition, the commenters based their estimates solely on the 

upper bound of EPA's estimates for the NPDES permits, and have ignored 

the mix of low-cost and high-cost facilities that is likely to exist. 

EPA believes that the commenters' estimate is a hypothetical ``worstcase'' scenario that does not apply to the typical facility and may not 

apply to any facilities. EPA believes that the costs of the storm water 

requirements for the proposed chemicals will be relatively minor. 

Again, EPA has revised the RIA to qualitatively discuss the linkage 

between EPCRA section 313 reporting and the NPDES storm water, but it 

has not made any quantitative estimates of these costs.

 d. Executive order 12856. Executive Order 12856, signed by the 

President in August 1993, extends the coverage of EPCRA to federal 

facilities. In addition, section 3-303(a) of the Executive Order states 

that ``Each federal agency shall establish a plan and goals for 

eliminating or reducing the unnecessary acquisition by that agency of 

products containing extremely hazardous substances or toxic chemicals'' 

(emphasis added). The Executive Order defines ``toxic chemical'' as a 

substance on the list described in section 313 of EPCRA. Many 

commenters contend that the cost to the federal government and the 

private sector of complying with Executive Order 12856 for the 

chemicals being added to EPCRA section 313 will be $1.5 billion per 

year.

 EPA does not believe that the effects of Executive Order 12856 

should have a bearing on the decision-making regarding the addition of 

toxic chemicals to EPCRA section 313. EPA believes that following the 

commenters line of reasoning would discourage the federal government 

from ever making any changes in procurement, for whatever reason, 

because doing so might have an impact on a supplier. Furthermore, EPA 

believes that there is insufficient data to make any estimate of the 

effects of the Executive Order, and that the resources required to make 

such an estimate would exceed the value of the information.

 EPA notes that section 3-303(a) of the Executive Order does not 

require the elimination of toxic chemicals in federal procurement. If 

the performance characteristics of a toxic chemical or product 

containing a toxic chemical are critical in the required tasks, federal 

agencies may continue to purchase it. Each federal agency must make its 

own determination whether a particular toxic chemical is necessary in a 

particular use.
 The Executive Order requires that federal agencies eliminate or 

reduce the unnecessary procurement of extremely hazardous substances or 

toxic chemicals. None of the commenters identify which toxic chemicals 

are being unnecessarily purchased by the federal government, and which 

federal agencies are making these unnecessary purchases. Without such 

information, EPA cannot verify the commenters' claim that the addition 

of chemicals to EPCRA section 313 will create significant impacts as a 

result of the Executive Order. If these chemicals are not being 

purchased by the federal government, or are not being purchased 

unnecessarily, there will not be an impact.

 The commenters' estimate of $1.5 billion in costs is based solely 

on a series of assumptions, which are not supported by data. EPA does 

not believe that the commenter's analysis was based on a careful 

analysis of any factual information. EPA has no data with which to 

replace these assumptions. Given EPA's belief that effect of the 

Executive Order should not have a bearing on the rulemaking (as well as 

the limitations of the Executive Order, the small amount of procurement 

that would be affected, and the ability of producers to sell to private 

sector clients or manufacture substitutes), EPA does not believe that 

there is a need to develop any data on these factors.

 The Executive Order states that ``the environmental, energy and 

economic benefits of energy and water use reductions are very 

significant,'' and that ``the federal government has the opportunity to 

realize significant economic as well as environmental benefits of 

pollution prevention.'' The Executive Order provided a mandate for the 

federal government to reduce its unnecessary use of toxic chemicals. 

EPA believes that the proposal to add chemicals to the section 313 list 

complements this mandate. Furthermore, EPA hopes that federal agencies 

will comply with the spirit of the Order, and reduce their unnecessary 

use of toxic and hazardous chemicals, whether or not these chemicals 

are listed on the EPCRA section 313 list. EPA believes that, by 

definition, the social benefits cannot exceed the social costs for an 

unnecessary toxic chemical, and social welfare can be improved by 

switching to a substitute product. Therefore, EPA believes that any 

actions federal agencies take to meet their obligations under Executive 

Order 12856 will have a positive net benefit.

 3. Benefits. Many commenters assert that the RIA did not show any 

benefits to adding chemicals to the EPCRA section 313 list of 

chemicals. The commenters appear to have made these statements because 

EPA did not make a quantitative estimate of the benefits associated 

with the rule.

 There are two types of benefits associated with EPCRA section 313. 
The first type of benefit is due to improvements in understanding, 

awareness, and decision-making related to the provision and 

distribution of information. The second type of benefits derive from 

changes in behavior that result from the information reported to TRI. 

These benefits include reduced environmental and health risks, and 

reduced treatment and disposal costs: These changes in behavior come at 

some cost to society. Because the current state of knowledge about the 

economics of information is not highly developed, EPA has not attempted 

to quantify the pure information benefits of adding chemicals to the 

EPCRA section 313 list. Because of the inherent uncertainty in the 

chain of events, EPA has also not attempted to quantify the benefits or 

the costs of the changes in behavior that result from the information. 

EPA does not believe that there are adequate methodologies to make 

reasonable quantitative estimates of either type of benefits. However, 

EPA believes that its qualitative discussion of the effects of the 

current TRI program show that such benefits do exist. The information 

on the additional chemicals is expected to improve scientific 

understanding of the environment and health risks, foster greater 

community awareness of industrial activities, and allow Federal, state, 

and local authorities to make better informed decisions on acceptable 

levels of toxic chemicals in communities.

 Instead, EPA has drawn its conclusions about the net benefits of 

adding chemicals to EPCRA section 313 by inference. In enacting EPCRA 

and the PPA, Congress implicitly determined that the net benefits of 

reporting was positive for the original list of 320 chemicals and 

categories. EPA's interpretation of the statutory toxicity criteria is 

more stringent than Congress' original determination because EPA has 

deleted 12 chemicals from the original list of 320 chemicals and 

categories developed by Congress. EPA believes that all of the 

chemicals being finalized meet the statutory toxicity criteria of 

section 313, and are at least as toxic as some of the chemicals for 

which Congress believed there were net benefits due to reporting. Thus, 

by inference, the net benefits of reporting for the chemicals added in 

this rulemaking should be positive as well.

 EPA believes that the experience of the past 5 years shows that 

reporting under EPCRA section 313 has produced real gains in 

understanding about exposure to toxic chemicals. EPA sees no reason why 

the information on the additional chemicals will provide less 

understanding than the currently reported chemicals have provided.

 4. Small business. Under the Regulatory Flexibility Act (5 U.S.C. 

sections 601 - 612), agencies must prepare an analysis of small 

business impacts for proposed rules. Many commenters contend that small 
business impacts were understated in the RIA, and they question EPA's 

conclusion that the rule will not have a significant impact on a 

substantial number of small entities. EPA believes that the commenters 

have significantly overestimated the costs of the rule, and that the 

commenters' estimates of small business impacts are not valid. EPA has 

provided additional analysis in the RIA for the final rule that 

demonstrates that the rule will not have significant cost impacts on 

small entities.

 EPA believes that, whether or not the proposed rule would have had 

significant cost impacts on small entities, the Agency has subsequently 

met its obligations under the Regulatory Flexibility Act. Where a 

proposed rule would have significant impacts on small entities, the Act 

requires EPA to identify and consider (but not necessarily adopt) 

alternatives that minimize the impact on these entities, while 

accomplishing the stated objectives of the applicable statute.

 Elsewhere in this issue of the Federal Register, EPA is finalizing 

a rule establishing an alternate threshold for low-levels of TRI 

chemicals in waste that would otherwise meet the reporting requirements 

under EPCRA section 313. Such facilities can submit an annual 

certification statement in lieu of a TRI Form R. EPA estimates that 

facilities will require an average of 34 hours to comply with the 

requirements for a certification statement, compared to 53 hours for a 

TRI Form R. The alternate reporting threshold will apply to the 

chemicals being added under EPCRA section 313 by this rule as well as 

chemicals currently listed under EPCRA section 313.

 EPA's guidelines for implementing the Regulatory Flexibility Act 

state that ``The alternatives considered for the purpose of fulfilling 

the Act's requirements need not be restricted in applicability to small 

entities. Regulatory alternatives that prove to be more cost-effective 

for small entities often will be more cost-effective for larger 

entities as well. For example, alternatives that place lesser burden on 

facilities with lower emission levels, lower production levels, etc., 

should be analyzed in conjunction with fulfilling the Act's 

requirements even though such alternatives may not ease the burden on 

all (or even most) small entities and may benefit large entities as 

well as small ones.''

 Because EPA has considered, and adopted, an alternative that places 

lesser burden on facilities with lower emission levels, EPA believes 

that it has met the requirements of the Regulatory Flexibility Act. The 

alternate threshold will provide significant relief for small 

businesses that will report for the proposed chemicals, which is the 

intent of the Act.
 5. Reporting burden. Many commenters report that the time required 

for compliance with EPCRA section 313 is higher than that estimated in 

the RIA. Commenters estimates of the time required to prepare a TRI 

Form R and perform the necessary recordkeeping vary from 91 to 2,000 

hours, compared with EPA's estimate of 53 hours.

 The unit time estimates used by EPA are average values. EPA 

recognizes that large multi-divisional, multi-departmental facilities 

may require more than the average time to comply. As with any average, 

some facilities will be above the average and others will be below it. 

However, there are many other facilities subject to the rule that are 

not large, multi-divisional or multi-departmental. These facilities 

will typically have a simpler compliance process.

 The variability among facilities is evident in comments on the rule 

submitted by a large chemical manufacturing company, that provided 

estimates showing that it spends an average of 28 hours for each TRI 

Form R that is submitted to compile information, perform calculations, 

prepare the TRI Form R and maintain records. This includes the time 

spent on compliance determination for chemicals that are below 

threshold levels. This is less than EPA's estimate of 53 hours for the 

same activities.

 While some of the commenters may require more time than average to 

comply with the rule, other companies require less time than average. 

EPA believes that its time estimates are a reasonable average for the 

manufacturing sector as a whole.

V. Rulemaking Record

 The record supporting this final rule is contained in the docket 

number OPPTS-400082B. All documents, including an index of the docket, 

are available in the TSCA Nonconfidential Information Center (NCIC), 

also known as the TSCA Public Document Office, from noon to 4 p.m., 

Monday through Friday, excluding legal holidays. TSCA NCIC is located 

at EPA Headquarters, Rm. NE-B607, 401 M St., SW., Washington, DC 20460.

VI. References

 (1) Colborn, T., F.S. fom Saal A.M. Soto. Developmental Effects of 

Endocrine-Disrupting Chemicals in Wildlife and Humans. Environmental 

Health Perspectives 101:378-384.

 (2) DeRosa, Stara and Durkin Ranking Chemicals Based on Chronic 

Toxicity Data, Tox. and Ind. Health, Vol. 1, No.4, (1985)

 (3) NAS/NRC. Risk Assessment in the Federal Government: Managing 
the Process. National Academy Press, Washington, DC (1983)

 (4) USEPA/OHEA. Risk Assessment Guidelines for Carcinogen Risk. 

U.S. Environmental Protection Agency, Cincinnati, OH. (1987).

 (5) USEPA/OHEA. The Risk Assessment Guidelines of 1986. U.S. 

Environmental Protection Agency, Washington, DC (1987)

 (6) USEPA/OHEA. Guidelines for Developmental Toxicity Risk 

Assessment. U.S. Environmental Protection Agency, Washington, DC (1991) 

[56 FR 63805]

 (7) USEPA/OHEA. Draft Report: Principles of Neurotoxicity Risk 

Assessment; Notice. U.S. Environmental Protection Agency, Washington, 

DC (1993) [58 FR 41556]

 (8) USEPA/OPP. EPTC-RS-DCI. Evaluation of Two-Year Chronic Rat 

Study (Accession Nos. 254335, 254336, 254337, 254338, and Addendum to 

Final Report (Accession Nos. 258076, 260057). U. S. Environmental 

Protection Agency, Washington, DC (1986)

 (9) USEPA/OPP. Support Document for the Addition of Chemicals from 

Federal Insecticide, Fungicide, Rodenticide Act (FIFRA) Active 

Ingredients to EPCRA Section 313. U. S. Environmental Protection 

Agency, Washington, DC (1993).

 (10) USEPA/OPP. Triallate: Subchronic Neurotoxicity Study in Rats. 

U.S. Environmental Protection Agency, Washington, DC (1994).

 (11) USEPA/OPPT. Revised Draft Hazard Assessment Guidelines for 

Listing Chemicals on the Toxic Release Inventory. U. S. Environmental 

Protection Agency, Washington, DC (1992).

 (12) USEPA/OPPT. Support Document for the Addition of Chemicals 

from Section 112(b) of the Clean Air Act Amendments and Chlorinated 

Paraffins to EPCRA section 313. U. S. Environmental Protection Agency, 

Washington, DC (1993).

 (13) USEPA/OPPT. Support Document for the Health and Ecological 

Toxicity Review of TRI Expansion Chemicals. U. S. Environmental 

Protection Agency, Washington, DC (1993).

 (14) USEPA/OPPT. Response to Comments Received on the January 12, 

1994 Proposed Rule to Expand the EPCRA Section 313 List. U. S. 

Environmental Protection Agency, Washington, DC (1994).

VII. Regulatory Assessment Requirements

A. Executive Order 12866

 Under Executive Order 12866 (58 FR 51735, October 4, 1993) the 

Agency must determine whether the regulatory action is ``significant'' 

and therefore subject to review by the Office of Management and Budget 
(OMB) and the requirements of the Executive Order. Under section 3(f), 

the order defines as ``significant'' those regulatory actions likely to 

lead to a rule (1) Having an annual effect on the economy of $100 

million or more, or adversely and materially affecting a sector of the 

economy, productivity, competition, jobs, the environment, public 

health or safety, or State, local or tribal governments or communities 

(also referred to as ``economically significant''); (2) creating 

serious inconsistency or otherwise interfering with an action taken or 

planned by another agency; (3) materially altering the budgetary 

impacts of entitlements, grants, user fees, or loan programs; or (4) 

raising novel legal or policy issues arising out of legal mandates, the 

President's priorities, or the principles set forth in this Executive 

Order.

 EPA has prepared a Regulatory Impact Analysis (RIA) in conjunction 

with this rulemaking. A copy of this document (titled ``Regulatory 

Impact Analysis of the Final Rule to Add Various Chemicals and Chemical 

Categories to the EPCRA Section 313 List of Toxic Chemicals'') is 

available in the TSCA NCIC (See Unit V. of this preamble), for review 

and copying.

 EPA has estimated that the total costs to industry of adding the 

new chemicals to the EPCRA section 313 list is approximately $99 

million in the first year and $49 million each year thereafter. Costs 

to EPA are approximately $1 million per year.

 Table 2.-Summary of Cost Comparison Between Proposed and Final Rule 

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

 Final Rule with

 Proposed Rule Final Rule Alternate 

 Threshold 

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

Number of 313 286<SUP>1 286 

chemicals and 

chemical 

categories 

Number of new 2,404 1,225 1,225 

facilities 

Total number of 7,049 3,509 3,509 

facilities 

Number of TRI 28,196 14,036 10,548 

Form Rs 

submitted 

Number of annual 0 0 3,488 
certifications 

submitted 

First year $160.4 million $99 million $92.8 million 

industry costs 

Subsequent year $88.5 million $48.8 million $44.3 million 

industry costs 

EPA Costs $2.1 million $1.1 million $0.9 million 

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

 Source-RIA. The results for the alternate threshold are based on 

a 500 pound level of total waste.

 <SUP>1This includes 39 chemicals as part of two delineated 

categories.

 The costs for the final rule are different from the costs for the 

proposed rule, as shown in Table 2. There are two reasons for this 

change. First, the number of chemicals and chemical categories added 

has decreased from 313 to 286, which reduced the number of reports that 

would be submitted. Second, the number of reports estimated for one 

chemical, water dissociable nitrate compounds (reportable only when in 

aqueous solution), was increased from 2,146 to 3,066 to account for 

facilities that create water dissociable nitrate compounds in aqueous 

solution through on-site biological treatment of wastewater.

 Elsewhere in this issue of the Federal Register, EPA is finalizing 

a rule establishing an alternate threshold for facilities with low 

amounts of a listed toxic chemical in waste (see Unit II. of this 

preamble). Qualifying facilities would be eligible to submit an annual 

certification statement instead of a TRI Form R. Because the time 

required for the alternate threshold is less than the time required for 

a TRI Form R, the cost of compliance with this rule will be lowered as 

a result. The effect of the alternate threshold on the chemicals being 

added by this rule is demonstrated in Table 2. Further information on 

the effect of the alternate threshold is presented elsewhere in this 

issue of the Federal Register.

 The costs described in Table 2 represent only those actions that 

are required by this rule. There are other requirements that are linked 

to reporting under EPCRA section 313, but which are not required by 

this rule. There are 13 states that place a fee or tax on facilities 

that file a TRI Form R or report to EPA under EPCRA section 313, and 7 

states that mandate pollution prevention plans from such facilities. 

EPA has also created special requirements for certain facilities with 

NPDES storm water permits that report under EPCRA section 313.
 Adding chemicals and chemical categories to the EPCRA section 313 

list may cause some facilities to incur additional costs through these 

linked requirements. These costs have not been monetized, but they 

should not be significant. The linked fees and taxes are transfers, and 

not social costs, and many of the reporting facilities will not be 

located in the 13 states with fees and taxes. Also, the NPDES and 

pollution prevention planning requirements are most likely to create 

costs for facilities that are new reporters. There will be 

approximately 1,225 new reporters as a result of this rule, although 

not all of these will be subject to the NPDES requirements, or be 

located in states with pollution prevention planning requirements. The 

linkage to the NPDES requirements is limited to about two dozen of the 

new chemicals, not all 286 chemicals and chemical categories being 

added.

 The market failure that this rule is intended to correct is the 

externality created by the lack of information available to citizens 

about the releases and transfers of toxic chemicals in their 

communities. Taking no action would allow this externality (and the 

resultant social costs) to continue. It is expected that this 

rulemaking will generate benefits by providing citizens with access to 

information that otherwise would not be available to them. The benefits 

of the rule itself are limited to improvements in understanding, 

awareness and decision-making related to the provision and distribution 

of information.

 EPA believes that the rulemaking can reasonably be anticipated to 

indirectly yield health and environmental benefits by leading to 

reductions in the releases and transfers of toxic chemicals. These 

changes in behavior come at some cost to industry. The net benefits of 

the follow-on activities are the difference between the benefits of 

decreased chemical releases and transfers, and the costs of the actions 

needed to achieve them. As noted above, EPA has not quantified the 

benefits of this rule or the follow-on activities.

 This action was submitted to OMB for review, as required by 

Executive Order 12866, and any comments or changes made in response to 

OMB suggestions or recommendations have been documented in the public 

record.

B. Regulatory Flexibility Act

 The Regulatory Flexibility Act of 1980 requires each Federal agency 

to perform a Regulatory Flexibility Analysis for all rules that are 

likely to have a ``significant impact on a substantial number of small 
entities.'' EPA investigated the potential impact of the proposed rule 

on small businesses, and has prepared a Final Regulatory Flexibility 

Analysis (FRFA). This assessment has been included as part of the RIA 

and is summarized below.

 In assessing small business impacts, EPA calculated the costs 

incurred by two hypothetical facilities that are supplier notification 

facilities reporting to the TRI for the first time. Facilities were 

assumed to file only Form Rs, instead of any annual certification 

statements. Thus, the results are based on conservative assumptions. 

The first facility files a report for a single new chemical, while the 

other files reports for four new chemicals. For each hypothetical 

facility, annual regulatory costs were calculated and compared to 

average annual sales.

 The cost impact ratios were calculated based on the average annual 

sales of those facilities currently reporting under EPCRA section 313

for which annual sales and employee figures could be obtained from Dun 

Bradstreet. The Dun Bradstreet data base was used instead of Census 

data on the assumption that facilities that report under EPCRA section 

313 are not uniformly distributed throughout the entire population of 

facilities in each size category. EPA believes that it is reasonable to 

assume that facilities reporting under EPCRA section 313 have, on 

average, larger annual sales than the typical facility in an industry. 

Therefore, the annual sales of current reporters should be a more 

appropriate measure than the sales of all facilities in an industry.

 A small business was defined as having fewer than 50 employees. 

Although a more detailed break-down of size categories would have

allowed for a closer examination of the potential impact on even 

smaller facilities, the total number of observations in the matched 

data base was too small to allow for additional categories.

 EPA often uses a cost impact percentage of one percent as a 

threshold measure below which facilities are not considered to be 

significantly impacted as a result of a regulation. Under the scenario 

in which facilities are assumed to submit one TRI Form R, the cost 

impact percentages are well below one percent for all employee size 

classes in all SICs. The highest cost impact percentage is 0.4 percent 

for small facilities in Standard Industrial Classification (SIC) codes 

25 (Furniture) and 31 (Leather) in the first year of reporting.

 Under the scenario in which facilities are assumed to submit four 

TRI Form Rs, cost impact percentages in the first year of reporting are 

above one percent only for small facilities in SIC codes 25 (1.2 

percent) and 31 (1.1 percent). Cost impact percentages are below 0.8 

percent for all industries in subsequent years.
 The higher impact rates for the hypothetical facilities occur in 

industry sectors where there have historically been a relatively small 

number of establishments reporting. Approximately 8 percent of all 

facilities in SIC code 25 (Furniture) and 10 percent of all facilities 

in SIC code 31 (Leather) currently report to EPCRA section 313 

(compared to 57 percent of all facilities in the chemical industry). It 

is reasonable that large and medium businesses are more highly 

represented in these percentages than small businesses, because they 

would be more likely to exceed the EPCRA section 313 thresholds. In 

addition, facilities in SIC 25 and 31 have typically submitted fewer 

than four reports each, and would be less likely to submit four reports 

for the new chemicals than facilities in other industries.

 Thus, cost impacts for facilities potentially affected by the rule 

were not found to be of sufficient magnitude to cause significant 

impacts. Although EPA has found that the rule does not result in 

significant impacts on small facilities, EPA has separately developed 

alternatives to meet the goals of the Regulatory Flexibility Act (i.e., 

to accomplish the objectives of EPCRA section 313 while minimizing the 

economic impact on small entities). EPA proposed a rule establishing an 

alternative reporting threshold for low-level releases and transfers 

(July 28, 1994, 59 FR 38524). The proposal requested comment on five 

different levels for the alternate reporting threshold. This rule is 

being finalized elsewhere in today's issue of the Federal Register.

C. Paperwork Reduction Act

 The collection of information and other requirements under section 

313 of EPCRA and section 6607 of the PPA are covered under OMB approval 

number 2070-0093, which was issued on May 14, 1992. While this approval 

normally would have expired on November 30, 1992, it remains in effect 

pursuant to the 1993 Department of Veteran Affairs and Housing and 

Urban Development and Independent Agencies Appropriations Act, Pub. L. 

102-389, signed October 6, 1992, which states that:

 Notwithstanding the Paperwork Reduction Act of 1980 or any 

requirements thereunder the Environmental Protection Agency Toxic 

Chemical Release Inventory TRI Form R and instructions, revised 1991 

version issued May 19, 1992, and related requirements (OMB No. 2070-

0093), shall be effective for reporting under section 6607 of the 

Pollution Prevention Act of 1990 (Public Law 101-508) and section 

313 of the Superfund Amendments and Reauthorization Act of 1986 

(Public Law 99-499) until such time as revisions are promulgated 

pursuant to law.
 This final rule adds chemicals to the list of toxic chemicals 

subject to reporting under section 313 of EPCRA and section 6607 of the 

PPA and does not change the elements of the TRI reporting form, its 

instructions, or related requirements. Accordingly, the TRI Form R and 

instructions and related requirements remain in effect, as provided by 

Pub. L. 102-389.

 The industry reporting burden for collecting this information is 

estimated to average 53 hours per respondent annually, including time 

for reviewing instructions, searching existing data sources, gathering 

and maintaining the data needed, and completing and reviewing the 

collection of information. The actual burden to a specific facility may

deviate from this estimate depending on the complexity of the 

facility's operations and the profile of the release.

List of Subjects in 40 CFR Part 372

 Environmental protection, Community right-to-know, Reporting and 

recordkeeping requirements, Toxic chemicals.

 Dated: November 22, 1994.

Carol M. Browner,

Administrator.

 Therefore, 40 CFR part 372 is amended to read as follows:

Part 372--[AMENDED]

 1. The authority citation for part 372 continues to read as 

follows:

 Authority: 42 U.S.C. 11013 and 11028.

 2. In Sec. 372.65 by adding chemicals to paragraph (a) 

alphabetically, to paragraph (b) by CAS no. sequence, and to paragraph 

(c) by alphabetically adding six categories to read as follows:

Sec. 372.65 Chemicals and chemical categories to which the part 

applies.

 * * * * *
 (a) * * *

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

 Effective 

 Chemical Name CAS No. Date 

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

Abamectin [Avermectin B1] 71751-41-2 1/1/95

Acephate (Acetylphosphoramidothioic 30560-19-1 1/1/95

acid O,S-dimethyl ester) 

 

 ******* 

Acifluorfen, sodium salt [5-(2-Chloro- 62476-59-9 1/1/95

4-(triflouromethyl)phenoxy)-2-nitrobenzoic acid, sodium salt] 

 

 ******* 

Alachlor 15972-60-8 1/1/95

Aldicarb 116-06-3 1/1/95

 

 ******* 

d-trans-Allethrin [d-trans- 28057-48-9 1/1/95

Chrysanthemic acid of d-allethrone] 

Allylamine 107-11-9 1/1/95

 

 ******* 

Aluminum phosphide 20859-73-8 1/1/95

Ametryn (N-Ethyl-N'-(1-methylethyl)-6- 834-12-8 1/1/95

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

diamine) 

 

 ******* 

Amitraz 33089-61-1 1/1/95

 

 ******* 

Anilazine [4,6-dichloro-N-(2- 101-05-3 1/1/95

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

 

 ******* 

Atrazine (6-Chloro-N-ethyl-N'-(1- 1912-24-9 1/1/95

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

diamine) 

 
 ******* 

Bendiocarb [2,2-Dimethyl-1,3- 22781-23-3 1/1/95

benzodioxol-4-ol methylcarbamate] 

Benfluralin (N-Butyl-N-ethyl-2,6- 1861-40-1 1/1/95

dinitro-4- 

(trifluoromethyl)benzenamine) 

Benomyl 17804-35-2 1/1/95

 

 ******* 

Bifenthrin 82657-04-3 1/1/95

 

 ******* 

Bis(tributylin) oxide 56-35-9 1/1/95

Boron trichloride 10294-34-5 1/1/95

Boron trifluoride 7637-07-2 1/1/95

Bromacil (5-Bromo-6-methyl-3-(1- 314-40-9 1/1/95

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

pyrimidinedione) 

Bromacil, lithium salt [2,4-(1H,3H)- 53404-19-6 1/1/95

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

(1-methylpropyl), lithium salt] 

Bromine 7726-95-6 1/1/95

1-Bromo-1-(bromomethyl)-1,3- 35691-65-7 1/1/95

propanedicarbonitrile 

 

 ******* 

2-Bromo-2-nitropropane-1,3-diol 52-51-7 1/1/95

(Bronopol) 

 

 ******* 

Bromoxynil (3,5-Dibromo-4- 1689-84-5 1/1/95

hydroxybenzonitrile) 

Bromoxynil octanoate (Octanoic acid, 1689-99-2 1/1/95

2,6-dibromo-4-cyanophenyl ester) 

Brucine 357-57-3 1/1/95

 

 ******* 

C.I. Acid Red 114 6459-94-5 1/1/95

 

 ******* 

C.I. Direct Blue 218 28407-37-6 1/1/95

 
 ******* 

Carbofuran 1563-66-2 1/1/95

 

 ******* 

Carboxin (5,6-Dihydro-2-methyl-N- 5234-68-4 1/1/95

phenyl-1,4-oxathiin-3-carboxamide) 

 

 ******* 

Chinomethionat [6-Methyl-1,3- 2439-01-2 1/1/95

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

 

 ******* 

Chlorendic acid 115-28-6 1/1/95

Chlorimuron ethyl [Ethyl-2-[[[(4- 90982-32-4 1/1/95

chloro-6-methoxyprimidin-2-yl)- 

carbonyl]-amino]sulfonyl]benzoate] 

 

 ******* 

1-(3-Chloroallyl)-3,5,7-triaza-1- 4080-31-3 1/1/95

azoniaadamantane chloride 

p-Chloroaniline 106-47-8 1/1/95

 

 ******* 

3-Chloro-2-methyl-1-propene 563-47-3 1/1/95

p-Chlorophenyl isocyanate 104-12-1 1/1/95

Chloropicrin 76-06-2 1/1/95

 

 ******* 

3-Chloropropionitrile 542-76-7 1/1/95

 

 ******* 

p-Chloro-o-toluidine 95-69-2 1/1/95

2-Chloro-1,1,1-trifluoro-ethane (HCFC- 75-88-7 1/1/95

133a) 

Chlorotrifluoromethane (CFC-13) 75-72-9 1/1/95

3-Chloro-1,1,1-trifluoro-propane 460-35-5 1/1/95

(HCFC-253fb) 

Chlorpyrifos methyl [O,O-dimethyl-O- 5598-13-0 1/1/95

(3,5,6-trichloro-2- 

pyridyl)phosphorothioate 

Chlorsulfuron [2-chloro-N-[[4-methoxy- 64902-72-3 1/1/95

6-methyl-1,3,5-triazin-2- 
yl)amino]carbonyl]benzenesulfonamide 

] 

 

 ******* 

Crotonaldehyde 4170-30-3 1/1/95

Cyanazine 21725-46-2 1/1/95

 

 ******* 

Cycloate 1134-23-2 1/1/95

 

 ******* 

Cyclohexanol 108-93-0 1/1/95

Cyfluthrin [3-(2,2-Dichloroethenyl)- 68359-37-5 1/1/95

2,2-dimethylcyclopropanecarboxylic 

acid, cyano(4-fluoro-3- 

phenoxyphenyl)methyl ester] 

Cyhalothrin [3-(2-Chloro-3,3,3- 68085-85-8 1/1/95

trifluoro-1-propenyl)-2,2- 

dimethylcyclopropanecarboxylic acid 

cyano(3-phenoxyphenyl)methyl ester] 

 

 ******* 

Dazomet(Tetrahydro-3,5-dimethyl-2H- 533-74-4 1/1/95

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

Dazomet, sodium salt [Tetrahydro-3,5- 53404-60-7 1/1/95

dimethyl-2H-1,3,5-thiadiazine-2- 

thione, ion(1-), sodium] 

2,4,-DB 94-82-6 1/1/95

2,4-D butoxyethyl ester 1929-73-3 1/1/95

2,4-D butyl ester 94-80-4 1/1/95

2,4-D chlorocrotyl ester 2971-38-2 1/1/95

 

 ******* 

Desmedipham 13684-56-5 1/1/95

2,4-D 2-ethylhexyl ester 1928-43-4 1/1/95

2,4-D 2-ethyl-4-methylpentyl ester 53404-37-8 1/1/95

 

 ******* 

Diazinon 333-41-5 1/1/95

 

 ******* 

2,2-Dibromo-3-nitrilopropionamide 10222-01-2 1/1/95
 

 ******* 

Dicamba (3,6-Dichloro-2- 1918-00-9 1/1/95

methyoxybenzoic acid) 

Dichloran [2,6-Dichloro-4- 99-30-9 1/1/95

nitroaniline] 

 

 ******* 

3,3'-Dichlorobenzidine 612-83-9 1/1/95

dihydrochloride 

3,3'-Dichlorobenzidine sulfate 64969-34-2 1/1/95

 

 ******* 

trans-1,4-Dichloro-2-butene 110-57-6 1/1/95

1,2-Dichloro-1,1-difluoroethane (HCFC- 1649-08-7 1/1/95

132b) 

 

 ******* 

Dichlorofluoromethane (HCFC-21) 75-43-4 1/1/95

 

 ******* 

Dichloropentafluoropropane 127564-92-5 1/1/95

1,1-dichloro-1,2,2,3,3- 13474-88-9 1/1/95

pentafluoropropane (HCFC-225cc) 

1,1-dichloro-1,2,3,3,3- 111512-56-2 1/1/95

pentafluoropropane (HCFC-225eb) 

1,2-dichloro-1,1,2,3,3- 422-44-6 1/1/95

pentafluoropropane (HCFC-225bb) 

1,2-dichloro-1,1,3,3,3- 431-86-7 1/1/95

pentafluoropropane (HCFC-225da) 

1,3-dichloro-1,1,2,2,3- 507-55-1 1/1/95

pentafluoropropane (HCFC-225cb) 

1,3-dichloro-1,1,2,3,3- 136013-79-1 1/1/95

pentafluoropropane (HCFC-225ea) 

2,2-dichloro-1,1,1,3,3- 128903-21-9 1/1/95

pentafluoropropane (HCFC-225aa) 

2,3-dichloro-1,1,1,2,3- 422-48-0 1/1/95

pentafluoropropane (HCFC-225ba) 

3,3-dichloro-1,1,1,2,2- 422-56-0 1/1/95

pentafluoropropane (HCFC-225ca) 

Dichlorophene [ 2,2'-Methylene-bis(4- 97-23-4 1/1/95

chlorophenol)] 
 

 ******* 

trans-1,3-Dichloropropene 10061-02-6 1/1/95

 

 ******* 

Diclofop methyl [2-[4-(2,4- 51338-27-3 1/1/95

Dichlorophenoxy)phenoxy]propanoic 

acid, methyl ester] 

 

 ******* 

Dicyclopentadiene 77-73-6 1/1/95

 

 ******* 

Diethatyl ethyl 38727-55-8 1/1/95

 

 ******* 

Diflubenzuron 35367-38-5 1/1/95

Diglycidyl resorcinol ether 101-90-6 1/1/95

Dimethipin [2,3,-Dihydro-5,6-dimethyl- 55290-64-7 1/1/95

1,4-dithiin-1,1,4,4-tetraoxide] 

Dimethoate 60-51-5 1/1/95

 

 ******* 

3,3'-Dimethoxybenzidine 20325-40-0 1/1/95

dihydrochloride (o-Dianisidine 

dihydrochloride) 

3,3'-Dimethoxybenzidine hydrochloride 111984-09-9 1/1/95

(o-Dianisidine hydrochloride) 

Dimethylamine 124-40-3 1/1/95

Dimethylamine dicamba 2300-66-5 1/1/95

 

 ******* 

3,3'-Dimethylbenzidine 612-82-8 1/1/95

dihydrochloride (o-Tolidine 

dihydrochloride) 

3,3'-Dimethylbenzidine 41766-75-0 1/1/95

dihydrofluoride (o-Tolidine 

dihydrofluoride) 

 

 ******* 

Dimethyl chlorothiophosphate 2524-03-0 1/1/95

Dimethyldichlorosilane 75-78-5 1/1/95
N,N-Dimethylformamide 68-12-2 1/1/95

 

 ******* 

2,6-Dimethylphenol 576-26-1 1/1/95

 

 ******* 

Dinitrobutyl phenol (Dinoseb) 88-85-7 1/1/95

Dinocap 39300-45-3 1/1/95

 

 ******* 

Diphenamid 957-51-7 1/1/95

Diphenylamine 122-39-4 1/1/95

 

 ******* 

Dipotassium endothall [7- 2164-07-0 1/1/95

Oxabicyclo(2.2.1)heptane-2,3- 

dicarboxylic acid, dipotassium salt] 

Dipropyl isocinchomeronate 136-45-8 1/1/95

Disodium cyanodithioimidocarbonate 138-93-2 1/1/95

2,4-D isopropyl ester 94-11-1 1/1/95

2,4-Dithiobiuret 541-53-7 1/1/95

Diuron 330-54-1 1/1/95

Dodine [Dodecylguanidine monoacetate] 2439-10-3 1/1/95

2,4,-DP 120-36-5 1/1/95

2,4-D propylene glycol butyl ether 1320-18-9 1/1/95

ester 

2,4-D sodium salt 2702-72-9 1/1/95

 

 ******* 

Ethoprop [Phosphorodithioic acid O- 13194-48-4 1/1/95

ethyl S,S-dipropyl ester] 

 

 ******* 

Ethyl dipropylthiocarbamate [EPTC] 759-94-4 1/1/95

 

 ******* 

Famphur 52-85-7 1/1/95

Fenarimol [.alpha.-(2-Chlorophenyl)- 60168-88-9 1/1/95

.alpha.-4-chlorophenyl)-5- 

pyrimidinemethanol] 

Fenbutatin oxide (Hexakis(2-methyl-2- 13356-08-6 1/1/95

phenyl-propyl)distannoxane) 
Fenoxaprop ethyl [2-(4-((6-Chloro-2- 66441-23-4 1/1/95

benzoxazolylen)oxy)phenoxy)propanoic 

acid,ethyl ester] 

Fenoxycarb [2-(4- 72490-01-8 1/1/95

Phenoxyphenoxy)ethyl]carbamic acid 

ethyl ester] 

Fenpropathrin [2,2,3,3- 39515-41-8 1/1/95

Tetramethylcyclopropane carboxylic 

acid cyano(3-phenoxy-phenyl)methyl 

ester] 

Fenthion [O,O-Dimethyl O-[3-methyl-4- 55-38-9 1/1/95

(methylthio)phenyl]ester, 

phosphorothioic acid] 

Fenvalerate [4-Chloro-alpha-(1- 51630-58-1 1/1/95

methylethyl)benzeneacetic acid 

cyano(3-phenoxyphenyl)methyl ester] 

Ferbam [Tris(dimethylcarbamo- 14484-64-1 1/1/95

dithioato-S,S')iron] 

Fluazifop-butyl [2-[4-[[5- 69806-50-4 1/1/95

(Trifluoromethyl)-2-pyridinyl]oxy]- 

phenoxy]propanoic acid, butyl ester] 

Fluorine 7782-41-4 1/1/95

Fluorouracil (5-Fluorouracil) 51-21-8 1/1/95

Fluvalinate [N-[2-Chloro-4- 69409-94-5 1/1/95

(trifluoromethyl)phenyl]-DLvaline(+)-cyano (3- 

phenoxyphenyl)methyl ester] 

Folpet 133-07-3 1/1/95

Fomesafen [5-(2-Chloro-4- 72178-02-0 1/1/95

(trifluoromethyl)phenoxy)-Nmethylsulfonyl)-2-nitrobenzamide] 

 

 ******* 

alpha-Hexachlorocyclohexane 319-84-6 1/1/95

 

 ******* 

n-Hexane 110-54-3 1/1/95

Hexazinone 51235-04-2 1/1/95

Hydramethylnon [Tetrahydro-5,5- 67485-29-4 1/1/95

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

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

(trifluoromethyl)phenyl]ethenyl]-2- 
propenylidene]hydrazone] 

 

 ******* 

Imazalil [1-[2-(2,4-Dichlorophenyl)-2- 35554-44-0 1/1/95

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

3-Iodo-2-propynyl butylcarbamate 55406-53-6 1/1/95

Iron pentacarbonyl 13463-40-6 1/1/95

 

 ******* 

Isodrin 465-73-6 1/1/95

Isofenphos [2-[[Ethoxyl[(1- 25311-71-1 1/1/95

methylethyl)amino]phosphinothioyl]ox 

y]benzoic acid 1-methylethyl ester] 

 

 ******* 

Lactofen [5-(2-Chloro-4- 77501-63-4 1/1/95

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

ethoxy-1- methyl-2-oxoethyl ester] 

 

 ******* 

Linuron 330-55-2 1/1/95

Lithium carbonate 554-13-2 1/1/95

Malathion 121-75-5 1/1/95

 

 ******* 

Mecoprop 93-65-2 1/1/95

2-Mercaptobenzothiazole (MBT) 149-30-4 1/1/95

 

 ******* 

Merphos 150-50-5 1/1/95

Metham sodium (Sodium 137-42-8 1/1/95

methyldithiocarbamate) 

 

 ******* 

Methazole [2-(3,4-Dichlorophenyl)-4- 20354-26-1 1/1/95

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

dione] 

Methiocarb 2032-65-7 1/1/95

Methoxone (4-Chloro-2-methylphenoxy) 94-74-6 1/1/95

acetic acid (MCPA)) 

Methoxone-sodium salt ((4-chloro-2- 3653-48-3 1/1/95

methylphenoxy) acetate sodium salt) 
 

 ******* 

Methyl isothiocyanate 556-61-6 1/1/95

[Isothiocyanatomethane] 

2-Methyllactonitrile 75-86-5 1/1/95

 

 ******* 

N-Methylolacrylamide 924-42-5 1/1/95

Methyl parathion 298-00-0 1/1/95

N-Methyl-2-pyrrolidone 872-50-4 1/1/95

Methyltrichlorosilane 75-79-6 1/1/95

Metiram 9006-42-2 1/1/95

Metribuzin 21087-64-5 1/1/95

Mevinphos 7786-34-7 1/1/95

 

 ******* 

Molinate (1H-Azepine-1-carbothioic 2212-67-1 1/1/95

acid, hexahydro-S-ethyl ester) 

 

 ******* 

Monuron 150-68-5 1/1/95

 

 ******* 

Myclobutanil [.alpha.-Butyl-.alpha.- 88671-89-0 1/1/95

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

propanenitrile] 

Nabam 142-59-6 1/1/95

Naled 300-76-5 1/1/95

 

 ******* 

Nitrapyrin (2-Chloro-6- 1929-82-4 1/1/95

(trichloromethyl) pyridine) 

 

 ******* 

p-Nitroaniline 100-01-6 1/1/95

 

 ******* 

Norflurazon [4-Chloro-5-(methylamino)- 27314-13-2 1/1/95

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

pyridazinone] 

 

 ******* 
Oryzalin [4-(Dipropylamino)-3,5- 19044-88-3 1/1/95

dinitrobenzenesulfonamide] 

 

 ******* 

Oxydemeton methyl [S-(2- 301-12-2 1/1/95

(ethylsulfinyl)ethyl) o,o-dimethyl 

ester phosphorothioic acid] 

Oxydiazon [3-[2,4-Dichloro-5-(1- 19666-30-9 1/1/95

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

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

one] 

Oxyfluorfen 42874-03-3 1/1/95

Ozone 10028-15-6 1/1/95

Paraquat dichloride 1910-42-5 1/1/95

 

 ******* 

Pebulate [Butylethylcarbamothioic 1114-71-2 1/1/95

acid S-propyl ester] 

Pendimethalin [N-(1-Ethylpropyl)-3,4- 40487-42-1 1/1/95

dimethyl-2,6-dinitrobenzenamine] 

 

 ******* 

Pentobarbital sodium 57-33-0 1/1/95

 

 ******* 

Perchloromethyl mercaptan 594-42-3 1/1/95

Permethrin [3-(2,2-Dichloroethenyl)- 52645-53-1 1/1/95

2,2-dimethylcyclopropanecarboxylic 

acid, (3-phenoxyphenyl)methyl ester] 

Phenanthrene 85-01-8 1/1/95

 

 ******* 

Phenothrin [2,2-Dimethyl-3-(2-methyl- 26002-80-2 1/1/95

1-propenyl)cyclopropanecarboxylic 

acid (3-phenoxyphenyl)methyl ester] 

1,2-Phenylenediamine 95-54-5 1/1/95

1,3-Phenylenediamine 108-45-2 1/1/95

1,2-Phenylenediamine dihydrochloride 615-28-1 1/1/95

1,4-Phenylenediamine dihydrochloride 624-18-0 1/1/95

 

 ******* 

Phenytoin 57-41-0 1/1/95
 

 ******* 

Phosphine 7803-51-2 1/1/95

 

 ******* 

Picloram 1918-02-1 1/1/95

 

 ******* 

Piperonyl butoxide 51-03-6 1/1/95

Pirimiphos methyl [O-(2- 29232-93-7 1/1/95

(Diethylamino)-6-methyl-4- 

pyrimidinyl)-O,Odimethylphosphorothioate] 

 

 ******* 

Potassium bromate 7758-01-2 1/1/95

Potassium dimethyldithiocarbamate 128-03-0 1/1/95

Potassium N-methyldithiocarbamate 137-41-7 1/1/95

Profenofos [O-(4-Bromo-2- 41198-08-7 1/1/95

chlorophenyl)-O-ethyl-S-propyl 

phosphorothioate] 

Prometryn [N,N'-Bis(1-methylethyl)-6- 7287-19-6 1/1/95

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

diamine] 

Propachlor [2-Chloro-N-(1- 1918-16-7 1/1/95

methylethyl)-N-phenylacetamide] 

 

 ******* 

Propanil [N-(3,4- 709-98-8 1/1/95

Dichlorophenyl)propanamide] 

Propargite 2312-35-8 1/1/95

Propargyl alcohol 107-19-7 1/1/95

Propetamphos [3- 31218-83-4 1/1/95

[[(Ethylamino)methoxyphosphinothioyl 

]oxy]-2-butenoic acid, 1-methylethyl 

ester] 

Propiconazole [1-[2-(2,4- 60207-90-1 1/1/95

Dichlorophenyl)-4-propyl-1,3- 

dioxolan-2-yl]- methyl-1H-1,2,4,- 

triazole] 

 

 ******* 
Quizalofop-ethyl [2-[4-[(6-Chloro-2- 76578-14-8 1/1/95

quinoxalinyl)oxy]phenoxy]propanoic 

acid ethyl ester] 

Resmethrin [[5-(Phenylmethyl)-3- 10453-86-8 1/1/95

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

methyl-1- 

propenyl)cyclopropanecarboxylate]] 

 

 ******* 

Sethoxydim [2-[1-(Ethoxyimino)butyl]- 74051-80-2 1/1/95

5-[2-(ethylthio)propyl]-3-hydroxy-2- 

cyclohexen-1-one] 

 

 ******* 

Simazine 122-34-9 1/1/95

Sodium azide 26628-22-8 1/1/95

Sodium dicamba [3,6-Dichloro-2- 1982-69-0 1/1/95

methoxybenzoic acid, sodium salt] 

Sodium dimethyldithiocarbamate 128-04-1 1/1/95

Sodium fluoroacetate 62-74-8 1/1/95

Sodium nitrite 7632-00-0 1/1/95

Sodium pentachlorophenate 131-52-2 

Sodium o-phenylphenoxide 132-27-4 1/1/95

 

 ******* 

Sulfuryl fluoride [Vikane] 2699-79-8 1/1/95

Sulprofos [O-Ethyl O-[4- 35400-43-2 1/1/95

(methylthio)phenyl]phosphorodithioic 

acid S-propyl ester] 

Tebuthiuron [N-[5-(1,1-Dimethylethyl)- 34014-18-1 1/1/95

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

dimethylurea] 

Temephos 3383-96-8 1/1/95

Terbacil [5-Chloro-3-(1,1- 5902-51-2 1/1/95

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

pyrimidinedione] 

 

 ******* 

1,1,1,2-Tetrachloro-2-fluoroethane 354-11-0 1/1/95

(HCFC-121a) 

1,1,2,2-Tetrachloro-1-fluoroethane 354-14-3 1/1/95

(HCFC-121) 
 

 ******* 

Tetracycline hydrochloride 64-75-5 1/1/95

Tetramethrin [2,2-Dimethyl-3-(2- 7696-12-0 1/1/95

methyl-1- 

propenyl)cyclopropanecarboxylic acid 

(1,3,4,5,6,7-hexahydro-1,3-dioxo-2Hisoindol-2-yl)methyl ester] 

 

 ******* 

Thiabendazole [2-(4-Thiazolyl)-1H- 148-79-8 1/1/95

benzimidazole] 

 

 ******* 

Thiobencarb [Carbamic acid, 28249-77-6 1/1/95

diethylthio-, s-(p-chlorobenzyl)] 

 

 ******* 

Thiodicarb 59669-26-0 1/1/95

Thiophanate ethyl [[1,2- 23564-06-9 1/1/95

Phenylenebis(iminocarbonothioyl)]bis 

carbamic acid diethyl ester] 

Thiophanate-methyl 23564-05-8 1/1/95

Thiosemicarbazide 79-19-6 1/1/95

 

 ******* 

Triadimefon [1-(4-Chlorophenoxy)-3,3- 43121-43-3 1/1/95

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

butanone] 

Triallate 2303-17-5 1/1/95

 

 ******* 

Tribenuron methyl [2-(((((4-Methoxy-6- 101200-48-0 1/1/95

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

methylamino)carbonyl)amino)sulfonyl)- 

, methyl ester] 

Tributyltin fluoride 1983-10-4 1/1/95

Tributyltin methacrylate 2155-70-6 1/1/95

S,S,S-Tributyltrithiophosphate (DEF) 78-48-8 1/1/95

 

 ******* 

Trichloroacetyl chloride 76-02-8 1/1/95
 

 ******* 

1,2,3-Trichloropropane 96-18-4 1/1/95

Triclopyr, triethylammonium salt 57213-69-1 1/1/95

Triethylamine 121-44-8 1/1/95

Triforine [N,N'-[1,4-Piperazinediyl- 26644-46-2 1/1/95

bis(2,2,2-trichloroethylidene)] 

bisformamide] 

 

 ******* 

Trimethylchlorosilane 75-77-4 1/1/95

2,3,5-Trimethylphenyl methylcarbamate 2655-15-4 1/1/95

Triphenyltin chloride 639-58-7 1/1/95

Triphenyltin hydroxide 76-87-9 1/1/95

 

 ******* 

Vinclozolin [3-(3,5-Dichlorophenyl)-5- 50471-44-8 1/1/95

ethenyl-5-methyl-2,4- 

oxazolidinedione] 

 

 ******* 

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

 (b) * * *

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

 Effective 

 CAS No. Chemical Name Date 

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

 

 ******* 

51-03-6 Piperonyl butoxide 1/1/95

51-21-8 Fluorouracil (5-Fluorouracil) 1/1/95

 

 ******* 

52-51-7 2-Bromo-2-nitropropane-1,3-diol 1/1/95

 (Bronopol) 

 

 ******* 

52-85-7 Famphur 1/1/95

 

 ******* 
55-38-9 Fenthion [O,O-Dimethyl O-[3-methyl-4- 1/1/95

 (methylthio)phenyl] ester, 

 phosphorothioic acid] 

 

 ******* 

56-35-9 Bis(tributyltin) oxide 1/1/95

 

 ******* 

57-33-0 Pentobarbital sodium 1/1/95

57-41-0 Phenytoin 1/1/95

 

 ******* 

60-51-5 Dimethoate 1/1/95

 

 ******* 

62-74-8 Sodium fluoroacetate 1/1/95

 

 ******* 

64-75-5 Tetracycline hydrochloride 1/1/95

 

 ******* 

68-12-2 N,N-Dimethylformamide 1/1/95

 

 ******* 

75-43-4 Dichlorofluoromethane (HCFC-21) 1/1/95

 

 ******* 

75-72-9 Chlorotrifluoromethane (CFC-13) 1/1/95

75-77-4 Trimethylchlorosilane 1/1/95

75-78-5 Dimethyldichlorosilane 1/1/95

75-79-6 Methyltrichlorosilane 1/1/95

75-86-5 2-Methyllactonitrile 1/1/95

75-88-7 2-Chloro-1,1,1-trifluoroethane (HCFC- 1/1/95

 133a) 

76-02-8 Trichloroacetyl chloride 1/1/95

76-06-2 Chloropicrin 1/1/95

 

 ******* 

76-87-9 Triphenyltin hydroxide 1/1/95

 

 ******* 

77-73-6 Dicyclopentadiene 1/1/95
 

 ******* 

78-48-8 S,S,S-Tributyltrithiophosphate (DEF) 1/1/95

 

 ******* 

79-19-6 Thiosemicarbazide 1/1/95

 

 ******* 

85-01-8 Phenanthrene 1/1/95

 

 ******* 

88-85-7 Dinitrobutyl phenol (Dinoseb) 1/1/95

 

 ******* 

93-65-2 Mecoprop 1/1/95

94-11-1 2,4-D isopropyl ester 1/1/95

 

 ******* 

94-74-6 Methoxone (4-Chloro-2-methylphenoxy) 1/1/95

 acetic acid (MCPA) 

 

 ******* 

94-80-4 2,4-D butyl ester 1/1/95

94-82-6 2,4-DB 1/1/95

 

 ******* 

95-54-5 1,2-Phenylenediamine 1/1/95

 

 ******* 

95-69-2 p-Chloro-o-toluidine 1/1/95

 

 ******* 

96-18-4 1,2,3-Trichloropropane 1/1/95

 

 ******* 

97-23-4 Dichlorophene [ 2,2'-Methylene-bis(4- 1/1/95

 chlorophenol)] 

 

 ******* 

99-30-9 Dichloran [2,6-Dichloro-4- 1/1/95

 nitroaniline] 

 
 ******* 

100-01-6 p-Nitroaniline 1/1/95

 

 ******* 

101-05-3 Anilazine [4,6-dichloro-N-(2- 1/1/95

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

 

 ******* 

101-90-6 Diglycidyl resorcinol ether 1/1/95

 

 ******* 

104-12-1 p-Chlorophenyl isocyanate 1/1/95

 

 ******* 

106-47-8 p-Chloroaniline 1/1/95

 

 ******* 

107-11-9 Allylamine 1/1/95

 

 ******* 

107-19-7 Propargyl alcohol 1/1/95

 

 ******* 

108-45-2 1,3-Phenylenediamine 1/1/95

 

 ******* 

108-93-0 Cyclohexanol 1/1/95

 

 ******* 

110-54-3 n-Hexane 1/1/95

110-57-6 trans-1,4-Dichloro-2-butene 1/1/95

 

 ******* 

115-28-6 Chlorendic acid 1/1/95

 

 ******* 

116-06-3 Aldicarb 1/1/95

 

 ******* 

120-36-5 2,4-DP 1/1/95

 

 ******* 
121-44-8 Triethylamine 1/1/95

 

 ******* 

121-75-5 Malathion 1/1/95

122-34-9 Simazine 1/1/95

122-39-4 Diphenylamine 1/1/95

 

 ******* 

124-40-3 Dimethylamine 1/1/95

 

 ******* 

128-03-0 Potassium dimethyldithiocarbamate 1/1/95

128-04-1 Sodium dimethyldithiocarbamate 1/1/95

 

 ******* 

131-52-2 Sodium pentachlorophenate 1/1/95

132-27-4 Sodium o-phenylphenoxide 1/1/95

 

 ******* 

133-07-3 Folpet 1/1/95

 

 ******* 

136-45-8 Dipropyl isocinchomeronate 1/1/95

137-41-7 Potassium n-methyldithiocarbamate 1/1/95

137-42-8 Metham Sodium 1/1/95

138-93-2 Disodium cyanodithioimidocarbonate 1/1/95

 

 ******* 

142-59-6 Nabam 1/1/95

148-79-8 Thiabendazole [2-(4-Thiazolyl)-1H- 1/1/95

 benzimidazole] 

149-30-4 2-Mercaptobenzothiazole 1/1/95

150-50-5 Merphos 1/1/95

150-68-5 Monuron 1/1/95

 

 ******* 

298-00-0 Methyl parathion 1/1/95

300-76-5 Naled 1/1/95

301-12-2 Oxydemeton methyl [s-(2- 1/1/95

 (Ethylsulfinyl)ethyl)o,o-dimethyl 

 ester phosphorothioic acid] 

 
 ******* 

314-40-9 Bromacil (5-Bromo-6-methyl-3-(1- 1/1/95

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

 pyrimidinedione) 

319-84-6 alpha-Hexachlorocyclohexane 1/1/95

330-54-1 Diuron 1/1/95

330-55-2 Linuron 1/1/95

333-41-5 Diazinon 1/1/95

 

 ******* 

354-11-0 1,1,1,2-Tetrachloro-2-fluoroethane 1/1/95

 (HCFC-121a) 

354-14-3 1,1,2,2-Tetrachloro-1-fluoroethane 1/1/95

 (HCFC-121) 

357-57-3 Brucine 1/1/95

422-44-6 1,2-dichloro-1,1,2,3,3- 1/1/95

 pentafluoropropane (HCFC-225bb) 

422-48-0 2,3-dichloro-1,1,1,2,3- 1/1/95

 pentafluoropropane (HCFC-225ba) 

422-56-0 3,3-dichloro-1,1,1,2,2- 1/1/95

 pentafluoropropane (HCFC-225ca) 

431-86-7 1,2-dichloro-1,1,3,3,3- 1/1/95

 pentafluoropropane (HCFC-225da) 

460-35-5 3-chloro-1,1,1-trifluoropropane (HCFC- 1/1/95

 253fb) 

 

 ******* 

465-73-6 Isodrin 1/1/95

 

 ******* 

507-55-1 1,3-dichloro-1,1,2,2,3- 1/1/95

 pentafluoropropane (HCFC-225cb) 

 

 ******* 

533-74-4 Dazomet (Tetrahydro-3,5-dimethyl-2H- 1/1/95

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

 

 ******* 

541-53-7 2,4-Dithiobiuret 1/1/95

 

 ******* 

542-76-7 3-Chloropropionitrile 1/1/95
 

 ******* 

554-13-2 Lithium carbonate 1/1/95

556-61-6 Methyl isothiocyanate 1/1/95

 [Isothiocyanatomethane] 

563-47-3 3-Chloro-2-methyl-1-propene 1/1/95

 

 ******* 

576-26-1 2,6-Dimethylphenol 1/1/95

 

 ******* 

594-42-3 Perchloromethyl mercaptan 1/1/95

 

 ******* 

612-82-8 3,3'-Dimethylbenzidine 1/1/95

 dihydrochloride (o-Tolidine 

 dihydrochloride) 

612-83-9 3,3'-Dichlorobenzidine 1/1/95

 dihydrochloride 

 

 ******* 

615-28-1 1,2-Phenylenediamine dihydrochloride 1/1/95

 

 ******* 

624-18-0 1,4-Phenylenediamine dihydrochloride 1/1/95

 

 ******* 

639-58-7 Triphenyltin chloride 1/1/95

 

 ******* 

709-98-8 Propanil [N-(3,4- 1/1/95

 Dichlorophenyl)propanamide] 

 

 ******* 

759-94-4 Ethyl dipropylthiocarbamate (EPTC) 1/1/95

834-12-8 Ametryn (N-Ethyl-N'-(1-methylethyl)-6- 1/1/95

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

 diamine) 

872-50-4 N-Methyl-2-pyrrolidone 1/1/95

 

 ******* 

924-42-5 N-Methylolacrylamide 1/1/95
957-51-7 Diphenamid 1/1/95

 

 ******* 

1114-71-2 Pebulate [Butylethylcarbamo-thioic 1/1/95

 acid S-propyl ester] 

 

 ******* 

1134-23-2 Cycloate 1/1/95

 

 ******* 

1320-18-9 2,4-D propylene glycol butyl ether 1/1/95

 ester 

 

 ******* 

1563-66-2 Carbofuran 1/1/95

1649-08-7 1,2-dichloro-1,1-difluoroethane (HCFC- 1/1/95

 132b) 

1689-84-5 Bromoxynil (3,5-Dibromo-4- 1/1/95

 hydroxybenzonitrile) 

1689-99-2 Bromoxynil octanoate (Octanoic acid, 1/1/95

 2,6-dibromo-4-cyanophenyl ester) 

 

 ******* 

1861-40-1 Benfluralin(N-Butyl-N-ethyl-2,6- 1/1/95

 dinitro-4- 

 (trifluoromethyl)benzenamine) 

 

 ******* 

1910-42-5 Paraquat dichloride 1/1/95

1912-24-9 Atrazine (6-Chloro-N-ethyl-N'-(1- 1/1/95

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

 diamine) 

1918-00-9 Dicamba (3,6-Dichloro-2- 1/1/95

 methyoxybenzoic acid) 

1918-02-1 Picloram 1/1/95

1918-16-7 Propachlor [2-Chloro-N-(1- 1/1/95

 methylethyl)-N-phenylacetamide] 

1928-43-4 2,4-D 2-ethylhexyl ester 1/1/95

1929-73-3 2,4-D butoxyethyl ester 1/1/95

1929-82-4 Nitrapyrin (2-Chloro-6- 1/1/95

 (trichloromethyl)pyridine) 

 
 ******* 

1982-69-0 Sodium dicamba [3,6-Dichloro-2- 1/1/95

 methoxybenzoic acid, sodium salt] 

1983-10-4 Tributyltin fluoride 1/1/95

2032-65-7 Methiocarb 1/1/95

2155-70-6 Tributyltin methacrylate 1/1/95

2164-07-0 Dipotassium endothall [7- 1/1/95

 Oxabicyclo(2.2.1)heptane-2,3- 

 dicarboxylic acid, dipotassium salt] 

 

 ******* 

2212-67-1 Molinate (1H-Azepine-1-carbothioic 1/1/95

 acid, hexahydro-S-ethyl ester) 

 

 ******* 

2300-66-5 Dimethylamine dicamba 1/1/95

 

 ******* 

2303-17-5 Triallate 1/1/95

2312-35-8 Propargite 1/1/95

2439-01-2 Chinomethionat [6-Methyl-1,3- 1/1/95

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

2439-10-3 Dodine [Dodecylguanidine monoacetate] 1/1/95

2524-03-0 Dimethyl chlorothiophosphate 1/1/95

 

 ******* 

2655-15-4 2,3,5-Trimethylphenyl methylcarbamate 1/1/95

2699-79-8 Sulfuryl Fluoride [Vikane] 1/1/95

2702-72-9 2,4-D sodium salt 1/1/95

 

 ******* 

2971-38-2 2,4-D chlorocrotyl ester 1/1/95

 

 ******* 

3383-96-8 Temephos 1/1/95

3653-48-3 Methoxone - sodium salt (4-Chloro-2- 1/1/95

 methylphenoxy acetate sodium salt) 

 

 ******* 

4080-31-3 1-(3-Chloroallyl)-3,5,7-triaza-1- 1/1/95

 azoniaadamantane chloride 

4170-30-3 Crotonaldehyde 1/1/95
 

 ******* 

5234-68-4 Carboxin (5,6-Dihydro-2-methyl-N- 1/1/95

 phenyl-1,4-oxathiin-3-carboxamide) 

5598-13-0 Chlorpyrifos methyl [O,O-dimethyl-O- 1/1/95

 (3,5,6-trichloro-2- 

 pyridyl)phosphorothioate] 

5902-51-2 Terbacil [5-Chloro-3-(1,1- 1/1/95

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

 pyrimidinedione] 

6459-94-5 C.I. Acid Red 114 1/1/95

 

 ******* 

7287-19-6 Prometryn [N,N'-Bis(1-methylethyl)-6- 1/1/95

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

 diamine] 

 

 ******* 

7632-00-0 Sodium nitrite 1/1/95

7637-07-2 Boron trifluoride 1/1/95

 

 ******* 

7696-12-0 Tetramethrin [2,2-Dimethyl-3-(2- 1/1/95

 methyl-1-propenyl)cyclopropane- 

 carboxylic acid (1,3,4,5,6,7- 

 hexahydro-1,3-dioxo-2H-isoindol-2- 

 yl)methyl ester] 

 

 ******* 

7726-95-6 Bromine 1/1/95

7758-01-2 Potassium bromate 1/1/95

7782-41-4 Fluorine 1/1/95

 

 ******* 

7786-34-7 Mevinphos 1/1/95

7803-51-2 Phosphine 1/1/95

 

 ******* 

9006-42-2 Metiram 1/1/95

10028-15-6 Ozone 1/1/95

 

 ******* 
10061-02-6 trans-1,3-Dichloropropene 1/1/95

10222-01-2 2,2-Dibromo-3-nitrilopropionamide 1/1/95

10294-34-5 Boron trichloride 1/1/95

10453-86-8 Resmethrin [[5-(Phenylmethyl)-3- 1/1/95

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

 methyl-1- 

 propenyl)cyclopropanecarboxylate]] 

 

 ******* 

13194-48-4 Ethoprop [Phosphorodithioic acid O- 1/1/95

 ethyl S,S-dipropyl ester] 

13356-08-6 Fenbutatin oxide (hexakis(2-methyl-2- 1/1/95

 phenylpropyl)distannoxane) 

13463-40-6 Iron pentacarbonyl 1/1/95

13474-88-9 1,1-Dichloro-1,2,2,3,3- 1/1/95

 pentafluoropropane (HCFC-225cc) 

13684-56-5 Desmedipham 1/1/95

14484-64-1 Ferbam [Tris(dimethylcarbamo- 1/1/95

 dithioato-S,S')iron] 

15972-60-8 Alachlor 1/1/95

 

 ******* 

17804-35-2 Benomyl 1/1/95

19044-88-3 Oryzalin [4-(Dipropylamino)-3,5- 1/1/95

 dinitrobenzene-sulfonamide] 

19666-30-9 Oxydiazon [3-[2,4-Dichloro-5-(1- 1/1/95

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

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

 one] 

20325-40-0 3,3'-Dimethoxybenzidine 1/1/95

 dihydrochloride (Dianisidine 

 dihydrochloride) 

20354-26-1 Methazole [2-(3,4-Dichlorophenyl)-4- 1/1/95

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

 dione] 

 

 ******* 

20859-73-8 Aluminum phosphide 1/1/95

21087-64-5 Metribuzin 1/1/95

21725-46-2 Cyanazine 1/1/95

22781-23-3 Bendiocarb [2,2-Dimethyl-1,3- 1/1/95

 benzodioxol-4-ol methylcarbamate] 
23564-05-8 Thiophanate methyl 1/1/95

23564-06-9 Thiophanate ethyl [[1,2- 1/1/95

 Phenylenebis(iminocarbonothioyl)]bis 

 carbamic acid diethyl ester] 

25311-71-1 Isofenphos [2-[[Ethoxyl[(1- 1/1/95

 methylethyl)amino]phosphinothioyl]ox 

 y]benzoic acid 1-methylethyl ester] 

26002-80-2 Phenothrin [2,2-Dimethyl-3-(2-methyl- 1/1/95

 1-propenyl)cyclopropanecarboxylic 

 acid (3-phenoxyphenyl)methyl ester] 

 

 ******* 

26628-22-8 Sodium azide 1/1/95

26644-46-2 Triforine [N,N'-[1,4- 1/1/95

 Piperazinediylbis(2,2,2- 

 trichloroethylidene)] bisformamide] 

27314-13-2 Norflurazon [4-Chloro-5-(methylamino)- 1/1/95

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

 pyridazinone] 

28057-48-9 d-trans-Allethrin [d-trans- 1/1/95

 Chrysanthemic acid of d-allethrone] 

28249-77-6 Thiobencarb [Carbamic acid, 1/1/95

 diethylthio-, s-(p-chlorobenzyl)] 

28407-37-6 C.I. Direct Blue 218 1/1/95

29232-93-7 Pirimiphos methyl [O-(2- 1/1/95

 (Diethylamino)-6-methyl-4- 

 pyrimidinyl)-O,O-dimethyl 

 phosphorothioate] 

30560-19-1 Acephate (Acetylphosphoramidothioic 1/1/95

 acid O,S-dimethyl ester) 

31218-83-4 Propetamphos [3- 1/1/95

 [[(Ethylamino)methoxyphosphino- 

 thioyl]oxy]-2-butenoic acid, 1- 

 methylethyl ester] 

33089-61-1 Amitraz 1/1/95

34014-18-1 Terbuthiuron [N-[5-(1,1- 1/1/95

 Dimethylethyl)-1,3,4-thiadiazol-2- 

 yl)-N,N'- dimethylurea] 

 

 ******* 

35367-38-5 Diflubenzuron 1/1/95

35400-43-2 Sulprofos [O-Ethyl O-[4- 1/1/95
 (methylthio)phenyl]phosphorodithioic 

 acid S-propyl ester] 

35554-44-0 Imazalil [1-[2-(2,4-Dichlorophenyl)-2- 1/1/95

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

35691-65-7 1-Bromo-1-(bromomethyl)-1,3- 1/1/95

 propanedicarbonitrile 

38727-55-8 Diethatyl ethyl 1/1/95

 

 ******* 

39300-45-3 Dinocap 1/1/95

39515-41-8 Fenpropathrin [2,2,3,3- 1/1/95

 Tetramethylcyclopropane carboxylic 

 acid cyano(3-phenoxyphenyl)methyl 

 ester] 

40487-42-1 Pendimethalin [N-(1-Ethylpropyl)-3,4- 1/1/95

 dimethyl-2,6-dinitrobenzen-amine] 

41198-08-7 Profenofos [O-(4-Bromo-2- 1/1/95

 chlorophenyl)-O-ethyl-S-propyl 

 phosphorothioate] 

41766-75-0 3,3'-Dimethylbenzidine 1/1/95

 dihydrofluoride (ortho-Tolidine 

 dihydrofluoride) 

42874-03-3 Oxyfluorfen 1/1/95

43121-43-3 Triadimefon [1-(4-Chlorophenoxy)-3,3- 1/1/95

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

 butanone] 

50471-44-8 Vinclozolin [3-(3,5-Dichlorophenyl)-5- 1/1/95

 ethenyl-5-methyl-2,4- 

 oxazolidinedione] 

51235-04-2 Hexazinone 1/1/95

51338-27-3 Diclofop methyl [2-[4-(2,4- 1/1/95

 Dichlorophenoxy)phenoxy]propanoic 

 acid, methyl ester] 

51630-58-1 Fenvalerate 1/1/95

52645-53-1 Permethrin [3-(2,2-Dichloroethenyl)- 1/1/95

 2,2-dimethylcyclopropanecarboxylic 

 acid, (3-phenoxyphenyl)methyl ester] 

53404-19-6 Bromacil, lithium salt [2,4-(1H,3H)- 1/1/95

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

 (1-methylpropyl), lithium salt] 

53404-37-8 2,4-D 2-ethyl-4-methylpentyl ester 1/1/95

53404-60-7 Dazomet, sodium salt [Tetrahydro-3,5- 1/1/95
 dimethyl-2H-1,3,5-thiadiazine-2- 

 thione, ion(1-), sodium] 

55290-64-7 Dimethipin [2,3,-Dihydro-5,6-dimethyl- 1/1/95

 1,4-dithiin 1,1,4,4-tetraoxide] 

55406-53-6 3-Iodo-2-propynyl butylcarbamate 1/1/95

57213-69-1 Triclopyr, triethylammonium salt 1/1/95

59669-26-0 Thiodicarb 1/1/95

60168-88-9 Fenarimol [.alpha.-(2-Chlorophenyl)- 1/1/95

 .alpha.-4-chlorophenyl)-5-pyrimidine- 

 methanol] 

60207-90-1 Propiconazole [1-[2-(2,4- 1/1/95

 Dichlorophenyl)-4-propyl-1,3- 

 dioxolan-2-yl]-methyl-1H-1,2,4,- 

 triazole] 

62476-59-9 Acifluorfen, sodium salt [5-(2-Chloro- 1/1/95

 4-(triflouromethyl)phenoxy)-2-nitro- 

 benzoic acid, sodium salt] 

62924-70-3 Flumetralin [2-Chloro-N-(2,6-dinitro- 1/1/95

 4-(trifluoromethyl)-phenyl)-N-ethyl- 

 6-fluorobenzenemethanamine] 

 

 ******* 

64902-72-3 Chlorsulfuron [2-chloro-N-[[4-methoxy- 1/1/95

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

 carbonyl]benzenesulfonamide] 

64969-34-2 3,3'-Dichlorobenzidine.sulfate 1/1/95

66441-23-4 Fenoxaprop ethyl [2-(4-((6-Chloro-2- 1/1/95

 benzoxazolylen)oxy)phenoxy) 

 propanoic acid, ethyl ester] 

67485-29-4 Hydramethylnon [Tetrahydro-5,5- 1/1/95

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

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

 (trifluoromethyl)phenyl]ethenyl]-2- 

 propenylidene]hydrazone] 

68085-85-8 Cyhalothrin [3-(2-Chloro-3,3,3- 1/1/95

 trifluoro-1-propenyl)-2,2- 

 dimethylcyclopropanecarboxylic acid 

 cyano(3-phenoxyphenyl)methyl ester] 

68359-37-5 Cyfluthrin [3-(2,2-Dichloro-ethenyl)- 1/1/95

 2,2-dimethylcyclo-propanecarboxylic 

 acid, cyano(4-fluoro-3- 

 phenoxyphenyl)methyl ester] 
69409-94-5 Fluvalinate [N-[2-Chloro-4- 1/1/95

 (trifluoromethyl)phenyl]-DL- 

 valine(+)-cyano(3- 

 phenoxyphenyl)methylester] 

69806-50-4 Fluazifop-butyl [2-[4-[[5- 1/1/95

 (Trifluoromethyl)-2-pyridinyl]oxy]- 

 phenoxy]propanoic acid, butyl ester] 

71751-41-2 Abamectin [Avermectin B1] 1/1/95

72178-02-0 Fomesafen [5-(2-Chloro-4- 1/1/95

 (trifluoromethyl)phenoxy)-N- 

 methylsulfonyl)-2- nitrobenzamide] 

72490-01-8 Fenoxycarb [2-(4- 1/1/95

 Phenoxyphenoxy)ethyl]carbamic acid 

 ethyl ester] 

74051-80-2 Sethoxydim [2-[1-(Ethoxyimino)butyl]- 1/1/95

 5-[2-(ethylthio)propyl]-3-hydroxy-2- 

 cyclohexen-1-one] 

76578-14-8 Quizalofop-ethyl [2-[4-[(6-Chloro-2- 1/1/95

 quinoxalinyl)oxy]phenoxy] propanoic 

 acid ethyl ester] 

77501-63-4 Lactofen [5-(2-Chloro-4- 1/1/95

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

 ethoxy-1-methyl-2-oxoethyl ester] 

82657-04-3 Bifenthrin 1/1/95

88671-89-0 Myclobutanil [.alpha.-Butyl-.alpha.- 1/1/95

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

 1-propanenitrile] 

 

 ******* 

90982-32-4 Chlorimuron ethyl [Ethyl-2-[[[(4- 1/1/95

 chloro-6-methoxyprimidin-2-yl)- 

 carbonyl]-amino]sulfonyl]benzoate] 

101200-48-0 Tribenuron methyl [2-(((((4-Methoxy-6- 1/1/95

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

 methylamino)carbonyl)amino)sulfonyl)- 

 , methyl ester] 

111512-56-2 1,1-dichloro-1,2,3,3,3- 1/1/95

 pentafluoropropane (HCFC-225eb) 

111984-09-9 3,3'-Dimethoxybenzidine hydrochloride 1/1/95

 (Dianisidine dihydrochloride) 

127564-92-5 Dichloropentafluoropropane 1/1/95

128903-21-9 2,2-Dichloro-1,1,1,3,3- 1/1/95
 pentafluoropropane (HCFC-225aa) 

136013-79-1 1,3-Dichloro-1,1,2,3,3- 1/1/95

 pentafluoropropane (HCFC-225ea) 

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

 (c) * * *

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

 Effective 

 Category Name Date 

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

 

 ******* 

Diisocyanates (This category includes only those chemicals 

listed below) 1/1/95

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

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

 002556-36-7 1,4-Cyclohexane diisocyanate 

 134190-37-7 Diethyldiisocyanatobenzene 

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

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

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

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

 000139-25-3 3,3'-Dimethyldiphenylmethane-4,4'- 

 diisocyanate 

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

004098-71-0 Isophorone diisocyanate 

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

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

 000101-68-8 Methylenebis(phenylisocyanate) (MDI) 

 003173-72-6 1,5-Naphthalene diisocyanate 

 000123-61-5 1,3-Phenylene diisocyanate 

 000104-49-4 1,4-Phenylene diisocyanate 

 009016-87-9 Polymeric diphenylmethane diisocyanate 

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

 015646-96-5 2,4,4-Trimethylhexamethylene diisocyanate 

 

 ******* 

Nicotine and salts 1/1/95

Nitrate compounds (water dissociable; reportable only when 

in aqueous solution) 1/1/95

 
 ******* 

Polychlorinated alkanes: Includes those chemicals defined 

by the following formula: 1/1/95

 C<INF>xH<INF>2x-yCl<INF>y 

where x = 10 to 13; 

 y = 3 to 12; and 

 where the average chlorine content ranges from 40-70% 

 with the limiting molecular formulas C<INF>10H<INF>19Cl<INF>3 and 

 C<INF>13H<INF>16Cl<INF>12. 

 

 ******* 

Polycyclic aromatic compounds (PACs): (This category 

includes only those chemicals listed below) 1/1/95

 00056-55-3 Benz(a)anthracene 

 00218-01-9 Benzo(a)phenanthrene 

 00050-32-8 Benzo(a)pyrene 

 00205-99-2 Benzo(b)fluoranthene 

 00205-82-3 Benzo(j)fluoranthene 

 00207-08-9 Benzo(k)fluoranthene 

 00189-55-9 Benzo(rst)pentaphene 

 00226-36-8 Dibenz(a,h)acridine 

 00224-42-0 Dibenz(a,j)acridine 

 00053-70-3 Dibenzo(a,h)anthracene 

 05385-75-1 Dibenzo(a,e)fluoranthene 

 00192-65-4 Dibenzo(a,e)pyrene 

 00189-64-0 Dibenzo(a,h)pyrene 

 00191-30-0 Dibenzo(a,l)pyrene 

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

 00057-97-6 7,12-Dimethylbenz(a)anthracene 

 00193-39-5 Indeno[1,2,3-cd]pyrene 

 03697-24-3 5-Methylchrysene 

 05522-43-0 1-Nitropyrene 

 

 ******* 

Strychnine and salts 1/1/95

 

 ******* 

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

[FR Doc. 94-29376 Filed 11-23-94; 4:03 pm]

BILLING CODE 6560-50-F