[Federal Register Volume 59, Number 229 (Wednesday, November 30, 1994)]
[Unknown Section]
[Page 0]
From the Federal Register Online via the Government Publishing Office [www.gpo.gov]
[FR Doc No: 94-29376]
[[Page Unknown]]
[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
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ENVIRONMENTAL PROTECTION AGENCY
40 CFR Part 372
[OPPTS-400082B; FRL-4922-2]
RIN 2070-AC47
Addition of Certain Chemicals; Toxic Chemical Release Reporting;
Community Right-to-Know
AGENCY: Environmental Protection Agency (EPA).
ACTION: Final rule.
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SUMMARY: EPA is adding 286 chemicals and chemical categories, which
include 39 chemicals as part of two delineated categories, to the list
of toxic chemicals subject to reporting under section 313 of the
Emergency Planning and Community Right-to-Know Act of 1986 (EPCRA) and
section 6607 of the Pollution Prevention Act of 1990 (PPA). The
additions of these chemicals and chemical categories are based on their
acute human health effects, carcinogenicity or other chronic human
health effects, and/or their adverse effects on the environment. EPA is
taking this action pursuant to its authority to add to the list those
chemicals and chemical categories that meet the EPCRA section 313(d)(2)
criteria for addition to the list of toxic chemicals. EPCRA section 313
reporting for the newly listed chemicals and chemical categories will
be required beginning with the 1995 calendar year. As such, the first
reports for the added chemicals and chemical categories must be
submitted to EPA and States by July 1, 1996.
EFFECTIVE DATE: This rule is effective November 22, 1994.
FOR FURTHER INFORMATION CONTACT: Maria J. Doa, Project Manager, 202-
260-9592, for specific information regarding this final rule. For
further information on EPCRA section 313, contact the Emergency
Planning and Community Right-to-Know Information Hotline, Environmental
Protection Agency, Mail Stop 5101, 401 M St., SW., Washington, DC
20460, Toll free: 800-535-0202, TDD: 800-553-7672.
SUPPLEMENTARY INFORMATION:
I. Introduction
A. Statutory Authority
This rule is issued under section 313(d) of the Emergency Planning
and Community Right-to-Know Act of 1986 (EPCRA), 42 U.S.C. 11001 et
seq.. EPCRA is also referred to as Title III of the Superfund
Amendments and Reauthorization Act of 1986.
B. Background
Section 313 of EPCRA requires certain facilities manufacturing,
processing, or otherwise using listed toxic chemicals to report their
environmental releases of such chemicals annually. Beginning with the
1991 reporting year, such facilities also must report pollution
prevention and recycling data for such chemicals, pursuant to section
6607 of the Pollution Prevention Act, 42 U.S.C. 13106. Section 313
established an initial list of toxic chemicals that was composed of
more than 300 chemicals and 20 chemical categories. Section 313(d)
authorizes EPA to add or delete chemicals from the list, and sets forth
criteria for these actions. Under section 313(e), any person may
petition EPA to add chemicals to or delete chemicals from the list. EPA
issued a statement of petition policy and guidance in the Federal
Register of February 4, 1987 (52 FR 3479), to provide guidance
regarding the recommended content and format for petitions. On May 23,
1991 (56 FR 23703), EPA issued guidance regarding the recommended
content of petitions to delete individual members of the section 313
metal compound categories.
II. Background
On January 12, 1994 (59 FR 1788), EPA issued a proposal in the
Federal Register to add 313 chemicals and chemical categories to the
list of toxic chemicals under EPCRA section 313 based on their acute
human health effects, carcinogenicity or other chronic human health
effects, and/or their environmental effects. EPA's decision to add the
chemicals and chemical categories in today's rule to the section 313
list is based on a further assessment, in light of public comments of
both the relative toxicity of the chemicals--the potency of the
chemical's inherent toxicity--and a careful consideration of the type
of adverse effect the chemical causes or can reasonably be anticipated
to cause. Under section 313(d)(2)(A) (acute human toxicity), the effect
must be ``significant.'' Under section 313(d)(2)(B) the effect must
either be cancer or teratogenicity, or some other ``serious or
irreversible'' chronic health effect. Under section 313(d)(2)(C)
(environmental toxicity) the effect must be ``significant'' and ``of
sufficient seriousness in the judgment of the Administrator'' to
warrant reporting.
The statute does not specify how serious or significant an effect
must be in order for a chemical to be listed under any of the criteria.
This determination is left to the EPA's discretion and scientific
judgment. The Agency recognizes that not every adverse effect is
sufficiently significant or serious to satisfy the criteria. For
chemicals with effects that satisfy the criteria, Congress made it
clear in section 313 that communities have a right to know about
releases of such chemicals. The Agency's goal in implementing section
313 is to ensure that the communities are provided with that release
information to allow them to further educate themselves and, if
appropriate, take or recommend action.
A brief description of the selection process follows, however, a
detailed description of EPA's methodology and rationale for the
proposed addition of these chemicals and chemical categories can be
found in the proposed rule.
1. Development of the chemical addition list. As a starting point
for screening candidates for addition to the toxic chemical list under
EPCRA section 313, EPA chose to examine the lists of chemicals
regulated or identified, as of concern, under various environmental
statutes including: Section 112(b) of the Clean Air Act (CAA) as
amended in 1990 (Hazardous Air Pollutants); (2) section 602(b) of the
CAA (Class II ozone depleting substances); (3) section 307(a) of the
Clean Water Act (CWA) (Priority Pollutant List); (4) Federal
Insecticide, Fungicide, and Rodenticide Act (FIFRA) Active Ingredients,
including Special Review, Canceled/Denied or Suspended, and Restricted
Use Pesticides; (5) section 302 of EPCRA (Extremely Hazardous
Substances); (6) section 102 of the Comprehensive Environmental
Response, Compensation, and Liability Act (CERCLA); (7) section 3001 of
the Resource Conservation and Recovery Act (RCRA) and chemicals listed
at 40 CFR 261.33(e) and Appendix VIII; (8) section 1412 of the Safe
Drinking Water Act as amended; (9) certain chemicals subject to the
Toxics Substance Control Act (Existing Chemicals); and (10) the State
of California Safe Drinking Water and Toxic Enforcement Act of 1986
(Proposition 65) (List of Chemicals Known to the State to Cause
Reproductive Toxicity); and/or those chemicals designated as possible,
probable, or known carcinogens in the Monographs of the International
Agency for Research on Cancer (IARC) and the 6th Annual Report on
Carcinogens of the National Toxicology Program (NTP), U.S. Department
of Health and Human Services (DHHS).
2. Screening of chemicals. To prioritize chemicals for possible
addition to EPCRA section 313, EPA applied a human health and
ecotoxicity screen and a production volume screen, which are described
below.
a. Toxicity screen. A toxicity screen is a limited review of
readily available toxicity data that is used for a preliminary
categorization of a chemical during the process of selecting candidates
for possible listing under EPCRA section 313. The toxicity screen is
used to identify chemicals for further consideration and does not
reflect a final determination for listing a chemical under EPCRA
section 313. Such a determination can only be made after a hazard
assessment is conducted (See Unit II.3. of this preamble). The
chemicals identified above were screened for four general effect
categories: Acute human health effects, cancer, other chronic human
health effects, and ecological effects.
The screening criteria associated with each of the effect areas
used in the toxicity screen are discussed in detail in the Revised
Draft Hazard Assessment Guidelines for Listing Chemicals on the Toxic
Release Inventory (Draft Hazard Assessment Guidelines), (Ref. 11).
Based on the results of this screen, the chemicals were preliminarily
placed in one of three screening categories defined in the Draft Hazard
Assessment Guidelines: ``high priority;'' ``medium priority;'' or ``low
priority.''
Chemicals that were categorized as ``low priority'' during the
screening process were not considered further as candidates for
addition to the EPCRA section 313 list in this rulemaking.
b. Production volume screen. EPCRA section 313(f) establishes
reporting thresholds of either 25,000 or 10,000 pounds per facility per
year related to the amount of a chemical that is manufactured,
processed, or otherwise used. EPA anticipates that the addition of
chemicals manufactured, imported, processed, or used in quantities less
than the EPCRA section 313 activity thresholds would not result in the
submission of Toxic Release Inventory (TRI) reports. Thus, EPA elected
to focus its attention on chemicals likely to yield reports and also
screened potential candidates for the likelihood of meeting the EPCRA
section 313 volume thresholds. Chemicals for which there were no data
to indicate that the chemical is likely to meet or exceed the EPCRA
section 313 volume thresholds were not considered further as possible
candidates for addition to the section 313 list at this time.
3. Hazard evaluation. After completing the screening phase, EPA
conducted a thorough hazard assessment for each of the addition
candidates that resulted from the above analyses and determined based
on the weight-of-the evidence if there was sufficient evidence to
establish that the candidate chemical met the statutory criteria for
addition to EPCRA section 313. To make this determination, EPA senior
scientists reviewed readily available toxicity information on each
chemical for each of the following effect areas: acute human health
effects; cancer; other chronic human effects; and environmental
effects. In addition, EPA reviewed, where appropriate, information on
the environmental fate of the chemical.
The hazard assessment was conducted in accordance with relevant EPA
guidelines for each adverse human health or environmental effect (e.g.,
the appropriate guidelines for hazard evaluation of chemical
carcinogens and for the type of evidence required to substantiate a
determination of carcinogenicity are the Assessment Guidelines for
Carcinogen Risk (Ref. 4)). During this assessment the number, severity,
and significance of the effects induced by the chemical, the dose level
causing the effect, and the quality and quantity of the available data,
including the nature of the data (e.g., human epidemiological,
laboratory animal, field or workplace studies) and confidence level in
the existing data base, were all considered. Where a careful review of
the scientific data for a particular chemical results in a high level
of confidence that the chemical causes an adverse effect at relatively
low dose levels, EPA believes that this evidence is sufficient for
listing the chemical under section 313. EPA also believes that where a
review of the scientific data indicates that the chemical will cause
various adverse effects at moderate dose levels, the total weight-of-
the-evidence indicates that there is sufficient evidence for listing
the chemical under EPCRA section 313. EPA believes that both types of
chemicals described above exhibit moderately high to high toxicity
based on a hazard assessment.
EPA also conducted an analysis of exposure for each chemical or
chemical category proposed for listing under EPCRA section 313(d)(2)(A)
(i.e., based on adverse acute human health effects), and, where
appropriate, under section 313(d)(2)(C) (i.e., based on adverse
ecological effects). For chemicals listed under EPCRA section
313(d)(2)(A), this analysis included estimated concentrations of the
chemical at or beyond the facility site boundary through the use of
estimated releases and modelling techniques. EPA did not conduct an
analysis of exposure for the chemicals proposed for listing under
section 313(d)(2)(B) because these chemicals exhibit moderately high to
high toxicity based on a hazard assessment (see Unit IV.B. for a
discussion of the use of exposure). As discussed more thoroughly in
Unit IV.B. of this preamble, EPA does not believe that it is
appropriate to factor exposure into the listing decisions for the
chemicals being listed pursuant to section 313(d)(2)(B) in this
rulemaking.
Following a review and analysis of the information available about
each chemical in this final rule (including information provided
through public comment) by senior Agency scientists, the Agency
concludes that for each of the chemicals listed one or more of the
EPCRA section 313 listing criteria are met. Moreover, the adverse
effects associated with each of the chemicals being listed today are
serious and significant. In some cases the effects are extreme, such as
cancer or death. In others, the effects are serious and lasting,
including, for example, impairment of a fetus' or an offspring's
physical development, neurological effects inhibiting motor abilities
or mental processes or impairing the ability to reproduce, or the
sustainability of a fragile ecosystem such as an estuary. For a number
of chemicals in the final rule, there is more than one adverse effect.
It is important to understand that although an adverse effect is
known or can be reasonably anticipated to be caused by a chemical on
the section 313 list, a release of a chemical into a community does not
necessarily mean that the effect will occur. Exposure and dose are also
important factors in determining whether an adverse effect occurs and
how serious the manifestation will be. The listing of a chemical on the
section 313 list does not mean that a particular community will
experience these adverse effects. Instead the purpose for listing a
chemical is to ensure that the public gets information about releases
of such chemicals. Thus, EPA believes that for chemicals that typically
do not affect solely one or two species but rather affect changes
across a whole ecosystem and for which there is well-documented
evidence supporting the adverse effects, that their addition to the
EPCRA section 313 list is warranted even though the severity of the
adverse effects that they induce will be dependent upon site-specific
characteristics. Once EPA makes release data available through TRI, the
community may then make its own determination on the importance of
these releases (and their potential adverse effects).
The expansion of the EPCRA section 313 toxic chemical list is the
first phase of the expansion of the TRI program. EPA plans to issue a
proposed rule in early 1995 expanding the scope of industry sectors
that would be subject to EPCRA section 313. EPA's initial analysis for
this effort is focused on industrial sectors which have activities
related to manufacturing that result in significant releases of
chemicals listed on EPCRA section 313. EPA is also considering further
expanding right-to-know by investigating the feasibility of adding data
on exposure to and use of chemicals at TRI facilities. The Agency
believes that the collection of this type of data would provide a
greater understanding of risk reduction and pollution prevention
opportunities.
In conjunction with these expansion activities, the Agency is also
considering situations where data of lesser value can be removed from
the TRI system. Elsewhere in this issue of the Federal Register, EPA is
promulgating a rule establishing an alternate threshold for facilities
with low annual reportable amounts of listed toxic chemicals. This
alternate threshold will provide considerable relief for facilities
which generate ``small'' amounts of EPCRA section 313 chemicals in
reportable amounts. This relief will offset the increased burden that
this expansion rule may impose. The alternate threshold for
manufacture, or process, or otherwise use for each of the chemicals
meeting the facility category will be an amount greater than one
million pounds per year. If a facility meets the alternate threshold
criteria, that facility will not be required to file a complete TRI
report (Form R), but will be required to submit an annual certification
statement for each chemical meeting these conditions for the reporting
year for which these conditions were met and maintain records
supporting calculations made to determine these conditions. EPA
estimates that this alternate threshold provides the option to convert
approximately 20,100 Form R reports to certification statements.
III. Summary of Final Rule
In this action, EPA is adding 286 chemicals and chemical
categories, which includes 39 chemicals as part of two delineated
categories, to the EPCRA section 313 list. EPA finds that each of these
chemicals and chemical categories meets one or more of the EPCRA
section 313(d)(2) criteria. Additionally, EPA believes that each of
these chemicals can reasonably be anticipated to be manufactured or
imported in quantities of at least 10,000 pounds (the EPCRA section 313
otherwise use reporting threshold) by at least one facility. Therefore,
the Agency believes that the listing of these chemicals can reasonably
be anticipated to generate EPCRA section 313 reports and that adding
these chemicals to the toxic chemical list is appropriate.
The proposed rule and record supporting the rulemaking contain
information on EPA's review of these chemicals, including the toxicity
evaluation. This background information will not be repeated here in
the final rule. However, to the extent that comments were received on
these issues, those comments are addressed in this document. In
addition to general comment and comment addressing a broad number of
chemicals, EPA received specific technical comments on 110 of the
chemicals and chemical categories. Detailed responses to comments are
contained in Response to Comments Received on the January 12, 1994
Proposed Rule to Expand the EPCRA Section 313 List (Response to Comment
Document, Ref. 14). Summaries of responses to comments on selected
chemicals appear in units IV.F. and IV.G. of this preamble. Table 1
lists the chemicals that EPA has determined meet the statutory criteria
of EPCRA section 313(d)(2) and are therefore being added to the toxic
chemical list. Each of the chemicals and chemical categories listed
below were found to meet the statutory criteria described in EPCRA
section 313(d)(2)(A)-(C). This means that the Agency has made a finding
that the chemical is known to cause an effect, or is reasonably
anticipated to do so. It does not necessarily mean that the chemical is
known to cause a given effect. The specific criterion or criteria that
the chemical meets are also listed in Table 1 below.
Table 1.--Chemicals Being Added to the EPCRA Section 313 List
----------------------------------------------------------------------------------------------------------------
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-nitro-
benzoic acid, sodium salt)
Alachlor 015972-60-8 X
Aldicarb 000116-06-3 X
d-trans-Allethrin [d-trans- 028057-48-9 X
Chrysanthemic acid of d-allethrone]
Allylamine 000107-11-9 X
Aluminum phosphide 020859-73-8 X
Ametryn (N-Ethyl-N'-(1-methylethyl)-6- 000834-12-8 X X
(methylthio)-1,3,5,-triazine- 2,4
diamine)
Amitraz 033089-61-1 X
Anilazine (4,6-Dichloro-N-(2- 000101-05-3 X X
chlorophenyl)-1,3,5-triazin-2-amine)
Atrazine (6-Chloro-N-ethyl-N'-(1- 001912-24-9 X
methylethyl)-1,3,5,-triazine-2,4-
diamine)
Bendiocarb (2,2-Dimethyl-1,3- 022781-23-3 X X
benzodioxol-4-ol methylcarbamate)
Benfluralin (N-Butyl-N-ethyl-2,6- 001861-40-1 X
dinitro-4-(trifluoromethyl)
benzenamine)
Benomyl 017804-35-2 X
Bifenthrin 082657-04-3 X X
Bis(tributyltin) oxide 000056-35-9 X X
Boron trichloride 010294-34-5 X
Boron trifluoride 007637-07-2 X
Bromacil (5-Bromo-6-methyl-3-(1- 000314-40-9 X
methylpropyl)-2,4(1H,3H)-
pyrimidinedione)
Bromacil lithium salt (2,4(1H,3H)- 053404-19-6 X
Pyrimidinedione, 5-bromo-6-methyl-3 (1-
methylpropyl), lithium salt)
Bromine 007726-95-6 X
1-Bromo-1-(bromomethyl)-1,3- 035691-65-7 X
propanedicarbonitrile
2-Bromo-2-nitropropane-1,3-diol 000052-51-7 X
(Bronopol)
Bromoxynil (3,5-Dibromo-4- 001689-84-5 X
hydroxybenzonitrile)
Bromoxynil octanoate (Octanoic acid, 001689-99-2 X
2,6-dibromo-4-cyanophenyl ester)
Brucine 000357-57-3 X
C.I. Acid Red 114 006459-94-5 X
C.I. Direct Blue 218 028407-37-6 X
Carbofuran 001563-66-2 X
Carboxin (5,6-Dihydro-2-methyl-N-phenyl- 005234-68-4 X
1,4-oxathiin-3-carboxamide)
Chinomethionat (6-Methyl-1,3- 002439-01-2 X
dithiolo[4,5-b]quinoxalin-2-one)
Chlorendic acid 000115-28-6 X
Chlorimuron ethyl (Ethyl-2-[[[(4-chloro- 090982-32-4 X
6-methoxyprimidin-2-yl)-carbonyl]-
amino]sulfonyl]benzoate)
1-(3-Chloroallyl)-3,5,7-triaza-1- 004080-31-3 X
azoniaadamantane chloride
p-Chloroaniline 000106-47-8 X
3-Chloro-2-methyl-1-propene 000563-47-3 X
p-Chlorophenyl isocyanate 000104-12-1 X
Chloropicrin 000076-06-2 X
3-Chloropropionitrile 000542-76-7 X
p-Chloro-o-toluidine 000095-69-2 X
2-Chloro-1,1,1-trifluoroethane (HCFC- 000075-88-7 X X
133a)
Chlorotrifluoromethane (CFC-13) 000075-72-9 X X
3-Chloro-1,1,1-trifluoropropane(HCFC- 000460-35-5 X X
253fb)
Chlorpyrifos methyl (O,O-Dimethyl-O- 005598-13-0 X X
(3,5,6-trichloro-2-
pyridyl)phosphorothioate)
Chlorsulfuron (2-Chloro-N-[[(4-methoxy- 064902-72-3 X
6-methyl-1,3,5-triazin-2-yl)
amino]carbonyl]benzenesulfonamide)
Crotonaldehyde 004170-30-3 X
Cyanazine 021725-46-2 X
Cycloate 001134-23-2 X
Cyclohexanol 000108-93-0 X
Cyfluthrin (3-(2,2-Dichloroethenyl)-2,2- 068359-37-5 X X
dimethylcyclopropanecarboxylic acid,
cyano(4-fluoro-3-
phenoxyphenyl)methylester)
Cyhalothrin (3-(2-Chloro-3,3,3- 068085-85-8 X
trifluoro-1-propenyl)-2,2-
Dimethylcyclopropanecarboxylic acid
cyano(3-phenoxyphenyl)methyl ester)
Dazomet (Tetrahydro-3,5-dimethyl-2H- 000533-74-4 X
1,3,5-thiadiazine-2-thione)
Dazomet sodium salt (2H-1,3,5- 053404-60-7 X
Thiadiazine-2-thione, tetrahydro-3,5-
dimethyl-, ion(1-), sodium)
2,4-DB 000094-82-6 X
2,4-D butoxyethyl ester 001929-73-3 X
2,4-D butyl ester 000094-80-4 X
2,4-D chlorocrotyl ester 002971-38-2 X
Desmedipham 013684-56-5 X
2,4-D 2-ethylhexyl ester 001928-43-4 X
2,4-D 2-ethyl-4-methylpentyl ester 053404-37-8 X
Diazinon 000333-41-5 X X
2,2-Dibromo-3-nitrilopropionamide 010222-01-2 X
Dicamba (3,6-Dichloro-2-methyoxybenzoic 001918-00-9 X
acid)
Dichloran (2,6-Dichloro-4-nitroaniline) 000099-30-9 X
3,3'-Dichlorobenzidine dihydrochloride 000612-83-9 X
3,3'-Dichlorobenzidine sulfate 064969-34-2 X
trans-1,4-Dichloro-2-butene 000110-57-6 X
1,2-Dichloro-1,1-difluoroethane (HCFC- 001649-08-7 X X
132b)
Dichlorofluoromethane (HCFC-21) 000075-43-4 X X
Dichloropentafluoropropane 127564-92-5 X X
1,3-Dichloro-1,1,2,3,3- 136013-79-1 X X
pentafluoropropane (HCFC-225ea)
2,2-Dichloro-1,1,1,3,3- 128903-21-9 X X
pentafluoropropane (HCFC-225aa)
1,1-Dichloro-1,2,3,3,3- 111512-56-2 X X
pentafluoropropane (HCFC-225eb)
1,1-Dichloro-1,2,2,3,3- 013474-88-9 X X
pentafluoropropane (HCFC-225cc)
1,3-Dichloro-1,1,2,2,3- 000507-55-1 X X
pentafluoropropane (HCFC-225cb)
1,2-Dichloro-1,1,3,3,3- 000431-86-7 X X
pentafluoropropane (HCFC-225da)
3,3-Dichloro-1,1,1,2,2- 000422-56-0 X X
pentafluoropropane (HCFC-225ca)
2,3-Dichloro-1,1,1,2,3- 000422-48-0 X X
pentafluoropropane (HCFC-225ba)
1,2-Dichloro-1,1,2,3,3- 000422-44-6 X X
pentafluoropropane (HCFC-225bb)
Dichlorophene (2,2'-Methylenebis(4- 000097-23-4 X X
chlorophenol)
trans-1,3-Dichloropropene 010061-02-6 X
Diclofop methyl (2-[4-(2,4- 051338-27-3 X
Dichlorophenoxy)
phenoxy]propanoicacid, methyl ester)
Dicyclopentadiene 000077-73-6 X
Diethatyl ethyl 038727-55-8 X
Diflubenzuron 035367-38-5 X X
Diglycidyl resorcinol ether 000101-90-6 X
Diisocyanates, consisting of: NA X
1,3-Bis(methylisocyanate) cyclohexane 038661-72-2
1,4-Bis(methylisocyanate) cyclohexane 010347-54-3
1,4-Cyclohexane diisocyanate 002556-36-7
Diethyldiisocyanatobenzene 134190-37-7
4,4'-Diisocyanatodiphenyl ether 004128-73-8
2,4'-Diisocyanatodiphenyl sulfide 075790-87-3
3,3'-Dimethoxybenzidine-4,4'- 000091-93-0
diisocyanate
3,3'-Dimethyl-4,4'-diphenylene 000091-97-4
diisocyanate
3,3'-Dimethyl diphenylmethane-4,4'- 000139-25-3
diisocyanate
Hexamethylene-1,6-diisocyanate 000822-06-0
Isophorone diisocyanate 004098-71-0
Methylenebis(phenyl isocyanate) 000101-68-8
4-Methyldiphenylmethane-3,4- 075790-84-0
diisocyanate
1,1-Methylene bis(4- 005124-30-1
isocyanatocyclohexane)
1,5-Naphthalene diisocyanate 003173-72-6
1,3-Phenylene diisocyanate 000123-61-5
1,4-Phenylene diisocyanate 000104-49-4
Polymeric diphenylmethane 009016-87-9
diisocyanate
2,2,4-Trimethylhexamethylene 016938-22-0
diisocyanate
2,4,4-Trimethylhexamethylene
diisocyanate 015646-96-5
Dimethipin (2,3,-Dihydro-5,6-dimethyl- 055290-64-7 X
1,4-dithiin 1,1,4,4-tetraoxide)
Dimethoate 000060-51-5 X
3,3'-Dimethoxybenzidine dihydrochloride 020325-40-0 X
(o-Dianisidine dihydrochloride)
3,3'-Dimethoxybenzidine hydrochloride 111984-09-9 X
(o-Dianisidine hydrochloride)
Dimethylamine 000124-40-3 X
Dimethylamine dicamba 002300-66-5 X
3,3'-Dimethylbenzidine dihydrochloride 000612-82-8 X
(o-Tolidine dihydrochloride)
3,3'-Dimethylbenzidine dihydrofluoride 041766-75-0 X
(o-Tolidine dihydrofluoride)
Dimethyl chlorothiophosphate 002524-03-0 X
Dimethyldichlorosilane 000075-78-5 X
N,N-Dimethylformamide 000068-12-2 X
2,6-Dimethylphenol 000576-26-1 X
Dinitrobutyl phenol (Dinoseb) 000088-85-7 X X
Dinocap 039300-45-3 X X
Diphenamid 000957-51-7 X
Diphenylamine 000122-39-4 X
Dipotassium endothall (7- 002164-07-0 X
Oxabicyclo(2.2.1)heptane-2,3-
dicarboxylic acid, dipotassium salt)
Dipropyl isocinchomeronate 000136-45-8 X
Disodium cyanodithioimidocarbonate 000138-93-2 X
2,4-D isopropyl ester 000094-11-1 X
2,4-Dithiobiuret 000541-53-7 X
Diuron 000330-54-1 X X
Dodine (Dodecylguanidine monoacetate) 002439-10-3 X
2,4-DP (Dichlorprop) 000120-36-5 X
2,4-D propylene glycol butyl ether 001320-18-9 X
ester
2,4-D sodium salt 002702-72-9 X
Ethoprop (Phosphorodithioic acid O- 013194-48-4 X X
ethyl S,S-dipropyl ester)
Ethyl dipropylthiocarbamate (EPTC) 000759-94-4 X X
Famphur 000052-85-7 X X
Fenarimol (.alpha.-(2-Chlorophenyl)- 060168-88-9 X
.alpha.-4-chlorophenyl)-5-
pyrimidinemethanol)
Fenbutatin oxide (hexakis(2-methyl-2- 013356-08-6 X X
phenylpropyl)distannoxane)
Fenoxaprop ethyl (2-(4-((6-Chloro-2- 066441-23-4 X X
benzoxazolylen)oxy)phenoxy)propanoic
acid,ethyl ester)
Fenoxycarb (2-(4- 072490-01-8 X
Phenoxyphenoxy)ethyl]carbamic acid
ethyl ester)
Fenpropathrin (2,2,3,3- 039515-41-8 X X
Tetramethylcyclopropane carboxylic
acid cyano(3-phenoxyphenyl)methyl
ester)
Fenthion (O,O-Dimethyl O-[3-methyl-4- 000055-38-9 X X
(methylthio) phenyl] ester,
phosphorothioic acid)
Fenvalerate (4-Chloro-alpha-(1- 051630-58-1 X X
methylethyl)benzeneacetic acid cyano(3-
phenoxyphenyl)methyl ester)
Ferbam (Tris(dimethylcarbamodithioato- 014484-64-1 X X
S,S')iron)
Fluazifop butyl (2-[4-[[5- 069806-50-4 X
(Trifluoromethyl)-2-pyridinyl]oxy]-
phenoxy]propanoic acid, butyl ester)
Fluorine 007782-41-4 X
Fluorouracil (5-Fluorouracil) 000051-21-8 X
Fluvalinate (N-[2-Chloro-4- 069409-94-5 X X
(trifluoromethyl)phenyl]-DL-valine(+)-
cyano (3-phenoxyphenyl)methyl ester)
Folpet 000133-07-3 X X
Fomesafen (5-(2-Chloro-4- 072178-02-0 X
(trifluoromethyl)phenoxy)-N
methylsulfonyl)-2-nitrobenzamide)
alpha-Hexachlorocyclohexane 000319-84-6 X X
n-Hexane 000110-54-3 X
Hexazinone 051235-04-2 X X
Hydramethylnon (Tetrahydro-5,5-di- 067485-29-4 X X
methyl-2(1H)- pyrimidinone[3-[4-
(trifluoromethyl)phenyl]-1-[2-[4-
(trifluoromethyl) phenyl]ethenyl]-
2propenylidene]hydrazone)
Imazalil (1-[2-(2,4-Dichlorophenyl)-2- 035554-44-0 X
(2-propenyloxy)ethyl]-1H-imidazole)
3-Iodo-2-propynyl butylcarbamate 055406-53-6 X
Iron pentacarbonyl 013463-40-6 X
Isodrin 000465-73-6 X
Isofenphos (2-[[Ethoxyl[(1- 025311-71-1 X X
methylethyl)amino]phosphinothioyl]oxy]
benzoic acid 1-methylethyl ester)
Lactofen (5-(2-Chloro-4- 077501-63-4 X
(trifluoromethyl)phenoxy)-2-nitro-2-
ethoxy-1-methyl-2-oxoethyl ester)
Linuron 000330-55-2 X
Lithium carbonate 000554-13-2 X
Malathion 000121-75-5 X X
Mecoprop 000093-65-2 X
2-Mercaptobenzothiazole (MBT) 000149-30-4 X
Merphos 000150-50-5 X
Metham sodium (Sodium 000137-42-8 X
methyldithiocarbamate)
Methazole (2-(3,4-Dichlorophenyl)-4- 020354-26-1 X
methyl-1,2,4-oxadiazolidine-3,5-dione)
Methiocarb 002032-65-7 X
Methoxone ((4-Chloro-2-methylphenoxy) 000094-74-6 X
acetic acid) (MCPA)
Methoxone sodium salt ((4-Chloro-2- 003653-48-3 X
methylphenoxy) acetate sodium salt)
Methyl isothiocyanate 00556-61-6 X
2-Methyllactonitrile 000075-86-5 X
N-Methylolacrylamide 000924-42-5 X
Methyl parathion 000298-00-0 X X
N-Methyl-2-pyrrolidone 000872-50-4 X
Methyltrichlorosilane 000075-79-6 X
Metiram 009006-42-2 X
Metribuzin 021087-64-5 X
Mevinphos 007786-34-7 X
Molinate (1H-Azepine-1 carbothioic 002212-67-1 X
acid, hexahydro-S-ethyl ester)
Monuron 000150-68-5 X
Myclobutanil (.alpha.-Butyl-.alpha.-(4- 088671-89-0 X
chlorophenyl)-1H-1,2,4-triazole-1-
propanenitrile)
Nabam 000142-59-6 X
Naled 000300-76-5 X X
Nicotine and salts NA X
Nitrapyrin (2-Chloro-6- 001929-82-4 X
(trichloromethyl)pyridine)
Nitrate compounds (water dissociable) NA X
p-Nitroaniline 000100-01-6 X
Norflurazon (4-Chloro-5-(methylamino)-2- 027314-13-2 X
[3-(trifluoromethyl)phenyl]-3(2H)-
pyridazinone)
Oryzalin (4-(Dipropylamino)-3,5- 019044-88-3 X
dinitrobenzenesulfonamide)
Oxydemeton methyl (S-(2- 000301-12-2 X
(Ethylsulfinyl)ethyl) O,O-dimethyl
ester phosphorothioic acid)
Oxydiazon (3-[2,4-Dichloro-5-(1- 019666-30-9 X
methylethoxy)phenyl]-5-(1,1-
dimethylethyl)-1,3,4-oxadiazol-2(3H)-
one)
Oxyfluorfen 042874-03-3 X X
Ozone 010028-15-6 X X
Paraquat dichloride 001910-42-5 X
Pebulate (Butylethylcarbamothioic acid 001114-71-2 X
S-propyl ester)
Pendimethalin (N-(1-Ethylpropyl)-3,4- 040487-42-1 X
dimethyl-2,6-dinitrobenzenamine)
Pentobarbital sodium 000057-33-0 X
Perchloromethyl mercaptan 000594-42-3 X
Permethrin (3-(2,2-Dichloroethenyl)-2,2- 052645-53-1 X X
dimethylcyclopropanecarboxylic acid,
(3-phenoxyphenyl)methyl ester)
Phenanthrene 000085-01-8 X
Phenothrin (2,2-Dimethyl-3-(2-methyl-1- 026002-80-2 X X
propenyl) cyclopropanecarboxylic acid
(3-phenoxyphenyl)methyl ester)
1,2-Phenylenediamine 000095-54-5 X
1,3-Phenylenediamine 000108-45-2 X
1,2-Phenylenediamine dihydrochloride 000615-28-1 X
1,4-Phenylenediamine dihydrochloride 000624-18-0 X
Phenytoin 000057-41-0 X
Phosphine 007803-51-2 X
Picloram 001918-02-1 X
Piperonyl butoxide 000051-03-6 X
Pirimiphos methyl (O-(2-(Diethylamino)- 029232-93-7 X
6-methyl-4- pyrimidinyl)-O,O-dimethyl
phosphorothioate)
Polychlorinated alkanes NA X X
Polycyclic aromatic compounds (PACs) NA X
consisting of:
Benz(a)anthracene 000056-55-3
Benzo(a)phenanthrene 000218-01-9
Benzo(a)pyrene 000050-32-8
Benzo(b)fluoranthene 000205-99-2
Benzo(j)fluoranthene 000205-82-3
Benzo(k)fluoranthene 000207-08-9
Benzo(rst)pentaphene 000189-55-9
Dibenz(a,h)acridine 000226-36-8
Dibenz(a,j)acridine 000224-42-0
Dibenzo(a,h)anthracene 000053-70-3
Dibenzo(a,e)fluoranthene 005385-75-1
Dibenzo(a,e)pyrene 000192-65-4
Dibenzo(a,h)pyrene 000189-64-0
Dibenzo(a,l)pyrene 000191-30-0
7H-Dibenzo(c,g)carbazole 00194-59-2
7,12-Dimethyl benz(a)anthracene 000057-97-6
Indeno[1,2,3-cd]pyrene 000193-39-5
5-Methylchrysene 003697-24-3
1-Nitropyrene 005522-43-0
Potassium bromate 007758-01-2 X
Potassium dimethyldithiocarbamate 000128-03-0 X
Potassium N-methyldithiocarbamate 000137-41-7 X
Profenofos (O-(4-Bromo-2-chlorophenyl)- 041198-08-7 X
O-ethyl-S-propyl phosphorothioate)
Prometryn (N,N'-Bis(1-methylethyl)-6- 007287-19-6 X
methylthio-1,3,5-triazine-2,4-diamine)
Propachlor (2-Chloro-N-(1-methylethyl)- 001918-16-7 X
N-phenylacetamide)
Propanil (N-(3,4- 000709-98-8 X
Dichlorophenyl)propanamide)
Propargite 002312-35-8 X X
Propargyl alcohol 000107-19-7 X
Propetamphos (3- 031218-83-4 X
[(Ethylamino)methoxyphosphinothioyl]ox
y]-2-butenoic acid, 1-methylethyl
ester)
Propiconazole (1-[2-(2,4- 060207-90-1 X
Dichlorophenyl)-4-propyl-1,3-dioxolan-
2-yl]-methyl-1H-1,2,4,-triazole)
Quizalofop-ethyl (2-[4-[(6-Chloro-2- 076578-14-8 X
quinoxalinyl)oxy]phenoxy] propanoic
acid ethyl ester)
Resmethrin ([5-(Phenylmethyl)-3- 010453-86-8 X X
furanyl]methyl 2,2-dimethyl-3-(2-
methyl-1-
propenyl)cyclopropanecarboxylate])
Sethoxydim (2-[1-(Ethoxyimino)butyl]-5- 074051-80-2 X
[2-(ethylthio)propyl]-3-hydroxyl-2-
cyclohexen-1-one)
Simazine 000122-34-9 X
Sodium azide 026628-22-8 X
Sodium dicamba (3,6-Dichloro-2- 001982-69-0 X
methoxybenzoic acid, sodium salt)
Sodium dimethyldithiocarbamate 000128-04-1 X
Sodium fluoroacetate 000062-74-8 X X
Sodium nitrite 007632-00-0 X
Sodium pentachlorophenate 000131-52-2 X X
Sodium o-phenylphenoxide 000132-27-4 X
Strychnine and salts NA X
Sulfuryl fluoride (Vikane) 002699-79-8 X
Sulprofos (O-Ethyl O-[4- 035400-43-2 X X
(methylthio)phenyl]phosphorodithioic
acid S propyl ester)
Tebuthiuron (N-[5-(1,1-Dimethylethyl)- 034014-18-1 X
1,3,4-thiadiazol-2-yl)- N,N'-
dimethylurea)
Temephos 003383-96-8 X
Terbacil (5-Chloro-3-(1,1- 005902-51-2 X
dimethylethyl)-6-methyl- 2,4 (1H,3H)-
pyrimidinedione)
1,1,1,2-Tetrachloro-2-fluoroethane 000354-11-0 X X
(HCFC-121a)
1,1,2,2-Tetrachloro-1-fluoroethane 000354-14-3 X X
(HCFC-121)
Tetracycline hydrochloride 000064-75-5 X
Tetramethrin (2,2-Dimethyl-3-(2-methyl- 007696-12-0 X X
1-propenyl) cyclopropanecarboxylic
acid (1,3,4,5,6,7-hexahydro-1,3-dioxo-
2H-isoindol-2-yl)methyl ester)
Thiabendazole (2-(4-Thiazolyl)-1H- 000148-79-8 X X
benzimidazole)
Thiobencarb (Carbamic acid, diethylthio- 028249-77-6 X
, S-(p-chlorobenzyl))
Thiodicarb 059669-26-0 X X
Thiophanate ethyl ([1,2- 023564-06-9 X
Phenylenebis(iminocarbonothioyl)]
biscarbamic acid diethyl ester)
Thiophanate-methyl 023564-05-8 X
Thiosemicarbazide 000079-19-6 X
Triadimefon (1-(4-Chlorophenoxy)-3,3- 043121-43-3 X
dimethyl-1-(1H-1,2,4-triazol-1-yl)-2-
butanone)
Triallate 002303-17-5 X
Tribenuron methyl (2-(4-Methoxy-6- 101200-48-0 X
methyl-1,3,5-triazin-2-yl)-
methylamino)carbonyl)amino)sulfonyl)-,
methyl ester)
Tributyltin fluoride 001983-10-4 X
Tributyltin methacrylate 002155-70-6 X
S,S,S-Tributyltrithiophosphate (DEF) 000078-48-8 X X
Trichloroacetyl chloride 000076-02-8 X
1,2,3-Trichloropropane 000096-18-4 X
Triclopyr triethylammonium salt 057213-69-1 X
Triethylamine 000121-44-8 X
Triforine (N,N'-[1,4-Piperazinediylbis- 026644-46-2 X
2,2,2-trichloroethylidene)]
bisformamide)
Trimethylchlorosilane 000075-77-4 X
2,3,5-Trimethylphenyl methylcarbamate 002655-15-4 X
Triphenyltin chloride 000639-58-7 X X
Triphenyltin hydroxide 000076-87-9 X X
Vinclozolin (3-(3,5-Dichlorophenyl)-5- 050471-44-8 X
ethenyl-5-methyl-2,4-oxazolidinedione)
----------------------------------------------------------------------------------------------------------------
EPA is deferring final action on 40 chemicals and one chemical
category until a later date. These chemicals and the comments received
on them raised particularly difficult technical or policy issues which
will require additional time to address. The Agency does not believe
that it would be in the spirit of community right-to-know to delay
final action on the remaining 286 chemicals and chemical categories,
pending completion of work on the more limited group. In a future
rulemaking, EPA will make a final determination as to whether these
chemicals should be added to EPCRA section 313. The public comment that
has been received specific to these deferred chemicals will be
addressed as part of the future rulemaking discussed above. These
chemicals follow:
o-benzyl-p-chlorophenol
butylate
butylated hydroxyanisole (BHA)
calcium hypochlorite
caprolactam
carbon monoxide
cyromazine
dichloromethylphenylsilane
dithiopyr
2,4-D 2-octyl ester
flumetralin
iprodione
isophorone
man made mineral fibers
methylene bis(thiocyanate)
nitric oxide
nitrogen dioxide
nine polycyclic aromatic compounds, specifically:
carbazole
cyclopenta(cd)pyrene
dibenz(a,c)anthracene
dibenz(a,j)anthracene
2-methylchrysene
3-methylchrysene
4-methylchrysene
6-methylchrysene
2-methylfluoranthene
phosphorus oxychloride
phosphorus pentachloride
phosphorus pentasulfide
phosphorus pentoxide
primsulfuron
sodium chlorite
sodium hypochlorite
sodium 2-pyridinethiol-1-oxide
sulfur dioxide
sulfur trioxide
tefluthrin
thiabendazole, hypophosphite salt
trichloroethylsilane
trichlorophenylsilane
vanadium pentoxide
Based on an evaluation of the public comments received and a
reanalysis of the available data cited in the proposed rule, EPA has
determined that three chemicals, clomazone, 5-chloro-2-(2,4-
dichlorophenoxy)phenol, and tetrasodium ethylenediaminetetraacetate,
that were proposed for listing do not have sufficient evidence of
toxicity at this time to meet the statutory criteria of EPCRA
section313(d)(2) and thus are not listed in this final rule. Summaries
of responses to chemical-specific comments for these chemicals appear
in unit IV.G. of this preamble.
IV. Summary of Public Comment
The public comment period for the proposed rule closed April 12,
1994. On March 9, 1994, EPA held a public meeting on the proposed
addition of chemicals and chemical categories. Two hundred and sixty-
six comments were received, including 136 from industry, 60 from trade
associations, 32 from environmental groups, 15 from private citizens, 3
from Federal agencies, 7 from State agencies and 13 from other public
interest groups, labor groups, universities, and associations. In
addition to general comment and comment addressing a broad number of
chemicals, EPA received specific technical comments on 110 of the
chemicals and chemical categories. Detailed responses to all comments,
except those comments specific to chemicals for which final action is
being deferred, are contained in the Response to Comment Document (Ref.
14).
In addition to a number of comments supporting the concept of
chemical expansion, EPA received comments in the following major areas:
EPA's screening process used to identify potential candidates and the
Agency's use of the Draft Hazard Assessment Guidelines (Ref. 11); the
use of exposure in determining if a chemical meets the statutory
criteria of EPCRA section 313; listing of categories; the addition of
chemicals that are regulated by the Food and Drug Administration (FDA);
the addition of chemicals that are regulated under FIFRA; duplicative
reporting; general technical comments; and chemical-specific comments.
A. Comments on EPA's Screening Process Used to Identify Potential
Candidates for Addition to EPCRA Section 313 and on EPA's Use of the
Draft Hazard Assessment Guidelines
1. Screening based on toxicity. Monsanto, Zeneca Incorporated, and
the National Oilseed Processors Association contend that the use of
minimum effective doses (MEDs) to screen chemicals as potential
candidates for addition to the EPCRA section 313 list was unrealistic
and overly broad as a screening tool. One of these commenters also
contended that EPA based its proposed addition on toxicity screening
only.
EPA believes that the commenter may have misunderstood the use of
the MED screening criteria. The MED screen is not intended, and is not
used by EPA, as a surrogate for the actual statutory listing criteria.
The MED was used as a screening tool during the preliminary review of
several thousand candidate chemicals, because MED values were available
and they are based on experimental values. MEDs are not equivalent to
lowest-observed-adverse-effect levels (LOAELs). MEDs are generally
derived from LOAELs from chronic toxicity studies using a log
transformation and as such a MED is a single value based upon the best
available study. Satisfying the MED screening criteria, however, does
not mean that a chemical will necessarily be added to the list. In
every case, the Agency determines that at least one of the section
313(d)(2) criteria is met before a chemical is listed. For example,
isoprene, 1,3-dichloropropane, and dichlorodimethylmethane passed the
toxicity screen, but upon a more detailed review, were determined not
to meet the criteria of EPCRA section 313(d)(2) and thus were not
proposed for addition.
EPA believes that MEDs are useful as a screening tool and that the
methodology has been adequately reviewed both internal and external to
the Agency. The MED system was first presented in a peer reviewed
article by DeRosa, et. al (Ref. 2). The MED methodology has been used
by EPA in programs other than EPCRA section 313. For example, the MED
methodology is integral to the reportable quantity (RQ) scoring system
as utilized by EPA in CERCLA section 102. The RQ scoring system scheme
is described in several Federal Register documents (April 4, 1985, 50
FR 13456; September 29, 1986, 51 FR 34535; and March 16, 1987, 52 FR
8140). Further, the Superfund Amendments and Reauthorization Act of
1986 (SARA) required EPA and the Agency for Toxic Substances and
Disease Registry (ATSDR) to develop a list of 275 hazardous substances
most commonly found at facilities on the National Priorities List (NPL)
and considered to present the most significant threat to human health
at those sites or at other facilities where releases may occur. During
development of criteria to select the first list of 100, the RQ
methodology (as discussed in the Draft Hazard Assessment Guidelines,
Ref. 11) was selected as one of the evaluation tools used to develop
the initial list, and the annual updates. When the initial list was
published (April 17, 1987, 52 FR 12866) a summary of the methodology
used to develop the list was provided.
Monsanto believes that the use of an MED of 500 mg/kg/day as the
upper limit of the ``may be sufficient'' category of the screening
criteria required an unrealistically high dose to have been used for
toxicity testing.
EPA agrees that the upper bound for the medium priority category
may warrant reconsideration. EPA will address this issue and other
comments received on the Draft Hazard Assessment Guidelines (Ref. 11),
when the Agency finalizes that document. However, none of the chemicals
proposed for listing in the proposed rule had MEDs that approached this
upper bound. Of the chemicals proposed for addition pursuant to EPCRA
section 313(d)(2)(B), greater than 93 percent had MED values that were
in the range for the high priority category; the remaining chemicals
(less than 7 percent) had MEDs in the lowest fifth of the medium
priority category range, i.e., MEDs only slightly greater than the high
priority category range. EPA reiterates that the MED screen is not
intended, and is not used by EPA, as a surrogate for the actual
statutory listing criteria. Additions to EPCRA section 313 are based on
a hazard assessment, and, where appropriate, an analysis of exposure,
to determine whether the chemical meets one or more of the EPCRA
section 313(d)(2) listing criteria.
The Natural Resources Defense Council supports the health and
environmental effects screening criteria used by EPA as a reasonable
basis to screen chemicals as candidates for possible addition to EPCRA
section 313.
The Agency agrees with this commenter in its support of the use of
the screening criteria and believes that the screening criteria provide
a reasonable basis to make a preliminary evaluation of chemicals for
possible addition to the EPCRA section 313 list. EPA also agrees with
the commenter's statement that the specific screening values are
consistent with established risk assessment procedures applied in other
EPA programs.
2. Screening based on production volume. Eastman Chemical Company
states that, in addition to the use of a production volume screen, the
Agency should consider the number of TRI Form Rs that would likely be
submitted subsequent to listing. If the number is considered to be
minimal (perhaps 5, 10, 15 or more reports), then EPA should balance
the public's right-to-know with the economic burden placed on an
industry.
EPA adopted a production volume screen for the development of the
proposed rule to screen out those chemicals for which no reports are
expected to be submitted. The Agency believes that it has the
discretion to not include such chemicals at this time. If chemicals
that did not meet the production volume screen were listed, there would
be an economic burden for firms that would have to determine that they
did not exceed the reporting threshold, without providing any
information to the public.
While the Agency has determined to not list chemicals for which no
reports would be submitted, EPA believes that it is appropriate to add
chemicals to EPCRA section 313 for which even a small number of reports
are likely to be submitted nationally. In such cases, the reporting
facilities will still provide important information to the surrounding
communities. Even though a particular chemical may only be
manufactured, processed, or otherwise used at a relatively small number
of facilities, the data provided in the TRI Form R reports by these
facilities could represent significant information in the communities
in which the facilities are located. The Agency believes that it would
be inconsistent with the public's right-to-know not to list chemicals
even if only a low number of reports is expected.
3. Use of the Draft Hazard Assessment Guidelines. Six industry
trade organizations and three companies contend that EPA's use of the
Draft Hazard Assessment Guidelines (Ref. 11) was inappropriate. The
commenters state that the use of the term ``draft guidelines''
indicates that the document requires additional review. Therefore, they
believe that EPA should refrain from using the document to support this
rulemaking.
It is appropriate for EPA to use the Draft Hazard Assessment
Guidelines (Ref. 11), as it did in this rule, in considering whether to
list a chemical on the section 313 list. The Draft Hazard Assessment
Guidelines are an embodiment of internal EPA practices that have been
used in listing determinations that have evolved since the inception of
the TRI program. The Draft Hazard Assessment Guidelines do not
constitute a set of rules for adding or deleting chemicals to or from
the list: the Draft Hazard Assessment Guidelines are an explanation of
the process and general standards for evaluating chemicals against the
EPCRA section 313 listing criteria. These Draft Hazard Assessment
Guidelines notwithstanding, EPA has evaluated every chemical proposed
for addition directly against the EPCRA section 313 statutory criteria,
and has taken into consideration comments submitted by the public
specific to those chemicals (responses to those chemical-specific
comments are found in the Response to Comment Document, (Ref. 14);
summaries of most significant chemical-specific comments are found in
units IV.F. and IV.G. of this preamble).
B. Use of Exposure Assessments
One of the most significant issues raised by commenters relates to
the Agency's consideration of hazard, exposure, and risk in
interpreting the section 313(d)(2) criteria. Specifically, a number of
commenters believe that EPA's interpretation of the EPCRA section
313(d)(2)(B) criterion, chronic human health effects, and the section
313(d)(2)(C) criterion, ecological effects, has been overly
restrictive. The commenters contend that EPA should conduct risk
assessments and make a formal determination that a chemical poses a
risk (i.e., a combination of exposure and hazard) before adding it to
the EPCRA section 313 list. The commenters argue that the following
factors support their contention: (1) The statutory criteria include an
implicit exposure and thus risk component; (2) the legislative history
illustrates Congress' intent that exposure considerations were to be an
integral part of determining whether a chemical should be listed on the
EPCRA section 313 list; and (3) EPA should consider exposure in
conjunction with section 313(d)(2)(B), chronic human health effects,
and for all listings pursuant to section 313(d)(2)(C), ecological
effects, because there is precedent for the use of exposure in previous
listing and delisting actions.
In light of the many comments received on this issue, EPA has
reviewed its positions in this area, and agrees with many of the
commenters that there are limited circumstances under which it is
appropriate for EPA to consider exposure factors for listing decisions
under section 313(d)(2). The Agency believes that exposure
considerations are appropriate in making determinations (1) under
section 313(d)(2)(A), (2) under section 313(d)(2)(B) for chemicals that
exhibit low to moderately low toxicity based on a hazard assessment
(i.e., those chemicals for which the value of listing on the EPCRA
section 313 list on hazard alone is marginal), and (3) under section
313(d)(2)(C) for chemicals that are low or moderately ecotoxic but do
not induce well-documented serious adverse effects as described below.
The Agency believes that exposure considerations are not appropriate in
making determinations (1) under section 313(d)(2)(B) for chemicals that
exhibit moderately high to high human toxicity (These terms, which do
not directly correlate to the numerical screening values reflected in
the Draft Hazard Assessment Guidelines, are defined in unit II.) based
on a hazard assessment, and (2) under section 313(d)(2)(C) for
chemicals that are highly ecotoxic or induce well-established adverse
environmental effects. For chemicals which induce well-established
serious adverse effects, e.g., chlorofluorocarbons, which cause
stratospheric ozone depletion, EPA believes that an exposure assessment
is unnecessary. EPA believes that these chemicals typically do not
affect solely one or two species but rather cause changes across a
whole ecosystem. EPA believes that these effects are sufficiently
serious because of the scope of their impact and the well-documented
evidence supporting the adverse effects.
EPA, however, disagrees with those commenters who suggest that EPA
must include a risk assessment component to EPCRA section 313
determinations. Specifically, EPA does not agree with the commenters
about the extent to which exposure must be considered in making
determinations under sections 313(d)(2)(B) and (C). This is primarily
because EPA does not agree with the commenters' understanding of EPCRA
section 313. Risk assessment may be pertinent and appropriate for use
under statutes that control the manufacture, use, and/or disposal of a
chemical, such as the Clean Air Act or the Toxic Substances Control
Act. However, EPCRA section 313 is an information collection provision
that is fundamentally different from other environmental statutes that
control or restrict chemical activities.
EPCRA section 313 charges EPA with collecting and disseminating
information on releases, among other waste management data, so that
communities can estimate local exposure and local risks; risks which
can be significantly different than those which would be assessed using
generic exposure considerations. The intent of EPCRA section 313 is to
move the determination of what risks are acceptable from EPA to the
communities in which the releases occur. This basic local empowerment
is a cornerstone of the right-to-know program.
EPCRA section 313 establishes an information collection and
dissemination program, the burden it imposes is significantly less than
the burden imposed by a statute which controls the manufacture, use,
and/or disposal of a chemical. EPCRA section 313 requires that a
facility use the best available information to prepare each chemical-
specific TRI report. However, the statute does not require that the
facility conduct monitoring or emissions measurements to determine
these quantities. A facility must only estimate, to the best of its
ability, the quantitative information it reports. This is in contrast
to other environmental statutes that may require a facility to monitor
releases, change its manufacturing process, install specific waste
treatment technology, or dispose of wastes in a certain manner. As
such, the Agency believes that the standard that must be met to require
information submission under EPCRA section 313 is less than that to
regulate a chemical under a statute such as the Clean Air Act.
EPA believes that its position regarding the use of hazard,
exposure, and risk in listing decisions is consistent with the purpose
and legislative history of EPCRA section 313, as illustrated in the
following passage from the Conference report:
The Administrator, in determining to list a chemical under any
of the above criteria, may, but is not required to conduct new
studies or risk assessments or perform site-specific analyses to
establish actual ambient concentrations or to document adverse
effects at any particular location. (H. Rep. 99-962, 99th Cong., 2nd
Sess., p. 295 (Oct. 3, 1986) ).
This passage indicates Congress did not intend to require EPA to
conduct new studies, such as exposure studies, or perform risk
assessments, and therefore did not consider these activities to be
mandatory components of all section 313 decisions. EPA believes that
this statement combined with the plain language of the statutory
criteria clearly indicate that Congress intended that the decision of
whether and how to consider exposure under EPCRA section 313(d)(2)(B)
and (C) should be left to the Agency's discretion. EPA has carefully
considered when and how to use exposure to fully implement the right-
to-know provisions of EPCRA. The Agency believes that in this final
rule, EPA has appropriately used the discretion provided to it to
assure the addition of chemicals that meet the right-to-know objectives
of EPCRA section 313 while not unduly burdening the regulated
community.
EPCRA section 313 specifically requires that exposure be considered
for listing a chemical pursuant to section 313(d)(2)(A). The statute
mandates that EPA consider whether ``a chemical is known to cause or
can reasonably be anticipated to cause significant adverse acute human
health effects at concentration levels that are reasonably likely to
exist beyond facility site boundaries.'' EPA has, and will continue to
look at exposures reasonably likely to exist beyond facility site
boundaries when making a listing determination pursuant to EPCRA
section 313(d)(2)(A).
The statute is silent on the issue of exposure considerations for
the section 313(d)(2)(B) and (C) criteria. The language of section 313
does not prohibit EPA from considering exposure factors when making a
finding under either section 313(d)(2)(B) or section 313(d)(2)(C).
However, the language of sections 313(d)(2)(B) and (C) does not require
the type of exposure assessment and/or risk assessment argued by the
commenters. EPA believes that it has the discretion under both section
313(d)(2)(B) and section 313(d)(2)(C) to consider, where appropriate,
those exposure factors that may call into question the validity of
listing of any specific chemical on TRI. In exercising this discretion,
EPA considers it appropriate to employ exposure considerations to a
limited extent in making determinations under EPCRA section
313(d)(2)(C) because this criterion requires the Agency to find a
``significant adverse effect on the environment of sufficient
seriousness, in the judgment of the Administrator to warrant
reporting'' under EPCRA section 313. This language recognizes the
possibility that under certain circumstances, a chemical that could
theoretically cause an adverse effect on the environment is unlikely to
cause one of a magnitude sufficient to warrant listing. Moreover,
because of the limitation on the number of chemicals listed pursuant to
only section 313(d)(2)(C) that may be listed, EPA believes that it is
appropriate to use both hazard and exposure factors as prioritizing
considerations in these listing decisions. Therefore, to meet its
obligation under section 313(d)(2)(C), in cases where a chemical is low
or moderately ecotoxic, EPA may look at certain exposure factors
(including pollution controls, the volume and pattern of production,
use, and release, environmental fate, as well as other chemical
specific factors, and the use of estimated releases and modeling
techniques) to determine if listing is reasonable, i.e., could the
chemical ever be present at high enough concentrations to cause a
significant adverse effect upon the environment to warrant listing
under section 313(d)(2)(C). Of the chemicals being added in today's
action pursuant to section 313(d)(2)(C), all but one are highly
ecotoxic. These highly ecotoxic chemicals are being added to the EPCRA
section 313 list pursuant to section 313(d)(2)(C) based on their
hazard. The other chemical, which is moderately ecotoxic, is being
added to the EPCRA section 313 list pursuant to section 313(d)(2)(C)
based on both its hazard and an exposure assessment for this chemical.
For listing determinations made pursuant to EPCRA section
313(d)(2)(B), in instances where the hazard assessment indicates that
the value of listing on EPCRA section 313 on hazard alone is marginal
(i.e., a chemical is of low toxicity and unrealistic exposures would be
necessary for it to pose a risk to communities), EPA may use exposure
considerations in its listing decisions. Only chemicals for which the
hazard assessments indicate moderately high to high toxicity are being
added in today's action to the EPCRA section 313 list pursuant to
section 313(d)(2)(B). None of these chemicals are chemicals for which
the consideration of exposure factors would be appropriate.
Through this rulemaking, EPA is clarifying its position regarding
the use of hazard, exposure, and risk in listing decisions under EPCRA
section 313. EPA will consider exposure factors when making
determinations under section 313(d)(2)(A) (acute human toxicity). In
addition, EPA has discretion to consider exposure factors where
appropriate for determinations under sections 313(d)(2)(B) (chronic
human toxicity) and (C) (environmental toxicity), and that there is a
broader range of circumstances in which exposure will be considered
under section 313(d)(2)(C) than under (B).
EPA has reviewed its past listing decisions in light of this
clarification, and believes that its prior listing determinations have
been consistent in the consideration of exposure in 31 of the 32
listing/delisting determinations previous to this action, including a
number of deletions of low toxicity chemicals that Congress placed on
the initial EPCRA section 313 list. EPA is currently reviewing the one
exception, inorganic fluorides, to determine if additional action is
warranted. EPA will continue to evaluate petitions according to this
clarification and will delete chemicals that do not meet the statutory
criteria.
C. Addition of Categories
Six industry trade organizations, 7 companies, and the Department
of Energy contend that section 313 does not provide EPA the statutory
authority to list chemical categories. Some of the commenters contend
that the intent of Congress was for EPA to review individual chemicals.
Therefore, the commenters believe that EPA should list all chemicals
individually. General Electric, American Iron and Steel Institute, and
Eastman Chemical Company further contend that, based on legal precedent
(citing AFL-CIO vs. OSHA, 965 F.2d 9262 (11th Cir. 1992)), EPA does not
have the authority to list chemical categories or specific groups of
chemicals.
EPA believes that the statutory authority to add ``a chemical'' to
the list may be reasonably interpreted to include the authority to list
groups or categories of chemicals. Indeed, this interpretation is
supported by the initial list of chemicals and chemical categories
adopted by Congress in section 313(c). In that initial list, Congress
included 20 chemical categories, mainly metal compounds, but also
categories of organic chemicals such as chlorophenols. Nothing in
section 313 or its legislative history indicates or even suggests that
Congress intended to preclude EPA from adding chemical categories to
the list where the appropriate findings can be made.
Where, as with the categories being added in this final rule, EPA
determines that the primary purpose of TRI--providing information to
the community about the release of chemicals--is most appropriately
served by listing a category of chemicals, EPA has the discretion to
list a category rather than individual chemicals. Of course, in adding
a category to the list, EPA must comply with the statutory criteria.
The Agency believes it satisfies the statutory criteria to add a
category to the list by identifying the toxic effect of concern for at
least one member of the category and then showing why that effect may
reasonably be expected to be caused by all other members of the
category. A specific justification for each of the categories included
in the final rule has been provided in the preamble of the January 12,
1994 proposed rule, in the docket supporting this rulemaking, and in
the Response to Comment Document (Ref. 14).
Several commenters raised policy concerns and suggested that there
would be regulatory difficulties associated with adding chemical
categories. These are addressed below.
One commenter suggested that the regulated community would face
uncertainty in deciding which chemicals belong in the category. In this
final rule, EPA has described the categories in sufficient detail to
alleviate uncertainty regarding their membership. Of course, the Agency
will work with the public and the regulated community to develop, as
appropriate, any interpretations and guidance the Agency determines are
necessary to facilitate accurate reporting for these categories.
One commenter questions how to properly report a chemical which
could be considered part of a category and which is also specifically,
individually listed. Threshold determinations should be made for the
individually-listed chemical rather than for the category. The current
EPCRA section 313 list contains some individually-listed chemicals that
also meet the definition of an EPCRA section 313 listed category. For
example, pentachlorophenol is listed individually on EPCRA section 313
but also meets the definition of the chlorophenol category. In these
situations, threshold determinations should be made for the chemical as
an individual entity rather than as a member of the category. A
facility would not count the quantities manufactured, processed, or
otherwise used toward threshold determinations for both the individual
listing and the category listing, but rather only toward the individual
chemical threshold.
One commenter contends that categories will lead to inadvertent
non-compliance with reporting requirements. EPA does not believe that
this is a significant concern. Because the categories being added to
the EPCRA section 313 list today each consist of chemicals that are
similar chemically and in effect, EPA believes that these categories
will not be difficult for the public or industry to understand or for
the Agency to administer. In addition, there are already categories on
the current list, and EPA has not experienced a significant problem of
the sort suggested by the commenter. The Congressional objective of
providing information is outweighed by any possible problems that some
facilities might have with inadvertent noncompliance.
One commenter states that the use of categories will artificially
lower the thresholds for reporting chemicals within the category. The
Agency believes that calculating the thresholds based on the category
(i.e., a sum of the activities for each individual category member) is
appropriate and not ``artificially lower.'' As described above,
categories are placed on the EPCRA section 313 list where each of the
members can be expected to cause similar effects because all members of
the category have a similar functional group or exhibit a similar
characteristic. For each of the categories added in today's rule, EPA
believes that because each member of the category has this similar
functional group or exhibits a similar characteristic, each member of
the category can be reasonably anticipated to cause similar adverse
effects. The members of the category are not randomly selected, but are
closely related and warrant being reported as a category. These
chemicals in aggregate can reasonably be anticipated to cause an
aggregate impact of the adverse effect associated with each member of
the category. Thus, it is appropriate to apply the reporting thresholds
to the category regardless of whether the threshold amount is
attributable to one member of the category or to individual members in
aggregate.
One commenter believes that listing broad categories where the
individual members have diverse properties and cause diverse effects
does not constitute ``good science.'' The Agency agrees that a category
must be rationally constructed both in terms of similarity in the
properties of the individual members and in terms of their effects.
There is, of course, no requirement that the properties across category
members be absolutely identical. EPA agrees that the members of a
category be reasonably expected to elicit the same type of effect or
related effects in order for a category to satisfy the statutory
listing criteria. Furthermore, EPA agrees that determinations to list a
category, as with listing an individual chemical are to be based on
``good science.'' EPA has applied these principles to the categories
being added in the final rule.
D. Policy Issues
There are several policy issues which were consistently raised in
comments on specific chemicals and general comment on the entire
proposed rule. For purposes of this final rule, EPA addresses these
issues in this unit of the preamble and not in unit IV.F. of the
preamble in the responses to chemical-specific comments. Detailed
responses to comments on specific individual chemicals are available in
the Response to Comments Document (Ref. 14).
1. The addition of chemicals that may be released in small
quantities. Many commenters object to the addition of many of the
chemicals to the EPCRA section 313 list because they do not believe
that there will be significant releases of these chemicals. Therefore,
they contend there will not be significant exposure to these chemicals
and the associated risks will be low.
EPA believes that the chemicals added today meet the EPCRA section
313(d)(2) criteria and should be included on the EPCRA section 313
list. The quantity of a chemical released is not part of the statutory
criteria. The purpose of EPCRA section 313 is to collect data on the
quantity released so that local communities can make their own
determinations about exposure.
Congress intended EPCRA section 313 to address the lack of
information on toxic chemicals in communities by providing information
on releases of toxic chemicals. The public can then use this release
information with site-specific information and the appropriate
attributes of a chemical to evaluate exposure. EPA considers it
inappropriate under the right-to-know program to supplant the public's
power to make risk determinations on a community level by the Agency's
use of specified levels of potential releases, exposure, or risk as
screening criteria to exclude chemicals from the EPCRA section 313
list. By listing chemicals that present a hazard and providing TRI data
on these chemicals to the public, EPA allows the public to make the
determination as to whether there is a risk in their community.
Furthermore, any exposure assessment conducted by EPA would be
conducted from a national perspective and may not truly represent the
risks to a specific community. (For a more detailed discussion on the
Agency's use of exposure see Unit IV.B. of this preamble).
2. The addition of chemicals that are regulated by FDA. Eli Lily
and Company, National Agricultural Chemical Association, Pharmeceutical
Manufacturers Association, and Hoffman-La Roche state that chemicals
which are regulated by the FDA should not be added to EPCRA section
313. The commenters argue that the FDA approves a drug only after
extensive testing and a determination that the benefits to the patients
outweigh the risks. The commenters further state that access to these
drugs is controlled because they can only be obtained through a medical
doctor.
EPA agrees that the drug testing and approval process conducted by
the FDA is extensive and necessary to protect the public health and
well-being. However, as discussed above, the purpose of listing these
chemicals under EPCRA section 313 is to provide information on the
release, transfer, and waste management activities occurring in the
community. This is a different function that addresses different issues
than those addressed by FDA. Furthermore, while the main use of these
chemicals is pharmaceutical in nature, that does not mean that they are
not a hazard in other contexts. EPA agrees that in controlled
situations (e.g., a doctor's prescription) ingestion of a drug is
likely to have certain intended benefits. However, outside of this
controlled situation, any adverse effects are not balanced by the
benefits received from the use of the drug. Further, EPCRA section 313
will collect information on the release and disposal of these
chemicals, which is not covered by the regulation of the use of a
chemical as a drug.
3. Chemicals regulated under FIFRA. Several commenters do not
support the addition of chemicals regulated under FIFRA to the EPCRA
section 313 list of toxic chemicals because, they contend, the major
route of exposure, agricultural field use, has been addressed through
FIFRA regulation which establishes safety factors and use directions
allowing for safe use. They further contend that the use of these
chemicals has been determined not to present an unreasonable risk and
therefore, listing pesticides under EPCRA section 313 is unnecessary.
FIFRA regulations require that the Agency determine that pesticidal
uses of a chemical do not cause ``unreasonable adverse effects on the
environment'' which is defined in FIFRA section 2(bb) as ``any
unreasonable risk to man or the environment taking into account the
economic, social, and environmental costs and benefits of the use of
pesticides'' (7 U.S.C. section 136(bb)). FIFRA is a regulatory statute,
and the impacts of regulation can be immediate and direct (e.g.,
banning of a chemical), and as such EPA examines not only the hazards
presented by the chemical, but also the specific exposure scenarios,
and weighs the risks against the benefits of the chemical. The
``unreasonable adverse effects'' determination under FIFRA is specific
to the intentional use of the chemical as a pesticide and does not
address other uses or releases of the chemical that may result from
manufacture, processing, or other use. Furthermore, a determination
under FIFRA that the use of a chemical will not result in an
``unreasonable adverse effect'' is not a determination that the
chemical is not hazardous or that the use of the chemical is without
risk. Finally, EPCRA section 313 was not enacted to serve the same
purpose as FIFRA. Listing on EPCRA section 313 provides communities
with some of the information required to determine what risks may
result from the manufacture, processing and non-pesticidal use of a
chemical, information not generally provided through FIFRA.
4. Duplicative reporting. Many commenters believe that listing some
of the chemicals proposed will result in duplicative regulation that
will be unduly burdensome and of little benefit. One other commenter,
Westinghouse Electric Corporation, states that EPA should utilize
existing sources of information to avoid duplicative reporting.
Congress did not intend that the chemicals listed under EPCRA
section 313 be limited to those that are not regulated under other
environmental statutes and for which no information is collected
pursuant to other requirements. The initial list of chemicals that
Congress included in section 313 consisted of substances regulated
under RCRA, CWA, SDWA, CERCLA, FIFRA, and CAA. Further, as
Representative Edgar stated in the House of Representatives debate on
the Conference bill:
With respect to the contents of the toxic release form,
estimates of releases into each environmental medium must be
provided. This shall include any releases into the air, water, and
land, as well as releases from waste treatment and storage
facilities. This shall include all releases of toxic chemicals into
surface waters whether or not such releases are pursuant to the
Clean Water Act permits. (132 Cong. Rec. H9561, October 8, 1986)
EPA believes that the chemicals being added today meet the toxicity
criteria of EPCRA section 313(d)(2) and, therefore, should be added to
the EPCRA section 313 list. EPA further believes that the EPCRA section
313 requirements do not duplicate other regulatory program
requirements. EPCRA was not enacted to serve the same purpose as other
regulatory programs but to collect and disseminate information to the
public. Nor is EPCRA section 313 intended to regulate how a chemical
may be used, the amount of chemical a facility manufactures, processes,
otherwise uses, and releases, what media the chemical is released to,
or how the chemical is disposed. Therefore, TRI, as an information
collection and dissemination program, is not designed to directly
impose controls for the protection of human health or the environment
in the same manner as other regulatory programs. The benefit of TRI is
that it empowers the public, through access to release, transfer, and
waste management data on toxic chemicals, to make determinations about
risks in their communities based on TRI data, site-specific
information, and the properties of the chemicals.
E. General Technical Comments
1. Maternal toxicity. A number of commenters argued that for
certain chemicals in animal tests, the only evidence for developmental
toxicity occurred at maternally toxic doses (that is, doses that were
high enough to induce toxicity in the mother), and, therefore,
developmental toxicity cannot be used as a basis for listing these
chemicals under EPCRA section 313. EPA disagrees that fetal effects
only in the presence of maternal toxicity demonstrate that a given
substance does not present a developmental hazard. Although the
developmental effects may have been seen in the presence of reversible
maternal effects, the developmental effects may be more permanent and
cannot be treated as only secondary to reversible maternal toxicity.
With regard to adverse effects in the presence of maternal toxicity,
EPA believes that developmental effects at maternal toxicity are ``. .
.toxic manifestations and as such are generally considered a reasonable
basis for Agency regulation and/or risk assessment'' (Ref 6). This
approach has particular relevance in situations where reversible
maternal toxicity may occur in the presence of irreversible adverse
fetal effects. The Agency does not distinguish between fetal effects
observed in the presence of maternal toxicity or those observed without
concomitant maternal toxicity. Both maternal and fetal toxicity are of
concern to the Agency, and are within the criteria of EPCRA section
313(d)(2). Thus, EPA will use the effect, maternal or fetal, which is
most sensitive to set LOAELs and no-observed-adverse-effect levels
(NOAELs). If both occur at the same level, the LOAELs and NOAELs for
both are the same. When the LOAEL is the same for the adult and
developing organisms, it may simply indicate that both are sensitive to
that dose level, rather than that the developmental effects result only
from maternal toxicity. Moreover, whether developmental effects are
secondary to maternal toxicity or not, the maternal effects may be
reversible while effects on offspring may be permanent. There are
several agents known to produce adverse developmental effects at
minimally toxic doses in adult humans (e.g., tobacco smoking, alcohol,
isotretinoin).
2. Use of IRIS and other secondary sources. Several commenters
object to EPA's use of the Agency's Integrated Risk Information System
(IRIS) data base, the Agency's Office of Pesticide Programs' 1988 TOX-
One-Liners data base, Registry of Toxic Effects of Chemical Substances
(RTECS) data base, and the Aquatic Information Retrieval (AQUIRE) data
base. The commenters contend that in relying on these sources the
Agency ignores other pertinent data that may be in its possession. They
contend that EPA should have examined the primary sources, rather than
relying on data bases which are summaries of studies. Specifically,
some commenters claim that there are many studies in EPA's possession,
but not included in the 1988 TOX-One-Liner data base, that appear not
to have been considered in the review process, because they have not
yet been reviewed by EPA's Office of Pesticide Programs. The commenters
contend that reliance on IRIS or the 1988 TOX-One-Liner data base does
not constitute a detailed analysis and careful examination of the
available data on a chemical.
EPA disagrees with the commenters. EPA's use of the Agency's IRIS
data base for EPCRA section 313 purposes does constitute a hazard
evaluation. That data base generally provides information against which
EPA can evaluate the section 313(d)(2) criteria. The information
contained in the IRIS data base represents the Agency's weight-of-
evidence hazard assessment for chemicals contained in the data base.
The information was developed after the Agency's thorough scientific
review of the available data. Therefore, by relying on information in
the IRIS data base in the review of chemicals for listing on EPCRA
section 313, EPA made statutory determinations based on hazard
assessments conducted by the Agency.
Although the 1988 TOX-One-Liners were used as part of the Agency's
evaluation of the toxicity of a candidate chemical, a number of other
sources were also used. These include decision documents from a number
of Agency and EPA internal peer review groups, deliberations of the
FIFRA Scientific Advisory Panel, and reference to data evaluation
records for studies used in support of listing. Therefore, evaluations
of the toxicity of individual chemicals has been made on the entire
data base and did not rely only on the 1988 TOX-One-Liners data base.
Furthermore, inclusion of all of the detailed studies in the docket was
not possible, because of the proprietary nature of some of the
information. However, in cases where relevant information was used in
support of the listing decision, but was not included in the 1988 TOX
One-Liners data base (which is the most recent sanitized version of the
data base), sanitized versions of the additional sources were included
in the docket. In those cases where only the 1988 TOX-One-Liners data
base or other similar sources were cited, no additional data not
described in the 1988 TOX-One-Liners, RTECS, or the AQUIRE data bases
was considered to be relevant to this listing. For a few chemicals it
has become apparent based on comments received that EPA's analysis did
not include studies which are in EPA's possession but which EPA has not
reviewed. The Agency is deferring the final action on these chemicals
until such studies can be reviewed.
3. Testing at toxic doses. A number of commenters stated that
pesticides which are registered under FIFRA should not be listed under
EPCRA section 313 because the testing conducted to obtain a pesticide
registration under the FIFRA review process requires testing at dose
levels ``virtually guaranteed to produce a toxicological effect.''
It is not EPA's position that chemicals registered as pesticides
under FIFRA should be precluded from listing simply because these
chemicals were tested at doses which are designed to produce toxic
effects. The commenters are correct that the FIFRA standard study
design attempts to set the doses at levels which bracket the minimal
toxic dose, and, therefore, the high dose(s) by design produces an
effect. The purpose of this study design under FIFRA is to determine
the potential for toxicity of the chemical, whether the responses are
dose-related and, depending on the effects produced, the degree of
toxicity. Because virtually any chemical substance can elicit a
toxicological response at some dose level, the mere presence of the
toxic response is not used in isolation in listing decisions under
EPCRA section 313. Rather, it is the relative severity of the effect,
the presence of a dose/response relationship, and whether the effect is
manifested at relatively low doses which are considered in determining
the hazard of the chemical, and in making listing determinations under
EPCRA section 313.
4. Precursor chemicals. CRF AG Products Company, Monsanto, FMC
Corporation, Eastman Chemical Company, and the Chemical Manufacturers
Association question EPA's authority to list precursor chemicals (i.e.,
a chemical that reacts in vivo or in the environment to generate
another chemical that produces the toxic effect supporting the listing)
on the EPCRA section 313 list. The commenters believe that a chemical
should only be added to the list based on the toxicity of the chemical
itself. Further they contend that nowhere in the legislative history is
there any indication that post-release transformation products,
degradation products, or products of chemical reactions are legitimate
bases for adding chemicals to the EPCRA section 313 list.
The EPCRA section 313(d)(2) listing criteria each state that EPA
may list a chemical that it determines ``causes or may reasonably be
anticipated to cause'' the relevant adverse human health or
environmental effects. EPA believes that this language allows EPA to
consider the effects caused by the degradation products of a listed
chemical. Where it may reasonably be anticipated, based on available
data, that the listed chemical would readily degrade into another
chemical that would cause the adverse effect, EPA is acting reasonably
and within its grant of authority in listing the precursor to the toxic
degradation product.
Furthermore, one could also view the effects caused by the
degradation product as effects indirectly caused by the listed
chemical. EPA believes it is within its authority to consider both the
direct and indirect adverse human health and environmental effects of a
chemical in making a listing determination. Based on the statutory
language and legislative history, EPA interprets EPCRA section
313(d)(2) to include toxic effects indirectly caused by a listed
chemical. The statute and the legislative history do not specifically
preclude EPA from considering indirect effects in deciding whether a
chemical meets the toxicity criteria under section 313. In the absence
of specific congressional intent on the issue, it is reasonable for EPA
to consider indirect effects in light of the broad statutory purpose to
inform the public about releases of toxic chemicals to the environment.
Were EPA to exclude indirect effects from consideration it would ill-
serve the purpose of the statute by precluding public access to
information about chemicals that, albeit, indirectly cause a wide range
of adverse health and environmental effects.
There is precedent for the Agency to consider the ``indirect''
toxicity of a chemical being considered for listing. Indirect toxicity
was the basis for the granting of two petitions, one to add seven
chlorofluorocarbons and halons (August 30, 1990, 55 FR 31594) and a
second to add hydrochlorofluorocarbons to the EPCRA section 313 list
(December 1, 1993, 58 FR 64936). EPA also used indirect toxicity in
support of its denial of petitions to delete certain volatile organic
chemicals from the section 313 list, specifically, the ethylene and
propylene petition (January 27, 1989, 54 FR 4072) and the cyclohexane
petition (March 15, 1989, 54 FR 10668).
5. Use of studies conducted by routes other than oral, inhalation,
or dermal. Several commenters maintain that intraperitoneal,
intravenous, or subcutaneous injection (injection into the abdomen, a
vein, or under the skin, respectively) has minimal relevance for
evaluating potential human exposure from industrial situations and
should not be used to support an EPCRA section 313 listing decision.
One commenter contends that, if considered at all, intraperitoneal
injection is a form of exposure that should be considered in
establishing a section 313(d)(2)(A) finding of acute effects, not a
section 313(d)(2)(B) finding of chronic effects.
EPA disagrees with the commenters. In making section 313 listing
decisions, the Agency cannot ignore the possible significance of any
existing data, including data from intraperitoneal, intravenous, or
subcutaneous injection studies. Although it is preferable to have
toxicity data from the common routes of human exposure, EPA believes
that for hazard assessment under EPCRA section 313, the Agency should
use all available information to identify the hazard associated with a
chemical. This comment relates to five chemicals (bromacil lithium
salt, fluorouracil, pentobarbital sodium, tetracycline hydrochloride,
and sodium nitrite) that are being added to the section 313 list today.
For three of these chemicals, bromacil lithium salt, fluorouracil, and
sodium nitrite, any data from intraperitoneal or other injection routes
of exposure are supplemented by data from other, non-injection exposure
routes. For example, in addition to chronic dog and rat injection
studies to support the chronic hematological concerns of sodium
nitrite, there are human oral data. For bromacil lithium salt,
intraperitoneal injection studies in rats are supplemented by gavage
studies in mice to support the developmental concerns for this
chemical. In addition to the developmental effects observed in the
offspring of women receiving fluorouracil intravenously, developmental
abnormalities in mice, rats and hamsters receiving fluorouracil orally
were used to support the developmental toxicity finding. For both
pentobarbital sodium and tetracycline hydrochloride, the studies cited
in the proposed rule in support of the developmental effects of these
chemicals are either studies in which the chemical was administered via
injection or studies in which the chemical was administered via another
route. However, because both of these chemicals are commonly
administered orally, and are efficacious by this route (orally), there
is reason to extrapolate the effects observed in injection studies to
effects by other routes. The proposed rule and the Response to Comment
Document (Ref. 14) contain information on EPA's review of these
chemicals, including the toxicity evaluation. This background
information will not be repeated here in the final rule. Based on EPA's
reanalysis of the available information in the proposed rule for these
five chemicals, EPA has sufficient evidence to determine that bromacil
lithium salt, fluorouracil, pentobarbital sodium, tetracycline
hydrochloride, and sodium nitrite have sufficient evidence to meet the
statutory listing criteria under EPCRA section 313(d)(2)(B).
6. Use of acute studies to support a chronic finding. Several
commenters object to the use of data from acute studies to support a
finding of chronic toxicity. The commenters contend that there is no
correlation between transient acute impact and chronic toxicity that is
appropriate to industrial chemicals as a whole. The commenters contend
that, if a chemical exhibits transient acute but not chronic effects,
it should not be listed based on chronic toxicity, unless additional
data on chronic effects are also used in the determination to list the
chemical.
EPA agrees with the commenter that if a chemical exhibits acute
toxic effects, it should be listed based on acute effects unless
additional data on adverse effects after long-term exposure are
available. This comment relates to three of the chemicals (bromine, 2-
bromo-2-nitropropane-1,3-diol, and sodium nitrite) that are being added
to the section 313 list today. For these chemicals, any data from acute
studies are supplemented by chronic toxicity information. In chronic
toxicity studies, bromine produced upper respiratory irritation and
neurological symptoms. In chronic toxicity studies, 2-bromo-2-
nitropropane-1,3-diol produced various effects including lesions of the
stomach mucosa, ulceration, raised areas and excrescences,
inflammation, epithelial hyperplasia and hyperkeratosis, and congested
vessels of the mucosa of the gastrointestinal (G.I.) tract. Sodium
nitrite induced, in a chronic study in mice, reduced motor activity and
major electroencephalogram (EEG) changes in treated animals. The
proposed rule and the Response to Comment Document (Ref. 14) contain
information on EPA's review of these chemicals, including the toxicity
evaluation. This background information will not be repeated here in
the final rule. A summary of the response to comments for these
chemicals is provided in Unit IV.F. of this preamble.
7. Use of cholinesterase inhibition as a measure of neurotoxicity.
Several commenters expressed concern that the Agency has used a
chemical's effect of inhibiting plasma, red blood cell (RBC) or brain
cholinesterase activity as a basis for listing chemicals on the EPCRA
section 313 list. These commenters feel that this effect is not an
adequate indicator of neurotoxicity.
The Agency believes that inhibition of plasma, RBC, or brain
cholinesterase activity is an appropriate indicator to assess the
toxicity of potential neurotoxicants (Ref. 7). In order for the normal
activity of the nervous system to be altered by a toxic chemical, the
chemical must enter the body, reach the tissue target site(s), and be
maintained at a sufficient concentration for a period of time in order
for an adverse effect to occur. Biochemical changes precede the more
overt, physiological changes associated with neurotoxicity, and are
more easily detectable. Acetylcholinesterase (AChE) is the enzyme that
inactivates or terminates the effect of the neurotransmitter
(acetylcholine) on its target. When this enzyme is inhibited,
acetylcholine is built up in the body, and may result in loss of
appetite, anxiety, muscle twitching, paralysis, or other neurotoxic
effects. Thus, one can assess the signs and symptoms of systemic
poisoning by many neurotoxins from their biochemical mechanism of
action, such as the inhibition of AChE. Because of the severity of
these effects, EPA takes a cautious approach by using a measure of
cholinesterase activity as an indicator of neurotoxicity.
The comments concerning cholinesterase inhibition relate to six of
the chemicals that are being added to the section 313 list today. The
proposed rule and the Response to Comment Document (Ref. 14) contain
information on EPA's review of these chemicals, including the toxicity
evaluation. This background information will not be repeated here.
Based on comments received and EPA's reanalysis of the available
information in the proposed rule for these six chemicals, EPA has
sufficient evidence to determine that acephate, cycloate, diazinon,
ethyl dipropylthiocarbamate, pirimphos methyl, and profenofos meet the
statutory listing criteria under EPCRA section 313(d)(2)(B) based on
available neurotoxicity data for these chemicals.
8. Use of certain studies for hazard assessment. Several commenters
argue that EPA should not use studies in support of listing a chemical
on the EPCRA section 313 list, if these studies have been determined to
be insufficient for use in risk assessments under FIFRA or TSCA. For
example, the commenters point to studies EPA considered in this
rulemaking in conducting hazard assessments even though the studies
when submitted for use under FIFRA or TSCA were determined by EPA to be
of ``low confidence.'' EPA believes its use of these studies for
section 313 purposes is appropriate. The ``low confidence''
determination under FIFRA or TSCA applies to the use of the studies for
purposes of risk assessment associated with regulations that impose
controls. The data base for a chemical may be rated low confidence
because of shortcomings such as lack of experimental detail. Although
these studies may be of limited value for purposes of risk assessment
in support of regulatory controls, when considered together, they
present a sufficient weight-of-evidence as to the hazard associated
with the chemical. As additions to EPCRA section 313 made pursuant to
EPCRA section 313(d)(2)(B) are not based on the kind of risk assessment
needed for regulatory controls, EPA believes that such studies can be
used to support listing.
9. Docket was incomplete for certain chemicals. Several commenters
contend that the docket information supporting the listing of certain
chemicals is incomplete. Other commenters contend that, overall, the
docket is too general and limited. Responses to comments about the
evidence provided in the docket for specific chemicals are provided in
the Response to Comment Document (Ref. 14).
In the public docket supporting this rulemaking, EPA included
copies of EPA's support documents (Refs. 9, 12, and 13) for the
proposed rule and copies of the main references cited in those
documents. The primary references that are cited in these main
reference documents were not themselves included. However, these
reference documents are published material, readily accessible, and are
in the public domain. EPA believes that the docket material for both
the proposed and final rules contains the appropriate information to
support the addition of these chemicals to the EPCRA section 313 list
and to have provided the public an adequate basis on which to comment
on the proposed rule.
F. Chemical-Specific Comments for Chemicals that Are Being Finalized in
Today's Action
The Agency received comments on 110 of the 313 specific chemicals
included in the proposed rule. This unit of the preamble summarizes the
most significant of those comments and the Agency's responses. More
detailed responses are included in the Response to Comment Document
(Ref. 14). Neither this unit of the preamble nor the Response to
Comment Document addresses comments specific to chemicals that have
been deferred for final action. These comments will be addressed in a
separate rulemaking specific to those chemicals.
1. Abamectin. One commenter, Merck, states that primates are less
sensitive to the acute effects of abamectin and its analog, ivermectin,
than rodents. The commenter implies that because humans are primates,
abamectin should be less toxic in humans than in rodents. The commenter
further contends that ivermectin and abamectin have been used safely in
animals and humans.
Abamectin interferes with gamma-aminobutyric acid (GABA)
transmission and, as such, produces neurotoxic clinical signs such as
tremors, ataxia, convulsions, or coma that are more severe in rodents
and dogs than primates. EPA agrees that the available studies indicate
that the sensitivity as well as doses required to produce neurotoxic
effects vary from rodents to primates by a 20-fold factor. However,
abamectin was proposed for addition to the EPCRA section 313 list based
on developmental effects rather than neurotoxicity. There are no
developmental studies with abamectin in primates. Therefore, EPA
believes that the rodent studies cited in the proposed rule provide
sufficient evidence that abamectin can reasonably be anticipated to
cause developmental toxicity in humans.
When administered in therapeutic doses, the Agency does not dispute
the animal and human safety and efficacy of ivermectin and abamectin,
but the safety of a 0.2 to 0.3 mg/kg single therapeutic dose does not
diminish the findings of the developmental, reproductive, neurotoxic,
chronic, and carcinogenic animal studies with abamectin which in some
cases demonstrate serious compound-related effects at higher than
therapeutic doses in all species tested.
The same commenter states that although the aquatic toxicity data
cited for the proposed listing of abamectin under EPCRA section 313 are
accurate and valid, it may be inappropriate to list abamectin under
EPCRA section 313 based on the environmental fate of this chemical,
because of environmental fate factors which were not presented by EPA
in the proposed rule.
EPA agrees with the commenter that the aquatic toxicity values
presented in the proposed rule are accurate and valid. EPA disagrees
that the environmental fate of abamectin will negate the chemical's
ecological toxicity. EPA believes that the environmental fate factors
presented by the commenter may reduce, but do not eliminate, the
potential for adverse effects on aquatic organisms because the chemical
is extremely acutely toxic to aquatic organisms.
EPA reaffirms that there is sufficient evidence for listing
abamectin on the EPCRA section 313 list pursuant to EPCRA section
313(d)(2)(B) based on the available developmental toxicity data and
pursuant to EPCRA section 313(d)(2)(C) based on the available
ecotoxicity data. Therefore, EPA is finalizing the addition of
abamectin on the EPCRA section 313 list.
2. Alachlor. Monsanto states that at the highest dose tested in the
chronic mouse study cited in the proposed rule, EPA concluded there was
an increase in lung tumors in females. Monsanto believes that other
regulatory agencies have disagreed with this conclusion. The commenter
contends that these tumors occur spontaneously in mice with a fairly
high and variable frequency and a possible slight increase in a common
rodent tumor at the highest dose tested does not represent a risk to
humans receiving, at most, trace level exposure.
The Agency has concluded that there was statistically significant
increase (the increase was greater than that which would be expected to
occur spontaneously) in lung tumors in female CD-1 mice at 2 dose
levels which were relevant to potential carcinogenicity to humans. The
commenter provides no specifics to support its contention that ``other
regulatory agencies have disagreed with this conclusion'' nor is the
Agency aware of any.
The commenter further states that the Support Document for the
Health and Ecological Toxicity Review of TRI Expansion Chemicals (Ref.
13) also incorrectly listed the dose levels (``[greater than] 42 mg/kg/
day'') producing tumors in rats in the 2-year rat feeding study cited
in the proposed rule. The commenter argues that significant increases
in thyroid and stomach tumors were observed only at 126 mg/kg/day, the
highest dose tested; this dose level also produced severe, excessive
toxicity. Thus, the commenter concludes that the dose-response curves
for the stomach and thyroid tumors are exceptionally steep, with
increased incidences observed only at a dose which exceeded the Maximum
Tolerated Dose (MTD).
EPA believes that the Support Document for the Health and
Ecological Toxicity Review of TRI Expansion Chemicals (Ref. 13)
correctly states the toxic dose levels in the 2-year rat feeding study
as being greater than or equal to 42 mg/kg/day. In this study, nasal
tumors were significantly increased at 42 mg/kg/day and above and the
stomach and thyroid follicular cell tumors at 126 mg/kg/day. The Agency
agrees that the 126 mg/kg/day dose level probably exceeded the MTD;
however, upon reconsideration of the carcinogenicity data, the Agency
determined that the MTD is between 42 mg/kg/day and 126 mg/kg/day.
Although the MTD was exceeded by the highest dose (126 mg/kg/day),
significant effects were seen at 42 mg/kg/day, which does not exceed
the MTD. Therefore, EPA believes that the 2-year chronic dog study
cited in the proposed rule is a valid measure of the oncogenic
potential of alachlor.
The commenter cites a chronic rat feeding study, not cited by EPA
in the proposed rule, in which 5 to 6 months of alachlor administration
followed by 19 months on control diet did not produce a significant
increase in stomach or thyroid tumors in rats. The commenter believes
that this information is consistent with the results of a study, not
cited by EPA in the proposed rule, in which a close structural
chloroacetanilide analog of alachlor has been shown to be a promoter
but not an initiator of stomach tumors. The commenter did not further
identify this study.
Although in the chronic rat feeding study referred to by Monsanto,
the specific group which received alachlor in the diet for 5 to 6
months in this study, and then control diet as a recovery period did
not develop stomach or thyroid tumors, the other groups on study which
continued to receive alachlor in the diet developed both stomach and
thyroid tumors as well as nasal turbinate tumors. Therefore, the
failure to develop stomach tumors after 5 to 6 months treatment
reflects the time frame required for tumor development rather than
indicating a lack of carcinogenic response.
The commenter also discusses the mechanism of carcinogenicity for
alachlor. The commenter states that the mechanism is nongenotoxic and
hormonally mediated. The commenter argues that the mechanism exhibits a
threshold and that nasal turbinate tumors in particular are not
relevant to humans.
The Agency acknowledges the mechanism of carcinogenicity may be
hormonally mediated. However, the mechanism does not alter the fact
that the tumors are relevant to potential carcinogenesis in man.
Mechanism of tumor development relates to the appropriate model by
which cancer risk is calculated. However, mechanism has no impact on
the determination of carcinogenicity hazard. In determining cancer
classification, EPA does not assume that the specific types of tumors
seen in animals will develop in humans. However, EPA believes that the
development of tumors, such as nasal turbinates, in animals
demonstrates the potential for tumor development in humans.
The same commenter states that two epidemiology studies, not cited
by EPA in the proposed rule, have been conducted on alachlor
manufacturing workers. The commenter contends that neither study
indicates an increase in tumors in humans due to exposure to alachlor.
The commenter believes that these studies provide important additional
evidence indicating that the tumors produced in rats by alachlor are
not produced in humans and should have been considered by the Agency.
Epidemiological studies are used by the Agency in the overall
evaluation of the carcinogenic potential of a chemical, along with
other evidence. However, the studies cited by the commenter are based
on a small sample size. Studies of this type cannot verify the levels
and duration of exposure and represent results from a heterogeneous
population. In addition, one of the two studies apparently only focused
on tumors resulting in death of the study subjects and may reflect an
under estimation of tumor incidence. Therefore, in the face of evidence
of carcinogenicity in two adequately performed bioassays in two
species, the epidemiology data, although pertinent, do not negate the
importance of the animal data in the studies relied upon in the
proposed rule.
EPA reaffirms that there is sufficient evidence for listing
alachlor on the EPCRA section 313 list pursuant to EPCRA section
313(d)(2)(B) based on the available carcinogenicity data for this
chemical. Therefore, EPA is finalizing the addition of alachlor on the
EPCRA section 313 list.
3. Ametryn. Ciba-Geigy Corporation objects to listing ametryn under
EPCRA section 313 on the basis of liver effects, stating that
hepatotoxicity was observed only at high dose levels (100 and 500 mg/
kg/day) in subchronic studies.
The Agency believes that the LOEL of 100 mg/kg/day is sufficiently
low given the seriousness of the effect (hepatic toxicity) to justify
listing on the EPCRA section 313 list. Thus, EPA reaffirms that there
is sufficient evidence for listing ametryn on the EPCRA section 313
list pursuant to EPCRA section 313(d)(2)(B) based on the available
hepatotoxicity data for this chemical, and pursuant to EPCRA section
313(d)(2)(C) based on the available environmental toxicity data.
Therefore, EPA is finalizing the addition of ametryn on the EPCRA
section 313 list.
4. Amitraz. Nor-Am Chemical Company states that in the 2-year
beagle dog feeding study cited in the proposed rule, contrary to EPA's
conclusions, the only effects seen in the high dose (1.0 mg/kg/day)
group were a small but insignificant increase in blood glucose and in
one animal slight hypothermia during weeks 52 and 79.
EPA disagrees with the commenter. EPA has re-evaluated this study,
and determined that in this study amitraz induced significant changes
in blood chemistry (increased blood glucose). Hypothermia occurred not
only at the times noted by the commenter, but also on days 1 and 2, and
in one dog 3 hours after dosing, which returned to normal within 24
hours, at the 1.0 mg/kg/day level, the LOEL. As noted in the proposed
rule, these findings were supported by similar results obtained in a
90-day feeding study in dogs cited in the proposed rule.
Nor-Am disagrees with the Agency's conclusion that the NOAEL for
fetotoxicity was 5 mg/kg/day in the 3-generation rat reproduction study
cited in the proposed rule. The commenter believes that while there was
a slight decrease in the mean litter size at birth in the 20 mg/kg/day
dose group and decreased pup viability in the 5 and 20 mg/kg/day dose
groups post partum, there was no direct evidence of fetotoxicity. Nor-
Am states that the effect on litter size was only significant in the
third generation animals at 5 mg/kg/day, and may have been due to an
effect on lactation.
EPA's reanalysis of this data indicates that there was a decrease
in litter size and pup survival at 5 mg/kg/day in all 3 generations and
a slight reduction in pup weight in the F1 and F2
generations. Thus, there was direct evidence of fetotoxicity.
The commenter contends that the rabbit teratology study reported by
the Agency in the proposed rule was considered by EPA to be invalid
(i.e., significantly flawed) due to high abortion rates in all groups,
inadequately small group sizes, and lack of assessment of fetuses. The
commenter argues that the low incidence of anomalies upon which the
NOAEL of 1 mg/kg/day was based were within historical control ranges
and failed to show any clear dose-related effect. The commenter claims
that a subsequent study, not cited by EPA in the proposed rule,
revealed no effects on fetal morphology at doses up to 12 mg/kg/day
while maternal toxicity was found at 3 mg/kg/day and above; no NOEL
could be established. The commenter claims that this subsequent study,
not cited by EPA in the proposed rule, should have been considered by
EPA.
EPA disagrees. The rabbit teratology study cited by EPA in the
proposed rule was never declared by EPA to be invalid (i.e., seriously
flawed). Upon reanalysis of the rabbit teratology study, EPA determined
that although this study does not fully satisfy the guidelines for
study conduct under FIFRA, it is sufficient for the purposes of hazard
assessment, with a NOEL and LOEL for maternal and developmental
toxicity of 5 and 25 mg/kg/day, respectively. As described in the
proposed rule, at 25 mg/kg/day, the following effects were seen:
Decreased litter size and increased pre and post-implantation losses,
decreased maternal body weight gain, and increased abortions. The high
abortion rate is indicative of maternal toxicity. Although the abortion
rates were higher than the control, enough animals remained at
sacrifice to evaluate the toxicity potential of this chemical, and to
support the finding that amitraz can reasonably be anticipated to cause
developmental toxicity.
The subsequent study cited by the commenter was also considered by
EPA. This study also does not fully satisfy the guidelines for study
conduct under FIFRA. Although the fetotoxic effects observed in the
initial study (cited in the proposed rule) were not reproduced in the
subsequent study referred to by the commenter and not cited in the
proposed rule, this does not invalidate the results obtained in the
initial study. Both studies were considered by EPA in determining the
developmental toxicity of amitraz.
EPA reaffirms that there is sufficient evidence for listing amitraz
on the EPCRA section 313 list pursuant to EPCRA section 313(d)(2)(B)
based on the chronic toxicity and developmental toxicity data for this
chemical. Therefore, EPA is finalizing the addition of amitraz on the
EPCRA section 313 list.
5. Atrazine. Ciba-Geigy Corporation objects to the listing of
atrazine under EPCRA section 313 based on increased incidence of
mammary tumors in female Sprague-Dawley rats because the commenter
contends that this tumor type is not indicative of potential
carcinogenicity in humans. The commenter states that the effect is
species (rat) and strain (Sprague-Dawley) specific. Further, the
commenter states epidemiology data from Ciba-Geigy manufacturing and
use indicate no evidence of carcinogenicity in a human population
exposed for up to 30 years. Ciba-Geigy did not provide EPA with a copy
of this study but did discuss the results in their comments.
While epidemiology data are considered in the weight of the
evidence for carcinogenicity, the current classification is based upon
a positive finding in a well conducted animal study as described in the
Risk Assessment Guidelines of 1986 (Ref. 5). Atrazine has been
classified as a category C chemical by EPA's OPP Carcinogenicity Peer
Review Committee and the Scientific Advisory Panel (EPA, 1988). The use
of mammary tumor data for hazard assessment purposes, even when only
one strain of test animal has been demonstrated to be positive, is
consistent with current Agency policy. The Agency considers the cancer
classification to be sufficient basis for listing of atrazine.
EPA reaffirms that there is sufficient evidence for listing
atrazine on the EPCRA section 313 list pursuant to EPCRA section
313(d)(2)(B) based on the available carcinogenicity data. Therefore,
EPA is finalizing the addition of atrazine on the EPCRA section 313
list.
6. Bendiocarb. Nor-Am Chemical Company states that bendiocarb does
not meet the criteria of EPCRA section 313(d)(2)(C) due to its
environmental fate. The commenter alleges that it has been shown not to
accumulate in soil, water, or plants and has a relatively short half-
life (a few days). Nor-Am Chemical Company also contends that
bendiocarb is rapidly broken down by hydrolysis to a biologically
inactive product. As a result, the commenter states that there is no
clear evidence of adverse effects on the environment associated with
bendiocarb.
EPA disagrees that the environmental fate of bendiocarb will negate
the chemical's ecological toxicity. EPA believes that the environmental
fate factors presented by the commenter may reduce but do not eliminate
the potential for adverse effects on aquatic organisms and birds
because the chemical induces environmental toxicity at low dose levels.
Thus, EPA believes that the chemical can reasonably be anticipated to
cause a significant adverse effect on the environment.
EPA reaffirms that there is sufficient evidence for listing
bendiocarb on the EPCRA section 313 list pursuant to EPCRA section
313(d)(2)(B) based on neurological toxicity data for this chemical, and
pursuant to EPCRA section 313(d)(2)(C) based on the available
environmental toxicity data. Therefore, EPA is finalizing the addition
of bendiocarb on the EPCRA section 313 list.
7. Bifenthrin. FMC Corporation does not support the addition of
bifenthrin under EPCRA section 313 because ``EPA overstates the
neurological and [developmental effects] of bifenthrin. The
neurological effects to which EPA referred were tremors or twitching,
neurological signs that did not persist for the entire duration of the
studies.'' EPA agrees with the commenter regarding the developmental
toxicity potential or lack thereof, but disagrees with the commenter
regarding the neurological hazards. In addition to the tremors or
twitching effects cited by the commenter, more severe symptoms,
including clonic convulsions and death, occur in the studies referred
to by the commenters that are cited in the proposed rule, at dose
levels only slightly higher than those causing slight or occasional
tremors and/or twitching. In a rat developmental toxicity study by
gavage, cited in the proposed rule, the maternal LOEL based on tremors
was 2 mg/kg/day; the NOEL was 1 mg/kg/day. The MTD of 2 mg/kg/day was
established on the basis of findings in a rat pilot study (included as
part of the chronic rat study cited in the proposed rule) in which
there were 3 deaths out of 10 animals at 2.5 mg/kg/day. With regard to
the comment concerning the transitory nature of the effects, although
they may be transitory in nature, this does not diminish the
significance of the adverse effects. In particular, neurotoxic effects
leading to convulsion may result in more permanent, underlying damage
which is not reversible upon cessation of immediate signs and symptoms.
Therefore, the Agency concludes that the neurological effects due to
bifenthrin are of sufficient seriousness to warrant listing.
EPA reaffirms that there is sufficient evidence for listing
bifenthrin on the EPCRA section 313 list pursuant to EPCRA section
313(d)(2)(B) based on the available neurological toxicity data, and
pursuant to EPCRA section 313(d)(2)(C) based on the available
environmental toxicity data. Therefore, EPA is finalizing the addition
of bifenthrin on the EPCRA section 313 list.
8. Bromine. Great Lakes Chemical Corporation and Albemarle
Corporation believe that bromine does not meet the listing criteria of
EPCRA section 313. They contend that the Agency has failed to show that
chronic exposure to bromine causes serious or irreversible effects.
They also contend that the time-weighted average (TWA) of 0.1 part per
million (ppm) established by the National Institute of Occupational
Safety and Health (NIOSH) will protect against the acute effects of
exposure. They believe, therefore, that the addition of bromine to the
EPCRA section 313 list should not be finalized.
NIOSH established the TWA for bromine for acute effects. However,
the Agency is not listing bromine on the EPCRA section 313 list on the
basis of its acute effects but on the basis of the adverse effects it
induces after chronic exposure. These effects include functional
neurologic effects and abnormalities in respiratory and endocrine
systems. In humans, chronic exposure to bromine can cause severe
irritation of the skin, mucous membranes and respiratory tract,
gastroenteritis, and death. This severe irritation which can lead to
death through either, or both, respiratory or gastroenteric irritation
is the primary endpoint of concern although neurologic signs and
symptoms which include dizziness, headache, and ``feelings of
oppression'' along with other functional disturbances of the central
nervous system (CNS) may also occur after exposure to bromine.
EPA reaffirms that there is sufficient evidence for listing bromine
on the EPCRA section 313 list pursuant to EPCRA section 313(d)(2)(B)
based on the available chronic toxicity data for this chemical.
Therefore, EPA is finalizing the addition of bromine on the EPCRA
section 313 list.
9. 2-Bromo-2-nitropropane-1,3-diol (Bronopol). Boots Microcheck
contends that 2-bromo-2-nitropropane-1,3-diol presents only a moderate
acute hazard, but does not present a chronic hazard. Therefore, the
commenter concludes that the compound should not be listed under EPCRA
section 313 pursuant to EPCRA section 313(d)(2)(B).
Although the Agency agrees with the commenter that 2-bromo-2-
nitropropane-1,3-diol presents a moderate acute hazard, EPA does not
agree that the chemical is not a chronic toxicant. The effects noted in
both acute and chronic studies, cited in the proposed rule, indicate
irritation due to exposure to the compound. However, differing
expressions of irritation are obtained depending upon the level of
material to which the test animals were exposed and the duration of
exposure. In the acute studies cited in the proposed rule, the acute
gastric effects were seen at relatively high doses. In the chronic
studies, cited in the proposed rule, the effects, described below, were
noted following repeated oral exposure to lower doses of 2-bromo-2-
nitropropane-1,3-diol. The NOEL for chronic oral exposure in rats was
10 mg/kg/day, with effects including lesions of the stomach mucosa,
ulceration, raised areas and excrescences. In a 13-week study in rats
cited in the proposed rule, effects included inflammation, epithelial
hyperplasia and hyperkeratosis, and congested vessels of the mucosa of
the G.I. tract. The chronic studies cited in the proposed rule show
that irritation was caused by a repeated number of low doses. In these
chronic studies multiple doses were required before irritation
occurred. Further, the type of irritation caused by acute and chronic
exposure are different. Therefore, the irritation due to chronic
exposure to 2-bromo-2-nitropropane-1,3-diol is distinguishable from
that caused by acute exposure. EPA believes that the effects observed
in the longer term studies are serious and potentially irreversible.
EPA reaffirms that there is sufficient evidence for listing 2-
bromo-2-nitropropane-1,3-diol on the EPCRA section 313 list pursuant to
EPCRA section 313(d)(2)(B) based on the available chronic toxicity data
for this chemical. Therefore, EPA is finalizing the listing of 2-bromo-
2-nitropropane-1,3-diol on the EPCRA section 313 list.
10. Carboxin. Zeneca Incorporated and Uniroyal Chemical oppose the
listing of carboxin. The commenters claim that the effect of renal
toxicity noted by EPA in the proposed rule was seen only in rat feeding
studies and not in a chronic dog feeding study. Thus, they claim it
appears to be a species-specific effect that may not be relevant to
man.
EPA disagrees with the conclusions of the commenters. Because
direct human testing is generally unavailable, animals are commonly
accepted as surrogates for toxicity testing to predict potential
hazard(s) to humans. Exceptions occur only in a few rare cases where
effects have been determined to be species-specific (e.g.,
2-globulin). It should be noted that the actual
number of species tested with carboxin is limited and, therefore, it is
premature to state that the renal toxicity of carboxin is species-
specific. Significantly, the commenters did not provide any additional
evidence to support their contention that the renal toxicity is
species-specific. EPA uses information from the most sensitive species
to evaluate potential human hazard(s), as a conservative assumption.
EPA reaffirms that there is sufficient evidence for adding carboxin
on the EPCRA section 313 list pursuant to EPCRA section 313(d)(2)(B)
based on the available renal toxicity data for this chemical.
Therefore, EPA is finalizing the listing of carboxin on the EPCRA
section 313 list.
11. 1-(3-Chloroallyl)-3,5,7-triaza-1-azoniaadamantane chloride. Dow
Chemical Company notes that, in the dog study cited in the proposed
rule, the test material was administered in gelatin capsules due to
problems with palatability. They argue that this mode of administration
is unusual and introduces the confounding factor of what is in essence
a bolus administration (given all at one time) of the chemical, and
results in an artificially lowered NOEL.
The Agency does not agree that this mode of administration is
unusual. EPA frequently reviews dog studies in which the test material
is administered by capsule. In addition, dog studies rarely permit ad
libitum feeding as used in rat studies, even when dietary incorporation
is the means of dose administration. Dogs generally receive a measured
amount of food that they rapidly consume. Therefore, bolus
administration closely approximates actual behavior in dogs. The
concern that capsule administration produces an apparently altered
response is not a confounding factor in the study cited in the proposed
rule, and therefore the reported NOEL does not need to be raised as
suggested by the commenter.
The same commenter contends that the effects used as a basis for
listing occurred only in dogs and only in a single study, and,
therefore, are not relevant to humans.
Because direct human testing is generally unavailable, animals are
commonly accepted in the scientific and regulatory communities as
surrogates for toxicity testing to predict potential hazard to humans,
except in a few rare cases where effects have been determined to be
species-specific (e.g., 2-globulin). In the interest
of being protective, EPA uses information from the most sensitive
species to evaluate potential human hazard. In addition, results
demonstrated in a single well-conducted study are sufficient and can
serve as a basis for listing on the section 313 list.
The same commenter states that the LOEL in the study was based upon
a slight, reversible effect in the liver of a single animal. The study,
the commenter argues, should have been considered in toto rather than
relying on a single effect. The commenter implies that EPA should have
set the LOEL at a higher dose.
The commenter is incorrect. The LOEL of 15 mg/kg/day is correct.
This LOEL was based upon obliterative vasculitis and perivasculitis in
one animal. However, these effects are not commonly seen in dogs, yet
in the study cited in the proposed rule, they occurred in seven of
eight dogs at 30 mg/kg/day, the dose next highest to the LOEL. EPA
considers the effects seen in this study to be serious effects.
EPA reaffirms that there is sufficient evidence for listing 1-(3-
chloroallyl)-3,5,7-triaza-1-azoniaadamantane chloride on the EPCRA
section 313 list pursuant to EPCRA section 313(d)(2)(B) based on the
available chronic toxicity data for this chemical. Therefore, EPA is
finalizing the addition of 1-(3-chloroallyl)-3,5,7-triaza-1-
azoniaadamantane chloride on the EPCRA section 313 list.
12. Chlorosilanes. Silicones Environmental Health and Safety
Council and General Electric oppose the listing of the six
chlorosilanes that were proposed for addition
(dichloromethylphenylsilane, dimethyldichlorosilane,
methyltrichlorosilane, trichloroethylsilane, trichlorophenylsilane, and
trimethylchlorosilane) arguing that they undergo rapid hydrolysis and
are not expected to be found in the atmosphere in appreciable
concentrations. The commenters further state that EPA estimated
conditions in its exposure assessment that greatly exceed actual
conditions.
Based on these comments, EPA conducted revised exposure assessments
for each of the chlorosilanes. These revisions support EPA's initial
finding that dimethyldichlorosilane, methyltrichlorosilane, and
trimethylchlorosilane can reasonably be anticipated to be present at
facility boundaries in concentration levels that would cause a
significant adverse effect. EPA believes that the exposure assessments
were based on reasonable release estimates and reasonable worst-case
concentration modeling. Details of this analysis are provided in the
Response to Comment Document (Ref. 14). Thus EPA reaffirms that there
is sufficient evidence to list dimethyldichlorosilane,
methyltrichlorosilane, and trimethylchlorosilane on the EPCRA section
313 list pursuant to EPCRAsection 313(d)(2)(A). Therefore, EPA is
finalizing the listings for dimethyldichlorosilane,
methyltrichlorosilane, and trimethylchlorosilane on the EPCRA section
313 list.
The revised exposure assessments for dichloromethylphenylsilane,
trichloroethylsilane, and trichlorophenylsilane, however, indicate that
these chemicals are not individually present at facility boundaries in
concentration levels that would cause a significant adverse effect.
However, two or more of these chemicals are usually produced together
and as a category are reasonably anticipated to be present at facility
boundaries in concentration levels that would cause a significant
adverse effect. Therefore, EPA is deferring the individual listings of
these three chemicals for consideration as a category possibly to be
added at a later date.
13. Crotonaldehyde. Eastman Chemical and Monsanto believe that
crotonaldehyde should not be added to the EPCRA section 313 list
because of inadequate data on human health. Furthermore, they contend
that crotonaldehyde does not meet the criteria for listing as a
carcinogen as put forth in the Risk Assessment Guidelines for
Carcinogen Risk (Ref. 4) because it was tested in a single sex, single
species experiment. The commenters further believe that EPA's statement
that crotonaldehyde did not induce tumors at the high dose, because at
that high dose crotonaldehyde is cytotoxic, is a contention which is
not supported by scientific evidence. They believe that overall the
weight of evidence for carcinogenicity, including reactivity and
mutagenicity, is insufficient to support listing.
EPA agrees that the human carcinogenicity data are inadequate but
feels that the available animal data are adequate to support a concern
for carcinogenicity. The Agency accepts the single-sex, single species
testing of crotonaldehyde as being sufficient for listing because these
data are supported by strong evidence of mutagenicity in Salmonella
typhimurium; a statistically significant increase in the number of both
benign and malignant tumors in low dose animals and induced altered
liver foci but not tumor formation in the high dose group.
Crotonaldehyde is known to be severely cytotoxic with the capacity to
induce cell death and alter cellular macromolecules. It caused gross
degeneration, chromosome breakage and reciprocal translocations in
Drosophila melanogaster and gross degeneration and polyploidy in all
stages of spermatogenesis in mouse seminiferous tubules thus showing
that is has ample ability to interact with cellular DNA and cause
severe disruption in chromosome structure and cellular integrity. It is
logical to assume that if crotonaldehyde is capable of such damage in
the mammalian testis which is protected by the blood/testis barrier, it
can also cause severe toxicity and cell death in the liver which has no
such protection from toxic agents. Absent evidence to the contrary,
which the commenter did not provide, EPA continues to believe that
failure to observe tumor formation is due to cell death before tumors
could develop. Based on these findings, the Agency believes that the
weight of evidence for crotonaldehyde is sufficient for listing. EPA
reaffirms that there is sufficient evidence for listing crotonaldehyde
on the EPCRA section 313 list pursuant to EPCRA section 313(d)(2)(B)
based on available carcinogenicity and mutagenicity data for this
chemical. Therefore, EPA is finalizing the addition of crotonaldehyde
on the EPCRA section 313 list.
14. Cycloate. Zeneca Incorporated contends that in the 3-generation
rat feeding study, cited in the proposed rule as being of unknown
duration, the distended myelin sheath demyelination and nerve fiber
loss at the LOEL of 3.0 mg/kg/day occurred only after extensive
exposure and as such would not be relevant to a toxic release type of
short exposure.
The effects described in this study are considered to be both
serious and irreversible. Adverse effects that are induced by a
chemical after repeated long-term exposures and are a valid basis for
listing under EPCRA section 313.
The same commenter states that the 3-generation rat reproduction
study cited in the proposed rule was replaced by a more recent (1990)
2-generation rat reproduction study, also cited in the proposed rule,
in which the toxic effects on pup survival (LOEL of 50 mg/kg/day) and
pup body weight (LOEL of 20 mg/kg/day) occurred at doses which were
maternally toxic as well.
EPA considered both studies in its evaluation of cycloate. As
described in unit IV.E. of this preamble, developmental effects seen in
developing organisms are considered to be adverse whether or not they
occur at doses that are also maternally toxic.
EPA reaffirms that there is sufficient evidence for listing
cycloate on the EPCRA section 313 list pursuant to EPCRA section
313(d)(2)(B) based on the available neurological and developmental
toxicity data. Therefore, EPA is finalizing the addition of cycloate on
the EPCRA section 313 list.
15. Cyclohexanol. Monsanto opposes the listing of cyclohexanol
because concentrations that led to tremors, central nervous system
depression, lethargy, or hypothermia in rabbits, as cited in the
proposed rule, are above the level of MED that EPA identified in the
Draft Hazard Assessment Guidelines (Ref. 11) as high priority or
moderate priority. Furthermore, the concentrations that led to
reproductive impacts in rats were above the MED level of high priority.
In addition, Monsanto states that the Industrial Health Foundation
submitted to EPA's TSCA office the results of a 2-generation
reproduction study demonstrating a NOEL of 500 ppm in air which should
have been considered. The commenter claims that EPA has also not
demonstrated that the effects mentioned, or concentrations at which
they occurred, were serious or irreversible.
EPA agrees that the concentrations that led to tremors, central
nervous system depression, lethargy, or hypothermia in rabbits are
above the level of MED that EPA identifies in the Draft Hazard
Assessment Guidelines (Ref. 11) as high priority for listing. However,
while the 2,500 mg/kg/day dermal exposure is above the moderate
priority MED guideline, the 997 ppm (438 mg/kg/day) is within this
category. In addition to the neurotoxicity effects, as cited in the
proposed rule, cyclohexanol also induces renal, hepatic, and myocardial
effects at moderate dose levels (for example, inhalation of 0.59 mg/L
of cyclohexanol induced degenerative changes in the livers and kidneys
of rabbits). EPA considers these effects to be serious. In this case,
based on a weight-of-evidence approach, EPA believes that cyclohexanol
presents a sufficient hazard to warrant listing under EPCRA section 313
even though the reported values for neurotoxicity effects are in excess
of the MEDs placing a chemical in the high priority grouping.
EPA disagrees that the concentrations that led to reproductive
impacts in rats and gerbils (15 mg/kg) as described in the proposed
rule are above the MED range for high priority listing. EPA reiterates
the overall reproductive toxicity of this chemical, based on a weight-
of-evidence, supports the addition of cyclohexanol to the EPCRA section
313 list.
The chemical tested in the 2-generation reproduction study
submitted to the Agency by the Industrial Health Foundation, cited by
the commenter, was cyclohexanone not cyclohexanol as claimed by the
commenter.
EPA reaffirms that there is sufficient evidence for listing
cyclohexanol pursuant to EPCRA section 313 pursuant to EPCRA section
313(d)(2)(B) based on the available chronic neurological, hepatic,
renal, myocardial, and reproductive toxicity data for this chemical.
Therefore, EPA is finalizing the addition of cyclohexanol on the EPCRA
section 313 list.
16. Cyhalothrin. Zeneca Incorporated contends that the
neurotoxicity signs observed in the 6-month and 1-year dog studies
cited in the proposed rule occurred at doses that were ``otherwise
toxic as well'' and do not provide any evidence of a specific
neurotoxicity. Zeneca Incorporated implies that the presence of
``otherwise toxic'' signs reduces the significance of the neurotoxicity
observed in the cited study.
The phrase ``otherwise toxic as well'' was not defined by the
commenter. The clinical signs of neurotoxicity observed in the dogs at
3.5 mg/kg/day (ataxia, muscle tremors, and convulsions in the 1-year
study cited in the proposed rule) and at 10 mg/kg/day (unsteadiness and
trembling in the 6-month study cited in the proposed rule) are
considered by EPA to be evidence of physiological neurotoxicity.
Although there were no pathologic changes in the nervous tissue, EPA
considers these effects to be serious because they often precede
pathologic neurotoxicity. With the exception of liquid feces, there
were no reported toxic findings other than those related to
neurotoxicity.
EPA reaffirms that there is sufficient evidence for listing
cyhalothrin on the EPCRA section 313 list pursuant to EPCRA section
313(d)(2)(B) based on the available neurological toxicity data.
Therefore, EPA is finalizing the addition of cyhalothrin on the EPCRA
section 313 list.
17. Desmedipham. Nor-Am Chemical states that methemoglobin
formation, which is cited by EPA as the basis for listing, is an
entirely reversible effect which occurs only after prolonged and
consistent exposure. Therefore, the commenter concludes that this
finding, by itself, should not be used.
Based on the 90-day dog study, cited in the proposed rule, EPA
considers 150 ppm to be a NOAEL. Methemoglobin values were only
minimally higher than control levels and were not associated with an
increase in Heinz bodies. In the 1-year dog feeding study, after 13
weeks treatment at 300 ppm, methemoglobin was seen associated with
histopathological changes (hemosiderin and hemopoiesis). While
methemoglobinemia may be a reversible effect, it is nevertheless a
serious effect, and in some cases irreversible damage may occur as a
result of methemoglobinemia. Methemoglobinemia interfers with the
oxygenating capacity of blood resulting in an undersupply of oxygen to
the tissues. Therefore, methemoglobinemia is a toxic effect and not
simply an indicator of exposure to desmedipham as concluded by the
commenter.
Therefore, EPA reaffirms that there is sufficient evidence for
listing desmedipham on the EPCRA section 313 list pursuant to EPCRA
section 313(d)(2)(B) based on the available hematological toxicity
data. Therefore, EPA is finalizing the addition of desmedipham on the
EPCRA section 313 list.
18. 2,2-Dibromo-3-nitrilopropionamide. Dow Chemical Company and
Rohm Haas state that the corrosivity and irritancy of the 2,2-dibromo-
3-nitrilopropionamide (DBNPA) solutions to the esophagus, pharynx,
trachea, and lungs led to development of dyspnea in rats. The
commenters imply that the dyspnea in rats should be discounted because
it was caused by the method of administration rather than the toxicity
of the chemical.
The Agency agrees that the dyspnea observed in the 4-week and 13-
week rat gavage studies cited in the proposed rule may have been due to
severe irritation of the trachea and lungs from accidental or
incidental delivery of small amounts of the DBNPA dosing solutions into
the larynx, pharynx, trachea, and/or lungs during the procedure.
However, this suggestion of possible cause can be neither refuted nor
confirmed based upon the available data. Dyspnea is the basis for the
LOEL in the study. One of the commenters agrees that DBNPA is
corrosive, particularly to the eyes and, at the least, is severely
irritating to the respiratory tract. This is consistent with the
effects observed in the two subject studies. The Agency considers the
finding of dyspnea in the 4- and 13-week studies to be of sufficient
seriousness to warrant listing on the EPCRA section 313 list.
EPA reaffirms that there is sufficient evidence for listing 2,2-
dibromo-3-nitrilopropionamide on the EPCRA section 313 list pursuant to
EPCRA section 313(d)(2)(B) based on the available chronic respiratory
toxicity data. Therefore, EPA is finalizing the addition of 2,2-
dibromo-3-nitriloproprionamide on the EPCRA section 313 list.
19. Diclofop-methyl. Nor-Am Chemical and Hoechst-Celanese contend
that EPA interpreted the doses administered by gavage as diet
concentrations (ppm) in the rat teratology study cited in the proposed
rule. One commenter states the Agency should provide clarifications
concerning ``mortality'' of the pups and the calculation of the actual
test substance intake at different stages during the in-life phases
during development in the 3-generation rat reproduction study.
The commenter is correct in stating that the Agency erred in
interpreting gavage doses as ppm in the rat teratology study. However,
EPA still believes that the doses at which adverse effects occur are
sufficiently low and the adverse effects reported are of sufficient
seriousness to warrant listing. The developmental NOEL is 10 mg/kg/day
and the LOEL is 32 mg/kg/day based on an increased incidence of a
number of variations and malformations, as described in the proposed
rule. While the maternal effects on body weight and food consumption at
32 mg/kg/day are transient and reversible, some of the developmental
effects at this dose are irreversible. In the 3-generation rat
reproduction study cited in the proposed rule, a decrease in pups born
alive in the F1a, reduced pup weights (F1a and 2a) and
general retardation of physical development (F1a and 2a) was
noted in offspring at 100 ppm (5 mg/kg/day). The commenter considers
the LOEL for this study to be 6.7 mg/kg/day. This dose resulted in
decreased parental food consumption and body weight and there were no
post partum pup mortalities. Additionally, there were no effects on
fertility at the LOEL at any time during the three generations.
The commenters further stated that EPA should ``consider the
validity'' of the 30-day rat study cited in the proposed rule because
heart, kidney, and adrenal weights were increased only at doses with no
histopathological correlates and were due to the pharmacodynamic lipid
metabolism of the test material by the liver.
The increased relative heart, liver, and kidney weights at 80 ppm
(4 mg/kg/day) in the 30-day rat feeding study is further substantiated
by a recent 90-day rat feeding study cited in the proposed rule with a
LOEL of 80 ppm and a NOEL of 20 ppm (1 mg/kg/day). In the recent 90-day
study cited in the proposed rule, absolute and relative liver and
kidney weight was increased in males and relative liver and kidney
weight was increased in females at 80 ppm. These increased organ
weights are evidence of a compound-related effect. The Agency
interprets Hoechst-Celanese's own statements regarding the 30-day rat
feeding study that ``increased liver weights and centrilobular
enlargement of hepatic cells at dietary concentrations of 80 ppm and
higher'' as evidence of toxicity.
Hoechst-Celanese also contends that the effects in the renal cortex
observed in the 90-day dog study cited in the proposed rule at 250 ppm
(15 and 13.4 mg/kg/day in males and females, respectively) did not
occur at the highest concentration tested in the 1-year dog study (80
ppm, 4-5mg/kg/day) indicating that the finding in the 90-day study was
not test substance related.
EPA believes that the effects occurring in the renal cortex in the
90-day dog study at 13 to 15 mg/kg/day may not have appeared in the 1-
year dog study, since the highest dose tested was 4-5 mg/kg/day. If
higher doses were employed in the 1-year study, then renal effects
could possibly have occurred. However, the results of the 1-year study
do not negate the 90-day results, since the dose levels used in the 90-
day study were so much higher.
Hoechst-Celanese also states that the Agency used an invalid
(flawed) reproductive toxicity study to support the listing. The
commenter indicates that the study was compromised by infection of the
rat colony with RCV/SDA virus. They further state that another
reproductive toxicity study, which EPA did not cite in the proposed
rule, should have been evaluated in which the fetotoxic NOEL was 30 mg/
kg/day instead of greater than 5 mg/kg/day as in the original study.
The Agency does not find the original study to be invalid. The data
were considered to be valid for regulatory purposes. In addition, the
Agency found the fetotoxic NOEL in the study referred to by the
commenter, not cited by EPA in the proposed rule, to be 5 mg/kg/day,
not 30 mg/kg/day as stated by the commenter.
EPA reaffirms that there is sufficient evidence for listing
diclofop-methyl on the EPCRA section 313 list pursuant to EPCRA section
313(d)(2)(B) based on the available developmental, hepatic, and renal
toxicity data. Therefore, EPA is finalizing the addition of diclofop-
methyl on the EPCRA section 313 list.
20. Diisocyanates. EPA originally proposed to list three
diisocyanates (hexamethylene-1,6-diisocyanate, isophorone diisocyanate,
and 1,1-methylene bis(4-isocyanatocyclohexane) on the basis of acute
toxicity pursuant to EPCRA section 313(d)(2)(A). As an alternative, EPA
proposed to create a delimited diisocyanates category containing these
3 diisocyanates and 17 other diisocyanates based on chronic pulmonary
irritation pursuant to EPCRA section 313(d)(2)(B). EPA is finalizing
addition of the delimited diisocyanate category based on chronic
pulmonary toxicity and therefore has not addressed comments concerning
the acute toxicity of any of the diisocyanates. EPA believes that
diisocyanates are best added as a category because the members of this
category are structurally similar (i.e., each contains the diisocyanate
functionality), they induce a similar toxic effect (chronic pulmonary
irritation), and their toxicity is due to the diisocyanate portion of
the molecule common to all members.
Chemical Manufacturers Association Hexamethylene-1,6-Diisocyanate
Panel, Dow Chemical Company, Monsanto, Olin Chemicals, Sealed Air
Corporation, Huls America Incorporated, and the Diisocyanates Panel of
the Chemical Manufacturers Association oppose EPA's alternative
proposal to create a diisocyanate category and believe that individual
diisocyanates should be evaluated and included on the EPCRA section 313
list only if the diisocyanate independently satisfies the statutory
listing criteria. The commenters state that in adding a broad category
of diisocyanates, EPA ignores its statutory mandate to evaluate the
individual toxicity of each chemical and to evaluate the exposure
potential to the EPCRA community by each individual chemical. The
commenters contend that the category would mislead the public as to the
amount and type of toxic chemicals to which communities may be exposed.
The commenters contend that data collected in aggregate is confusing
and difficult to use or interpret. Commenters state that adding a
category of diisocyanates based upon the isocyanate functionality is
based on the chronic effects associated with exposures to a limited
number of diisocyanates and that this method unjustifiably equates
toxicity across an entire class of chemicals that have different
properties and effects. Commenters state that diisocyanates encompass a
diverse group of chemicals which vary significantly in physical and
chemical properties and in potential toxicity. Commenters state that
the available evidence on the pulmonary effects or toxicity of
individual diisocyanates (toluene diisocyanate,
methylenebis(phenylisocyanate), and isophorone diisocyanate) does not
support the addition of a diisocyanates category. The commenters also
state that EPA has not cited any data to support the assertions that
diisocyanates cause these effects. Commenters state that individual
diisocyanates have been shown to respond differently in mutagenicity
studies and that other toxicological differences would be expected
among individual diisocyanates, because of differences in their ability
to penetrate membranes, the capacity of organisms to metabolize them,
the specific reactivity of the 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 F1A
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 substance-
related, 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 n-
hexane 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 n-
hexane 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 n-
hexane 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/m3 (58 ppm, LOAEL(ADJ) of 73 mg/m3) 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 n-
hexane 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 n-
hexane 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 non-
neoplastic 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-iodo-
2-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-iodo-
2-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 dose-
dependent.
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 (F2a) 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 (F2b), 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 N-
methyl-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., 2-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 (SOx), nitric oxide
and nitrogen dioxide (NOx), 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 -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 -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 short-
chain chlorinated paraffins. Some of the flaws that the commenters
allege concern the studies used to support the listing of the short-
chain species and included: (1) Kidney tumors in male rats may be due
to binding to 2-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 short-
chain 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, 2-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 2-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 short-
chain 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 non-
genotoxic 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 -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 -olefins.
The commenters further contend that chlorinated paraffins and
chlorinated -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 -
olefins are distinctly different chemicals with different physical/
chemical properties. The main difference between chlorinated paraffins
and chlorinated -olefins that EPA is aware of is that
chlorinated paraffins, typically manufactured from paraffin mixtures,
are also mixtures whereas individual chlorinated -olefins can
be manufactured in moderate to high purity. The issue is whether a pure
chlorinated -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 -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 C12H19Cl7 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 C12H19Cl7 and an average molecular weight of
approximately 411.
The commenters claim that the chlorine positions in chlorinated
-olefins differ significantly compared to the chlorine
positions in chlorinated paraffins. EPA does not believe that
chlorination at carbons 1 and 2 of the -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 -olefins differ significantly
from the variations possible within these two groups of substances.
Since for the -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 -
olefins, especially as the degree of chlorination decreases.
The commenters' claim that chlorinated -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 -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
C10 to C30 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
-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 -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 -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 -olefin and a paraffin of the same chain
length. The physical properties of chlorinated -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 -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: CxH2x-yCly; 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
C10H19Cl3 and C13H16Cl12.
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 post-
implantation 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 ``worst-
case'' 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 2861 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.
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-nitro-
benzoic 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]-DL-
valine(+)-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)-N-
methylsulfonyl)-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,O-
dimethylphosphorothioate]
*******
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-2H-
isoindol-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
CxH2x-yCly
where x = 10 to 13;
y = 3 to 12; and
where the average chlorine content ranges from 40-70%
with the limiting molecular formulas C10H19Cl3 and
C13H16Cl12.
*******
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
