FLUORIDE ACTION NETWORK PESTICIDE PROJECT
Return to FAN's Pesticide Homepage
Note from FAN:
In the January 12, 1994 Federal Register Notice, EPA proposed the following fluorine and organofluorine chemicals for addition to TRI. This Notice was exceedingly long and we present only excerpts.EPA's proposal for 313 chemicals as new additions to TRI is worth the read. It is available at: http://www.epa.gov/tri/frnotices/59fr1788.htm. EPA presents information on each chemical, or class of chemicals (eg, CFCs).
Pesticides
Acifluorfen sodium salt (62476-59-9)
Benfluralin (1861-40-1)
Bifenthrin (82657-04-3)
Boron trifluoride (7637-07-2)
Cyfluthrin (68359-37-5)
Cyhalothrin (68085-85-8)
Dichlorofluoromethane (HCFC-21) (75-43-4)
Diflubenzuron (35367-38-5)
Dithiopyr (97886-45-8)
Fluazifop butyl (69806- 50-4)
Flumetralin (62924-70-3)
Fluvalinate (69409-94- 5)
Fomesafen (72178-02-0)
Hydramethylnon (67485-29-4)
Lactofen (77501-63-4)
Norflurazon ( 27314-13-2)
Oxyfluorfen (42874-03-3)
Primisulfuron methyl (86209-51-0)
Sodium fluoroacetate (62-74-8)
Sulfuryl fluoride (Vikane) (2699-79-8)
Tefluthrin (79538-32-2)
Tributyltin fluoride (1983-10-4)Other
Chlorotrifluoromethane (CFC-13) (75-72-9)
2-Chloro-1,1,1-trifluoroethane (HCFC-133a) (75- 88-7)
3-Chloro-1,1,1-trifluoropropane (HCFC-253fb) (460-35-5)
Dichloropentafluoropropane (127564-92-5)
1,3-Dichloro-1,1,2,3,3-pentafluoropropane (HCFC-225ea) (136013-79-1)
2,2-Dichloro-1,1,1,3,3-pentafluoropropane (HCFC-225aa) (128903-21-9)
1,1-Dichloro-1,2,3,3,3-pentafluoropropane (HCFC-225eb) (111512-56-2)
1,1-Dichloro-1,2,2,3,3-pentafluoropropane (HCFC-225cc) (13474-88-9)
1,3-Dichloro-1,1,2,2,3-pentafluoropropane (HCFC-225cb) (507-55-1)
1,2-Dichloro-1,1,3,3,3-pentafluoropropane (HCFC-225da) (431-86-7)
3,3-Dichloro-1,1,1,2,2-pentafluoropropane (HCFC-225ca) (422-56-0)
2,3-Dichloro-1,1,1,2,3-pentafluoropropane (HCFC-225ba) (422-48-0)
1,2-Dichloro-1,1,2,3,3-pentafluoropropane (HCFC-225bb) (422-44-6
1,2-Dichloro-1,1-difluoroethane (HCFC-132b) (1649-08-7)
3,3'-Dimethylbenzidine dihydrofluoride (o-Tolidine dihydrofluoride) (41766-75-0)
Fluorine (7782-41-4)
* 5-Fluorouracil (CAS No. 000051-21-8)
1,1,1,2-Tetrachloro-2-fluoroethane (HCFC-121a) (354-11-0)
1,1,2,2-Tetrachloro-1-fluoroethane (HCFC-121) (354-14- 3)* 5-Fluorouracil: major use is pharmaceutical. It was used as an insect chemosterilant.
http://www.epa.gov/tri/frnotices/59fr1788.htm
[Federal Register: January 12, 1994]
_______________________________________________________________________
Part IV
Environmental Protection Agency
_______________________________________________________________________
40 CFR Part 372
Addition of Certain Chemicals; Toxic Chemical Release Reporting;
Community Right-to-Know; Proposed Rule
ENVIRONMENTAL PROTECTION AGENCY
40 CFR Part 372
[OPPTS-400082; FRL-4645-6]
RIN 2070-AC47
Addition of Certain Chemicals; Toxic Chemical Release Reporting;
Community Right-to-Know
AGENCY: Environmental Protection Agency (EPA).
ACTION: Proposed rule.
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SUMMARY: EPA is proposing to add 313 chemicals and chemical categories
to the list of toxic chemicals required to be reported on under section
313 of the Emergency Planning and Community Right-to-Know Act of 1986
and section 6607 of the Pollution Prevention Act of 1990. The proposed
addition of these chemicals and chemical categories is based on their
acute human health effects, carcinogenicity or other chronic human
health effects, and/or their environmental effects. EPA believes that
these chemicals and chemical categories meet the EPCRA section
313(d)(2) criteria for addition to the list of toxic chemicals.
DATES: Written comment on this proposed rule must be received on or
before April 12, 1994. The public meeting will take place on March 2,
1994, at 1 p.m. and adjourn by 5 p.m.
ADDRESSES: Written comments should be submitted in triplicate to: OPPT
Docket Clerk, TSCA Document Receipt Office (7407), Office of Pollution
Prevention and Toxics, Environmental Protection Agency, Rm. E-G99, 401
M St., SW., Washington, DC 20460. Comments containing information
claimed as confidential must be clearly marked as confidential business
information (CBI). If CBI is claimed, three additional sanitized copies
must also be submitted. Nonconfidential versions of comments on this
proposed rule will be placed in the rulemaking record and will be
available for public inspection. Comments should include the docket
control number for this proposal, OPPTS-400082. Unit VI. of this
preamble contains additional information on submitting comments
containing information claimed as CBI.
The public meeting will be held at the: Environmental Protection
Agency, Auditorium, Education Center, 401 M St., SW., Washington, DC.
FOR FURTHER INFORMATION CONTACT: Maria J. Doa, 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 or Toll free TDD: 800-553-7672, Attention: Docket
Number OPPTS-400082.
SUPPLEMENTARY INFORMATION:
I. Introduction
A. Statutory Authority
This proposed rule is issued under sections 313(d) and (e)(1) of
the Emergency Planning and Community Right-to-Know Act of 1986 (EPCRA),
42 U.S.C. 11023. 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. When enacted,
section 313 established an initial list of toxic chemicals that was
comprised of more than 300 chemicals and 20 chemical categories.
Section 313(d) authorizes EPA to add chemicals to 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 has added to and deleted chemicals from
the original statutory 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 submitting petitions.
EPA must respond to petitions within 180 days either by initiating a
rulemaking or by publishing an explanation of why the petition is
denied. 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. Explanation for Expansion of the EPCRA Section 313 Chemical
List
A. General Rationale
The Toxics Release Inventory (TRI), through the public access
provisions of EPCRA, has proven to be one of the most powerful forces
in empowering the Federal government, State governments, industry,
environmental groups, and the general public, to fully participate in
an informed dialogue about the environmental impacts of toxic chemicals
in the United States.
A major section of EPCRA, which Congress passed in 1986, resulted
in the creation of the Toxics Release Inventory. TRI is a publicly
available data base that provides quantitative information on toxic
chemical releases, transfers, recycling, and disposal. With the
collection of this information for the first time in 1987, came the
ability for the public, government, and the regulated community to
understand the magnitude of chemical emissions in the United States; to
compare chemical releases and transfers of chemical wastes among
States, industries, facilities, and environmental media; and perhaps
most importantly, to assess the need to reduce and where possible,
eliminate these releases and transfers. TRI enables all interested in
environmental progress to establish credible baselines, to set
realistic goals, and to measure progress over time, in meeting those
goals. The TRI system has become a neutral yardstick by which progress
can be measured by all interested parties.
The original list of chemicals for which reporting was required
consisted of 320 chemicals and chemical categories. The list was a
combination of the Maryland Chemical Inventory Report List of Toxic or
Hazardous Substances and the New Jersey Environmental Hazardous
Substance List. The combination of these two lists provided a sound and
logical starting point for the national TRI program. Recognizing
however that the list would need to be a dynamic one, EPCRA
specifically authorizes additions to and deletions from the list. To
date, EPA has added 16 chemicals to the list and has deleted 12
chemicals from the list.
With 5 years experience behind the program, EPA, other federal
agencies, Congress, and the public have recognized the need to expand
the TRI list beyond the original chemicals and chemical categories and
beyond the relatively limited reporting universe. (Currently reporting
is only required from facilities that fall within the manufacturing
Standard Industrial Classification (SIC) codes 20 through 39 that meet
certain thresholds).
While the data on the chemicals that are covered have allowed the
public and private sectors to be informed and involved in environmental
decisionmaking as they never were before, it has become increasingly
evident to those same constituents that they have access to information
on a relatively small number of important chemicals. Congress has
echoed this recognition in the Right-to-Know More bills that were put
forward in the 102nd Congress. EPA and State regulatory agencies have
integrated TRI information as a critical component in their
environmental decisionmaking and in many cases are constrained by the
lack of similar information on chemicals of concern not covered by the
TRI. While the TRI has been successful in focusing attention on the
initial list of chemicals and in many cases fostering emissions
reductions and prevention activities, that same focus has highlighted
the need to expand beyond that initial list and to include additional
chemicals that exhibit similar toxicity characteristics. This proposal
is one of the first in a series of actions that EPA plans to use to
expand the coverage of the TRI. This first phase will focus on adding
chemicals, followed by a second phase that will identify additional
facilities for inclusion. EPA is considering a third phase, which would
look at modification of the data elements currently required by TRI.
In conjunction with these expansion activities EPA has been
considering whether other adjustments are needed in the scope of the
TRI program. EPA received petitions from the Small Business
Administration and the American Feed Industry Association seeking an
exemption for ``small sources'' (i.e, those facilities that file TRI
forms with zero or small release estimates). EPA previously put those
petitions out for public comment and, on review, believes there is
substantial merit to the general concerns raised in the petitions.
The Agency's plan for proceeding on the small source issue would
include the following steps. EPA is examining four options for
establishing a small release exemption from the TRI reporting
obligation: Cutoffs at zero, 500 pounds, 1,000 pounds, and 5,000
pounds. EPA will provide the public with a report on these four options
by the end of January. This analysis will consider what data might not
be available at both the national and community level, and the cost
savings to the government and to industry of the four exemption levels.
EPA plans to hold a public meeting in February for discussion of the
report. Based on this feedback, EPA will then design a regulatory
strategy that will align the small source issue with final action on
today's proposal. The Agency's objective will be to minimize
unnecessary data collection and reporting by facilities, including for
the chemicals identified in today's proposal.
B. Development of the Chemical Addition Candidates
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: (1) 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 (f) 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).
In addition, EPA considered 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).
From this initial group of substances, EPA excluded chemicals that
are already listed on section 313 or are already reportable under one
of the EPCRA section 313 categories. For example, ``cyanide, total'' is
listed under section 307(a) of the CWA. This listing is considered to
be a subset of the EPCRA section 313 cyanide compounds category and the
hydrogen cyanide listing. EPA decided not to propose listing these
types of chemicals separately because they are already reportable under
one of the existing section 313 categories. 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. The results of the toxicity screen for a subset of these
chemicals were presented at a public meeting on May 29, 1992 (Ref. 4).
Other chemicals were also removed from consideration for this
rulemaking because they are the subjects of two recently published
EPCRA petition responses. On March 4, 1992, EPA received a petition
from Governor Mario M. Cuomo of New York and the Natural Resources
Defense Council (NRDC) to add 80 chemicals and 2 chemical categories to
the list of toxic chemicals under section 313 of EPCRA. All of these
chemicals and chemical categories appear on the RCRA list of hazardous
wastes under 40 CFR 261.33(f) and as such are a subset of the chemicals
screened by EPA. EPA responded to the petition in a proposed rulemaking
on September 8, 1992 (57 FR 41020) and in a final rule adding 22
chemicals on November 30, 1993 (58 FR 63500).
On December 3, 1991, EPA received a petition from the NRDC, Friends
of the Earth, and the Environmental Defense Fund to add
hydrochlorofluorocarbons (HCFCs) to the list of toxic chemicals under
section 313 of EPCRA. The HCFCs are listed under section 602(b) of the
CAA as Class II ozone depleting substances and as such are a subset of
the chemicals screened by EPA. EPA responded to the petition in a
proposed rulemaking on June 24, 1992 (57 FR 28159) and in a final rule
adding 11 HCFCs on November 30, 1993 (58 FR 63496). An additional 16
HCFCs not added to the TRI list by the November 30, 1993 final rule are
proposed for addition in this rulemaking (See Unit IV.B.135. of this
preamble).
1. Toxicity screen. A toxicity screen is a limited review of
readily available toxicity data (e.g., information in data bases and
other secondary sources) 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.B.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. 6). The
numerical screening values reflected in the Draft Hazard Assessment
Guidelines were developed to capture, in the ``sufficient for listing''
screening category, the majority of chemicals already listed on various
CERCLA and EPCRA lists, and thus known or suspected to be toxic and/or
hazardous. These Draft Hazard Assessment Guidelines contain guidance
for both the screening and hazard assessments of chemicals and are
available for review in the docket associated with this rulemaking.
This draft document was distributed at a public meeting on May 29,
1992. A final version of these guidelines has not yet been developed.
Requests for further information about these draft guidelines should be
addressed to the person identified under ``FOR FURTHER INFORMATION
CONTACT.''
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: ``sufficient;'' ``may be
sufficient;'' or ``insufficient.'' EPA received comment in response to
the Draft Hazard Assessment Guidelines that objected to the Agency's
use of the terms ``sufficient,'' ``may be sufficient,'' and
``insufficient'' as titles for the toxicity screening categories. The
commenter claimed that these terms are appropriate only for the results
of a hazard assessment. The commenter stated that these terms should
not be used for screening categories because the toxicity screen only
identifies chemicals for further consideration. EPA agrees that the
screening categories only reflect a preliminary determination on each
chemical, and therefore, to avoid further confusion, will refer to the
screening categories as ``high priority,'' ``medium priority,'' and
``low priority'' to reflect the difference between a toxicity screen
and a hazard assessment. These terms will be used throughout this
document in reference to the toxicity screening categories. 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.
2. Production volume screen. EPCRA section 313(f) establishes
reporting thresholds related to the amount of a chemical that is
manufactured, processed, or otherwise used. [The EPCRA section 313
manufacture (includes import) and processing thresholds are 25,000
pounds per facility per year. The otherwise use threshold is 10,000
pounds per facility per year]. EPA anticipates that the addition of
chemicals manufactured, imported, processed, or used in quantities less
than the EPCRA section 313 volume thresholds would not result in the
submission of TRI reports. Thus, EPA elected to initially focus its
attention on chemicals likely to yield reports. Accordingly, EPA 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.
Production volume data on each of the chemicals were gathered
primarily from two sources: (1) The TSCA Chemical Update System (1990);
and (2) the FIFRA Section 7 Tracking System. On June 12, 1986 (51 FR
21438), EPA promulgated a rule pursuant to section 8(a) of TSCA which
required manufacturers and importers to report every 4 years, subject
to certain threshold production quantities and other exclusions, the
quantities of chemicals they produced (40 CFR part 710). Among the
exceptions to the inventory update rule (IUR) reporting were polymers,
biological products, inorganic substances, and chemicals produced at
less than 10,000 pounds, all with certain limitations. Data from the
IUR is maintained in EPA's TSCA Chemical Update System (CUS).
Section 7 of FIFRA provides the Agency with annual production
information on registered pesticides. EPA regulations implementing
FIFRA section 7 (40 CFR part 167) require all manufacturers of
pesticidal products (which includes formulated pesticides, active
ingredients, and devices) to submit an annual report detailing the
amount of each type of pesticidal product manufactured, sold and
distributed during the past year, and estimated to be manufactured,
imported, and processed during the current year (40 CFR 167.85).
For industrial inorganic compounds not subject to FIFRA or
available on CUS, information from the public literature was used,
supplemented with information from companies.
3. Hazard evaluation. EPA conducted a hazard evaluation 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 Guidelines for Carcinogen Risk
Assessment (Ref. 2)). The guidelines that were used for each effect are
Agency guidelines that are identified in the Draft Hazard Assessment
Guidelines (Ref. 6). During this assessment the 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. On the other hand, where a
review of the scientific data indicates that the chemical will cause
various adverse effects at moderate dose levels, EPA believes, based on
the total weight-of-the-evidence, that there is sufficient evidence for
listing the chemical under EPCRA section 313.
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 requests comment on
its approach in considering exposure as a part of its evaluation of
these chemicals under sections 313(d)(2)(A) and (C).
Based on this analysis for each of the chemicals proposed for
listing, EPA determined that one or more of the statutory criteria were
met. A discussion of EPA's interpretation of the EPCRA section 313
criteria is given in Unit III. of this preamble. A discussion of the
evidence supporting EPA's proposal to add each of the chemicals to
EPCRA section 313 is presented in Unit IV. of this preamble and in the
record supporting this proposed rule.
4. Other considerations. EPA excluded certain chemicals and
chemical categories from consideration for proposed listing under EPCRA
section 313 in this rulemaking for a number of reasons. Some chemicals
were identified only as environmental degradation products rather than
chemicals that are manufactured, processed, or otherwise used by a
facility. These chemicals will only be present in the environment as a
result of the release into the environment of precursor chemicals. If
the degradation product meets the toxicity criteria of EPCRA section
313, the precursor chemical may be considered for listing on EPCRA
section 313. The degradation product would not be considered for
listing on EPCRA section 313 because a facility subject to EPCRA
section 313 is only required to file a TRI report for a chemical that
it manufactures, processes, or otherwise uses, within the facility
boundaries. Therefore, EPA does not believe that it is appropriate to
consider listing such chemicals at this time.
Some of the lists reviewed by EPA included listings that
represented waste streams from particular processes. These waste
streams, such as coke oven emissions, are not discrete chemicals or
chemical categories, but contain a wide range of chemicals, many of
which are currently listed individually on EPCRA section 313. The focus
of this rulemaking is on the addition of specific chemicals and
chemical categories and, as such, EPA believes that these waste streams
are inappropriate for listing under EPCRA section 313 at this time.
EPA also excluded chemicals whose only identified toxicity concern
was a result of their status as a volatile organic compound (VOC). VOCs
contribute to the formation of tropospheric ozone which causes a number
of health-related and environmental problems. EPA continues to believe
that VOCs meet the listing criteria of EPCRA section 313. However, EPA
intends to address the issue of how VOCs should be listed on EPCRA
section 313 separately. Therefore, chemicals whose only identified
toxicity concern is due to their status as VOCs were excluded from
consideration at this time.
EPA also identified chemicals that are routinely manufactured,
processed, or otherwise used at levels far below the reporting
thresholds of EPCRA section 313. These chemicals are not expected to
ever be manufactured, processed, or otherwise used in quantities at or
above these reporting thresholds. In this proposed rulemaking, EPA is
attempting to add chemicals to EPCRA section 313 that are manufactured,
processed, or otherwise used in quantities greater than the EPCRA
section 313 volume thresholds and thus would result in the submission
of TRI reports. Consequently, chemicals that are manufactured,
processed, or otherwise used in quantities less than the EPCRA section
313 volume thresholds were excluded from further consideration at this
time, because no reports would be filed under EPCRA section 313 for
such chemicals.
Some of the chemicals that are manufactured, processed, or
otherwise used below the EPCRA section 313 activity thresholds,
particularly those 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. 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 may reconsider in the future the issue of
listing such chemicals in a manner which would result in the submission
of TRI reports. EPA requests comment on the following: Is it
appropriate to list such chemicals on EPCRA section 313? 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 exemptions (40 CFR part 372.38),
would be required to insure that release and transfer information would
be collected?
III. EPCRA Section 313 Statutory Criteria
EPCRA section 313(d)(2) sets out criteria for adding chemicals to
the list of chemicals subject to reporting under section 313(a). For a
chemical (or category of chemicals) to be added to the EPCRA section
313(c) list of toxic chemicals, the Administrator must determine
whether, in her judgement, there is sufficient evidence to establish
any one of the following:
(A) The 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 as a result of continuous, or frequently
recurring, releases.
(B) The chemical is known to cause or can reasonably be anticipated
to cause in humans--
(i) cancer or teratogenic effects, or
(ii) serious or irreversible--
(I) reproductive dysfunctions,
(II) neurological disorders,
(III) heritable genetic mutations, or
(IV) other chronic health effects.
(C) The chemical is known to cause or can reasonably be anticipated
to cause, because of--
(i) its toxicity,
(ii) its toxicity and persistence in the environment, or
(iii) its toxicity and tendency to bioaccumulate in the
environment, a significant adverse effect on the environment of
sufficient seriousness, in the judgement of the Administrator, to
warrant reporting under this section.
To remove a chemical from the section 313(c) list, the
Administrator must determine that there is not sufficient evidence to
establish any of the criteria described above as required by EPCRA
section 313(d)(3). Thus, the criteria for listing or delisting a
chemical are identical. However, whereas EPA can add a chemical if only
one of the criteria is met, it can only delete a chemical if none of
the criteria are met.
To ascertain whether there is sufficient or insufficient evidence
to determine that the statutory criteria are met for listing a
chemical, EPA conducts a hazard assessment on the chemical and
determines based on the weight-of-the-evidence, whether the chemical
can reasonably be anticipated to cause any of the adverse effects
specified in EPCRA section 313(d)(2). The hazard analysis is described
above in Unit II.B.3. of this preamble. EPA's interpretation of the
specific statutory criteria follows.
1. Section 313(d)(2)(A) (acute human health effects). To determine
whether the section 313(d)(2)(A) ``acute human health effects''
criterion is met, EPA must examine the adverse effects associated with
the chemical, the ``concentration levels'' which would cause acute
human health effects, and the likelihood of such levels existing
``beyond facility site boundaries as a result of continuous, or
frequently recurring, releases.'' Such a determination may include,
among other factors, consideration of production processes, workplace
procedures, pollution controls, and the volume and pattern of
production, use, and release, as well as other chemical-specific
factors. EPA believes that to make the section 313(d)(2)(A)
determination it must demonstrate that a chemical can reasonably be
anticipated to be released in quantities that result in concentration
levels, or within a reasonable margin of exposure of the concentration
levels, that would be expected to cause acute human health effects
beyond the facility site boundary. The margin of exposure applied is
dependent upon the type of hazard data (e.g., data in animals versus
human) and the confidence in this hazard data base for acute effects
(e.g., sufficiency of the hazard data). However, EPA is not required to
make a facility-specific finding, nor is it necessary for EPA to
demonstrate that these concentration levels or effects occur at or near
any particular facility (Ref. 1). Furthermore, ``EPA 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'' (Ref. 1). Nor is
EPA limited to considering concentration levels and potential acute
human health effects at the ``fenceline.'' Rather, the phrase ``beyond
facility site boundaries'' reflects Congress' recognition that the
``highest concentration to which persons outside the site boundary may
be exposed'' could occur at ``any point outside the boundaries of the
site on which the facility is located,'' including, for example, where
an air emissions plume cools and settles to the ground (Ref. 1).
Therefore, EPA believes that to make a finding under EPCRA section
313(d)(2)(A), the Agency may estimate concentrations at or beyond the
facility site boundary through the use of estimated releases and
modelling techniques. The term ``continuous or frequently recurring
releases'' is included only to distinguish routine releases that are a
normal consequence of the operation of a facility from the episodic and
accidental releases that are subject to EPCRA section 304 (Ref. 1). As
such, EPA believes that episodic and accidental releases are not
pertinent in a determination that a chemical meets the section
313(d)(2)(A) criterion.
2. Section 313(d)(2)(B) (chronic human health effects). In contrast
to the section 313(d)(2)(A) criterion, section 313(d)(2)(B) does not
require consideration of either the nature and frequency of releases or
concentration levels at facility site boundaries. Rather, section
313(d)(2)(B) is focused solely on whether the chemical is known or can
reasonably be anticipated to cause cancer, teratogenicity, or other
serious or irreversible chronic human health effects. Consequently, EPA
believes that it is sufficient to consider only the toxicity of the
subject chemical to make the section 313(d)(2)(B) determination.
3. Section 313(d)(2)(C) (environmental effects). The section
313(d)(2)(C) criterion requires EPA to consider a chemical's potential
to cause significant adverse effects on the environment. The statute
directs EPA to base its determination on a consideration of the
toxicity of the chemical, either alone or in combination with the
persistence of the chemical or the potential for the chemical to
bioaccumulate. Congress intended that EPA consider a broad range of
environmental effects when making a determination under section
313(d)(2)(C).
In determining what constitutes a significant adverse effect on
the environment...the Administrator should consider the extent to
which the toxic chemical causes or can reasonably be anticipated to
cause any of the following adverse reactions, even if restricted to
the immediate vicinity adjacent to the site: (1) Gradual or sudden
changes in the composition of animal life or plant life, including
fungal or microbial organisms in an area. (2) Abnormal number of
deaths of organisms (e.g. fish kills). (3) Reduction of the
reproductive success or the vigor of a species. (4) Reduction in
agricultural productivity, whether crops or livestock. (5)
Alterations in the behavior or distribution of a species. (6) Long
lasting or irreversible contamination of components of the physical
environment, especially in the case of groundwater, and surface
water and soil resources that have limited self-cleansing capability
(Ref. 1).
EPA believes that the environmental effects criterion inherently
contains a limited exposure component because of the statutory
requirement for EPA 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. Unlike
section 313(d)(2)(B), where EPA only has to determine whether certain
kinds of effects are ``known or reasonably anticipated'' to occur,
section 313(d)(2)(C) requires EPA to find the effect to be of
sufficient seriousness to warrant reporting, which implies the
possibility that under certain circumstances, a chemical that could
theoretically cause a significant adverse effect on the environment is
unlikely to cause one of a magnitude to warrant listing.
The extent to which exposure is factored into EPA's determination
depends upon the inherent toxicity of a chemical, and a variety of
other chemical-specific characteristics. EPA believes that when a
chemical is inherently extremely toxic, that is, it is toxic at very
low dose levels, an exposure assessment is not necessary because even
minimal releases of such a chemical may reasonably be anticipated to
result in significant adverse environmental effects. In such cases, EPA
could rely on toxicity alone under section 313(d)(2)(C)(i) as a basis
for listing.
However, for chemicals that exhibit adverse effects upon the
environment solely based on toxicity at moderately low doses, EPA
believes that consideration of potential exposure is warranted because
minimal releases may not result in significant adverse effects upon the
environment. These exposure considerations may include, among other
factors, 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 modelling techniques.
EPCRA sections 313(d)(2)(C)(ii) and (iii) allow EPA to consider the
impacts of other characteristics of a chemical. Where a chemical
exhibits significant adverse effects in the environment based on
toxicity and persistence or toxicity and bioaccumulation at very low to
moderately low dose levels, EPA believes that exposure considerations
are not required in addition to those considerations implicit in
evaluation of the chemical's potential for persistence and
bioaccumulation. This is because even minimal releases of the chemical
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.
Therefore, evaluation of a chemical's persistence or bioaccumulation
potential may be considered the functional equivalent of an exposure
analysis.
In addition, for chemicals which induce well-established 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 affect changes across a whole ecosystem. EPA
believes that these effects are of sufficient seriousness that
additional exposure considerations are not warranted because of the
scope of their impact and the well-documented evidence supporting the
adverse effects. EPA requests comment on its approach for considering
exposure as a part of its evaluation for listing of these chemicals
under section 313(d)(2)(C).
In Unit IV.B. of this preamble, EPA identifies each of the
chemicals proposed for addition to EPCRA section 313 and the specific
statutory criteria upon which the proposed addition is based.
IV. EPA's Technical Review
A. Introduction
Data on the chemicals and chemical categories were reviewed for
evidence indicating adverse acute and chronic toxicity,
carcinogenicity, mutagenicity, developmental and reproductive effects,
neurotoxicity, and environmental effects. Information on the
environmental fate was also reviewed.
For each chemical proposed for addition to EPCRA section 313 in
this rulemaking, EPA conducted an extensive hazard assessment, and,
where appropriate, an analysis of exposure, to determine whether the
chemical met one or more of the EPCRA section 313(d)(2) listing
criteria. This hazard assessment is discussed in detail in Unit II.B.3
of this preamble. Only after this careful review was a final
determination made as to whether one of the EPCRA section 313(d)(2)
listing criteria was met for each individual chemical or chemical
category proposed for listing below. EPA need only show that one of the
listing criteria is met in order to list a chemical or chemical
category under EPCRA section 313. The information summarized below for
each chemical or chemical category represents the key data elements
that lead EPA to believe that there is sufficient evidence to establish
that one of the section 313(d)(2) listing criteria is met. A more
extensive review of the existing data base for each chemical or
chemical category proposed for listing, which reflects the entire
weight-of-the-evidence considered by EPA, is contained in following
support documents: Support Document for the Addition of Chemicals from
Federal Insecticide, Fungicide, Rodenticide Act (FIFRA) Active
Ingredients to EPCRA Section 313 (Ref 3); Physical Properties and
Environmental Fate of Some TRI Expansion Chemicals (Ref. 5); 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.
7); and Support Document for the Health and Ecological Toxicity Review
of TRI Expansion Chemicals (Ref. 8). These support documents contain a
complete list of the references (which can be found in the public
record for this proposed rulemaking) that were used in support of these
proposed additions.
A list of the 313 chemicals and chemical categories and their
Chemical Abstract Service (CAS) number, where appropriate, follows.
A limited discussion of the health and environmental effects
associated with each of the 313 chemicals and chemical categories is
provided below in Unit IV.B. of this preamble. Each chemical is
identified by chemical name, CAS No., and the list(s) from which the
chemical originated. These lists are designated as follows:
CAA HAP: Clean Air Act section 112(b) ``Hazardous Air
Pollutants.''
CAA OD: Clean Air Act section 602(b) Class II ozone depleters.
CAL: 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.''
CERCLA: Comprehensive Environmental Response, Compensation, and
Liability Act section 102.
CWA PPL: Clean Water Act section 307(a) ``Priority Pollutant
List.''
EPCRA EHS: EPCRA section 302 ``Extremely Hazardous Substances.''
FIFRA AI: Federal Insecticide, Fungicide, and Rodenticide Act
(FIFRA) ``Active Ingredients.''
FIFRA SR: FIFRA ``Special Review, Canceled/Denied or Suspended,
and Restricted Use Pesticides.''
IARC: Monographs of the International Agency for Research on
Cancer.
NTP: The 6th Annual Report on Carcinogens of the National
Toxicology Program.
RCRA APP8: Resource Conservation and Recovery Act (RCRA)
Chemicals listed at 40 CFR part 261 Appendix VIII.
RCRA P: RCRA Chemicals listed at 40 CFR part 261.33(e).
SDWA: Safe Drinking Water Act section 1412.
TSCA: Toxic Substances Control Act ``Existing Chemicals.''
EPA requests comment on the sufficiency of the evidence for each of
the chemicals proposed for addition. In addition, EPA requests comment
on any issues that may be specific to any of the individual chemicals
or chemical categories. For example, should chemicals be listed on
EPCRA section 313 that meet the EPCRA section 313 criteria but whose
only use is as a drug product.
B. Chemicals Proposed for Addition to EPCRA Section 313
3. Acifluorfen sodium salt (5-(2-chloro-4-
(triflouromethyl)phenoxy)-2-nitro-benzoic acid, sodium salt) (CAS No.
062476-59-9) (FIFRA AI) (Ref. 3). Acifluorfen is classified as a Group
B2 compound, i.e., the chemical is a probable human carcinogen.
Acifluorfen produced an increased incidence of combined malignant and
benign liver tumors in two different strains of mice. The compound also
displayed positive mutagenic activity in several non-mammalian test
systems, and is structurally similar to four other diphenyl ether
herbicide compounds which caused increased incidences of liver tumors
in two different strains of mice. EPA believes that there is sufficient
evidence for listing acifluorfen sodium salt on EPCRA section 313
pursuant to EPCRA section 313(d)(2)(B) based on the available
carcinogenicity data.
14. Benfluralin (N-butyl-N-ethyl-2,6-dinitro-4(trifluoromethyl)
benzenamine) (CAS No. 001861-40-1) (FIFRA AI) (Ref. 3). Increased
relative liver weights, decreased red blood cell counts and decreased
hematocrit and hemoglobin levels were observed in dogs orally
administered benfluralin at a dose of 125 mg/kg/day for 2 years. The
NOAEL was 25 mg/kg/day. Based on the NOAEL, EPA has established an oral
RfD of 0.003 mg/kg/day. EPA believes that there is sufficient evidence
for listing benfluralin on EPCRA section 313 pursuant to EPCRA section
313(d)(2)(B) based on the available hematological toxicity data for
this chemical.
17. Bifenthrin (CAS No. 082657-04-3) (FIFRA AI) (Ref. 3). Tremors
or head and forelimb twitching were noted in dogs, rats and rabbits
exposed to various doses. NOEL values based on the appearance of
tremors (often transient) ranged from 1 to 2.67 mg/kg/day. The oral RfD
for bifenthrin was based on a 1year beagle dog feeding study, in which
the LOEL, based on tremors observed during weeks 15 to 29, was 3.0 mg/
kg/day and the NOEL was 1.5 mg/kg/day. The RfD based on this NOEL was
0.015 mg/kg/day.
In a rat teratology study, an increased incidence of hydroureter
(without hydronephrosis) was noted in fetuses at 2 mg/kg/day (LOEL).
The NOEL was 1 mg/kg/day.
EPA believes that there is sufficient evidence for listing
bifenthrin on EPCRA section 313 pursuant to EPCRA section 313(d)(2)(B)
based on the available neurological and developmental toxicity data.
Aquatic acute toxicity values for bifenthrin include a bluegill 96-
hour LC<INF>50 of 0.35 ppb, a rainbow trout 96-hour LC<INF>50 of 0.15
ppb, a sheepshead minnow LC<INF>50 of 17.5 ppb, and a daphnid 48-hour
EC<INF>50 of 1.6 ppb. EPA believes that there is sufficient evidence
for listing bifenthrin on EPCRA section 313 pursuant to EPCRA section
313(d)(2)(C) based on the available environmental toxicity data.
20. Boron trifluoride (CAS No. 007637-07-2) (EPCRA EHS) (Ref. 8).
Boron trifluoride is a colorless gas that is corrosive to tissues due
to its rapid hydrolysis to hydrofluoric acid and boric acid. The
principal acute effect in animals is irritation of the mucous membranes
of the respiratory tract and eyes; post mortem examination also
revealed pneumonia and degenerative changes in renal tubules. The
kidneys are most severely affected because boric acid concentrates in
this organ. Exposure of six animal species to 0.28 mg/L of boron
trifluoride for 4 to 7 hours a day, 5 days a week killed all animals
within 30 days. Rats, rabbits, and guinea pigs were exposed to boron
trifluoride via inhalation. Guinea pigs died of respiratory failure
after being exposed to 0.036 mg/L for 19 days; rats experienced
fluorosis of the teeth at this concentration. All three species were
minimally affected at 0.004 mg/L. In a 2-week rat inhalation study, all
animals died after 6 daily exposures to 0.18 mg/L. Rats exposed to
0.024 mg/L showed signs of respiratory irritation, increased lung
weights, and depressed liver weights. Rats exposed to 0.17 mg/L of
boron trifluoride 6 hours/day, 5 days a week for 13 weeks developed
necrosis of the proximal tubular epithelium of the kidneys. Guinea pigs
exposed to 0.035 mg/L, 7 hours/day, 5 days a week for 3 months
developed severe pneumonitis and pulmonary changes indicating chemical
irritation.
EPA believes that there is sufficient evidence for listing boron
trifluoride on EPCRA section 313 pursuant to section 313(d)(2)(B) based
on the available chronic toxicity data for this chemical.
50. Chlorotrifluoromethane (CFC-13) (CAS No. 000075-72-9) (CAA OD)
(Ref. 8). Chlorofluorocarbons, including chlorotrifluoromethane (CFC-
13) are known to release chlorine radicals into the stratosphere.
Chlorine radicals act as catalysts to reduce the net amount of
stratospheric ozone.
Stratospheric ozone shields the earth from ultraviolet-B (UV-B)
radiation (i.e., 290 to 320 nanometers). Decreases in total column
ozone will increase the percentage of UV-B radiation, especially at its
most harmful wavelengths, reaching the earth's surface.
Exposure to UV-B radiation has been implicated by laboratory and
epidemiologic studies as a cause of two types of nonmelanoma skin
cancers: squamous cell cancer and basal cell cancer. Studies predict
that for every 1 percent increase in UV-B radiation, nonmelanoma skin
cancer cases would increase by about 1 to 3 percent.
Recent epidemiological studies, including large case control
studies, suggest that UV-B radiation plays an important role in causing
malignant melanoma skin cancer. Recent studies predict that for each 1
percent change in UV-B intensity, the incidence of melanoma could
increase from 0.5 to 1 percent.
Studies have demonstrated that UV-B radiation can suppress the
immune response system in animals, and, possibly, in humans. Increases
in exposure to UV-B radiation are likely to increase the incidence of
cataracts and could adversely affect the retina.
Aquatic organisms, particularly phytoplankton, zooplankton, and the
larvae of many fishes, appear to be susceptible to harm from increased
exposure to UV-B radiation because they spend at least part of their
time at or near the surface of waters they inhabit.
Increased UV-B penetration has been shown to result in adverse
impacts on plants. Field studies on soybeans suggest that yield
reductions could occur in some cultivars of soybeans, while evidence
from laboratory studies suggest that two out of three cultivars are
sensitive to UV-B. Because this increased UV-B radiation can be
reasonably anticipated to lead to cancer and other chronic human health
58. Cyfluthrin (3-(2,2-Dichloroethenyl)-2,2-
dimethylcyclopropanecarboxylic acid, cyano(4-fluoro-3-
phenoxyphenyl)methyl ester) (CAS No. 068359-37-5) (FIFRA AI) (Ref. 3).
In a 14-day rat study, oral administration of 60 mg/kg/day produced
tremors, uncoordinated gait, salivation, slight brain hemorrhages,
necrosis of the skeletal muscle fibers, and death. The NOEL was not
defined. In another study, salivation, straddled gait, axonal
degeneration of sciatic nerve, microtubular dilation, and mitochondria
degeneration in the sciatic and femoral nerves were observed in rats
administered 80 mg/kg/day orally for 5 days and 40 mg/kg/day for the
following 9 days. No NOEL was established.
Liver and adrenal weight increases were observed in rats orally
administered 40 to 80 mg/kg/day for 28 days. The highest dose of 80 mg/
kg/day was reduced to 40 mg/kg/day. The NOEL was 20 mg/kg/day. Liver
weight changes and urobilinogen and ketone bodies in the urine were
observed in rats fed 15 mg/kg/day for 28 days. No NOEL was established.
In a 28-day mouse feeding study, increased liver weight was observed at
50 mg/kg/day (LOEL). The NOEL was 15 mg/kg/day. Inflammatory foci in
the kidneys of females were observed at 7.5 mg/kg/day in a 2-year rat
feeding study. The NOEL was 2.5 mg/kg/day. Based on the NOEL of the
study, an oral RfD of 0.025 mg/kg/day was determined. Increased
alkaline phosphatase activity was observed in males at 7.5 mg/kg/day in
a 23-month mouse feeding study.
EPA believes that there is sufficient evidence for listing
cyfluthrin on EPCRA section 313 pursuant to EPCRA section 313(d)(2)(B)
based on the available neurological, hepatic, and renal toxicity data.
Aquatic acute toxicity values for cyfluthrin include a rainbow
trout 96-hour LC<INF>50 of 0.68 ppb, a bluegill 96-hour LC<INF>50 of
1.5 ppb, and a daphnid 48-hour EC<INF>50 of 0.14 ppb. EPA believes that
there is sufficient evidence for listing cyfluthrin on EPCRA section
313 pursuant to EPCRA section 313(d)(2)(C) based on the available
environmental toxicity data.
59. Cyhalothrin (3-(2-chloro-3,3,3-trifluoro-1-propenyl)-2,2-
dimethylcyclopropanecarboxylic acid cyano(3-phenoxyphenyl)methyl ester)
(CAS No. 068085-85-8) (FIFRA AI) (Ref. 3). Cyhalothrin administered
orally (in capsules) to dogs at 10 mg/kg/day for 26 weeks produced
occasional disturbances of the nervous system (unsteadiness and/or
muscular trembling). The NOEL for these effects was not defined. In a
1-year dog study, ataxia, muscle tremors, and convulsions were observed
following oral administration at 3.5 mg/kg/day. Abnormal gait and
convulsions were observed at 0.5 mg/kg/day. The LOEL of the study was
0.5 mg/kg/day and the NOEL was 0.1 mg/kg/day. EPA believes that there
is sufficient evidence for listing cyhalothrin on EPCRA section 313
pursuant to EPCRA section 313(d)(2)(B) based on the available
neurological toxicity data.
83. Diflubenzuron (CAS No. 035367-38-5) (FIFRA SR) (Ref. 8). In a
2-year study in which beagle dogs received diflubenzuron daily in
gelatin capsules, the LOAEL for increases in sulfhemoglobin and
methemoglobin was 10 mg/kg/day and the NOAEL was 2 mg/kg/day. EPA has
derived an oral RfD of 0.02 mg/kg/day for this chemical from this
study. Similar effects were noted in two separate 2-year rat feeding
studies (the LOAEL was 7.8 to 8 mg/kg/day; the NOAEL was 2 mg/kg/day),
and in a lifetime oral study in mice (the LOAEL was 12 mg/kg/day; the
NOAEL was 2.4 mg/kg/day). EPA believes that there is sufficient
evidence for listing diflubenzuron on EPCRA section 313 pursuant to
EPCRA section 313(d)(2)(B) based on the available hematological
toxicity data.
Measured aquatic acute toxicity data for diflubenzuron include a
48-hour LC<INF>50 of 4.55 ppb for daphnids. EPA believes that there is
sufficient evidence for listing diflubenzuron on EPCRA section 313
pursuant to EPCRA section 313(d)(2)(C) based on the environmental
toxicity data for this chemical.
92. 3,3'-Dimethylbenzidine dihydrofluoride (o-Tolidine
dihydrofluoride) (CAS No. 041766-75-0) (TSCA) (Ref. 8). Neither IARC or
EPA has classified 3,3'-dimethylbenzidine dihydrofluoride with respect
to carcinogenicity. In a bioassay conducted by NTP, however, 3,3'-
dimethylbenzidine dihydrochloride was found to be carcinogenic in both
mice and rats. Male and female mice exposed to concentrations of 5 to
140 ppm (0.952 to 6.6 mg/kg/day) in drinking water for 112 weeks
developed lung alveolar cell adenoma and adenocarcinoma. Male and
female F344 rats exposed to concentrations of 30 to 150 ppm (4.2 to 21
mg/kg/day) in drinking water for 60 to 61 weeks developed tumors in the
gastrointestinal tract, liver, lung, and oral cavity. Tumors in the
skin, Zymbal's gland, preputial gland in males, clitoral gland and
mammary gland in females, and leukemia in females were also noted in
this study. EPA believes that there is sufficient evidence for listing
3,3'-dimethylbenzidine dihydrofluoride on EPCRA section 313 pursuant to
EPCRA section 313(d)(2)(B) based on its potential to cause cancer in
humans and on the carcinogenicity data for 3,3'-dimethylbenzidine
dihydrochloride.
106. Dithiopyr (2-(difluoromethyl)-4-(2-methylpropyl)-6-
(trifluoromethyl)-3,5-pyridinedicarbothioic acid S,S-dimethyl ester)
(CAS No. 097886-45-8) (FIFRA AI) (Ref. 3). In a 2-generation rat
reproduction study, decreased body weight, diffuse hepatocellular
swelling, and ``white spots'' on the livers were observed in the
offspring of rats administered greater than or equal to 16.4 mg/kg/day.
The NOEL values were 1.7 mg/kg/day. In a 13-week rat feeding study, the
LOEL of 6.62 mg/kg/day produced diffuse hepatocellular swelling. The
NOEL was 0.662 mg/kg/day. In a 13-week dog feeding study, increased
alkaline phosphatase, discolored livers, and cholestasis was observed
at 10 mg/kg/day (LOEL). The NOEL was 1 mg/kg/day. In addition, at 30
mg/kg/day, increased serum glutamic-pyruvic transaminase and serum
glutamic oxaloacetic transaminase, increased liver and kidney weights,
and decreased cholesterol and albumin were observed. EPA believes that
there is sufficient evidence for listing dithiopyr on EPCRA section 313
pursuant to EPCRA section 313(d)(2)(B) based on the available hepatic
and renal toxicity data.
124. Fluazifop butyl (2-[4-[[5-(trifluoromethyl)-2-pyridinyl]oxy]-
phenoxy]propanoic acid, butyl ester) (CAS No. 069806-50-4) (FIFRA AI)
(Ref. 3). A 3-month rat feeding study demonstrated hepatocyte
hypertrophy in males (the LOEL was 5 mg/kg/day; the NOEL was 0.5 mg/kg/
day). In a 1-year feeding study, dogs had changes in serum alkaline
phosphatase and alanine aminotransferase and/or alanine
sulfatransferase (the LOEL was 25 mg/kg/day; the NOEL was 5 mg/kg/day).
Similar changes were also reported in dogs following 3 months exposure
in their diet (the LOEL was 125 mg/kg/day). In a carcinogenicity study,
male mice fed 20 ppm (2.6 mg/kg/day, the LOEL) had an increased
incidence of hepatocyte hypertrophy. The NOEL was 5 ppm or 0.65 mg/kg/
day. Male and female mice exposed to a higher dose of 80 ppm (10.4 mg/
kg/day) had increased liver weight (relative and absolute) and
hypertrophy of periacinal hepatocytes. Males in this dose group also
had increased pigmentation in hepatocytes and Kupffer cells.
In a teratogenicity study in Sprague-Dawley rats exposed via oral
gavage, delayed ossification and an increased incidence of hydroureter
were observed in fetuses (the fetotoxic LOEL was 5 mg/kg/day; the NOEL
1 mg/kg/day) and a teratogenic LOEL of 200 mg/kg/day (the NOEL was 10
mg/kg/day) was determined based on the incidence of diaphragmatic
hernia. Maternal toxicity was observed in this study at doses higher
than those causing fetotoxicity and included reduced body weight gain
and decreased gravid uterus (the maternal LOEL was 200 mg/kg/day; the
NOEL was 10 mg/kg/day). In a 2-generation reproductive toxicity dietary
study in Wistar rats, the reproductive LOEL of 250 ppm (12.5 mg/kg/day;
the NOEL was 80 ppm or 4 mg/kg/day) was based on reduced litter sizes,
reduced viability, reduced testis and epididymis weights and tubular
atrophy in offspring. Fetotoxicity (delayed ossification and eye
opacities) was also demonstrated in New Zealand White rabbits (the LOEL
was 30 mg/kg/day; the NOEL was 10 mg/kg/day). EPA believes that there
is sufficient evidence for listing fluazifop butyl on EPCRA section 313
pursuant to EPCRA section 313(d)(2)(B) based on the available hepatic
and developmental toxicity data for this chemical.
125. Flumetralin (2-chloro-N-(2,6-dinitro-4-(trifluoromethyl)-
phenyl)-N-ethyl-6-fluorobenzenemethanamine) (CAS No. 062924-70-3)
(FIFRA AI) (Ref. 3). Aquatic acute toxicity values for flumetralin
include a daphnid 48-hour EC<INF>50 of greater than 2.8 ppb, a bluegill
sunfish 96-hour LC<INF>50 of greater than 3.2 ppb, and a rainbow trout
96-hour LC<INF>50 of greater than 3.2 ppb. EPA believes that there is
sufficient evidence for listing flumetralin on EPCRA section 313
pursuant to EPCRA section 313(d)(2)(C) based on the available
environmental toxicity data for this chemical.
126. Fluorine (CAS No. 007782-41-4) (CERCLA; EPCRA EHS; RCRA APP8;
RCRA P) (Ref. 8). Inhalation of fluorine causes initial coughing,
choking and chills, which is followed 1 or 2 days later with pulmonary
edema. Fluorine has a strong caustic action on mucous membranes, eyes
and skin. In human volunteers exposed to 100 ppm (0.16 mg/L) for 30
seconds, much irritation to the nose and eyes was reported. In acute
inhalation studies in animals, lethality occurs at a fairly uniform
level and is the result of pulmonary edema. Following 1 hour exposures
in mice, rats or guinea pigs, the inhalation LC<INF>50 values ranged
from 150 to 185 ppm (0.23 to 0.29 mg/L). The LC<INF>50 for rabbits
following a 30-minute exposure was 270 ppm (0.42 mg/L). EPA's exposure
analysis indicates that fluorine concentrations are likely to exist
beyond facility site boundaries, as a result of continuous, or
frequently recurring releases, at levels that can reasonably be
anticipated to cause significant adverse acute human health effects.
EPA believes that there is sufficient evidence for listing fluorine on
EPCRA section 313 pursuant to EPCRA section 313(d)(2)(A) based on the
available acute toxicity and exposure data for this chemical.
127. Fluorouracil (5-Fluorouracil) (CAS No. 000051-21-8) (CAL;
EPCRA EHS) (Ref. 8). A major use of fluorouracil is in the palliative
treatment of carcinoma of the colon, rectum, breast, stomach, and
pancreas that is not amenable to surgery or irradiation. The major
toxic effects of fluorouracil are on the normal, rapidly proliferating
tissues particularly of the bone marrow and lining of the
gastrointestinal tract. Leukopenia, predominantly of the
granulocytopenic type, thrombocytopenia, and anemia occur commonly with
intravenous fluorouracil therapy at doses ranging from 6 to 12 mg/kg.
Pancytopenia and agranulocytosis also have occurred.
Developmental abnormalities or other effects on newborns were
reported in offspring of women receiving 150 or 240 mg/kg fluorouracil
intravenously during weeks 11 to 14 or 20 to 31 of pregnancy. In
addition, maternal toxicity to the reproductive organs, toxicity to the
fetus, and developmental abnormalities have been reported in mice,
rats, and hamsters receiving oral, intraperitoneal, or intramuscular
doses of fluorouracil ranging from 10 to 700 mg/kg.
Chronic neurotoxic effects were noted in dogs fed fluorouracil at a
dietary dose of 2 mg/kg/day for 6 months. In this study, animals were
examined at the end of 3 months and 6 months. At the end of the
experiment, or at death, the brain was removed and examined (only one
dog survived the entire 6-month period). Histological sections of the
brain showed the presence large multiple monolocular vacuoles in the
wall of the fornix of the third ventricle.
EPA believes that there is sufficient evidence for listing
fluorouracil on EPCRA section 313 pursuant to EPCRA section
313(d)(2)(B) based on the toxicity of this substance to bone marrow,
and on the developmental and chronic neurotoxicity data for this
chemical.
128. Fluvalinate (N-[2-chloro-4-(trifluoromethyl)phenyl]DL-
valine(+)- cyano (3-phenoxyphenyl)methyl ester) (CAS No. 069409-94-5)
(FIFRA AI) (Ref. 3). Delayed ossification and decreased weight and
length of fetuses were observed in offspring of rats orally
administered 50 mg/kg/day (LOEL) on days 6 to 15 of gestation. The NOEL
was 10 mg/kg/day. These effects were observed at doses that produced
maternal toxicity. Curved tibia and fibula were observed in the
offspring of rabbits orally administered 125 mg/kg/day (LOEL). The NOEL
was 25 mg/kg/day. In a 2-generation reproduction study, a decrease in
pup weight and growth were observed in offspring of rats orally
administered 5 mg/kg/day (LOEL). The NOEL was 1 mg/kg/day.
Significantly decreased weight and survival were observed in offspring
of rats orally administered 25 mg/kg/day.
In a range finding study, dietary administration of 50 mg/kg/day
for 30 days produced skin lesions in rats. The NOEL was not determined.
A 2-year rat feeding study was terminated at 64 weeks due to dermal
lesions produced in animals at 15 mg/kg/day. The NOEL was 2 mg/kg/day.
Dietary administration of 10 mg/kg/day (LOEL for effect) to mice for 2
years produced scabbing and dermal abrasion. No NOEL for these effects
was established. An increase in plantar ulcers was observed in rats fed
2.5 mg/kg/day (LOEL) for 2 years. The NOEL was 1 mg/kg/day. Decreases
in body weight gain were also observed in this study. Based on the NOEL
of the study, an oral RfD of 0.01 mg/kg/day was derived. In a 2-
generation rat reproduction study, dietary administration of 5 mg/kg/
day produced decreased body weight gain and skin lesions in parents and
offspring.
Dietary administration of 2.5 mg/kg/day to rats for 13 weeks
produced anemia in blood parameters (decreased hematocrit, hemaglobin,
and red blood cells). The NOEL was 1.0 mg/kg/day. Dietary
administration of 30 mg/kg/day (LOEL) to rats for 3 months produced
decreased hemoglobin, hematocrit, and red blood cell count in rats. The
NOEL was 3 mg/kg/day.
EPA believes that there is sufficient evidence for listing
fluvinate on EPCRA section 313 pursuant to EPCRA section 313(d)(2)(B)
based on the available developmental, dermal, and hematological
toxicity data for this chemical.
Aquatic acute toxicity values for fluvalinate include a daphnid 48-
hour EC<INF>50 of 0.40 ppb, a bluegill sunfish 96-hour LC<INF>50 of 0.9
ppb, a rainbow trout 96-hour LC<INF>50 of 2.9 ppb, and a sheepshead
minnow 96-hour LC<INF>50 of 10.8 ppb. EPA believes that there is
sufficient evidence for listing fluvinate on EPCRA section 313 pursuant
to EPCRA section 313(d)(2)(C) based on the available environmental
toxicity data for this chemical.
130. Fomesafen (5-(2-chloro-4-(trifluoromethyl)phenoxy)-N
methylsulfonyl)-2-nitrobenzamide) (CAS No. 072178-02-0) (FIFRA AI)
(Ref. 3). Decreased plasma cholesterol and triglycerides and increased
liver weights (reversible at 7 days post-treatment) were observed at 50
mg/kg/day (only dose tested) when administered in the diet of rats for
4 weeks. In a 90-day rat study, dietary administration of 5 mg/kg/day
(LOEL) produced alterations in lipid metabolism and increases in liver
weight. The NOEL was 0.25 mg/kg/day. In a 26-week dog study, dietary
administration of 25 mg/kg/day (LOEL) produced alterations in lipid
metabolism and liver changes (changes not defined). The NOEL was 1 mg/
kg/day. Liver toxicity (increased liver masses, discolored hepatocytes,
and pigmented Kupffer cells) was observed in a 2-year rat feeding study
at 50 mg/kg/day (LOEL). The NOEL was 5 mg/kg/day. Metabolism studies
have shown that fomesafen accumulates in the liver. EPA believes that
there is sufficient evidence for listing fomesafen on EPCRA section 313
pursuant to EPCRA section 313(d)(2)(B) based on the available hepatic
toxicity data for this chemical.
135. Hydramethylnon (tetrahydro-5,5-dimethyl-2(1H)-pyrimidinone[3-
[4- (trifluoromethyl)phenyl]-1-[2-[4(trifluoromethyl) phenyl]ethenyl]-
2-propenylidene]hydrazone) (CAS No. 067485-29-4) (FIFRA AI) (Ref. 3).
In a 90-day dog feeding study, testicular atrophy was observed at 6 mg/
kg/day (LOEL). The NOEL was 3 mg/kg/day. In a 90-day rat study, dietary
administration of 5 mg/kg/day (LOEL) produced testicular atrophy. The
NOEL was 2.5 mg/kg/day. Dietary administration of 6.5 mg/kg/day for 18
months produced testicular lesions in mice. The NOEL was 2.75 mg/kg/
day. In a 2-year rat study, dietary administration of 5 mg/kg/day
produced decreased testicular weight and testicular atrophy. The NOEL
was 2.5 mg/kg/day. In a 3-generation rat reproduction study, oral
administration of 5 mg/kg/day produced male infertility. The NOEL was
2.5 mg/kg/day.
Decreased fetal weight was observed in the offspring of rats
administered 30 mg/kg/day (LOEL). The NOEL was 10 mg/kg/day. Increased
post implantation loss and decreased fetal viability were observed in
the offspring of rabbits administered 15 mg/kg/day (LOEL). The NOEL was
5 mg/kg/day. Vertebral anomalies were seen in the offspring of rabbits
administered 10 mg/kg/day (LOEL). The NOEL was 5 mg/kg/day.
Dietary administration of 1 mg/kg/day (LOEL) for 6 months to dogs
produced increased absolute and relative liver weights. The NOEL was
0.33 mg/kg/day. Based on the NOEL of the study, an oral RfD of 0.0003
mg/kg/day was derived.
EPA believes that there is sufficient evidence for listing
hydramethylnon on EPCRA section 313 pursuant to EPCRA section
313(d)(2)(B) based on the available reproductive, developmental, and
hepatic toxicity data for this chemical.
The 96-hour LC<INF>50 in the Chanel Catfish was 90 ppb.
Bioaccumulation factors in bluegill sunfish are 1300 for the whole
fish, 780 for the fillet, and 1900 for viscera. EPA believes that there
is sufficient evidence for listing hydramethylon on EPCRA section 313
pursuant to EPCRA section 313(d)(2)(C) based on the available
environmental toxicity data and the potential for bioaccumulation.
136. Hydrochlorofluorocarbons (CAA OD) (Ref. 8).
Hydrochlorofluorocarbons are known to release chlorine radicals into
the stratosphere. Chlorine radicals act as catalysts to reduce the net
amount of stratospheric ozone.
Stratospheric ozone shields the earth from ultraviolet-B (UV-B)
radiation (i.e., 290 to 320 nanometers). Decreases in total column
ozone will increase the percentage of UV-B radiation, especially at its
most harmful wavelengths, reaching the earth's surface.
Exposure to UV-B radiation has been implicated by laboratory and
epidemiologic studies as a cause of two types of nonmelanoma skin
cancers: squamous cell cancer and basal cell cancer. Studies predict
that for every 1 percent increase in UV-B radiation, nonmelanoma skin
cancer cases would increase by about 1 to 3 percent.
Recent epidemiological studies, including large case control
studies, suggest that UV-B radiation plays an important role in causing
malignant melanoma skin cancer. Recent studies predict that for each 1
percent change in UV-B intensity, the incidence of melanoma could
increase from 0.5 to 1 percent.
Studies have demonstrated that UV-B radiation can suppress the
immune response system in animals, and, possibly, in humans. Increases
in exposure to UV-B radiation are likely to increase the incidence of
cataracts and could adversely affect the retina.
Aquatic organisms, particularly phytoplankton, zooplankton, and the
larvae of many fishes, appear to be susceptible to harm from increased
exposure to UV-B radiation because they spend at least part of their
time at or near the surface of waters they inhabit.
Increased UV-B penetration has been shown to result in adverse
impacts on plants. Field studies on soybeans suggest that yield
reductions could occur in some cultivars of soybeans, while evidence
from laboratory studies suggest that two out of three cultivars are
sensitive to UV-B.
Because this increased UV-B radiation can be reasonably anticipated
to lead to cancer and other chronic human health effects and
significant adverse environmental effects, EPA believes there is
sufficient evidence for listing the following HCFCs that are
commercially viable on EPCRA section 313 pursuant to EPCRA sections
313(d)(2)(B) and (C). EPA is proposing that the following HCFCs be
added individually to EPCRA section 313:
Dichloropentafluoropropane (CAS No. 127564-92-5)
1,3-Dichloro-1,1,2,3,3-pentafluoropropane (HCFC-225ea) (CAS No.
136013-79-1)
2,2-Dichloro-1,1,1,3,3-pentafluoropropane (HCFC-225aa) (CAS No.
128903-21-9)
1,1-Dichloro-1,2,3,3,3-pentafluoropropane (HCFC-225eb) (CAS No.
111512-56-2)
1,1-Dichloro-1,2,2,3,3-pentafluoropropane (HCFC-225cc) (CAS No.
13474-88-9)
1,3-Dichloro-1,1,2,2,3-pentafluoropropane (HCFC-225cb) (CAS No.
000507-55-1)
1,2-Dichloro-1,1,3,3,3-pentafluoropropane (HCFC-225da) (CAS No.
000431-86-7)
3,3-Dichloro-1,1,1,2,2-pentafluoropropane (HCFC-225ca) (CAS No.
000422-56-0)
2,3-Dichloro-1,1,1,2,3-pentafluoropropane (HCFC-225ba) (CAS No.
000422-48-0)
1,2-Dichloro-1,1,2,3,3-pentafluoropropane (HCFC-225bb) (CAS No.
000422-44-6)
Dichlorofluoromethane (HCFC-21) (CAS No. 000075-43-4)
1,1,1,2-Tetrachloro-2-fluoroethane (HCFC-121a) (CAS No. 000354-11-
0)
1,1,2,2-Tetrachloro-1-fluoroethane (HCFC-121) (CAS No. 000354-14-3)
1,2-Dichloro-1,1-difluoroethane (HCFC-132b) (CAS No. 001649-08-7)
2-Chloro-1,1,1-trifluoroethane (HCFC-133a) (CAS No. 000075-88-7)
3-Chloro-1,1,1-trifluoropropane (HCFC-253fb) (CAS No. 000460-35-5).
145. Lactofen (5-(2-chloro-4-(trifluoromethyl)phenoxy)-2-nitro-2-
ethoxy-1-methyl-2-oxoethyl ester) (CAS No. 077501-63-4) (FIFRA AI)
(Ref. 3). Lactofen meets the criteria of an EPA Group B2 compound,
i.e., a probable human carcinogen. This conclusion was based on an
increased incidence of hepatocellular carcinomas in males and combined
incidence of hepatocellular adenomas and carcinomas in both sexes of
CD-1 mice following dietary administration of lactofen. In CD rats,
there was increased incidence of liver neoplastic nodules in both
sexes. Four structurally similar chemicals, acifluorfen, nitrofen,
oxyfluorfen, and fomesafen, all produced hepatocellular tumors in
rodents.
Results of several subchronic and chronic studies indicated the
liver and kidney as target organs for lactofen. Increased absolute and
relative liver weight and hepatocytomegaly (the LOEL was 1.5 mg/kg/day;
the NOEL was not determined) were observed in male mice fed lactofen
for 78 weeks. At 37.5 mg/kg/day, there was also an increased incidence
of cataracts and renal pigmentation. Based on the LOEL, an oral RfD of
0.002 mg/kg/day was derived. Renal dysfunction and decreased hemoglobin
and hematocrit levels and red blood cell counts (the LOEL was 25/75 mg/
kg/day; the NOEL was 5 mg/kg/day) were observed in a 1-year feeding
study in dogs. Increased renal and hepatic pigmentation (the LOEL was
50 mg/kg/day; the NOEL was 25 mg/kg/day) were noted in a 2-year feeding
study in rats. In a 90-day mouse study, increased alkaline phosphatase,
serum glutamate oxaloacetate transaminase (SGOT), and serum gleutanic
pyruvic transaminase (SGPT) activities, increased liver weight, hepatic
necrosis, biliary hyperplasia, decreased hematocrit and hemoglobin
levels and red blood cell counts, extramedullary hematopoiesis, and
kidney nephrosis and fibrosis (the LOEL was 26 mg/kg/day; the NOEL was
not determined) were seen. Decreased hemoglobin and hematocrit levels,
decreased red blood cell counts, and brown pigment in the kidney and
liver (the LOEL was 50 mg/kg/day) were noted in a 90-day feeding study
in rats.
EPA believes that there is sufficient evidence for listing lactofen
on EPCRA section 313 pursuant to EPCRA section 313(d)(2)(B) based on
the available carcinogenicity data and hepatic, renal, and
hematological toxicity data for this chemical.
180. Norflurazon (4-Chloro-5-(methylamino)-2-
[3(trifluoromethyl)phenyl]-3(2H)-pyridazinone) (CAS No. 027314-13-2)
(FIFRA AI) (Ref. 3). Congestion of the liver, hepatocyte swelling and
increased liver weights, and increase in colloid vacuole in the thyroid
were observed in dogs fed 450 ppm (10.25 mg/kg/day) norflurazon for 6
months. The NOEL was 150 ppm (3.75 mg/kg/day). An oral RfD of 0.04 mg/
kg/day has been determined. Increased relative liver weight and
hypertrophy of the thyroid with depletion of colloid were seen in rats
fed 2,500 ppm (125 mg/kg/day) norflurazon for 90 days. The NOEL was 500
ppm (25 mg/kg/day). Hepatic hyperplasia and hypertrophy and increased
relative liver weight were noted in a 28-day feeding study in rats. The
LOEL was 1,000 ppm (50 mg/kg/day) and the NOEL was 500 ppm (25 mg/kg/
day). Increased relative liver weight and diffuse and smooth granular
livers were seen in a 28-day feeding study in mice. The LOEL was 2,520
ppm (328 mg/kg/day) and the NOEL was 420 ppm (55 mg/kg/day). EPA
believes that there is sufficient evidence for listing norflurazon on
EPCRA section 313 pursuant to EPCRA section 313(d)(2)(B) based on the
available hepatic and thyroid toxicity data.
184. Oxyfluorfen (CAS No. 042874-03-3) (FIFRA SR) (Ref. 8).
Oxyfluorfen is a phenoxyphenyl-type herbicide. Several chronic oral
toxicity studies suggest that oxyfluorfen may be hepatotoxic. Hepatic
effects (e.g. increased absolute liver weight, necrosis, regeneration,
and hyperplastic nodules) were observed in mice fed diets containing
greater than 3 mg/kg/day oxyfluorfen for 20 months (the NOEL was 0.3
mg/kg/day). Based on these findings, an oral RfD value of 0.003 mg/kg/
day was derived. This study was supported by other chronic feeding
studies that demonstrated increases in liver weight, alkaline
phosphatase activity, and bile pigmented hepatocytes (the LOEL was 15
mg/kg/day; the NOEL was 2.5 mg/kg/day) in dogs, and minimal hypertrophy
of centrilobular hepatocytes (the LOEL was 40 mg/kg/day; the NOEL was 2
mg/kg/day) in rats. EPA believes that there is sufficient evidence for
listing oxyfluorfen on EPCRA section 313 pursuant to EPCRA section
313(d)(2)(B) based on the hepatotoxic effects of this chemical.
The estimated chronic MATC values for fish and daphnids are 9 ppb
and 20 ppb oxyfluorfen, respectively. The estimated log K<INF>ow is
6.1. EPA believes that there is sufficient evidence for listing
oxyfluorfen on EPCRA section 313 pursuant to EPCRA section 313(d)(2)(C)
based on the environmental toxicity data and potential for
bioaccumulation for this chemical
211. Primisulfuron (methyl 2-[[[[[4,6-bis(difluoromethoxy)2-
pyrimidinyl]-amino] carbonyl] amino]sulfonyl] benzoate) (CAS No.
086209-51-0) (FIFRA AI) (Ref. 3). In a 90-day dog feeding study,
reduced thyroid weights accompanied by colloid depletion and
parafollicular hyperplasia and anemia were observed at the LOEL of 25
mg/kg/day. The NOEL was 0.625 mg/kg/day. In a 1-year dog study, dietary
administration of 250/125 mg/kg/day (LOEL: the dose was changed after
week 10 in the study) produced thyroid hyperplasia, anemia, increased
platelet levels, vacuolar changes, and increased absolute and relative
liver weights. The NOEL was 25 mg/kg/day. In an 18-month study in mice,
dietary administration of 1.7 mg/kg/day produced increased absolute and
relative liver weights in females. No NOEL was established. Based on
this study, an oral RfD of 0.006 mg/kg/day was derived. In a 2-year
mouse study, increases in absolute and relative liver weights were
observed at 408 mg/kg/day in males and 1.7 mg/kg/day in females. The
systemic LOEL and NOEL in males was 408 mg/kg/day and 40.2 mg/kg/day,
respectively. The systemic LOEL in females was 1.7 mg/kg/day and a NOEL
could not be established. EPA believes that there is sufficient
evidence for listing primisulfuron on EPCRA section 313 pursuant to
EPCRA section 313(d)(2)(B) based on the available thyroid and liver
toxicity data for this chemical.
Plant toxicity values include a duckweed 14-day EC<INF>50 of 0.27
ppb and an algae 7-day EC<INF>50 of 24 ppb. EPA believes that there is
sufficient evidence for listing primisulfuron on EPCRA section 313
pursuant to EPCRA section 313(d)(2)(C) based on the available
environmental toxicity data for this chemical.
228. Sodium fluoroacetate (CAS. No. 000062-74-8) (CERCLA; EPCRA
EHS; FIFRA SR; RCRA APP8; RCRA P) (Ref. 8). In a 13-week oral study in
rats, gavage administration of sodium fluoroacetate (0.02 mg/kg/day)
resulted in decreased testis weight and altered spermatogenesis in
males (the NOAEL was 0.05 mg/kg/day). In addition, increased heart
weight was noted in females and males administered 0.20 mg/kg/day of
sodium fluoroacetate. The increase in heart weight, however, was only
accompanied by subacute, minimal inflammation (not dose-related). Also,
fluorocitrate levels were significantly increased after 4 weeks in
males administered 0.50 mg/kg/day and after 13 weeks in both male and
female rats administered 0.20 or 0.50 mg/kg/day. The testicular and
cardiac effects were reported to be consistent with those noted in the
literature.
A case study reported a deliberate ingestion of an unspecified dose
of sodium fluroacetate by a healthy female. The woman experienced
nausea, vomiting, and abdominal pain 30 minutes after ingestion, with
subsequent seizures occurring 60 minutes after the initial onset of
symptoms. Neurological examination after 2 weeks revealed severe
cerebellar dysfunction. By 18 months, memory disturbances and
depressive behavior persisted. Inhalation exposure to unspecified
levels of sodium fluoroacetate caused salivation, loss of speech,
violent convulsions, and coma in a male worker. The patient ultimately
recovered. Neurological effects have also been reported in rats in a
13-week oral study. Four of 20 female rats treated with 0.50 mg/kg/day
(the highest dose tested) exhibited convulsions at day 79, with no
recurrences for the remainder of the study. An estimated lethal dose of
sodium fluoroacetate in humans ranges from 5 to 10 mg/kg.
EPA believes that there is sufficient evidence for listing sodium
fluoroacetate on EPCRA section 313 pursuant to EPCRA section
313(d)(2)(B) based on the neurologic, reproductive, and myocardial
toxicity data for this chemical.
Measured oral LD<INF>50 values of fluoroacetate in the house
sparrow, redwinged blackbird, starling and golden eagle are 3.0, 4.22,
2.37, and 1.25 to 5 mg/kg, respectively. In addition, measured acute
toxicity data for mammalian wildlife include an oral LD<INF>50 of 0.22
to 0.44 mg/kg for mule deer, an oral LD<INF>50 of 1.41 mg/kg for male
ferrets, and an oral LD<INF>50 of 0.5 to 1.0 mg/kg for bears. EPA
believes that there is sufficient evidence for listing sodium
fluoroacetate on EPCRA section 313 pursuant to EPCRA section
313(d)(2)(C) based on the environmental toxicity data for this
chemical.
237. Sulfuryl fluoride (Vikane) (CAS No. 002699-79-8) (FIFRA AI)
(Ref. 3). The primary effects of sulfuryl fluoride in humans are
respiratory irritation and central nervous system depression, followed
by excitation and possibly convulsions. Rabbits exposed via inhalation
(6 hours/day, 5 days/week, for 2 weeks) to sulfuryl fluoride showed
hyperactivity, convulsions and vacuolation of the cerebrum at 600 ppm
(2.5 mg/L). Renal lesions were present in all rats exposed by
inhalation (6 hours/day, 5 days/week, for 2 weeks) to 600 ppm (2.5 mg/
L) sulfuryl fluoride. Minimal renal changes were noted in rats exposed
to 300 ppm (1252 mg/L), whereas no effects occurred at 100 ppm (4.2 mg/
L). Convulsions at near lethal concentrations were reported in rabbits,
mice, and rats. In a 30-day inhalation study, loss of control, tremors
of the hind quarters, and histopathological changes in the lung, liver,
and kidney were reported in rabbits exposed to 400 ppm (1.6 mg/L) for 7
hours/day, 5 days/week for 5 weeks. The NOEL was 200 ppm (0.83 mg/L).
Cerebral vacuolation and/or malacia and inflammation of nasal tissues
were observed in rabbits exposed by inhalation to 100 or 300 ppm (0.4
or 1.25 mg/L) for 13 weeks. The NOEL was 30 ppm (0.125 mg/L). Rats
exposed by inhalation to 100 to 600 ppm (0.4 to 0.25 mg/L) sulfuryl
fluoride for 13 weeks developed mottled teeth (indicative of fluoride
toxicity), renal and respiratory effects, and cerebral vacuolation. EPA
believes that there is sufficient evidence for listing sulfuryl
fluoride on EPCRA section 313 pursuant to EPCRA section 313(d)(2)(B)
based on the available neurological, renal, and respiratory toxicity
data for this chemical.
.
240. Tefluthrin (CAS No. 079538-32-2) (FIFRA AI) (Ref. 3). Delayed
ossification was seen in the offspring of rats administered 5 mg/kg/day
(LOEL) orally on days 7 through 16 of gestation. The NOEL was 3 mg/kg/
day.
In a 3-month rat study, dietary administration of 10 mg/kg/day
produced plasma, red blood cell, and brain cholinesterase inhibition.
The NOEL was 5 mg/kg/day. In a 6-month dog study, dietary
administration of 10 mg/kg/day (LOEL) produced plasma cholinesterase
inhibition. The NOEL was 1 mg/kg/day.
In a 21-day rat dietary study, administration of 20 mg/kg/day (LOEL
for females) produced decreased platelet counts, increased white blood
cell, lymphocyte, and neutrophil counts in males and females. The NOEL
for females was 5 mg/kg/day. Increased absolute and relative liver
weights were observed at 5 mg/kg/day in males, thus no NOEL could be
established for males. Dietary administration of 10 mg/kg/day (LOEL)
for 3 months to rats produced increased absolute liver weights,
decreased bilirubin levels, and hepatocellular hypertrophy. The NOEL
was 5 mg/kg/day. In a 6-month dog study, dietary administration of 10
mg/kg/day (LOEL) produced hepatotoxicity (effects not reported). The
NOEL was 1 mg/kg/day. In a 2-year mouse study, dietary administration
of 13.5 mg/kg/day produced liver necrosis. The NOEL was 3.4 mg/kg/day.
EPA believes that there is sufficient evidence for listing
tefluthrin on EPCRA section 313 pursuant to EPCRA section 313(d)(2)(B)
based on the available developmental, neurological, hepatic, and
hematological toxicity data for this chemical.
Aquatic acute toxicity values for tefluthrin include a rainbow
trout 96-hour LC<INF>50 of 0.06 ppb, a bluegill 96-hour LC<INF>50 of
0.13 ppb, a sheepshead minnow 96-hour LC<INF>50 of 0.13 ppb, a daphnid
48-hour EC<INF>50 of 0.07 ppb, and a mysid 96-hour EC<INF>50 of 0.053
ppb. EPA believes that there is sufficient evidence for listing
teflurin on EPCRA section 313 pursuant to EPCRA section 313(d)(2)(C)
based on the available environmental toxicity data for this chemical.
256. Tributyltin fluoride (CAS No. 001983-10-4) (FIFRA AI) (Ref.
3). Aquatic acute toxicity values for tributyltin fluoride include a
bleak fish 96-hour LC<INF>50 of 2.3 ppb, an algae 72-hour EC<INF>50 of
9.3 ppb, and a Harpacticoid copepod 96-hour LC<INF>50 of 0.8 ppb. EPA
believes that there is sufficient evidence for listing tributyltin
fluoride on EPCRA section 313 pursuant to EPCRA section 313(d)(2)(C)
based on the available environmental toxicity data.
IX. References
(1) U.S. Congress, House of Representatives. ``Conference Report
No. 962,'' 99th Cong., 2nd Session. 294 (1986).
(2) USEPA/OHEA. Risk Assessment Guidelines for Carcinogen Risk.
U.S. Environmental Protection Agency, Cincinnati, OH. (1987).
(3) 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).
(4) USEPA/OPPT. Issue Paper Prepared for the Public Meeting on
Expansion of the Toxic Release Inventory. U. S. Environmental
Protection Agency, Washington, DC (1993).
(5) USEPA/OPPT. Physical Properties and Environmental Fate of Some
TRI Expansion Chemicals. U. S. Environmental Protection Agency,
Washington, DC (1993).
(6) USEPA/OPPT. Revised Draft Hazard Assessment Guidelines for
Listing Chemicals on the Toxic Release Inventory. U. S. Environmental
Protection Agency, Washington, DC (1992).
(7) 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, D.C. (1993).
(8) USEPA/OPPT. Support Document for the Health and Ecological
Toxicity Review of TRI Expansion Chemicals. U. S. Environmental
Protection Agency, Washington, DC (1993).
List of Subjects in 40 CFR Part 372
Environmental protection, Community right-to-know, Reporting and
recordkeeping requirements, Toxic chemicals
Dated: January 6, 1994.
Carol M. Browner,
Administrator.
Therefore it is proposed that 40 CFR part 372 be amended to read as
follows:
Part 372--[AMENDED]
1. The authority citation for part 372 would continue 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 four categories to read as follows:
Sec. 372.65 Chemicals and chemical categories to which the part
applies.
* * * * *
(a) * * *
------------------------------------------------------------------------
Effective
Chemical Name CAS No. Date
------------------------------------------------------------------------
*******
Acifluorfen, sodium salt [5-(2-Chloro- 62476-59-9 1/1/95
4-(triflouromethyl)phenoxy)-2-nitro-
benzoic acid, sodium salt]
*******
Benfluralin (N-Butyl-N-ethyl-2,6- 1861-40-1 1/1/95
dinitro-4-
(trifluoromethyl)benzenamine)
*******
Bifenthrin 82657-04-3 1/1/95
Boron trifluoride 7637-07-2 1/1/95
p-Chloroaniline 106-47-8 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)
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]
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)
Diflubenzuron 35367-38-5 1/1/95
3,3'-Dimethylbenzidine 41766-75-0 1/1/95
dihydrofluoride (o-Tolidine
dihydrofluoride)
Dithiopyr [2-(Difluoromethyl)-4-(2- 97886-45-8 1/1/95
methylpropyl)-6-(trifluoromethyl)-
3,5-pyridinedicarbothioic acid S,S-
dimethyl ester]
Fluazifop-butyl [2-[4-[[5- 69806-50-4 1/1/95
(Trifluoromethyl)-2-pyridinyl]oxy]-
phenoxy]propanoic acid, butyl ester]
Flumetralin [2-Chloro-N-(2,6-dinitro- 62924-70-3 1/1/95
4-(trifluoromethyl)phenyl)-N-ethyl-6-
fluorobenzenemethanamine]
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]
Fomesafen [5-(2-Chloro-4- 72178-02-0 1/1/95
(trifluoromethyl)phenoxy)-N-
methylsulfonyl)-2-nitrobenzamide]
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]
Lactofen [5-(2-Chloro-4- 77501-63-4 1/1/95
(trifluoromethyl)phenoxy)-2-nitro-2-
ethoxy-1- methyl-2-oxoethyl ester]
Norflurazon [4-Chloro-5-(methylamino)- 27314-13-2 1/1/95
2-[3-(trifluoromethyl)phenyl]-3(2H)-
pyridazinone]
Oxyfluorfen 42874-03-3 1/1/95
Primisulfuron [Methyl 2-[[[[[4,6- 86209-51-0 1/1/95
bis(difluoromethoxy)-2-pyrimidinyl]-
amino]carbonyl]amino]sulfonyl]benzoa
te]
Sodium fluoroacetate 62-74-8 1/1/95
Sulfuryl fluoride [Vikane] 2699-79-8 1/1/95
Tefluthrin 79538-32-2 1/1/95
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)
Tributyltin fluoride 1983-10-4 1/1/95
51-21-8 Fluorouracil (5-Fluorouracil) 1/1/95
62-74-8 Sodium fluoroacetate 1/1/95
75-43-4 Dichlorofluoromethane (HCFC-21) 1/1/95
75-72-9 Chlorotrifluoromethane (CFC-13) 1/1/95
75-88-7 2-Chloro-1,1,1-trifluoroethane (HCFC- 1/1/95
133a)
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)
3
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)
507-55-1 1,3-dichloro-1,1,2,2,3- 1/1/95
pentafluoropropane (HCFC-225cb)
1861-40-1 Benfluralin(N-Butyl-N-ethyl-2,6- 1/1/95
dinitro-4-
(trifluoromethyl)benzenamine)
1983-10-4 Tributyltin fluoride 1/1/95
2699-79-8 Sulfuryl Fluoride [Vikane] 1/1/95
7637-07-2 Boron trifluoride 1/1/95
7782-41-4 Fluorine 1/1/95
27314-13-2 Norflurazon [4-Chloro-5-(methylamino)- 1/1/95
2-[3-(trifluoromethyl)phenyl]- 3(2H)-
pyridazinone]
35367-38-5 Diflubenzuron 1/1/95
42874-03-3 Oxyfluorfen 1/1/95
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]
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]
72178-02-0 Fomesafen [5-(2-Chloro-4- 1/1/95
(trifluoromethyl)phenoxy)-N-
methylsulfonyl)-2- nitrobenzamide]
77501-63-4 Lactofen [5-(2-Chloro-4- 1/1/95
(trifluoromethyl)phenoxy)-2-nitro-2-
ethoxy-1-methyl-2-oxoethyl ester]
79538-32-2 Tefluthrin
82657-04-3 Bifenthrin 1/1/95
86209-51-0 Primisulfuron [Methyl 2-[[[[[4,6- 1/1/95
bis(difluoromethoxy)-2-pyrimidinyl]-
amino]carbonyl]amino]sulfonyl]benzoa
te]
97886-45-8 Dithiopyr [2-(Difluoromethyl)-4-(2- 1/1/95
methylpropyl)-6-(trifluoro-methyl)-
3,5-pyridinedicarbothioic acid S,S-
dimethyl ester]
111512-56-2 1,1-dichloro-1,2,3,3,3- 1/1/95
pentafluoropropane (HCFC-225eb)
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)
------------------------------------------------------------------------
[FR Doc. 94-753 Filed 1-11-94; 3:34 pm]
BILLING CODE 6560-50-F