Wednesday
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
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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.
SUMMARY: EPA is proposing to add 313
chemicals and chemical categories to
tho 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
those 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
mooting will take place on March 2,
1994, at 1 p.m. and adjourn by 5 p.m.
ADDRESSES: Written comments should
bo submitted in triplicate to: OPPT
Docket Clerk, TSCA Document Receipt
Office (7407), Office of Pollution
Prevention and Toxics, Environmental
Protection Agency, Rm. E-G99,401M
St., SW., Washington, DC 20460.
Comments containing information
claimed as confidential must be clearly
marked as confidential business
information (CBI). If GDI 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, 401M
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, 401M 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)(l) 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 m 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
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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 H
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
VIE; (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 (LARC) 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
toxicitv 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^ the
petition in a proposed rulemaking on
September 8, 1992 (57 FR 41020) and in
a final rule adding 22 chemicals on
No%'ember 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 60 2 (b) of
the CAA as Class n 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 H.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
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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," "maybe 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 HI.
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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?
m. 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,
(n) neurological disorders,
(in) 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
H.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-
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specific factors. EPA believes that to
make the section 3l3(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. Sect/on 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
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Federal Register / Vol. 59, No. 8 / Wednesday, January 12, 1994 / Proposed Rules 1793
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.
1. Abamectin (Avermectin Bl) (CAS No.
071751-41-2)
2. Acephate (Acetylphosphoramidothioic
acid O,S-dimethyl ester) (CAS No. 030560-
19-1)
3. Acifluorfen sodium salt (5-(2-Chloro-4-
(triflouromethyl)phenoxy)-2-nitro-benzoic
acid, sodium salt) (CAS No. 062476-59-9)
4. Alachlor (CAS No. 015972-60-8)
5. Aldicarb (CAS No. 000116-06-3)
6. d-trans-Allethrin [d-trans-Chrysanthemic
acid of d-allethrone] (CAS No. 028057-48-9)
7. Allylamine (CAS No. 000107-11-9)
8. Aluminum phosphide (CAS No. 020859-
73-8)
9. Ametryn (N-Ethyl-N'-(l-methylethyl)-6-
(methylthio)-l,3,5,triazine- 2,4 diamine)
(CAS No. 000834-12-8)
10. Amitraz (CAS No. 033089-61-1)
11. Anilazine (4,6-Dichloro-N-(2-
chlorophenyl)-! ,3,5-triazin-2-amine) (CAS
No. 000101-05-3)
12. Atrazine (6-Chloro-N-ethyl-N'-(l-
methylethyl)-l,3,5,triazine-2,4-diamme)
(CAS No. 001912-24-9) -
13. Bendiocarb (2,2-Dimethyl-l,3-
benzodioxol-4-ol methylcarbamate) (CAS No.
022781-23-3)
14. Benfluralin (N-Butyl-N-ethy 1-2,6-
dinitro-4-(trifluoromethyl) benzenamine)
(CAS No. 001861-40-1)
15. Benomyl (CAS No. 017804-35-2)
16. o-Benzyl-p-chlorophenol (CAS No.
000120-32-1)
17. Bifenthrin (CAS No. 082657-04-3)
18. Bis(tributyltin) oxide (CAS No. 000056-
35-9)
19. Boron trichloride (CAS No. 010294-34-
5)
20. Boron trifluoride (CAS No. 007637-07-
2)
21. Bromacil (5-Bromo-6-methyl-3-(l-
methylpropyl)-2,4-(lH,3H)-pyrimidinedione)
(CAS No. 000314-40-9)
22. Bromacil lithium salt (2,4-(lH,3H)-
Pyrimidinedione, 5-bromo-6-methyl-3-(l-
methylpropyl), lithium salt) (CAS No.
053404-19-6)
23. Bromine (CAS No. 007726-95-6)
24. l-Bromo-l-(bromomethyl)-l,3-
propanedicarbonitrile (CAS No. 035691-65-7)
25. 2-Bromo-2-nitropropane-l,3-diol
(Bronopol) (CAS No. 000052-51-7)
26. Bromoxynil (3,5-Dibromo-4-
hydroxybenzonitrile) (CAS No. 001689-84-5)
27. Bromoxynil octanoate (Octanoic acid,
2,6-dibromo-4-cyanophenyl ester) (CAS No.
001689-99-2)
28. Brucine (CAS No. 000357-57-3)
29. Butylate (Bis-2-
methylpropyljcarbamothioic acid S-ethyl
ester) (CAS No. 002008-41-5)
30. Butylated hydroxyanisole (CAS No.
025013-16-5)
31. C.I. Acid Red 114 (CAS No. 006459-94-
5)
32. C.I. Direct Blue 218 (CAS No. 028407-
37-6)
33. Calcium hypochlorite (CAS No.
007778-54-3)
34. Caprolactam (CAS No. 000105-60-2)
35. Carbofuran (CAS No. 001563-66-2)
36. Carbon monoxide (CAS No. 000630-08-
0)
37. Carboxin (5,6-Dihydro-2-methyl-N-
phenyl-1,4-oxathiin-3-carboxamide) (CAS
No. 005234-68-4)
38. Chinomethionat (6-Methyl-l,3-
dithiolo[4,5-b]quinoxalin-2-one) (CAS No.
002439-01-2)
39. Chlorendic acid (CAS No. 000115-28-
6)
40. Chlorimuron ethyl (Ethyl-2-[[[(4-chloro-
6-methoxyprimidin-2-yl)-carbonyl]-
amino]sulfonyl]benzoate) (CAS No. 090982-
32-4)
41. Chlorinated paraffins
42. l-(3-Chloroallyl)-3,5,7-triaza-l-
azoniaadamantane chloride (CAS No,
004080-31-3)
43. p-Chloroaniline (CAS No. 000106-47-8)
44. 5-Chloro-2-(2,4-
dichlorophenoxyjphenol (CAS No. 003380-
34-5)
45. 3-Chloro-2-methyl-l-propene (CAS No.
000563-47-3)
46. p-Chlorophenyl isocyanate (CAS No.
000104-12-1)
47. Chloropicrin (CAS No. 000076-06-2)
48. 3-Chloropropionitrile (CAS No.
000542-76-7)
49. p-Chloro-o-toluidine (CAS No. 000095-
69-2)
50. Chlorotrifluoromethane (CFC-13) (CAS
No. 000075-72-9)
51. Chlorpyrifos methyl (O.O-Dimethyl-O-
(3,5,6-trichloro-2-pyridyl)phosphorothioate)
(CAS No. 005598-13-0)
52. Chlorsulfuron (2-Chloro-N-[[(4-
methoxy-6-methyl-l,3,5-triazin-2-
yl)amino]carbonyl]benzenesulfonamide)
(CAS No. 064902-72-3)
53. Clomazone (2-[(2-
Chlorophenyl)methyl]-4,4-dimethyl-3-
isoxazolidinone) (CAS No. 081777-89-1)
54. Crotonaldehyde (CAS No. 004170-30-3)
55. Cyanazine (CAS No. 021725-46-2)
56. Cycloate (CAS No. 001134-23-2)
57. Cyclohexanol (CAS No. 000108-93-0)
58. Cyfluthrin (3-(2,2-Dichloroethenyl)-2,2-
dimethylcyclopropanecarboxylicacid,
cyano(4-fluoro-3-phenoxyphenyl)methyl
ester) (CAS No. 068359-37-5)
59. Cyhalothrin (3-(2-Chloro-3,3,3-
trifluoro-l-propenyl)-2,2-
dimethylcyclopropanecarboxylicacid
cyano(3-phenoxyphenyl)methyl ester) (CAS
No. 068085-85-8)
60. Cyromazine (N-Cyclopropyl-1,3,5-
triazine-2,4,6-triamine) (CAS No. 066215-27-
8)
61. Dazomet (Tetrahydro-3,5-dimethyl-2H-
l,3,5-thiadiazine-2-thione) (CAS No. 000533-
74-4)
62. Dazomet, sodium salt (2H-1,3,5-
Thiadiazine-2-thione, tetrahydro-3,5-
dimethyl-, ion(l-), sodium) (CAS No. 053404-
60-7)
63. 2,4-DB (CAS No. 000094-82-6)
64. 2,4-D butoxyethyl ester (CAS No.
001929-73-3)
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1794
Federal Register / Vol. 59, No. 8 / Wednesday, January 12, 1994 / Proposed Rules
65.2,4-D butyl ester (CAS No. 000094-80-
4)
66.2,4-D chlorocrotyl ester (CAS No.
002971-38-2)
67. Desmedipham (CAS No. 013684-56-5)
68. 2,4-D 2-othylhexyl ester (CAS No.
001928-43-4)
69. 2,4-D 2-ethyl-4-mDthylpentyl ester
(CAS No. 053404-37-8)
70. DIazinon (CAS No. 000333-41-5)
71.2,2-Dibromo-3-nitrilopropionamide
(CAS No. 010222-01-2)
72. Dicamba (3,6-Dichloro-2-
mcthyoxybenzoic acid) (CAS No. 001918-00-
9}
73. Dichloran (2,6-Dichloro-4-nitroaniline)
(CAS No. 000099-30-9)
74. 3,3'-Dichlorobenzidine dihydrochloride
(CAS No. 000612-83-9)
75.3,3'-Dlchlorobenzidine sulfate (CAS
No. 064969-34-2)
76. trans-l,4-D5chloro-2-butene (CAS No.
000110-57-6)
77. DIchloromethylphenylsilane (CAS No.
000149-74-6)
78. DIchloropheno (2,2'-Methylenebis(4-
chlorophenol) (CAS No. 000097-23-4)
79. trans-l,3-Dichloropropene (CAS No.
010061-02-6)
80. Didofop methyl (2-[4-(2,4-
Dichlorophenoxy) phenoxylpropanoic acid,
methyl ester) (CAS No. 051338-27-3)
81. Dicydopentadiene (CAS No. 000077-
73-6)
82. Diethatyl ethyl (CAS No. 038727-55-8)
83. Diflubenzuron (CAS No. 035367-38-5)
84. Diglycidyl resorcinol ether (CAS No.
000101-90-6)
85. Dimethipin (2,3,-Dihydro-5,6-dimethyl-
1,4-dithiin 1,1,4,4-tetraoxide) (CAS No.
055290-64-7)
86. Dimethoate (CAS No. 000060-51-5)
87. 3,3'-Dimethoxybenzidine
dlhydrochlorido (o-Dianisidino
dihydrochloride) (CAS No. 020325-40-0)
88. 3.3'-Dlraelhoxybenzidino
hydrochlorido (o-Dianisidine hydrochloride)
(CAS No. 111984-09-9)
89. Diraethylamine (CAS No. 000124-40-3)
90. Dimothylamine dicamba (CAS No.
002300-66-5)
91. 3,3'-Dimethylbenzidine
dihydrochloride (c-Tolidine
dihydrochlorido) (CAS No. 000612-82-8)
92.3,3'-Dimethylbenzidine
dihydrofluorido (o-Tolidine dihydrofluoride)
(CAS No. 041766-75-0)
93. Dimethyl chlorothiophosphate (CAS.
No. 002524-03-0)
94. Dimethyldichlorosilane (CAS No.
000075-78-5)
95. N,N-DImethylfonnamide (CAS No.
000068-12-2)
96.2,6-Dimethylphenol (CAS No. 000576-
26-1)
97. Dinocap (CAS No. 039300-45-3)
98. Dinoscb (CAS No. 000088-85-7)
99. Diphenamid (CAS No. 000957-51-7)
100. Diphenylamine (CAS No. 000122-39-
4)
101. Dipotassium endothall (7-
Oxab!cyck>(2.2.1)heptane-213-dicarboxylic
add, dipotassium salt) (CAS No. 002164-07-
0)
102. Dipropyl isocinchomeronate (CAS No.
000136-45-8)
103. Disodium cyanodithioimidocaibonate
(CAS No. 000138-93-2)
104. 2,4-D isopropyl ester (CAS No.
000094-11-1)
105. 2,4-Dithiobiuret (CAS No. 000541-53-
7)
106. Dithiopyr (2-(Difluoromethyl)-4-(2-
methylpropyl)-6-(trifluoromethyl)-3,5-
pyridinedicarbothioic acid S,S-dimethyl
ester) (CAS No. 097886-45-8)
107. Diuron (CAS No. 000330-54-1)
108. 2,4-D 2-octyl ester (CAS No. 001917-
97-1)
109. Dodine (Dodecylguanidine
mohoacetate) (CAS No. 002439-10-3)
110. 2,4-DP (Dichlorprop) (CAS No.
000120-36-5)
111. 2,4-D propylene glycol butyl ether
ester (CAS No. 001320-18-9)
112. 2,4-D sodium salt (CAS No. 002702-
72-9)
113. Ethoprop (Phosphorodithioic acid O-
ethyl S,S-dipropyl ester) (CAS No. 013194-
48-4)
114. Ethyl dipropylthiocarbamate (EPTC)
(CAS No. 000759-94-4)
115. Famphur (CAS No. 000052-85-7)
116. Fenarimol (.alpha.-(2-Chlorophenyl)-
.alpha.-4-chlorophenyl)-5-
pyrimidinemethanol) (CAS No. 060168-88-9)
117. Fenbutatin oxide (hexakis(2-methyl-2-
phenylpropyl)distannoxane) (CAS No.
013356-08-6)
118. Fenoxaprop ethyl (2-(4-((6-Chloro-2
benzoxazolylen)oxy)phenoxy)propanoicacid,
ethyl ester) (CAS No. 066441-23-4)
119. Fenoxycarb (2-(4-
Phenoxyphenoxy)ethyl]carbamic acid ethyl
ester) (CAS No. 072490-01-8)
120. Fenpropathrin (2,2,3,3-
Tetramethylcyclopropane carboxylic acid
cyano(3-phenoxyphenyl)methyl ester) (CAS
No. 039515-41-8)
121. Fenthion (O.O-Dimethyl O-[3-methyl-
4-(methylthio) phenyl] ester,
phosphorothioic acid) (CAS No. 000055-38-9)
122. Fenvalerate (4-Chloro-alpha-(l-
methylethyljbenzeneacetic acid cyano(3-
phenoxyphenyl)methyl ester) (CAS No.
051630-58-1)
123. Ferbam
(Tris(dimethylcarbamodithioato-S,S')iron)
(CAS No. 014484-64-1)
124. Fluazifop butyl (2-[4-[[5-
(Trifluoromethyl)-2-pyridinyl]oxy]-
phenoxylpropanoic acid, butyl ester) (CAS
No. 069806-50-4)
125. Flumetralin (2-Chloro-N-(2,6-dinitro-
4-(trifluoromethyl)phenyl)-N-ethyl-6-
fluorobenzenemethanamine) (CAS No.
062924-70-3)
126. Fluorine (CAS No. 007782-41-4)
127. Fluorouracil (5-Fluorouracil) (CAS
No. 000051-21-8)
128. Fluvalinate (N-[2-Chloro-4-
(trifluoromethyl)phenyl]-DL-valine(+)-cyano
(3-phenoxyphenyl)methyl ester) (CAS No.
069409-94-5)
129. Folpet (CAS No. 000133-07-3)
130. Fomesafen (5-(2-Chloro-4-
(trifluoromethyl)phenoxy)-N
methylsulfonyl)-2-nitrobenzamide) (CAS No.
072178-02-0)
131. alpha-Hexachlorocyclohexane (CAS
NO. 000319-84-6)
132. Hexamethylene-l,6-diisocyanate (CAS
No. 000822-60-0)
133. n-Hexane (CAS No. 000110-54-3)
134. Hexazinone (CAS No. 051235-04-2)
135. Hydramethymon (Tetrahydro-5,5-
dimethyl-2(lH)pyrimidinone[3-[4-
(trifluoromethyl)phenyl]-l-[2-
[4(trifluoromethyl)phenyl]ethenyl]-2
propenylidenejhydrazone) (CAS No. 067485-
29-4)
136—151. Hydrochlorofluorocarbons,
specifically:
136. Dichloropentafluoropropane (CAS No.
127564-92-5)
137. l,3-Dichloro-l,l,2,3,3-
pentafluoropropane (HCFC-225ea) (CAS No.
136013-79-1)
138. 2,2-Dichloro-l,l,l,3,3-
pentafluoropropane (HCFC-225aa) (CAS No.
128903-21-9)
139. l,l-Dichloro-l,2,3,3,3-
pentafluoropropane (HCFC-225eb) (CAS No.
111512-56-2)
140. l,l-Dichloro-l,2,2,3,3-
pentafluoropropane (HCFC-225cc) (CAS No.
13474-88-9)
141. l,3-Dichloro-l,l,2,2,3-
pentafluoropropane (HCFC-225cb) (CAS No.
000507-55-1)
142. l,2-Dichloro-l,l,3,3,3-
pentafluoropropane (HCFC-225da) (CAS No.
000431-86-7)
143. 3,3-Dichloro-l,l,l,2,2-
pentafluoropropane (HCFC-225ca) (CAS No.
000422-56-0)
144. 2,3-Dichloro-l,l,l,2,3-
pentafluoropropane (HCFC-225ba) (CAS No.
000422-48-0)
145. l,2-Dichloro-l,l,2,3,3-
pentafluoropropane (HCFC-225bb) (CAS No.
000422-44-6)
146. Dichlorofluoromethane (HCFC-21)
(CAS No. 000075-43-4)
147. l,l,l,2-Tetrachloro-2-fluoroethane
(HCFC-121a) (CAS No. 000354-11-0)
148.1,1,2,2-Tetrachloro-l-fluoroethane
(HCFC-121) (CAS No. 000354-14- 3)
149. l,2-Dichloro-l,l-difluoroethane
(HCFC-132b) (CAS No. 001649-08-7)
150. 2-Chloro-l,l,l-trifluoroethane (HCFC-
133a) (CAS No. 000075-88-7)
151. 3-Chloro-l,l,l-trifluoropropane
(HCFC-253fb) (CAS No. 000460-35-5)
152. Imazalil (l-[2-(2,4-Dichlorophenyl)-2-
(2-propenyloxy)ethyljlH-imidazole)(CAS
No. 035554-44-0)
153. 3.-Iodo-2-propynyl butylcarbamate
(CAS No. 055406-53-6)
154. Iprodione (3-(3,5-Dichlorophenyl)-N-
(l-methylethyl)-2,4-dioxo-l-
imidazolidinecarboxamide) (CAS No.
036734-19-7)
155. Iron pentacarbonyl (CAS No. 013463-
40-6)
156. Isodrin (CAS No. 000465-73-6)
157. Isofenphos (2-[[Ethoxyl[(l-
methylethyl)
amino]phosphinothioyl]oxy]benzoic acid 1-
methylethyl ester) (CAS No. 025311-71-1)
158. Isophorone (CAS No. 000078-59-1)
159. Isophorone diisocyanate (CAS No.
004098-71-9)
160. Lactofen (5-(2-Chloro-4-
(trifluoromethyl)phenoxy)-2-nitro-2-ethoxy-
l-methyl-2-oxoethyl ester) (CAS No. 077501-
63-4)
161. Linuron (CAS No. 000330-55-2)
162. Lithium carbonate (CAS No. 000554-
13-2)
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1795
163. Malathion (CAS No. 000121-75-5)
164. Man-made mineral fibers
165. Mecoprop (CAS No. 000093-65-2)
166. 2-Mercaptobenzothiazole (MBT) (CAS
No. 000149-30-4)
167. Merphos (CAS No. 000150-50-5)
168. Metham sodium (Sodium
methyldithiocarbamate) (CAS No. 000137-42-
8)
169. Methazole (2-(3,4-Dichlorophenyl}-4-
methyl-l,2,4-oxadiazolidine-3,5-dione) (CAS
No. 020354-26-1)
170. Methiocarb (CAS No. 002032-65-7)
171. Methoxone ((4-Chloro-2-
methylphenoxy) acetic acid) (MCPA) (CAS
No. 000094-74-6)
172. Methoxone sodium salt ((4-Chloro-2-
methylphenoxy) acetate sodium salt) (CAS
No. 003653-48-3)
173. l,l-Methylenebis(4-
isocyanatocyclohexane) (CAS No. 005124-30-
1)
174. Methylene bis(thiocyanate) (CAS No.
006317-18-6)
175. Methyl isothiocyanate (CAS No.
00556-61-6)
176. 2-Methyllactonitrile (CAS No. 000075-
86-5)
177. N-Methylolacrylamide (CAS No. -
000924-42-5)
178. Methyl parathion (CAS No. 000298-
00-0)
179. N-Methyl-2-pyrrolidone (CAS No.
000872-50-4)
180. Methyltrichlorosilane (CAS No.
000075-79-6)
181. Metiram (CAS No. 009006-42-2)
182. Metribuzin (CAS No. 021087-64-5)
183. Mevinphos (CAS No. 007786-34-7)
184. Molinate (IH-Azepine-l-carbothioic
acid, hexahydro-S-ethyl ester) (CAS No.
002212-67-1)
185. Monuron (CAS No. 000150-68-5)
186. Myclobutanil (.alpha.-Butyl-.alpha.-(4-
chlorophenyl)-lH-l,2,4-triazole-l-
propanenitrile) (CAS No. 088671-89-0)
187. Nabam (CAS No. 000142-59-6)
188. Naled (CAS No. 000300-76-5)
189. Nicotine and salts
190. Nitrapyrin (2-Chloro-6-
(trichloromethyl) pyridine) (CAS No. 001929-
82-4)
191. Nitrate ion (CAS No. 014797-55-8)
192. Nitric oxide (CAS No. 010102-43-9)
193. p-Nitroaniline (CAS No. 000100-01-6)
194. Nitrogen dioxide (CAS No. 010102-44-
0)
195. Norflurazon (4-Chloro-5-
(methylamino)-2-[3(trifluoromethyl)phenylJ-
3(2H)-pyridazinone) (CAS No. 027314-13-2)
196. Oryzalin (4-(Dipropylamino)-3,5-
dinitrobenzenesulfonamide) (CAS No.
019044-88-3)
197. Oxydemeton methyl (S-(2-
(Ethylsulfinyl)ethyl) O,O-dimethyl ester
phosphorothioic acid) (CAS No. 000301-12-2)
198. Oxydiazon (3-l2,4-Dichloro-5-(l-
methylethoxy)phenyl]-5(l,l-dimethylethyl)-
l,3,4-oxadiazol-2(3H)-one) (CAS No. 019666-
30-9)
199. Oxyfluorfen (CAS No. 042874-03-3)
200. Ozone (CAS No. 010028-15-6)
201. Paraquat dichloride (CAS No. 001910-
42-5)
202. Pebulate (Butylethylcarbamothioic
acid S-propyl ester) (CAS No. 001114-71-2)
203. Pendimethalin (N-(l-Ethylpropyl)-3,4-
dimethyl-2,6-dinitrobenzenamine) (CAS No.
040487-42-1)
204. Pentobarbital sodium (CAS No.
000057-33-0)
205. Perchloromethyl mercaptan (CAS No.
000594-42-3)
206. Permethrin (3-(2,2-Dichloroethenyl)-
2,2-dimethylcyclopropanecarboxylic acid, (3-
phenoxyphenyl)methyl ester) (CAS No.
052645-53-1)
207. Phenanthrene (CAS No. 000085-01-8)
208. Phenothrin (2,2-Dimethyl-3-(2-methyl-
1-propenyl) cyclopropanecarboxylic acid (3-
phenoxyphenyl)methyl ester) (CAS No.
026002-80-2)
209.1,2-Phenylenediamine (CAS No.
000095-54^5)
210.1,3-Phenylenediamine (CAS No.
000108-45-2)
211.1,2-Phenylenediamine
dihydrochloride (CAS No. 000615-28-1)
212.1,4-Phenylenediamine
dihydrochloride (CAS No. 000624-18-0)
213. Phenytoin (CAS No. 000057-41-0)
214. Phosphine (CAS No. 007803-51-2)
215. Phosphorus oxychloride (CAS No.
010025-87-3)
216. Phosphorus pentachloride (CAS No.
010026-13-8)
217. Phosphorus pentasulfide (CAS No.
001314-80-3)
218. Phosphorus pentoxide (CAS No.
001314-56-3)
219. Picloram (CAS No. 001918-02-1)
220. Piperonyl butoxide (CAS No. 000051-
03-6)
221. Pirimiphos methyl (O-(2-
(Diethylamino)-6-rnethyl-4-pyrimidinyl)-O,O-
dimethyl phosphorothioate) (CAS No.
029232-93-7)
222— 249. Polycyclic aromatic compounds
(PACs) including:
222. Benz(a)anthracene (CAS No. 000056-
55-3)
223. Benzo(a)phenanthrene (CAS No.
000218-01-9)
224. Benzo(a)pyrene (CAS No. 000050-32-
8)
225. Benzo(b)fluoranthene (CAS No.
000205-99-2)
226. Benzo(j)fluoranthene (CAS No.
000205-82-3)
227. Benzo(k)fluoranthene (CAS No.
000207-08-9)
228. Benzo(rst)pentaphene (CAS No.
000189-55-9)
229. Carbazole (CAS No. 000086-74-8)
230. Cyclopenta(cd)pyrene (CAS No.
027208-37-3)
231. Dibenz(a,h)acridine (CAS No. 000226-
36-8)
232. Dibenz(a,j)acridine (CAS No. 000224-
42-0)
233. Dibenz(a,c)anthracene (CAS No.
000215-58-7)
234. Dibenz(a,j)anthracene (CAS No.
000224-41-9)
235. Dibenzo(a,h)anthracene (CAS No.
000053-70-3)
236. Dibenzo(a,e)fluoranthene (CAS No.
005385-75-1)
237. Dibenzo(a,e)pyrene (CAS No. 000192-
65-4)
238. Dibenzo(a,h)pyrene (CAS No. 000189-
64-0)
239. Dibenzo(a,l)pyrene (CAS No. 000191-
30-0)
240. 7H-Dibenzo(c,g)carbazole (CAS No.
000194-59-2)
241. 7,12-Dimethylbenz(a)anthracene (CAS
No. 000057-976)
242. Indeno[l,2,3-cd]pyrene (CAS No.
000193-39-5)
243. 2-Methylchrysene (CAS No. 003351-
32-4)
244. 3-Methylchrysene (CAS No. 003351-
31-3)
245. 4-Methylchrysene (CAS No. 003351-
30-2)
246. 5-Methylchrysene (CAS No. 003697-
24-3)
247. 6-Methylchrysene (CAS No. 001705-
85-7)
248. 2-Methylfluoranthene (CAS No.
033543-31-6)
249.1-Nitropyrene (CAS No. 005522-43-0)
250. Potassium bromate (CAS No. 007758-
01-2)
251. Potassium dimethyldithiocarbamate
(CAS No. 000128-03-0)
252. Potassium N-methyldithiocarbamate
(CAS No. 000137-41-7)
253. Primisulfuron (Methyl 2-[[[[[4,6-
bis(difluoromethoxy)-2pyrimidinyl]-
amino]carbonyl]amino]sulfonyl]benzoate)
(CAS No. 086209-51-0)
254. Profenofos (O-(4-Bromo-2-
chlprophenyl)-O-ethyl-S-propyl
phosphorothioate) (CAS No. 041198-08-7)
255. Prometryn (N,N'-Bis(l-methylethyl)-6-
methylthio-l,3,5-triazine-2,4-diamine) (CAS
No. 007287-19-6)
256. Propachlor (2-Chloro-N-(l-
methylethyl)-N-phenylacetamide) (CAS No.
001918-16-7)
257. Propanil (N-(3,4-
Dichlorophenyl)propanamide) (CAS No.
000709-98-8)
258. Propargite (CAS No. 002312-35-8)
259. Propargyl alcohol (CAS No. 000107-
19-7)
260. Propetamphos (3-
[(Ethylamino)methoxyphosphinothioyl]oxy]-
2-butenoic acid, 1-methylethyl ester) (CAS
No. 031218-83-4)
261. Propiconazole (l-[2-(2,4-
Dichlorophenyl)-4-propyl-l,3-dioxolan-2-yl]-
methyl-lH-l,2,4,-triazole) (CAS No. 060207-
90-1)
262. Quizalofop-ethyl (2-[4-[(6-Chloro-2-
quinoxalinyl) oxylphenoxy] propanoic acid
ethyl ester) (CAS No. 076578-14-8)
263. Resmethrin ([5-(Phenylmethyl)-3-
furanyl]methyl 2,2-dimethyl-3-(2-methyl-l-
propenyl) cyclopropanecarboxylate]) (CAS
No. 010453-86-8)
264. Sethoxydim (2-[l-
(Ethoxyimino)butyl]-5-[2(ethylthio)propyl]-3-
hydroxyl-2-cyclohexen-l-one) (CAS
No.074051-80-2)
265. Simazine (CAS No. 000122-34-9)
266. Sodium azide (CAS No. 026628-22-8)
267. Sodium chlorite (CAS No. 007758-19-
2)
268. Sodium dicamba (3,6-Dichloro-2-
methoxybenzoic acid, sodium salt) (CAS No.
001982-69-0)
269. Sodium dimethyldithiocarbamate
(CAS No. 000128-04-1)
270. Sodium fluoroacetate (CAS. No.
000062-74-8)
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Federal Register / Vol. 59, No. 8 / Wednesday, January 12, 1994 / Proposed Rules
271. Sodium hypochlorite (CAS No.
007681-52-9)
272. Sodium nitrite (CAS No. 007632-00-0)
273. Sodium pentachlorophenate (CAS No.
000131-52-2)
274. Sodium o-phonylphenoxide (CAS No.
000132-27-4)
275, Sodium 2-pyridinethiol-l-oxide (CAS
No. 015922-78-8)
276. Strychnine and salts
277. Sulfur dioxide (CAS No. 007446-09-5)
278. Sulfur trioxide (CAS No. 007446-11-
9)
279. Sulfuryl fluoride (Vikane) (CAS No.
002699-79-8)
280. Sulprofos (O-Ethyl O-[4-
(mcthylth!o)phenyl]phosphorodithioicacid
S- propyl estor) (CAS No. 035400-43-2)
281. Tebuthiuron (N-[S-(1,1-
Dlmethylcthyl)-l,3,4-thiadiazol-2-yl)-N,N>-
dimethylurea) (CAS No. 034014-18-1)
282. Tofluthrin (CAS No. 079538-32-2)
283. Tomcphos (CAS No. 003383-96-8)
284. Terbacil (5-Chloro-3-(l.l-
dImothylethyl)-6-methyl-2,4-(lH,3H)-
pyrlmldlnedione) (CAS No. 005902-51-2)
285. Tetracyclino hydrochloride (CAS No.
000064-75-5)
286. Tctramothrin (2,2-Dimethyl-3-(2-
methyl-1-propenyl) cyclopropanecarboxylic
aeld(l,3,4,5,6,7-hexahydro-l,3-dioxo-2H-
isoIndol-2-yl)methyl ester) (CAS No. 007696-
12-0)
287. Tetrasodium
cthylcnediaminetotraacetate (CAS No.
000054-02-8)
288. Thiabendazole (2-(4-Thiazolyl)-lH-
bcnzlmldazole) (CAS No. 000148-79-8)
289. Thiabendazole, hypophosphite salt (2-
(4-ThiazoIyl) benzimidazole, hypophosphite
salt) (CAS No. 028558-32-9)
290. Thiobencarb (Carbamic acid,
diethylthio-, S-(p-chlorobenzyl)) (CAS No.
028249-77-6)
291. Thlodicarb (CAS No. 059669-26-0)
292. Thiophanate ethyl ([1,2-Phenylenebis
(iminocarbonothioyl)] biscarbamic acid
diethyl ester) (CAS No. 023564-06-9)
293. Thiophanate-methyl (CAS No.
023564-05-8)
294. Thlosemicaibazide (CAS No. 000079-
19-6)
295, Triadimofon (l-(4-Chlorophenoxy)-
3,3-dimethyl-l-(lH-l,2,4-triazol-l-yl)-2-
butanone) (CAS No. 043121-43-3)
296. Triallate (CAS No. 002303-17-5)
297. Tribenuron methyl (2-(((((4-Methoxy-
6-methyl-l,3,5-triazin-2-yl)-
mothylamino)carbonyl)amino)sulfonyl)-,
methyl estor) (CAS No. 101200-48-0)
298. Tributyltin fluoride (CAS No. 001983-
10-4)
299. Tributyltin methacrylate (CAS No.
002155-70-6)
300. S,S,S-Trlbutyltrithiophosphate (DBF)
(CAS No. 000078-48-8)
301. Trichloroacetyl chloride (CAS No.
000076-02-8)
302.Trichloroethylsilane (CAS No.
000115-21-9)
303. Trichlorophenylsilane (CAS No.
000098-13-5)
304.1,2,3-Trichloropropane (CAS No.
000096-18-4)
305. Triclopyr triethylammonium salt
(CAS No. 057213-69-1)
306. Triethylamine (CAS No. 000121-44-8)
307. Triforine (N,N'-[1,4-
Piperazinediylbis(2,2,2-trichloroethylidene)]
bisformamide) (CAS No. 026644-46-2)
308. Trimethylchlorosilane (CAS No.
000075-77-4)
309. 2,3,5-Trimethylphenyl
methylcarbamate (CAS No. 002655-15-4)
310. Triphenyltin chloride (CAS No.
000639-58-7)
311. Triphenyltin hydroxide (CAS No.
000076-87-9)
312. Vanadium pentoxide (CAS No.
001314-62-1)
313. Vinclozolin (3-(3,5-Dichlorophenyl)-5-
ethenyl-5-methyl-2,4-oxazolidinedione) (CAS
No. 050471-44-8)
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
1. Abamectin (avermectin Bl) (CAS
No. 071751-41-2) (FIFRA AI) (Ref. 3).
This compound induces developmental
toxicity in several species with the
mouse being the most sensitive species.
Increased retinal folds in weanlings,
decreased viability and lactation
indices, and decreased body weight
were noted in a two-generation rat
reproduction study. The lowest-
observed-effect level (LOEL) was 0.4
milligram per kilogram per day (mg/kg/
day) and the no-observed-effect level
(NOEL) was 0.12 mg/kg/day. Based on
the NOEL, EPA derived a reference dose
(RfD) of 0.0004 mg/kg/day. EPA believes
that there is sufficient evidence for
listing abamectin on EPCRA section 313
pursuant to EPCRA section 313(d)(2)(B)
based on the available developmental
toxicity data.
Aquatic acute toxicity values for
abamectin include a bluegill 96-hour
LCso of 9.6 parts per billion (ppb), a
rainbow trout 96-hour LCso of 3.6 ppb,
and a daphnid 48-hour LCso of 0.34
ppb. EPA believes that there is sufficient
evidence for listing abamectin on
EPCRA section 313 pursuant to EPCRA
section 313(d)(2)(C) based on the
available environmental toxicity data.
2. Acephate
(acetylphosphoramidothioic acid O,S-
dimethyl ester) (CAS No. 030560-19-1)
(FIFRA AI) (Ref. 3). In a 28-month
feeding study in rats, inhibition of brain,
plasma, and red blood cell
cholinesterase activities was observed at
50 parts per million (ppm) (2.5 mg/kg/
day). The NOEL for this study was 5
ppm (0.25 mg/kg/day). Similar findings
were noted in a 2-year feeding study in
dogs. The LOEL for this study was 100
ppm (2.5 mg/kg/day) and the NOEL was
30 ppm (0.75 mg/kg/day). EPA believes
that there is sufficient evidence for
listing acephate on EPCRA section 313
pursuant to EPCRA section 313(d)(2)(B)
based on the available neurotoxicity
data for this chemical.
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
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Federal Register / Vol. 59, No. 8 7 Wednesday, January 12, 1994 / Proposed Rules 1797
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.
4. ;WacMor(CASNo. 015972-60-8)
(FIFRA SR) (Ref. 8). Alachlor is an
aniline-type herbicide. Dose-related
hemolytic anemia with reductions in
red blood cell counts, hematocrit and
hemoglobin, as well as hemosiderosis in
the liver, spleen and kidney occurred in
male dogs orally exposed to alachlor for
1—year. The LOEL based on these effects
was 3.0 mg/kg/day, and the NOEL was
1.0 mg/kg/day. Effects in female dogs in
the same study were not demonstrated
as clearly as in males but were
considered suggestive of anemia. EPA
derived an oral RfD of 0.01 mg/kg/day
from this study.
In a three-generation reproduction
study in rats, chronic nephritis and
increased relative and absolute kidney
weights were reported in F2 adult males
and F3 pups. The LOEL was 10 mg/kg/
day, and the NOEL was 3 mg/kg/day.
Rabbits (Dutch Belted strain) that
received alachlor via oral gavage during
gestation days 6 to 27 had an increased
rate of preimplantation loss (49 percent)
and offspring with increased incidences
of developmental malformations
including major vessel variations,
presacral vertebrae, and rudimentary
and full 13th ribs. The increased
incidence of rudimentary and full 13th
ribs was dose-related, and a lowest-
observed-adverse-effect level (LOAEL)
of 10 mg/kg/day was determined based
on this effect. The no-observed-adverse
effect level (NOAEL) was not
determined.
EPA has classified alachlor as a
category Group B2 compound, i.e., the
chemical is a probable human
carcinogen. In a 2—year rat feeding study
with Long-Evans rats, there were
increased incidences of nasal turbinate
tumors, malignant stomach tumors and
thyroid follicular adenomas and
carcinomas in both sexes at doses
greater than or equal to 42 mg/kg/day.
In an 18-month study in female CD-I
mice, bronchiolar tumors occurred at an
increased incidence at 200 mg/kg/day.
EPA believes that there is sufficient
evidence for listing alachlor on EPCRA
section 313 pursuant to EPCRA section
313(d)(2)(B) based on the chronic
toxicity and carcinogenicity data for this
chemical.
5. Aldicarb (CAS No. 000116-06-3)
(CERCLA; EPCRA EHS; FIFRA SR;
RCRA APP8; RCRA P) (Ref. 8). Aquatic
acute toxicity test data for aldicarb
include a measured 96-hour LCso of 50
ppb for bluegill and a measured 48-
hour LCso of 70 ppb for daphnid. In
addition, the measured 48-hour ECso for
daphnid is 51 ppb. Measured terrestrial
acute toxicity data for wildlife include
an oral LDso for female mallard ducks of
3.4 milligram per kilogram (mg/kg) and
an oral LDso for California quail of 2.58
mg/kg in males and 4.67 mg/kg in
females. EPA believes that there is
sufficient evidence for listing aldicarb
on EPCRA section 313 pursuant to
EPCRA section 313(d)(2)(C) based on
the environmental toxicity data for this
chemical.
6. d-trans-AHethrin [d-trans-
Chrysanthemic acid of dallethrone]
(CAS No. 028057-48-9) (FIFRA AI) (Ref.
3). Centrilobular hydropic degeneration
of the liver (LOEL was 1,000 ppm or 25
mg/kg/day; the NOEL was 200 ppm or
5 mg/kg/day) was seen in dogs fed
allethrin for 3 months. Increases in
serum liver enzymes in female rats and
increased liver weights in male and
female rats (the LOEL was 250 mg/kg/
day; the NOEL was 1,500 ppm or 75 mg/
kg/day) were observed in rats fed
allethrin for 3 months. Histopathology
data were not presented in this study.
Taken together, the results of these
studies indicate hepatotoxic potential
for d-trans-allethrin. EPA believes that
there is sufficient evidence for listing d-
trans-allethrin on EPCRA section 313
pursuant to EPCRA section 313(d)(2)(B)
based on the available hepatic toxicity
data.
7. Allylamine (CAS No. 000107-11-9)
(EPCRA EHS) (Ref. 8). Repeated
inhalation exposure to 5 ppm (0.011
mg/L) allylamine for 50 exposures of 7
hours caused liver and renal damage
and myocarditis in rats. Congestion of
the liver and kidney was observed in
rats, rabbits, and dogs exposed to 5 or
20 ppm (0.011 or 0.044 milligram per
liter (mg/L)) allylamine for 8 hours/day,
5 days/week, for 1—year. EPA believes
that there is sufficient evidence for
listing allylamine on EPCRA section 313
pursuant to EPCRA section 313(d)(2)(B)
based on the hepatotoxicity and
nephrotoxicity data for this chemical.
8. Aluminum phosphide (CAS No.
020859-73-8) (CERCLA; EPCRA EHS;
RCRA APP8; RCRA P) (Ref. 8). The
median lethal dose of aluminum
phosphide in humans is 20 mg/kg. The
acute inhalation toxicity of aluminum
phosphide is attributed to phosphine
gas resulting from decomposition of
aluminum phosphide on contact with
moisture in the air. Symptoms of
phosphine poisoning include
restlessness, headache, dizziness,
fatigue, chest tightness, nausea,
vomiting, lethargy, stupor, coma,
convulsions, lowered blood pressure,
pulmonary edema and respiratory
failure; disorders of the kidney, liver,
heart and brain can also occur. In female
CFT-Wistar rats exposed to phosphine
gas generated from aluminum
phosphide pellets in distilled water, 100
percent mortality was observed after a
6-hour exposure to 40 ppm (0.1 mg/L),
and exposure to 20 to 40 ppm (0.05 to
0.1 mg/L) for 6 hours resulted in 33
percent mortality. Symptoms of toxicity
reported in these animals included
dyspnea, loss of muscular coordination,
polyuria, and paralysis.
EPA's exposure analysis indicates that
aluminum phosphide 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 aluminum
phosphide on EPCRA section 313
pursuant to EPCRA section 313(d)(2)(A)
based on the available acute toxicity and
exposure data for this chemical.
9. Ametryn (N-Ethyl-N'-(l-
methylethyl)-6-(methylthio) 1,3,5,-
triazine- 2,4-diamine) (CAS No. 000834-
12-8) (FIFRA AI) (Ref. 3). Fatty
degeneration of the liver was observed
in rats administered 100 mg/kg/day
ametryn by gavage, 6 days per week for
13 weeks. The NOEL was 10 mg/kg/day
(8.6 mg/kg/day adjusted for duration). In
another study, hepatic effects (severe
vascular congestion, centrilobular liver
necrosis and fatty degeneration of
individual liver cells) were observed in
rats that died following gavage
administration of 500 mg/kg/day
ametryn for 6 days per week for 28 days.
The NOEL was 250 mg/kg/day. EPA
believes that there is sufficient evidence
for listing ametryn on EPCRA section
313 pursuant to EPCRA section
313(d)(2)(B) based on the available
hepatotoxicity data for this chemical.
The 72-hour ECso for green algae is. 14
ppb. Ametryn is a herbicide and may be
expected to affect nontarget plants such
as algae. EPA believes that there is
sufficient evidence for listing ametryn
on EPCRA section 313 pursuant to
EPCRA section 313(d)(2)(C) based on
the available environmental toxicity
data for this chemical.
10. Amitraz (CAS No. 033089-61-1)
(FIFRA SR) (Ref. 8). Amitraz is an
aniline-type insecticide. In a 2-year
beagle dog feeding study, effects noted
at the LOAEL dose (1.0 mg/kg/day) at
various times during the study included
significantly increased mean blood
glucose concentration, slight
hypothermia, and slight central nervous
system depression (the latter effect
occurred immediately after dosing on
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days 1 and 2). The NOAEL in this study
was 0.25 mg/kg/day and the oral RED
derived from the NOAEL was 0.0025
mg/kg/day. These findings were
supportedby similar results obtained in
a 90-day feeding study in dogs. In
studies with rats or mice exposed to
amitraz from 90 days to 2 years,
LOAELs less than or equal to 12 mg/kg/
day were derived based on effects that
included decreased body weight gain
and changes in organ (brain or heart)
weight (the NOELs were less than or
equal to 3 mg/kg/day).
A three-generation reproduction study
in rats demonstrated decreased litter
size and increased mortality during
suckling. The fetotoxic LOAEL in this
study was 5 mg/kg/day and the NOAEL
was 1.6 mg/kg/day. In a teratology study
in rabbits, a fetotoxicity LOAEL of 5 mg/
kg/day and NOAEL of 1 mg/kg/day were
based on the incidences of cleft palate
and meningocoele associated with small
ears and displaced toes.
EPA believes that there is sufficient
evidence for listing amitraz on EPCRA
section 313 pursuant to EPCRA section
313(d)(2)(B) based on the chronic
toxicity and developmental toxicity data
for this chemical.
11. Anilazine (4,6-dichloro-N-(2-
chlorophenyl)-l,3,5-triazm-2-amine)
(CAS No. 000101-05-3) (FIFRA AI) (Ref.
3). When anilazine was administered to
rats, maternal reproductive parameters
were not affected. The systemic
maternal NOEL was 150 mg/kg and the
LOEL was 500 mg/kg, based on
decreased body weight gain. The
developmental NOEL was 1,500 mg/kg,
which was the highest dose tested. In
rabbits, the maternal toxicity NOEL was
15 mg/kg and the LOEL was 40 mg/kg,
based on increased mortalities and
decreased body weight gain (also
decreased percentage of pregnant does
at 75 mg/kg). The developmental NOEL
was 40 mg/kg and the LOEL was 75 mg/
kg, based on increased fetal mortality,
decreased fetal weight, and increased
postimplantation loss and inhibited
ossification (phalanges). EPA believes
that there is sufficient evidence for
listing anilazine on EPCRA section 313
pursuant to EPCRA section 313(d)(2)(B)
based on the available developmental
toxicity data.
Aquatic acute toxicity values for
anilazine include a scud (Gammarus)
96-hour LCso of 0.27 ppb and an oyster
96-hour ECso (growth) of 46 ppb. EPA
believes that there is sufficient evidence
for listing anilazine on EPCRA section
313 pursuant to EPCRA section
313(d)(2)(C) based on the available
environmental toxicity data.
12. Atrazine (6-chloro-N-ethyl-N'-(l-
methylethyl)-l,3,5,-triazine-2,4-diamine)
(CAS No. 001912-24-9) (FIERA AI) (Ref.
3). Based on sufficient evidence of
carcinogenicity in animals, the
International Agency for Research on
Cancer (IARC) has classified atrazine as
a Group 2B compound; i.e., the
chemical is possibly carcinogenic to
humans. Administration of atrazine to
Sprague Dawley rats was associated
with an increased incidence of
mammary gland fibroadenomas and
adenocarcinomas in female rats. A
hormonal mechanism may be involved
in the induction of mammary tumors by
atrazine. Therefore there is sufficient
evidence for listing atrazine on EPCRA
section 313 pursuant to EPCRA section
313(d)(2)(B) based on the available
carcinogenicity data for this chemical.
13. Bendiocarb (2,2-dimethyl-l,3-
benzodioxol-4-olmethylcarbamate)
(CAS No. 022781-23-3) (FIFRA AI) (Ref.
3). Depressed blood cholinesterase
levels were reported in numerous
species. In a developmental toxicity
study in rats, cholinergic signs were
observed in maternal animals at 4 mg/
kg/day (LOEL). The maternal NOEL was
1 mg/kg/day; no adverse effects were
observed in fetuses. A LOEL of 2.5 mg/
kg/day for cholinesterase inhibition was
reported in dogs in a 4-month dietary
study. The NOEL was 0.5 mg/kg/day.
Decreases in cholinesterase activity
were observed in female rats fed 20, 30,
or 40 mg/kg/day for 28 days. No NOEL
was established in this study. However,
no details regarding clinical signs or
histopathological changes in neural
tissue were reported. EPA believes that
there is sufficient evidence for listing
bendiocarb on EPCRA section 313
pursuant to EPCRA section 313(d)(2)(B)
based on the available neurological
toxicity data for this chemical.
Aquatic acute toxicity values for
bendiocarb include a mysid 96-hour
ECso of 6.7 ppb and a daphnid 48-hour
ECso of 29.2 ppb. Avian acute toxicity
values include a mallard duck LDso of
3.1 mg/kg. EPA believes that there is
sufficient evidence for listing
bendiocarb on EPCRA section 313
pursuant to EPCRA section 313(d)(2)(C)
based on the available environmental
toxicity 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.
15. Benomyl (CAS No. 017804-35-2)
(CAL; FIFRA SR) (Ref. 8). In a three-
generation study in rats, a dietary level
of 25 mg/kg/day of benomyl resulted in
decreased weanling weights. The no-
effect level was 5 mg/kg/day.
Microphthalmia (the LOEL was 62.5
mg/kg/day; the NOEL was 30 mg/kg/
day) was reported in a rat
developmental toxicity study. Decreased
fetal weight (the LOEL was 62.5 mg/kg/
day; the NOEL was 30 mg/kg/day) was
observed in another rat developmental
toxicity study. The developmental
effects were observed at doses that were
not toxic to the maternal animal.
Anomalies consisting of supra occipital
scars, subnormal vertebral centrum,
supernumary ribs, and cleft palate were
reported in an oral developmental
toxicity study in mice (the LOEL was
100 mg/kg/day; the NOEL was 50 mg/
kg/day). An increase in the incidence of
anomalies including encephalocele,
hydrocephalus, microphthalmia, and
anophthalmia was noted following
administration of benomyl to rats by
intubation during the first 20 days of
pregnancy at doses of 125, 250, and 500
mg/kg. The developmental effects were
always associated with death and were
considered to be the cause of death. EPA
believes that there is sufficient evidence
for listing benomyl on EPCRA section
313 pursuant to EPCRA section
313(d)(2)(B) based on the developmental
toxicity data for this chemical.
16. o-Benzyl-p-chlorophenol (CAS No.
000120-32-1) (FIFRA AI) (Ref. 3). In a
16-day oral rat study, dose-related
increases in liver and kidney weights
(absolute and relative) and nephrosis
were observed at a dose level of greater
than or equal to 62.5 mg/kg/day. A
NOEL was not established. When the
compound was administered by gavage
for 13 weeks, rats developed multifocal
dilation of renal tubules and increased
liver weights (16 percent) at 240 mg/kg/
day. The NOEL was 120 mg/kg/day. In
a 90-day oral study, mice receiving 30
mg/kg/day developed kidney lesions.
Increased liver weights were also noted.
No NOEL was established in this study.
EPA believes that there is sufficient
evidence for listing o-benzyl-p-
chlorophenol on EPCRA section 313
pursuant to EPCRA section 313(d)(2)(B)
based on the available hepatic and renal
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
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1799
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
lyear 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
LCso of 0.35 ppb, a rainbow trout 96-
hour LCso of 0.15 ppb, a sheepshead
minnow LCso of 17.5 ppb, and a
daphnid 48-hour EC50 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.
18. Bis(tributyltin) oxide (CAS No.
000056-35-9) (FIFRA AI) (Ref. 3).
Adverse effects on the immune system
were reported in rats exposed to various
doses of bis(tributyltin) oxide for a
duration as short as 4 weeks. SPF-
derived Wistar rats were fed the
compound for 17 months. In this study,
a LOEL of 0.25 mg/kg/day and a NOEL
of 0.025 mg/kg/day were based on
immunotoxicity manifested as
decreased resistance to Trichinella
spiralis, reduced natural killer (NK) cell
activity in the spleen and reduced
macrophage function. The RfD derived
from this NOEL was 0.00003 mg/kg/day.
Similar immunological effects were
reported in 4- and 6-week rat feeding
studies with 20 and 80 ppm (1 and 4
mg/kg/day; the LOEL was 1 mg/kg/day).
Li rats that received dietary levels (of
a range of doses that included 50 mg/
kg/day) for 106 weeks, kidney function
was decreased and serum levels of
alanine aminotransferase, aspartate
aminotransferase and alkaline
phosphatase were increased. At the end
of the 2—year study, nephrosis and
vacuolization and pigmentation of the
proximal tubular epithelium were
reported in animals administered 50
mg/kg/day. On the basis of marginal
effects at 5 mg/kg/day (LOEL), a NOEL
of 0.5 mg/kg/day was established.
EPA believes that there is sufficient
evidence for listing bis(tributyltin) oxide
on EPCRA section 313 pursuant to
EPCRA section 313(d)(2)(B) based on
the available immunological and renal
toxicity data.
Aquatic acute toxicity values for
bis(tributyltin) oxide include a bluegill
96—hour LCso of 7.6 ppb, a rainbow trout
96-hour LCso 6.9 ppb, a measured
fathead minnow 96-hour LCso of 2.7
ppb, and a daphnid 48-hour LCso of
1.67 ppb. EPA believes that there is
sufficient evidence for listing
bis(tributyltin) oxide on EPCRA section
313 pursuant to EPCRA section
313(d)(2)(C) based on the available
environmental toxicity data.
19. Boron trichloride (CAS No.
010294-34-5) (EPCRA EHS) (Ref. 8).
Boron trichloride is corrosive to the skin
and mucosal tissue due to its rapid
hydrolysis to hydrochloric acid and
boric acid, the former acid being the
corrosive species. Single, relatively large
doses of boron administered through
any route affects the central nervous
system causing depressed circulation,
diarrhea, vomiting, shock, and coma.
The kidneys are the most severely
affected organ. Symptoms of acute
irritation of the upper airways were
observed in humans at exposure levels
of greater than or equal to 0.004 mg/L.
Inhalation of 0.48 mg/L of boron
trichloride proved fatal to certain
laboratory animals. Inhalation of 0.096
mg/L of boron trichloride for 7 hours
produced adverse effects on the
respiratory tract, and weight loss.
EPA's exposure analysis indicates that
boron trichloride 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 boron
trichloride on EPCRA section 313
pursuant to EPCRA section 313(d)(2)(A)
based on the available acute toxicity and
exposure data for this chemical.
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.
21. Bromacil (5-bromo-6-methyl-3-(l-
methylpropyl)-2,4-(lH,3H)-
pyrimidinedione) (CAS No. 000314-40-
9) (FIFRA AI) (Ref. 3). Increased thyroid
activity was seen in male and female
rats fed 5,000 ppm (250 mg/kg/day)
bromacil for 90 days. In a 2—year dietary
study, thyroid hyperplasia was seen in
female rats fed 1,250 ppm (62.5 mg/kg/
day). Thyroid follicular adenoma was
observed in one female. EPA believes
that there is sufficient evidence for
listing bromacil on EPCRA section 313
pursuant to EPCRA section 313(d)(2)(B)
based on the available thyroid toxicity
data for this chemical.
22. Bromacil lithium salt (2,4-
(lH,3H)-pyrimidinedione, 5-bromo-6-
methyl-3-(l-methylpropyl), lithium salt)
(CAS No. 05340419-6) (FIFRA AI) (Ref.
3). Bromacil lithium salt will dissociate
into bromacil, which is soluble in
aqueous systems and lithium ion.
Defects of the palate, eye, and external
ear were reported in the offspring of rats
administered 50 mg lithium chloride
intraperitoneally on gestation days 1, 4,
7, and 9 followed by 20 mg/day until
day 17. Cleft palates were also observed
in mouse fetuses when mothers were
gavaged with 300 to 465 mg/kg/day
lithium carbonate on gestation day 6 to
15. An increase in Ebstein's anomaly
was reported among offspring of women
taking lithium; cardiovascular defects
were found in 212 offspring exposed in
utero to lithium therapy.
Increased thyroid activity was seen in
male and female rats fed 5,000 ppm (250
mg/kg/day) bromacil for 90 days. In a 2—
year dietary study, thyroid hyperplasia
was seen in female rats fed 1,250 ppm
(62.5 mg/kg/day). Thyroid follicular
adenoma was observed in one female.
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EPA believes that there is sufficient
evidence for listing bromacil lithium
salt on EPCRA section 313 pursuant to
EPCRA section 313(d)(2)(B) based on
the available developmental and thyroid
toxicity data.
23. Bromine (CAS No. 007726-95-6)'
(EPCRA EHS) (Ref. 8). Rats fed bromine
at a dose of 0.01 mg/kg/day for 6 months
experienced changes in their reflexes
and blood indexes. Rats, mice, and
rabbits inhaling 0.001 mg/kg/day for 4
months developed functional
abnormalities of the respiratory,
nervous, and endocrine systems. Data
on the acute and chronic effects of
bromine in humans are limited.
Bromine is very corrosive to the eyes,
skin, and mucous membranes in either
the liquid or vapor form. A
concentration of 10 ppm of bromine in
air is intolerable in humans, and can
cause severe irritation of the upper
respiratory tract. Other clinical
symptoms include neurologic,
dermatologic, and gastrointestinal
effects. The maximum concentration
allowable in humans for a 0.5 to 1-hour
exposure to bromine is 4 ppm. Bromine
can cause lacrimation at concentrations
less than 1 ppm. Chronic exposure to
bromine (estimated concentration at 0.6
ppm) can result in eye irritation, upper
respiratory irritation, coughing, and
headache. Neurological symptoms have
also been reported following chronic
exposure to bromine.
EPA believes that there is sufficient
evidence for listing bromine on EPCRA
section 313 pursuant to EPCRA section
313(d)(2)(B) based on the available
chronic toxicity data for this chemical.
24. l-Bromo-l-(bromomethyl)-l,3-
propanedicarbonitrile (CAS No. 035691-
65-7) (FIFRA AI) (Ref. 3). In a 3-month
dietary study where rats were
administered 83.5,500, and 3,000 ppm
(4,25, and 150 mg/kg/day) 1-bromo-l-
(bromomethyl)-l,3-
propanedicarbonitrile, a NOEL of 83.5
ppm (4 mg/kg/day) and a LOEL of 500
ppm (25 mg/kg/day) were established
(based on neonatal splenic
hematopoiesis, decreased parental body
weight and food consumption,
increased male urinary epithelial cells,
amorphous casts, and crystals). At 3,000
Spm (150 mg/kg/day) there was
ecreased lactase dehydrogenase,
increased total cholesterol, total protein,
and albumin, elevated female organ-to-
body weight ratio for thyroid, liver,
spleen, ovaries, and pituitary. In a 13-
week dietary study in beagle dogs
(administered 167,1,000, and 4,000
ppm; 4,25, and 100 mg/kg/day) the
LOEL was greater than 167 ppm (4 mg/
kg/day) (increased male thyroid and
female ovary organ to body weight
ratio). At 1,000 ppm (25 mg/kg/day), the
same signs were seen as at 167 ppm (4
mg/kg/day), plus diarrhea and increased
organ to body weight ratio of thyroid,
heart, liver, and adrenals. At 4,000 ppm
(100 mg/kg/day), emesis and ataxia in
males, decreased body weight gain/food
consumption, decreased hematocrit,
hemoglobin, immature red blood cells,
and alkaline phosphatase,
extramedullary hematopoiesis in the
liver and spleen, thyroid enlargement
with follicular cell hyperplasia,
increased organ to body weight ratios
for thyroid, adrenals, liver and spleen
were seen. In a 13-week dietary study
where beagle dogs were administered
167 ppm (4 mg/kg/day), thyroid
stimulating hormone (TSH)-stimulated
T3 and T4 increased in both sexes.
Thyroids were enlarged (both sexes)
with absolute weights and organ to body
weight ratios increased in females.
EPA believes that there is sufficient
evidence for listing 1-bromo-l-
(bromomethyl)-l,3-
propanedicarbonitrile on EPCRA section
313 pursuant to EPCRA section
313(d)(2)(B) based on the available
toxicity data for this chemical.
25. 2-Bromo-2-nitropropane-l,3-diol
(bronopol) (CAS No. 000052-51-7)
(FIFRA AI) (Ref. 3). Severe irritation was
reported in the gastrointestinal tracts of
rats, mice or dogs administered single or
multiple oral doses of 2-bromo-2-
nitropropane-l,3-diol. In an acute oral
study in mice, the LDso of 374 mg/kg
resulted in ulceration of the stomach
and duodenum, thickening of the
intestinal wall, and adhesions of the
stomach to the liver. Severe gastric
irritation was reported in dogs
administered a single oral dose of 250
mg/kg. The NOEL was 100 mg/kg.
Superficial ulceration with epithelial
hyperplasia and hyperkeratosis, and
congested vessels in the gastrointestinal
mucosa, was observed in rats fed 80 mg/
kg/day (LOEL) in their diet for 13
weeks. The NOEL was 20 mg/kg/day.
Vomiting was noted in dogs fed 20 mg/
kg/day in their diet for 13 weeks. The
NOEL in this study was 8 mg/kg/day. In
addition, blood was noted in the urine
of these dogs. Mortality, irritation of the
gastrointestinal tract, ulceration and
stomach lesions were reported in a 2—
year dietary study in rats fed 40 mg/kg/
day. The NOEL was 10 mg/kg/day. EPA
believes that there is sufficient evidence
for listing 2-bromo-2-nitropropane-l,3-
diol on EPCRA section 313 pursuant to
EPCRA section 313(d)(2)(B) based on
the available toxicity data.
26. Bromoxynil (3,5-dibromo-4-
hydroxybenzonitrile) (CAS No. 001689-
84-5) (FIFRA AI) (Ref. 3).
Developmental effects (hydrocephalus,
microphthalmia, anophthalmia and
severe defects in ossification of the
skull) were observed in rabbits
administered 6Qjmg/kg/day bromoxynil
by gavage. The NOEL was 30 mg/kg/
day. Developmental toxicity (increases
in all forms of supernumerary ribs) was
also observed in rats at 5 mg/kg/day.
The NOEL was 1.5 mg/kg/day. The
maternal LOEL (based on body weight
loss) was 30 mg/kg/day. Several other
developmental studies indicate
potential developmental toxicity of
bromoxynil. EPA believes that there is
sufficient evidence for listing
bromoxynil on EPCRA section 313
pursuant to EPCRA section 313(d)(2)(B)
based on the available developmental
toxicity data for this chemical.
27. Bromoxynil octanoate (octanoic
acid, 2,6-dibromo-4-cyanophenyl ester)
(CAS No. 001689-99-2) (FIFRA AI) (Ref.
3). Bromoxynil octanoate hydrolyzes to
yield bromoxynil and octanol. In a
dermal developmental toxicity study,
bromoxynil octanoate was
developmentally toxic to rat fetuses
(increased incidences of supernumerary
ribs) at 15 mg/kg/day (LOEL). The NOEL
was 10 mg/kg/day. The maternal LOEL
for decreased body weight gain was 20
mg/kg/day. The NOEL was 15 mg/kg/
day. Developmental effects
(hydrocephalus, microphthalmia,
anophthalmia and severe defects in
ossification of the skull) were observed
in rabbits administered 60 mg/kg/day
bromoxynil by gavage. The NOEL was
30 mg/kg/day. Developmental toxicity
(increases in all forms of supernumerary
ribs) was also observed in rats at 5 mg/
kg/day. The NOEL was 1.5 mg/kg/day.
The maternal LOEL (based on body
weight loss) was 30 mg/kg/day. EPA
believes that there is sufficient evidence
for listing bromoxynil octanoate on
EPCRA section 313 pursuant to EPCRA
section 313(d)(2)(B) based on the
available developmental toxicity data
for bromoxynil and bromoxynil
octanoate.
28. Brucine (CAS No. 000357-57-3)
(CERCLA; RCRA APP8; RCRA P) (Ref.
8). Brucine is an alkaloid similar in
structure to strychnine. It is capable of
causing death or permanent injury due
to exposures in normal use. In humans,
brucine can cause central and
peripheral paralysis, convulsions, and
respiratory failure. A potentially lethal
oral dose in small children is 5 to 10
mg. The lethal oral dose for an adult
may be as low as 30 mg. The acute oral
LDso in rabbits is 4 mg/kg.
EPA's exposure analysis indicates that
brucine concentrations are likely to
exist beyond facility site boundaries, as
a result of continuous, or frequently
recurring releases, at levels that can
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reasonably be anticipated to cause
significant adverse acute human health
effects. EPA believes that there is
sufficient evidence for listing brucine on
EPCRA section 313 pursuant to EPCRA
section 313(d)(2)(A) based on the
available acute toxicity and exposure
data for this chemical.
29. Butylate (Bis-2-
methylpropyl)carbamothioic acid S-
ethyl ester) (CAS No. 002008-41-5)
(FIFRA AI) (Ref. 3). In a 2-year feeding
study in mice, hepatic (cellular
infiltrates, focal necrosis) and renal
effects (amyloidosis, chronic nephritis,
lymphocytic foci) were observed at 80
mg/kg/day. The NOEL was 20 mg/kg/
day. In a separate study, liver
pericholangitis was observed in rats fed
180 mg/kg/day for 56 weeks. The NOEL
was 30 mg/kg/day. An increased relative
liver weight was observed in male dogs
fed 25 mg/kg/day for 1-year. The NOEL
was 5 mg/kg/day. Based on the NOEL,
EPA has established a chronic oral RfD
of 0.05 mg/kg/day. EPA believes that
there is sufficient evidence for listing
butylate on EPCRA section 313 pursuant
to EPCRA section 313(d)(2)(B) based on
the available hepatic and renal toxicity
data for this chemical.
30. Butylated hydroxyanisole (CAS
No. 025013-16-5) (CAL; IARC; NTP)
(Ref. 8). Butylated hydroxyanisole is
classified by IARC as a Group 2B
compound; i.e., the chemical is possibly
carcinogenic to humans. Butylated
hydroxyanisole has been shown to
induce gastrointestinal tumors in rats
and hamsters. EPA believes that there is
sufficient evidence for listing butylated
hydroxyanisole on EPCRA section 313
pursuant to EPCRA section 313(d)(2)(B)
based on the carcinogenicity data for
this chemical.
31. C.I. Acid Red 114 (CAS No.
006459-94-5) (TSCA) (Ref. 8). In a 2-
year bioassay conducted by the National
Toxicology Program (NTP) in which
F344 rats were exposed to C.I. Acid Red
114 via drinking water, hepatocellular
carcinomas of the liver, tumors of the
skin, and adenomas or carcinomas in
the ZymbaPs gland of both sexes were
observed. In the same study, female rats
also had increased incidences of
adenoma or carcinoma in the clitoral
gland, and squamous cell papilloma or
carcinoma in the oral cavity. The
exposure concentrations in this study
ranged from 70 to 300 ppm (9.8 to 42
mg/kg/day) for males and from 150 to
600 ppm (21 to 84 mg/kg/day) for
females. EPA believes that there is
sufficient evidence for listing C.I. Acid
Red 114 on EPCRA section 313 pursuant
to EPCRA section 313(d)(2)(B) based on
the carcinogenicity data for this
chemical.
32. C.J. Direct Blue 218 (CAS No.
028407-37-6) (NTP) (Ref. 8). In an NTP
bioassay, there was clear evidence of
carcinogenicity of C.I. Direct Blue 218 in
male and female B6C3F1 mice based on
significantly increased incidence of
hepatocellular adenomas and
carcinomas. In a 2—year NTP feeding
study in rats, there was some evidence,
of carcinogenicity in male F344 rats
based on a significant increase in the
incidence of squamous cell papillomas
of the pharynx in the high dose group
(500 mg/kg/day). EPA believes that
there is sufficient evidence for listing
C.I. Direct Blue 218 on EPCRA section
313 pursuant to EPCRA section
313(d)(2)(B) based on the
carcinogenicity data for this chemical.
33. Calcium hypochlorite (CAS No.
007778-54-3) (CERCLA) (Ref. 8). Aquatic
acute toxicity data for calcium
hypochlorite include a 96-hour
measured LCso for rainbow trout of 60
ppb and a 96—hour measured LCso for
the Atlantic silverside of 37 ppb. EPA
believes that there is sufficient evidence
for listing calcium hypochlorite on
EPCRA section 313 pursuant to EPCRA
section 313(d)(2)(C) based on the
available ecotoxicity data for this
chemical.
34. Caprolactam (CAS No. 000105-60-
2) (CAA HAP) (Ref. 7). Rats were
administered caprolactam by oral
gavage at doses of 0,100, 500, and 1,000
mg/kg/day on gestation days 6 through
20. This resulted in a LOAEL of 1,000
mg/kg/day and a NOAEL of 500 mg/kg/
day for fetal resorption. Rabbits were
administered caprolactam by oral
gavage at doses of 0, 50,150, and 250
mg/kg/day on gestation days 6 through
28. This resulted in a LOAEL of 150 mg/
kg/day for maternal and fetal body
weight depression. In addition, a slight
increase in the severity of spontaneous
nephropathy (10,000 ppm) was
observed in male rats of the first
parental generation fed 10,000 ppm of
caprolactam in a three-generation
reproductive study, resulting in a
NOAEL of 1,000 ppm (50 mg/kg/day).
Mean body weights and food
consumption were reduced in both
parental generations at 5,000 and 10,000
ppm. Body weights of offspring were
also reduced at these dietary
concentrations (the LOAEL was 250 mg/
kg/day). EPA believes that there is
sufficient evidence for listing
caprolactam on EPCRA section 313
pursuant to EPCRA section 313(d)(2)(B)
based on the available developmental
toxicity data for this chemical.
35. Carbofuran (CAS No. 001563-66-
2) (CERCLA; EPCRA EHS; FIFRA SR)
(Ref. 8). Aquatic acute toxicity test data
for carbofuran include a measured 96-
hour LCso for bluegill of 80 ppb. In
addition, the measured 48-hour ECso for
daphnids is 35 ppb. Measured terrestrial
acute toxicity data for wildlife include
an oral LDso for mallard ducks of 0.397
mg/kg for females and 0.480 mg/kg for
males and an oral LDso for female ring-
necked pheasants of 4.15 mg/kg. EPA
believes that there is sufficient evidence
for listing carbofuran on EPCRA section
313 pursuant to EPCRA section
313(d)(2)(C) based on the environmental
toxicity data for this chemical.
36. Carbon monoxide (CAS No.
000630-08-0) (CAL) (Ref. 8).
Cardiovascular (e.g., electrocardiograph
changes, atrial fibrillation, ventricular
arrhythmias) and neurological (e.g.,
headache, dizziness, convulsions, and
coma) effects were reported in humans
exposed to carbon monoxide. In
humans, histological effects in the brain
include extensive demyelination of
white matter, and necrosis.
Neuropsychiatric disorders have also
been reported. Persistant
electrocardiograph changes, and
degeneration of myocardial muscle
fibers, hemorrhage and necrosis were
observed following inhalation exposure
of dogs to 100 ppm (0.11 mg/L) carbon
monoxide, 5.5 hours/day, 6 days/week,
for 11 weeks. Some of the dogs showed
disturbances in gait and in postural and
position reflexes. The toxicity of carbon
monoxide results from its combination
with hemoglobin in the blood to form
carboxyhemoglobin which is a poor
oxygen carrier. Thus, oxygen delivery
by the blood is severely compromised,
which leads to tissue hypoxia and
possibly tissue poisoning, resulting in
the toxic effects (including death)
known for this substance.
Infants born to women who survive
acute exposure to high concentrations of
carbon monoxide during pregnancy
often display neurological sequelae and
gross brain damage. Exposure of
pregnant rats to 150 ppm (0.17 mg/L)
carbon monoxide caused reduced pup
growth rate, and altered behavior (poor
performance on negative geotaxis and
homing tests) in pups.
EPA oelieves that there is sufficient
evidence for listing carbon monoxide on
EPCRA section 313 pursuant to EPCRA
section 313(d)(2)(B) based on the
available chronic neurological,
myocardial, and developmental toxicity
data for this chemical.
Carbon monoxide is regulated under
Title I of the CAA (Provisions for
Attainment and Maintenance of
National Ambient Air Quality
Standards). In addition to this proposal
to add carbon monoxide to EPCRA
section 313, in Units IV.B.179. and 235,
EPA is proposing to add two other
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1802 Federal Register / Vol. 59, No. 8 / Wednesday, January 12, 1994 / Proposed Rules
chemicals, nitrogen dioxide and sulfur
dioxide, that are regulated under Title I
of the CAA. Sulfur dioxide is also
regulated under Title IV of the CAA
(Acid Deposition Control). Extensive
data, which are highly technical, are
collected on these chemicals as required
by the CAA. EPA requests comment on
the following: (1) Is the information
collected under the CAA sufficient for
public right-to-know purposes; and (2)
suggestions on how the data collected
on these chemicals pursuant to CAA
Titles I and IV could be used to meet the
purposes of EPCRA section 313.
37. Carboxin (5,6-dihydro-2-methyl-N-
phenyI-l,4~oxathiin-3-carboxamide)
(CAS No. 005234-68-4) (FIFRA AI) (Ref.
3). Decreased body weight gain and food
consumption, increased mortality, and
reduced kidney, heart and spleen
weights were observed in rats fed 600
ppm (30 mg/kg/day) carboxin for 2
years. The NOEL is 200 ppm (10 mg/kg/
day). A similar NOEL was estabh'shed in
a three-generation rat reproduction
study. Based on the NOEL, EPA
established an oral RfD of 0.01 mg/kg/
day. In a 90-day feeding study in rats,
degeneration of the kidneys was seen at
600 ppm (30 mg/kg/day). The NOEL
was 10 mg/kg/day. EPA believes that
there is sufficient evidence for listing
carboxin on EPCRA section 313
pursuant to EPCRA section 313(d)(2)(B)
based on the available renal toxicity
data for this chemical.
38. Chinomethionat (6-methyl-l,3-
dithiolo[4,5-bJquinoxalin-2-one)(CAS
No. 002439-01-2) (FIFRA AI) (Ref. 3).
Increases in liver weight, liver protein,
and both total liver and microsomal
RNA levels, as well as inhibition of
mixed-function oxidase enzymes (e.g.,
N-demethylase, cytochrome P-450) were
noted in rats administered 75 mg/kg/day
by oral gavage for 4 days or in female
rats administered 75 mg/kg/day in their
diet for 21 days. Liver enlargement was
reported in rats fed 10 mg/kg/day in
their diet for 35 days. The increase in
liver size was attributed to increased
cellular protein and an increase in water
content. Rats exposed orally to 2,700
mg/kg for 90 days (30 mg/kg/day) had
changes in liver weight and effects on
the hepatic microsomal oxidases as well
as weight loss or decreased body weight
gain. In a 1-year dog study, the NOEL
was established at 0.6 mg/kg/day for the
test material in the diet. The LOEL was
1.9 mg/kg/day as indicated by extra
medullary hematopoietic nodules in the
liver.
In a developmental toxicity study in
rats, increased resorption and decreased
fetal weight were reported at 37.5 mg/
kg/day (the highest dose tested). The
NOEL was 12.5 mg/kg/day. In another
developmental study in rats given 30
mg/kg/day in carboxy methyl cellulose
by gavage from gestation day 6 to 20,
cleft palate, anasarca and micrognathia
was observed.
EPA believes that there is sufficient
evidence for listing chinomethionat on
EPCRA section 313 pursuant to EPCRA
section 313(d)(2)(B) based on the
available hepatic and developmental
toxicity data.
39. Chlorendic acid (CAS No. 000115-
28-6) (NTP) (Ref. 8). Based on sufficient
evidence of carcinogenicity in animals
IARC classified chlorendic acid as a
Group 2B compound; i.e., it is possibly
carcinogenic in humans. In an NTP
bioassay, there was clear evidence of
liver carcinogenicity in both rats and
mice. EPA believes that there is
sufficient evidence for listing chlorendic
acid on EPCRA section 313 pursuant to
EPCRA section 313(d)(2)(B) based on
the carcinogenicity data for this
chemical.
40. ChlotimuTon ethyl (ethyl-2-[[[(4-
chloro-6-methoxyprimidin-2-yl)-
carbonyl]-amino]sulfonyl]benzoate)
(CAS No. 090982-32-4) (FIFRA AI) (Ref.
3). In a 1-year dog study, dietary •
administration of 37.5 mg/kg/day
(LOEL) produced an increase in white
blood cells in both sexes, a decrease in
red blood cells, hematocrit, and
hemoglobin in females, and an increase
in alkaline phosphatase in males. The
NOEL was 6.25 mg/kg/day. Based on the
NOEL, an oral RfD of 0.02 mg/kg/day
was derived. This study was given a
high confidence rating. In a 2-year rat
feeding study, changes in hematology
parameters were observed at the LOEL
of 125 mg/kg/day. The NOEL was 12.5
mg/kg/day. In an 18-month mouse
feeding study, centrilobular
hepatocellular hypertrophy was
observed at 90 days at 187.5 mg/kg/day
(LOEL). The NOEL was 18.75 mg/kg/
day. EPA believes that there is sufficient
evidence for listing chlorimuron ethyl
on EPCRA section 313 pursuant to
EPCRA section 313(d)(2)(B) based on
the available hematological toxicity
data.
41. Chlorinated paraffins category
(CAA HAP) (Ref. 7). Chlorinated
paraffins are defined as mixtures of
linear saturated chlorinated
hydrocarbons obtained through the
partial chlorination of paraffin, olefin,
or acetylene feedstocks which have an
average chain length of 10 to 30 carbon
atoms and contain average chlorine
levels ranging from 40 to 70 percent by
weight. Chlorinated paraffins can be
described by the general formula:
CxHjx-y+zCly where x ranges from 10 to
30 and y ranges from 3 to 26. Both 58
percent-chlorinated, short-chain (10 to
12 carbons) and 43 percent-chlorinated,
long-chain (22 to 26 carbons)
chlorinated paraffins were tested in rats
and mice by gavage in a 2-year
bioassay. The 58 percent-chlorinated,
short-chain (10 to 12 carbons)
chlorinated paraffins were carcinogenic
in rats and mice: dosed male and female
mice showed increased incidences of
liver tumors, dosed male rats had
increased incidences of kidney tubular
cell hyperplasia and adenomas or
adenocarcinomas (combined), and
dosed female rats and mice showed
increased thyroid gland follicular cell
neoplasms, indicating an EPA Group B2
classification, i.e., a probable human
carcinogen. The 43 percent-chlorinated,
long-chain (22 to 26 carbons)
chlorinated paraffins were carcinogenic
in male mice showing an increased
incidence of malignant lymphomas, and
marginal increase in hepatocellular
neoplasms in female mice and adrenal
gland pheochromocytomas in female
rats, indicating an EPA Group B2
category classification, i.e., the chemical
is a probable human carcinogen. EPA
believes that there is sufficient evidence
for listing chlorinated paraffins on
EPCRA section 313 pursuant to EPCRA
section 313(d)(2)(B) based on the
available carcinogenicity data for these
chemicals.
The following ecotoxicity data (LCsoS
followed by experiment duration in
parenthesis) have been reported for
short chain (10 to 13 carbons) and
intermediate chlorination (59 percent
chlorine) chlorinated paraffins:
daphnid, 46 ppb (48-hour); mysid
shrimp, 14 ppb (96-hour); marine algae,
42 ppb (96-hour); daphnid, 2 ppb and
9 ppb (21-day chronic study); and
midge, 78 ppb (49-day chronic study).
Ranges of chronic toxicity values are as
follow: Freshwater invertebrates, 2 to
162 ppb; freshwater fish, 3 to 17.2 ppb;
marine invertebrates, 2.4 to 24 ppb; and
marine fish, 2.4 ppb to 620.5 ppm.
Chlorinated paraffins are persistent with
a half-life of greater than 30 days in the
environment. EPA believes that there is
sufficient evidence for listing the
category chlorinated paraffins on
EPCRA section 313 pursuant to EPCRA
section 313(d)(2)(C) based on the
available ecotoxicity data for these
chemicals and their persistence in the
environment.
EPCRA section 313 requires threshold
determinations for chemical categories
to be based on the total of all chemicals
in the category manufactured,
processed, or otherwise used. For
example, a facility that manufactures
three members of a chemical category
would count the total amount of all
three chemicals manufactured towards
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1803
the manufacturing threshold for that
category. When filing reports for
chemical categories the releases are
determined in the same manner as the
thresholds. One report if filed for the
category and all releases are reported on
this form.
42.1 -(3-Chloroallyl)-3,5,7-triaza-l -
azoniaadamantane chloride (CAS No.
004080-31-3) (FIFRA AI) (Ref. 3).
Decrease in heart weight, obliterative
vasculitis, and perivasculitis of the
hepatic blood vessels were observed in
dogs orally administered l-(3-
chloroallyl)-3,5,7-triaza-l-
azoniaadamantane for 90 days. The
NOEL was 7.5 mg/kg/day; the LOEL was
15 mg/kg/day. EPA believes that there is
sufficient evidence for listing l-(3-
chloroallyl)-3,5,7-triaza-l-
azoniaadamantane chloride on EPCRA
section 313 pursuant to EPCRA section
313(d)(2)(B) based on the available
chronic toxicity data for l-(3-
chloroallyl)-3,5,7-triaza-l-
azoniaadamantane.
43. p-Chloroaniline (CAS No. 000106-
47-8) (CERCLA; RCRA APP8; RCRA P)
(Ref. 8). In a 78-week study in which
rats were fed p-chloroaniline, non-
neoplastic proliferative lesions of the
splenic capsule (focal fibrosis with
subcapsular mesenchymal proliferation)
were observed. The LOAEL was 12.5
mg/kg/day (the lowest dose tested) and
the RfD derived from this data is 0.004
mg/kg/day. EPA believes that there is
sufficient evidence for listing p-
chloroaniline on EPCRA section 313
pursuant to section 313(d) (2)(B) based
on the chronic toxicity data for this
chemical.
44. 5-Chloro-2-(2,4-
dichlorophenoxyjphenol (CAS No.
003380-34-5) (FIFRA AI) (Ref. 3). In a 3-
month dog feeding study, decreased red
blood cell and hemoglobin values,
increased serum alkaline phosphatase,
jaundice, and increased liver weight
were observed at 25 mg/kg/day (LOEL).
No NOEL could be established. In
another 3-month dog feeding study, the
LOEL of 25 mg/kg/day produced
morphologic changes in the liver (focal
acidophilic granular degeneration of
cytoplasm). The NOEL was 12.5 mg/kg/
day. In a 3-month rat feeding study, 125
mg/kg/day (LOEL) produced increased
liver weights in males. The NOEL was
50 mg/kg/day. At 150 mg/kg/day
(LOEL), decrease in triglycerides,
increase in creatinine, decrease in red
blood cells, increase in spleen and heart
weight, and cytomegaly were observed
in another 3-month rat feeding study
(NOEL was 50 mg/kg/day). In a 2-year
study, dietary administration of 15 mg/
kg/day produced decreases in red blood
cells, hemoglobin concentration, and
hematocrit as well as hepatic necrosis in
males. At 50 mg/kg/day, there were
decreases in red blood cells in females.
EPA believes that there is sufficient
evidence for listing 5-chloro-2-(2,4-
dichlorophenoxy)phenol on EPCRA
section 313 pursuant to EPCRA section
313(d)(2)(B) based on the available
hematological toxicity data for this
chemical.
45. 3-Chloro-2-methyl-l-propene
(CAS No. 000563-47-3) (NTP) (Ref. 8). In
an NTP gavage bioassay there was clear
evidence of carcinogenicity from 3-
chloro-2-methyl-l-propene in rats and
mice. The substance induced adrenal
cortex, testicular and gastrointestinal
tumors in rats and adrenal cortex and
gastrointestinal tumors in mice. EPA
believes that there is sufficient evidence
for listing 3-chloro-2-methyl-l-propene
on EPCRA section 313 pursuant to
EPCRA section 313(d)(2)(B) based on
the carcinogenicity data for this
chemical.
46. p-Chlorophenyl isocyanate (CAS
No. 000104-12-1) (TSCA) (Ref. 8). p-
Chlorophenyl isocyanate is very lethal
following inhalation. The 4—hour mouse
inhalation LCSo value is 0.053 mg/L. In
addition, isocyanates as a class are
generally severe skin, eye, and
respiratory irritants following acute
exposure.
EPA's exposure analysis indicates that
p-chlorophenyl isocyanate
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 p-chlorophenyl isocyanate on
EPCRA section 313 pursuant to EPCRA
section 313(d)(2)(A) based on the
available acute toxicity and exposure
data for this chemical.
47. Chloropicrin (CAS No. 000076-06-
2) (FIFRA AI) (Ref. 3). Measured aquatic
acute toxicity data for chloropicrin
include a rainbow trout 96-hour LCso of
16.5 ppb, a bluegill 96-hour LC50 of 105
ppb, and a 48-hour EC50 of 80 ppb. EPA
believes that there is sufficient evidence
for listing chloropicrin on EPCRA
section 313 pursuant to EPCRA section
313(d)(2)(C) based on the available
environmental toxicity data for this
chemical.
48. 3-Chloropropionitrile (CAS No.
000542-76-7) (CERCLA; EPCRA EHS;
RCRA APP8; RCRA P) (Ref. 8). 3-
Chloropropionitrile is metabolized by
hepatic cytochrome P450 enzymes to
release cyanide. The substance is
readily absorbed both dermally and
orally. The mouse oral LDso is 51.3 mg/
EPA's exposure analysis indicates that
3-chloropropionitrile 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 3-
chloropropionitrile on EPCRA section
313 pursuant to EPCRA section
313(d)(2)(A) based on the available
acute toxicity and exposure data for this
chemical.
49. p-Chloro-o-toluidine (CAS No.
000095-69-2) (IARC; NTP) (Ref. 8). p-
Chloro-o-toluidine is classified as a
Group B2 carcinogen by EPA; i.e., the
compound is a probable human
carcinogen. It is classified as a Group 2B
carcinogen by IARC; i.e., a possible
human carcinogen. Epidemiology
studies are inadequate in evaluating the
carcinogenic potential of 4-chloro-o-
toluidine hydrochloride in humans. In a
long-term feeding study by NCI, p-
chloro-o-toluidine hydrochloride
induced hemangiomas,
hemangiosarcomas, and vascular tumors
in mice. An increase in the incidence of
pituitary chromophobe adenomas was
observed in female rats following
dietary administration. EPA believes
that there is sufficient evidence for
listing p-chloro-o-toluidine on EPCRA
section 313 pursuant to EPCRA section
313(d)(2)(B) based on the available
carcinogenicity 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
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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 he
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, there is sufficient evidence for
listing chlorotrifluoromethane (CFC-13)
on EPCRA section 313 pursuant to
EPCRA sections 313(d)(2)(B) and (C).
51. Chlorpyrifos methyl (O,O-
dimethyl-O-{3,5,6-trichloro-2-
pyiidyf)phosphorothioate) (CAS No.
005598-13-0) (FIFRA AI) (Ref. 3).
Humans experienced a 10 percent
reduction in plasma cholinesterase
activity after 10 dermal exposures to 10
mg/kg/day and a 47 percent reduction
after 4 dermal exposures to 25 mg/kg/
day (exposures were for 12 hours per
day). Rabbits experienced a 97 to 100
percent reduction in plasma
cholinesterase activity after 5 dermal
exposures to 10 mg/kg/day for 12 hours
a day or 2 dermal exposures to 25 mg/
kg/day for 12 hours a day. In a 2-year
rat feeding study, red blood cell and
plasma cholinesterase inhibition were
observed at 1 mg/kg/day (LOEL). The
NOEL was 0.1 mg/kg/day. In a 2-year
dog feeding study, plasma
cholinesterase inhibition was observed
at 1 mg/kg/day (LOEL). The NOEL was
0.1 mg/kg/day. The oral rat LDjo is
between 1,159 mg/kg and 3,833 mg/kg.
Lethargy, ataxia, diarrhea, salivation,
and tremors were observed in these
studies. EPA believes that there is
sufficient evidence for listing
chlorpyrifos methyl on EPCRA section
313 pursuant to EPCRA section
313(d)(2)(B) based on the available
neurological toxicity data.
Aquatic acute toxicity values for
chlorpyrifos methyl include a daphnid
48-hour LCjo of 1.11 ppb and a rainbow
trout 96-hour LCso of 12.6 ppb. EPA
believes that there is sufficient evidence
for listing chlorpyrifos methyl on
EPCRA section 313 pursuant to EPCRA
section 313(d)(2)(C) based on the
available environmental toxicity data.
52. Chlorsulfuron (2-chloro-N-[[(4-
methoxy-6-methyl-l,3,5-triazin-2-
yl)amino]carbonyl]benzenesulfonamide)
(CAS No. 064902-72-3) (FIFRA AI) (Ref.
3). In a rabbit developmental study, an
increased incidence of fetal resorptions
was observed at the LOEL of 75 mg/kg/
day. The NOEL was 25 mg/kg/day.
ui a 3-generation rat reproduction
study, a decrease in fertility index was
observed at 125 mg/kg/day (LOEL). The
NOEL was 25 mg/kg/day. EPA believes
that there is sufficient evidence for
listing chlorsulfuron on EPCRA section
313 pursuant to EPCRA section
313(d)(2)(B) based on the available
developmental and reproductive
toxicity data for this chemical.
53. Clomazone (2-[(2-
chlorophenyl)methyl]-4,4-dimethyl-3-
isoxazolidinone) (CAS No. 081777-89-1)
(FIFRA AI) (Ref. 3). In a 90-day dog
feeding study, increased cholesterol and
increased absolute and relative liver
weights were observed at 62.5 mg/kg/
day (LOEL). The NOEL was 12.5 mg/kg/
day. Dietary administration of 62.5 mg/
kg/day (LOEL) to dogs for 1-year also
produced increased cholesterol and
increased liver weights. The NOEL was
12.5 mg/kg/day. In a 90-day mouse
feeding study, megalocytosis of the liver
cells was seen at 2.6 mg/kg/day (LOEL).
No NOEL was established. In a 2—year
rat feeding study, elevated cholesterol
levels and liver-to-body weight ratios
were observed at 21.5 mg/kg/day
(LOEL). The NOEL was 4.3 mg/kg/day.
Dietary administration of 62.5 mg/kg/
day (LOEL) to dogs for 1-year increased
cholesterol and liver weights. The NOEL
was 12.5 mg/kg/day.
In a two-generation reproduction
study, decreased pup viability, reduced
survival, decreased body weight, and
nonfunctional limbs were observed in
the offspring of rats that were orally
administered 50 mg/kg/day (LOEL). The
NOEL was 5 mg/kg/day.
EPA believes that there is sufficient
evidence for listing clomazone on
EPCRA section 313 pursuant to EPCRA
section 313(d)(2)(B) based on the
available hepatic and developmental
toxicity data.
54. Crotonaldehyde (CAS No. 004170-
30-3) (RCRA APP8) (Ref. 8).
Crotonaldehyde has been tested for
carcinogenicity in one animal study.
When Crotonaldehyde was administered
to male F344 rats at 0, 42, or 421 mg/
L for 113 weeks, there was a statistically
significant increase in the incidence of
hepatocellular neoplasms (benign and
malignant combined) in the low dose
group. The lack of tumorigenic effects at
the high-dose group is believed to be
due to the hepatotoxicity observed in
this group. At high dose,
Crotonaldehyde is cytotoxic; cells died
before neoplasms are manifested.
Crotonaldehyde and other alpha, beta-
unsaturated carbonyls are chemically
reactive compounds which can readily
react with cellular macromolecules such-
as DNA and proteins. Mutagenicity
studies in a slightly modified
preincubation Ames test have clearly
shown that Crotonaldehyde is
mutagenic. EPA believes that there is
sufficient evidence for listing
Crotonaldehyde on EPCRA section 313
pursuant to EPCRA section 313(d)(2)(B)
based on the available carcinogenicity
and mutagenicity data for this chemical.
55. Cyanazine (CAS No. 021725-46-2)
(CAL; FIFRA SR) (Ref. 8). Cyanazine is
a triazihe-type herbicide. In a three-
generation reproduction study in Long-
Evans rats, Fsb female weanlings had
increased relative brain weights and
decreased relative kidney weights. The
LOAEL was 4.05 mg/kg/day and the
NOAEL was 1.35 mg/kg/day. In rabbits
that received cyanazine in gelatin
capsules during gestation days 6 to 18,
there was increased postimplantation
loss, decreased litter size, and
alterations in ossification. In addition,
there were increased malformations in
the offspring, including anophthalmia/
microphthalmia, dilated brain
ventricles, dome cranium and
thoracoschisis (the LOAEL was 2 mg/kg/
day; the NOAEL was 1 mg/kg/day).
Similar developmental effects were
reported in Fischer 344 rats
administered cyanazine during gestation
days 6 to 15 (the LOAEL was 25 mg/kg/
day; the NOAEL 5 was mg/kg/day), EPA
believes that there is sufficient evidence
for listing cyanazine on EPCRA section
313 pursuant to EPCRA section
313(d)(2)(B) based on the developmental
toxicity data for this chemical.
56. Cycloate (CAS No. 001134-23-2)
(FIFRA AI) (Ref. 3). Cycloate, a
carbamate pesticide, is a cholinesterase
inhibitor. Symptoms of poisoning
include salivation, lacrimation,
convulsions, and death. Depressed
plasma cholinesterase was observed in a
9-week rat inhalation study at 0.0025
mg/L. The NOEL was less than 0.0025
mg/L. Decreased serum cholinesterase
(in males and females) and Wallerian
degeneration of nerve fibers in spinal
cord and sciatic nerve (females) were
observed at 0.12 mg/L in a 10-week rat
inhalation study (cholinesterase NOEL
is 0.012 mg/L). In both inhalation
studies, animals were exposed for 6
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hours/day, 5 days/week. Plasma, red
blood cell, and brain cholinesterase
inhibition was reported in rats fed 8 mg/
kg/day for 2 years. The NOEL was less
than 8 mg/kg/day. Dose-related
neuropathy and muscle myopathy were
observed. In a 2—year rat feeding study,
distended myelin sheath demyelination
and nerve fiber loss occurred at 3 mg/
kg/day (LOEL). The NOEL was 0.5 mg/
kg/day.
Decreased weight and survival were
observed in the offspring of rats orally
administered 24 mg/kg/day (LOEL) and
72 mg/kg/day of cycloate, respectively
(duration and frequency of dosing not
reported). The reproductive NOEL was
8 mg/kg/day. Decreased pup weight was
observed at 20 mg/kg/day and decreased
pup survival was observed at 50 mg/kg/
day in a 2-generation rat reproduction
study. The NOEL values for these
endpoints were 2.5 mg/kg/day and 20
mg/kg/day, respectively.
EPA believes that there is sufficient
evidence for listing cycloate on EPCRA
section 313 pursuant to EPCRA section
313(d)(2)(B) based on the available
neurological and developmental toxicity
data.
57. Cyclohexanol (CAS No. 000108-
93-0) (TSCA) (Ref. 8). Four rabbits
exposed to 997 ppm (4 mg/L) for 11
days (6 hours/day, 5 days/week) and a
rabbit receiving dermal applications of
approximately 2,500 mg/kg/day for 10
days (1 hour/day) developed tremors,
central nervous system depression,
lethargy or hypothermia.
Microscopic or degenerative changes
were observed in the livers and kidneys
of rabbits inhaling 145 ppm (0.59 mg/L)
of cyclohexanol for 50 days (6 hours/
day, 5 days/week), or repeated doses at
272 ppm (1.1 mg/L). In addition,
degenerative myocardial effects were
observed at this exposure level.
Repeated inhalation exposure to higher
doses (997 to 1,229 ppm; 4 to 5 mg/L)
in rabbits resulted in degenerative
changes in the brain and heart as well
as liver and kidneys.
Reproductive effects including
testicular atrophy, loss of Type A
spermatogonia, spermatocytes and
spermatozoa, "shrinkage" of
seminiferous tubules and Leydig cells,
reductions in RNA protein, sialic acid,
and glycogen in testes, epididymis and
seminal vesicles and increased
testicular cholesterol and alkaline
phosphatase were observed in male rats
or gerbils exposed to 15 mg/kg of
cyclohexanol for 21 to 37 days. These
changes were accompanied with
decreased fertility, and occurred at
exposure levels which had no effect on
the liver or kidney.
EPA believes that there is sufficient
evidence for listing cyclohexanol on
EPCRA section 313 pursuant to EPCRA
section 313(d)(2)(B) based on4he
chronic neurological, hepatic, renal,
myocardial, and reproductive toxicity
data for this chemical.
58. Cyfluthrin (3-(2,2-
Dichloroethenyl)-2,2-
dimethylcyclopropanecarboxylicacid,
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 LCso of 0.68 ppb, a bluegill 96-
hour LC50 of 1.5 ppb, and a daphnid 48-
hour ECso 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-
dimethylcyclopropanecarboxylicacid
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.
60. Cyromazine (N-cyclopropyl-1,3,5-
triazine-2,4,6-triamine) (CAS No.
066215-27-8) (FIFRA AI) (Ref. 3). In a 6-
month dog feeding study, 7.5 mg/kg/day
(LOEL) produced changes in hematocrit
and hemoglobin levels. The NOEL was
0.75 mg/kg/day. Based on the NOEL, ah
oral RfD of 0.0075 mg/kg/day was
derived. In a 90-day dog feeding study,
the LOEL of 25 mg/kg/day produced an
increase in relative liver weights in
males. The NOEL was 7.5 mg/kg/day. In
a 90-day rat feeding study, the LOEL of
15 mg/kg/day produced a decrease in
relative liver weights in males. The
NOEL was 1.5 mg/kg/day. EPA believes
that there is sufficient evidence for
listing cyromazine on EPCRA section
313 pursuant to EPCRA section
313(d)(2)(B) based on the available
hematological toxicity data.
61. Dazomet (tetrahydro-3,5-dimethyl-
2H-l,3,5-thiadiazine-2-thione) (CAS No.
000533-74-4) (FIFRA AI) (Ref. 3).
Animals fed dazomet at a dietary dose
of 40 ppm for 2 years showed focal
necrosis and fatty metamorphosis of the
liver. Rats fed 30.3 mg/kg/day
experienced decreased weight gain and
changes in liver weight. Renal focal
tubular necrosis was seen in rats fed 10
ppm (0.5 mg/kg/day) for 2 years. EPA
believes that there is sufficient evidence
for listing dazomet on EPCRA section
313 pursuant to EPCRA section
313(d)(2)(B) based on the available
hepatic and renal toxicity data for this
chemical.
62. Dazomet sodium salt (tetrahydro-
3,5-dimethyl-2H-l,3,5-thiadiazine-2-
thione, ion(l-), sodium) (CAS No.
053404-60-7) (FIFRA AI) (Ref. 3). The
available toxicity data is on dazomet.
Rats fed 80 ppm for 2 years (4 mg/kg/
day) showed focal necrosis and fatty
metamorphosis of the liver. Rats fed
30.3 mg/kg/day experienced decreased
weight gain and changes in liver weight.
Renal focal tubular necrosis was seen in
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rats fed 10 ppm (0.5 mg/kg/day) for 2
years. EPA believes that there is
sufficient evidence for listing dazomet
sodium on EPCRA section 313 pursuant
to EPCRA section 313(d)(2){B) based on
the available renal toxicity data for its
free add, dazomet.
63. 2,4-DB (CAS No. 000094-82-6)
(FIFRA SR) (Ref. 8). 2,4-DB (4-(2,4-
dichlorophenoxyjbutanoic acid) is a 2,4-
dichlorophenoxy-type herbicide. In a
study involving beagle dogs fed a diet
containing 2,4-DB for 90 days, a LOAEL
of 25 mg/kg/day was determined, based
on internal hemorrhaging and mortality
observed during the first 3 to 9 weeks
of treatment. The NOAEL in this study
was 8 mg/kg/day. At this dose level,
slight increases in liver weights were
observed, but unaccompanied by any
gross or histopathologic lesions. EPA
has derived an oral RfD of 0.008 mg/kg/
day from the LOAEL. In a subchronic rat
feeding study, the LOAEL and NOAEL
values determined were higher (the
LOAEL was approximately 80 to 100
mg/kg/day; the NOAEL was
approximately 25 to 30 mg/kg/day), and
were based on severe liver and kidney
damage.
In the above-mentioned subchronic
(90-day) dog feeding study, it was
observed that the animals exposed to
doses of 2,4-DB at 25 mg/kg/day (the
LOAEL) and higher exhibited
aspermatogenesis within the first 3 to 9
weeks of treatment. The offspring of rats
orally exposed to 17 mg/kg of 2,4-DB
during days 1 to 7 of gestation
developed abnormalities. There was
also an increase in stillbirths at this
dose level. In a separate study, offspring
of rats orally exposed to 416 mg/kg on
days 5 or 9 of gestation exhibited
increased preirnplantation loss and/or
developmental toxicity.
EPA believes that there is sufficient
evidence for listing 2,4-DB on EPCRA
section 313 pursuant to EPCRA section
313(d)(2)(B) based on the hepatic,
reproductive, and developmental
toxicity data for this chemical.
64.2,4-D butoxyethyl ester (CAS No.
001929-73-3) (CERCLA; FIFRA AI;
IARC) (Ref. 8). 2,4-D butoxyethyl ester is
a 2,4-dichlorophenoxy-type herbicide.
In mammals, the butoxyethyl ester of
2,4-D is hydrolyzed to yield the free
acid, 2,4-D. Therefore, the toxicity of
2,4-D butoxyethyl ester is expected to be
similar to that of 2,4-D, in which the
kidney, liver, and nervous system are
the primary targets of injury. EPA
believes that there is sufficient evidence
for listing 2,4-D butoxyethyl ester on
EPCRA section 313 pursuant to EPCRA
section 313(d)(2)(B) oased on the known
chronic effects of its metabolite 2,4-D.
65. 2,4-D butyl ester (CAS No. 000094-
80-4) (CERCLA; FIFRA AI; IARC) (Ref.
8). 2,4-D butyl ester is a 2,4-
dichlorophenoxytype herbicide. In
mammals, the butyl ester of 2,4-D is
hydrolyzed to yield the free acid, 2,4-D.
Therefore, the toxicity of 2,4-D butyl
ester is expected to be similar to that of
2,4-D, in which the kidney, liver, and
nervous system are the primary targets
of injury. EPA believes that there is
sufficient evidence for listing 2,4-D
butyl ester on EPCRA section 313
pursuant to EPCRA section 313(d)(2)(B)
based on the known toxic effects of its
metabolite 2,4-D.
66. 2,4-D chlorocrotyl ester (CAS No.
002971-38-2) (CERCLA; FIFRA AI;
IARC) (Ref. 8). 2,4-D chlorocrotyl ester
is a 2,4-dichlorophenoxy-type herbicide.
In mammals, the chlorocrotyl ester of
2,4-D is hydrolyzed to yield the free
acid, 2,4-D. Therefore, the toxicity of
2,4-D chlorocrotyl ester is expected to
be similar to that of 2,4-D, in which the
kidney, liver and nervous system are the
primary targets of injury. T2PA believes
that there is sufficient evidence for
listing 2,4-D chlorocrotyl ester on
EPCRA section 313 pursuant to EPCRA
section 313(d)(2)(B) based on the known
toxic effects of its metabolite 2,4-D.
67. Desmedipham (CAS No. 013684-
56-5) (FIFRA AI) (Ref. 3). In a 90-day
dog study, groups of four beagles/sex
were fed diets containing 0 to 5.24 mg/
kg/day. This caused increased
methemoglobin at 5.24 mg/kg/day
(LOEL). EPA believes that there is
sufficient evidence for listing
desmedipham on EPCRA section 313
pursuant to EPCRA section 313(d)(2)(B)
based on the available hematological
toxicity data.
68.2,4-D 2-ethylhexyl ester (CAS No.
001928-43-4) (CERCLA; FIFRA AI;
IARC) (Ref. 8). 2,4-D 2-ethylhexyl ester
is a 2,4-dichlorophenoxy-type herbicide.
The 2-ethylhexyl moiety contains eight
carbons and, therefore, is an isooctyl
group. Developmental toxicity following
maternal exposure to 2,4-D isooctyl
esters has been demonstrated in the rat
and mouse. Fetotoxicity occurred in
offspring of rats exposed to 528 mg/kg
during gestation days 8 through 11. Rats
orally exposed to doses as low as 302
mg/kg during gestation days 9 through
12 had musculoskeletal abnormalities.
Exposure to a lower dose (188 mg/kg)
for a longer period during gestation
(days 6 through 15) caused
developmental effects on homeostasis
and effects on newborn growth
statistics. In mice, 438 mg/kg
administered orally during gestation
days 8 to 12 also caused effects on
newborn growth statistics.
EPA believes that there is sufficient
evidence for listing 2,4-D 2-ethylhexyl
ester on EPCRA section 313 pursuant to
EPCRA section 313(d)(2)(B) based on
the developmental toxicity data for 2,4-
D isooctyl esters, and on the toxic
effects of its metabolite 2,4-D.
The aquatic acute toxicity data for 2,4-
D isooctyl esters include a measured
48-hour LCso of 8.8 ppm for bluegill. In
addition, 2,4-D isooctyl esters are
expected to bioaccumulate based on the
estimated log KOW of 6.6. EPA believes
that there is sufficient evidence for
listing 2,4-D 2-ethylhexyl ester on
EPCRA section 313 pursuant to EPCRA
section 313(d)(2)(C) based on the
available environmental toxicity data
and the potential for bioaccumulation.
69. 2,4-D 2-ethyl-4-methylpentyl ester
(CAS No. 053404-37-8) (CERCLA;
FIFRA AI; IARC) (Ref. 8). 2,4-D 2-ethyl-
4-methylpentyl ester is a 2,4-
dichlorophenoxy-type herbicide. The 2-
ethyl-4-methylpentyl ester moiety
contains eight carbons and, therefore, is
an isooctyl group. Developmental
toxicity following maternal exposure to
2,4-D isooctyl esters has been
demonstrated in the rat and mouse.
Fetotoxicity occurred in offspring of rats
exposed to 528 mg/kg during gestation
days 8 through 11. Rats orally exposed
to doses as low as 302 mg/kg during
gestation days 9 through 12 had
musculoskeletal abnormalities.
Exposure to a lower dose (188 mg/kg)
for a longer period during gestation
(days 6 through 15) caused
developmental effects on homeostasis
and effects on newborn growth
statistics. In mice, 438 mg/kg
administered orally during gestation
days 8 through 12 also caused effects on
newborn growth statistics.
EPA believes that there is sufficient
evidence for listing 2,4-D 2-ethyl-4-
methylpentyl ester on EPCRA section
313 pursuant to EPCRA section
313(d)(2)(B) based on the developmental
toxicity data for 2,4-D isooctyl esters,
the toxic effects of its metabolite 2,4-D.
The aquatic acute toxicity data for 2,4-
D isooctyl esters include a measured
48-hour LCso of 8.8 ppm for bluegill. In
addition, 2,4-D isooctyl esters are
expected to bioaccumulate based on the
estimated log KOW of 6.6. EPA believes
that there is sufficient evidence for
listing 2,4-D 2-ethyl-4-methylpentyl
ester on EPCRA section 313 pursuant to
EPCRA section 313(d)(2)(C) based on
the available environmental toxicity
data and the potential for
bioaccumulation.
70. Diazinon (CAS No. 000333-41-5)
(CERCLA; FIFRA SR) (Ref. 8). Diazinon,
' an organophosphate insecticide, causes
plasma cholinesterase inhibition and
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central nervous system depression.
Significant inhibition of plasma
cholinesterase was observed in two men
administered five doses of 0.025 mg/kg/
day. Diazinon administered to men at
doses of 0.05 mg/kg/day for 28 days
caused a 35 to 40 percent reduction in
plasma cholinesterase. A NOEL for
cholinesterase inhibition of 0.02 mg/kg/
day was identified from several
controlled studies in humans. Clinical
symptoms of diazinon poisoning
include headache, nausea, sweating,
vomiting, and diarrhea all of which are
indicative of neurotoxicity. Plasma
cholinesterase inhibition (93 percent)
and red blood cell inhibition (90
percent) occurred in monkeys orally
exposed to diazinon in doses of 5 mg/
kg/day for 52 weeks. The NOEL for
inhibition of cholinesterase in this study
was 0.05 mg/kg/day and the LOEL was
0.5 mg/kg/day.
Urogenital defects in the offspring of
female rats orally administered diazinon
at doses of 26.4 mg/kg on days 12 to 15
of gestation has been reported. Diazinon
also induced musculoskeletal
abnormalities in offspring when
administered orally to mothers at doses
of 45 mg/kg on days 8 to 12 of gestation.
Post-implantation mortality was
increased in female rats administered
63.5 mg/kg on day 10 of gestation.
Similar reproductive and developmental
effects were observed in mice. Oral
administration of 3.96 mg/kg of
diazinon (days 1 to 22 of gestation)
caused decreased litter size and delayed
behavioral effects in the newborn. Doses
of 0.210 mg/kg and 3.78 mg/kg
administered orally on days 1 to 21 of
gestation caused abnormalities in the
immune and reticuloendothelial system
and biochemical and metabolic
abnormalities of the offspring,
respectively.
EPA believes that there is sufficient
evidence for listing diazinon on EPCRA
section 313 pursuant to EPCRA section
313(d)(2)(B) based on the developmental
and chronic neurotoxicity data for this
chemical.
Measured aquatic acute toxicity data
for diazinon include a 96-hour LCso for
rainbow trout of 90 ppb and a daphnid
96-hour LCso of 0.90 ppb. In addition,
measured terrestrial wildlife acute
toxicity data for diazinon include an
oral LDso for male mallard ducks of 3.54
mg/kg and an oral LD50 for male
pheasants of 4.33 mg/kg. EPA believes
that there is sufficient evidence for
listing diazinon on EPCRA section 313
pursuant to EPCRA section 313(d)(2)(C)
based on the environmental toxicity
data for this chemical.
71. 2,2-Dibromo-3-
nitrilopropionamide (CAS No. 010222-
01-2) (FIFRA AI) (Ref. 3). Oral
administration of 50 mg/kg/day (LOEL)
to rats for 4 weeks produced dyspnea
and weight loss. The NOEL was 25 mg/
kg/day. Oral administration of 30 mg/
kg/day to rats for 13 weeks produced
dyspnea. The NOEL was 13 mg/kg/day.
These data may be indicative of direct
effects of the compound on the
respiratory system. EPA believes that
there is sufficient evidence for listing
2,2-dibromo-3-nitrilopropionamide on
EPCRA section 313 pursuant to EPCRA
section 313(d)(2)(B) based on the
available chronic respiratory data.
72. Dicamba (3,6-Dichloro-2-
methyoxybenzoic acid) (CAS No.
001918-00-9) (FIFRA AI) (Ref. 3).
Decreased fetal body weights and
increased post-implantation loss was
observed in the offspring of rabbits
receiving 10 mg/kg/day of dicamba on
days 6 through 18 of gestation. The
LOEL was 10 mg/kg/day and NOEL was
3 mg/kg/day. Based on the NOEL, EPA
derived an oral RiD value of 0.03 mg/
kg/day. In a separate study, disorders of
oxidative phosphorylation and focal
necrosis in the heart were observed in
newborn rats following transplacental
exposure to dicamba. In a
developmental toxicity study, an
increase in skeletal malformations was
seen in the offspring of rats orally
administered 64 mg/kg/day on days 6
through 19 of gestation. EPA believes
that there is sufficient evidence for
listing dicamba on EPCRA section 313
pursuant to EPCRA section 313(d)(2)(B)
based on the available developmental
toxicity data for this chemical.
73. Dichloran (2,6-Dichloro-4-
nitroaniline) (CAS No. 000099-30-9)
(FIFRA AI) (Ref. 3). Dichloran, an
aniline, is a potential inducer of
methemoglobinemia. Either single or
repeated oral doses of dichloran
produced enlarged livers and induction
of microsomal enzymes in the rat. Dogs
fed 21 mg/kg/day had increases in
serum transaminases. In Rhesus
monkeys, where dichloran does not
induce hepatic enzymes, 160 mg/kg/day
for 3 months caused hepatic
centrilobular fatty infiltration and death.
Inhalation exposure to 0.17 mg/L
produced elevated cholesterol levels
and increased liver weight in a 3-month
rabbit study and increased liver weight
in a 21-day rat study. In a 2-year mouse
study, dietary administration of 102.7
mg/kg/day (LOEL) produced
centrilobular hepatocyte enlargement,
focal necrosis, acute inflammatory Cell
infiltration, vacuolization of
centrilobular hepatocytes, increased
weight of the liver and increased
incidence of erythropoiesis in males.
The NOEL was 30 mg/kg/day. EPA
believes that there is sufficient evidence
for listing dichloran on EPCRA section
313 pursuant to EPCRA section
313(d)(2)(B) based on the available
hepatic toxicity data.
74. 3,3'-Dichlorobenzidine
dihydrochloride (CAS No. 000612-83-9)
(TSCA) (Ref. 8). IARC has classified
3,3'dichlorobenzidine (o-
dichlorobenzidine) as a group 2B
compound, i.e. this chemical is possibly
carcinogenic in humans. IARC uses the
generic name 3,3'-dichlorobenzidine
interchangeably with 3,3'-
dichlorobenzidine dihydrochloride. The
dihydrochloride salt of 3,3'-
dichlorobenzidine is expected to be
equally as toxic as the free base (3,3'-
dichlorobenzidine). EPA believes that
there is sufficient evidence for listing
3,3'-dichlorobenzidine dihydrochloride
on EPCRA section 313 pursuant to
EPCRA section 313(d)(2)(B) based on its
potential to cause cancer in humans.
75. 3,3'-Dichlorobenzidine sulfate
(CAS No. 064969-34-2) (TSCA) (Ref. 8).
IARC has classified 3,3'-
dichlorobenzidine (o-
dichlorobenzidine) as a group 2B
compound, i.e. this chemical is possibly
carcinogenic in humans. The sulfate salt
of 3,3'dichlorobenzidine is expected to
be equally as toxic as the free base (3,3'-
dichlorobenzidine). EPA believes that
there is sufficient evidence for listing
3,3'-dichlorobenzidine sulfate on
EPCRA section 313 pursuant to EPCRA
section 313(d)(2)(B) based on its
potential to cause cancer in humans.
76. trans-l,4-Dichloro-2-butene (CAS
No. 000110-57-6) (EPCRA EHS) (Ref. 8).
Mortality in two of six rats was observed
following inhalational exposure to 62
ppm (0.34 mg/L) for 4 hours. An acute
inhalation LC5o in rats was 86 ppm (0.44
mg/L). EPA's exposure analysis
indicates that trans-l,4-dichloro-2-
butene 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 trans-1,4-
dichloro-2-butene on EPCRA section
313 pursuant to EPCRA section
313(d)(2)(A) based on the available
acute toxicity and exposure data for this
chemical.
77. Dichloromethylphenylsilane (CAS
No. 000149-74-6) (EPCRA EHS) (Ref. 8).
As a class, chlorinated silanes are very
corrosive to the skin and mucous
membranes and liberate hydrochloric
acid in the presence of water. The 2-
hour mouse inhalation LCso value for
dichloromethylphenylsilane is 0.17 mg/
L. EPA's exposure analysis indicates
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1808 Federal Register / Vol. 59, No. 8 / Wednesday, January 12, 1994 / Proposed Rules
that dichloromethylphenylsilane
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 dichloromethylphenylsilane
on EPCRA section 313 pursuant to
EPCRA section 313(d)'(2)(A) based on
the available acute toxicity and
exposure data for this chemical.
78. Dichlorophene (2,2'-
methylenebis(4-chlorophenol) (CAS No.
000097-23-4) (FIFRA AI) (Ref. 3).
Increased incidence of microphthalmia
was observed in the offspring of rats
administered 25 mg/kg/day (teratogenic
LOEL). The NOEL was 5.0 mg/kg/day. A
dose of 75 mg/kg/day (fetotoxic LOEL)
produced delayed ossification of
vertebral centra and sternaebrae,
reduced body weight and length, and
increased resorptions in rat fetuses. The
fetotoxic NOEL was 5.0 mg/kg/day. No
other developmental studies were
available. EPA believes that there is
sufficient evidence for listing
dichlorophene on EPCRA section 313
pursuant to EPCRA section 313(d)(2)(B)
based on the available developmental
toxicity data.
Aquatic acute toxicity values for
dichlorophene include a measured 48-
hour LCjo of 50 ppb for Spicodioptomus
(calanoid copipod). EPA believes that
there is sufficient evidence for listing
dichlorophene on EPCRA section 313
pursuant to EPCRA section 313(d)(2)(C)
based on the available environmental
toxicity data.
79. trans-l,3-Dichloropropene (CAS
No. 010061-02-6) (CERCLA; CWA PPL)
(Ref. 8). Clinical reports have
documented the occurrence of
histiocytic lymphoma in two firemen
and acute myelomonocytic leukemia in
a farmer exposed accidently to 1,3-
dichloropropene. Information on the
isomer or isomer mixture (i.e., trans/cis
isomers) was not specified. The
lymphoma and leukemia were refractory
to treatment, and all three men died.
There is evidence that 1,3-
dichloropropene may cause cancer in
rats and mice after oral exposure. In a
2-year gavage study, rats treated with 25
or 50 mg/kg/day 1,3-dichloropropene
(53 percent ris isomer, 45 percent trans
isomer, 1 percent epiehlorhydrin)
developed squamous cell papillomas
and carcinomas of the forestomach.
Male rats also developed neoplastic
nodules of the liver. Female mice that
received 50 or 100 mg/kg/day developed
squamous cell papillomas and
carcinomas of the forestomach,
transitional cell carcinomas of the
urinary bladder, and an increased
incidence of alveolar/bronchiolar
adenomas. A statistically significant
increase in bronchloalveolar adenomas
was noted in male mice exposed to 60
ppm (272 mg/L) 1,3-dichloropropene
vapors (50 percent cis isomer, 43
percent trans isomer). This benign lung
tumor was not seen in female mice or
in male or female rats. IARC assigned
1,3-dichloropropene to Group 2B, i.e.,
possibly carcinogenic in humans. EPA
believes that there is sufficient evidence
for listing trans-l,3-dichloropropene on
EPCRA section 313 pursuant to EPCRA
section 313(d)(2)(B) based on the
available carcinogenicity data for 1,3-
dichloropropene (unspecified isomer).
80. Didofop methyl (2-[4-(2,4-
dichlorophenoxy) phenoxyjpropanoic
add, methyl ester) (CAS No. 051338-27-
3) (FIFRA AI) (Ref. 3). In a rat teratology
study, increased resorptions, reduced
body weights, and dilation of the renal
pelvis or distension of the ureter in
offspring were reported in rats fed 1.6
mg/kg/day (LOEL). The NOEL was 0.5
mg/kg/day. Increased pup mortality was
observed at 5 mg/kg/day (LOEL) in a 3-
generation rat reproduction study. The
NOEL was 1.5 mg/kg/day.
In a 30-day rat feeding study,
increased relative heart, liver, and
kidney weights were observed at the
LOEL of 4 mg/kg/day. No NOEL was
established. Jaundice, increased
bilirubin, increased serum glutamic-
pyruvic transaminase and serum
glutamic-oxaloacetic transaminase, and
increased liver and kidney weights were
observed in a 30-day dog feeding study
at 50 mg/kg/day. The NOEL was 12.5
mg/kg/day. In a 90-day rat feeding
study, elevated liver weights and
centrilobular enlargement of hepatic
cells were observed at 4 mg/kg/day. The
NOEL was 1.6 mg/kg/day. Dogs fed 6.25
mg/kg/day for 90 days had increased
hpid content and focal changes in the
renal cortex. The NOEL was 2 mg/kg/
day. EPA believes that there is sufficient
evidence for listing diclofop methyl on
EPCRA section 313 pursuant to EPCRA
section 313(d)(2)(B) based on the
available developmental, hepatic, and
renal toxicity data.
81. Dicyclopentadiene (CAS No.
000077-73-6) (TSCA) (Ref. 8).
Convulsions were reported in rats or
mice following inhalation of
dicyclopentadiene at dosage levels of
332 or 145 ppm (1.8 or 0.78 mg/L),
respectively, for 1 or 2 days. The
reported acute oral LD5o in rats is 353
mg/kg. Animals at this dose level had
convulsions and muscle weakness. In a
90-day inhalation study in dogs,
neurotoxic symptoms observed
included diarrhea, excessive salivation
and lack of control of hind quarters. The
NOAEL in this study was 8.9 ppm
(0.048 mg/L); no LOEL was reported.
EPA believes that there is sufficient
evidence for listing dicyclopentadiene
on EPCRA section 313 pursuant to
EPCRA section 313(d)(2)(B) based on
the chronic neurotoxicity data for this
82. Die'thatyl ethyl (CAS No. 038727-
55-8) (FIFRA AI) (Ref. 3). In a 2-year
study, groups of six beagles/sex were
given doses orally from 0 to 31.25 mg/
kg/day. The lowest dose (0.25 mg/kg/
day) produced a positive Coombs test.
EPA believes that there is sufficient
evidence for listing diethatyl ethyl on
EPCRA section 313 pursuant to EPCRA
section 313(d)(2)(B) based on the
available hematological toxicity data for
this chemical.
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
LCso 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.
84. Diglycidyl resorcinol ether (CAS
No. 000101-90-6) (IARC; NTP) (Ref. 8).
Diglycidyl resorcinol ether is classified
by IARC as a Group 2B compound, i.e.,
it is possibly carcinogenic in humans. In
an NTP bioassay, rats orally
administered 12 mg/kg of diglycidyl
resorcinol ether 5 days a week for 103
weeks developed squamous cell
papillomas and squamous cell
carcinomas of the stomach. Mice orally
administered 50 mg/kg 5 days a week
for 103 weeks developed squamous cell
carcinomas and squamous cell
papillomas of the stomach. Mice orally
administered 70.5 mg/kg/day of
diglycidyl resorcinol ether for 2 years
developed blood lymphomas and
Hodgkin's disease. Mice receiving
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1809
dermal applications of diglycidyl
resorcinol ether for 1-year developed
skin tumors. EPA believes that there is
sufficient evidence for listing diglycidyl
resorcinol ether on EPCRA section 313
pursuant to EPCRA section 313(d)(2)(B)
based on the carcinogenicity data for
this chemical.
85. Dimethipin (2,3,-Dihydro-5,6-
dimethyl-l,4-dithiin 1,1,4,4-tetraoxide)
(CAS No. 055290-64-7) (FIFRA AI) (Ref.
3). In a 1—year dog feeding study,
decreased erythrocyte, hemoglobin, and
hematocrit levels as well as increased
platelet levels were observed at 75 mg/
kg/day. The LOEL for systemic toxicity
based on decreased body weight was 7.5
mg/kg/day. No NOEL could be
established. In a 2-year rat feeding
study, increased absolute and relative
liver weights were observed at 10 mg/
kg/day (LOEL). The NOEL was 2 mg/kg/
day. Based on the NOEL in the study,
EPA established an oral RfD of 0.02 mg/
kg/day. EPA believes that there is
sufficient evidence for listing ,
dimethipin on EPCRA section 313
pursuant to EPCRA section 313(d)(2)(B)
based on the available hematological
and hepatic toxicity data.
86. Dimethoate (CAS No. 000060-51-
5) (CERCLA; EPCRA EHS; FIFRA SR;
RCRA APP8; RCRA P) (Ref. 8).
Dimethoate is an organophosphate
insecticide. In humans, dimethoate
causes typical symptoms of
cholinesterase inhibition (sweating,
diarrhea, salivation, headache, difficulty
in breathing, etc.). In a controlled
human study, subjects were
administered dimethoate for 57 days.
Whole blood and erythrocyte
cholinesterase inhibition was observed
from day 20 on. The NOEL was 0.202
mg/kg/day, and the LOEL was 0.434 mg/
kg/day. In another study in which
humans were administered dimethoate
for 57 days, the NOEL for cholinesterase
inhibition was 15 mg/day (0.2 mg/kg
based on a 70 kg person). The LOEL was
not specified. Cholinergic symptoms
reflective of cholinesterase inhibition
following dimethoate administration
have also been observed in laboratory
animals. A 2-year feeding study in rats
determined the NOEL and LOEL for
plasma and brain cholinesterase
inhibition to be 0.05 and 0.5 mg/kg/day,
respectively.
Dimethoate was tested for
developmental effects in Wistar rats.
Cygon 4E (47.3 percent dimethoate, 52.7
percent unspecified constituents) was
administered to pregnant females on
days 6 to 15 of gestation. The NOEL for
developmental effects was 6 mg/kg/day.
At a LOEL of 12 mg/kg/day, an increase
in the incidence of wavy ribs was
observed in the fetuses. An increase in
offspring mortality occurred in a five-
generation chronic feeding study (actual
doses were 9.5 to 10.5 mg/kg/day) in
male and female CD-I mice. At 12 mg/
kg/day (120 mg/kg, gestation days 6 to
15), musculoskeletal abnormalities were
observed in the rat offspring. EPA
believes that there is sufficient evidence
for listing dimethoate on EPCRA section
313 pursuant to EPCRA section
313(d)(2)(B) based on the available
developmental and neurotoxicity data
for this chemical.
87. 3,3'-Dimethoxybenzidine
dihydrochloride (o-Dianisidine
dihydrochloride) (CAS No. 020325-40-0)
(TSCA) (Ref. 8). IARC has classified 3,3'-
dimethoxybenzidine (o-dianisidine) as a
Group 2B compound, i.e., this chemical
is possibly carcinogenic. In an NTP
carcinogenicity bioassay, increases in
neoplasms of the skin, oral cavity, large
intestine, liver, uterus, and cervix were
noted in rats administered this chemical
in drinking water at dose levels of 6,12,
or 21 mg/kg/day in males and 7,14, or
23 mg/kg/day in females. The
dihydrochloride salt of o-dianisidine is
expected to be equally as toxic as the
free base (o-dianisidine). EPA believes
that there is sufficient evidence for
listing 3,3'-dimethoxybenzidine
dihydrochloride on EPCRA section 313
pursuant to EPCRA section 313(d)(2)(B)
based on its potential to cause cancer in
humans.
88. 3,3'-Dimethoxybenzidine
hydrochloride (o-Dianisidine
hydrochloride) (CAS No. 111984-09-9)
(TSCA) (Ref. 8). IARC has classified 3,3'-
dimethoxybenzidine (o-dianisidine) as a
Group 2B compound, i.e., this chemical
is possibly carcinogenic. In an NTP
carcinogenicity bioassay, increases in
neoplasms of die skin, oral cavity, large
intestine, liver, uterus and cervix were
noted in rats administered this.chemical
in drinking water at dose levels of 6,12,
or 21 mg/kg/day in males and 7,14, or
23 mg/kg/day in females. The
hydrochloride salt of o-dianisidine is
expected to be equally as toxic as the
free base (o-dianisidine). EPA believes
that there is sufficient evidence for
listing 3,3'dimethoxybenzidine
hydrochloride on EPCRA section 313
pursuant to EPCRA section 313(d)(2)(B)
based on its potential to cause cancer in
humans.
89. Dimethylamine (CAS No. 000124-
40-3) (TSCA) (Ref. 8). Dimethylamine is
corrosive to the mucous membranes,
respiratory tract and eyes of treated
animals. B6C3F1 mice and F344 rats
exposed to 10 to 175 ppm (0.018 to 0.32
mg/L) dimethylamine via inhalation for
6 to 12 months developed dose-related
lesions in the respiratory and olfactory
epithelium. Significant decreases in
body weight occurred in high-dose (175
ppm; 0.32 mg/L) animals of both
species, and some of the high-dose mice
died following exposure.
Centrilobular fatty degeneration and
necrosis of parenchymal cells were
reported in mice, rats, rabbits or guinea
pigs administered 97 or 183 ppm (0.18
or 0.34 mg/L) dimethylamine via
inhalation for 18 to 20 weeks. Increased
liver weight without any
histopathological changes were reported
following 8-month oral exposure of rats
to 0.35 mg/kg/day and guinea pigs
exposed to 3.5 mg/kg/day.
Rats administered oral doses of
dimethylamine as low as 0.035 mg/kg
for 8 months exhibited changes in
conditional reflexes including marked
attenuation of the excitation process and
speedier extinction of the positive
reflex.
EPA believes that there is sufficient
evidence for listing dimethylamine on
EPCRA section 313 pursuant to EPCRA
section 313(d)(2)(B) based on the
chronic respiratory-, hepatic, and
neurological toxicity of this chemical.
90. Dimethylamine dicamba (CAS No.
002300-66-5) (FIFRA AI) (Ref. 3). In a
pilot rabbit developmental toxicity
study, an increase in early and late fetal
resorptions was observed in animals
receiving the LOEL of 1.0 mg/kg/day.
The NOEL was 0.5 mg/kg/day (oral
doses, days 6 to 18 of gestation). In
another study, increased post-
implantation loss was observed in
rabbits receiving the LOEL of 10 mg/kg/
day (oral doses, days 6 to 18 of
gestation). Developmental toxicity was
also observed at doses of 10 mg/kg/day
in studies with dicamba. EPA believes
that there is sufficient evidence for
listing dimethylamine dicamba on
EPCRA section 313 pursuant to EPCRA
section 313(d)(2)(B) based on the
available developmental toxicity data
for this chemical.
91. 3,3'-Dimethylbenzidine
dihydrochloride (o-Tolidine
dihydrochloride) (CAS No. 000612-82-8)
(TSCA) (Ref. 8). In a bioassay conducted
by NTP, 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 (0.95 to
26.6 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
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gland in females, and leukemia in
Females were also noted in this study.
EPA believes that there is sufficient
evidence for listing 3,3'-
dimothylbenzidine dihydrochloride on
EPCRA section 313 pursuant to EPCRA
section 313(d)(2)(B) based on its
potential to cause cancer in humans.
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 carcinogenic!ty data for 3,3'-
dimethylbenzidine dihydrochloride.
93. Dimethyl chlorothiophosphate
(CAS. No. 002524-03-0) (EPCRA EHS)
(Ref. 8). In a dominant lethal study,
male rats were administered dimethyl
chlorothiophosphate by gavage for 5
consecutive days and mated to
untreated females. The LOEL of 7.5 mg/
kg/day was determined based on an
increase in preimplantation losses and
dead implants. No NOEL for dimethyl
chlorothiophosphate was determined
from this study. EPA believes that there
is sufficient evidence for listing
dimethyl chlorothiophosphate on
EPCRA section 313 pursuant to EPCRA
section 313(d)(2)(B) based on the
developmental toxicity data for this
chemical.
94. Dimethyldichlorosilane (CAS No.
000075-78-5) (CERCLA; EPCRA EHS)
(Ref. 8). As a class, however, chlorinated
silanes are very corrosive to the skin
and mucous membranes and liberate
hydrochloric acid in the presence of
water. Dimethyldichlorosilane causes
severe bums and the vapor is harmful
to humans. The 2-hour mouse
inhalation LCso value is 0.30 mg/L.
EPA's exposure analysis indicates that
dimethyldichlorosilane 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
dimethyldichlorosilane on EPCRA
section 313 pursuant to EPCRA section
313(d)(2)(A) based on the available
acute toxicity and exposure data for this
chemical.
95. N,N-Dimethylformamide (CAS No.
000068-12-2) (CAA HAP) (Ref. 7). In
humans, N,N-dimethylformamide
(DMF) produced an increase in
subjective symptoms suggestive of mild
liver dysfunction in workers and
changes in objective measurements of
liver damage (serum enzymes and liver
enlargement) via inhalation exposure,
resulting in a LOAEL of 22 mg/m3
(adjusted LOAEL of 7.9 mg/m3)).
Although there are several additional
studies which are generally inadequate
when considered individually, taken
together, these studies demonstrate that
DMF exposure is associated with
hepatic toxicity in humans. Several
animal inhalation studies further
support the hepatotoxic effects of DMF.
EPA believes that there is sufficient
evidence for listing N,N-
dimethylformamide on EPCRA section
313 pursuant to EPCRA section
313(d)(2)(B) based upon the available
hepatotoxicity data for this chemical.
96.2,6-Dimethylphenol (000576-26-1)
(TSCA) (Ref. 8). Oral administration of
2,6-dimethylphenol to rats for 8 months
produced histologic lesions (the LOEL
was 6.0 mg/kg/day; the NOEL was 0.6
mg/kg/day) in the liver, kidneys, and
spleen. Another supporting oral study
in rats that also reported histological
lesions in the liver and kidneys (the
LOEL was 6.0 mg/kg/day; the NOEL was
0.06 mg/kg/day) of rats following
subchronic oral administration of 2,6-
dimethylphenol. EPA believes that there
is sufficient evidence for listing 2,6-
dimethylphenol on EPCRA section 313
pursuant to EPCRA section 313(d)(2)(B)
based on the hepatotoxicity and
nephrotoxicity data for this chemical.
97. Dinocap (CAS No. 039300-45-3)
(CAL; FIFRA SR) (Ref. 8). Dinocap is a
dinitrophenyl-type fungicide. In mice,
oral administration of 25 mg/kg/day of
dinocap on days 7 to 16 of gestation has
been shown to increase post-
implantation mortality and reduce
newborn viability. Oral administration
of 5.0 mg/kg/day to pregnant mice
produced developmental toxicity in the
offspring (administration of 10 mg/kg/
day resulted in abnormalities of the
musculoskeletal and hepatobiliary
system in the offspring). In the same
study, oral administration of 20 mg/kg/
day on days 7 to 16 of gestation
produced craniofacial abnormalities in
offspring. In the same study, behavioral
abnormalities and delayed growth were
observed in offspring of mice receiving
12 mg/kg/day on days 7 to 16 of
gestation. EPA believes that there is
sufficient evidence for listing dinocap
on EPCRA section 313 pursuant to
EPCRA section 313(d)(2)(B) based on
the developmental toxicity data for this
chemical.
Measured aquatic acute toxicity data
for dinocap indicate that the LC5o for
rainbow trout is 15 ppb and the LC^o for
bluegill is 20 ppb. EPA believes that
there is sufficient evidence for listing
dinocap on EPCRA section 313 pursuant
to EPCRA section 313(d)(2)(C) based on
the environmental toxicity data for this
chemical.
98. Dinoseb (CAS No. 000088-85-7)
(CAL; EPCRA EHS; FIFRA SR; RCRA
APP8; RCRA P; SDWA) (Ref. 8). Dinoseb
is a dinitrophenyl-type herbicide and
insecticide. In a three generation
reproduction study dinoseb produced
decreased pup weights (the LOEL was 1
mg/kg/day; the NOEL was not
determined) in the Fib, Fja, and Fsa
pups. The Fib pup weights diminished
(combined sexes) by day 21 at dose
levels greater than 1 mg/kg/day. Other
studies have shown biologically and
statistically significant increases in
developmental malformations and/or
anomalies (the LOEL was 10 mg/kg/day;
the NOEL was 3 mg/kg/day), and an
increased incidence of an absence of
ossification for a number of skeletal
sites and supernumerary ribs (the LOEL
was not specified; the NOEL was 3 mg/
kg/day). Dinoseb administered by
gavage to rabbits from days 6 to 18 of
gestation produced neural tube defects
(the LOEL was 10 mg/kg/day; the NOEL
was 3 mg/kg/day).
The fertility index in male rats was
reduced in a reproductive study in
animals fed dinoseb at dose levels of
15.6 mg/kg/day at 22.2 mg/kg/day over
an 11-week period. Decreased seminal
vesicle weight, decreased sperm count
and increased incidence of abnormal
sperm were noted at dose levels of 9.1
mg/kg/day and higher. The NOEL was
3.8 mg/kg/day.
• EPA believes that there is sufficient
evidence for listing dinoseb on EPCRA
section 313 pursuant to EPCRA section
313(d)(2)(B) based on the developmental
and reproductive toxicity data for this
chemical.
Aquatic acute toxicity data for
.dinoseb include a measured fat-head
minnow 96—hour LCso of 88 ppb. EPA
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believes that there is sufficient evidence
for listing dinoseb on EPCRA section
313 pursuant to EPCRA section
313(d)(2)(C) based on the environmental
toxicity data for this chemical.
99. Diphenamid (CAS No. 000957-51-
7) (FIFRA SR) (Ref. 8). Diphenamid is a
diphenylacetamide-type herbicide. In a
2-year study in dogs fed diphenamid,
an increase in liver weight and an
increase in portal macrophages and
fibroblasts were seen at the LOEL of 10
mg/kg/day. The NOEL was 3 mg/kg/day.
Based on the NOEL, an RfD of 0.03 mg/
kg/day was derived. In a 2—year study
in rats fed diphenamid, an increase in
liver weight was seen at the LOEL of 30
mg/kg/day; the NOEL was 10 mg/kg/
day. Although, no histopathological
changes were reported in these studies,
biochemical changes accompanied by
histo-pathological changes were
observed in a 2-generation study in rat
pups. EPA believes that there is
sufficient evidence for listing
diphenamid on EPCRA section 313
pursuant to EPCRA section 313(d)(2)(B)
based on the available hepatotoxicity
data for this chemical.
100. Diphenylamine (CAS No.
000122-39-4) (RCRA APP8) (Ref. 8).
Increased liver and kidney weights were
noted in dogs that received 25 mg/kg/
day (the LOAEL) of diphenylamine in
their feed for 2 years. The NOAEL in
this study was 2.5 mg/kg/day and the
oral RfD was 0.025 mg/kg/day.
Pronounced anemia and decreased body
weight gain were also noted in these
animals. The hepatotoxicity induced by
diphenylamine is manifested by
peripherolobular fat changes and
increased lipids. Vacuolar degeneration
and hepatocyte necrosis were reported
in rats or guinea pigs that received 2,or
4 percent (i.e., 1,000 or 2,000 mg/kg/day
for rats and 800 to 1,600 mg/kg/day for
guinea pigs) of diphenylamine in die
diet for 6 months. In another 2-year rat
study, changes reported in the kidney in
diphenylamine-fed animals included
epithelial necrosis in the proximal
tubule, cystic dilatation of tubules, and
interstitial inflammation.
EPA believes that there is sufficient
evidence for listing diphenylamine on
EPCRA section 313 pursuant to EPCRA
section 313(d)(2)(B) based on the
chronic hepatic and renal toxicity data
for this chemical.
101. Dipotassium endothall (7-
oxabicyclo(2.2.1)heptane-2,3-
dicarboxylic acid, dipotassium salt)
(CAS No. 002164-07-0) (FIFRA AI) (Ref.
3). In a 2-year dog feeding study,
increased absolute and relative weight
of the stomach and small intestine was
observed at 6 mg/kg/day (LOEL). The
NOEL was 2 mg/kg/day. An oral RfD of
0.02 mg/kg/day was derived based on
the NOEL. EPA believes that there is
sufficient evidence for listing dipossium
endothall on EPCRA section 313
pursuant to EPCRA section 313(d)(2)(B)
based on the available chronic toxicity
data for this chemical.
102. Dipropyl isocinchomeronate
(CAS No. 000136-45-8) (FIFRA AI) (Ref.
3). Dipropyl isocinchomeronate has
been classified by EPA as a Group B2
compound, i.e., a probable human
carcinogen. This classification is based
on the findings of multiple malignant
and benign tumors in the rat (liver
adenomas and carcinomas in both sexes,
kidney carcinomas in both sexes, benign
testes tumors in males and uterine
tumors in females), and multiple
malignant tumors in the mouse (liver
adenomas and carcinomas in both sexes
and lung/bronchiolar adenomas and
carcinomas in males). EPA believes that
there is sufficient evidence for listing
dipropyl isocinchomeronate on EPCRA
section 313 pursuant to EPCRA section
313(d)(2)(B) based on the available
carcinogenicity toxicity data.
103. Disodium
cyanodithioimidocarbonate (CAS No.
000138-93-2) (FIFRA AI) (Ref. 3). Rats
administered disodium
cyanodithioimidocarbonate by gavage
on gestation days 6 to 15 demonstrated
increased skeletal variations in
offspring. The NOEL is 6 mg/kg, and the
LOEL is 18 mg/kg. In a rabbit teratology
study, increased resorptions were
observed in rabbits administered the
compound by gavage on gestation days
6 to 18. The NOEL is 3 mg/kg, and the
LOEL is 10 mg/kg. EPA believes that
there is sufficient evidence for listing
disodium cyanodithioimidocarbonate
on EPCRA section 313 pursuant to
EPCRA section 313(d)(2)(B) based on
the available developmental toxicity
data.
104. 2,4-D isopropyl ester (CAS No.
000094-11-1) (CERCLA; FIFRA AI:
IARC) (Ref. 8). 2,4-D isopropyl ester is
a 2,4-dichlorophenoxy-type herbicide.
In mammals, the isopropyl ester of 2,4-
D is hydrolyzed to yield the free acid,
2,4-D. Therefore, the toxicity of 2,4-D
isopropyl ester is expected to be similar
to that of 2,4-D, in which the kidney,
liver, and nervous system are the
primary targets of injury. 2,4-D is
presently included in the EPCRA
section 313 list of toxic chemicals. EPA
believes that there is sufficient evidence
for listing 2,4-D isopropyl ester on
EPCRA section 313 pursuant to EPCRA
section 313(d)(2)(B) based on the known
toxic effects of its metabolite 2,4-D.
105. 2,4-Dithiobiuret (CAS No.
000541-53-7) (CERCLA; EPCRA EHS;
RCRA APP8; RCRA P) (Ref. 8). In
experimental animals, 2,4-dithiobiuret
is a highly toxic substance that causes
death through respiratory depression
and respiratory failure. Rats receiving 1
mg/kg/day for 6 days suffered from
delayed onset of neuromuscular
depression. Rats given 2,4-dithiobiuret
for 52 days showed signs of muscle
weakness after a latency period of 3 to
4 days. The NOEL was determined to be
0.125 mg/kg/day. The LOEL was 0.25
mg/kg/day. The cause of the muscle
weakness was depressed neuromuscular
transmission. EPA believes that there is
sufficient evidence for listing 2,4-
dithiobiuret on EPCRA section 313
pursuant to EPCRA section 313(d)(2)(B)
based on the chronic neurotoxicity data
for this chemical.
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.
107. Diuron (CAS No. 000330-54-1)
(CERCLA) (Ref. 8). In a 2-year study in
dogs administered diuron,
sulfhemoglobin (an abnormal blood
pigment) was detected following doses
as low as 3.125 mg/kg/day (LOAEL).
The NOAEL was 0.625 mg/kg/day.
Higher doses (6.25 and 31.25 mg/kg/
day) caused decreased red blood cell,
hemoglobin, and hematocrit values. The
highest dose tested (31.25 mg/kg/day)
also caused an increase in erythrogenic
activity in the bone marrow,
hemosiderosis in the spleen, increased
liver weight, and body weight loss. EPA
has derived an oral RfD of 0.002 mg/kg/
day for this chemical from this study.
Similar effects (anemia, increased
erythrogenic activity in the bone
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marrow, and abnormal pigments in the
blood) were also observed in rats
exposed orally to doses as low as 6.25
mg/kg/day for 2 years, or to 250 mg/kg/
day for 90 days. In a 7-week study, rats
receiving diuron doses of greater than or
equal to 10 mg/kg/day had decreased
red blood cells and significantly
increased methemoglobinemia.
Offspring of Wistar rats fed diuron
during days 6 to 15 of gestation showed
developmental toxicity, that included
malformed ribs, extra ribs, and delayed
ossification. The developmental LOAEL
in this study was 100 mg/kg/day. No
NOAEL was determined. Maternal and
fetal body weights decreased at 400 mg/
kg/day. In a three-generation
reproduction study in rats fed diuron at
6.25 mg/kg/day, decreased body weights
were reported in the Fjb and Fsa litters.
EPA believes that there is sufficient
evidence for listing diuron on EPCRA
section 313 pursuant to EPCRA section
313(d)(2)(B) based on the available
hematological and developmental
toxicity data for this chemical.
The measured aquatic toxicity data for
diuron includes a 1.5-hour ECso of
0.010 ppm (10 ppb) for marine green
algae. EPA believes that there is
sufficient evidence for listing diuron on
EPCRA section 313 pursuant to EPCRA
section 313(d)(2)(C) pased on the
environmental toxicity data for this
chemical.
108. 2,4-D 2-octyl ester (CAS No.
001917-97-1) (CERCLA; FIFRA AI;
IARC) (Ref. 8). 2,4-D 2-octyl ester is a
2,4-dichlorophenoxy-type herbicide.
The 2-octyl moiety contains eight
carbons and, therefore, is an isooctyl
group.
Developmental toxicity following
maternal exposure to 2,4-D isooctyl
esters has been demonstrated in the rat
and mouse. Fetotoxicity occurred in
offspring of rats exposed to 528 mg/kg
during gestation days 8 to 11. Rats orally
exposed to doses as low as 302 mg/kg
during gestation days 9 through 12 had
musculoskeletal abnormalities.
Exposure to a lower dose (188 mg/kg)
for a longer period during gestation
(days 6 through 15) caused
developmental effects on homeostasis
and effects on newborn growth
statistics. In mice, 438 mg/kg
administered orally during gestation
days 8 through 12 also caused effects on
newborn growth statistics.
EPA believes that there is sufficient
evidence for listing 2,4-D 2-octyl ester
on EPCRA section 313 pursuant to
EPCRA section 313(d)(2)(B) based on
the developmental toxicity data for 2,4-
D isooctyl esters, and the toxic effects of
its metabolite 2,4-D.
The aquatic acute toxicity data for 2,4-
D isooctyl esters include a measured
48-hour LCso of 8.8 ppm for bluegill. In
addition, 2,4-D isooctyl esters are
expected to bioaccumulate based on the
estimated log K<,w of 6.6. EPA believes
that there is sufficient evidence for
listing 2,4-D isooctyl esters on EPCRA
section 313 pursuant to section EPCRA
313(d)(2)(C) based on the available
environmental toxicity data and the
potential for bioaccumulation.
109. Dodine (dodecylguanidine
monoacetate) (CAS No. 002439-10-3)
(FIFRA AI) (Ref. 3). Aquatic acute
toxicity values for dodine include a
daphnid 48-hour ECso of 17.8 ppb. EPA
believes that there is sufficient evidence
for listing dodine on EPCRA section 313
pursuant to EPCRA section 313(d)(2)(C)
based on the available environmental
toxicity data.
110. 2,4-DP (dichlorprop) (CAS No.
000120-36-5) (FIFRA SR; IARC) (Ref. 8).
2,4-DP (2-(2,4-
dichlorophenoxyjpropionic acid) is a
2,4-dichlorophenoxy-type herbicide.
Developmental toxicity has been
reported in rats and mice administered
oral doses of 2,4-DP as low as 20 mg/
kg during gestation days 4 through 18.
Behavioral changes and physical effects
were observed in newborn rats, while
increased post-implantation loss was
observed in the mothers. Exposure of
mice to much higher doses (3,000 and
4,000 mg/kg) for shorter durations (i.e.,
gestation days 6 through 15) caused
musculoskeletal abnormalities and
fetotoxicity.
EPA believes that there is sufficient
evidence for listing 2,4-DP on EPCRA
section 313 pursuant to EPCRA section
313(d)(2)(B) based on the available
developmental toxicity data for this
chemical.
111. 2,4-D propylene glycol butyl
ether ester (CAS No. 001320-18-9)
(CERCLA; FIFRA AI; IARC) (Ref. 8). 2,4-
D propylene glycol butyl ether ester is
a 2,4-dichlorophenoxy-type herbicide.
In mammals, the propylene glycol butyl
ether ester is expected to hydrolyze to
yield the free acid, 2,4-D. Therefore, the
toxicity of 2,4-D propylene glycol butyl
ether ester is expected to be similar to
that of 2,4-D, in which the kidney, liver,
and nervous system are the primary
targets of injury. EPA believes that there
is sufficient evidence for listing 2,4-D
propylene glycol butyl ether ester on
EPCRA section 313 pursuant to EPCRA
section 313(d)(2)(B) based on the
chronic toxicity data for this chemical.
112. 2,4-D sodium salt (CAS No.
002702-72-9) (CERCLA; FIFRA AI;
IARC) (Ref. 8). 2,4-D sodium salt is a
2,4-dichlorophenoxy-type herbicide. In
mammals, the sodium salt is expected to
hydrolyze to yield the free acid, 2,4-D.
Therefore, the toxicity of 2,4-D sodium
salt is expected to be similar to that of
2,4-D, in which the kidney, liver, and
nervous system are the primary targets
of injury. 2,4-D is presently included in
the EPCRA section 313 list of toxic
chemicals. EPA believes that there is
sufficient evidence for listing 2,4-D
sodium salt ester on EPCRA section 313
pursuant to EPCRA section 313(d)(2)(B)
based on the systemic toxicity data for
this chemical.
113. Ethoprop (phosphorodithioic
acid O-ethyl S,S-dipropyl ester) (CAS
No. 013194-48-4) (FIFRA AI) (Ref. 3).
Ethoprop is acutely toxic to animals.
The acute oral LDso in rats is 5.62 mg/
kg/day. Clinical signs of toxicity
observed in animals at this dose level
included depression, salivation,
inactivity, convulsions and prostration.
Similar signs were reported at the 4-
hour inhalation LCso of 0.12 mg/L in
rats. In a 2-year rat chronic feeding
study, plasma, red blood cell, and brain
cholinesterase inhibition were observed
in both sexes at 0.5 mg/kg/day. The
NOEL was 0.05 mg/kg/day. Similar
results were reported in a chronic
dietary study in mice at 0.1 mg/kg/day.
The NOEL was 0.01 mg/kg/day. The two
chronic studies together with the results
of acute studies indicate the potential
neurotoxicity of ethoprop. EPA believes
that there is sufficient evidence for
listing ethoprop on EPCRA section 313
pursuant to EPCRA section 313(d)(2)(B)
based on the available neurological
toxicity data.
Aquatic acute toxicity values for
ethoprop include a mysid 96-hour LCso
of 7.5 ppb, a shrimp 96-hour LCso of 13
ppb, and a daphnid 48-hour ECso of 93
ppb. Avian acute and dietary toxicity
data include a ring-necked pheasant 14-
day LD50 of 4.2 mg/kg and a mallard
duck 14-day LDSO of 12.6 mg/kg. EPA
believes that there is sufficient evidence
for listing ethoprop on EPCRA section
313 pursuant to EPCRA section
313(d)(2)(C) based on the available
environmental toxicity data for this
chemical.
114. Ethyl dipropylthiocarbamate
(EPTC) (CAS No. 000759-94-4) (FIFRA
AI) (Ref. 3). EPTC is a cholinesterase
inhibitor. Workers exposed to EPTC
complained of headache, malaise,
nausea, and impaired working ability.
Poisoned animals exhibited salivation,
lacrimation, blepharospasm, and
depression. Neuropathy was observed in
rats orally administered 25 mg/kg/day
for 2 years. The LOEL was 25 mg/kg/day
and the NOEL was 5 mg/kg/day.
Decreased brain cholinesterase activity
was observed in female rats orally
administered 15 mg/kg/day (LOEL). The
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1813
NOEL was 3 mg/kg/day. The 4-hour
inhalation rat and cat lowest-lethal-
concentration values are 0.2 mg/L and
0.4 mg/L, respectively. Somnolence and
salivation were observed in exposed
animals. The dermal rabbit LDSO is
10,000 mg/kg. Depressed righting
reflexes, prostration, and clonic
convulsions were observed.
In a 2-year dietary rat study,
degenerative cardiomyopathy was
observed in males receiving 9 mg/kg/
day of EPTC. No NOEL was established.
This effect was observed in females at
36 mg/kg/day. The NOEL was 18 mg/kg/
day. In a 2-generation rat reproduction
study, parental toxicity included
cardiomyopathy observed in rats orally
administered 10 mg/kg/day. Based on
the NOEL of 2.5 mg/kg/day, EPA
derived an oral RfD of 0.025 mg/kg/day.
In a 2-year dietary rat study, chronic
myocarditis was observed at the LOEL
of 125 mg/kg/day. The NOEL was 25
mg/kg/day.
An increased incidence of fetal
resorptions, increased incidence of fetal
retardations, and decreased fetal body
weights were observed in rats receiving
300 mg/kg/day of EPTC on days 6 to 15
of gestation. The LOEL was 300 mg/kg/
day and the NOEL was 100 mg/kg/day.
The NOEL was 10 mg/kg/day. In a 2-
generation rat reproduction study,
decreased pup weight was observed in
both generations at 40 mg/kg/day. The
NOEL was 10 mg/kg/day.
EPA believes that there is sufficient
evidence for listing EPTC on EPCRA
section 313 pursuant to EPCRA section
313(d)(2)(B) based on the available
neurological, cardiovascular, and
reproductive toxicity data for this
115. Famphur (CAS No. 000052-85-7)
(CERCLA; FIFRA AI; RCRA APP8;
RCRA P) (Ref. 8). Famphur is a
thiophosphate-type cholinesterase
inhibitor. In a 90-day feeding study, rats
given diets supplemented with famphur
showed decreased plasma and brain
cholinesterase activity at 1.25 mg/kg/
day, and decreased whole blood
cholinesterase activity at 0.15 mg/kg/
day. A bull was treated with famphur
for 43 days before signs of neurotoxicity
appeared. The symptoms, including
paresis of all four limbs, were attributed
to focal cervical or diffuse spinal cord
lesions. Calves receiving 60.75 mg/kg
showed marked inhibition of whole
blood cholinesterase. EPA believes that
there is sufficient evidence for listing
famphur on EPCRA section 313
pursuant to EPCRA section 313(d)(2)(B)
based on the chronic neurotoxicity
known for this chemical.
Measured terrestrial wildlife acute
toxicity data for famphur indicate that
the oral LDso values for the redwinged
blackbird and the starling are 1.78 mg/
kg and 4.22 mg/kg, respectively. In
addition, the measured oral LDso for
mallard ducks is 3.45 mg/kg (based on
35 percent active ingredient). EPA
believes that there is sufficient evidence
for listing famphur on EPCRA section
313 pursuant to EPCRA section
313(d)(2)(C) based on the environmental
toxicity data for this chemical.
116. Fenarimol (.alpha.-(2-
chlorophenyl)-.alpha.-4-chlorophenyl)-
5-pyrimidinemethanol) (CAS No.
060168-88-9) (FIFRA AI) (Ref. 3). In a 3-
month mouse feeding study, liver
weights were increased in males at
levels greater than or equal to 620 ppm
(80.6 mg/kg/day) and in females at
levels greater than 1,100 ppm (143 mg/
kg/day). At higher doses (143 to 260 mg/
kg/day), decreased total bilirabin,
hepatomegaly, and/or periportal fatty
liver changes were observed. Mice
exposed to dietary levels of 78 mg/kg/
day for 1-year had increased liver
weight and slight fatty changes. One
year feeding studies in Wistar rats also
resulted in increased liver weights (the
LOEL was 17.5 mg/kg/day; the NOEL
was 6.5 mg/kg/day). In a 2—year feeding
study with Wistar rats, fatty changes in
the liver were observed at 17.5 mg/kg/
day (LOEL). The NOEL was 6.5 mg/kg/
day. A 2—year feeding study in mice
resulted in fatty liver changes. The
LOEL was 78 mg/kg/day and the NOEL
was 22.1 mg/kg/day. EPA believes that
there is sufficient evidence for listing
fenarimol on EPCRA section 313
pursuant to EPCRA section 313(d)(2)(B)
based on the available hepatic toxicity
data.
117. Fenbutatin oxide (hexakis(2-
methyl-2-phenylpropyl)distannoxane)
(CAS No. 013356-08-6) (FIFRA AI) (Ref.
3). In a rat teratology study, the LOEL
for developmental toxicity (toxic to
zygote) was 60 mg/kg/day and the NOEL
was 30 mg/kg/day. In a rabbit teratology
study, oral administration of 5 mg/kg/
day produced intrauterine lethality and
was also toxic to maternal animals. The
NOEL was 1 mg/kg/day. In a 3-
generation rat reproduction study,
administration of 15 mg/kg/day (LOEL)
produced decreased viability index. The
NOEL was 5 mg/kg/day. EPA believes
that there is sufficient evidence for
listing fenbutatin oxide on EPCRA
section 313 pursuant to EPCRA section
313(d)(2)(B) based on the available
developmental toxicity data for this
chemical.
Aquatic acute toxicity values for
fenbutatin oxide include a rainbow trout
96—hour LCso of 1.7 ppb, a fathead
minnow 96-hour LCso of 1.9 ppb, a
daphnid 48-hour ECso of 3.1 ppb, a
bluegill sunfish 96-hour of LC5o of 4.8
ppb, and a sheepshead minnow 96—hour
LC5o of 20.8 ppb. Avian acute toxicity
values include a quail oral LDso of 0.007
mg/kg. EPA believes that there is
sufficient evidence for listing fenbutatin
oxide on EPCRA section 313 pursuant to
EPCRA section 313(d)(2)(C) based on
the available environmental toxicity
data for this chemical.
118. Fenoxaprop ethyl (2-(4-((6-
chloro-2-
benzoxazolylen)oxy)phenoxy)propanoic
acid,ethyl ester) (CAS No. 066441-23-4)
(FIFRA AI) (Ref. 3). In a 30-day mouse
feeding study, liver weight increases
were observed (LOEL 20 ppm or 2.6 mg/
kg/day and NOEL 10 ppm or 1.3 mg/kg/
day). In a 32-day rat feeding study,
changes in the liver and kidney as well
as altered lipid metabolism and
decreased cholesterol were observed.
The LOEL in the rat study was 80 ppm
(4 mg/kg/day). The NOEL was 20 ppm
(1 mg/kg/day). Inflammatory changes in
the kidney (chronic interstitial
nephritis) were reported in dogs that
received a 3-month feeding of 80 ppm
(2 mg/kg/day, the LOEL). The NOEL
was 16 ppm or 0.4 mg/kg/day.
Decreased serum lipids and cholesterol
were reported in rats exposed for 2 years
to dietary levels greater than or equal to
180 ppm (9 mg/kg/day, the LOEL). The
NOEL in this study was 30 ppm (1.5
mg/kg/day).
In a developmental toxicity study,
fetotoxic effects (slightly impaired
growth and delayed ossification) were
reported at 100 mg/kg/day. The NOEL
was 32 mg/kg/day. These effects were
observed at doses that were also toxic to
maternal animals. In a 2-generation
reproductive toxicity feeding study in
rats, decreased survival, decreased body
weight at study termination, and
significant changes in kidney and liver
weights were reported in the Faa and F2b
litters. The fetotoxic LOEL in this study
was 5 ppm (0.25 mg/kg/day, the lowest
dose tested). The LOEL and NOEL for
maternal toxicity (increased kidney and
liver weights) were 80 ppm (4 mg/kg/
day) and 30 ppm (1.5 mg/kg/day),
respectively. Thus, the fetotoxic effects
were observed at doses lower than those
that produced maternal toxicity.
EPA believes that there is sufficient
evidence for listing fenoxaprop ethyl on
EPCRA section 313 pursuant to EPCRA
section 313(d)(2)(B) based on the
available renal and developmental
toxicity data for this chemical.
Aquatic acute toxicity values for
fenoxaprop ethyl include a mysid 96-
hour ECso of 98 ppb. EPA believes that
there is sufficient evidence for listing
fenoxaprop ethyl on EPCRA section 313
pursuant to EPCRA section 313(d)(2)(C)
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based on the available environmental
toxicity data.
119. Fenoxycarb (2-(4-
phenoxyphenoxyJethyUcarbamic acid
ethyl ester) (CAS No. 072490-01-8)
(FEFRA AI) (Ref. 3). Liver changes
(including fatty changes, glycogen
depletion, hepatocyte hypertrophy and
multinucleated hepatocytes) were
reported in mice (the LOEL was 80 mg/
kg/day; the NOEL was not determined)
and rats (the LOEL was 300 mg/kg/day;
the NOEL was 100 mg/kg/day) following
3-month dietary exposures. Dose-
related changes in the liver of male rats,
including increased relative liver
weight, focal necrosis, centrilobular
hypertrophy and pigmented histiocytes,
were reported after the first year of a 2—
year oncogenicity study. The LOEL for
these effects was 600 ppm (30 mg/kg/
day) and the NOEL was 200 ppm (10
mg/kg/day). Male and female rats
exposed to a higher dose (1,800 ppm or
90 mg/kg/day) in this study had
increased alkaline phosphatase and
reduced platelets and white blood cells,
and fibrosis was present in the hepatic
lesions in the males.
In a reproduction study in rats, delays
in pinna unfolding and eye opening
were reported at 10 mg/kg/day.
EPA believes that there is sufficient
evidence for listing fenoxycarb on
EPCRA section 313 pursuant to EPCRA
section 313(d)(2)(B) based on the
available hepatic and developmental
toxicity data for this chemical.
120. Fenpropathrin (2,2,3,3-
tetramethylcyclopropane carboxylic
acid cyano(3-phenoxyphenyl)methyl
ester) (CAS No. 039515-41-8) (FIFRA AI)
(Ref. 3). In a 1—year feeding study,
tremors were noted in dogs exposed to
6.25 mg/kg/day. The NOEL was 2.5 mg/
kg/day. In a developmental toxicity
study in rats, signs of neurotoxicity
reported in the pregnant dams included
ntaxia, tremors, convulsions,
lacrimation, prostration of death. The
LOEL for maternal toxicity was 10 mg/
kg/day and the NOEL was 6 mg/kg/day
In 2-year dietary studies in rats and
mice, body tremors and increased
mortality were observed in male rats
(the LOEL was 30 mg/kg/day; the NOEL
was 22.5 mg/kg/day), whereas only
marginally increased hyperactivity was
noted in female mice (the LOEL was
65.2 mg/kg/day; the NOEL was 16.2 mg/
kg/day). EPA believes that there is
sufficient evidence for listing
fenpropathrin on EPCRA section 313
pursuant to EPCRA section 313(d)(2)(B)
based on the available neurological
toxicity data for this chemical.
Aquatic acute toxicity values for
fenpropathrin include a rainbow trout
96-hour LCso of 2.3 ppb, a bluegill 96-
hour LCso of 2.2 ppb, a sheepshead
minnow 96—hour LCso of 3.1 ppb, and
a daphnid 48-hour ECso of 0.53 ppb.
EPA believes that there is sufficient
evidence for listing fenpropathrin on
EPCRA section 313 pursuant to EPCRA
section 313(d)(2)(C) based on the
available environmental toxicity data for
this chemical.
121. Fenthion (O,O-dimethyl O-[3-
methyl-4-(methylthio) phenyl] ester,
phosphorothioic acid) (CAS No. 000055-
38-9) (FIFRA AI) (Ref. 3). In cases of
human poisonings from fenthion
exposure, reported cholinergic
manifestations included the following:
A man who ingested 257 mg/kg had an
increased pulse rate (no effect on blood
pressure) and gastrointestinal symptoms
including diarrhea and nausea or
vomiting; a woman that ingested 525
mg/kg experienced muscle contraction
or spasticity, respiratory depression,
and miosis; a woman that ingested an
unspecified amount of fenthion did not
exhibit the initial cholinergic crisis until
5 days postexposure, and symptoms
(primarily psychosis) recurred 24 days
later. Similar signs of toxicity,
characteristic of organophosphate
poisoning, were observed in rats that
were fed 300 ppm (15 mg/kg/day).
Symptoms reported in these rats
included spasms, nervousness,
salivation and diarrhea as well as
ophthalmological symptoms such as
eyeball protrusion and corneal turbidity.
LOEL and NOEL values for
cholinesterase inhibition from animal
studies of various durations include the
following: In a 28-day feeding study in
rats, the LOEL was 10 ppm (0.5 mg/kg/
day) and the NOEL was 5 ppm (0.65 mg/
kg/day) for brain cholinesterase
inhibition; in another 28-day rat feeding
study, plasma and erythrocyte
cholinesterase recovered 2 weeks
postexposure. The LOEL for
cholinesterase inhibition in a 30-day
inhalation study in rats was 0.163 mg/
L. In a 63-day rat feeding study,
significant cholinesterase inhibition
occurred by day 3 at 25 mg/kg/day. In
a 16-week feeding study in rats, tie
LOEL for cholinesterase inhibition was
5 ppm in females (0.65 mg/kg/day) and
the NOEL was 3 ppm (0.15 mg/kg/day).
EPA believes that there is sufficient
evidence for listing fenthion on EPCRA
section 313 pursuant to EPCRA section
313(d)(2)(B) based on the available
neurological toxicity data for this
chemical.
Aquatic acute toxicity values for
fenthion include a daphnid 48-hour
LCso of 0.62 ppb for immobilization.
Acute toxicity values for other non-
standard aquatic invertebrates range
from a 48-hour ECso of 0.024 ppb for
brown shrimp to a 96-hour ECso of 110
ppb for scud. Avian acute toxicity
values include a male mallard duck oral
LDso of 5.94 mg/kg, a male bobwhite
quail LDso of 4 mg/kg, and a mourning
dove oral LDSO of 4.63 mg/kg. EPA
believes that there is sufficient evidence
for listing fenthion on EPCRA section
313 pursuant to EPCRA section
313(d)(2)(C) based on the available
environmental toxicity data for this
chemical.
122. Fenvalerate (4-chloro-aIpha-(l-
methylethyljbenzeneacetic acid
cyano(3-phenoxyphenyl)methyl ester)
(CAS No. 051630-58-1) (FIFRA AI) (Ref.
3). Excitement and ataxia were observed
in rats administered fenvalerate at the
oral LDso dose of 70.2 mg/kg. The oral
mouse LDso for fenvalerate is 185 mg/kg.
Tremor, convulsions, and ataxia were
observed in this study. Neurological
dysfunctions consisting of jerky leg
movements, exaggerated flexion of the
hind limb, and unsteady gait were
observed in rats fed 7.5 mg/kg/day
(LOEL) of fenvalerate for 13 weeks. The
NOEL was 2.5 mg/kg/day. Based on the
NOEL of the study, EPA derived an oral
RfD of 0.0025 mg/kg/day. Peripheral
nerve and spinal cord lesions were
observed in rats orally administered 360
a 6-month dog feeding study,
normocytic anemia, increased serum
cholesterol levels, and hepatic
microgranulomatosis were observed in
animals administered fenvalerate at 6.25
mg/kg/day (LOEL). No NOEL was
defined. In a 2-year mouse feeding
study, multifocal granulomata in the
liver was observed in males and females
fed fenvalerate at 7.5 and 37.5 mg/kg/
day, respectively. The male NOEL was
1.5 mg/kg/day and the female NOEL
was 7.5 mg/kg/day. In a 20-month
mouse feeding study, decreased
erythrocyte count, increased mean cell
volume of the blood, and granulomatous
changes in the liver were observed at 15
mg/kg/day (LOEL). The NOEL was 4.5
mg/kg/day.
EPA believes that there is sufficient
evidence.for listing fenvalerate on
EPCRA section 313 pursuant to EPCRA
section 313(d)(2)(B) based on the
available neurological, hepatic, and
hematological toxicity data for this
chemical.
Measured aquatic acute toxicity data
for fenvalerate include a bluegill 96-
hour LCso of 0.26 ppb, a fathead
minnow 96-hour LCso of 0.33 ppb, a
rainbow trout 96-hour LCso of 1.2 ppb,
an Atlantic salmon 96-hour LCso of 1.2
ppb, and a sheepshead minnow 96-hour
LCso of 4.4 ppb. In addition, the 48-
hour LCso for daphnids is 0.05 ppb. EPA
believes that there is sufficient evidence
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1815
for listing fenvalerate on EPCRA section
313 pursuant to EPCRA section
313(d)(2)(C) based on the environmental
toxicity data for this chemical.
123. Ferbam
(tris(dimethylcarbamodithioato-
S,S')iron) (CAS No. 014484-64-1)
(FIFRA AI) (Ref. 3). In an 80-week
feeding study in rats, females fed 96 mg/
kg/day had ataxia that progressed to
hind limb paralysis. The NOEL was not
determined. Symptoms of neurotoxicity
reported in mice following acute oral
exposure included somnolence,
excitement and ataxia, although the
doses at which these signs occurred
were much higher (the LDso in this
study was 3,400 mg/kg). EPA believes
that there is sufficient evidence for
listing ferbam on EPCRA section 313
pursuant to EPCRA section 313(d)(2)(B)
based on the available neurological
toxicity data.
Aquatic acute toxicity values for
ferbam include a daphnid 48-hour LCso
of 90 ppb, a 96-hour LC50 of 52 ppb for
the eastern oyster, and a guppy 96-hour
LC50 of 90 ppb. EPA believes that there
is sufficient evidence for listing ferbam
on EPCRA section 313 pursuant to
EPCRA section 313(d)(2)(C) based on
the available environmental toxicity
data for this chemical.
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
ECso of greater than 2.8 ppb, a bluegill
sunfish 96-hour LC5o of greater than 3.2
ppb, and a rainbow trout 96—hour LCso
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 LC50
values ranged from 150 to 185 ppm
(0.23 to 0.29 mg/L). The LC50 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
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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
ECso of 0.40 ppb, a bluegill sunfish 96-
hour LCso of 0.9 ppb, a rainbow trout
96-hour LCso of 2.9 ppb, and a
sheepshead minnow 96-hour LCjo 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.
129. Folpet (CAS No. 000133-07-3)
(CAL) (Ref. 8). Folpet is classified as a
Group B2 compound by EPA; i.e., the
substance is a probable human
carcinogen. Folpet has been shown to
Induce carcinoma and adenoma of the
duodenum in both sexes of CD-I and
B6C3F1 mice. EPA believes that there is
sufficient evidence for listing folpet on
EPCRA section 313 pursuant to EPCRA
section 313(d)(2)(B) based on the
available carcinogenicity data for this
chemical.
Aquatic acute toxicity test data for
folpet include a measured 96-hour LCso
of 39 ppb for rainbow trout, and a
measured 96-hour LCso of 72 ppb (0.072
ppm) for bluegill. EPA believes that
there is sufficient evidence for listing
folpet on EPCRA section 313 pursuant
to EPCRA section 313(d)(2)(C) based on
the environmental toxicity data for this
chemical.
130. Fomesafen (5-(2-chloro-4-
(trifluoromethyl)phenoxy)-N
methylsulfonyI)-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.
131. alpha-Hexachlorocyclohexane
(CAS No. 000319-84-6) (CERCLA; CWA
PPL; FIFRA SR) (Ref. 8). alpha-
Hexachlorocyclohexane is classified by
EPA as a Group B2 compound; i.e., the
substance is a probable human
carcinogen. Although human data are
limited, there is a case report of acute
leukemia in a Japanese sanitation
employee following occupational
exposure to alpha-
hexachlorocyclohexane and DDT. alpha-
Hexachlorocyclohexane has been shown
in dietary studies to cause an increase
in the incidence of liver tumors in five
mouse strains and in Wistar rats. EPA
believes that there is sufficient evidence
for listing alpha-hexachlorocyclohexane
on EPCRA section 313 pursuant to
EPCRA section 313(d)(2)(B) based on
the carcinogenicity data for this
chemical.
Measured aquatic acute toxicity test
data for alpha-hexachlorocyclohexane
include a 48-hour ECso of 800 ppb for
daphnids. This chemical is expected to
bioaccumulate in aquatic systems
because the measured bioconcentration
factor (BCF) for rainbow trout is 1950.
EPA believes that there is sufficient
evidence for listing alpha-
hexachlorocyclohexane on EPCRA
section 313 pursuant to EPCRA section
313(d)(2)(C) based on the environmental
toxicity data for this chemical and its
potential for bioaccumulation.
132.Hexamethylene-l,6-diisocyanate
or Diisocyanates category (CAS No.
000822-60-0) (CAA HAP) (Ref. 7).
Hexamethylene-l,6-diisocyanate(HDI)
is extremely toxic via the inhalation
route. The rat LCso for HDI ranges from
56 (385 mg/m3) to 45 ppm (310 mg/m3).
The mouse LCso for HDI is 4 ppm (30
mg/m3). HDI also induces irritation of
the upper respiratory tract in mice after
acute exposure. The mouse LOAEL was
0.062 ppm (0.43 mg/m3) for a 3-hour
exposure. A NOAEL was not
established. Acute exposures to HDI
vapors may induce pulmonary irritation
in the rat at 60 mg/m3, but data were
insufficient to generate a LOAEL or
NOAEL for this effect.
Although the data are insufficient to
evaluate the potential for HDI to
produce pulmonary hypersensitivity,
indirect evidence suggests that
inhalation of monomeric HDI may cause
pulmonary sensitivity. In addition, data
are insufficient to evaluate the potential
for HDI to elicit an allergic reaction in
previously sensitized animals or people;
however, indirect evidence suggests that
inhalation of monomeric HDI may elicit
allergic responses (i.e., asthma,
alveolitis) in isocyanate-sensitized
individuals.
EPA's exposure analysis indicates that
HDI 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
hexamethylene-l,6-diisocyanate on
EPCRA section 313 pursuant to EPCRA
section 313(d)(2)(A) based on the
available acute toxicity and exposure
data for this chemical.
EPA is proposing to list HDI as an
individual chemical on EPCRA section
313. In addition, in Units IV.B.144. and
158. of this preamble, EPA is proposing
to individually list isophorone
diisocyanate and 1,1-methylene bis(4-
isocyanatocyclohexane) on EPCRA
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1817
section 313. As an alternative proposal
to the individual listing of HDI,
isophorone diisocyanate, and 1,1-
methylene bis(4-
isocyanatocyclohexane), EPA is
proposing to create a diisocyanates
category that includes HDI, isophorone
diisocyanate, 1,1-methylene bis(4-
isocyanatocyclohexane), and 16 other
diisocyanates.
EPCRA section 313 requires threshold
determinations for chemical categories
to be based on the total of all chemicals
in the category manufactured,
processed, or otherwise used. For
example, a facility that manufactures
three members of a chemical category
would count the total amount of all
three chemicals manufactured towards
the manufacturing threshold for that
category. When filing reports for
chemical categories, the releases are
determined in the same manner as the
thresholds. One report is filed for the
category and all releases ate reported on
this form.
The chemicals selected for this
proposed category are members of the
diisocyanates category under review by
EPA's Office of Pollution Prevention
and Toxics. This category has been
defined as monomeric diisocyanates of
molecular weight less than or equal to
300, plus polymeric diphenylmethane
diisocyanate (which is only 40 to 60
percent polymerized). Chemicals were
included in this category based on
similar chronic and acute adverse
respiratory effects. The following
chemicals are the proposed members of
the EPCRA section 313 diisocyanates
category:
l,3-Bis(methylisocyanate)cyclohexane
(CAS No. 038661-72-2)
l,4-Bis(methylisocyanate)cyclohexane
(CAS No. 010347-54-3)
1,4-Cyclohexane diisocyanate (CAS
No. 002556-36-7)
Diethyldiisocyanatobenzene (CAS No.
134190-37-7)
4,4'-Diisocyanatodiphenyl ether (CAS
No. 004128-73-8)
2,4'-Diisocyanatodiphenyl sulfide
(CAS No. 075790-87-3)
3,3 '-Dimethoxybenzidine-4,4'-
diisocyanate (CAS No. 000091-93-0)
3,3 '-Dimethyl-4,4'-diphenylene
diisocyanate (CAS No. 000091-97-4)
3,3'-Dimethyldiphenylmethane-4,4'-
diisocyanate (CAS No. 000139-25-3)
Hexamethylene-l,6-diisocyanate (CAS
No. 000822-06-0)
Isophorone diisocyanate (CAS No.
004098-71-0)
4-Methyldipheny lmethane-3,4-
diisocyanate (CAS No. 075790-84-0)
1,1-Methylene bis(4-
isocyanatocyclohexane) (CAS No.
005124-30-1)
1,5-Naphthalene diisocyanate (CAS
No. 003173-72-6)
1,3-Phenylene diisocyanate (CAS No.
000123-61-5) -- I -•
1,4-Phenylene diisocyanate (CAS No.
000104-49-4)
Polymeric diphenylmethane
diisocyanate (CAS No. 009016-87-9)
2,2,4-Trimethylhexamethylene
diisocyanate (CAS No. 016938-22-0)
2,4,4-Trimethylhexamethylene
diisocyanate (CAS No. 015646-96-5)
These diisocyanates represent a
category of chemicals that may effect
many organ systems. However, the
primary toxicity target for diisocyanates
is the upper and lower respiratory tract
resulting in chronic pulmonary
irritation. Diisocyanates are also known
respiratory and dermal sensitizing
agents. Both acute and chronic effects
may result from acute or chronic
exposures. These effects may be
immune- or non-immune mediated.
EPA believes that diisocyanates should
be listed as a category because it is the
isocyanate functionality that is
responsible for the observed chronic
pulmonary irritation associated with
exposures to members of this category.
The other part of the molecule does not
mitigate to any large degree the
observed toxic effects. EPA believes that
there is sufficient evidence for listing
diisocyanates as a category on EPCRA
section 313 pursuant to EPCRA section
313(d)(2)(B) based on the available
toxicity data for members of the
category.
Currently there are four other
diisocyanates listed on EPCRA section
313, these are:
Toluene-2,4-diisocyanate (CAS No.
000584-84-9)
Toluene-2,6-diisocyanate (CAS No.
000091-08-7)
Toluenediisocyanate (mixed isomers)
(CAS No. 026471-62-5)
Methylenebis(phenylisocyanate) (CAS
No. 000101-68-8)
EPA intends to maintain the
individual listings for the three toluene
diisocyanate compounds. In addition to
the effects discussed above, these
compounds have been classified as
probable carcinogens. EPA intends to
continue to individually list
diisocyanates that are possible of
probable carcinogens.
Methylenebis(phenylisocyanate) has not
been shown to be a carcinogen and EPA
is proposing to remove it as an
individually listed chemical, and add it
to the diisocyanates category if the
alternative proposal for creation of the
category is finalized.
EPA requests comment on the
alternative proposal to create a
diisocyanates category and what other
diisocyanates should be included in
such a category.
133. n-Hexane (CAS No. 000110-54-3)
(CAA HAP) (Ref. 7). In an epidemiology
study, no neurological abnormalities
were noted in workers. However,
neurophysiological tests showed that
the mean motor nerve conduction
velocities of the exposed group was
significantly decreased over the values
for the control group. Also, the residual
latency of motor nerve conduction of
the posterior tibial nerve in the exposed
group was significantly slowed when
compared with the nonexposed group.
A LOAEL of 204 mg/m3 (58 ppm,
LOAEL(ADJ) of 73 mg/m3) was
established for these
electrophysiological alterations in
humans. The alterations observed are
consistent with n-hexane-induced
peripheral neuropathy observed in other
studies in humans and in animals. EPA
believes that there is sufficient evidence
for listing n-hexane on EPCRA section
313 pursuant to EPCRA section
313(d)(2)(B) based upon the available
neurotoxicity data for this chemical.
134. Hexazinone (CAS No. 051235-04-
2) (FIFRA AI) (Ref. 3). In a 2-year mouse
feeding study, liver hypertrophy,
hyperplastic nodules and focal necrosis
were observed at 375 mg/kg/day (LOEL).
The NOEL was 30 mg/kg/day. In a 90-
day feeding study in dogs, decreased
body weight, increased alkaline
phosphatase activity, decreased
albumin/globulin ratio and increased
absolute and relative liver weights were
noted in both sexes at 5,000 ppm (125
mg/kg/day; LOEL). The NOEL was 1,000
ppm (25 mg/kg/day). EPA believes that
there is sufficient evidence for listing
hexazinone on EPCRA section 313
pursuant to EPCRA section 313(d)(2)(B)
based on the available toxicity data for
this chemical.
Measured aquatic acute toxicity test
data for hexazinone include an ECso of
7 ppb for S. capricomutum. EPA
believes that there is sufficient evidence
for listing hexazinone on EPCRA section
313 pursuant to EPCRA section
313(d)(2)(C) based on the available
environmental toxicity data for this
chemical.
135. Hydramethylnon (tetrahydro-5,5-
dimethyl-2(lH)-pyrimidinone[3-[4-
(trifluoromethyl)phenyl]-l -[2-
[4(trifluoromethyl)phenyl]ethenyI]-2-
propenylidenejhydrazone) (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
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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 LCso 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). Hydrochlorofluofocarbons
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
epldemiologic 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)
l,3-Dichloro-l,l,2,3,3-
pentafluoropropane (HCFC-225ea) (CAS
No. 136013-79-1)
2,2-Dichloro-l,l,l,3,3-
pentafluoropropane (HCFC-225aa) (CAS
No. 128903-21-9)
l.l-Dichloro-1,2,3,3,3-
pentafluoropropane (HCFC-225eb) (CAS
No. 111512-56-2)
l,l-Dichloro-l,2,2,3,3-
pentafluoropropane (HCFC-225cc) (CAS
No. 13474-88-9)
l,3-Dichloro-l,l,2,2,3-
pentafluoropropane (HCFC-225cb) (CAS
No. 000507-55-1)
l,2-Dichloro-l,l,3,3,3-
pentafluoropropane (HCFC-225da) (CAS
No. 000431-86-7)
3,3-Dichloro-l,l,l,2,2-
pentafluoropropane (HCFC-225ca) (CAS
No. 000422-56-0)
2,3-Dichloro-l,l,l,2,3-
pentafluoropropane (HCFC-225ba) (CAS
No. 000422-48-0)
1,2-0101110X0-1,1,2,3,3-
pentafluoropropane (HCFC-225bb) (CAS
No. 000422-44-6)
Dichlorofluoromethane (HCFC-21)
(CAS No. 000075-43-4)
l,l,l,2-Tetrachloro-2-fluoroethane
(HCFC-121a) (CAS No. 000354-11-0)
1,1,2,2-Tetrachloro-l-fluoroethane
(HCFC-121) (CAS No. 000354-14-3)
1,2-Dichloro-l ,1-difluoroethane
(HCFC-132b) (CAS No. 001649-08-7)
2-Chloro-l,l,l-trifluoroethane(HCFC-
133a) (CAS No. 000075-88-7)
3-Chloro-l,l,l-trifluoropropane
(HCFC-253fb) (CAS No. 000460-35-5).
137. Imazalil (l-[2-(2,4-
dichlorophenyl)-2-(2-
propenyloxy)ethyl]-lH-imidazole)(CAS
No. 035554-44-0) (FIFRA AI) (Ref. 3). In
a rat teratology study, increased
maternal mortality, decreased litter size,
and increased number of dead fetuses
were observed in animals administered
40 mg/kg/day (LOEL). The NOEL was 10
mg/kg/day. Stillbirths and altered live
birth index were observed in rats orally
administered 80 mg/kg/day days 16
through 22 of gestation and 21 days post
gestation. Altered lactation index was
observed in rats orally administered 20
mg/kg/day on days 16 through 22 of
gestation and 21 days post gestation.
Post-implantation loss was observed in
rabbits orally administered 0.63 mg/kg/
day on days 6 through 18 of gestation.
Altered viability index was observed in
rabbits orally administered 2.5 mg/kg/
day on days 6 through 18 of gestation.
EPA believes that there is sufficient
evidence for listing imazalil on EPCRA
section 313 pursuant to EPCRA section
313(d)(2)(B) based on the available
developmental toxicity data for this
chemical.
138. 3-Iodo-2-propynyl
butylcarbamate (CAS No. 055406-53-6)
(FIFRA AI) (Ref. 3). In a 90-day rat
study, oral administration of 50 mg/kg/
day (LOEL) produced increased liver-to-
body-weight ratios. The NOEL was 20
mg/kg/day. In a 2-year rat study, dietary
administration of 40 and 80 mg/kg/day
produced significant non-neoplastic
pathological changes in the stomach. No
NOEL was established; the LOEL was 20
mg/kg/day. Based on this study, EPA
derived an oral RfD of 0.07 mg/kg/day.
EPA believes that there is sufficient
evidence for listing 3-iodo-2-propynyl
butylcarbamate on EPCRA section 313
pursuant to EPCRA section 313(d)(2)(B)
based on the available chronic toxicity
data for this chemical.
139. Iprodione (3-(3,5-
dichlorophenyl)-N-(l-methylethyl)-2,4-
dioxo-1-imidazolidinecarboxamide)
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1819
(CAS No. 036734-19-7) (FIFRA AI) (Ref.
3). Increased red blood cell Heinz
bodies and decreased prostate weight
(the LOEL was 15 mg/kg/day; the NOEL
was 4.2 mg/kg/day) were observed in
dogs fed iprodione for 1—year. Increased
Heinz bodies were also seen in females
at 15 mg/kg/day. At 90 mg/kg/day,
increased liver weight was noted in
male and female dogs. Based on the
NOEL, an oral RfD of 0.04 mg/kg/day
was derived. In another 1-year feeding
study in dogs, decreased red blood cell
counts and hemoglobin and hematocrit
levels (the LOEL was 600 ppm or 15 mg/
kg/day; the NOEL was 100 ppm or 2.5
mg/kg/day) were observed. At 3,600
ppm (90 mg/kg/day), increased absolute
and relative liver weights and increase
liver alkaline phosphatase, serum
glutamic-pyruvic transaminase, serum
glutamic-oxaloacetic transaminase, and
lactate dehydrogenase activities were
noted. Decreased red blood cell count
and decreased hemoglobin and
hematocrit levels (the LOEL was 24.6
mg/kg/day in males, 26.4 mg/kg/day in
females; the NOEL was 17.5 mg/kg/day
in males, 18.4 mg/kg/day in females).
EPA believes that there is sufficient
evidence for listing iprodione on EPCRA
section 313 pursuant to EPCRA section
313(d)(2)(B) based on the available
hematological and hepatic toxicity data
for this chemical.
Acute aquatic toxicity data include a
green algae 120-hour EC5o of 21 ppb.
EPA believes that there is sufficient
evidence for listing iprodione on EPCRA
section 313 pursuant to EPCRA section
313(d)(2)(C) based on the available
environmental toxicity data for this
chemical.
140. Iron pentacarbonyl (CAS No.
013463-40-6) (EPCRA EHS) (Ref. 8).
Humans exposed to high concentrations
of iron pentacarbonyl immediately
experience headache and dizziness.
These effects are followed 12 to 36
hours after exposure by symptoms such
as fever, cyanosis, cough, and shortness
of breath. In humans, iron
pentacarbonyl has also been known to
cause adverse effects on the respiratory
and central nervous system, liver, and
kidney. The rat oral LDso is 25 mg/kg
and the rat inhalation LCso value is
0.044 mg/L. The 4-hour inhalation
LCioo in mice is 0.007 mg/L. The rabbit
oral LDso is 12 mg/kg. EPA's exposure
analysis indicates that iron
pentacarbonyl 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 iron
pentacarbonyl on EPCRA section 313
pursuant to EPCRA section 313(d)(2)(A)
based on the available acute toxicity and
exposure data for this chemical.
141. Isodrin (CAS No. 000465-73-6)
(CERCLA; EPCRA EHS; RCRA APP8;
RCRA P) (Ref. 8). Measured aquatic
acute toxicity data for isodrin include a
24-hour LCso of 12 ppb for bluegills and
a 24-hour LCso of 6 ppb for minnows.
EPA believes that there is sufficient
evidence for listing isodrin on EPCRA
section 313 pursuant to EPCRA section
313(d)(2)(C) based on the environmental
toxicity data for this chemical.
142. Isofenphos (2-[[ethoxyl[(l-
methylethyl) ammo] phosphinothioyl]
oxy] benzole acid 1-methylethyl ester)
(CAS No. 025311-71-1) (FIFRA AI) (Ref.
3). In a 108-week feeding study in mice,
inhibition of brain cholinesterase (the
LOEL was 100 ppm or 13 mg/kg/day;
the NOEL was 10 ppm or 1.3 mg/kg/
day) and plasma cholinesterase (the
LOEL was 10 ppm or 1.3 mg/kg/day; the
NOEL was 0.13 mg/kg/day) was
observed. Inhibition 'of red blood cell
cholinesterase (the LOEL was 10 ppm or
0.5 mg/kg/day; the NOEL was 1 ppm or
0.05 mg/kg/day) was seen in a 2—year
feeding study in rats. Other studies (14—
and 90-day feeding studies in dogs, 30-
and 90-day studies in rats, and a 3—
week inhalation study in rats) also
demonstrate cholinesterase (plasma, red
blood cell or brain) inhibition in rats
and dogs. EPA believes that there is
sufficient evidence for listing
isophenphos on EPCRA section 313
pursuant to EPCRA section 313(d)(2)(B)
based on the available neurological
toxicity data for this chemical.
Aquatic acute toxicity values for
isofenphos include a daphnid 48—hour
ECso of 1.6 ppb and a mysid 96-hour
ECso of 1.7 ppb. EPA believes that there
is sufficient evidence for listing
isofenphos on EPCRA section 313
pursuant to EPCRA section 313(d)(2)(C)
based on the available environmental
toxicity data.
143. Isophorone (CAS No. 000078-59-
1) (CAA HAP) (Ref. 7). Isophorone has
been shown to cause neurotoxic effects
in humans exposed to atmospheric
concentrations of 5 to 8 ppm. After
being exposed for 1 month, workers
complained of fatigue and malaise.
Neurotoxicity was also observed in
humans following acute exposure. At 40
to 85 ppm, effects included nausea,
headache, dizziness, faintness,
inebriation, and a feeling of suffocation.
Increasing exposure concentrations
resulted in increasing severity of
symptoms. Irritation and central
nervous system (CNS) depression were
observed at concentrations of 200 to 400
ppm. EPA believes that there is
sufficient evidence for listing
isophorone on EPCRA section 313
pursuant to EPCRA section 313(d)(2)(B)
based on the available neurotoxicity
data for this chemical.
144. Isophorone diisocyanate (CAS
No. 004098-71-9) (TSCA) (Ref. 8). The
4-hour inhalation LCso value of
isophorone diisocyanate in rats is 0.123
mg/L. The rat and mouse 3-hour
inhalation RD5o (50 percent reduction in
respiratory rate) values are 0.0046 mg/
L and 0.0019 mg/L, respectively. A 50-
year old man developed severe asthma
after exposure to an unspecified amount
of paint containing isophorone
diisocyanate. A 1-hour exposure to an
unspecified amount of the compound
caused eczema in three out of four
workers. In addition, isocyanates as a
class are generally severe skin, eye and
respiratory irritants. EPA's exposure
analysis indicates that isophorone
diisocyanate 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
isophorone diisocyanate on EPCRA
section 313 pursuant to EPCRA section
313(d)(2)(A) based on the available
acute toxicity and exposure data for this
chemical.
As detailed in Unit IV.B.132. of this
preamble, as an alternative proposal to
the individual listing of HDI,
isophorone diisocyanate, and 1,1-
methylene bis(4-
isocyanatocyclohexane), EPA is
proposing to create a diisocyanates
category that includes HDI, isophorone
diisocyanate, 1,1-methylene bis(4-
isocyanatocyclohexane), and 16 other
diisocyanates.
145. Lactofen (5-(2-chloro-4-
(trifluoromethyl)phenoxy)-2-nitro-2-
ethoxy-l-methyl-2-oxoethyI 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-I 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.
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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 RED 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) \vere noted in a 2—year
feeding study in rats. In a 90-day mouse
study, increased alkaline phosphatase,
serum glutamate oxaloacetate
transaminase (SCOT), and serum
gleutanic pyruvic transaminase (SGPT)
activities, increased liver weight,
hepatic necrosis, biliary hyperplasia,
decreased hematocrit and hemoglobin
levels and red blood cell counts,
exlramcdullary 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.
146.1/nuron (CAS No. 000330-55-2)
(FTFRA SR) (Ref. 8). The appearance of
sulfhcmoglobin in the blood of dogs,
rats, or mice exposed to linuron has
been reported. In fact, available animal
data from feeding studies of various
durations (30 days to 2 years) with
linuron as well as from studies with
structurally similar urea-based
herbicides indicate that the presence of
sulfhemoglobin (abnormal blood
pigment) and morphological changes in
red blood cells provide the most
sensitive indicator of exposure to
linuron. In a 2—year feeding study with
beagle dogs, the LOAEL, based on the
presence of the sulfhemoglobin, was
0.625 mg/kg/day. This was the lowest
dose tested. Red blood cell counts were
decreased in dogs exposed to higher
doses of linuron. EPA has derived an
oral RfD of 0.002 mg/kg/day for linuron
from this study. Similar findings were
reported in two separate 2-year rat
feeding studies. In one of these studies,
the LOAEL was 31.25 mg/kg/day and
the NOAEL was 6.25 mg/kg/day. These
values were based on spleen and bone
marrow changes indicative of
hemolysis, and an increase in mortality
and growth retardation. In the other 2-
year rat study, a LOAEL of 2.5 mg/kg/
day (the lowest dose tested) was based
on decreased red blood cell counts and
reticulocytosis. Elevated sulfhemoglobin
levels were reported in rats exposed for
as little as 30 days to 150 mg/kg/day.
This exposure level also caused severe
growth retardation and increased
mortality. The LOAEL for decreased
body weight gain was 15 mg/kg/day and
the NOAEL was 3 mg/kg/day. Chronic
administration of linuron at 4 mg/kg/
day to rats caused hypochromic anemia,
decreased cholinesterase and peroxidase
activities in the blood.
A LOAEL of 31.25 mg/kg/day was
established in a 3-generation
reproductive toxicity study in which
linuron (in the diet) caused reduced
weanling weights, reduced liver and
kidney weights, liver atrophy, and
reduced pup survival. In a separate
developmental toxicity study in rats
administered linuron orally, a LOAEL of
31.25 mg/kg/day was based on an
increased incidence of fetal resorptions.
The LOAEL for maternal toxicity in this
study was 6.25 mg/kg/day (NOAEL 2.50
mg/kg/day), and was based on
decreased food consumption and
decreased body weight gain. An oral
teratology study in rabbits indicated a
LOAEL of 5 mg/kg/day (lowest dose
tested) based on decreased fetal body
weight, decreased litter size and an
increase in skull malformations.
EPA believes that there is sufficient
evidence for listing linuron on EPCRA
section 313 pursuant to EPCRA section
313(d)(2)(B) based on the hematological
and developmental toxicity data for this
chemical.
147. Lithium carbonate (CAS No.
000554-13-2) (CAL) (Ref. 8). A major use
of lithium carbonate is in the treatment
of manic episodes of manic-depressive
illness. Decreases in the number of
implantations, number of live fetuses
and fetal body weight, and increases in
resorptions and various limb/skeletal
anomalies were reported in the offspring
of Wistar rats that received 100 mg/kg
(the fetotoxic LOEL; the fetotoxic NOEL
was 50 mg/kg) during gestation days 6
through 15. Offspring of mice that
received 465 mg/kg/day during
gestation days 6 through 15 had
increased craniofacial abnormalities.
Fetal death and reductions in litter size
were also noted. EPA believes that there
is sufficient evidence for listing lithium
carbonate on EPCRA section 313
pursuant to EPCRA section 313(d)(2)(B)
based on the available developmental
toxicity data for this chemical.
148. Malathion (CAS No. 000121-75-
5) (CERCLA) (Ref. 8). Malathion is a
phosphorothioate insecticide.'Its
insecticidal properties are due to
cholinesterase inhibition. A 42-year old
woman ingested a minimum of 120 ml
of a 50 percent solution (approximately
850 mg/kg). She quickly became
comatose, cyanotic, flaccid, devoid of
tendon reflexes, and miotic. Her serum
cholinesterase activity was 22 percent of
normal for 9 days and her red blood cell
cholinesterase activity was 10 to 25
percent of normal for 45 days. Thirty-
five cases of poisoning by ingestion
were reported in India. The symptoms
observed were cyanosis, excess
salivation, pinpoint pupils, pulmonary
edema, and electrocardiographic
abnormalities; all of which are
indicative of cholinesterase inhibition.
Autopsy of the fatalities indicated
damage to the myocardium. In a 56-day
study in which men were orally
administered malathion, the NOEL for
neurotoxic effects was 0.23 mg/kg/day
and the LOEL was 0.34 mg/kg/day.
Plasma and red blood cell
cholinesterase inhibition was observed
at 0.34 mg/kg/day; however, no clinical
signs of overt toxicity were noted at this
dose. Based on the NOEL, EPA has
derived an oral RfD of 0.02 mg/kg/day
for this chemical. Cholinesterase
inhibition symptoms have also been
observed in experimental animals
exposed to malathion. EPA believes that
there is sufficient evidence for listing
malathion on EPCRA section 313
pursuant to EPCRA section 313(d)(2)(B)
based on the chronic neurotoxicity data
for this chemical.
Measured aquatic acute toxicity data
for malathion include a 96-hour LCso of
68 ppb for rainbow trout, a 96-hour
LCso of 51 ppb for sheepshead minnow,
and a 96—hour LCso of 76 ppb for lake
trout. In addition, the measured 48-
hour ECso for daphnids is 0.9 ppb. EPA
believes that there is sufficient evidence
for listing malathion on EPCRA section
313 pursuant to EPCRA section
313(d)(2)(C) based on the environmental
toxicity data for this chemical.
149. Man-made mineral fibers
category (CAA HAP) (Ref. 7). Man-made
mineral fibers are synthetic, amorphous
(noncrystalline) fibers which consist of
three major groups: Glass fibers; mineral
wool fibers (which includes mainly rock
wool and slag wool); and refractory
ceramic fibers. Health concerns for these
fibers are based on the morphological
and toxicologic similarities with
asbestos, a known human carcinogen,
causing lung cancer and mesotheliomas
in humans and non-malignant
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respiratory diseases (e.g. lung fibrosis).
Injection studies, in which glass wool
and glass microfibers were directly
placed into the respiratory airways, the
pleural or abdominal cavities of
laboratory animals, have shown
consistent evidence of carcinogenesis.
Experimental studies have shown
evidence of carcinogenesis by injection
of rock wool and slag wool. IARC has
classified glass wool, rock wool, and
slag wool fibers as Group 2B
compounds, i.e., possible human
carcinogens. EPA has classified
refractory ceramic fibers as Group B2
compounds, i.e., probable human
carcinogen. EPA believes that there is
sufficient evidence for listing man-made
mineral fibers as a category on EPCRA
section 313 pursuant to EPCRA section
313(d)(2)(B) based on the available
carcinogenicity data for these fibers.
EPCRA section 313 requires threshold
determinations for chemical categories
to be based on the total of all chemicals
in the category manufactured,
processed, or otherwise used. For
example, a facility that manufactures
three members of a chemical category
would count the total amount of all
three chemicals manufactured towards
the manufacturing threshold for that
category. When filing reports for
chemical categories, the releases are
determined in the same manner as the
thresholds. One report is filed for the
category and all releases are reported on
this form.
EPA considered a number of options
for listing man-made mineral fibers on
EPCRA section 313. In 1977, the
National Institute for Occupational
Safety and Health (NIOSH)
recommended that exposures to fibers
be limited to 3 fibers per cubic
centimeters (f/cc) for fibers that are less
than 3.5 micrometers in diameter and
longer than 10 micrometers in length.
NIOSH has since commented that in
order to protect workers from lung
cancer it will be necessary to lower the
exposure to 0.2 f/cc for fibrous glass. In
1992, the Occupational Safety and
Health Administration (OSHA)
proposed a 1 f/cc 8-hour time-weighted
average (TWA) limit for respirable fibers
of fibrous glass, including refractory
ceramic fibers. Respirable fibers are
generally defined as fibers with a
diameter of less than 3.5 micrometers
whose length is at least 3 times the
diameter (i.e., an aspect ratio (fiber
length divided by fiber diameter) of 3 or
greater). In order to ease the burden of
reporting, EPA considered listing fibers
based on an aspect ratio that simply
discriminates between particles and
fibers. This, however, seemed to be
overly inclusive in that it would cover
nonrespirable as well as respirable
fibers. EPA also considered using a
diameter criteria without an aspect ratio
but this option also appears to be too
inclusive since it may include particles
as well as fibers. EPA is proposing to list
man-made mineral fibers as a category
that includes glass microfibers, glass
wool fibers, rock wool fibers, slag wool
fibers, and refractory ceramic fibers that
have a diameter less than 3.5
micrometers and an aspect ratio greater
than 3. This definition is consistent
with both the NIOSH and OSHA
recommendations and is limited to
fibers that are respirable. EPA requests
comment on this definition of man-
made mineral fibers and any other
options for defining a fibers category.
150. Mecoprop (CAS No. 000093-65-2)
(IARC) (Ref. 8). Mecoprop is a mono-
chloro, mono-methylphenoxy
isopropanoic acid type herbicide. IARC
has assigned mecoprop to Group 2B,
i.e., it is possibly carcinogenic to
humans.
In several animal studies, changes in
liver or kidney weights were the most
sensitive indicators of mecoprop
toxicity. In a 90-day rat feeding study,
the LOAEL was 9 mg/kg/day and the
NOAEL was 3 mg/kg/day. At 26 mg/kg/
day, the changes in organ weights were
accompanied by decreased glucose
levels in males and increased creatinine
levels in females. EPA has derived an
oral RfD of 0.001 mg/kg/day from this
study.
EPA believes that there is sufficient
evidence for listing mecoprop on
EPCRA section 313 pursuant to EPCRA
section 313(d)(2)(B) based on the
hepatic and renal toxicity data for this
chemical.
151. 2-Mercaptobenzothiazole (MET)
(CAS No. 000149-30-4) (TSCA) (Ref. 8).
The 21-day maximum acceptable
toxicant concentration (MATC) for
daphnids range from 240 to 470 ppb.
The 60-day MATC for rainbow trout
range from 41 to 78 ppb. EPA's exposure
analysis indicates that releases of 2-
mercaptobenzothiazole will result in
concentration levels that can reasonably
be anticipated to cause significant
adverse environmental effects. EPA
believes that there is sufficient evidence
for listing 2-mercaptobenzothiazole on
EPCRA section 313 pursuant to EPCRA
section 313(d)(2)(C) based on the
available environmental toxicity data
and exposure data for this chemical.
152. Merphos (CAS No. 000150-50-5)
(FIFRA SR) (Ref. 8). Merphos is a
thiophosphate-type cholinesterase
inhibitor. Delayed neurotoxic effects
have been reported in a 28-year old man
following accidental exposure to the
chemical over a period of 3 days.
Fourteen days later, he developed
complete facial diplegia and decreased
conduction velocity in his nerve fibers.
He recovered completely. Both
immediate and delayed neurotoxic
effects following exposure to merphos
have been reported in experimental
animals. In a 3—month hen feeding
study the NOEL for neurotoxic effects
was 0.1 mg/kg/day and the LOEL was
0.5 mg/kg/day. At 0.5 mg/kg, hens
showed delayed neurotoxicity, ataxia,
and equivocal changes in the spinal
cord and peripheral nerves. Based on
the NOEL, EPA derived an oral RfD of
0.00003 mg/kg/day for this chemical. In
a 112-day rat feeding study, females
showed red blood cell cholinesterase
inhibition at the LOEL of 0.25 mg/kg/
day. The NOEL was 0.1 mg/kg/day. In
a 90-day rat feeding study, animals
showed reduced brain cholinesterase
activity at the LOEL of 3.8 mg/kg/day.
The NOEL was 1.8 mg/kg/day. In a 90-
day dog feeding study, plasma
cholinesterase inhibition was observed
at the LOEL of 2.5 mg/kg/day. The
NOEL was 0.75 mg/kg/day. Fourteen
cattle and 20 sheep administered single
doses of merphos (25 to 200 mg/kg) or
10 daily doses of merphos (2.5 mg/kg/
day) showed emaciation, diarrhea, and
depression of blood cholinesterase.
Ingested merphos is rapidly metabolized
to n-butyl mercaptan within the
gastrointestinal tract. n-Butyl mercaptan
has been shown to be responsible for the
acute neurotoxic effects of merphos.
Thus, oral exposure to merphos is
expected to cause acute neurotoxic
symptoms while dermal exposure to
merphos is expected to cause delayed
neurotoxic symptoms. EPA believes that
there is sufficient evidence for listing
merphos on EPCRA section 313
pursuant to EPCRA section 313(d)(2)(B)
based on the chronic neurotoxicity data
for this chemical.
153. Metham sodium (sodium
methyldithiocarbamate) (CAS No.
000137-42-8) (FIFRA AI) (Ref. 3).
Postimplanatation loss was observed in
rabbits administered metham sodium at
30 mg/kg/day (LOEL) on days 6 to 18 of
gestation. The NOEL was 10 mg/kg/day
(4.2 mg/kg/day based on active
ingredient). In rats fed metham sodium,
increased variations, retardations, and
anomalies were reported at doses of 10
mg/kg/day (LOEL) administered on days
6 to 15. The NOEL was less than or
equal to 10 mg/kg/day (less than or
equal to 4.2 mg/kg/day based on active
ingredient). Although neither study was
considered to be fully adequate due to
study design and reporting deficiencies,
the weight of evidence indicates that
metham sodium induces developmental
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1822 Federal Register / Vol. 59, No. 8 / Wednesday, January 12, 1994 / Proposed Rules
toxicity. In addition, metham sodium is
metabolized to carbon disulfide, a
potent developmental toxicant. EPA
believes that there is sufficient evidence
for listing metham sodium on EPCRA
section 313 pursuant to EPCRA section
313(d)(2)(B) based on the available
developmental toxicity data for this
chemical and its metabolite, carbon
disulfide,
154. Methazole (2-(3,4-
dlchlorophenyl)-4-methyl-l,2,4-
oxadiazolidine-3,5-dione) (CAS No.
020354-26-1) (FIFRA AI) (Ref. 3).
Rabbits receiving 30 or 60 mg/kg/day by
gavage on days 6 to 18 of gestation
exhibited increased embryolethality.
The NOEL was 10 mg/kg/day. EPA
believes that there is sufficient evidence
for listing methazole on EPCRA section
313 pursuant to EPCRA section
313(dj(2)(B) based on the available
developmental toxicity data for this
chemical.
155. Methiocarb (CAS No. 002032-65-
7) (CERCLA; EPCRA EHS) (Ref. 8).
Measured terrestrial acute toxicity data
for wildlife include an oral LDSO of 4.6
mg/kg for red-winged blackbirds. EPA
believes that there is sufficient evidence
for listing methiocarb on EPCRA section
313 pursuant to EPCRA section
313(d](2)(C) based on the environmental
toxicity data for this chemical.
156. Methoxone ((4-Chloro-2-
metliylphenoxy) acetic acid) (MCPA)
(CAS No. 000094-74-6) (FIFRA SR;
IARC) (Ref. 8). Methoxone is a
chlorophenoxy-type herbicide. Animal
studies indicate that the kidney and
liver are the primary target organs of
methoxone toxicity. Beagle dogs fed
diets containing methoxone for 1-year
developed liver toxicity, which was
demonstrated by increased liver weights
associated with alterations in serum
glutamate-pyruvate transaminase, serum
glutamate-oxaloacetate transaminase,
bilirubin, triglyceride and cholesterol
levels. These effects occurred at doses of
0.75 mg/kg/day (LOAEL) and higher.
The NOAEL was 0.15 mg/kg/day.
Kidney changes in the treated animals
included deposition of kidney pigment
in the proximal tubular epithelium (the
LOAEL was 0.75 mg/kg/day; the NOAEL
was 0.15 mg/kg/day), and was
accompanied by alterations in
creatinine, urea, and potassium levels.
EPA derived an oral RfD of 0.0005 mg/
kg/day from this study. Similar changes
suggesting liver and kidney toxicity
were reported in another 90-day dog
feeding study (the LOAEL was 3 mg/kg/
day; the NOAEL was 1 mg/kg/day) and
in rats in a 90-day feeding study (the
LOAEL was 7.5 mg/kg/day; the NOAEL
was 2.5 mg/kg/day).
EPA believes that there is sufficient
evidence for listing methoxone on
EPCRA section 313 pursuant to EPCRA
section 313(d)(2)(B) based on the
available hepatic and renal toxicity data
for this chemical.
157. Methoxone sodium salt ((4-
chloro-2-methylphenoxy) acetate
sodium salt) (CAS No. 003653-48-3)
(FIFRA SR; IARC) (Ref. 8). Methoxone
sodium salt is a chlorophenoxy-type
herbicide. Animal studies indicate that
the kidney and liver are the primary
target organs of methoxone toxicity.
Beagle dogs fed diets containing
methoxone for 1—year developed liver
toxicity, which was demonstrated by
increased liver weights associated with
alterations in serum glutamate-pyruvate
transaminase, serum glutamate-
oxaloacetate transaminase, bilirubin,
triglyceride and cholesterol levels.
These effects occurred at doses of 0.75
mg/kg/day (LOAEL) and higher. The
NOAEL was 0.15 mg/kg/day. Kidney
changes in the treated animals included
deposition of kidney pigment in the
proximal tubular epithelium (the
LOAEL was 0.75 mg/kg/day; the NOAEL
was 0.15 mg/kg/day), and was
accompanied by alterations in
creatinine, urea, and potassium levels.
EPA derived an oral RfD of 0.0005 mg/
kg/day from this study. Similar changes
suggesting liver and kidney toxicity
were reported in another 90-day dog
feeding study (the LOAEL was 3 mg/kg/
day; the NOAEL was 1 mg/kg/day) and
in rats in a 90-day feeding study (the
LOAEL was 7.5 mg/kg/day; the NOAEL
was 2.5 mg/kg/day).
EPA believes that there is sufficient
evidence for listing methoxone sodium
salt on EPCRA section 313 pursuant to
EPCRA section 313(d)(2)(B) based on its
potential to cause cancer and on the
available hepatic and renal toxicity data
for this chemical.
158.1,1-Methylene bis(4-
isocyanatocyclohexane) (CAS No.
005124-30-1) (TSCA) (Ref. 8). The 5-
hour rat inhalation LCjo value for 1,1-
methylenebis(4-isocyanatocyclohexane)
is 0.21 mg/L. The 3-hour mouse
inhalation RDso (50 percent reduction in
respiratory rate) value is 0.027 mg/L. In
addition, isocyanates as a class are
generally severe skin, eye, and
respiratory irritants. EPA's exposure
analysis indicates that 1,1-
methylenebis(4-isocyanatocyclohexane)
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 l,l-methylenebis(4-
isocyanatocyclohexane) on EPCRA
section 313 pursuant to EPCRA section
313(d)(2)(A) based on the available
acute toxicity and exposure data for this
chemical.
As detailed in Unit IV.B.132. of this
preamble, as an alternative proposal to
the individual listing of HDI,
isophorone diisocyanate, and 1,1-
methylene bis(4-
isocyanatocyclohexane), EPA is
proposing to create a diisocyanates
category that includes HDI, isophorone
diisocyanate, 1,1-methylene bis(4-
isocyanatocyclohexane), and 16 other
diisocyanates.
159. Methylene bis(thiocyanate) (CAS
No. 006317-18-6) (FIFRA AI) (Ref. 3).
The minimal human lethal dose for
methylene bis(thiqcyanate) is 15 to 30 g
(214 to 429 mg/kg), although fatalities
have been reported at 300 mg (4.3 mg/
kg). Clinical effects may include
decreased blood pressure, apnea,
cerebral excitation, convulsions, coma,
vomiting, diarrhea, abdominal
cramping, albuminuria, skin rashes,
exfoliative dermatitis, muscle weakness,
goiter, and toxic psychosis. The
intravenous mouse LDso is 3-6 mg/kg.
The subcutaneous rabbit DLo is 20 mg/
kg; convulsions and lowered blood
pressure were observed in this study.
EPA believes that there is sufficient
evidence for listing methylene
bis(thiocyanate) on EPCRA section 313
pursuant to EPCRA section 313(d)(2)(B)
based on the available neurological
toxicity data for this chemical.
160. Methyl isothiocyanate (CAS No.
00556-61-6) (FIFRA AI) (Ref. 3). Aquatic
acute toxicity values for methyl
isothiocyanate include a fish 96-hour
LC50 of 94 ppb, a 96-hour LCso of 130
ppb for bluegills, and a daphnid 48-
hour LC5o of 55 ppb. EPA believes that
there is sufficient evidence for listing
methyl isothiocyanate on EPCRA
section 313 pursuant to EPCRA section
313(d)(2)(C) based on the available
environmental toxicity data.
161. 2-Methyllactonitrile (CAS No.
000075-86-5) (CERCLA; EPCRA EHS;
RCRA APP8; RCRA P) (Ref. 8). 2-
Methyllactonitrile belongs to a class of
substances known as the cyanohydrins.
Cyanohydrins are generally quite toxic
because they can release hydrogen
cyanide. An oral dose of 5 mg/rat
(approximately 14 mg/kg) of 2-
methyllactonitrile administered twice
weekly for 3 to 8 months produced liver
and kidney lesions. Inhalation of 10.2
mg/L twice weekly for 3 to 8 months
(duration of each individual exposure
not reported) produced kidney lesions,
desquamation of the bronchial
epithelium, and bronchial ulcerations.
EPA believes that there is sufficient
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Federal Register / Vol. 59, No. 8 / Wednesday, January 12, 1994 / Proposed Rules 1823
evidence for listing 2-methyllactonitrile
on EPCRA section 313 pursuant to
EPCRA section 313(d)(2)(B) based on
the chronic toxic effects to the liver,
kidney, and bronchi caused by this
chemical.
l62..N-Methylolacrylamide (CAS No.
000924-42-5) (CAL) (Ref. 8). There was
clear evidence of carcinogenicity from
N-methylolacrylamide in a 2—year study
using B6C3F1 mice administered the
substance by oral gavage. In both sexes,
there were increased incidences of
Harderian gland adenomas or
carcinomas, hepatocellular adenomas or
carcinomas, and alveolar or bronchiolar
adenomas and carcinomas. There was
also an increase in ovarian granulosa
cell tumors. EPA believes that there is
sufficient evidence for listing N-
methylolacrylamide on EPCRA section
313 pursuant to EPCRA section
313(d)(2)(B) based on the
carcinogenicity data for this chemical.
163. Methyl parathion (CAS No.
000298-00-0) (CERCLA; FIFRA SR;
RCRA APP8; RCRA P) (Ref. 8). Methyl
parathion is a thiophosphate-type
cholinesterase inhibitor. Methyl
parathion is highly toxic when
administered to experimental animals at
low doses. The rat and mouse oral LDso
values are reported to be 6.01 mg/kg and
18 mg/kg, respectively. The rat and
mouse 4-hour inhalation LCso values are
reported to be 0.034 mg/L and 0.12 mg/
L, respectively, at which symptoms of
cholinesterase inhibition were observed.
Human volunteers showed a 37
percent decrease in red blood cell
cholinesterase activity following oral
administration of 0.43 mg/kg/day of
methyl parathion for 10 days. The LOEL
was 0.43 mg/kg/day and the NOEL was
0.31 mg/kg/day. In a 90-day dog feeding
study, brain, red blood cell, and plasma
cholinesterase inhibition was observed
at the LOEL of 1.0 mg/kg/day. The
NOEL was 0.3 mg/kg/day. In a chronic
rat feeding study, plasma and
erythrocyte cholinesterase were
inhibited throughout the study and
brain cholinesterase was depressed at
the termination of the study at 2.5 mg/
kg/day. The NOEL for systemic toxicity
was 0.025 mg/kg/day. An adequate
NOEL for neurologic changes was not
defined. Overt signs of cholinergic
toxicity (tremors, abnormal gait,
alopecia) were observed in the animals
at a dose of 2.5 mg/kg/day. Histologic
examination revealed evidence of
peripheral neuropathy in animals
administered this dose. EPA has derived
an oral RfD of 0.00025 mg/kg/day based
on the systemic NOEL for this chemical.
Hepatocellular swelling,
degeneration, and fatty change have
been observed in humans acutely
intoxicated with methyl parathion.
Hepatocellular changes were observed
in patients that survived for 28 hours to
9 days after intoxication. Methyl-
parathion was orally administered to
rats in increasing doses for 36 days
(starting with 0.37 mg/kg/day and
increasing by a factor of 1.5 on every 4th
day). Weight loss, hyperglycemia, and
macrocytic anemia, all secondary to
hepatbtoxicity, were observed.
EPA believes that there is sufficient
evidence for listing methyl parathion on
EPCRA section 313 pursuant to EPCRA
section 313(d)(2)(B) based on the
chronic neurotoxicity and hepatic
toxicity data for this chemical.
Measured aquatic acute toxicity data
for methyl parathion include a 48-hour
ECso of 0.14 ppb for daphnids and a 96-
hour LCso of 15 ppb for crayfish. EPA
believes that there is sufficient evidence
for listing methyl parathion on EPCRA
section 313 pursuant to EPCRA section
313(d)(2)(C) based on the available
environmental toxicity data for this
chemical.
164. N-Methyl-2-pyrrolidone (CAS No.
000872-50-4) (TSCA) (Ref. 8). In a 2-
generation reproductive study, there
was evidence of reproductive toxicity in
the Fi generation after exposure to 50
mg/kg/day (LOAEL; no NOAEL was
established). Exposure to 50 mg/kg/day
or more resulted in significant
reductions in the male fertility index
and in the female fecundity index. In
addition, exposure to 500 mg/kg/day
resulted in an increased incidence of
dams with decreased corpora lutea.
There was also evidence of
developmental toxicity in both
generations after exposure to 500 mg/kg/
day as demonstrated by reduced litter
size, reduced postnatal survival, and
reduced pup weight.
Maternal toxicity (significant
reduction in mean body weight gain)
was observed in rabbits receiving 175
mg/kg by gavage on days 6 through 18
of gestation (The NOAEL was 55 mg/kg/
day). Exposure to 540 mg/kg/day
(LOAEL) resulted in developmental
toxicity as demonstrated by a significant
increase in resorptions, and
malformations (misshapen skull bone
and cardiovascular malformations). The
NOAEL for developmental toxicity was
175 mg/kg/day.
EPA believes that there is sufficient
evidence for listing N-
methylpyrrolidone on EPCRA section
313 pursuant to EPCRA section
313(d)(2)(B) based on the available
developmental and reproductive
toxicity data for this chemical.
165. Methyltrichlorosilane (CAS No.
000075-79-6) (EPCRA EHS) (Ref. 8). As
a class, chlorinated silanes are very
corrosive to the skin and mucous
membranes and liberate hydrochloric
acid in the presence of water.
Methyltrichlorosilane causes severe
burns and the vapor is harmful to
humans. The 2—hour mouse inhalation
LC50 value is 0.180 mg/L. EPA's
exposure analysis indicates that
methyltrichlorosilane 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
methyltrichlorosilane on EPCRA section
313 pursuant to EPCRA section
313(d)(2)(A) based on the available
acute toxicity and exposure data for this
chemical.
166. Metiram (CAS No. 009006-42-2)
(FIFRA SR) (Ref. 8). Metiram is an
ethylene bisdithiocarbamate (EBDG)
fungicide. Evidence suggests that
ethylene bisthiocarbamate fungicides
and ethylenethiourea (a common
contaminant, metabolite, and
degradation product of these fungicides)
cause cancer and adverse
developmental effects in experimental
animals. In a 2-year diet study,
ethylenethiourea caused liver adenomas
and carcinomas in mice, and thyroid
follicular cell adenomas and carcinomas
in mice and rats. A NOAEL of less than
or equal to 5 mg/kg has been reported
for ethylenethiourea, based on a rat
developmental toxicity study.
Ethylenethiourea caused delayed
ossification or hardening of the parietal
bone in pups. EPA believes that there is
sufficient evidence for listing metiram
on EPCRA section 313 pursuant to
EPCRA section 313(d)(2)(B) based on
the carcinogenicity and developmental
toxicity data for ethylenethiourea, a
metabolite and degradation product of
metiram.
In Unit IV.B.172. of this preamble,
EPA is proposing to add another
ethylene bisdithiocarbamate (EBDC),
nabam. An additional two EBDCs, zineb
and maneb, are currently individually
listed on the EPCRA section 313 list of
toxic chemicals. The category of EBDCs
has recently been added to EPCRA
section 313 (December 1,1993, 58 FR
63500). EPA requests comment on the
following: (1) Should the individual
EBDCs, metiram and nabam, be added
individually to EPCRA section 313 even
though they are members of the EBDC
category, which is listed on EPCRA
section 313; and (2) should the
individual listings for two EBDCs, zineb
and maneb, be deleted and added as
members of the newly created EBDC
category.
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167. Metribuzin (CAS No. 021087-64-
5) (FIFRA AI) (Ref. 3). In a rabbit
teratology study, the NOEL for maternal
and fetotoxicity was 15 mg/kg/day, and
tha LOEL was 45 mg/kg/day.
Developmental effects including
irregular spinus process and decreased
pup body weight were observed in rats
treated with metribuzin (Sencor) during
gestation day 7 to 19 at 85 mg/kg/day
(LOEL). The NOEL for developmental
toxicity was 30 mg/kg/day. The LOEL
and NOEL for maternal toxicity were 30
and 10 mg/kg/day, respectively.
In a 2-year dog feeding study, adverse
effects observed at 1,500 ppm (37.5 mg/
kg/day; LOEL) included weight
reduction, increased mortality,
hematologic changes, and liver/kidney
damage. The systemic NOEL was 100
Epm (2.5 mg/kg/day). In a 2-year rat
Kjding study, decreased weight gain,
mortality, and pathological changes in
the liver and kidney were observed at
300 ppm (15 mg/kg/day). The NOEL
was 100 ppm (5 mg/kg/day).
EPA believes that there is sufficient
evidence for listing metribuzin on '
EPCRA section 313 pursuant to EPCRA
section 313(d)(2)(B) based on the
available hepatic, renal, and
developmental toxicity data for this
chemical.
168. Mevinphos (CAS No. 007786-34-
7) (CERCLA; EPCRA EHS) (Ref. 8).
Measured aquatic acute toxicity values
for movinphos include a 96-hour LC5o
of 70 ppb forbluegills, and a 96-hour
LCso of 0.16 ppb for daphnids.
Measured acute avion toxicity data
include a pheasant oral LDjo of 1.37 mg/
kg, a mallard duck oral LDjo of 4.63 mg/
kg, and a sharp-tailed grouse oral LDj0
of 1.34 mg/kg. EPA believes that there
is sufficient evidence for listing
mevinphos on EPCRA section 313
pursuant to EPCRA section 313(d)(2)(C)
based on the environmental toxicity
data for this chemical.
169. Molinate (lH-azepine-1-
carbothioic acid, hexahydro-S-ethyl
ester) (CAS No. 002212-67-1) (FIFRA AI)
(Ref 3). In a rat developmental toxicity
study, adverse effects observed
following administration of molinate at
35 mg/kg/day (LOEL) included
increased post-implantation loss, lower
fetal body weight, increased incidence
of runts, and external/soft tissue/
skeletal variants; the NOEL was 2.2 mg/
kg. In a rabbit developmental study,
adverse effects such as an increase in
the number of abortions, and a decrease
in the number of females with live
fetuses were noted at 200 mg/kg/day.
The NOEL was 20 mg/kg/day. The
developmental effects were observed at
levels which were toxic to maternal
animals.
In a rat fertility test, reductions in
fertility, dose-related altered sperm
morphology, and a reduction in the
number of viable fetuses were observed
following administration of molinate.
The NOEL was 0.2 mg/kg/day and the
LOEL was 4 mg/kg/day. Based on the
NOEL of the study, an oral RfD of 0.002
mg/kg/day was derived. In a 90-day
study in male rats, the lowest toxic oral
dose of 324 mg/kg produced adverse
effects on spermatogenesis, male
fertility, and viability index. The 20-day
inhalation male rat lowest-toxic
contentration (TCLo) is 0.0006 mg/L. At
this exposure level adverse effects on
spermatogenesis and male fertility index
were reported. In a 2-generation rat
reproduction study, the reproductive
NOEL was 0.3 mg/kg/day, and the LOEL
was 2.5 mg/kg/day based on reduced
fecundity and increased incidence of
ovarian vacuolation/hypertrophy. In a
3-month rat inhalation study, testicular
degeneration and abnormal spermatozoa
were observed at 0.002 mg/L (LOEL). No
NOEL was determined.
In a 2—year study in rats fed molinate,
adverse effects seen at 0.35 mg/kg/day
included degeneration and
demyelination of the sciatic nerve and
skeletal muscle atrophy/reserve cell
hyperplasia; no NOEL was determined.
In a 1—year study in dogs administered
molinate orally, adverse effects observed
at 50 mg/kg/day included anemia, loss
of ability to bark, ataxia, splayed hind
limbs, vacuolation of the medulla,
demyelination of the pons and spinal
cord, tremors, and eosinophilic bodies
in the nervous system.
EPA believes that there is sufficient
evidence for listing molinate on EPCRA
section 313 pursuant to EPCRA section
313(d)(2)(B) based on the available
developmental, reproductive, and
neurological toxicity data for this
chemical.
170. Monuron (CAS No. 000150-68-5)
(FIFRA SR) (Ref. 8). The measured
aquatic toxicity data for monuron
include a 1.5-hour ECso of 90 ppb and
a 10-day ECso of 100 ppb for marine
algae. EPA believes that there is
sufficient evidence for listing monuron
on EPCRA section 313 pursuant to
EPCRA section 313(d)(2)(C) based on
the environmental toxicity data for this
chemical.
171. Myclobutanil (alpha-butyl-alpha-
(4-chlorophenyl)-lH-l,2,4-triazole-l-
propanenitrile) (CAS No. 088671-89-0)
(FIFRA AI) (Ref. 3). Hepatocellular
hypertrophy (the LOEL was 5.9 mg/kg/
day; the NOEL was 0.3 mg/kg/day) was
seen in a 90-day feeding study in dogs.
In another 90-day feeding study,
hepatocellular necrosis and hypertrophy
(the LOEL was 147.2 mg/kg/day; the
NOEL was 49.1 mg/kg/day) were
observed in rats. Hepatocellular
hypertrophy (the LOEL was 14.3 mg/kg/
day in males and 15.7 mg/kg/day in
females; the NOEL was 3.1 mg/kg/day in
males and 3.83 mg/kg/day in females)
was noted in a 1-year feeding study in
dogs. Hepatic effects (centrilobular
hepatocytic hypertrophy, kupffer cell
pigmentation, periportal vacuolation
and altered foci) were observed in mice
fed 75 mg/kg/day myclobutanil for 2
years. At 15 mg/kg/day, increased liver
mixed function oxidase (the NOEL was
3 mg/kg/day) was also seen.
Testicular atrophy (the LOEL was 9.84
mg/kg/day; the NOEL was 2.49 mg/kg/
day) was observed in a 2-year chronic
feeding study in rats. The seminiferous
tubules were frequently devoid of
spermatid formation and germinal
epithelial cells. Based on the NOEL, an
oral RfD of 0.025 mg/kg/day was
derived. Testicular atrophy (the LOEL
was 46.4 mg/kg/day; the NOEL was 9.28
mg/kg/day) was also noted in a 2-
generation reproduction study.
In a developmental toxicity study in
rats, increased resorption and decreased
viability were observed at 93.8 mg/kg/
day (LOEL). The NOEL was 31.3 mg/kg/
day. In a developmental toxicity study
in rabbits, an increased number of
resorptions per litter, reduced viability
index, and reduced litter size were
observed at 200 mg/kg/day (LOEL). The
NOEL was 60 mg/kg/day.
EPA believes that there is sufficient
evidence for listing myclobutanil on
EPCRA section 313 pursuant to EPCRA
section 313(d)(2)(B) based on the
available hepatic, reproductive, and
developmental toxicity data for this
chemical.
172. Nabam (CAS No. 000142-59-6)
(FIFRA SR) (Ref. 8). Nabam is an
ethylene bisthiocarbamate fungicide.
Evidence suggests that ethylene
bisthiocarbamate fungicides and
ethylenethiourea (a common
contaminant, metabolite, and
degradation product of these fungicides)
cause cancer and adverse
developmental effects in experimental
animals. In a 2—year diet study
ethylenethiourea caused liver adenomas
and carcinomas in mice, and thyroid
follicular cell adenomas and carcinomas
in mice and rats. A NOAEL of less than
or equal to 5 mg/kg has been reported
for ethylenethiourea, based on a rat
developmental toxicity study.
Ethylenethiourea caused delayed
ossification or hardening of the parietal
bone in pups. EPA believes that there is
sufficient evidence for listing nabam on
EPCRA section 313 pursuant to EPCRA
section 313(d)(2)(B) based on the
carcinogenicity and developmental
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toxicity data for ethylenethiourea, a
metabolite and degradation product of
nabam.
173. Naled (GAS No. 000300-76-5)
(CERCLA; FIFRA SR) (Ref. 8). Naled is
an organophosphate-type cholinesterase
inhibitor. In a human acute poisoning
case, toxic symptoms included
abdominal cramps, hypersecretion,
emesis, perspiration, anxiety, vertigo
and horizontal nystagmus, and persisted
for 4 months. In a 2—year rat feeding
study the NOEL for neurotoxic effects
was 0.2 mg/kg/day and the LOEL was
2.0 mg/kg/day. It was observed in this
study that, at 2.0 mg/kg/day, brain
cholinesterase activity was inhibited by
approximately 24 percent. At 10.0 mg/
kg/day, brain cholinesterase activity was
inhibited by approximately 60 percent,
and both plasma and red blood cell
cholinesterase were also inhibited.
Based on the NOEL, EPA has an oral
RfD of 0.002 mg/kg/day for this
chemical. In a 1-year feeding study
using dogs as the test species, plasma
and red blood cell cholinesterase
activity were inhibited at 2.0 mg/kg/day.
The NOEL was 0.2 mg/kg/day and the
LOEL was 2.0 mg/kg/day.
In a 2-generation reproduction study
of naled in rats, the NOEL was 6 mg/kg/
day. At 18 mg/kg/day, decreased litter
size, survival, and pup body weight
were observed.
EPA believes that there is sufficient
evidence for listing naled on EPCRA
section 313 pursuant to EPCRA section
313(d)(2)(B) based on the chronic
neurotoxicity and reproductive toxicity
data for this chemical.
Measured aquatic acute toxicity
values for naled include a 48—hour ECso
of 0.35 ppb for daphnids and a 96-hour
LCso of 87 ppb for lake trout. EPA
believes that there is sufficient evidence
for listing naled on EPCRA section 313
pursuant to EPCRA section 313(d)(2)[C)
based on the environmental toxicity
data for this chemical.
174. Nicotine and salts (CAL;
CERCLA; EPCRA EHS; FIFRA AI; RCRA
APP8; RCRA P) (Ref. 8). Nicotine salts
will dissociate in aqueous solutions to
yield soluble nicotine. Nicotine is
highly toxic in humans. The estimated
lethal oral dose in adults is
approximately 40 to 60 mg. The onset of
toxicity is rapid. Symptoms include
nausea, salivation, abdominal pain,
vomiting, diarrhea, headache, weakness,
sweating, and confusion. Nicotine
markedly stimulates the central nervous
system, causing tremors and
convulsions. The stimulation is
followed by depression, and death
resulting from paralysis of respiratory
muscles. Nicotine can also activate
parasympathetic ganglia and cholinergic
nerve endings resulting in
gastrointestinal hyperactivity.
Skeletal defects and occasional cleft
palates were observed in mice injected
with 25 mg/kg nicotine on gestation
days 9 to 11. Reduced size in the
newborn of rats and limb deformities in
the offspring of swine were reported in
swine and rats following oral exposure
to 1,058 ppm nicotine (approximately
53 mg/kg/day). Deformities were found
in some rabbit fetuses when dams were
administered nicotine at a dose of 20
mg/kg 5 times during pregnancy.
Pregnant swine fed aqueous leaf extracts
of tobacco at the rate of 16 and 32 mg/
kg nicotine produced arthrogrypotic
newborn pigs.
EPA believes that there is sufficient
evidence for listing nicotine and its salts
as a category on EPCRA section 313
pursuant to EPCRA section 313(d)(2)(B)
based on the developmental toxicity
data for these substances.
EPCRA section 313 requires threshold
determinations for chemical categories
to be based on the total of all chemicals
in the category manufactured,
processed, or otherwise used. For
example, a facility that manufactures
three members of a chemical category
would count the total amount of all
three chemicals manufactured towards
the manufacturing threshold for that
category. When filing reports for
chemical categories, the releases are
determined in the same manner as the
thresholds. One report if filed for the
category and all releases are reported on
this form.
175. Nitrapyrin (2-chloro-6-
(trichloromethyl) pyridine) (CAS No.
001929-82-4) (FIFRA AI) (Ref. 3). In a 1-
year study hi dogs fed nitrapyrin
adverse effects noted included increased
cholesterol and alkaline phosphatase,
increased absolute and relative liver
weight and panlobular/centrilobular
hepatocellular hypertrophy. The NOEL
was 3 mg/kg/day and the LOEL was 15
mg/kg/day. In a 10—week reproductive
rat study, adverse effects observed
included increased incidence of fetal
liver hypertrophy and vacuolization at
75 mg/kg/day (LOEL). The NOEL was 20
mg/kg/day. In a 90-day rat feeding
study, hepatocellular fatty change and
necrosis, renal tubule epithelial cell
swelling and increasingly severe
interstitial nephritis were observed at 50
mg/kg/day. The NOEL was 15 mg/kg/
day. In a 2-year rat feeding study, an
increase in glomerulonephropathy was
observed hi males dosed with 60 mg/kg/
day and an increase in hepatic
hypertrophy and vacuolization was
observed in males and females dosed
with 60 mg/kg/day. The NOEL was 20
mg/kg/day.
Increased incidence of crooked hyoid
bone and craniofacial abnormalities
were observed in the offspring of rabbits
orally administered nitrapyrin at 30 mg/
kg/day (LOEL) on days 6 through 18 of
gestation. The NOEL was 10 mg/kg/day.
Decreased weight and hypertrophy and
vacuolization of the liver were observed
in offspring of rats dosed with 75 mg/
kg/day (LOEL) for 10 weeks prior to
mating. The NOEL was 20 mg/kg/day.
EPA beh'eves that there is sufficient
evidence for listing nitrapyrin on
EPCRA section 313 pursuant to EPCRA
section 313(d)(2)(B) based on the
available renal, hepatic, and
developmental toxicity data for this
chemical.
176. Nitrate ion (CAS No. 014797-55-
8) (SDWA) (Ref. 8). Nitrate refers to the
nitrate ion (NO3-). Infantile
methemoglobinemia occurs in human
infants exposed to aqueous solutions of
nitrate ion and can progress to cyanosis
and death. Based on numerous
epidemiological and clinical studies,
EPA has determined a LOAEL of 1.8 to
3.2 mg/kg/day and a NOAEL and RfD of
1.6 mg/kg/day, corresponding to 10 mg/
L nitrate-nitrogen or 44 mg/L nitrate ion
in drinking water. Infants weighing an
average of 4 kg (0 to 3 months of age)
are the most sensitive population to
nitrate-induced methemoglobinemia.
This is primarily due to their higher
stomach pH which favors the growth of
nitrate-reducing bacteria, the
immaturity of their metabolic enzyme
systems, and reduced capacity of their
erythrocytes to reduce methemoglobin
to hemoglobin. EPA believes that there
is sufficient evidence for listing nitrate
ion on EPCRA section 313 pursuant to
EPCRA section 313(d)(2)(B) based on
the available hematological toxicity data
for this chemical.
In nitrogen-limited waters, nitrates
have the potential to cause increased
algal growth leading to eutrophication
in the aquatic environment. (Nitrate-
nitrogen is the form of nitrogen most
available to plants.) Studies of estuarine
water at several locations along the
eastern coast of the United States have
indicated that low concentrations of
dissolved nitrogen (e.g., nitrate) limit
primary production of plants.
Additions of nitrate to such estuarine
systems stimulate primary production of
plants and can produce changes in the
dominant species of plants, leading to
cultural eutrophication and ultimately
to deterioration of water quality,
including algal blooms.
It has been determined that lakes with
a spring maximum concentration of
more than 300 ug/L of inorganic
nitrogen (e.g., nitrates) could be
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1826 Federal Register / Vol. 59, No. 8 / Wednesday, January 12, 1994 / Proposed Rules
expected to have algal nuisances in the
summer.
Toxic effects result from oxygen
depletion as the algae die and decay.
Toxic effects have also been related to
the release of decay products or direct
excretion of toxic substances from
sources such as blue-green algae.
EPA believes that there is sufficient
evidence for listing nitrate ion on
EPCRA section 313 pursuant to EPCRA
section 313(d)(2)(C) based on the
available environmental toxicity data.
177. Nitric oxide (CAS No. 010102-43-
9) (CERCLA; EPCRA EHS; RCRA APP8;
RCRA P) (Ref. 8). The acute toxicity of
nitric oxide has been rated high. Nitric
oxide causes death or permanent injury
after very short exposure to small
quantities. Exposure to nitric oxide can
result in acute and chronic changes of
the pulmonary system including
pulmonary edema, pneumonitis,
bronchitis, bronchiolitis, emphysema,
and methemoglobinemia. Neurologic
effects (fatigue, restlessness, anxiety,
mental confusion, lethargy, loss of
consciousness) have also been reported.
The effects of nitric oxide may be
related to the formation of
methemoglobin. EPA believes that there
is sufficient evidence for listing nitric
oxide on EPCRA section 313 pursuant to
EPCRA section 313(d)(2)(B) based on
the available neurological and
hematological toxicity data for this
chemical.
178. p-Nitroantiine (CAS No. 000100-
01-6) (CERCLA; RCRA APP8; RCRA P)
(Ref. 8). In a 14-day study in mice fed
p-nitroaniline in doses as low as 10 mg/
Kg, 5 days per week, methemoglobin
concentrations were found to be
significantly higher than those in
control animals. In the same study,
hematocrit values in mice that received
300 mg/kg, and total erythrocyte counts
in mice that received 100 or 300 mg/kg,
were significantly lower than those of
control animals. Similar effects were
observed in 13-week and 2-year mouse
studies. In the 2-year study, lesions
related to the administration of p-
nitroaniline occurred in the spleen,
liver, and bone marrow (primarily in
mice receiving 30 or 100 mg/kg) and
were observed at 9 and 15 months. In
addition, increases in the incidence or
severity of splenic congestion,
hematopoiesis, pigment (hemosiderin)
accumulation, Kupffer cell pigmentation
in the liver, and bone marrow
hypercellularity (hyperplasia). EPA
believes that there is sufficient evidence
for listing p-nitroaniline on EPCRA
section 313 pursuant to EPCRA section
313(d)(2)(B) based on the chronic
toxicity data for this chemical.
179. Nitrogen dioxide (CAS No.
010102-44-0) (CERCLA; EPCRA EHS;
RCRA APP8; RCRA P) (Ref. 8). Acid
precipitation occurs in large regions of
the Eastern United States and Canada,
Europe, and Japan. This widespread
occurrence of acid precipitation and dry
deposition results in large part from
man-made emissions of oxides of sulfur
and nitrogen (e.g., nitrogen dioxide).
These substances are transformed in the
atmosphere into sulfuric acid and nitric
acid, transported over great distances
and deposited on vegetation, soils,
surface waters, and materials. These
substances are transferred from the
atmosphere into ecosystems by the
absorption of gases, the impaction and
gravitational settling of fine aerosols and
coarse particles, and precipitation.
Acids contained in polluted snow are
released as contaminated meltwater.
The resulting release of pollutants can
cause major or rapid changes in the
acidity of streams and lake waters.
Interference with normal reproduction
in fish populations is induced by acidity
of lake and stream waters. Reproduction
of frogs and salamanders is also
inhibited by atmospheric acidification
of surface waters.
Atmospheric deposition of sulfuric
acid and nitric acid can cause serious
damage to crops and forests. Biological
effects include induction of necrotic
lesions, loss of nutrients due to leaching
from foliar organs, accelerated erosion
of waxes and leaf surfaces, and
interference with normal reproductive
processes. Acidification also decreases
the rate of many soil processes such as
nitrogen fixation and the breakdown of
organic matter.
EPA believes that there is sufficient
evidence for listing nitrogen dioxide on
EPCRA section 313 pursuant to EPCRA
section 313(d)(2)(C) based on the
available environmental toxicity data for
this chemical.
Nitrogen dioxide is regulated under
Title I of the CAA (Provisions for
Attainment and Maintenance of
National Ambient Air Quality
Standards). La addition to this proposal
to add nitrogen dioxide to EPCRA
section 313, in Units IV.B.36. and 235,
EPA is proposing to add two other
chemicals, carbon monoxide and sulfur
dioxide, that are regulated by Title I of
the CAA. Sulfur dioxide is also
regulated by Title IV of the CAA (Acid
Deposition Control). Extensive data,
which are highly technical, are collected
on these chemicals as required by the
CAA. EPA requests comment on the
following: (1) Is the information
collected under the CAA sufficient for
public right-to-know purposes; and (2)
suggestions on how the data collected
on these chemicals pursuant to CAA
Titles I and IV could be used to meet the
purposes of EPCRA section 313.
180. Noiflurazon (4-ChIoro-5-
(methylamino)-2-
[3(trifluoromethyl)phenyl]-3(2H)-
pyridazinone) (CAS No. 027314-13-2)
(FEFRA 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 i
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.
181. Oryzalin (4-(Dipropylamino)-3,5-
dinitrobenzene sulfonamide) (CAS No.
019044-88-3) (FIFRA AI) (Ref. 3).
Reduced hemoglobin and hematocrit
levels, decreased red blood cell count,
increased blood urea nitrogen (BUN)
and alkaline phosphatase and SGPT,
anemia, hepatic changes, splenic
hematopoiesis and hyperplastic bone
marrow were observed in dogs fed 56.25
mg/kg/day (the NOEL was 18.75 mgVkg/
day) for 3 months. Increases in serum
cholesterol levels, alkaline phosphatase
activity, and relative liver and kidney
weights and decreases in alanine
transaminase (the LOEL was 50 mg/kg/
day; the NOEL was 5 mg/kg/day) were
observed in dogs fed oryzalin for 1—year.
Decreased red blood cell count and
hematocrit and hemoglobin levels
(LOEL was 45 mg/kg/day; NOEL was 15
mg/kg/day) were noted in a 1-year
feeding study in rats. In a 2—year feeding
study in rats, decreased red blood cell
count and hematocrit and hemoglobin
levels, and increased BUN and liver and
kidney weights (the LOEL was 45 mg/
kg/day; the NOEL was 15 mg/kg/day)
were observed. EPA believes that there
is sufficient evidence for listing oryzalin
on EPCRA section 313 pursuant to
EPCRA section 313(d)(2)(B) based on
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1827
the available hepatic and hematological
toxicity data for this chemical.
182. Oxydemeton methyl (S-(2-
(Ethylsulfinyl)ethylj O,O-dimethyl ester
phosphorothioic acid) (CAS No. 000301-
12-2) (FIFRA AI) (Ref. 3). Two
multigeneration reproduction studies
indicate a variety of reproductive effects
at 2.1 to 2.5 mg/kg/day. These effects
include decreased litter size and
viability, decreased weight of the testes
and ovaries, and increased epididymal
vacuolation. The NOELs were 0.38 and
0.5 mg/kg/day. A NOEL of 0.9 mg/kg/
day was determined in a 5-day study in
the rat. The LOEL for decreased fertility
and epididymal sperm motility was 5
mg/kg/day.
Oxydemeton methyl can cause
inhibition of brain, plasma, and red
blood cell cholinesterase. In a 2-
generation reproduction study,
statistically significant inhibition of red
blood cell and brain cholinesterase
activity (the NOEL was less than 0.043
mg/kg/day) was observed in adult males
and females of the F° and F<
generations. In a 5-day feeding
(dominant lethal plus) study, inhibition
of plasma cholinesterase activity (the
LOEL was 1.5 mg/kg/day; the NOEL was
0.45 mg/kg/day) was observed. EPA
believes that there is sufficient evidence
for listing Oxydemeton methyl on
EPCRA section 313 pursuant to EPCRA
section 313(d)(2)(B) based on the
available reproductive and neurological
toxicity data for this chemical.
183. Oxydiazon (3-[2,4-Dichloro-5-(l-
methylethoxy)phenyl]5- (1,1-
dimethylethyl)-l,3,4-oxadiazol-2(3H)-
one) (CAS No. 019666-30-9) (FIFRA AI)
(Ref. 3). Rats given 40 mg/kg/day by
gavage on days 6 to 15 of gestation
exhibited increased fetal resorptions.
The NOEL was 12 mg/kg/day.
Increased liver and kidney weight
(associated with no pathology) and
increased alkaline phosphatase activity
were observed in rats fed 100 mg/kg/day
(the NOEL was 25 mg/kg/day) for 90
days. Increased levels of SGPT and
alkaline phosphatase activities and
increased liver weight (the LOEL was 5
mg/kg/day; the NOEL was 0.5 mg/kg/
day) were observed in a 2-year feeding
study in rats. Effects noted at 150 mg/
kg/day included liver pathology,
hemolytic anemia, increased kidney
weight, and pigment nephrosis. Based
on the NOEL, an oral RfD of 0.005 mg/
kg/day was derived. EPA believes that
there is sufficient evidence for listing
oxydiazon on EPCRA section 313
pursuant to EPCRA section 313(d)(2)(B)
based on the available developmental,
hepatic, and renal toxicity data for this
chemical.
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 KOW 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.
185. Ozone (CAS No. 010028-15-6)
(EPCRA EHS) (Ref. 8). Information from
a large number of studies of both
humans and animals indicate that ozone
can affect structure, function,
metabolism, pulmonary defense against
bacterial infection, and extrapulmonary
effects. Among these extrapulmonary
effects are: (1) Cardiovascular effects; .(2)
reproductive and teratological effects;
(3) central nervous system effects; (4)
alterations in red blood cell
morphology; (5) enzymatic activity; and
(6) cytogenetic effects on circulating
lymphocytes. EPA believes that there is
sufficient evidence for listing ozone on
EPCRA section 313 pursuant to EPCRA
section 313(d)(2)(B) based on the
available toxicity data for this chemical.
Effects of ozone on green plants
include injury to foliage, reductions in
growth, losses in yield, alterations in
reproductive capacity, and alterations in
susceptibility to pests and pathogens.
Based on the known interrelationships
of different components of ecosystems,
such effects, if of sufficient magnitude,
may potentially lead to irreversible
changes of sweeping nature to
ecosystems.
Measured aquatic acute toxicity
values for ozone include a 96-hour LCso
of 80 ppb for striped bass, a 96-hour
LCso of 30 ppb for channel catfish, and
a 96-hour LCso of 9.3 ppb for rainbow
trout. EPA believes that there is
sufficient evidence for listing ozone on
EPCRA section 313 pursuant to EPCRA
section 313(d)(2)(C) based on the
available ecotoxicity data for this
chemical.
186. Paraquat dichloride (CAS No.
001910-42-5) (EPCRA EHS; FIFRA SR)
(Ref. 8). Paraquat can cause death in
humans as a consequence of severe
injury to the lungs, or as a result of
kidney, liver, or heart failure. Following
exposure, death may .occur in 24 hours
or less. The acute oral LDso values for
paraquat are reported as 57,120, 25, 50
and 35 mg/kg in the rat, mouse, dog,
monkey, and cat, respectively. Chronic
pneumonitis (the LOEL was 0.93 mg/kg/
day; the NOEL was 0.45 mg/kg/day) was
reported in dogs fed diets containing
paraquat dichloride for 52 weeks. These
results are supported by the results of a
2—year feeding study in rats (the LOEL
was 3.75 mg/kg/day based on
nonneoplastic lung lesions; the NOEL
was 1.25 mg/kg/day) and a 90-day
feeding study in dogs (the LOEL was 1.5
mg/kg/day based on increased lung
weight, alveolitis, and alveolar collapse;
the NOEL was 0.5 mg/kg/day).
EPA believes that there is sufficient
evidence for listing paraquat dichloride
on EPCRA section 313 pursuant to
EPCRA section 313(d)(2)(B) based on
the chronic toxicity data for this
chemical.
187. Pebulate
(Butylethylcarbamothioic acid S-propyl
ester) (CAS No. 001114-71-2) (FIFRA AI)
(Ref. 3). In a 1-year dog feeding study,
a NOEL of greater than 5 mg/kg/day was
established due to abnormal behavior,
ataxia, convulsions, and neurological
effects in the brain and spinal cord at
100 mg/kg/day. EPA believes that there
is sufficient evidence for listing
pebulate on EPCRA section 313
pursuant to EPCRA section 313(d)(2)(B)
based on the available neurological
toxicity data.
188. Pendimethalin (N-(l-
Ethylpropyl)-3,4-dimethyl-2,6-
dinitrobenzenamine) (CAS No. 040487-
42-1) (FIFRA AI) (Ref. 3). Increased liver
weights and alkaline phosphatase
activity and hepatic lesions (the LOEL
was 50 mg/kg/day; the NOEL was 12.5
mg/kg/day) were observed in dogs fed
pendimethalin for 2 years. EPA derived
an oral RfD of 0.04 mg/kg/day.
Hypertrophy of the liver and increased
liver weights were observed in rats fed
5,000 ppm (250 mg/kg/day) for 3
months. The NOEL was 25 mg/kg/day.
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EPA believes that there is sufficient
evidence for listing pendimethalin on
EPCRA section 313 pursuant to EPCRA
section 313(d)(2)(B) based on the
available hepatic toxicity data.
189. Pentobarbital sodium (CAS No.
000057-33-0) (CAL) (Ref. 8).
Pentobarbital sodium is commonly used
as a sedative hypnotic. The average
adult sedative dose is 20 to 40 mg
orally. The average adult hypnotic dose
is 100 to 200 mg orally. Pentobarbital is
also used parenterally or rectally to
provide basal hypnosis for general,
spinal, or regional anesthesia. Like other
barbiturates, a common adverse effect to
using pentobabital sodium is central
nervous system depression. Chronic
exposure to pentobarbital sodium may
lead to psychological and physical
dependence.
Ihtraporitoneal injection of 20 mg/kg
on day 1 of pregnancy produced adverse
effects on fertility in rats. Intraperitoneal
injections of 80 mg/kg to rats on day 1
of pregnancy caused preimplantation
loss. Intraperitoneal injection of 94.5
mg/kg on day 2 of pregnancy decreased
fertility and caused fetal death in rats.
Intraperitoneal injection of 22 mg/kg on
day 10 of pregnancy caused adverse
effects in rat fetuses (details of study not
reported). Subcutaneous injection of 520
mg/kg of pentobarbital sodium on days
9 to 21, or administration of 30 mg/kg
on day 19 of pregnancy produced
abnormal behavioral effects in rat
offspring. Exposure to pentobarbital
sodium during pregnancy can cause
fetal addiction to the substance.
EPA believes that there is sufficient
evidence for listing pentobarbital
sodium on EPCRA section 313 pursuant
to EPCRA section 313(d)(2)(B)I based on
the developmental, reproductive, and
chronic neurological toxicity data for
this chemical.
190. Perchloromethyl mercaptan
(CAS No. 000594-42-3) (CERCLA;
EPCRA EHS) (Ref. 8). The rat oral LDjo
and 4-hour rat inhalation LCso values
for perchloromethyl mercaptan are 8.26
mg/kg and 0.26 mg/L, respectively. The
2-hour mouse inhalation LCso value is
reported to be 0.296 mg/L. In an eye
irritation test, 50 micrograms fug) (0.13
mg/kg/day) placed in a rabbit's eye for
24 hours produced a severe reaction.
EPA's exposure analysis indicates that
perchloromethyl mercaptan
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 perchloromethyl mercaptan
on EPCRA section 313 pursuant to
EPCRA section 313(d)(2)(A) based on
the available acute toxicity and
exposure data for this chemical.
191. Permethrin (3-(2,2-
Dichloroethenyl)-2,2-
dimethylcyclopropanecarboxylicacid,
(3-phenoxyphenyl)methyl ester) (CAS
No. 052645-53-1) (FIFRA AI) (Ref. 3).
Increased liver weights (the LOEL was
500 ppm or 25 mg/kg/day; the NOEL
was 100 ppm or 5 mg/kg/day) were
observed in rats fed permethrin for 2
years. Based on the NOEL, EPA derived
an oral RfD of 0.05 mg/kg/day.
Decreased alkaline phosphatase activity,
hepatocellular swelling, and increased
h'ver weight (the LOEL was 100 mg/kg/
day; the NOEL was 5 mg/kg/day) were
observed in dogs orally administered (in
capsules) permethrin for 1—year.
Tremors, excessive salivation,
convulsions, and incoordination were
noted'at 1,000 mg/kg/day. EPA believes
that there is sufficient evidence for
listing permethrin on EPCRA section
313 pursuant to EPCRA section
313(d)(2)(B) based on the available
hepatic toxicity data.
Aquatic acute toxicity values for
permethrin include a fathead minnow
96-hour LCso of 3.5 ppb, a rainbow trout
96-hour measured LCso of 0.62 ppb, a
bluegill 96-hour LCso of 2.52 ppb, an
Atlantic silverside 96—hour measured
LCso 2.2 ppb, and a daphnid 48-hour
LCso of 0.32 ppb. EPA believes that
there is sufficient evidence for listing
permethrin on EPCRA section 313
pursuant to EPCRA section 313(d)(2)(C)
based on the available environmental
toxicity data.
192. Phenanthrene (CAS No. 000085-
01-8) (CERCLA; CWA PP) (Ref. 8).
Measured aquatic acute toxicity data for
phenanthrene include a 48—hour LCso of
700 ppb for daphnids. The measured
28-day LCso for rainbow trout is 40 ppb,
and teratogenetic effects were noted.
The measured bioconcentration factor
(BCF) values include a fathead minnow
28-day BCF of 5,100 and a daphnid 24-
hour BCF of 1,165. EPA believes that
there is sufficient evidence for listing
phenanthrene on EPCRA section 313
pursuant to EPCRA section 313(d)(2)(C)
based on the available environmental
toxicity data for this chemical and its
potential to bioaccumulate.
193. Phenothrin (2,2-dimethyl-3-(2-
methyl-1-propenyl)
cyclopropanecarboxylic acid (3-
phenoxyphenyljmethyl ester) (CAS No.
026002-80-2) (FIFRA AI) (Ref. 3).
Hepatocellular enlargement and
increased absolute and relative liver
weights were observed in a chronic
feeding study in dogs. The LOEL was
27.7 mg/kg/day in males and 26.8 mg/
kg/day in females. The NOEL was 8.2
mg/kg/day in males and 7.1 mg/kg/day
in females. Hepatocellular hypertrophy
and increased relative liver weight (the
LOEL was 150 mg/kg/day; the NOEL
was 50 mg/kg/day) were observed in a
chronic oncogenicity study in rats.
Increased liver weight (the LOEL was
150 mg/kg/day, the NOEL was 45 mg/
kg/day) was noted in another chronic
oncogenicity feeding study in mice. EPA
believes that there is sufficient evidence
for listing phenothrin on EPCRA section
313 pursuant to EPCRA section
313(d)(2)(B) based on the available
hepatic toxicity data for this chemical.
Aquatic acute toxicity values for
phenothrin include a rainbow trout 96-
hour LCso of 16.7 ppb and a goldfish 48-
hour LCso of 100 ppb. EPA believes that
there is sufficient evidence for listing
phenothrin on EPCRA section 313
pursuant to EPCRA section 313(d)(2)(C)
based on the available environmental
toxicity data for this chemical.
194.1,2-Phenylenediamine (CAS No.
000095-54-5) (RCRA APP8) (Ref. 8). EPA
has classified 1,2-phenylenediamine as
a Group B2 compound, i.e., a probable
human carcinogen. 1,2—
Phenylenediamine dihydrochloride
appeared to be carcinogenic in both rats
and mice, as evidenced by an increased
incidence of hepatocellular carcinomas
in both species. A significantly
increased incidence of hepatocellular
carcinomas was observed in high dose
group male rats and mice, and female
mice of both treated groups. EPA
believes that there is sufficient evidence
for listing 1,2-phenylenediamine on
EPCRA section 313 pursuant to EPCRA
section 313(d)(2)(B) based on the
carcinogenicity data for 1,2-
phenylenediamine dihydrochloride.
195.1,3-Phenylenediamine (CAS No.
000108-45-2) (RCRA APP8) (Ref. 8).
Increased absolute and relative liver
weights and degenerative liver lesions
(the LOEL was 18 mg/kg/day; the NOEL
was 6.0 mg/kg/day) were noted in a 90-
day oral study in rats exposed to 1,3-
phenylenediamine. EPA believes that
there is sufficient evidence for listing
1,3-phenylenediamine on EPCRA
section 313 pursuant to EPCRA section
313(d)(2)(B) based on the hepatotoxicity
data for this chemical.
196.1,2-Phenylenediamine
dihydrochloride (CAS No. 000615-28-1)
(RCRA APP8) (Ref. 8). EPA has
classified 1,2—phenylenediamine as a
Group B2 compound, i.e., a probable
human carcinogen: 1,2-
Phenylenediamine dihydrochloride
appeared to be carcinogenic in both rats
and mice, as evidenced by an increased
incidence of hepatocellular carcinomas
in both species. A significantly
increased incidence of hepatocellular
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Federal Register / Vol. 59, No. 8 / Wednesday, January 12, 1994 / Proposed Rules 1829
carcinomas was observed in high dose
group male rats and mice, and female
mice of both treated groups. EPA
believes that there is sufficient evidence
for listing 1,2-phenylenediamine.
dihydrochloride on EPCRA section 313
pursuant to EPCRA section 313(d)(2)(B)
based on the carcinogenicity data for
this chemical.
197.1,4-Phenylenediamine
dihydrochloride (CAS No. 000624-18-0)
(RCRA APP8) (Ref. 8). Measured aquatic
acute toxicity for 1,4-phenylenediamine
include a fish 96-hour LC50 of 60 ppb.
EPA believes that there is sufficient
evidence for listing 1,4-
phenylenediamine dihydrochloride on
EPCRA section 313 pursuant to EPCRA
section 313(d)(2)(C) based on the
available environmental toxicity data for
1,4-phenylenediamine.
198. Phenytoin (CAS No. 000057-41-
0) (CAL; IARC; NTP) (Ref. 8). Phenytoin
is a hydantoin-type anticonvulsant, and
is used mainly in the prophylactic
management of tonic-clonic (grand mal)
seizures and partial seizures with
complex symptomatology. In doses used
to treat seizure disorders (i.e., 300 mg/
day in adults, 5 mg/kg/day in children)
phenytoin can cause adverse effects
such as constipation, dysphagia, nausea,
vomiting, anorexia and weight loss.
Ingestion of 4.5 g (64 mg/kg/day) by
adults and 0.6 g (60 mg/kg/day) by
children has produced transient coma
with motor restlessness. Ingestion of 11
mg/kg/day produced changes in motor
activity in a child (duration of study not
reported). Oral administration of 7.8
mg/kg/day for 4 days produced
encephalitis, hallucinations, and
irritability in a man. Ingestion of 7.6 mg/
kg/day for 2 weeks caused encephalitis,
hallucinations, and ataxia in a woman.
Phenytoin is classified as a Group 2B
compound by IARC; i.e., possible
human carcinogen. Ingestion of 16.5
mg/kg/day for 1-year produced
lymphoma including Hodgkin's disease
and skin tumors in a child. Oral
exposure to phenytoin produced
lymphoma in mice (doses and duration
of study not reported).
Oral administration of 5.9 mg/kg/day
to a woman for the first 39 weeks of
pregnancy induced kidney tumors in
the offspring. In another study, oral
administration of 5.9 mg/kg/day to a
woman for the first 39 weeks of
pregnancy induced brain tumors in the
offspring. Oral administration of 2 mg/
kg/day to a woman for 1—year produced
lymphoma including Hodgkin's disease.
Congenital malformation was reported
in 6.12 percent of births to 98 epileptic
mothers receiving phenytoin regularly
during the first 4 months of pregnancy.
Hypothrombinemia and hemorrhage has
occurred in newborns of mothers who
received phenytoin during pregnancy.
Oral doses of 4.0 to 5.9 mg/kg/day
administered to women for the first 39
weeks of pregnancy produced
craniofacial abnormalities, nervous
system disorders, and delayed physical
effects in their children. Doses of 2.0
mg/kg/day given to a woman for the first
39 weeks of pregnancy produced
abnormalities of skin, appendages, and
musculoskeletal system in her child as
well as other developmental
abnormalities. Oral doses of 5.0 mg/kg/
day produced biochemical and
metabolic abnormalities in the offspring.
Higher doses of phenytoin (130 mg/kg/
day) orally administered to rats
produced behavioral, growth,
musculoskeletal, and nervous system
abnormalities in the offspring.
EPA believes that there is sufficient
evidence for listing phenytoin on
EPCRA section 313 pursuant to EPCRA
section 313(d)(2)(B) based on the
chronic neurological and developmental
toxicity data and on the carcinogenicity
data for this chemical.
199. Phosphine (CAS No. 007803-51-
2) (CAA HAP) (Ref. 7). Available data on
phosphine indicate that its inhalation
LCso for rats is between 4 and 40 ppm
(the exposure time was 4 hours).
Phosphine is a highly-toxic gas with a
probable oral lethal dose of 5 mg/kg. An
air concentration of 3 ppm is safe for
long-term exposure, 500 ppm is lethal in
30 minutes, and a concentration of
1,000 ppm is lethal after a few breaths.
EPA's exposure analysis indicates that
phosphine 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 phosphine
on EPCRA section 313 pursuant to
EPCRA section 313(d)(2)(A) based on
the available acute toxicity and
exposure data for this chemical.
200. Phosphorus oxychloride (CAS
No. 010025-87-3) (CERCLA; EPCRA
EHS) (Refs. 5 and 8). Phosphorus
oxychloride reacts with water to yield
phosphoric acid and hydrochloric acid.
Phosphoric acid, as well as other
phosphates, have the potential to cause
increased algal growth leading to
eutrophication in the aquatic
environment.
Eutrophication may result when
nutrients, especially phosphates, enter
into an aquatic ecosystem in the
presence of sunlight and nitrogen. The
phosphate ion is a plant nutrient, which
can be a major limiting factor for plant
growth in freshwater environments. In
excess, phosphates can cause algal
blooms. Toxic effects result from oxygen
depletion as the algae die and decay.
Toxic effects have also been related to
the release of decay products or direct
excretion of toxic substances from
sources such as blue-green algae.
Laboratory studies indicate that
eutrophication may occur at phosphate
concentrations as low as 50 ppb in
lakes. The resulting oxygen depletion
and toxic decay products (e.g., hydrogen
sulfide) kill many invertebrates and fish.
Although green algae are more
sensitive to growth stimulation by
phosphates in fresh water, blue-green
algal blooms may cause greater damage.
At least three species of blue-green algae
are known to excrete toxins. Secretion
by cyanobacteria of dyalyzable
metabolites have inhibited the growth of
other species of algae and may result in
algal monoculture. When algal blooms
of these toxic species occur in a
reservoir, lake, slough, or pond, the cells
and toxins can become sufficiently
concentrated to cause illness or death in
invertebrates and vertebrates. Major
losses have been reported for cattle,
sheep, hogs, birds (domestic or wild)
and fishes, minor losses for dogs,
horses, small wild animals, amphibians,
and invertebrates.
Eutrophication may occur in slow
moving rivers, but is less likely in swift
rivers where rapid mixing occurs. Light
is the most important limiting factor
because rivers are murkier than lakes
thus, the chances of eutrophication in
swift rivers are slight. However, lakes
and reservoirs collect phosphates from
influent streams and store a fraction of
them within consolidated sediments,
thus serving as a phosphate sink.
The available information derived
from animal and controlled human
studies clearly indicates that exposure
to acid aerosols can produce health
effects of concern, particularly in
sensitive subgroups of the population
and after chronic exposure. The bulk of
these studies, however, have examined
sulfuric acid exposures. Data for other
acid species and mixtures are extremely
limited. However, as the effects appear
to be due to the acidity of the species,
this data should pertain to acid aerosols
consisting of other mineral acids, such
as hydrochloric acid. The effects seen
range from mild and transient changes,
such as small, reversible functional
effects in exercising asthmatics, to more
substantial effects that may have acute
or chronic health consequences, such as
persistently altered clearance and
structural changes that may be
suggestive of chronic lung disease. In
addition, there are some notable
consistencies in the health effects
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Federal Register / Vol. 59, No. 8 / Wednesday, January 12, 1994 / Proposed Rules
information across various studies and
disciplines.
EPA believes that there is sufficient
evidence for listing phosphorous
oxychloride on EPCRA section 313
pursuant to EPCRA sections 313(d)(2)(B)
and (C) based on the available chronic
human and environmental toxicity data
for its degradation products phoshoric
acid and hydrochloric acid.
201. Phosphorus pentachloride (CAS
No. 010026-13-8) (EPCRA EHS) (Refs. 5
and 8). Phosphorus pentachloride reacts
with water to yield phosphoric acid and
hydrochloric acid. As described in Unit
IV.B.200. of this preamble, phosphates,
including phosphoric acid, have the
potential to cause increased algal
growth leading to eutrophication and
fish kills in the aquatic environment.
The available information derived
from animal and controlled human
studies clearly indicates that exposure
to acid aerosols can produce health
effects of concern, particularly in
sensitive subgroups of the population
and alter chronic exposure. The bulk of
these studies, however, have examined
sulfuric acid exposures. Data for other
add species and mixtures are extremely
limited. However, as the effects appear
to be due to the acidity of the species,
this data should pertain to acid aerosols
consisting of other mineral acids, such
as hydrochloric acid. The effects seen
range from mild and transient changes,
such as small, reversible functional
effects hi exercising asthmatics, to more
substantial effects that may have acute
or chronic health consequences, such as
persistently altered clearance and
structural changes that may be
suggestive of chronic lung disease. In
addition, there are some notable
consistencies in the health effects
information across various studies and
disciplines.
EPA believes that there is sufficient
evidence for listing phosphorus
pentachloride on EPCRA section 313
pursuant to EPCRA sections 313(d)(2)(B)
and (C) based on the available chronic
human and environmental toxicity data
for its degradation products phoshoric
acid and hydrochloric acid.
202. Phosphorus pentasulfide (CAS
No. 001314-80-3) (CERCLA) (Refs. 5 and
8). Phosphorus pentasulfide reacts in
water to yield phosphoric acid and
hydrogen sulfide.
As described in Unit IV.B.200. of this
preamble, phosphates, including
phosphoric acid, have the potential to
cause increased algal growth leading to
eutrophication and fish kills in the
aquatic environment.
Acute exposures to large amounts of
hydrogen sulfide (approximately 250
ppm or more) have produced
pulmonary edema, unconsciousness,
respiratory paralysis, asphyxiation, and/
or death in some individuals. Similar
effects are also noted in animals. In a
subchronic study, inflammation of the
nasal mucosa occurred in mice
following 90-day inhalation of
hydrogen sulfide, resulting in a NOAEL
of 42.5 mg/m3 (30.5 ppm; Human
Equivalent Concentration (HEC) is 0.93
mg/ms) and a LOAEL of 110 mg/m3 (80
ppm; HEC is 2.4 mg/ms). Other
respiratory effects, such as alveolar
edema, infiltrates in the bronchioles,
cellular necrosis, hyperplasia, and
exfoliation in various respiratory
tissues, have been reported in rats.
Aquatic toxicity test data for hydrogen
sulfide show that measured fish 96-
hour LCso values range from 7 to 776
ppb.
EPA believes that there is sufficient
evidence for listing phosphorus
pentasulfide on EPCRA section 313
pursuant to EPCRA sections 313(d)(2)(B)
and (C) based on the available chronic
human and environmental toxicity data
for its degradation products, phosphoric
acid and hydrogen sulfide.
203. Phosphorus pentoxide (CAS No.
001314-56-3) (EPCRA EHS) (Refs. 5 and
8). Phosphorus pentoxide rapidly
hydrolyzes in the presence of water to
yield phosphoric acid.
As described in Unit IV.B.2pO. of this
preamble, phosphates, including
phosphoric acid, have the potential to
cause increased algal growth leading to
eutrophication and fish kills in the
aquatic environment. EPA believes that
there is sufficient evidence for listing
phosphorous pentoxide on EPCRA
section 313 pursuant to EPCRA section
313(d)(2)(C) based on the available
environmental toxicity data for its
degradation product phosphoric acid.
204. Picloram (CAS No. 001918-02-1)
(FIFRA AI; SDWA) (Ref. 8). Animal
studies in dogs, rats, or mice for various
durations (2 weeks to 2 years) have
indicated the liver as the primary target
of picloram toxicity. In a 6-month
feeding study in beagle dogs, a LOAEL
of 35 mg/kg/day and a NOAEL of 7 mg/
kg/day were determined for increased
liver weights (relative and absolute). At
a higher dose (175 mg/kg/day), there
were increases in serum alkaline
phosphatase concomitant with the
increases in liver weight. Other toxic
effects in the higher dosed animals
included reduced food consumption
and body weight. EPA has derived an
oral ROD of 0.07 mg/kg/day for this
chemical based on the findings of this
study. Hepatotoxicity has also been
reported in a 2-year rat feeding study.
The LOAEL was 60 mg/kg/day based on
changes in liver histopathology. The
NOAEL was 20 mg/kg/day.
Hepatotoxicity was also observed in a
90-day rat feeding study. The LOAEL
was 150 mg/kg/day based on changes in
liver histopathology, necrosis, and bile
duct proliferation. The NOAEL was 50
mg/kg/day. Increased liver weights were
also reported in mice following dietary
exposure to picloram for 13 weeks. The
LOAEL was 1,000 mg/kg/day. Liver
swelling was reported in rats
administered picloram in feed for 13
weeks. The LOAEL was 150 mg/kg/day.
EPA believes that there is sufficient
evidence for listing picloram on EPCRA
section 313 pursuant to EPCRA section
313(d)(2)(B) based on the available
hepatotoxicity data for this chemical.
205. Piperonyl butoxide (CAS No.
000051-03-6) (FIFRA SR) (Ref. 8).
Measured aquatic acute toxicity data for
piperonyl butoxide include a 96-hour
LCso of 3.4 ppb for rainbow trout and a
96-hour LC5o of 4.2 ppb for bluegill.
EPA believes that there is sufficient
evidence for listing piperonyl butoxide
on EPCRA section 313 pursuant to
EPCRA section 313(d)(2)(C) based on
the environmental toxicity data for this
chemical.
206. Pirimiphos methyl (O-(2-
(diethylamino)-6-methyl-4-pyrimidinyl)-
O,O-dimethyI phosphorothioate) (CAS
No. 029232-93-7) (FIFRA AI) (Ref. 3).
Pirimiphos methyl is a cholinesterase
inhibitor in humans and other
mammalian species. A mild and
transient decrease in plasma
cholinesterase activity was observed in
2 of 4 female humans given pirimiphos
methyl daily in a capsule at dose levels
of 0.25 mg/kg/day for 56 days. This
effect was not seen in 3 of 3 males. The
dose level of 0.25 mg/kg/day was
considered a NOEL for plasma
cholinesterase inhibition. Based on the
NOEL, an oral RfD of 0.01 mg/kg/day
was derived. The findings of the 56-day
study were corroborated by the 28-day
feeding study (capsule) with 5 male
human volunteers where 1 individual
showed borderline cholinesterase
depression. Inhibition of brain
cholinesterase (LOEL was 0.5 mg/kg/
day, the NOEL for cholinesterase
inhibition was not determined) was
observed in a 2—year feeding study in
dogs. Inhibition of plasma
cholinesterase activity (the LOEL was
2.5 mg/kg/day; the NOEL was 0.5 mg/
kg/day) was seen in a 2—year feeding
study in rats. No clinical signs were
reported for the above studies. EPA
believes that there is sufficient evidence
for listing pirimiphos methyl on EPCRA
section 313 pursuant to EPCRA section
^313(d)(2)(B) based on the available
"neurological toxicity data for this
chemical.
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1831
207. Polycyclic aromatic compounds
(PACs) (CAS No. NA) (CAA HAP) (Ref.
7). Polycyclic aromatic compounds are
a class of chemicals that include
polycyclic aromatic hydrocarbons,
azapolycyclic aromatic hydrocarbons,
thio-polycyclic aromatic hydrocarbons,
nijtroarenes, and others. PACs can be
formed in any combustion process that
involves the burning of fuels or, more
generally, materials containing carbon
and hydrogen. Some industrial sources
include coke ovens, catalytic cracking of
crude oil, carbon black production, and
iron and steel processes.
Materials containing mixtures of
PACs have been shown to be
carcinogenic. Several epidemiology
studies have shown increased.mortality
due to lung cancer in humans exposed
to coke-oven emissions, roofing-tar
emissions, and cigarette smoke. Each of
these mixtures contains benzo(a)pyrene,
benzo(a)anthracene,
benzo(b)fluoranthene,
benzo(a)phenanthrene, and
dibenzo(a,h)anthracene as well as other
potentially carcinogenic PACs and other
carcinogenic and potentially
carcinogenic chemicals, tumor
promoters, initiators, and co-
carcinogens such as nitrosoamines, coal
tar pitch, and creosote. Although it is
impossible to evaluate the contribution
of any individual PAC to the total
carcinogenic!ty of these mixtures to
humans, reports of this nature provide
qualitative evidence of the potential for
mixtures containing PACs to cause
cancer in humans. In addition, several
PACs caused cancer in animals when
orally (e.g., benz(a)anthracene,
benzo(a)pyrene, dibenz(a,h)anthracene),
dermally (e.g., benz(a)anthracene,
benzo(a)phenanthrene,
benzo(b)fluoranthene, benzo(a)pyrene,
dibenz(a,h)anthracene, and indeno
(l,2,3-cd)pyrene) or inhalationally (e.g.,
benzo(a)pyrene) exposed. EPA believes
that there is sufficient evidence for
listing these PACs on EPCRA section
313 pursuant to EPCRA section
313(d)(2)(B) based on the available
carcinogenicity data for these chemicals.
EPA is proposing to create a delimited
category for PACs that includes the
chemicals discussed below.
a. Benzo(b)fluoranthene (CAS No.
000205-99-2). Benzo(b)fluoranthene is
classified as a Group B2 compound by
EPA, i.e., the compound is a probable
human carcinogen. It is classified as a
Group 2B compound by IARC, i.e., the
compound is a possible human
carcinogen. Benzo(b)fluoranthene
produced tumors in mice after lung
implantation, intraperitoneal or
subcutaneous injection and skin
painting. EPA believes that there is
sufficient evidence for listing
benzo(b)fluoranthene on EPCRA section
313 pursuant to EPCRA section „
313(d)(2)(B) based on the available
carcinogenicity data for this chemical.
b. Benzo(})fluoranthene (CAS No.
000205-82-3). Benzo(j)fluoranthene is
classified as a Group 2B compound by
IARC, i.e., the compound is a possible
human carcinogen. In multiple skin
painting"assays and in a mouse-skin
initiation-promotion assay,.
benzo(j)fluoranthene produced tumors
in female mice. EPA believes that there
is sufficient evidence for listing
benzo(j)fluoranthene on EPCRA section
313 pursuant to EPCRA section
313(d)(2)(B) based on the available
carcinogenicity data for this chemical.
c. Benzo(k)fluoranthene (CAS No.
000207-08-9). Benzo(k)fluoranthene is
classified as a Group B2 compound by
EPA, i.e., the compound is a probable
human carcinogen. It is also classified
as a Group 2B compound by IARC, i.e.,
the compound is a possible human
carcinogen. Benzo(k)fluoranthene
produced tumors after lung
implantation in mice and when
administered with a promoting agent in
skin painting studies. Equivocal results
have been found in a lung adenoma
assay in mice. Benzo(k)fluoranthene is
mutagenic in bacteria. EPA believes that
there is sufficient evidence for listing
benzo(k)fluoranthene on EPCRA section
313 pursuant to EPCRA section
313(d)(2)(B) based on the available
carcinogenicity data for this chemical.
d. Carbazole (CAS No. 000086-74-8).
Mice fed a basal diet containing
carbazole showed a dose-related
increase in liver nodules and
hepatocellular carcinomas after oral
administration. EPA believes that there
.is sufficient evidence for listing
carbazole on EPCRA section 313
pursuant to EPCRA section 313(d)(2)(B)
based on the available carcinogenicity
data for this chemical.
e. Cyclopenta(cd)pyrene (CAS No.
027208-37-3). In a skin painting assay
and in several mouse-skin initiation-
promotion assays, cyclopenta(cd)pyrene
produced tumors in female mice.
Cyclopenta(cd)pyrene is also mutagenic
to Salmonella and mammalian cells in
vitro and induces morphologic
transformation in C3H10T1/2 cells in
vitro. EPA believes that there is
sufficient evidence for listing
cyclopenta(cd)pyrene on EPCRA section
313 pursuant to EPCRA section
313(d)(2)(B) based on the available
carcinogenicity data for this chemical.
f. Dibenz(a,c)anthracene (CAS No.
000215-58-7). In. a skin painting assay
and in several mouse-skin initiation-
promotion assays, dibenz(a,c)anthracene
produced tumors in female mice. EPA
believes that there is sufficient evidence
for listing dibenz(a,c)-anthracene on
EPCRA section 313 pursuant to EPCRA
section 313(d)(2)(B) based on the
available carcinogenicity data for this
chemical.
g. Dibenz(a,h)acridine (CAS No.
000226-36-8). Dibenz(a,h)acridine is
classified as a Group 2A compound by
IARC, i.e., the compound is a probable
human carcinogen. Dibenz(a,h)acridine
has been shown to be carcinogenic in
animals. EPA believes that there is
sufficient evidence for listing
dibenz(a,h)acridine on EPCRA section
313 pursuant to EPCRA section
313(d)(2)(B) based on the available
carcinogenicity data for this chemical.
h. Dibenz(a,j)acridine (CAS No.
000224-42-0). Dibenz(a,j)acridine is
classified as a Group 2B compound by
IARC, i.e., the compound is a possible
human carcinogen. Dibenz(a,j)acridine
has been shown to be carcinogenic in
animals. EPA believes that there is
sufficient evidence for listing
dibenz(a,j)acridine on EPCRA section
313 pursuant to EPCRA section
313(d)(2)(B) based on the available
carcinogenicity data for this chemical.
i. Dibenz(a,j)anthracene (CAS No.
000224-41-9). Dibenz(a,j)anthracene
produced tumors after subcutaneous
injection and after skin painting in
female mice. EPA believes that there is
sufficient evidence for listing
dibenz(a,j)anthracene on EPCRA section
313 pursuant to EPCRA section
313(d)(2)(B) based on the available
carcinogenicity data for this chemical.
j. Dibenzo(a,e)fluoranthene (CAS No.
005385-75-1). Dibenzo(a,e)fluoranthene
produced tumors in female mice after
mouse-skin initiation-promotion assay
and skin painting.
Dibenzo(a,e)fluoranthene also produced
tumors in both male and female mice
after subcutaneous injection. EPA
believes that there is sufficient evidence
for listing dibenzo(a,e)fluoranthene on
EPCRA section 313 pursuant to EPCRA
section 313(d)(2)(B) based on the
available carcinogenicity data for this
chemical.
k. Dibenzo(a,e)pyrene (CAS No.
000192-65-4). Dibenzo(a,e)pyrene is
classified as a Group 2B compound by
IARC, i.e., the compound is a possible
human carcinogen. Dibenzo(a,e)pyrene
has been shown to be carcinogenic in
animals. EPA believes that there is
sufficient evidence for listing
dibenzo(a,e)pyrene on EPCRA section
313 pursuant to EPCRA section
313(d)(2)(B) based on the available
carcinogenicity data for this chemical.
1. Dibenzo(a,h)pyrene (CAS No.
000189-64-0). Dibenzo(a,h)pyrene is
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1832 Federal Register / Vol. 59, No. 8 / Wednesday, January 12, 1994 / Proposed Rules
classified as a Group 2B compound by
IARC, i.e., the compound is a possible
human carcinogen. Dibenzo(a,h)pyrene
has been shown to be carcinogenic in
animals. EPA believes that there is
sufficient evidence for listing
dibenzo(a,h)pyrene on EPCRA section
313 pursuant to EPCRA section
313(d)(2)(B) based on the available
carcinogenicity data for this chemical.
m. Dwenzo(a,l)pyrene (CAS No.
000191-30-0). Dibenzo(a,l)pyrene is
classified as a Group 2B compound by
IARC, i.e., the compound is a possible
human carcinogen. Dibenzo(a,l)pyrene
produced tumors in both male and
female mice after subcutaneous (s.c.)
injection and tumors in female mice
after skin painting. EPA believes that
there is sufficient evidence for listing
dibenzo-(a,l)pyrene on EPCRA section
313 pursuant to EPCRA section
313(d)(2)(B) based on the available
carcinogenicity data for this chemical.
n. 7H-Dibenzo(c,g)carbazole (CAS No.
000194-59-2). 7H-Dibenzo(c,g)carbazole
is classified as a Group 2B compound by
IARC, i.e., the compound is a possible
human carcinogen. 7H-
Dibonzo(c,g)carbazole has been shown
to be carcinogenic in animals. EPA
believes that there is sufficient evidence
for listing 7H-dibenzo(c,g)carbazole on
EPCRA section 313 pursuant to EPCRA
section 313(d)(2)(B) based on the
available carcinogenicity data for this
chemical.
o. 2-Methylchiysene (CAS No.
003351-32-4). In a skin painting assay
and in a mouse-skin initiation-
promotion assay, 2-methylchrysene
produced tumors in female mice. EPA
believes that there is sufficient evidence
for listing 2-methylchrysene on EPCRA
section 313 pursuant to EPCRA section
313(d)(2)(B) based on the available
carcinogenicity data for this chemical.
p. 3-Methylchrysene (CAS No.
003351-31-3). In a skin painting assay
and in a mouse-skin initiation-
promotion assay, 3-methylchrysene
produced tumors in female mice. EPA
believes that there is sufficient evidence
for listing 3-methylchrysene on EPCRA
section 313 pursuant to EPCRA section
313(d)(2)(B) based on the available
carcinogenicity data for this chemical.
q. 4-Methylchrysene (CAS No.
003351-30-2). In a skin painting assay
and in a mouse-skin initiation-
promotion assay, 4-methylchrysene
produced tumors in female mice. EPA
believes that there is sufficient evidence
for listing 4-methylchrysene on EPCRA
section 313 pursuant to EPCRA section
313(d)(2)(B) based on the available
carcinogenicity data for this chemical.
r. 5-Methylchrysene (CAS No. 003697-
24-3). 5-Methylchrysene is classified as
a Group 2B compound by IARC, i.e., the
compound is a possible human
carcinogen. In a skin-painting assay and
in a mouse-skin initiation-promotion
assay, 5-methylchrysene produced
tumors in female mice. EPA believes
that there is sufficient evidence for
listing 5-methylchrysene on EPCRA
section 313 pursuant to EPCRA section
313(d)(2)(B) based on the available
carcinogenicity data for this chemical.
s. 6-Methylchrysene (CAS No. 001705-
85-7). In a skin painting assay and in a
mouse-skin initiation-promotion assay,
6-methylchrysene produced tumors in
female mice. EPA believes that there is
sufficient evidence for listing 6-
methylchrysene on EPCRA section 313
pursuant to EPCRA section 313(d)(2)(B)
based on the available carcinogenicity
data for this chemical.
t. 2-Methylfluoranthene (CAS No.
033543-31-6). In a skin painting assay,
2-methylfluoranthene produced benign
and malignant skin tumors in female
mice. In a female mouse-skin initiation-
promotion assay, 2-methylfluoranthene
produced skin papillomas. EPA believes
that there is sufficient evidence for
listing 2-methylfluoranthene on EPCRA
section 313 pursuant to EPCRA section
313(d)(2)(B) based on the available
carcinogenicity data for this chemical.
u. 1-Nitropyrene (CAS No. 005522-43-
0). 1-Nitropyrene is classified as a
Group 2B compound by IARC, i.e., the
compound is a possible human
carcinogen. 1-Nitropyrene produced
mammary adenocarcinomas and
squamous-cell carcinomas in a dose-
dependent manner by oral
administration in rats, papillomas (not
statistically significant) by skin
application in mice, and lung adenomas
by intratracheal instillation in hamsters. ,
In a s.c. injection study, 1-nitropyrene
produced tumors (i.e., one extraskeletal
osteosarcoma and seven malignant
fibrous histiocytomas) at the injection
site in male Fisher rats. In another s.c.
injection study, 1-nitropyrene produced
tumors at the injection site in both male
and female CD rats and mammary
tumors in females. EPA believes that
there is sufficient evidence for listing 1-
nitropyrene on EPCRA section 313
pursuant to EPCRA section 313(d)(2)(B)
based on the available carcinogenicity
data for this chemical.
In addition to the above compounds,
EPA proposes that the PAC category
also include the following seven PACs:
Benz(a)anthracene (CAS No. 000056-
55-3)
Benzo(a)phenanthrene (CAS No..
000218-01-9)
Benzo(a)pyrene (CAS No. 000050-32-
8)
Benzo(rst)pentaphene (CAS No.
000189-55-9)
Dibenzo(a,h)anthracene (CAS No.
000053-70-3)
7,12-Dimethylbenz(a)anthracene (CAS
No. 000057-97-6)
Indeno[l,2,3-cd]pyrene (CAS No.
000193-39-5)
These PACs were proposed for listing
individually in EPA's response to a
petition to add certain chemicals that
appear on the RCRA list of toxic wastes
under 40 CFR 261.33(f) to EPCRA
section 313 (57 FR 41020, September 8,
1992). These chemicals were proposed
for addition based on the available
carcinogenicity data. Due to the
similarities of these seven PACs to the
chemicals listed in Unit IV.B.207.a.
through IV.B.207.U. of this preamble,
EPA believes that these chemicals
should be added to EPCRA section 313
as part of the delineated PAC category
rather than listed individually.
EPCRA section 313 requires threshold
determinations for chemical categories
to be based on the total of all chemicals
in the category manufactured,
processed, or otherwise used. For
example, a facility that manufactures
three members of a chemical category
would count the total amount of all
three chemicals manufactured towards
the manufacturing threshold for that
category. When filing reports for
chemical categories the releases are
determined in the same manner as the
thresholds. One report is filed for the
category and all releases are reported on
this form. In the case of the delimited
PAC category, only the 28 chemicals
listed above would be included for
purposes of making the threshold
determinations and in filing reports on
releases.
The Clean Air Act Amendments
section 112(b) Hazardous Air Pollutants
list includes a listing for polycyclic
organic matter (POM) that includes
PACs. The definition given for the POM
category is broad and chemically non-
specific and may be delineated by test
method. For the purpose of listing under
EPCRA section 313, EPA considered the
following more chemically-specific
definition for a PAC category: "includes
all chemical species from the polycyclic
aromatic hydrocarbon, aza-polycyclic,
thio-polycyclic, or nitroarene families
where polycyclic means three or more
fused rings. More specifically, it means
any combination of three or more fused
six or five membered hydrocarbon rings
with at least two or more rings being
aromatic. The structure may contain
fused non-aromatic five-membered
rings, a ring nitrogen, a ring sulfur, one
or more attached nitro groups, or one or
more attached alkyl groups." As an
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1833
alternative to the delimited category,
EPA is proposing to add a PAC category
based on this broad definition. Although
this definition may include chemicals of
low or no concern, it may be less of a
burden for facilities to report their total
PACs rather than trying to determine
which and how much of the specific
PACs covered by the delimited category
they are producing and releasing. EPA
requests comment on the addition of the
delimited PACs category versus the
alternative PAC category based on the
broader definition.
208. Potassium bromate (CAS No.
007758-01-2) (IARC) (Ref. 8). IARC has
assigned potassium bromate to Group
2B, i.e., it is possibly carcinogenic to
humans. Male and female rats orally
exposed to 250 or 500 ppm (35 to 70
mg/kg/day) potassium bromate in
drinking water for 110 weeks had an
increased incidence of renal cell
adenomas and adenocarcinomas and, in
males, there was also an increased
incidence of mesothelioma in the
peritoneal cavity. EPA believes that
there is sufficient evidence for listing
potassium bromate on EPCRA section
313 pursuant to EPCRA section
313(d)(2)(B) based on the available
carcinogenicity data for this chemical.
209. Potassium
dimethyldithiocarbamate (CAS No.
000128-03-0) (FIFRA AI) (Ref. 3). New
Zealand White rabbits given 38 mg/kg/
day by gavage on days 6 to 18 of
gestation exhibited malalignment of
sternebrae, total postimplantation loss,
and fetal weight decrement. Also at this
dose level, various malformations
including adactyly, gastroschisis, short
tail, anal atresia, spina bifida,
atelectasis, costal cartilage anomaly,
vertebral anomaly with/without rib,
caudal vertebrea anomaly, and severe
sternebrae malalignment were observed
in 6 of 52 fetuses from 5 of 11 litters.
At the 77 mg/kg/day dose level, there
was severe fetal/embryo lethality. The
NOEL was 12.8 mg/kg/day. EPA
believes that there is sufficient evidence
for listing potassium
dimethyldithiocarbamate on EPCRA
section 313 pursuant to EPCRA section
313(d)(2)(B) based on the available
developmental toxicity data for this
chemical.
210. Potassium N-
methyldithiocarbamate (CAS No.
000137-41-7) (FIFRA AI) (Ref. 3). By
analogy to the analogue, potassium
dimethyldithiocarbamate, potassium N-
methyldithiocarbamate can reasonably
be anticipated to cause fetotoxicity,
postimplantation loss and
malformations. Data on potassium
dimethyldithiocarbamate follows. New
Zealand White rabbits given 38 mg/kg/
day by gavage.on days 6 to 18 of
gestation exhibited malalignment of
sternebrae, total postimplantation loss,
and fetal weight decrement. Also a't this
dose level various possible
malformations including adactyly,
gastroschisis, short tail, anal atresia,
spina bifida, atelectasis, costal cartilage
anomaly, vertebral anomaly with/
without rib, caudal vertebrea anomaly,
and severe sternebrae malalignment in 6
of 52 fetuses from 5 of 11 litters. At the
77 mg/kg/day dose level, there was
severe fetal/embryo lethality. The NOEL
was 12.8 mg/kg/day. EPA believes that
there is sufficient evidence for listing
potassium N-methyldithiocarbamate on
EPCRA section 313 pursuant to EPCRA
section 313(d)(2)(B) based on the
available developmental toxicity data
for potassium dimethyldithiocarbamate.
211. Primisulfuron (methyl 2-[[[[[4,6-
bis(difluoromethoxy)2-pyrimidinyl]-
amino] carbonyl] aminojsulfonyl]
benzoate) (CAS No. 086209-51-0)
(FIFRA AI) {Ref. 3). In a 90-day dog
parafollicular hyperplasi
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 ECso of 0.27 ppb and
an algae 7-day ECsp 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.
212. Profenofos (O-(4-bromo-2-
chlorophenyl)-O-ethyl-Spropyl
phosphorothioate) (CAS No. 041198-08-
7) (FIFRA AI) (Ref. 3). In a 6-month
feeding study in dogs, inhibition of
plasma and red blood cell
cholinesterase activities were observed
at 2 ppm (0.05 mg/kg/day). The NOEL
was 0.2 ppm (0.005 mg/kg/day). Based
on the NOEL, EPA derived an oral RfD
of 0.00005 mg/kg/day. Other studies (21,
28, and 90-day studies in rat, rabbit and
dog) also demonstrate cholinesterase
(plasma, red blood cell or brain)
inhibition in rats and mice. EPA
believes that there is sufficient evidence
for listing profenofos on EPCRA section
313 pursuant to EPCRA section
313(d)(2)(B) based on the available
neurological toxicity data.
213. Prometryn (N,N'-bis(l-
methylethyl)-6-methylthio-l,3,5-
triazine-2,4-diamine) (CAS No. 007287-
19-6) (FIFRA AI) (Ref. 3). Degenerative
changes in the liver and kidney, and
bone marrow atrophy (the LOEL was
37.5 mg/kg/day; the NOEL was 3.75 mg/
kg/day) were observed in dogs fed
prometryn for 2 years. Based on the
NOEL, EPA derived an oral RfD of 0.004
mg/kg/day. Fatty liver degeneration (the
LOEL was 500 mg/kg; the NOEL was
250 mg/kg) was observed in rats fed
prometryn for 28 days.
In a teratology study in rabbits, test
material was administered by gavage
from gestation day 7 to 19. Increased
abortions and late resorptions occurred
at 72 mg/kg/day. The NOEL was 12 mg/
kg/day.
EPA believes that there is sufficient
evidence for listing prometryn on
EPCRA section 313 pursuant to EPCRA
section 313(d)(2)(B) based on the
available hepatic, renal, bone marrow,
and developmental toxicity data.
214. Propachlor (2-chloro-N-(l-
methylethyl)-N-phenylacetamide)(CAS
No. 001918-16-7) (FIFRA AI) (Ref. 3). No
evidence of maternal toxicity was seen
in rabbits administered propachlor by
gavage at 0, 5,15, or 50 mg/kg/day on
days 7 to 19 of gestation. Statistically
significant increases in mean
resorptions/postimplantation loss with
corresponding decreases in the mean
number of viable fetuses were reported
at 15 and 50 mg/kg/day when compared
to controls. EPA believes that there is
sufficient evidence for listing
propachlor on EPCRA section 313
pursuant to EPCRA section 313(d)(2)(B)
based on the available developmental
toxicity data.
215. Propanil (N-(3,4-
dichlorophenyljpropanamide) (CAS No.
000709-98-8) (FIFRA AI) (Ref. 3).
Results of several subchronic and
chronic toxicity studies indicated the
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liver and spleen as the target organs for
propanil. Increased relative spleen
weight (the LOEL was 20 mg/kg/day; the
NOEL was 5 mg/kg/day) was noted in
female rats fed propanil for 2 years.
Based on the NOEL, EPA derived an
oral RfD of 0.005 mg/kg/day.
Histopathological changes (the LOEL
was 30 mg/kg/day; the NOEL was 25
mg/kg/day) in the liver and spleen were
observed in mice orally administered
propanil for 90 days. At higher dose
levels (i.e., 240 and 1,920 mg/kg/day)
cyanosis, methemoglobinemia, and
increased liver and spleen weight were
noted. In a 90-day rat study, increased
spleen weight (the LOEL was 50 mg/kg/
day; the NOEL was 16.5 mg/kg/day) was
seen in females. Decreased hemoglobin
levels was seen in males. Increased
SCOT and SAP activities (the LOEL was
100 mg/kg/day; the NOEL was 15 mg/
kg/day) were observed in dogs orally
administered propanil for 2 years. EPA
believes that there is sufficient evidence
for listing propanil on EPCRA section
313 pursuant to EPCRA section
313(d)(2)(B) based on the available
hepatic toxicity data.
216. Propargite (CAS No. 002312-35-
8) (CERCLA) (Ref. 8). In a
developmental toxicity study in which
rabbits were exposed via oral gavage to
doses greater than or equal to 6 mg/kg/
day (fetotoxic LOAEL) of propargite
during gestation days 6 to 18, delayed
ossification, increased fetal resorption,
decreased fetal viability and reductions
in fetal body weight were noted. The
maternal LOAEL in this study was also
6 mg/kg/day and was based on body
weight reductions. The NOEL for
maternal and fetal toxicity was 2 mg/kg/
day. Developmental effects (increased
incidence of missing sternebrae) were
also reported in offspring of rats
exposed orally during gestation days 6
to 15. The fetotoxicity LOAEL was 25
mg/kg/day and the NOAEL was 6 mg/
kg/day. EPA believes that there is
sufficient evidence for listing propargite
on EPCRA section 313 pursuant to
EPCRA section 313(d)(2)(B) based on
the developmental toxicity data for this
chemical.
Measured aquatic acute toxicity data
for propargite include a bluegill sunfish
LCjo of 31 ppb. EPA believes that there
is sufficient evidence for listing
propargite on EPCRA section 313
pursuant to EPCRA section 313(d)(2)(C)
based on the environmental toxicity
data for this chemical.
217. Propargyl alcohol (CAS No.
000107-19-7) (CERCLA; RCRAAPP8;
RCRA P) (Ref. 8). Histopathological
changes in the liver and kidney were
reported in a subchronic rat feeding
study following exposure to propargyl
alcohol in the diet for as little as 4
weeks. The liver changes included
increased organ weight, hepatocytic
megalocytosis with proliferation of bile
ducts and cytoplasmic vacuolization of
hepatocytes, as well as hematological
and serum enzyme changes indicative of
liver damage. The kidney weights were
increased in females only, and both
sexes had karyomegaly of the renal
tubular epithelial cells. The LOAEL for
these changes was 15 mg/kg/day and the
NOAEL was 5 mg/kg/day. EPA derived
an oral RfD of 0.002 mg/kg/day from
this study. EPA believes that there is
sufficient evidence for listing propargyl
alcohol on EPCRA section 313 pursuant
to EPCRA section 313(d)(2)(B) based on
the hepatotoxicity and nephrotoxicity
data for this chemical.
218. Propetamphos (3-
[[(Ethylamino)methoxyphosphinothioyl]
oxyJ-2-butenoic acid, 1-methylethyl
ester) (CAS No. 031218-83-4) (FIFRA AI)
(Ref. 3). Purebred beagle dogs were
given propetamphos for 52 weeks in
feed. A dose of 2.5 mg/kg/day caused
increased relative liver weight and
increased liver enzymes. Dogs given
12.5 mg/kg/day developed
hepatocellular necrosis. The NOEL was
0.5 mg/kg/day.
Redblood cell and plasma
cholinesterase inhibition were seen in a
2-week rat inhalation study at 1 mg/kg/
day (LOEL). No NOEL could be
established. Cholinesterase inhibition
was observed at 0.4 mg/kg/day in a 13-
week rat dietary study. The NOEL was
0.2 mg/kg/day. Cholinesterase
inhibition was also observed at 0.1 mg/
kg/day (LOEL) in a 6-month dog dietary
study. The NOEL was 0.05 mg/kg/day.
In a 92-week mouse feeding study, red
blood cell, brain, and plasma
cholinesterase were inhibited at 1.0 mg/
kg/day (LOEL). The NOEL was 0.5 mg/
kg/day. Based on this study, an oral RfD
of 0.005 mg/kg/day was derived. In a 2-
year dietary rat study, plasma
cholinesterase depression was observed
at 0.6 mg/kg/day (LOEL). The
cholinesterase NOEL was 0.3 mg/kg/
day. Alopecia and hyperflexia were
observed at 6 mg/kg/day (systemic
LOEL). The systemic NOEL was 0.6 mg/
kg/day. In a lifetime mouse study,
dietary administration of 1 mg/kg/day
produced plasma, red blood cell, liver,
and brain cholinesterase depression.
The NOEL was 0.05 mg/kg/day.
EPA believes that there is sufficient
evidence for listing propetamphos on
EPCRA section 313 pursuant to EPCRA
section 313(d)(2)(B) based on the
available hepatic and neurological
toxicity data for this chemical.
219. Propiconazole (l-[2-(2,4-
dichlorophenyl)-4-propyl-l,3-dioxolan-
2-yl]- methyl-lH-l,2,4,-triazole) (CAS
No. 060207-90-1) (FIFRA AI) (Ref. 3). In
a 2-generation rat reproduction study,
dietary administration of 25 mg/kg/day
produced an increased incidence of
hepatic clear cell change in parental
animals and administration of 125 mg/
kg/day produced an increased incidence
of hepatic lesions in offspring. The
parental NOEL was 5 mg/kg/day and the
developmental NOEL was 25 mg/kg/
day. In a 2—year mouse study, dietary
administration of 65 mg/kg/day (LOEL)
produced increased liver lesions and
liver weight in males, whereas,
administration of 325 mg/kg/day
produced increased liver tumors,
increased SGPT and SCOT levels,
increased liver weight, hepatocyte
enlargement, and vacuolation and fat
deposition in the liver of both sexes.
The NOEL was 13 mg/kg/day.
In a 3-month dog dietary study,
lymphoid follicles were observed in the
mucous membranes of the pyloric part
of the stomach at 6.25 mg/kg/day. The
NOEL was 1.25 mg/kg/day. In a 1-year
dog study, dietary administration of
6.25 mg/kg/day produced mild gastric
• mucosal irritation. The NOEL was 1.25
mg/kg/day. Based on the NOEL of the
study, an oral RfD of 0.013 mg/kg/day
was derived.
EPA believes that there is sufficient
evidence for listing propiconazole on
EPCRA section 313 pursuant to EPCRA
section 313(d)(2)(B) based on the
available hepatic and gastrointestinal
toxicity data for this chemical.
220. Quizalofop-ethyl (2-[4-[(6-chloro-
2-quinoxalinyl) oxyjphenoxy] propanoic
acid ethyl ester) (CAS No. 076578-14-8)
(FIFRA AI) (Ref. 3). In a 3-month rat
study, dietary administration of 6.4 mg/
kg/day produced changes in liver
weight and liver lesions. The NOEL was
2 mg/kg/day. In a 6-month dietary dog
study, 10 mg/kg/day produced testicular
atrophy in males. The NOEL was 2.5
mg/kg/day. Liver cell enlargement was
observed at 3.7 mg/kg/day in males and
4.6 mg/kg/day in females (LOELs) in a
2-year rat dietary study. The NOELs for
males and females were 0.9 mg/kg/day
and 1.1 mg/kg/day, respectively. Based
on the study, an oral RfD of 0.009 mg/
kg/day was derived. Increased liver
weights were observed in pregnant rats
in a teratology study. The maternal
LOEL was 100 mg/kg/day and the NOEL
was 30 mg/kg/day. No teratogenic NOEL
could be established. In a 2-generation
rat reproduction study, increased liver
weights and increased incidence of
eosinophilic changes in the liver were
observed in the offspring at 5 mg/kg/day
"(LOEL). The NOEL was 1.25 mg/kg/day.
EPA believes that there is sufficient
evidence for listing quizalofop-ethyl on
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Federal Register / Vol. 59, No. 8 / Wednesday, January 12, 1994 / Proposed Rules 1835
EPCRA section 313 pursuant to EPCRA
section 313(d)(2)(B) based on the
available reproductive and hepatic
toxicity data for this chemical.
221. Resmethrin ([5-(phenylmethyl)-3-
furanyl]methyl2,2-dimethyl-3-(2-
methyl-1 -propenyl)
cyclopropanecarboxylate]) (CAS No.
010453-86-8) (FIFRA AI) (Ref. 3). Oral
administration of 30 mg/kg/day (LOEL)
in capsules for 6 months produced
increases in liver weights in female
dogs. The NOEL was 10 mg/kg/day. In
a 2-year rat study, dietary
administration of 125 mg/kg/day
produced increases in liver weight and
pathological lesions. The NOEL was 25
mg/kg/day.
In a one-generation reproduction rat
study, administration of 25 mg/kg/day
(LOEL) in the diet produced an increase
in dead pups and lower pup weight
among survivors. No NOEL could be
established. In a 3-generation
reproduction rat study, dietary
administration of 25 mg/kg/day (LOEL)
produced an increase in pups cast dead
• and lower pup weight among survivors.
No NOEL could be established. Based
on the NOEL of the study, an oral RfD
of 0.03 mg/kg/day was derived.
Signs of neurotoxicity, including
piloerection, ataxia, sensory changes in
peripheral nerves, changes in locomotor
activity, salivation, tremors, and
convulsions were observed in rats, dogs,
mice, and rabbits given acute oral,
intravenous or intraperitoneal injections
greater than or equal to 160 mg/kg. In
a 3-month rat inhalation study, 0.1 mg/
L (LOEL) produced behavioral effects
and 1 mg/L produced decreased
locomotor activity, tremors, and other
behavioral changes. No NOEL could be
established.
EPA believes that there is sufficient
evidence for listing resmethrin on
EPCRA section 313 pursuant to EPCRA
section 313(d)(2)(B) based on the
available hepatic, reproductive, and
neurological toxicity data for this
chemical.
Aquatic acute toxicity values for
resmethrin include a rainbow trout 96-
hour LCso of 0.275 ppb (89 percent a.L),
a bluegill sunfish 96-hour LCso of 0.750
ppb (89 percent a.i.), a lake trout 96-
hour LCso of 1.7 ppb (84.5 percent a.i.),
and a fathead minnow 96—hour LCso of
3.0 ppb. EPA believes that there is
sufficient evidence for listing
resmethrin on EPCRA section 313
pursuant to EPCRA section 313(d)(2)(C)
based on the available environmental
toxicity data for this chemical.
222. Sethoxydim (2-[l-
(ethoxyimino)buty!]-5-
[2(ethylthio)propyl]-3-hydroxy-2-
cyclohexen-1-one) (CAS No. 074051-80-
2) (FIFRA AI) (Ref. 3). Mild anemia (the
LOEL was 17.5 mg/kg/day; the NOEL
was 8.9 mg/kg/day) was observed in
male dogs fed sethoxydim for 1—year.
Based on the NOEL, EPA derived an
oral RfD of 0.09 mg/kg/day. Swollen
liver cells (the LOEL was 117 mg/kg/
day; the NOEL was 45 mg/kg/day) were
seen in mice fed sethoxydim for 14
weeks. Pathological effects in the liver
(the LOEL was 45 mg/kg/day; the NOEL
was 15 mg/kg/day) were noted in rats
fed sethoxydim for 14 weeks.
Nonneoplastic liver lesions (the LOEL
was 54 mg/kg/day; the NOEL was 18
mg/kg/day) were observed in mice fed
sethoxydim for 2 years. Decreased
phenosulfophthalein (PSP) clearance
(the NOEL was greater than 3 mg/kg/
day; the LOEL not determined) was
noted in dogs given sethoxydim in the
diet for 26 weeks. Decreased PSP
clearance (the LOEL was 20 mg/kg/day;
the NOEL was 2 mg/kg/day) was also
noted in a 6-month feeding study in
dogs. EPA believes that there is
sufficient evidence for listing
sethoxydim on EPCRA section 313
pursuant to EPCRA section 313(d)(2)(B)
based on the available hematological,
hepatic, and renal toxicity data.
223. Simazine (CAS No. 000122-34-9)
(FIFRA SR; SDWA) (Ref. 8). Simazine is
a triazine-type herbicide. Chronic
exposure of sheep to low doses
(approximately 1.4 to 6 mg/kg/day) of
simazine caused fatty and granular
degeneration in the liver, and increased
SCOT and alkaline phosphatase.
Neuronophagia, diffuse kidney
degeneration, diffuse glial proliferation
and degeneration of ganglion cells in the
cerebrum and medulla were also
reported in these animals. Dogs that
received 1,500 ppm (37.5 mg/kg/day)
simazine in a 2-year feeding study also
had slight increases in serum alkaline
phosphatase and SCOT, indicative of
liver damage.
Sheep that received 1.4 mg/kg/day
simazine for 37 to 111 days had necrotic
changes in the germinal epithelium of
the testis and disturbances in
spermatogenesis.
EPA believes that there is sufficient
evidence for listing simazine on EPCRA
section 313 pursuant to EPCRA section
313(d)(2)(B) based on the hepatic, renal,
neurological, and reproductive toxicity
of this chemical.
224. Sodium azide (CAS No. 026628-
22-8) (CERCLA; EPCRA EHS; RCRA P)
(Ref. 8). Although not used clinically,
sodium azide is a direct acting
vasodilator. A reduction in blood
pressure was noted in hypertensive
patients orally exposed to sodium azide
during an investigation of the substance
in treating cancer. Reductions in blood
pressure were also reported in animals
following acute exposure. The minimal
hypotensive dose in humans has been
estimated to be approximately 0.2 to 0.4
|ig/kg (0.0002 to 0.0004 mg/kg). EPA
believes that there is sufficient evidence
for listing sodium azide on EPCRA
section 313 pursuant to EPCRA section
313(d)(2)(B) based on the ability of this
substance to lower blood pressure.
225. Sodium chlorite (CAS No.
007758-19-2) (FIFRA AI) (Ref. 3). A
decrease in erythrocyte half-life (the
LOEL was 100 ppm or 7.3 mg/kg/day;
the NOEL was 50 ppm or 3.65 mg/kg/
day) was observed in cats administered
sodium chlorite in the drinking water
for 90 days. Increase in glucose-6-
phosphatase dehydrogenase activity,
mean corpuscular volume (MCV),
osmotic fragility, and acanthocytes were
observed in mice administered 100 ppm
(19 mg/kg/day) in the drinking water for
30 days. In another 30-day drinking
water study, increased glucose-6-
phosphatase dehydrogenase activity,
MCV, and osmotic fragility were noted
in mice administered 100 ppm (19 mg/
kg/day). The NOEL was 1.9 mg/kg/day.
The results of in vitro studies show that
sodium chlorite can result in oxidative
damage to erythrocytes. EPA believes
that there is sufficient evidence for
listing sodium chlorite on EPCRA
section 313 pursuant to EPCRA section
313(d)(2)(B) based on the available
hematological toxicity data.
226. Sodium dicamba (3,6-Dichloro-2-
methoxybenzoic acid, sodium salt) (CAS
No. 001982-69-0) (FIFRA AI) (Ref. 3). No
toxicity data are available for sodium
dicamba. However, data are available on
dicamba as discussed below. In
solution, sodium dicamba will
dissociate into sodium ion and the
dicamba anion. Decreased fetal body
weights and increased postimplantation
loss were observed in the offspring of
rabbits receiving 10 mg/kg/day on days
6 through 18 of gestation. The LOEL was
10 mg/kg/day and NOEL was 3 mg/kg/
day. Based on the NOEL, EPA derived
an oral RfD value of 0.03 mg/kg/day. In
a separate study, disorders of oxidative
phosphorylation and focal necrosis in
the heart were observed in newborn rats
following transplacental exposure to
dicamba. In a developmental toxicity
study, an increase in skeletal
malformations was seen in the offspring
of rats orally administered 64 mg/kg/day
on days 6 through 19 of gestation. EPA
believes that there is sufficient evidence
for listing sodium dicamba on EPCRA
section 313 pursuant to EPCRA section
313(d)(2)(B) based on the available
developmental toxicity data for
dicamba.
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227. Sodium
dimethyldithiocarbamate (CAS No.
000128-04-1) (FIFRA AI) (Ref. 3). By
analogy to potassium
dimetnyldithiocarbamate, sodium
dimethyldithiocarbamate can
reasonably be anticipated to cause
fetotoxicity, postimplantation loss and
malformations. Data on potassium
dimethyldithiocarbamate follows. New
Zealand white rabbits given 38 mg/kg/
day by gavage on days 6 to 18 of
gestation exhibited malalignment of
slernebrao, total postimplantation loss,
and fetal weight decrement. Also at this
dose level, various possible
malformations including adactyly,
gastroschisis, short tail, anal atresia,
spina bifida, atelectasis, costal cartilage
anomaly, vertebral anomaly with/
without rib, caudal vertebrea anomaly,
and severe sternebrae malalignment in 6
of 52 fetuses from 5 of 11 litters. At the
77 mg/kg/day dose level, there was
severe fetal/embryo lethality. The NOEL
was 12.8 mg/kg/day. EPA believes that
there is sufficient evidence for listing
sodium dimethyldithiocarbamate on
EPCRA section 313 pursuant to EPCRA
section 313(d)(2)(B) based on the
available developmental toxicity data
for the analogue potassium
dimethyldithiocarbamate.
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,
Ravage 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 LDso 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
LDso of 0.22 to 0.44 mg/kg for mule
deer, an oral LDso of 1.41 mg/kg for male
ferrets, and an oral LDso 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.
229. Sodium hypochlorite (CAS No.
007681-52-9) (CERCLA) (Ref. 8). Aquatic
acute toxicity data for sodium
hypochlorite include a 96-hour
measured LCso of 100 ppb for bluegill
and a 96-hour measured LCso of 80 ppb
for fathead minnow. In addition, the 96-
hour measured LCso values for non-
standard test species range from 32 ppb
for coho salmon to 82 ppb for Pacific
sand lance. EPA believes that there is
sufficient evidence for listing sodium
hypochlorite on EPCRA section
313(d)(2)(C) based on the available
ecotoxicity data for this chemical.
230. Sodium nitrite (CAS No. 007632-
00-0) (CERCLA) (Ref. 8). Sodium nitrite
causes conversion (oxidation) of
hemoglobin to methemoglobin.
Methemoglobin cannot combine
reversibly with oxygen and its formation
can cause anemic hypoxia which may
lead to intense cyanosis. Infants are
particularly susceptible to this effect
because of their higher stomach pH,
immature enzyme systems, the reduced
capacity of newborn erythrocytes to
reduce methemoglobin to hemoglobin,
and the increased rate of nitrite-induced
oxidation of fetal hemoglobin to
methemoglobin (approximately twice
the rate of adult hemoglobin oxidation).
Coma and methemoglobinemia/
carboxyhemoglobinemia were reported
in a human that received sodium nitrite
(71 mg/kg) orally. In animal studies,
methemoglobinemia was reported in
dogs that received an intravenous dose
of 30 mg/kg sodium nitrite and in rats
administered a 10 mg/kg dose of sodium
nitrite subcutaneously.
Fetotoxicity (fetal death) was reported
following oral exposure of pregnant rats
to sodium nitrite (30 mg/kg/day) during
gestation days 1 through 22. In mice
exposed orally to 80 mg/kg/day during
gestation days 6 to 15 there was
increased preimplantation loss and fetal
death, and in mice exposed to a lower
dose (20 mg/kg/day) during gestation
days 1 to 14, abnormalities of the blood
or lymphatic system were reported in
offspring. In offspring of rats orally
exposed to 26 to 256 mg/kg/day during
pregnancy (gestation days 1 through 22)
and/or during lactation (20 to 21 days
after birth), effects on growth including
biochemical and/or metabolic changes
were noted.
EPA believes that there is sufficient
evidence for listing sodium nitrite on
EPCRA section 313 pursuant to EPCRA
section 313(d)(2)(B) based on the
available chronic hematological and
developmental toxicity data for this
chemical.
231. Sodium pentachlorophenate
(CAS No. 000131-52-2) (FIFRA AI) (Ref.
3). Pentachlorophenol has been
classified by EPA as a Group B2
compound, i.e., a probable human
carcinogen. This was based on
occurrence of increased combined
incidence of hemangiosarcomas, liver
tumors, and pheochromocytomas in
female mice. EPA believes that there is
sufficient evidence for listing sodium
pentachlorophenate on EPCRA section
313 pursuant to EPCRA section
313(d)(2)(B) based on the available
carcinogenicity data for its parent
compound, pentachlorophenol.
Aquatic acute toxicity values for
sodium pentachlorophenate include a
rainbow trout 96-hour LCso of 55 ppb,
a bluegill 96-hour LCso of 44 ppb, a
fathead minnow 96-hour LCso of 20
ppb, and a shrimp 96-hour LCso of 84
ppb. EPA believes that there is sufficient
evidence for listing sodium
pentachlorophenate on EPCRA section
313 pursuant to EPCRA section
313(d)(2)(C) based on the available
environmental toxicity data for this
chemical.
232. Sodium o-phenylphenoxide
(CAS No. 000132-27-4) (CERCLA; IARC)
(Ref. 8). Sodium o-phenylphenoxide has
been classified by IARC as a Group 2B
compound; i.e., the substance is
possibly carcinogenic in humans. EPA
believes that there is sufficient evidence
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Federal Register / Vol. 59, No. 8 / Wednesday, January 12, 1994 / Proposed Rules 1837
for listing sodium o-phenylphenoxide
on EPCRA section 313 pursuant to
EPCRA section 313(d)(2)(B) based on
the carcinogenicity data for this
chemical.
233. Sodium 2-pyridinethiol-l-oxide
(CAS No. 015922-78-8) (FIFRA AI) (Ref.
3). New Zealand white rabbits were
tested with test material dermally on
days 6 to 18 of gestation. At 0.5 mg/kg/
day, pups exhibited missing or defective
vertebrae, ribs and sternebrae. No NOEL
was established. EPA believes that there
is sufficient evidence for listing sodium
2-pyridinethiol-l-oxide on EPCRA
section 313 pursuant to EPCRA section
313(d)(2)(B) based on the available
developmental toxicity data for this
chemical.
234. Strychnine and salts (CERCLA;
EPCRA EHS; FIFRA SR; RCRA APP8;
RCRA P) (Ref. 8). Strychnine salts will
dissociate in aqueous solutions to yield
soluble strychnine. Strychnine, an
alkaloid, can cause violent convulsions
in humans. Other effects include
agitation, hypertonicity of muscles, and
painful muscle spasms. Renal failure
and respiratory paralysis generally
ensues, from severe or prolonged
convulsions. A potentially lethal oral
dose in a small child is 5 to 10 mg. The
lethal oral dose for an adult may be as
low as 30 mg. Similar effects have also
been reported in animals exposed at
lethal doses ranging from 0.25 to 2.35
mg/kg via oral and parenteral routes of
exposure. EPA's exposure analysis
indicates that strychnine and strychnine
salts 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 strychnine
and salts as a category on EPCRA
section 313 pursuant to EPCRA section
313(d)(2)(A) based on the available
acute toxicity and exposure data for this
chemical.
EPCRA section 313 requires threshold
determinations for chemical categories
to be based on the total of all chemicals
in the category manufactured,
processed, or otherwise used. For
example, a facility that manufactures
three members of a chemical category
would count the total amount of all
three chemicals manufactured towards
the manufacturing threshold for that
category. When filing reports for
chemical categories, the releases are
determined in the same manner as the
thresholds. One report if filed for the
category and all releases are reported on
this form.
235. Sulfur dioxide (CAS No. 007446-
09-5) (CERCLA; EPCRA EHS) (Ref. 8).
Acid precipitation occurs in large
regions of the Eastern United States and
Canada, Europe, and Japan. This
widespread occurrence of acid
precipitation and dry deposition results
in large part from man-made emissions
of oxides of sulfur (e.g., sulfur dioxide)
and oxides of nitrogen. These
substances are transformed in the
atmosphere into sulfuric acid and nitric
acid, transported over great distances
and deposited on vegetation, soils,
surface waters, and materials. These
substances are transferred from the
atmosphere into ecosystems by the
absorption of gases, the impaction and
gravitational settling of fine aerosols and
coarse particles and, precipitation.
Acids contained in polluted snow are
released as contaminated meltwater.
The resulting release of pollutants can
cause major or rapid changes in the
acidity of streams and lake waters.
Interference with normal reproduction
in fish populations is induced by acidity
of lake and stream waters. Reproduction
of frogs and salamanders is also
inhibited by atmospheric acidification
of surface waters.
Atmospheric deposition of sulfuric
acid and nitric acid can cause serious
damage to crops and forests. Biological
effects include induction of necrotic
lesions, loss of nutrients due to leaching
from foliar organs, accelerated erosion
of waxes and leaf surfaces, and
interference with normal reproductive
processes. Acidification decreases the
rate of many soil processes such as
nitrogen fixation and the breakdown of
organic matter.
EPA believes that there is sufficient
evidence for listing sulfur dioxide on
EPCRA section 313 pursuant to EPCRA
section 313(d)(2)(C) based on the
available environmental toxicity data for
this chemical.
Limited data on long-term human
exposure to sulfuric acid with respect to
occupational settings are available.
Recent studies suggest that sulfuric acid
aerosols at levels as low as 0.02 to 0.04
mg/m3 may cause significant effects on
lung function in humans. Effects noted
include increased risk of chronic
bronchitis in smokers and reduced
tracheobronchial clearance rate. Other
studies suggest that sulfuric acid at
concentrations as low as 0.04 mg/m3
may act synergistically with
copollutants such as ozone, NO2, and
metal particulates in causing decreased
pulmonary diffusing capacity and
bronchial hypersensitivity. These effects
are presumably attributable to the acidic
and oxidative properties of sulfuric
acid, and are therefore pH and
concentration dependent. EPA believes
that there is sufficient evidence for
listing sulfur dioxide on EPCRA section
313 pursuant to EPCRA section
313(d)(2)(B) based on the available
chronic toxicity data for sulfuric acid,
the hydrolysis product of sulfur dioxide.
Sulfur dioxide is regulated under
Title I of the CAA (Provisions for
Attainment and Maintenance of
National Ambient Air Quality
Standards) and Title IV of the CAA
(Acid Deposition Control). In addition
to this proposal to add sulfur dioxide to
EPCRA section 313, in Units IV.B.36.
and 179, EPA is proposing to add two
other chemicals, carbon monoxide and
nitrogen dioxide, that are regulated
under Title I of the CAA. Extensive data,
which are highly technical, are collected
on these chemicals as required by the
CAA. EPA requests comment on the
following: (1) Is the information
collected under the CAA sufficient for
public right-to-know purposes; and (2)
suggestions on how the data collected
on these chemicals pursuant to CAA
Titles I and IV could be used to meet the
purposes of EPCRA section 313.
236. Sulfur trioxide (CAS No. 007446-
11-9) (EPCRA EHS) (Ref. 8). IARC has
classified sulfur trioxide in Group 1, i.e.,
the chemical is carcinogenic to humans
based on sufficient evidence of
carcinogenicity in humans. EPA
believes that there is sufficient evidence
for listing sulfur trioxide on EPCRA
section 313 pursuant to section
313(d)(2)(B) based on the
carcinogenicity data for this chemical.
Acid precipitation occurs in large
regions of the Eastern United States and
Canada, Europe, and Japan. This
widespread occurrence of acid
precipitation and dry deposition results
in large part from man-made emissions
of oxides of sulfur (e.g., sulfur trioxide)
and oxides of nitrogen. These
substances are transformed in the
atmosphere into sulfuric acid and nitric
acid, transported over great distances
and deposited on vegetation, soils,
surface water, and materials. These
substances are transferred from the
atmosphere into ecosystems by the
absorption of gases, the impaction and
gravitational settling of fine aerosols and
coarse particles and., precipitation.
Acids contained in polluted snow are
released as contaminated meltwater.
The resulting release of pollutants can
cause major or rapid changes in the
acidity of streams and lake waters.
Interference with normal reproduction
in fish populations is induced by acidity
of lake and stream waters. Reproduction
of frogs and salamanders is also
inhibited by atmospheric acidification
of surface waters.
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Federal Register / Vol. 59, No. 8 / Wednesday, January 12, 1994 / Proposed Rules
Atmospheric deposition of sulfuric
add and nitric acid can cause serious
damage to crops and forests. Biological
effects include induction of necrotic
lesions, loss of nutrients due to leaching
from foliar organs, accelerated erosion
of waxes and leaf surfaces, and
interference with normal reproductive
processes. Acidification decreases the
rate of many soil processes such as
nitrogen fixation and the breakdown of
organic matter.
EPA believes that there is sufficient
evidence for listing sulfur trioxide on
EPCRA section 313 pursuant to EPCRA
section 313(d)(2)(C) based on the
available environmental toxicity data for
this chemical.
Limited data on long-term human
exposure to sulfuric acid with respect to
occupational settings are available.
Recent studies suggest that sulfuric acid
aerosols at levels as low as 0.02 to 0.04
mg/m' may cause significant effects on
lung function in humans. Effects noted
include increased risk of chronic
bronchitis in smokers and reduced
tracheobronchial clearance rate. Other
studies suggest that sulfuric acid at
concentrations as low as 0.04 mg/m3
may act synergistically with
copollutants such as ozone, NOz, and
metal particulates in causing decreased
pulmonary diffusing capacity and
bronchial hypersensitivity. These effects
are presumably attributable to the acidic
and oxidative properties of sulfuric
acid, and are therefore pH and
concentration dependent. EPA believes
that there is sufficient evidence for
listing sulfur trioxide on EPCRA section
313 pursuant to EPCRA section
313(d)(2)(B) based on the available
chronic toxicity data for sulfuric acid,
the hydrolysis product of sulfur
trioxide.
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.
238. Sulprofos (O-Ethyl O-[4-
(methylthio)phenyl] phosphorodithioic
acid S-propyl ester) (CAS No. 035400-
43-2) (FIFRA AI) (Ref. 3). The acute
dermal rabbit LDso is between 745 mg/
kg and 994 rag/kg. Ataxia, tremors, and
diarrhea were observed. In a 28-day
dietary study, administration of 1 mg/
kg/day produced decreased red blood
cell and brain cholinesterase activity.
The NOEL was 0.1 mg/kg. Dietary
administration of 15 mg/kg/day for 3
months produced hyperactivity in
female rats. The NOEL was 5 mg/kg/
day. In the same study, 5 mg/kg/day
produced red blood cell and brain
cholinesterase inhibition in both sexes.
The cholinesterase NOEL was 1.5 mg/
kg/day. Red blood cell and brain
cholinesterase inhibition, diarrhea,
vomiting, and some hind limb paralysis
were seen in dogs orally administered 5
mg/kg/day (LOEL) for 3 months. The
NOEL was 0.5 mg/kg/day. In a 22-
month dietary mouse study, plasma and
red blood cell cholinesterase were
inhibited at 3.25 mg/kg/day. The NOEL
was 0.325 mg/kg/day. Plasma, red blood
cell, and brain cholinesterase inhibition
were seen at a dietary administration of
2.5 mg/kg/day (LOEL) in a 2-year dog
study. The NOEL was 0.25 mg/kg/day.
Based on this study, an oral RfD of 0.003
mg/kg/day was derived. Dietary
administration of 3 mg/kg/day (LOEL)
produced plasma and red blood cell
cholinesterase depression in a 2-year rat
study. The NOEL was 0.3 mg/kg/day.
Increased unossified sternebrae were
observed in the offspring of rats given
10 mg/kg/day (LOEL) by gavage during
days 6 to 15 of gestation. No NOEL was
established.
EPA believes that there is sufficient
evidence for listing sulprofos on EPCRA
section 313 pursuant to EPCRA section
313(d)(2)(B) based on the available
neurological and developmental toxicity
data for this chemical.
The aquatic acute values for sulprofos
include bluegill 96-hour LC5o value of
1.03 ppm and 11 ppm (technical
product). The channel catfish
bioconcentration factor for whole fish is
704 to 1006. EPA believes that there is
sufficient evidence for listing sulprofos
on EPCRA section 313 pursuant to
EPCRA section 313(d)(2)(C) based on
the available environmental toxicity
data and the potential for
bioconcentration.
239. Tebuthiuron (N-[5-(l,l-
Dimethylethyl)-l,3,4-thiadiazol-2-yl)-
N,N'-dimethylurea) (CAS No. 034014-
18-1) (FIFRA AI) (Ref. 3).
Administration of 25 mg/kg/day (LOEL)
on days 6 through 18 of gestation
produced reduced body weights in
offspring of rabbits. The NOEL was 10
mg/kg/day. In a 3-month rat study,
dietary administration of 125 mg/kg/day
(LOEL) produced growth suppression
and pancreatic lesions. The NOEL was
50 mg/kg/day. In a 2-generation rat
reproduction study, depressed body
weight gain was observed in the female
parental generation at 14 mg/kg/day.
The NOEL was 7 mg/kg/day. Based on
the NOEL of the study, an oral RfD of
0.07 mg/kg/day was derived. In a 3-
generation rat reproduction study,
decreased body weight was observed in
the offspring of animals administered 20
mg/kg/day (LOEL). No NOEL was
established. Dietary administration of 40
mg/kg/day to rats for 2 years produced
growth suppression. The NOEL was 20
mg/kg/day. EPA believes that there is
sufficient evidence for listing
tebuthiuron on EPCRA section 313
pursuant to EPCRA section 313(d)(2)(B)
based on the available developmental
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 cefl,
lymphocyte, and neutrophil counts in
males and females. The NOEL for
females was 5 mg/kg/day. Increased
absolute and relative liver weights were
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1839
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 LCso of 0.06 ppb, a bluegill 96-
hour LCso of 0.13 ppb, a sheepshead
minnow 96-hour LCso of 0.13 ppb, a
daphnid 48-hour EC50 of 0.07 ppb, and
a mysid 96-hour EC5o 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.
241. Temephos (CAS No. 003383-96-
8) (FIFRA AI) (Ref. 3). Temephos is a
cholinesterase inhibitor in many
mammalian species. The LOELs at
which the cholinesterase inhibition was
observed ranged from 0.3 to 10 mg/kg/
day. However, human subjects that
ingested 256 mg/day for 5 days or 64
mg/day for 4 weeks showed no clinical
signs or effects on plasma or red blood
cell cholinesterase activities. Dietary
exposure of rats to 350 mg/kg/day for 90
days resulted in cholinesterase
inhibition only; no clinical signs were
reported. Rabbits and guinea pigs
tolerated 10 mg/kg/day for extended
periods without clinical effects, and
dogs tolerated 3 to 4 mg/kg/day, the
highest dose tested. EPA believes that
there is sufficient evidence for listing
temephos on EPCRA section 313
pursuant to EPCRA section 313(d)(2)(B)
based on the available neurological
toxicity data.
242. Terbacil (5-chloro-3-(l,l-
dimethylethyl)-6-methyl-2,4-(lH,3H)-
pyrimidinedione) (CAS No. 005902-51-
2) (FIFRA AI) (Ref. 3). Decreases in the
number of implantations and live
fetuses, were observed in rats
administered 62.5 mg/kg/day (LOEL)
orally for days 6 to 15. The NOEL was
12.5 mg/kg/day. Significantly reduced
body weights were observed in the
offspring of rabbits orally administered
600 mg/kg/day (LOEL) orally on days 6
to 18 of gestation. The NOEL was 200
mg/kg/day. '
In a 2-week rat dietary study,
administration of 1,000 mg/kg/day
produced increased absolute and
relative liver weights. In a 3-month rat
dietary study, administration of 25 mg/
kg/day (LOEL) produced increased liver
weights and vacuolization and
hypertophy of hepatocytes. The NOEL
was 5 mg/kg/day. In a 1-year dog study,
dietary administration of 48 mg/kg/day
to males and 12 (LOEL) and 48 mg/kg/
day to females produced increased
alkaline phosphatase and alanine
transaminase levels. The NOEL was 3
mg/kg/day. In a 2-year dog study,
dietary administration of 6.25 mg/kg/
day (LOEL) produced slight increases in
liver weights, elevated alkaline
phosphatase levels, and increased
thyroid-to-body-weight ratios. The
NOEL was 1.25 mg/kg/day. Based on the
NOEL, an oral RfD of 0.013 mg/kg/day
was established. Hypertrophy of
centrilobular hepatocytes was observed
in male mice administered 162.5 mg/kg/
day (LOEL) in the diet. The NOEL was
6.5 mg/kg/day.
EPA believes that there is sufficient
evidence for listing terbacil on EPCRA
section 313 pursuant to EPCRA section
313(d)(2)(B) based on the available
hepatic and developmental toxicity data
for this chemical.
243. Tetracycline hydrochloride (CAS
No. 000064-75-5) (CAL) (Ref. 8).
Tetracycline hydrochloride is widely
used as an antibiotic for the treatment
of many common infections. The
average oral adult dose for most
infections is 1 to 2 grams per day in
equally divided doses. The most
frequent adverse reactions to orally
administered tetracycline hydrochloride
are gastrointestinal effects including
nausea, vomiting, diarrhea, bulky loose
stools, and abdominal discomfort.
Photosensitivity, manifested as an
exaggerated sunburn reaction on sun-
exposed areas of the body has occurred
following oral therapy with tetracycline
hydrochloride. Photosensitivity
reactions of this type generally develop
within a few minutes to several hours
after sun exposure and usually persist 1
to 2 days after discontinuance of
tetracycline hydrochloride.
Manufacturers of tetracycline
hydrochloride state that this substance
should not be used in women during the
last half of pregnancy or in children
younger than 8 years of age unless other
appropriate drugs are ineffective or
contraindicated. The American
Academy of Pediatrics recommends that
tetracycline hydrochloride be used only
in children who are 9 years of age or
older, except under unusual
circumstances. Use of tetracycline
hydrochloride in pregnant women or
infants has resulted in retardation of
skeletal development and bone growth
in the fetus or child. Because
tetracycline hydrochloride localizes in
the dentin and enamel of developing
teeth, use of this substance during tooth
development may cause enamel
hypoplasia and permanent yellow-gray
to brown discoloration of the teeth. Use
of tetracycline hydrochloride may result
in discoloration of the deciduous teeth
of children if the substance is used
during pregnancy or in children up to
4 to 6 months of age. These effects are
most common following long-term use
of tetracycline hydrochloride but have
occured following repeated short-term
use. Premature infants treated with
tetracycline have demonstrated a 40
percent depression of bone growth. This
effect is readily reversible if exposure to
the substance is short.
Intraperitoneal injection of 85 mg/kg/
day on days 14 to 18 of gestation has
resulted in abortion and extra
embryonic structures in rat offspring.
Subcutaneous injection of 48 mg/kg/day
on days 16 through 20 of gestation and
intramuscular injection of 40 mg/kg/day
to rats on days 10 through 15 of
gestation resulted in embryo/
fetotoxicity. Exposure to 50 mg/kg/day
on days 7 to 15 of pregnancy resulted
in postimplantation loss and fetotoxicity
in rats. Exposure to 85 mg/kg/day on
days 7 to 15 of pregnancy resulted in
abortion in rats. Fetotoxicity was
observed in mice receiving 86 mg/kg/
day of tetracycline hydrochloride on
days 8 to 13 of gestation.
EPA believes that there is sufficient
evidence for listing tetracycline
hydrochloride on EPCRA section 313
pursuant to EPCRA section 313(d)(2)(B)
based on the available developmental
toxicity data and other chronic toxicity
data for this chemical.
244. Tetramethrin (2,2-Dimethyl-3-(2-
methyl-1 -propenyl)
cyclopropanecarboxylic acid
(l,3,4,5,6,7-hexahydro-l,3-dioxo-2-H-
isoindol-2-yl)methyl ester (CAS No.
007696-12-0) (FIFRA AI) (Ref. 3).
Depression, salivation, ataxia, lethargy,
and convulsions were observed in acute
rat studies in which the oral LDso values
were greater than or equal to 4,400 mg/
kg. Tremors, excitement, and increased
urine volume were observed in an acute
dermal rat study in which the LDso was
greater than 2,500 mg/kg. Tremors,
ataxia, dyspnea, gastointestinal
hypermotility, and diarrhea were
observed in rats and mice administered
tetramethrin subcutaneously or
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intraperitonealy. The LD5o was greater
than 500 mg/kg. In a 6-month dog
dietary study, administration of 62.5
mg/kg/day produced nervouseness and
tremors. The NOEL was 31.25 mg/kg/
day.
EPA believes that there is sufficient
evidence for listing tetramethrin on
EPCRA section 313 pursuant to EPCRA
section 313(d)(2)(B) based on the
available neurological toxicity data for
this chemical.
Aquatic acute toxicity values for
tetramethrin include a bluegill 96-hour
LCjo of 21 ppb (mixed isomers,
technical product) and 69 ppb. EPA
believes that there is sufficient evidence
for listing tetramethrin on EPCRA
section 313 pursuant to EPCRA section
313(d)(2)(C) based on the available
environmental toxicity data for this
chemical.
245. Tetrasodium
ethylenediaminetetraacetate (CAS No.
000064-02-8) (FIFRA AI) (Ref. 3).
Increased occurrence of 13th
rudimentary ribs was observed in the
offspring of rats orally administered 5
mg/kg/day (LOEL). No NOEL was
established and the dosing duration was
not reported. EPA believes that there is
sufficient evidence for listing
tetrasodium
ethylenediaminetetraacetate on EPCRA
section 313 pursuant to EPCRA section
313(d)(2)(B) based on the available
developmental toxicity data for this
chemical.
246. Thiabendazole (2-(4-Thiazolyl)-
iH-benzimidazole) (CAS No. 000148-79-
8) (FIFRA AI) (Ref. 3). Oral
administration of 600 mg/kg/day (LOEL)
to rats on days 6 through 15 of gestation
produced cleft palate and open eyes.
Musculoskeletal abnormalities were
observed in the offspring of mice orally
administered 240 mg/kg on day 9 of
gestation. Musculoskeletal
abnormalities were also observed in the
offspring of rats orally administered 296
mg/kg/day on days 8 through 15 of
gestation. Decreased litter size, and skin
abnormalities were observed in the
offspring of rats orally administered 667
mg/kg/day on days 8 through 15 of
gestation. Oral administration of 1,300
mg/kg/day produced musculoskeletal
abnormalities and fetal death in the
offspring of mice. Oral administration of
2,400 mg/kg/day on day 11 of gestation
produced craniofacial abnormalities in
the offspring of mice. EPA believes there
is sufficient evidence for listing
thiabendazole on EPCRA section 313
pursuant to EPCRA section 313(d)(2)(B)
based on the available developmental
toxicity data for this chemical.
Aquatic acute toxicity values for
thiabendazole include a rainbow trout
96-hour LCso of 560 ppb, a daphnid 48-
hour ECso of 0.31 ppb, and a mysid 96-
hour LCso of 340 ppb. EPA believes that
there is sufficient evidence for listing
thiabendazole on EPCRA section 313
pursuant to EPCRA section 313(d)(2)(C)
based on the available environmental
toxicity data.
247. Thiabendazole, hypophosphite
salt (2-(4-thiazolyl) benzimidazole,
hypophosphite salt) (CAS No. 028558-
32-9) (FIFRA AI) (Ref. 3). Few toxicity
data are available on thiabendazole,
hypophosphite salt. However, data are
available on the parent compound,
thiabendazole, as discussed below.
Oral administration of 600 mg/kg/day
(LOEL) to rats on days 6 through 15 of
gestation produced cleft palate and open
eyes. Musculoskeletal abnormalities
were observed in the offspring of mice
orally administered 240 mg/kg on day 9
of gestation. Musculoskeletal
abnormalities were also observed in the
offspring of rats orally administered 296
mg/kg/day on days 8 through 15 of
gestation. Decreased litter size and skin
abnormalities were observed in the
offspring of rats orally administered 667
mg/kg/day on days 8 through 15 of
gestation. Oral administration of 1,300
mg/kg/day produced musculoskeletal
abnormalities and fetal death in the
offspring of mice. Oral administration of
2,400 mg/kg/day on day 11 of gestation
produced craniofacial abnormalities in
the offspring of mice. EPA believes that
there is sufficient evidence for listing
thiabendazole hypophosphite salt on
EPCRA section 313 pursuant to EPCRA
section 313(d)(2)(B) based on the
available developmental toxicity data
for this chemical.
No laboratory data are available for
thiabendazole hypophosphite salt.
Ecotoxicity data are available for the
parent compound thiabendazole.
Aquatic acute toxicity values for
thiabendazole include a rainbow trout
96-hour LCso of 560 ppb, a daphnid 48-
hour ECso of 0.31 ppb, and a mysid 96-
hour LCso of 340 ppb. EPA believes that
there is sufficient evidence for listing
thiabendazole hypophosphite salt on
EPCRA section 313 pursuant to EPCRA
section 313(d)(2)(C) based on the .
available environmental toxicity data for
this chemical.
248. Thiobencarb (carbamic acid,
diethylthio-, s-(p-chlorobenzyl)) (CAS
No. 028249-77-6) (FIFRA AI) (Ref. 3).
Measured aquatic acute toxicity values
for thiobencarb include a chinook
salmon 96-hour LCso of 760 ppb, a
striped bass 96-hour LCso of 760 ppb, a
rainbow trout 96-hour LCso of 790 ppb,
and a green algae 72-hour ECso of 30
ppb (population reduction). EPA
believes that there is sufficient evidence
for listing thiobencarb on EPCRA
section 313 pursuant to EPCRA section
313(d)(2)(C) based on the available
environmental toxicity data.
249. Thiodicarb (CAS No. 059669-26-
0) (FIFRA AI) (Ref. 3). Thiodicarb is a
cholinesterase inhibitor in mammalian
species. In addition, hematological
effects have been observed in various
species. Tremors and pinpoint pupils
(the NOEL was less than 0.043 mg/L)
were noted in rats exposed by
inhalation to thiodicarb for 9 days.
Macrocytic anemia (the LOEL was 2 g/
kg; the NOEL was 1 g/kg) was observed
in a 21-day dermal study in rabbits. In
another 21-day dermal study, decreased
red blood cell counts and decreased
hemoglobin levels (the LOEL was 4 g/
kg/day; the NOEL was 1 g/kg/day) were
reported. Decreased plasma and red
blood cell cholinesterase activities (the
LOEL was 30 mg/kg/day; the NOEL was
10 mg/kg/day) were observed in rats fed
thiodicarb for 28 days. Decreased red
blood cell cholinesterase activity and
decreased hemoglobin levels (the LOEL
was 10 mg/kg/day; the NOEL was 3 mg/
kg/day) were seen in a 13-week feeding
study in rats. Inhibition of plasma and
red blood cell cholinesterase activities
(the LOEL was 45 mg/kg/day; the NOEL
was 15 mg/kg/day) was noted in dogs
fed thiodicarb for 6 months. Significant
hematological and clinical chemistry
values were also seen at 45 mg/kg/day
(the NOEL was 15 mg/kg/day).
Reductions in red blood cell
cholinesterase activity (the LOEL was
12.8 mg/kg/day; the NOEL was 4.5 mg/
kg/day) were also seen in a 1-year
feeding study in dogs. In addition,
decreased red blood cell and decreased
hemoglobin and hematocrit levels, and
increased relative spleen and liver
weights (the LOEL was 38.3 mg/kg/day;
the NOEL was 12.8 mg/kg/day) were
reported. EPA believes that there is
sufficient evidence for listing thiodicarb
on EPCRA section 313 pursuant to
EPCRA section 313(d)(2)(B) based on
the available neurological and
hematological toxicity data.
Aquatic acute toxicity values for
thiodicarb include a bluegill 96-hour
LCso of 1.47 ppm , a rainbow trout 96-
hour LCso of 2.65 ppm, a sheepshead
minnow 96-hour LCso of 530 ppb, a
daphnid 48-hour ECso of 27 ppb, a
mysid 96-hour LCso of 29.3 ppb, an
eastern oyster 96-hour LCso of 1.0 ppb,
and an algae 96-hour ECso of 450 ppb.
EPA believes that there is sufficient
evidence for listing thiodicarb on
EPCRA section 313 pursuant to EPCRA
section 313(d)(2)(C) based on the
available environmental toxicity data.
250. Thiophanate ethyl ([1,2-
phenylenebis (iminocarbonothioyl)]
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1841
biscarbamic acid diethyl ester) (CAS No.
023564-06-9) (FIFRA AI) (Ref. 3). In a 6-
month dog study, dietary administration
of 500 mg/kg/day (LOEL) produced
thyroid changes. The NOEL was 50 mg/
kg/day. Thyroid follicular hypertrophy
was observed at 50 mg/kg/day (LOEL) in
a rat 2-year dietary study. The NOEL
was 10 mg/kg/day. EPA believes that
there is sufficient evidence for listing
thiophanate ethyl on EPCRA section 313
pursuant to EPCRA section 313(d)(2)(B)
based on the available thyroid toxicity
data for this chemical.
251. Thiophanate-methyl (CAS No.
023564-05-8) (FIFRA SR) (Ref. 8).
Decreased spermatogenesis was
observed in male rats fed 32 mg/kg/day
thiophanate-methyl. The NOEL was 8
mg/kg/day. Other effects noted at the 32
mg/kg/day dose level included
decreased body weight and histological
evidence of hyperthyroidism.
In a 3-generation reproductive study
in rats, reduced litter weights were seen
at a daily dietary dose of 32 mg/kg
thiophanate-methyl. The NOEL was 8
mg/kg/day. A decrease in the number of
implantations was observed in mice
administered a limit dose of 1,000 mg/
EPA believes that there is sufficient
evidence for listing thiophanate-methyl
on EPCRA section 313 pursuant to
EPCRA section 313(d)(2)(B) based on
the reproductive toxicity data for this
chemical.
252. Thiosemicarbazide (CAS No.
000079-19-6) (CERCLA; EPCRA EHS;
RCRA APP8; RCRA P) (Ref. 8). The oral
LDsoS for thiosemicarbazide in rats and
dogs are 9.16 and 10 mg/kg,
respectively. The LDLo in the mouse is
94 mg/kg. Cats orally administered
thiosemicarbazide experienced
convulsions, salivation, and vomiting;
the LDso was 20 mg/kg. Intraperitoneal
injection of 2.5 mg/kg of
thiosemicarbazide produced
restlessness, running fits, and
convulsions in rabbits. EPA's exposure
analysis indicates that
thiosemicarbazide 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
thiosemicarbazide on EPCRA section
313 pursuant to EPCRA section
313(d)(2)(A) based on the available
acute toxicity and exposure data for this
chemical.
253. Triadimefon (l-(4-
chlorophenoxy)-3,3-dimethyl-l-(lH-
l,2,4-triazol-l-yl)-2-butanone) (CAS No.
043121-43-3) (FIFRA AI) (Ref. 3).
Decreased hematocrit, red blood cell
count, and hemoglobin volume were
observed in dogs orally administered 60
mg/kg/day (LOEL) for 13 weeks. No
NOEL was established. In a 2—year
dietary rat study, decreased hemoglobin
and erythrocyte counts were observed at
25 mg/kg/day (LOEL). The NOEL was
2.5 mg/kg/day. Based on the NOEL of
the study, an oral RfD of 0.03 mg/kg/day
was derived. Dietary administration of
25 mg/kg/day (LOEL) for 2 years to dogs
produced increased serum alkaline
phosphatase and N-demethylase activity
and increased liver weight. The NOEL
was 2.5 mg/kg/day. Increased
erythrocyte count, thrombocyte count,
hemoglobin, and hematocrit levels in
females and increased serum alkaline
phosphatase, serum glutamic-pyruvic
transaminase, serum glutamic-
oxaloacetic transaminase, liver weights,
and hyperplastic nodules in both sexes
were observed at 234 mg/kg/day in a 2-
year mouse dietary stujdy. The NOEL
was 6.5 mg/kg/day and the LOEL was 39
mg/kg/day. In another 2—year mouse
dietary study, administration of 234 mg/
kg/day produced hepatocellular
adenomas. Doses of 39 mg/kg/day in
males (LOEL) and 6.5 mg/kg/day in
females (LOEL) produced nonrieoplastic
and preneoplastic changes in the liver,
increased liver weights with correlating
effects on serum enzymes, and
hepatocellular hypertrophy. The NOEL
in males was 6.5 mg/kg/day and no
NOEL in females could be established.
Cleft palates were observed in the
offspring of rats orally administered 75
mg/kg/day (LOEL). The NOEL was 30
mg/kg/day. Increased incidence of
abnormal ribs, extra ribs, and distended
urinary bladders were observed in the
offspring of rats orally administered 90
mg/kg/day (LOEL). The NOEL was 30
mg/kg/day. Increases in fetal resorptions
were observed in rabbits given 100 mg/
kg/day by gavage (LOEL). The NOEL
was 30 mg/kg/day. Increased incidences
of incomplete ossification of pelvic
pubes and phalanges, and irregular
spinous processes were observed in the
offspring of rabbits orally administered
50 mg/kg/day (LOEL) on days 6 through
18 of gestation. The NOEL was 20 mg/
kg/day.
In a 3-generation rat reproduction
study, decreased fertility and decreased
litter size were observed at 90 mg/kg/
day (LOEL). The NOEL was 15 mg/kg/
day. In a 2-generation reproduction
study in rats, decreased pup weights,
decreased litter size, and decreased pup
viability were observed at 90 mg/kg/day
(LOEL). The NOEL was 2.5 mg/kg/day.
EPA believes that there is sufficient
evidence for listing triadimefon on
EPCRA section 313 pursuant to EPCRA
section 313(d)(2)(B) based on the
available hepatic, hematological,
developmental, and reproductive
toxicity data for this chemical.
254. Triallate (CAS No. 002303-17-5)
(FIFRA SR) (Ref. 8). Triallate, a
dithiocarbamate insecticide, is a
cholinesterase inhibitor. When triallate
was administered to rats at a dose of
147.1 mg/kg/day orally and to cats at a
dose of 0.028 mg/L/day (via aerosol) for
2 months, the animals developed fatal
morphological changes in neurons of
the cerebral cortex, subcortical area,
cerebellum, and spinal cord. Doses of 30
mg/kg/day caused head bobbing and
circling in pregnant rats. The NOEL was
7.5 mg/kg/day. The LOEL and NOEL for
liver effects in a 2—year study in dogs
fed diets containing triallate were 4.25
mg/kg/day and 1.28 mg/kg/day,
respectively. At 4.25 mg/kg/day an
increase in hemosiderin deposition and
serum alkaline phosphatase was
observed in both sexes, and an increase
in liver weight was observed in females.
Based on the NOEL, an oral RfD of 0.013
mg/kg/day was derived. In a hamster
chronic feeding study, decreased
triglycerides were seen in males at the
LOEL of 30 mg/kg/day. The NOEL was
5 mg/kg/day. Ninety-day feeding studies
in rats (10 mg/kg/day) and dogs (5 mg/
kg/day) showed no treatment related
adverse effects except for increased
liver-to-body-weight ratios in the dogs.
EPA believes that there is sufficient
evidence for listing triallate on EPCRA
section 313 pursuant to EPCRA section
313(d)(2)(B) based on the chronic
neurological and hepatic toxicity data
for this chemical.
255. Tribenuron methyl (2-(((((4-
methoxy-6-methyl-l,3,5-triazin-2-yl)-
methylamino)carbonyl)amino)sulfonyl)-
, methyl ester) (CAS No. 101200-48-0)
(FIFRA AI) (Ref. 3). In a 1-year feeding
study in dogs, elevated serum bilirubin
and aspartate aminotransferase (AST)
levels and increased urinary volume
were reported in males receiving 8.16
mg/kg/day (LOEL). The NOEL for males
was 0.79 mg/kg/day. The LOEL for
females was 52.02 mg/kg/day (the
highest dose tested) and was based on
increased serum creatinine and
transient increases in AST, globulin,
and serum bilirubin. These females had
an 18.2 percent decrease in body weight
gain. The NOEL for females was 8.18
mg/kg/day. The highest dose in males
(51.46 mg/kg/day) caused increases in
serum creatinine and a 20 percent
decrease in body weight gain. The oral
RfD, derived from the NOEL for males,
was 0.008 mg/kg/day. In a 90-day
feeding study, decreased absolute and
relative liver and kidney weights, serum
glucose, globulin and cholesterol levels
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1842 Federal Register / Vol. 59, No. 8 / Wednesday, January 12, 1994 / Proposed Rules
were observed in rats at 87.5 mg/kg/day
(LOEL). The NOEL was 5 mg/kg/day.
EPA believes that there is sufficient
evidence for listing tribenuron methyl
on EPCRA section 313 pursuant to
EPCRA section 313(d)(2)(B) based on
the available hepatic and renal toxicity
data for this chemical.
258. Tributyltin fluoride (CAS No.
001983-10-4) (FIFRA AI) (Ref. 3).
Aquatic acute toxicity values for
tributyltin fluoride include a bleak fish
96-hour LCso of 2.3 ppb, an algae 72-
hour ECso of 9.3 ppb, and a Harpacticoid
copepod 96-iour LCso 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.
257. Tributyltin methacrylate (CAS
No. 002155-70-6) (FIFRA AI) (Ref. 3).
Pregnant rats were given tributyltin
methacrylate by gavage on days 6 to 19
of gestation. Mean fetal weight and
maternal body weight gain were
decreased at 18 mg/kg/day. Fetal
rosorplions were also significantly
increased. The fetotoxic NOEL for this
study was 9 mg/kg/day. EPA believes
that there is sufficient evidence for
listing tributyltin methacrylate on
EPCRA section 313 pursuant to EPCRA
section 313(d)(2)(B) based on the
available developmental toxicity data
for this chemical.
25S.S,S,S-Tributyltrithiophosphate
(DBF) (CAS No. 000078-48-8) (FIFRA
AI) (Ref. 8). S.S.S-
Tributyltrithiophosphate (DEF) is a
cholinesterase inhibitor. Both
immediate and delayed neurotoxic
effects have been reported in humans
following exposure to DEF. The
exposure levels at which these effects
occurred, however, were not reported.
In a 3-month hen feeding study, the
NOEL for neurotoxic effects was 0.1 mg/
kg/day and the LOEL was 0.5 mg/kg/
day. At 0.5 mg/kg day, hens showed
delayed neurotoxicity, ataxia, and
equivocal changes in the spinal cord
and peripheral nerves. Based on the
NOEL, EPA has derived an oral RfD of
0.00003 mg/kg/day for this chemical. In
a 12-week dog feeding study, animals
showed over sensitivity to stimuli at
0.62 mg/kg/day; the NOEL was 0.12 mg/
kg/day. In the same study, the LOEL for
cholinesterase inhibition was 0.12 mg/
kg/day and a NOEL was not established.
Brain cholinesterase inhibition was
observed in a chronic rat feeding study
at 1.25 mg/kg/day. The NOEL was 0.25
mg/kg/day. EPA believes that there is
sufficient evidence for listing S,S,S-
tributyltrithiophosphate on EPCRA
section 313 pursuant to EPCRA section
313(d)(2)(B) based on the chronic
neurotoxicity data for this chemical.
Measured acute aquatic toxicity data
for S,S,S-tributyltrithiophosphate
include a rainbow trout 96-hour LCso of
660 ppb (0.660 ppm) and a bluegill 96-
hour LCso of 620 ppb (0.620 ppm). The
measured log K<,w is 5.7. EPA believes
that there is sufficient evidence for
listing S,S,S-tributyltrithiophosphate on
EPCRA section 313 pursuant to EPCRA
section 313(d)(2)(C) based on the
environmental toxicity data for this
chemical and its potential for
bioaccumulation.
259. Trichloroacetyl chloride (CAS
No. 000076-02-8) (EPCRA EHS) (Ref. 8).
Trichloroacetyl chloride is highly toxic
in humans by the oral and inhalation
routes of exposure. Numerous cases of
strong irritation of the eyes, skin, and
respiratory tract and fever, nausea, and
vomiting following exposure to
trichloroacetyl chloride have been
reported. The acute inhalation LCso
values for mice and rats are 0.445 mg/
L and 0.475 mg/L, respectively,
indicating that trichloroacetyl chloride
is highly toxic by inhalation in these
species. EPA's exposure analysis
indicates that trichloroacetyl chloride
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 trichloroacetyl chloride on
EPCRA section 313 pursuant to EPCRA
section 313(d)(2)(A) based on the
available acute toxicity and exposure
data for this chemical.
260. Trichloroethylsilane (CAS No.
000115-21-9) (EPCRA EHS) (Ref. 8).
Chlorinated silanes are very corrosive to
the skin and mucous membranes and
liberate hydrochloric acid in the
presence of water. Trichloroethylsilane
causes severe burns and the vapor is
harmful to humans. The mouse 2-hour
inhalation LCso value is 0.30 mg/L.
EPA's exposure analysis indicates that
trichloroethylsilane 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
trichloroethylsilane on EPCRA section
313 pursuant to EPCRA section
313(d)(2)(A) based on the available
acute toxicity and exposure data for this
chemical.
261. Trichlorophenylsilane (CAS No.
000098-13-5) (EPCRA EHS) (Ref. 8).
Chlorinated silanes are very corrosive to
the skin and mucous membranes and
liberate hydrochloric acid in the
presence of water.
Trichlorophenylsilane causes severe
burns and the vapor is harmful to
humans (concentration not specified).
The 2-hour mouse inhalation LCso
value is 0.33 mg/L. EPA's exposure
analysis indicates that
trichlorophenylsilane 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
trichlorophenylsilane on EPCRA section
313 pursuant to EPCRA section
313(d)(2)(A) based on the available
acute toxicity and exposure data for this
chemical.
262.1,2,3-Trichloropropane (CAS No.
000096-18-4) (RCRA APP8) (Ref. 8).
Results of a subchronic oral toxicity
study in rats and mice reveal that the
primary target organs for 1,2,3-
trichloropropane are the liver and
kidney. Renal and hepatic necrosis were
observed in rats administered 1,2,3-
trichloropropane by gavage for 17
weeks. The LOAEL was 16 mg/kg/day
and the NOAEL was 8 mg/kg/day for
hepatic effects. The LOAEL was 32 mg/
kg/day and the NOAEL was 16 mg/kg/
day for renal effects. Hepatic necrosis in
mice occurred at 125 mg/kg/day. The
NOAEL was 63 mg/kg/day. Less severe
renal necrotic changes were seen at 250
mg/kg/day. The NOAEL was 125 mg/kg/
day. The renal and hepatic lesions were
accompanied by increases in organ
weights and alterations in serum
enzymes that were indicative of hepatic
and renal toxicity. At lower dose levels
(the LOAEL was 16 mg/kg/day),
nonregenerative anemia (decreased
hematocrit, hemoglobin, and
erythrocyte count) was observed in rats.
The NOAEL was 8 mg/kg/day.
Nonregenerative anemia is considered
to be one of die most sensitive effects of
1,2,3-trichlpropropane.
The respiratory tract is a principal
target of inhaled 1,2,3-trichloropropane
in humans and animals. Irritation of the
eyes and throat has been reported in
humans acutely exposed (15 minutes) to
100 ppm (0.602 mg/L) of 1,2,3-
trichloropropane via inhalation.
Irritative effects on the olfactory
epithelium have been observed in rats
exposed by inhalation to 3 ppm (the
LOAEL was 0.018 mg/L; the NOAEL
was 0.006 mg/L) of 1,2,3-
trichloropropane for 11 days.
•Histological effects have also been seen
in the nasal cavity (the LOEL was 125
mg/kg/day; the NOAEL was 63 mg/kg/
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1843
day) in rats and in the bronchiolar
epithelium (the LOEL was 63 mg/kg/
day; the NOAEL was 32 mg/kg/day) in
mice that were exposed to 1,2,3-
trichloropropane by oral intubation for
17 weeks.
EPA believes that there is sufficient
evidence for listing 1,2,3-
trichloropropane on EPCRA section 313
pursuant to EPCRA section 313(d)(2)(B)
based on the hematological, respiratory,
hepatic, and renal toxicity data for this
chemical.
263. Triclopyr triethylammonium salt
(CAS No. 057213-69-1) (FIFRA AI) (Ref.
3). Degeneration of proximal tubules
(the LOEL was 20 mg/kg/day; the NOEL
was 5 mg/kg/day) was noted in male
and female rats fed triclopyr for 3
months. A LOEL of 2.5 mg/kg/day,
based on phenosulfophthalein (PSP)
excretion, was reported in dogs fed
triclopyr for 6 months. A similar effect
was also noted at the LOEL of 5 mg/kg/
day, determined in dogs fed triclopyr for
8 months. The NOEL was greater than
5 mg/kg/day. Significant increases in
absolute and relative kidney weights
were observed in rats fed 36 mg/kg/day
for 2 years. The NOEL was 12 mg/kg/
day. In a pharmacokinetic study,
reduced PSP excretion was seen in dogs
administered 5 mg/kg/day, whereas no
effect on PSP excretion was seen in
monkeys administered 20 mg/kg/day.
No details on the route and length of
exposure were provided. EPA believes
that there is sufficient evidence for
listing triclopyr triethylammonium salt
on EPCRA section 313 pursuant to
EPCRA section 313(d)(2)(B) based on
the available renal toxicity data.
264. Triethylamine (CAS No. 000121-
44-8) (CAA HAP) (Ref. 7). Triethylamine
is an acute irritant which causes eye and
nasal irritation and pulmonary toxicity
in mice and rats and is an acute eye
toxicant in man.
In a survey of workers exposed to
triethylamine, none of the workers
reported effects at 5 ppm. Slight to mild
effects were noted at concentrations
between 5 and 10 ppm and above 10
ppm workers reported visual
disturbances which included halo
vision and irritation of the eyes, nose,
and throat. In a separate report, eye
irritation and visual disturbances
consisting of foggy vision, blue haze or
halo vision (halo around lights) was
reported in 19 workers exposed to
triethylamine. Exact exposure levels
were not determined. The TWA in the
work place of those individuals who
complained of "blue haze" was 11 mg/
m3 with a range of 4 to 24 mg/ms. The
American Council of Government and
Industrial Hygienists (ACGIH) has set a
threshold limit value-time weighted
average (TLV-TWA) of 10 ppm and a
threshold limit value-short-term
exposure limit (TLV-STEL) of 15 ppm
based upon inhalation toxicity in guinea
pigs and rats and skin irritation and eye
injury in rabbits.
EPA's exposure analysis indicates that
triethylamine 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
triethylamine on EPCRA section 313
pursuant to EPCRA section 313(d)(2)(A)
based on the available acute toxicity and
exposure data for this chemical.
265. Triforine (N,N'-[1,4-
piperazinediylbis(2,2,2-
trichloroethylidene)] bisformamide)
(CAS No. 026644-46-2) (FIFRA AI) (Ref.
3). In a 2—year feeding study in rats,
anemia was reported. The LOEL, based
on this effect, was 3,125 ppm (156 mg/
kg/day) and the NOEL was 625 ppm
(31.25 mg/kg/day). Siderosis of Kupffer
cells and bone marrow cells was
reported in dogs exposed to triforine in
their diet for 2 years. The LOEL in this
study was 1,000 ppm (25 mg/kg/day)
and the NOEL was 100 ppm (2.5 mg/kg/
day). Effects on red blood cells,
hematocrit or hemoglobin were also
noted in dogs or rats in several 13-week
feeding studies. For example, dogs
exposed to a 20.6 percent a.i.
formulation of the compound for 13
weeks at dose levels that included 600
ppm (the LOEL, equivalent to 15 mg/kg/
day or 3.1 mg a.i./kg/day) and 100 ppm
(the NOEL, equivalent to 2.5 mg/kg/day
or 0.5 mg a.i./kg/day) had siderosis in
the liver, spleen, and bone marrow.
A decrease in mean relative weight of
offspring was observed in rabbits
exposed to 25 mg/kg triforine (the
fetotoxicity LOEL). The fetotoxicity
NOEL was 5 mg/kg. The LOEL and
NOEL for maternal toxicity in this
developmental toxicity study were also
25 mg/kg and 5 mg/kg, respectively, and
were based on reduced food intake and
body weight loss. Fetotoxicity
(decreased number of fetuses and
increased resorptions) was also reported
in the offspring of rats fed 1,600 mg/kg
(the fetotoxicity LOEL) for an
unspecified duration. The fetotoxicity
NOEL was 800 mg/kg.
EPA believes that there is sufficient
evidence for listing triforine on EPCRA
section 313 pursuant to EPCRA section
313(d)(2)(B) based on the available
hematological and developmental
toxicity data for this chemical.
266. Trimethylchlorosilane (CAS No.
000075-77-4) (EPCRA EHS) (Ref. 8).
Chlorinated silanes are very corrosive to
the skin and mucous membranes and
liberate hydrochloric acid in the
presence of water.
Trimethylchlorosilane causes severe
burns and the vapor is harmful to
humans. The mouse inhalation LCLo
value is 0.10 mg/L. EPA's exposure
analysis indicates that
trimethylchlorosilane 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
trimethylchlorosilane on EPCRA section
313 pursuant to EPCRA section
313(d)(2)(A) based on the available
acute toxicity and exposure data for this
chemical.
267. 2,3,5-Trimethylphenyl
methylcarbamate (CAS No. 002655-15-
4) (FIFRA AI) (Ref. 3). Cholinesterase
inhibition was reported in a series of
studies for this carbamate pesticide. In
dogs that received 2,000 ppm (50 mg/
kg/day) 2,3,5-trimethylphenyl
methylcarbamate in their diet for 14
days, there was inhibition of plasma and
red blood cell cholinesterases and also
weight loss. Brain cholinesterase was
slightly decreased in rats in a 2-year
feeding study at 200 ppm (10 mg/kg/
day). At 800 ppm (40 mg/kg/day), there
were fatty changes in the liver which
disappeared after 7.5 months. EPA
believes that there is sufficient evidence
for listing 2,3,5-trimethylphenyl
methylcarbamate on EPCRA section 313
pursuant to EPCRA section 313(d)(2)(B)
based on the available neurological
toxicity data for this chemical.
268. Triphenyltin chloride (CAS No.
000639-58-7) (EPCRA EHS) (Ref. 8). Oral
exposure of male rats to 380 mg/kg
triphenyltin chloride over 19 days
caused adverse effects on the testes,
epididymis, sperm duct, prostate gland,
seminal vesicle, Cowper's gland, and
accessory glands. EPA believes that
there is sufficient evidence for listing
triphenyltin chloride on EPCRA section
313 pursuant to EPCRA section
313(d)(2)(B) based on the reproductive
toxicity data for this chemical.
Measured aquatic acute toxicity data
for triphenyltin chloride include a 48-
hour LCso for carp of 55 ppb and a 72-
hour ECso (growth) for marine green
algae of 0.92 ppb. In addition, the
measured aquatic toxicity information
indicates a freshwater green algae 8-day
ECso (growth) of 2 ppb. EPA believes
that there is sufficient evidence for
listing triphenyltin chloride on EPCRA
section 313 pursuant to EPCRA section
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313(d](2)(C) based on the environmental
toxicity data for this chemical.
269. Triphenyltin hydroxide (CAS No.
000076-87-9) (FIFRA SR) (Ref. 8).
Triphenyltin hydroxide has been
classified by EPA as a Group B2
compound, i.e., a probable carcinogen.
This was based on the significant
increases in fetal pituitary gland
adenomas in female Wistar rats and
Leydig cell tumors in male Wistar rats
fed 1 or 4 mg/kg/day triphenyltin
hydroxide for 2 years. There were
significant increases of hepatocellular
adenomas and combined hepatocellular
(adenoma and/or carcinoma) tumars in
male and female NMRI mice fed 0.65,
2.6, or 10.4 mg/kg/day for 80 weeks.
In a developmental toxicity study in
rats, oral doses of 15 mg/kg of
triphenyltin hydroxide during gestation
days 1 to 7 prevented implantation.
When administered from day 8 and
onwards, the compound was fetolethal.
EPA believes that there is sufficient
evidence for listing triphenyltin
hydroxide on EPCRA section 313
pursuant to EPCRA section 313(d)(2)(B)
based on the carcinogenicity data and
the developmental toxicity data for this
chemical.
Measured aquatic acute toxicity data
for triphenyltin hydroxide include a
fathead minnow 96-hour LCso of 5.4
ppb, abluegill 96-hour LCso of 23 ppb,
a rainbow trout 96—hour LCso of 15 ppb,
and a marine green algae 72-hour LCso
of 13.9 ppb. EPA believes that there is
sufficient evidence for listing
triphenyltin hydroxide on EPCRA
section 313 pursuant to EPCRA section
313(d)(2)(C) based on the environmental
toxicity data for this chemical.
270. Vanadium pentoxide (CAS No.
001314-62-1) (CERCLA; EPCRA EHS;
RCRA APP8) (Ref. 8). Eighteen workers
exposed to vanadium pentoxide dusts at
concentration in excess of 0.5 mg/m3
(0.0005 mg/L) for a period of up to 2
weeks developed respiratory symptoms
that persisted for nearly 2 weeks after
removal from exposure. Inhalation of
unspecified levels of vanadium
pentoxide for 1 to 5 years produced
asthma in 3 of 20 workers. Mice and rats
exposed to 1 to 3 mg/m? (0.001 to 0.003
mg/L) vanadium pentoxide 6 hours/day
for 3 months developed histopathologic
changes in their lungs and had a
decrease in growth rate. EPA believes
that there is sufficient evidence for
listing vanadium pentoxide on EPCRA
section 313 pursuant to EPCRA section
313(d)(2)(B) based on the available
chronic respiratory toxicity data for this
chemical.
271. Vinclozolin (3-(3,5-
dichlorophenyl)-5-ethenyl-5-methyl-2,4-
oxazolidinedione) (CAS No. 050471-44-
8) (FIFRA AI) (Ref. 3). The results of a
3-month feeding study in Wistar rats
administered 4,500 ppm (225 mg/kg/
day; the only dose tested) indicate that
vinclozolin interacts with numerous
steroid hormones in male and female
animals. A broad spectrum of steroid
hormones were affected in these
animals, including increases in
adrenocorticotropic hormone, lutenizing
hormone, follicle stimulating hormone,
testosterone, corticosterone,
aldosterone, and
dehydroepiandrosterone and slight
decreases in estradiol levels in males.
Female rats had elevated
adrenocorticotropic hormone and
luteinizing levels and depressed
corticosterone and aldosterone levels,
while follicle stimulating hormone,
testosterone, dehydroepiandrosterone
and estradiol levels were comparable to
controls. After a 2—month recovery
period postdosing, all male hormone
levels were normal except for a slight
elevation in FSH, and all female
hormone levels were normal except for
a slight elevation in estradiol. The
endocrine changes also were reported in
developmental, subchronic, and chronic
toxicity studies.
A broad spectrum of organ changes
occurred in dogs exposed to vinclozolin
hi a 1-year feeding study. Males
administered 4.8 mg/kg/day (the LOEL
for males) had increases in testes
weights, increased bilirubin, and
prostate atrophy. The NOEL in males
was 2.4 mg/kg/day. Females in this
study had increased adrenal weights,
lipid accumulation in the adrenal
glands, and marginally increased
hemosiderin in the liver at 5.1 mg/kg/
day (the LOEL for females). The NOEL
for females was 2.5 mg/kg/day. At
higher doses (47 mg/kg/day in males
and 53 mg/kg/day in females), there
were increases in Weights of the liver,
spleen, testes, adrenal, and thyroid.
Cither effects included increased diffuse
hyperplasia of the Leydig cells, lipid
accumulation in the adrenal cortex, and
increased platelets in males, and in
females, slight increases in mean
corpuscular volume and mean
corpuscular hemoglobin concentration.
The oral RfD for this compound, 0.025
mg/kg/day, was based on the findings of
a 6-month feeding study with beagle
dogs, in which adrenal weights
(absolute and relative) were
significantly increased at 7.5 mg/kg/day
(the LOEL). The NOEL was 2.5 mg/kg/
day. Both males and females exposed to
higher doses (600 and 2,000 ppm, or 15 ,
and 50 mg/kg/day) had histological
changes in the adrenal glands, including
vacuolation of the zona fasciculata. hi
addition to effects on the adrenal gland,
males exposed to the LOEL dose and
higher had decreased absolute kidney
weights, and at 600 ppm, fat droplets in
the distal tubule were observed.
Pseudohermaphroditism (a decrease
in anal-genital distance) occurred in
male offspring of rats administered
doses of 50 mg/kg (the LOEL) and
higher by gavage. The developmental
NOEL was 15 mg/kg. The same effect
was noted in the offspring of rats that
received dermal applications of 180 mg/
kg/day (LOEL; the developmental NOEL
was 60 mg/kg/day) during gestation, and
also in a 2-generation reproduction
study in rats (the LOEL was 86 mg/kg/
day, the NOEL was 25 mg/kg/day).
Other developmental effects observed in
the latter study included developmental
delays, reduced male and female pup
weight, increased stillbirths and
increased pup mortality throughout
lactation.
EPA believes that there is sufficient
evidence for listing vinclozolin on
EPCRA section 313 pursuant to EPCRA
section 313(d)(2)(B) based on the
available endocrine, adrenal, renal,
hepatic, and developmental toxicity
data.
V. Rationale for Listing
EPA is proposing to add the chemical
substances identified in Unit IV.B. of
this preamble because EPA believes that
these chemicals meet the statutory
criteria for listing under section
313(d)(2) of EPCRA. The bases for these
determinations and the specific toxic
effects are summarized in Unit IV.B. of
this preamble and set forth in more
detail in the rulemaking record.
EPA intends to evaluate public
comment on this proposed rule and
issue a final rule by November 30,1994.
Reporting for the chemicals identified in
the final rule would be required for
activities during the 1995 calendar year.
Such reports would have to be
submitted to EPA and States by July 1,
1996.
VI. Rulemaking Record
The record supporting this proposed
rule is contained in docket number
OPPTS-400082. Nonconfidential
documents, including an index of the
docket, are available to the public in the
TSCA Nonconfidential Information
Center (NCIC), also known as the TSCA
Public Docket Office from 12 noon to 4
p.m., Monday through Friday, excluding
legal holidays. The TSCA Public Docket
Office is located at EPA Headquarters,
Rm. E-G102, 401 M St., SW.,
Washington, DC 20460.
Any person who submits comments
claimed as CBI must mark the
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1845
comments as "confidential," "CBI," or
other appropriate designation.
Comments not claimed as confidential
at the time of submission will be placed
in the public file. Any comments
marked as confidential will be treated in
accordance with the procedures in 40
CFR part 2. Any person submitting
comments claimed to be confidential
must prepare and submit a
nonconfidential public version of the
comments in triplicate that EPA can
place in the public file.
VII. Request for Public Comment
EPA requests comment on any aspect
of this proposal. EPA requests specific
comment as detailed in the following
paragraphs.
EPA requests comment on the
sufficiency of the evidence for each of
the chemicals proposed for addition in
Unit IV.B. of this preamble. In addition,
EPA requests comment on any issues
that may be specific to any of the
individual chemicals or chemical
categories.
EPA requests comment on whether it
would be appropriate to list persistent
bioaccumulative toxic chemicals that
are manufactured, processed, or
otherwise used below the current
reporting thresholds 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, would
be required to insure that release and
transfer information would be collected?
In Units IV.B.132., IV.B.144., and
IV.B.158., of this preamble, EPA is
proposing to add individually three
diisocyanates: hexamethylene-1,6-
diisocyante; isophbrone diisocyanatej
and 1,1-methylene bis(4-
isocyanatocyclohexane). EPA requests
comment on its alternative proposal in
Unit IV.B.132. of this preamble to create
a diisocyanates category rather than
adding diisocyanates individually to
EPCRA section 313. EPA also requests
comment on what diisocyanates, other
than those listed in IV.B.132. of this
preamble, should be included in such a
category.
EPA requests comment on its
proposed definition of man-made
mineral fibers, given in Unit IV.B.149. of
this preamble, and any other options for
defining a fibers category.
In Unit IV.B.166. and 172. of this
preamble, EPA is proposing to add two
ethylene bisdithiocarbamates (EBDCs):
metiram; and nabam. An additional two
EBDCs, zineb and maneb, are currently
listed on the EPCRA section 313 list of
toxic chemicals. The category of EBDCs
has recently been added to EPCRA
section 313 (December 1,1993; 58 FR
63500). EPA requests comment on the
following: (1) Should the individual
EBDCs, metiram and nabam, be added
individually to EPCRA section 313 even
though they are members of the EBDC
category, which is listed on EPCRA
section 313; and (2) should the
individual listings for two EBDCs, zineb
and maneb, be deleted and added as
members of the newly created EBDC
category?
EPA requests comment on whether
polycyclic aromatic compounds (PACs)
should be added as a delineated
category consisting of the PACs listed in
Unit IV.B.207. of this preamble or as a
category with the definition given in
Unit IV.B.207. of this preamble.
EPA requests comment on its
approach in considering exposure as a
part of its evaluation of certain
chemicals under sections 313(d)(2)(A)
and (C).
In Units IV.B.36,179., and 235. of this
preamble, EPA is proposing to add three
chemicals (sulfur dioxide, nitrogen
dioxide, and carbon monoxide) that are
regulated by Title I of the CAA
(Provisions for Attainment and
Maintenance of National Ambient Air
Quality Standards). In addition, sulfur
dioxide is regulated under Title IV of
the CAA (Acid Deposition Control).
Extensive data, which are highly
technical, are collected on these
chemicals as required by the CAA. EPA
requests comment on the following: (1)
Is the information collected under the
CAA sufficient for public right-to-know
purposes; and (2) suggestions on how
the data collected on these chemicals
pursuant to CAA Titles I and IV could
be used to meet the purposes of EPCRA
section 313.
Comments should be submitted to the
address listed under the ADDRESSES
unit. All comments must be received on
or before April 12,1994.
Vm. Public Meeting
EPA will hold a 1-day public meeting
to discuss the issues presented above.
The tentative agenda for this public
meeting will include a discussion of the
issues presented in Unit VII. of this
preamable.
Scheduling of oral statements will be
on a first come first served basis by
calling the telephone number listed
under FOR FURTHER INFORMATION
CONTACT. All statements will be made
part of the public record and will be
considered in the development of the
final rule.
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).
X. Regulatory Assessment
Requirements
A. Executive Order 12866
Under Executive Order 12866 (58 FR
51735, October 4,1993), the Agency
must determine whether the regulatory
action is "significant" and therefore
subject to the Office of Management and
Budget (OMB) and the requirements of
the Executive Order. Under section 3(f),
the order defines a "significant
regulatory action" as an action likely to
result in a rule (1) Having an annual
effect on the economy of $100 million
or more, or adversely and materially
affecting a sector of the economy,
productivity, competition, jobs, the
environment, public health or safety, or
State, local, or tribal governments or
communities (also referred to as
"economically significant"); (2) creating
serious inconsistency or otherwise
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1846
Federal Register / Vol. 59, No. 8 / Wednesday, January 12, 1994 / Proposed Rules
interfering with an action taken or
planned by another agency; (3)
materially altering the budgetary
impacts of entitlements, grants, user
fees, or loan programs; or (4) raising
novel legal or policy issues arising out
of legal mandates, the President's
priorities, or the principles set forth in
this Executive Order.
Pursuant to the terms of this
Executive Order, it has been determined
that this proposed rule is a "significant
regulatory action." As such, this action
was submitted to OMB for review, and
any comments or changes made in
response to OMB suggestions or
recommendations have been
documented in the public record.
B. Regulatory Flexibility Act
The Regulatory Flexibility Act of 1980
requires each Federal agency to perform
a Regulatory Flexibility Analysis for all
rules that are likely to have a
"significant impact on a substantial
number of small entities." The analysis
supporting this proposed rule estimated
the maximum cost that a small business
might incur, and calculated the cost
impact percentage (reporting costs
divided by average value of shipments)
for each employee size, class, and SIC
code.
Reporting costs are estimated at less
than one percent of the average value of
shipments per report in the first year,
and less than one-half of one percent of
the value of shipments per report in
subsequent years. The precise impacts
depend on how many reports an
individual small business submits.
However, experience with current
reporters indicates that small businesses
generally submit fewer reports per
facility than larger ones. Most of the
reports are anticipated to be submitted
from industries with the lowest impacts.
Because of this, no segment of the
manufacturing sector is likely to suffer
significant adverse effects due to this
rule, Therefore, EPA certifies that this
proposed rule will not have a significant
impact on a substantial number of small
entities.
C. Paperwork Reduction Act
The collection of information and
other requirements under section 313 of
EPCRA and section 6607 of the PPA are
covered under OMB approval number
2070-0093, which was issued on May
14,1992. While this approval normally
would have expired on November 30,
1992, it remains in effect pursuant to the
1993 Department of Veteran Affairs and
Housing and Urban Development and
Independent Agencies Appropriations
Act, Pub. L. 102-389, signed October 6,
1992, which states that:
Notwithstanding the Paperwork Reduction
Act of 1980 or any requirements thereunder
the Environmental Protection Agency Toxic
Chemical Release Inventory Form R and
Instructions, revised 1991 version issued
May 19,1992, and related requirements
(OMB No. 2070-0093), shall be effective for
reporting under section 6607 of the Pollution
Prevention Act of 1990 (Public Law 101508)
and section 313 of the Superfund
Amendments and Reauthorization Act of
1986 (Public Law 99-499) until such time as
revisions are promulgated pursuant to law.
This proposed rule adds chemicals to
the list of toxic chemicals subject to
reporting under section 313 of EPCRA
and section 6607 of the PPA and does
not change the elements of the TRI
reporting form, its instructions, or
related requirements. Accordingly, the
Form R and Instructions and related
requirements remain in effect, as
provided by Pub. L. 102-389.
The industry reporting burden for
collecting this information is estimated
to average 53 hours per respondent
annually, including time for reviewing
instructions, searching existing data
sources, gathering and maintaining the
data needed, and completing and
reviewing the collection of information.
The actual burden to a specific facility
may deviate from this estimate
depending on the complexity of the
facility's operations and the profile of
the release.
Send comments regarding this
collection of information, including
suggestions for reducing this burden, to
Chief, Information Policy Branch, 2131,
U.S. Environmental Protection Agency,
401 M St., SW., Washington, DC 20460;
and to the Office of Information and
Regulatory Affairs, Office of
Management and Budget, 726 Jackson
Place NW., Washington, DC 20503,
marked "Attention: Desk Officer for
EPA." The final rule will respond to any
OMB or public comments on this
collection of information.
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 § 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:
§ 372.65 Chemicals and chemical
categories to which the part applies.
*****
(a) * * *
Chemical Name
Abamectin [Avermectin B1]
Acephate (Acetylphosphoramidothioic acid O.S-dimethyl ester)
*******
Actfluorfen, sodium salt [5-(2-Chlorc-4-(triflouromethyl)phenoxy)-2-nitrc-benzoic acid, sodium salt]
*******
Atachtor
AkJIcarb
*******
d-trans-Allethrin fd-trans-Chrysanthemic acid of d-allethrone]
Alfylamlrw
* * * * *** *
Aluminum phosphide
Arnetryn(N-Ethyl-N'-(1-methylethyl)-6-(methylthio)-1,3,5,-triazine-2,4-d!amine)
*******
AmJtraz
CAS No.
71751-41-2
30560-19-1
62476-59-9
15972-60-8
116-06-3
28057-48-9
107-11-9
20859-73-8
834-12-8
33089-61-1
Effective
Date
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
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Federal Register / Vol. 59, No. 8 / Wednesday, January 12, 1994 / Proposed Rules
3847
Chemical Name
*******
Anilazine [4,6-dichloro-N-(2-chlorophenyl)-1 ,3,5-triazin-2-amine]
* * * * * * *
Atrazine (6-Chloro-N-ethyl-N'-(1 -methylethyl)-1 ,3,5,-triazine-2,4-diamine)
*******
Bendiocarb [2,2-Dimethyl-1 ,3-benzodioxol-4-ol methylcarbamate]
Benfluralin (N-Butyl-N-ethyl-2,6-dinitro-4-(trifluoromethyl)benzenamine)
Benomyl
*******
o-Benzyl-p-chlorophenol
*******
Bifenthrin
*******
Bis(tributylin) oxide
Boron trichloride
Boron trifluoride
Bromacil (5-Bromo-6-methy!-3-(1 -methylpropyl)-2,4-(1 H,3H)-pyrimidinedione)
Bromacil, lithium salt [2,4-(1 H,3H)-Pyrimidinedione, 5-bromo-6-methyl-3-(1-methylpropyl), lithium salt]
Bromine
1 -Bromo-1 -(bromomethyl)-l ,3-propanedicarbonitrile
*******
2-Bromo-2-nitropropane-1 ,3-diol (Bronopol)
*******
Bromoxynil (3,5-Dibromo-4-hydroxybenzonitrile)
Bromoxynil octanoate (Octanoic acid, 2,6-dibromo-4-cyanophenyl ester)
Brucine
*******
Butylate (Bis-2-methylpropyl)carbamothioic acid S-ethyl ester)
Butylated hydroxyanisole
* * * * * * *
C.I. Acid Red 114
*******
C.I. Direct Blue 21 8
*******
Calcium hypochlorite
Caprolactam
*******
Carbofuran
*******
Carbon monoxide
*******
Carboxin (5,6-Dihydro-2-methyl-N-phenyl-1 ,4-oxathiin-3-carboxamide)
*******
Chinomethionat [6-Methyl-1 ,3-dithiolo[4,5-b]quinoxalin-2-one]
*******
Chlorendic acid
Chlorimuron ethyl [Ethyl-2-[[[(4-chloro-6-methoxyprimidin-2-yl)-carbonyl]-amino]sulfonyl]benzoate]
*******
1 -(3-Chloroally l)-3,5,7-triaza-1 -azoniaadamantane chloride
p-Chloroaniline
*******
5-Chloro-2-(2,4-dichlorophenoxy)phenol
*******
3-Chloro-2-methyl-1 -propene
p-Chlorophenyl isocyanate
Cnloropicrin
*****-**
3-Chloropropionitrile
*******
p-Chloro-o-toluidine
CAS No.
101-05-3
1912-24-9
22781-23-3
1861-40-1
17804-35-2
120-32-1
82657-04-3
56-35-9
10294-34-5
7637-07-2
314-40-9
53404-19-6
7726-95-6
35691-65-7
52-51-7
1689-84-5
1689-99-2
357-57-3
2008-41-5
25013-16-5
6459-94-5
28407-37-6
7778-54-3
105-60-2
1563-66-2
630-08-0
5234-68-4
2439-01-2
115-28-6
90982-32-4
4080-31-3
106-47-8
3380-34-5
563-47-3
104-12-1
76-06-2
-
542-76-7
95-69-2
Effective
Date
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
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1848 Federal Register / Vol. 59, No. 8 / Wednesday, January 12, 1994 / Proposed Rules
Chemical Name
2-CWcfC-1,1,1-trifluorc-ethane (HCFC-133a)
Chtorotrinuoromethane (CFC-13)
3-Chloro-1,1,1-WHuorc-propane (HCFC-253fb)
CWorpyrifos methyl [O,O-aimethyl-O-(3,5,6-trichlorc-2-pyridyl)phosphorothioate
Chlorsuiluron [2-chlorc-N-[[4-methoxy-6-methyl-1,3,5-triazin-2-yl)amino]carbonyObenzenesulfonamide]
***** ^ * *
Ctomazon8[2-K2-Chlorophenyl)methyl]-4,4-dimethyl-3-isoxazolidinone]
CrotonaWehyde
Cyanazina
*******
Cyctoato
*******
Cydohexanol
Cyfluthrin [3-{2^-Dfchloroethenyl)-2,2-dimethylcyclopropanecarboxylic acid, cyano(4-fluoro-3-
phenoxyphenyljmethyl ester]
Cyhatothnn [3-{2-Chforo-3,3,3-trifluoro-1-propenyl)-2,2-dimethylcyclopropanecarboxylio acid cyano(3-
phenoxyphenyljmethyl ester]
Cyromazlne [N-CyctooropyH ,3,5-triazine-2,4,6-triamine]
* ' * * * * * *
Dazometfretrahydro-3,5-dimethyl-2H-1,3,5-thiadiazine-2-thione)
Dazomet, sodium salt [Tetrahydro-3,5-dimethyI-2H-1,3,5-thiadiazine-2-thione, ion(1-), sodium]
2,4,-DB
2,4-D butoxyelhyl ester
2,4-D butyl ester
2,4-D chtorocrotyl ester
*******
Desmedipham
2,4-D 2-ethylhexyl ester
2,4-D 2-elhyM-methy!pentyl ester
*******
Diajzinon
*******
2,2-Dft>romo-3-nitrilopfopionamide
*******
Dtearnba (3,6-DtohIorc-2-methyoxyben2oic acid)
Dtehloran (2,6-Dichloro-4-niferoaniline]
*******
3,3'-D!chlofobenzldine dihydrochloride
3.3'-DichlorobenzIdine sulfate
*******
trans-1 ,4-DlchIorc-2-butene
1^-Dfchloro-1,1-dinuoroethane (HCFC-132b)
*******
DJchtofoftuoromethane (HCFC-21)
*******
Dtehtofomethylphenylsilane
Dichtoropentafluoropropane
1,1-ro-1 ,1 ,1 ,3,3-pentafluoropropane HCFC-225aa
2,3-d»chloro-1,1,1^,3-perrtafluoropropane HCFC-225ba
3,3-dtehk>ro-1 ,1 ,1 ^^-pentafluorobropane (HCFC-225ca
DicWorophene [ 2^'-Methyleno-bis(4-chlorophenol)]
*******
trans-1 ,3-Dtchtoropropene
*******
Diclofop methyl [2-[4-{2,4-Dfchlorophenoxy)phenoxy]propanoic acid, methyl ester]
*******
Dteydopentadtene
*******
Diothatyl ethyl
CAS No.
75-88-7
75-72-9
460-35-5
5598-13-0
64902-72-3
81777-89-1
4170-30-3
21725-46-2
1134-23-2
108-93-0
68359-37-5
68085-85-8
66215-27-8
533-74-4
53404-60-7
94-82-6
1929-73-3
94-80-4
2971-38-2
13684-56-5
1928-43-4
53404-37-8
333-41-5
10222-01-2
1918-00-9
99-30-9
612-83-9
64969-34-2
110-57-6
1649-08-7
75-43-4
149-74-6
127564-92-5
13474-88-9
111512-56-2
422-44-6
431-86-7
507-55-1
136013-79-1
128903-21-9
422-48-0
422-56-0
97-23-4
10061-02-6
51338-27-3
77-73-6
38727-55-8
Effective
Date
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
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Federal Register / Vol. 59, No. 8 / Wednesday, January 12, 1994 / Proposed Rules
1849
Chemical Name
* * * * *-* *
Diflubenzuron
Diglycidyl resorcinol ether
Dimethipin [2,3,-Dihydro-5,6-dimethyl-1 ,4-dithiin-1 ,1 ,4,4-tetraoxide]
Dimethoate
******
3,3'-Dimethoxybenzidine dihydrochloride (o-Dianisidine dihydrochloride)
3,3'-Dimethoxybenzidine hydrochloride (o-Dianisidine hydrochloride)
Dimethylamine
Dimethylamine dicamba
*******
3,3'-Dimethylbenzidine dihydrochloride (o-Tolidine dihydrochloride)
3,3'-Dimethylbenzidine dihydrofluoride (o-Tolidine dihydrofluoride)
*******
Dimethyl chlorothiophosphate
Dimethyldichlorosilane
N,N-Dimethylformamide
*******
2f6-Dimethylphenol
*******
Dinocap
Dinoseb
*******
Diphenamid
Diphenylamine
*******
Dipotassium endothall [7-Oxabicyclo(2.2.1)heptane-2,3-dicarboxylic acid, dipotassium salt]
Dipropyl isocinchomeronate
Disodium cyanodithioimidocarbonate
2,4-D isopropyl ester
2,4-Dithiobiuret
Dithiopyr [2-(Difluoromethyl)-4-(2-methylpropyl)-6-(trifluoromethyl)-3,5-pyridinedicarbothioic acid S,S-di-
methyl ester]
Diuron
2,4-D. 2-octyl ester
Dodine [Dodecylguanidine monoacetate]
2,4,-DP
2,4-D propylene glycol butyl ether ester
2,4-D sodium salt
*******
Ethoprop [Phosphorodithioic acid O-ethyl S,S-dipropyl ester]
*******
Ethyl dipropylthiocarbamate [EPTC]
*******
Famphur
Fenarimol [.alpha.-(2-Chlorophenyl)-.alpha.-4-chlorophenyl)-5-pyrimidinemethanol]
Fenbutatin oxide (Hexakis(2-methyl-2-phenyl-propyl)distannoxane)
Fenoxaprop ethyl [2-(4-((6-Chloro-2-benzoxazolylen)oxy)phenoxy)propanoic acid.ethyl ester]
Fenoxycarb [2-(4-Phenoxyphenoxy)ethyl]carbamic acid ethyl ester]
Fenpropathrin [2,2,3,3-Tetramethylcyclopropane carboxylic acid cyano(3-phenoxy-phenyl)methyl ester]
Fenthion [O,O-Dimethyl O-[3-methyl-4-(methylthio)phenyl]ester, phosphorothioic acid]
Fenvalerate [4-Chloro-alpha-(1-methylethyl)benzeneacetic acid cyano(3-phenoxyphenyl)methyl ester]
Ferbam[Tris(dimethylcarbamo-dithioato-S,S')iron]
Fluazifop-butyl [2-[4-[[5-(Trifluoromethyl)-2-pyridinyf]oxy]-phenoxy]propanoic acid, butyl ester]
Flumetralin [2-Chloro-N-(2,6-dinitro-4-(trifluoromethyl)phenyO-N-ethyl-6-fluorobenzenemethanamine]
*******
Fluorine
Fluorouracil (5-Fluorouracil)
Fluvalinate [N-[2-Chlorc-4-(trifluoromethyl)phenyl]-DL-valine(+)-cyano (S-phenoxyphenyl)methyl ester]
Folpet
Fomesafen [5-(2-Chloro-4-(trifluoromethyl)phenoxy)-N-methylsulfonyl)-2-nitrobenzamide]
*******
alpha-Hexachlorocyclohexane
*******
Hexamethylene-1 ,6-diisocyanate
*******
n-Hexane
Hexazinone
CAS No.
35367-38-5
101-90-6
55290-64-7
60-51-5
20325-40-0
111984-09-9
124-40-3
2300-66-5
612-82-8
41766-75-0
2524-03-0
75-78-5
68-12-2
576-26-1
39300-45-3
88-85-7
957-51-7
122-39-4
2164-07-0
136^5-8
138-93-2
94-1 1-1
541-53-7
97886-45-8
330-54-1
1917-97-1
2439-10-3
120-36-5
1320-18-9
2702-72-9
13194-4&4
759-94-4
52-85-7
60168-88-9
13356-08-6
66441-23-4
72490-01-8
39515-41-8
55-38-9
51630-58-1
14484-64-1
69806-50-4
62924-70-3
7782-41-4
51-21-8
69409-94-5
133-07-3
72178-02-0
319-84-6
822-60-0
110-54-3
51235-04-2
Effective
Date
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1 /9&
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
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1850
Federal Register / Vol. 59, No. 8 / Wednesday, January 12, 1994 / Proposed Rules
Chemical Name
Hydramathylnon [Tetjariydrc-5,5-dirnethyl-2(1 H)-pyritnidinone[3-[4- (trifluoromethyl)phenyl]-1 -[2-[4-
(lrifluorometnyl)phenyOethenyl]-2-propenyliderte]hycfrazone]
*******
Imazalil [1-{2-(2,4-Dichlorophenyl)-2-(2-propenyloxy)ethyl]-1 H-imidazole]
3-Iodo-2-propynyl butytearbamate
lprodkme[3-(3,5-Dk;hicxyl[(1-methyiethyl)amino]phosphinothioyi]oxy]benzoic acid 1-methylethyl ester]
Isophorono
Isophororte diisocyanate
*******
Lactofen [5-(2-Chloro-4-(trinuoromethyl)phenoxy)-2-nitro-2-ethoxy-1- methyl-2-oxoethyl ester]
*******
Umtron
Lithium carbonate
Matotbton
*******
Mecoprop
2-Mercaptobenzothiazole (MBT)
*******
Merphos
Metnam sodium (Sodium methyklithiocarbamate)
*******
Melhazole [2-(3,4-DicWorophenyl)-4-methyl-1 ,2,4-oxadiazolidine-3,5-dione]
Methiocarb
Metboxone (4-Chtoro-2-methylphenoxy) acetic acid (MCPA))
MeJhoxone-sodium salt {(4-cnloro-2-methylphenoxy) acetate sodium salt)
*******
1,1'-Methy!ene bis(4-isocyanatocyclohexane)
*******
Mothylana bis(thiocyanate)
*******
Methyl teothfocyanate [Isothiocyanatomethane]
2-MetnyltactonRrHa
*******
N-Mothytolacrylamlde
Methyl parathfon
Mothyltrtohlorosilane
Metiram
Motribuzin
* * * * * * *
Mofinata (IH-Azepine-1-carbothioic acid, hexahydro-S^ethyl ester)
*******
Monuron
*******
Myclobutanll [.a^sha.-Butykalpha.-(4-chlorophenyl)-1 H-1 ,2,4-triazole-1-propanenitrile]
Nabam
Naled
*******
Nitropyrki (2-Chtoro-6-(trich!oromethyl) pyridine)
Nitrate ton
*******
Nitric oxkte
• * * * * * *
p-NitroanilifiQ
*******
NHrogen dfoxida
*******
Norflurazonf4-CWorc-5-(rnethylarnino)-2-[3-(trinuororrtethyl)phenyl]-3(2H)-pyridazinone]
CAS No.
67485-29-4
35554-44-0
55406-53-6
36734-19-7
13463-40-6
465-73-6
25311-71-1
78-59-1
4098-71-9
77501-63-4
330-55-2
554-13-2
121-75-5
93-65-2
149-30-4
150-50-5
137-42-8
20354-26-1
2032-65-7
94-74-6
3653-48-3
5124-30-1
6317-18-6
556-61-6
75-86-5
924-42-5
298-00-0
872-50-4
75-79-6
9006-42-2
21087-64-5
7786-34-7
2212-67-1
150-68-5
88671-89-0
142-59-6
300-76-5
1929-82-4
14797-55-8
10102-43-9
100-01-6
10102-44-0
27314-13-2
Effective
Date
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
•1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
-------
Federal Register / Vol. 59, No. 8 / Wednesday, January 12, 1994 / Proposed Rules 1851
Chemical Name
*******
Oryzalin [4-(Dipropylamino)-3,5-dinitrobenzenesulfonamide]
* * * * * * *
Oxydemeton methyl [S-(2-(ethylsulfinyl)ethyl) o,o-dimethyl ester phosphorothioic acid]
Oxydiazon[3-[2,4-Dichloro-5-(1-methylethoxy)phenyl]-5-(1,1-dimethylethyl)-1,3,4-oxadiazol-2(3H)-one]
Oxyfluorfen
Ozone
Paraquat dichloride
*******
Pebulate [Butylethylcarbamothioic acid S-propyl ester]
Pendimethalin [N-(1-Ethylpropyl)-3,4-dimethyi-2,6-dinitrobenzenamine]
*******
Pentobarbital sodium
*******
Perchloromethyl mercaptan
Permethrin [3-(2,2-Dichloroethenyl)-2,2-dimethylcyclopropanecarboxylic acid, (S-phenoxyphenyl)methyl
ester]
Phenanthrene
*******
Phenothrin [2,2-Dimethyl-3-(2-methyl-1 -propenyl)cyclopropanecarboxylic acid (3-phenoxyphenyl)methyl
ester]
1 ,2-Phenylenediamine
1 ,3-Phenylenediamine
1 ,2-Phenylenediamine dihydrochloride
1 ,4-Phenylenediamine dihydrochloride
*******
Phenytoin
*******
Phosphine
*******
Phosphorous oxychloride
Phosphorous pentachloride
Phosphorous pentasulfide
Phosphorous pentoxide
* * * * * * *
Picloram
* * * * * * *
Piperonyl butoxide
Pirimiphos methyl [O-(2-(Diethylamino)-6-methyl-4-pyrimidinyl)-O,O-dimethylphosphorothioate]
*******
Potassium bromate
Potassium dimethyldithiocarbamate
Potassium N-methyldithiocarbamate
Primisulfuron [Methyl 2-[[[[[4,6-bis(difluoromethoxy)-2-pyrimidinyl]- amino]carbonyl]amino]sulfonyl]benzoate]
Profenofos [O-(4-Bromo-2-chlorophenyl)-O-ethyl-S-propylphosphorothioate]
Prometryn [N.N'-Bisfl-methylethylJ-e-methylthio-l ,3,5-tnazine-2,4- diamine]
Propachlor [2-Chloro-N-(1 -methylethyl)-N-phenylacetamide]
*******
Propanil [N-(3,4-Dichlorophenyl)propanamide]
Propargite
Propargyl alcohol
Propetamphos [3-[[(Ethylamino)methoxyphosphinothioyl]oxy]-2-butenoic acid, 1-methylethyl ester]
Propiconazole [1 -[2-(2,4-Dichlorophenyl)-4-propyl-1 ,3-dioxolan-2-yl]- methyl-1 H-1 ,2,4,-triazole]
*******
Quizalofop-ethyl [2-[4-[(6-Chloro-2-quinoxalinyl)oxy]phenoxy]propanoic acid ethyl ester]
Resmethrin [[5-(Phenylmethyl)-3-furanyl]methyl 2,2-dimethyl-3-(2-methyl-1 -prc-
penyl)cyclopropanecarboxylate]]
* * * * * - * *
Sethoxydim [2-[1 -(Ethoxyimino)butyl]-5-[2-(ethylthio)propyl]-3-hydroxy-2-cyclohexen-1 -one]
* * * * * . * *
Simazine
Sodium azide
Sodium chlorite
Sodium dicamba [3,6-Dichloro-2-methoxybenzoic acid, sodium salt]
Sodium dimethyldithiocarbamate
Sodium fluoroacetate
CAS No.
19044-88-3
301-12-2
19666-30-9
42874-03-3
10028-15-6
1910^2-5
1114-71-2
40487-42-1
57-33-0
594-42-3
52645-53-1
85-01-8
26002-80-2
95-54-5
108-45-2
615-28-1
624-18-0
57-41-0
7803-51-2
10025-87-3
10026-13-8
1314-80-3
1314-56-3
1918-02-1
51-03-6
29232-93-7
7758-01-2
128-03-0
137-41-7
86209-51-0
41198-08-7
7287-19-6
1918-16-7
709-98-8
2312-35-8
107-19-7
31218-83-4
60207-90-1
76578-14-8
10453-86-8
74051-80-2
122-34-9
26628-22-8
7758-19-2
1982-69-0
128-04-1
62-74-8
Effective
Date
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
-------
1852
Federal Register / Vol. 59, No. 8 / Wednesday, January 12, 1994 / Proposed Rules
Chemical Name
Sodium hypochlorite
Sodium nitrite
Sodium pentachtorophenate
Sodium c-phenylphenoxide
Sodium 2-pyrldmetriiol-1 -oxide
*******
Sulfur dioxide
*******
Sulfur trioxida
Sulfuryt fluoride [Vtkane]
Sulpfcfos [O-Ethyl O-[4-(methylthio)phenyl]phosphorodithioic acid S-propyl ester]
Tebuthiuron [N-[5-(1 ,1-Dimethylethyi)-1 ,3,4-thiadiazol-2-yl)-N,N'-dimethylurea]
Tenuthrin
Temephos
TerbacU [5-Chtoro-3-(1 ,1-dimethylethyl)-6-methyl-2,4(1 H,3H)-pyrimidinedione]
*******
1 .1 ,1 ,2-Tetrachloro-2-fiuoroelhane (HCFC-1 21 a)
1 ,1 .2,2-Tetrachloro-1 -fluoroethane (HCFC-1 21 )
*******
Tetracycline hydrochloride
Tetramelhrin [2,2-Dirnethyl-3-(2-methyl-1-propenyl)cyclopropanecarboxylic acid (1 ,3,4,5,6,7-hexahydro-1 ,3-
d?oxo-2H-lsoindol-2-yl)methyl ester]
Tetrasodium cthylenediaminetetraacetate
*******
Thiabendazole [2-(4-Thiazolyl)-1H-benzimidazole]
Thiabendazole, hypophosphite salt [2-(4-Thiazolyl)benzimidazole, hypophosphite salt]
*******
Thiobencarb [Carbamic acid, diethylthio-, s-(p-chlorobenzyl)]
*******
TOodicarb
Trriophanate ethyl 111 ^-Phenylenebis(iminocarbonothioyl)]biscarbamic acid diethyl ester]
ThJophanate-methyl
Thtosemicarbazida
*******
Trtadimefon [1-(4-Chlorophenoxy)-3,3-dirnethyl-1 -(1 H-1 ,2,4-triazol-1 -yl)-2-butanone]
Triallate
*******
Tribenuron methyl [2-{((((4-Methoxy-6-methyl-1 ,3,5-triazin-2-yl)- methylamino)carbonyl)amino)sulfonyl)-,
methyl ester]
Tributymn fluoride
Tributyttin methacrylate
S.S.S-Tributyltrithfophosphate (DEF)
*******
Trtehtoroacetyl chloride
*******
TrJchloroethylsWane
*******
TricWorophenylsilane
1 A3-Trichloropropane
Trictopyr, triethylammonium salt
Triethylamine
Triforine [N,N'-[1 ,4-Piperazinediyl-bis(2,2,2-trichloroethylidene)] bisformamide]
*******
Trimelhylchlorosaane
2,3,5-Tnmethytohenyl methylcarbamate
Triphenyttin chforide
Tr^>henyrtin hydroxide.
*******
Vanadium pentoxide
Vinclozolin [3-{3.5-Oichlorophenyl)-5-ethenyl-5-methyl-2,4- oxazolidinedione]
*******
CAS No.
7681-52-9
7632-00-0
131-52-2
132-27-4
15922-78-8
7446-09-5
7446-11-9
2699-79-8
35400-43-2
34014-18-1
79538-32-2
3383-96-8
5902-51-2
354-11-0
354-14-3
64-75-5
7696-12-0
64-02-8
148-79-8
28558-32-9
28249-77-6
59669-26-0
23564-06-9
23564-05-8
79-19-6
43121-43-3
2303-17-5
101200-48-0
1983-10-4
2155-70-6
78-48-8
76-02-8
115-21-9
98-13-5
96-18-4
57213-69-1
121-44-8
26644-46-2
75-77-4
2655-15-4
639-58-7
76-87-9
1314-62-1
50471-44-8
Effective
Date
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
(b)
* * *
-------
Federal Register / Vol. 59, No. 8 / Wednesday, January 12, 1994 / Proposed Rules
1853
CAS No.
51-03-6
51-21-8
52-51-7
52-85-7
55-38-9
56-35-9
57-33-0
57-41-0
60-51-5
62-74-8
64-02-8
64-75-5
68-12-2
75-43-4
75-72-9
75-77-4
75-78-5
75-79-6
75-86-5
75-88-7
76-02-8
76-06-2
76-87-9
77-73-6
78-48-8
78-59-1
79-19-6
85-01-8
88-85-7
93-65-2
94-11-1
94-74-6
94-80^1
94-82-6
95-54-5
Chemical Name
*****
Piperonyl butoxide
Fluorouracil (5-Fluorouracil)
*****
2-Bromo-2-nitropropane-1 ,3-diol (Bronopol)
*****
Famphur
*****
Fenthion [O,O-Dimethyl O-[3-methyl-4-(methylthio)phenyl] ester,
*****
Bis(tributyltin) oxide
*****
Pentobarbital sodium
Phenytoin
*****
Dimethoate
*****
Sodium fluoroacetate
*****
Tetrasodium ethylenediaminetetraacetate
*****
Tetracycline hydrochloride
*****
N,N-Dimethylformamide
*****
Dichlorofluoromethane (HCFC-21)
*****
Chlorotrifluoromethane (CFC-13)
Trimethylchlorosilane
Dimethyldichlorosilane
Methyltrichlorosilane
2-Methyllactonitrile
2-Chloro-1 ,1 ,1 -trifluoroethane (HCFC-1 33a)
Trichloroacetyl chloride
Chloropicrin
*****
Triphenyltin hydroxide
*****
Dicyclopentadiene
*****
S,S,S-Tributyltrithiophosphate (DEF)
Isophorone
*****
Thiosemicarbazide
*****
Phenanthrene
*****
Dinoseb
*****
Mecoprop
2,4-D isopropyl ester
*****
Methoxone (4-Chlorc-2-methylphenoxy) acetic acid (MCPA)
*****
2,4-D butyl ester
2,4-DB
* * * * ' *
1 ,2-Phenylenediamine
* *
* *
* *
* *
phosphorothioic acid]
* *
* *
* *
* *
* *
* *
* *
* *
* *
* *
* *
* ••*
* *
* *
* *
* *
* *
* *
Effective
Date
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
-------
1854
Federal Register / Vol. 59, No. 8 / Wednesday, January 12, 1994 / Proposed Rules
CAS No.
95-69-2
96-18-4
97-23-4
98-13-5
99-30-9
100-01-6
101-05-3
101-90-6
104-12-1
105-60-2
106-47-8
107-11-9
107-19-7
108-45-2
108-93-0
110-54-3
110-57-6
115-21-9
115-28-6
116-06-3
120-32-1
120-36-5
121-44-8
121-75-5
122-34-9
122-39-4
124-40-3
128-03-0
128-04-1
131-52-2
132-27-4
133-07-3
Chemical Name
*****
p-Chloro-c-toluidine
*****
1 ,2,3-Trichloropropane
*****
DJchlorophene [ 2,2'-MethyIene-bis(4-chlorophenol)j
*****
Trlchlorophenylsitane
*****
Dichloran [2,&Dichloro-4-nitroaniIine]
*****
p-Nttroaniline
*****
Anilazine [4,6-dichloro-N-(2-chlorophenyl)-1 ,3,5-triazin-2-amine]
*****
Dkjlycidyl resorcinol ether
*****
p-Chlorophenyl isocyanate
*****
Caprolactam
*****
p-Chloroaniline
*****
Allylamine
*****
Propargyl alcohol
*****
1 ,3-Phenylenediamine
*****
Cyctohexanol
*****
n-Hexane
trans-1 ,4-Dichloro-2-butene
*****
Trichloroethylsilane
Chlorendic acid
*****
Aldtearb
*****
o-Benzyl-p-chlorophenol
2,4-DP
*****
Triethylamine
*****
Malathion
Slmazine
Diphenylamine
*****
Dimethylamine
*****
Potassium dimethyldithiocarbamate
Sodium dimethyldithiocarbamate
*****
Sodium pentachlorophenate
Sodium o-phenylphenoxide
*****
Folpet
* *
* *
* *.
* *
* *
* *
* *
* *
* *
* *
* *
* *
* ' *
* *
* *
* *
* *
* *
* *
* *
* *
* *
* *
* *
* *
Effective
Date
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
-------
Federal Register / Vol. 59, No. 8 / Wednesday, January 12, 1994 / Proposed Rules 1855
CAS No.
136-45-8
137-41-7
137-42-8
138-93-2
142-59-6
148-79-8
149-30-4
149-74-6
150-50-5
150-68-5
298-00-0
300-76-5
301-12-2
314-40-9
319-84-6
330-54-1
330-55-2
333-41-5
354-11-0
354-14-3
357-57-3
422-44-6
422-48-0
422-56-0
431-86-7
460-35-5
465-73-6
507-55-i
533-74-4
541-53-7
542-76-7
554-13-2
556-61-6
563-47-3
576-26-1
594-42-3
612-82-8
612-83-9
615-28-1
624-18-0
630-08-0
639-58-7
709-98-8
759-94-4
Chemical Name
*******
Dipropyl isocinchomeronate
Potassium n-methyldithiocarbamate
Metham Sodium
Disodium cyanodithioimidocarbonate
* * * * * * *
Nabam
Thiabendazole [2-(4-Thiazolyl)-1 H-benzimidazole]
2-Mercaptobenzothiazole
Dichloromethylphenylsilane
Merphos
Monuron
*******
Methyl parathion
Naled
Oxydemeton methyl [s-(2-(Ethylsulfinyl)ethyl)o,o-dimethyl ester phosphorothioic acid]
*******
Bromacil (5-Bromc-6-methyl-3-(1-methylpropyl)-2,4-(1H,3H)-pyrimidinedione)
alpha-Hexachlorocyclohexane
Diuron
Linuron
Diazinon
* * * - * * * *
1 ,1 ,1 ,2-Tetrachlorc-2-fluoroethane (HCFC-1 21 a)
1,1,2,2-Tetrachloro-1-fluoroethane(HCFC-121)
Brucine
1 ,2-dichloro-1 ,1 ,2,3,3-pentafluoropropane (HCFC-225bb
2,3-dichloro-1 ,1 ,1 ,2,3-pentafluoropropane (HCFC-225ba
3,3-dichloro-1 ,1 ,1 ,2,2-pentafluoropropane (HCFC-225ca
1 ,2-dichloro-1 ,1 ,3,3,3-pentafluoropropane (HCFC-225da
3-chloro-1 ,1 ,1-trifluoropropane (HCFC-253fb)
*******
Isodrin
*******
1 ,3-dichloro-1 ,1 ,2,2,3-pentafluoropropane (HCFC-225cb)
*******
Dazomet (Tetrahydro-3,5-dimethyl-2H-1 ,3,5-thiadiazine-2-thione)
*******
2,4-Dithiobiuret
*******
3-Chloropropionitrile
*******
Lithium carbonate
Methyl isothiocyanate [Isothiocyanatomethane]
3-Chloro-2-metnyl-1 -propene
*******
2,6-Dimethylphenol
* * * * * * *
Perchloromethyl mercaptan
*******
3,3'-Dimethylbenzidine dihydrochloride (o-Tolidine dihydrochloride)
3,3'-Dichlorobenzidine dihydrochloride
*******
1 ,2-Phenylenediamine dihydrochloride
* * * * * * *
1 ,4-Phenylenediamine dihydrochloride
*******
Carbon monoxide
*******
Triphenyltin chloride
*******
Propanil [N-(3,4-Dichlorophenyl)propanamide]
* * * * * * *
Ethyl dipropylthiocarbamate (EPIC)
Effective
. Date
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
-------
1856
Federal Register / Vol. 59, No. 8 / Wednesday, January 12, 1994 / Proposed Rules
CAS No.
822-60-0
834-12-8
872-50-4
924-42-5
957-51-7
1114-71-2
1134-23-2
1314-56-3
1314-62-1
1314-80-3
1320-18-9
1563-86-2
1649-08-7
1689-84-5
1689-99-2
1881-40-1
1910-42-S
1912-24-9
1917-97-1
1918-00-9
1918-02-1
1918-16-7
1928-43-4
1929-73-3
1929-82-4
1982-69-0
1983-10-4
2008-41-5
2032-65-7
2155-70-6
2164-07-0
2212-67-1
2300-66-5
2303-17-5
2312-35-8
2439-01-2
2439-103
2524-03-0
2655-15-4
2699-79-8
2702-72-9
2971-38-2
3380-34-5
3383-96-8
3653-48-3
4080-31-3
4098-71-9
4170-30-3
5124-30-1
Chemical Name
Hexamethylene-1,6-diisocyanate .
Ametryn (N-Ethyl-N'-(1 -methylethyl)-6-(methylthio)-1 ,3,5.-triazine-2,4-diamine)
N-MethyI-2-pyrrolidone
******
N-Methylolacrylamide
Diphenamid
******
Pebulate [Butylethylcarbamo-thioic acid S-propyl ester]
******
Cycloate
******
Phosphorous pentoxide
Vanadium pentoxide
Phosphorous pentasulfide
* * * * * *
2,4-D propylene glycol butyl ether ester
******
Carbofuran
1 ,2-dtehloro-1 ,1 -difluoroethane (HCFC-1 32b)
Bromoxynil (3,5-Dibromo-4-hydroxybenzonitrile)
Bromoxynil octanoate (Octanoic acid, 2,6-dibromo-4-cyanophenyl ester)
******
Benfluralin(N-Butyl-N-ethyl-2,6-dinitro-4-(trifluoromethyl)benzenamine)
******
Paraquat dichloride
Atrazlne (6-Chlofo-N-ethyl-N'-(1 -methylethyl)-1 ,3,5,-triazine-2,4-diamine)
2,4-D 2-octyl ester
Dicamba (3,6-Dichloro-2-methyoxybenzoic acid)
Ptetoram
Propachlor[2-Chloro-N-{1-methylethyl)-N-phenylacetamide]
2,4-D 2-ethylhexyl ester
2,4-D butoxyethyl ester
Nitrapyrin (2-Chloro-6-(trichloromethyl)pyridine)
******
Sodium dicamba [3,6-Dichloro-2-methoxybenzoic acid, sodium salt]
Tributyltin fluoride
Butylate (Bis-2-methylpropyl) carbamothioic acid S-ethyl ester)
Methiocarb
Tributyltin methacrylate
Dipotassium endothall [7-Oxabicyclo(2.2.1)heptane-2,3-dicarboxylic acid,
******
Molinate (1H-Azepine-1-carbothioic acid, hexahydro-S-ethyl ester)
* * * * * *
Dimethylamine dicamba
******
Triallate
Propargite
Chinomethionat [6-Methyl-1 ,3-dithiolo[4,5-b]quinoxalin-2-one]
Dodine [Dodecylguanidine monoacetate]
Dimethyl chlorothiophosphate
******
2,3.5-Trimethylphenyl methylcarbamate
Sulfuryl Fluonde [Vikane]
2,4-D sodium salt
******
2,4-D chlorocrotyl ester
*
*
*
*
*
*
*
*
dipotassium salt]
*
*
*
*
*
*******
5-Chloro-2-(2,4-dichlorophenoxy)phenol
Temephos
Methoxone - sodium salt (4-Chloro-2-methylphenoxy acetate sodium salt)
******
1 -(3-Chloroallyl)-3,5,7-triaza-1 -azoniaadamantane chloride
Isophorone diisocyanate
Crotonaldehyde
******
1 ,1'-Methylene bis(4-isocyanatocyclohexane)
*
*
Effective
Date
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
-------
Federal Register / Vol. 59, No. 8 / Wednesday, January 12, 1994 / Proposed Rules
1857
CAS No.
5234-68-4
5598-13-0
5902-51-2
6317-18-6
6459-94-5
7287-19-6
7446-09-5
7446-11-9
7632-00-0
7637-07-2
7681-52-9
7696-12-0
7726-95-6
7758-01-2
7758-19-2
7778-54-3
7782-41-4
7786-34-7
7803-51-2
9006-42-2
10025-87-3
10026-13-8
10028-15-6
10061-02-6
10222-01-2
10102-43-9
10102-44-0
10294-34-5
10453-86-8
13194-48-4
13356-08-6
13463-40-6
13474-88-9
13684-56-5
14484-64-1
14797-55-8
15922-78-8
15972-60-8
17804-35-2
19044-88-3
19666-30-9
20325-40-0
20354-26-1
20859-73-8
21087-64-9
21725-46-2
22781-23-3
23564-05-8 •
23564-06-9
25013-16-5
25311-71-1
26002-80-2
26628-22-8
26644-46-2
27314-13-2
Chemical Name
Carboxin (5,6-Dihydro-2-methyl-N-phenyl-1 ,4-oxathiin-3-carboxamide)
Chlorpyrifos methyl [O,O-dimethyl-O-(3,5,6-trichloro-2-pyridyl)phosphorothioate]
Terbacil [5-Chlorc-3-(1 ,1-dimethylethyl)-6-methyl-2,4-(1 H,3H)-pyrimidinedione]
Methylene bis(thiocyanate)
C.I. Acid Red 114
*******
Prometryn [N,N'-Bis(1-methylethyl)-6-methylthio-1,3,5-triazine-2,4-diamine]
*******
Sulfur dioxide
Sulfur trioxide
*******
Sodium nitrite
Boron trifluoride
*******
Sodium hypochlorite
Tetramethrin [2,2-Dimethyl-3-(2-methyl-1 -propeny IJcyclopropane-carboxylic acid (1 ,3,4,5,6,7-hexahydro-1 ,3-
dioxo-2H-isoindol-2-yl) methyl ester]
*******
Bromine
Potassium bromate
Sodium chlorite
Calcium hypochlorite
Fluorine
*******
Mevinphos
Phosphine
*******
Metiram
Phosphorous oxychloride
Phosphorous pentachloride
Ozone
* * * - * * * *
trans-1 ,3-Dichloropropene
2,2-Dibromo-3-nitrilopropionamide
Nitric oxide
Nitrogen dioxide
Boron trichloride
Resmethrin [[5-(Phenylmethyl)-3-furanyl]methyl 2,2-dimethyl-3-(2-methyl-1 -pro-
penyl)cyclopropanecarboxylate]]
*******
Ethoprop [Phosphorodithioic acid O-ethyl S,S-dipropyl ester]
Fenbutatin oxide (hexakis(2-methyl-2-phenylpropyl)distannoxane)
Iron pentacarbonyl
1 ,1-Dichloro-1 ,2,2,3,3-pentafluoropropane (HCFC-225cc)
Desmedipham
Ferbam [Trisfdimethylcarbamo-dithioato-S.S'Jiron]
Nitrate ion '
Sodium 2-pyridinethiol-1 -oxide
Alachlor
*******
Benomyl
Oryzalin [4-(Dipropylamino)-3,5-dinitrobenzene-sulfonamide]
Oxydiazon [3-[2,4-Dichlorc-5-(1-rnethylethoxy)phenyl]-5-(1 ,1-dimethylethyl)-1 ,3,4-oxadiazol-2(3H)-one]
3,3 -Dimethoxybenzidine dihydrochloride (Dianisidine dihydrochloride)
Methazole [2-(3,4-Dichlorophenyl)-4-methyI-1,2,4-oxadiazolidine-3,5-dione]
*******
Aluminum phosphide
Metribuzin
Cyanazine
Bendiocarb [2,2-Dimethyl-1,3-benzodioxol-4-ol methylcarbamate]
Thiophanate methyl
Thiophanate ethyl [[1 ,2-Phenylenebis(iminocarbonothioyl)]biscarbamic acid diethyl ester]
Butylated hydroxyanisole
Isofenphos [2-[[EthoxylI(1-methylethyl)amino]phosphinothioyl]oxy]benzoic acid 1-methylethyl ester]
Phenothrin [2,2-Dimethyl-3-(2-rnethyl-1-propenyl)cyclopropanecarboxylic acid (3-phenoxyphenyl)methyl
ester]
*******
Sodium azide
Triforine [N,N'-[1 ,4-Piperazinediylbis(2,2,2-trichloroethylidene)] bisformamide]
Norflurazon[4-Chloro-5-{methylamino)-2-[3-(trifluoromethyl)phenyl]-3(2H)-pyridazinone]
Effective
Date
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
-------
1858 Federal Register / Vol. 59, No. 8 / Wednesday, January 12, 1994 / Proposed Rules
CAS No.
28057-48-9
28249-77-6
28407-37-6
28558-32-9
29232-93-7
30560-19-1
31218-83-4
33089-61-1
34014-18-1
35367-38-5
35400-43-2
35554-44-0
35691-65-7
36734-19-7
38727-55-8
39300-45-3
39515-41-8
40487-42-1
41198-08-7
41766-75-0
42874-03-3
43121-43-3
50471-44-8
51235-04-2
51338-27-3
51630-58-1
52645-53-1
53404-19-6
53404-37-8
53404-60-7
55290-64-7
55406-53-6
57213-69-1
59669-26-0
60168-88-9
60207-90-1
62476-59-9
62924-70-3
64902-72-3
64969-34-2
66215-27-8
66441-23-4
67485-29-4
68085-85-8
68359-37-S
69409-94-5
69806-50-4
71751-41-2
72178-02-0
72490-01-8
74051-80-2
76578-14-8
77501-83-4
79538-32-2
81777-89-1
82657-04-3
86209-51-0
88671-89-0
90982-32-4
97886-45-8
101200-48-0
111512-56-2
111984-09-9
127564-92-5
128903-21-9
136013-79-1
Chemical Name
d-trans-AIIethrin [d-trans-Chrysanthemic acid of d-allethrone]
Thiobencarb [Carbamic acid, diethylthio-, s-(p-chlorobenzyl)]
C.I. Direct Blue 21 8
Thiabendazole, hypophosphite salt [2-{4-Thiazolyl)benzimidazole, hypophosphite salt]
Pirimiphos methyl [O-{2-(Diethylamino)-6-methyl-4-pyrimidinyl)-O,O-dimethyl phosphorothioate]
Acephate (Acetylphosphoramidothioic acid O.S-dimethyl ester)
Propetamphos [3-[[(Ethylamino)methoxyphosphino-thioyl]oxy]-2-butenoicacid, 1-methylethyl ester]
Amitraz
Terbuthiuron [N-[5-(1 ,1-Dimethylethyl)-1 ,3,4-thiadiazol-2-yl)-N,N'- dimethylurea]
Difiubenzuron
Sulprofos [O-Ethyl O-[4-(methylthio)phenyl]phosphorodithioic acid S-propyl ester]
Imazalil [1 -[2-(2.4-Dichlorophenyl)-2-(2-propenyloxy)ethyl]-1 H-imidazole]
1 -Bromo-1 -(bromomethyl)-! ,3-propanedicarbonitrile
Iprodione [3-{3,5-Dichlorophenyl)-N-(1 -methylethyl)-2,4-dioxo-1 -imidazolidine-carboxamide]
Diethatyl ethyl
*******
Oinocap
Fenpropathrin [2,2,3,3-Tetramethylcyclopropane carboxylic acid cyano(3-phenoxyphenyl)methyl ester]
Pendimethalin [N-(1 -Ethylpropyl)-3,4-dimethyl-2,6-dinitrobenzen-amine]
Profenofos[O-(4-Bromo-2-chlorophenyl)-O-etlwl-S-propyl phosphorothioate]
3.3'-Dimethylbenzidine dihydrofluoride (ortho-folidine dinydrofluoride)
Oxyfluorfen
Triadimefon[1-(4-Chlorophenoxy)-3.3-dimethyl-1-(1H-1,2,4-triazol-1-yl)-2-butanone]
VinclozoIin[3-(3,5-Dichlorophenyl)-5-ethenyl-5-methyl-2,4-oxazolidinedione]
Hexazinone '
Diclofop methyl [2-[4-(2,4-Dichlorophenoxy)phenoxy]propanoic acid, methyl ester]
Fenvalerate
Permethrin [3-(2,2-Dichloroethenyl)-2,2-dimethylcyclopropanecarboxylic acid, (3-phenoxyphenyl)methyl
ester]
Bromacil, lithium salt [2,4-(1H,3H)-Pyrimidinedione, 5-bromc-6-methyl-3- (1-methylpropyl), lithium salt]
2,4-D 2-ethyI-4-methylpentyI ester
Dazomet, sodium salt [Tetrahydro-3,5-dimethyl-2H-1,3,5-thiadiazine-2-thione, ion(1-), sodium]
Dimethipin [2.3,-Dihydro-5.6-dimethyl-1 ,4-dithiin 1 ,1 ,4,4-tetraoxide]
3-lodo-2-propynyl butylcarbamate
Trtelopyr, triethylammonium salt
Thiodicarb
Fenarimol [.alpha.-(2-Chlorophenyl)-.alpha.-4-chlorophenyl)-5-pyrimidine- methanol]
Propiconazole [1 -F2-(2,4-Dichlorophenyl)-4-propyl-1 ,3-dioxolan-2-yl]-methyl-1 H-1 ,2,4,-triazole]
Acifluorfen. sodium salt [5-(2-Chloro-4-(triflouromethyl)phenoxy)-2-nitro-benzoic acid, sodium salt]
Flumetralin [2-Chloro-N-(2,6-dinitro-4-(trifluoromethyl)-phenyl)-N-ethyl-6-fluorobenzenemethanamine]
Chlorsulfuron [2-chloro-N-[[4-methoxy-6-methyl-1,3,5-triazin-2-yl)amino] carbonyl]benzenesulfonamide]
3,3-Dichlorobenzidine.sulfate
Cyromazine [N-CyclopropyH ,3,5-triazine-2,4,6-triamine]
Fenoxaprop ethyl [2-(4-((6-Chloro-2-benzoxazolylen)oxy)phenoxy) propanoic acid, ethyl ester]
Hydramethylnon |Tetrahydro-5,5-dimethyl-2(1 H)-pynmidinone[3-[4- (trifluoromethyl)phenyl]-1-[2-[4-
(trifluoromethyl)phenyl]ethenyl]-2-propenylidene]hydrazone]
Cyhalothrin [3-(2-Chloro-3,3,3-trifluoro-1-propenyl)-2,2- dimethylcyclopropanecarboxylic acid cyano(3-
pnenoxyphenyl)methyl ester]
Cytluthrin [3-(2,2-Dichloro-ethenyl)-2,2-dimethylcyclo-propanecarboxylic acid, cyano(4-fluoro-3-
phenoxyphenyljmethyl ester]
Fluvalinate [N-[2-Chloro-4-(trifluoromethyl)phenyl]-DL-valine(+)-cyano(3-phenoxyphenyl)methylester]
Fluazifop-butyl [2-[4-[[5-(Trifluoromethyl)-2-pyridinyOoxy]-phenoxy]propanoic acid, butyl ester]
Abamectin [Avermectin B1]
Fomesafen [5-{2-Chloro-4-(trinuoromethyl)phenoxy)-N-methylsulfonyl)-2-nitrobenzamide]
Fenoxycarb [2-(4-Phenoxyphenoxy)ethyl]carbamic acid ethyl ester]
Sethoxydim [2-[1 -(Ethoxyimino)butyl]-5-[2-(ethylthio)propyl]-3-hydroxy-2-cyclohexen-1 -one]
Quizalofop-ethyl [2-[4-[(6-Chloro-2-quinoxalinyl)oxy]phenoxy] propanoic acid ethyl ester]
Lactofen [5-(2-Chloro-4-(trifluoromethyl)phenoxy)-2-nitro-2-ethoxy-1 -methyl-2-oxoethyl ester]
Tefluthrin
Clomazone [2-[(2-Chlorophenyl)methyl]-4,4-dimethyl-3-isoxazolidinone]
Bifenthrin
Primisulfuron [Methyl 2-[[[[[4,6-bis(difluoromethoxy)-2-pyrimidinyl]-amino]carbonyl]amino]sulfonyl]benzoate]
Myclobutanil [.alpha.-Butykalpha.-(4-chlorophenyl)-1 H-1 ,2,4-triazole- 1 -propanenitrile]
Cntorimuron ethyl [Ethyl-2-[[[(4-chloro-6-methoxyprimidin-2-yl)-carbonyO-amino]sulfonyl]benzoate]
Dithiopyr [2-(Dmuoromethyl)-4-(2-methylpropyl)-6-(trifluoro-methyl)-3,5-pyridinedicartx)thioic acid S,S-di-
Trftienuron methyl [2-(((((4-Methoxy-6-methyl-1 ,3,5-triazin-2-yl)- methylamino)carbonyl)amino)sulfonyl)-,
methyl ester]
1 ,1-dichloro-1 ,2,3,3,3-pentafluoropropane (HCFC-225eb)
S.S'-Dlmethoxybenzidine hydrochloride (Dianisidine dihydrochloride)
Dichloropentafluoropropane
2^2-Dichlorc-1 ,1,1 ,3,3-pentafluoropropane (HCFC-225aa)
1 ,3-Dichloro-1 ,1 ,2,3,3-pentafluoropropane (HCFC-225ea)
Effective
Date
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
4 /H me
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
H /H /QC
i/i/yo
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
• 1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
1/1/95
(c)
-------
Federal Register / Vol. 59, No. 8 / Wednesday, January 12, 1994 / Proposed Rules
1859
Category Name
Effective
Date
Chlorinated paraffins: Includes those chemicals defined by the following formula:
CxH2x-y+2Cly
where x = 10 to 30 and y = 3 to 26
*******
Man-made mineral fibers: Includes glass microfibers, glass wool fibers, rock wool fibers, slag wool fibers, and refractory ceramic
fibers that have a diameter less than 3.5 micrometers and an aspect ratio greater than 3.
*******
Nicotine and salts
*******
Polycyclic Aromatic Compounds (PACs): (This category includes only those chemicals listed below)
00056-55-3 Benz(a)anthracene
00218-01-9 Benzo(a)phenanthrene
00050-32-8 Benzo(a)pyrene
00205-99-2 Benzo(b)fluoranthene
00205-82-3 Benzo(j)fluoranthene
00207-08-9 Benzo(k)fluoranthene
00189-55-9 Benzo(rst)pentaphene
00086-74-8 Carbazole
27208-37-3 Cyclopenta(cd)pyrene
00226-36-8 Dibenz(a,h)acridine
00224-42-0 Dibenz(a,j)acridine
00215-58-7 Dibenz(a,c)anthracene
00224-41-9 D|benz(a,j)anthracene
00053-70-3 Dibenzo a,h)anthracene
1/1/95
1/1/95
1/1/95
1/1/95
05385-75-1 Dibenzo a,e
00192-65-4 Dibenzo a.e
fluoranthene
pyrene
00189-64-0 Dibenzo a,h pyrene
00191-30-0 Dibenzo a,l)pyrene
00194-59-2 7H-Dibenzo(c,g)carbazole
00057-97-6 7,12-Dimethylbenz(a)anthracene
00193-39-5 lndeno[1,2,3-cd]pyrene
03351-32-4 2-Methylchrysene
03351-31-3 3-Methylchrysene
03351-30-2 4-Methylchrysene
03697-24-3 5-Methylchrysene
01705-85-7 6-Methylchrysene
33543-31-6 2-Methylfluoranthene
05522-43-0 1-Nitropyrene
Strychnine and salts
1/1/95
[FR Doc. 94-753 Filed 1-11-94; 3:34 pm]
BILLING CODE 6560-60-F
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