[Federal Register Volume 59, Number 8 (Wednesday, January 12, 1994)]
[Unknown Section]
[Page 0]
From the Federal Register Online via the Government Publishing Office [www.gpo.gov]
[FR Doc No: 94-753]


[[Page Unknown]]

[Federal Register: January 12, 1994]


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Part IV





Environmental Protection Agency





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40 CFR Part 372




Addition of Certain Chemicals; Toxic Chemical Release Reporting; 
Community Right-to-Know; Proposed Rule
ENVIRONMENTAL PROTECTION AGENCY

40 CFR Part 372

[OPPTS-400082; FRL-4645-6]
RIN 2070-AC47

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

AGENCY: Environmental Protection Agency (EPA).

ACTION: Proposed rule.

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SUMMARY: EPA is proposing to add 313 chemicals and chemical categories 
to the list of toxic chemicals required to be reported on under section 
313 of the Emergency Planning and Community Right-to-Know Act of 1986 
and section 6607 of the Pollution Prevention Act of 1990. The proposed 
addition of these chemicals and chemical categories is based on their 
acute human health effects, carcinogenicity or other chronic human 
health effects, and/or their environmental effects. EPA believes that 
these chemicals and chemical categories meet the EPCRA section 
313(d)(2) criteria for addition to the list of toxic chemicals.

DATES: Written comment on this proposed rule must be received on or 
before April 12, 1994. The public meeting will take place on March 2, 
1994, at 1 p.m. and adjourn by 5 p.m.

ADDRESSES: Written comments should be submitted in triplicate to: OPPT 
Docket Clerk, TSCA Document Receipt Office (7407), Office of Pollution 
Prevention and Toxics, Environmental Protection Agency, Rm. E-G99, 401 
M St., SW., Washington, DC 20460. Comments containing information 
claimed as confidential must be clearly marked as confidential business 
information (CBI). If CBI is claimed, three additional sanitized copies 
must also be submitted. Nonconfidential versions of comments on this 
proposed rule will be placed in the rulemaking record and will be 
available for public inspection. Comments should include the docket 
control number for this proposal, OPPTS-400082. Unit VI. of this 
preamble contains additional information on submitting comments 
containing information claimed as CBI.
    The public meeting will be held at the: Environmental Protection 
Agency, Auditorium, Education Center, 401 M St., SW., Washington, DC.

FOR FURTHER INFORMATION CONTACT: Maria J. Doa, Emergency Planning and 
Community Right-to-Know Information Hotline, Environmental Protection 
Agency, Mail Stop 5101, 401 M St., SW., Washington, DC 20460, Toll 
free: 800-535-0202 or Toll free TDD: 800-553-7672, Attention: Docket 
Number OPPTS-400082.

SUPPLEMENTARY INFORMATION:

I. Introduction

A. Statutory Authority

    This proposed rule is issued under sections 313(d) and (e)(1) of 
the Emergency Planning and Community Right-to-Know Act of 1986 (EPCRA), 
42 U.S.C. 11023. EPCRA is also referred to as Title III of the 
Superfund Amendments and Reauthorization Act of 1986.

B. Background

    Section 313 of EPCRA requires certain facilities manufacturing, 
processing, or otherwise using listed toxic chemicals to report their 
environmental releases of such chemicals annually. Beginning with the 
1991 reporting year, such facilities also must report pollution 
prevention and recycling data for such chemicals, pursuant to section 
6607 of the Pollution Prevention Act, 42 U.S.C. 13106. When enacted, 
section 313 established an initial list of toxic chemicals that was 
comprised of more than 300 chemicals and 20 chemical categories. 
Section 313(d) authorizes EPA to add chemicals to or delete chemicals 
from the list, and sets forth criteria for these actions. Under section 
313(e), any person may petition EPA to add chemicals to or delete 
chemicals from the list. EPA has added to and deleted chemicals from 
the original statutory list.
    EPA issued a statement of petition policy and guidance in the 
Federal Register of February 4, 1987 (52 FR 3479), to provide guidance 
regarding the recommended content and format for submitting petitions. 
EPA must respond to petitions within 180 days either by initiating a 
rulemaking or by publishing an explanation of why the petition is 
denied. On May 23, 1991 (56 FR 23703), EPA issued guidance regarding 
the recommended content of petitions to delete individual members of 
the section 313 metal compound categories.

II. Explanation for Expansion of the EPCRA Section 313 Chemical 
List

A. General Rationale

    The Toxics Release Inventory (TRI), through the public access 
provisions of EPCRA, has proven to be one of the most powerful forces 
in empowering the Federal government, State governments, industry, 
environmental groups, and the general public, to fully participate in 
an informed dialogue about the environmental impacts of toxic chemicals 
in the United States.
    A major section of EPCRA, which Congress passed in 1986, resulted 
in the creation of the Toxics Release Inventory. TRI is a publicly 
available data base that provides quantitative information on toxic 
chemical releases, transfers, recycling, and disposal. With the 
collection of this information for the first time in 1987, came the 
ability for the public, government, and the regulated community to 
understand the magnitude of chemical emissions in the United States; to 
compare chemical releases and transfers of chemical wastes among 
States, industries, facilities, and environmental media; and perhaps 
most importantly, to assess the need to reduce and where possible, 
eliminate these releases and transfers. TRI enables all interested in 
environmental progress to establish credible baselines, to set 
realistic goals, and to measure progress over time, in meeting those 
goals. The TRI system has become a neutral yardstick by which progress 
can be measured by all interested parties.
    The original list of chemicals for which reporting was required 
consisted of 320 chemicals and chemical categories. The list was a 
combination of the Maryland Chemical Inventory Report List of Toxic or 
Hazardous Substances and the New Jersey Environmental Hazardous 
Substance List. The combination of these two lists provided a sound and 
logical starting point for the national TRI program. Recognizing 
however that the list would need to be a dynamic one, EPCRA 
specifically authorizes additions to and deletions from the list. To 
date, EPA has added 16 chemicals to the list and has deleted 12 
chemicals from the list.
    With 5 years experience behind the program, EPA, other federal 
agencies, Congress, and the public have recognized the need to expand 
the TRI list beyond the original chemicals and chemical categories and 
beyond the relatively limited reporting universe. (Currently reporting 
is only required from facilities that fall within the manufacturing 
Standard Industrial Classification (SIC) codes 20 through 39 that meet 
certain thresholds).
    While the data on the chemicals that are covered have allowed the 
public and private sectors to be informed and involved in environmental 
decisionmaking as they never were before, it has become increasingly 
evident to those same constituents that they have access to information 
on a relatively small number of important chemicals. Congress has 
echoed this recognition in the Right-to-Know More bills that were put 
forward in the 102nd Congress. EPA and State regulatory agencies have 
integrated TRI information as a critical component in their 
environmental decisionmaking and in many cases are constrained by the 
lack of similar information on chemicals of concern not covered by the 
TRI. While the TRI has been successful in focusing attention on the 
initial list of chemicals and in many cases fostering emissions 
reductions and prevention activities, that same focus has highlighted 
the need to expand beyond that initial list and to include additional 
chemicals that exhibit similar toxicity characteristics. This proposal 
is one of the first in a series of actions that EPA plans to use to 
expand the coverage of the TRI. This first phase will focus on adding 
chemicals, followed by a second phase that will identify additional 
facilities for inclusion. EPA is considering a third phase, which would 
look at modification of the data elements currently required by TRI.
    In conjunction with these expansion activities EPA has been 
considering whether other adjustments are needed in the scope of the 
TRI program. EPA received petitions from the Small Business 
Administration and the American Feed Industry Association seeking an 
exemption for ``small sources'' (i.e, those facilities that file TRI 
forms with zero or small release estimates). EPA previously put those 
petitions out for public comment and, on review, believes there is 
substantial merit to the general concerns raised in the petitions.
    The Agency's plan for proceeding on the small source issue would 
include the following steps. EPA is examining four options for 
establishing a small release exemption from the TRI reporting 
obligation: Cutoffs at zero, 500 pounds, 1,000 pounds, and 5,000 
pounds. EPA will provide the public with a report on these four options 
by the end of January. This analysis will consider what data might not 
be available at both the national and community level, and the cost 
savings to the government and to industry of the four exemption levels. 
EPA plans to hold a public meeting in February for discussion of the 
report. Based on this feedback, EPA will then design a regulatory 
strategy that will align the small source issue with final action on 
today's proposal. The Agency's objective will be to minimize 
unnecessary data collection and reporting by facilities, including for 
the chemicals identified in today's proposal.

B. Development of the Chemical Addition Candidates

    As a starting point for screening candidates for addition to the 
toxic chemical list under EPCRA section 313, EPA chose to examine the 
lists of chemicals regulated or identified, as of concern, under 
various environmental statutes including: (1) Section 112(b) of the 
Clean Air Act (CAA) as amended in 1990 (Hazardous Air Pollutants); (2) 
section 602(b) of the CAA (Class II ozone depleting substances); (3) 
section 307(a) of the Clean Water Act (CWA) (Priority Pollutant List); 
(4) Federal Insecticide, Fungicide, and Rodenticide Act (FIFRA) Active 
Ingredients, including Special Review, Canceled/Denied or Suspended, 
and Restricted Use Pesticides; (5) section 302 of EPCRA (Extremely 
Hazardous Substances); (6) section 102 of the Comprehensive 
Environmental Response, Compensation, and Liability Act (CERCLA); (7) 
section 3001 of the Resource Conservation and Recovery Act (RCRA) and 
chemicals listed at 40 CFR 261.33(e) and (f) and Appendix VIII; (8) 
section 1412 of the Safe Drinking Water Act as amended; (9) certain 
chemicals subject to the Toxics Substance Control Act (Existing 
Chemicals); and (10) the State of California Safe Drinking Water and 
Toxic Enforcement Act of 1986 (Proposition 65) (List of Chemicals Known 
to the State to Cause Reproductive Toxicity).
    In addition, EPA considered chemicals designated as possible, 
probable, or known carcinogens in the Monographs of the International 
Agency for Research on Cancer (IARC) and the 6th Annual Report on 
Carcinogens of the National Toxicology Program (NTP), U.S. Department 
of Health and Human Services (DHHS).
    From this initial group of substances, EPA excluded chemicals that 
are already listed on section 313 or are already reportable under one 
of the EPCRA section 313 categories. For example, ``cyanide, total'' is 
listed under section 307(a) of the CWA. This listing is considered to 
be a subset of the EPCRA section 313 cyanide compounds category and the 
hydrogen cyanide listing. EPA decided not to propose listing these 
types of chemicals separately because they are already reportable under 
one of the existing section 313 categories. To prioritize chemicals for 
possible addition to EPCRA section 313, EPA applied a human health and 
ecotoxicity screen and a production volume screen, which are described 
below. The results of the toxicity screen for a subset of these 
chemicals were presented at a public meeting on May 29, 1992 (Ref. 4).
    Other chemicals were also removed from consideration for this 
rulemaking because they are the subjects of two recently published 
EPCRA petition responses. On March 4, 1992, EPA received a petition 
from Governor Mario M. Cuomo of New York and the Natural Resources 
Defense Council (NRDC) to add 80 chemicals and 2 chemical categories to 
the list of toxic chemicals under section 313 of EPCRA. All of these 
chemicals and chemical categories appear on the RCRA list of hazardous 
wastes under 40 CFR 261.33(f) and as such are a subset of the chemicals 
screened by EPA. EPA responded to the petition in a proposed rulemaking 
on September 8, 1992 (57 FR 41020) and in a final rule adding 22 
chemicals on November 30, 1993 (58 FR 63500).
    On December 3, 1991, EPA received a petition from the NRDC, Friends 
of the Earth, and the Environmental Defense Fund to add 
hydrochlorofluorocarbons (HCFCs) to the list of toxic chemicals under 
section 313 of EPCRA. The HCFCs are listed under section 602(b) of the 
CAA as Class II ozone depleting substances and as such are a subset of 
the chemicals screened by EPA. EPA responded to the petition in a 
proposed rulemaking on June 24, 1992 (57 FR 28159) and in a final rule 
adding 11 HCFCs on November 30, 1993 (58 FR 63496). An additional 16 
HCFCs not added to the TRI list by the November 30, 1993 final rule are 
proposed for addition in this rulemaking (See Unit IV.B.135. of this 
preamble).
    1. Toxicity screen. A toxicity screen is a limited review of 
readily available toxicity data (e.g., information in data bases and 
other secondary sources) that is used for a preliminary categorization 
of a chemical during the process of selecting candidates for possible 
listing under EPCRA section 313. The toxicity screen is used to 
identify chemicals for further consideration and does not reflect a 
final determination for listing a chemical under EPCRA section 313. 
Such a determination can only be made after a hazard assessment is 
conducted (See Unit II.B.3. of this preamble). The chemicals identified 
above were screened for four general effect categories: Acute human 
health effects, cancer, other chronic human health effects, and 
ecological effects.
    The screening criteria associated with each of the effect areas 
used in the toxicity screen are discussed in detail in the Revised 
Draft Hazard Assessment Guidelines for Listing Chemicals on the Toxic 
Release Inventory (Draft Hazard Assessment Guidelines), (Ref. 6). The 
numerical screening values reflected in the Draft Hazard Assessment 
Guidelines were developed to capture, in the ``sufficient for listing'' 
screening category, the majority of chemicals already listed on various 
CERCLA and EPCRA lists, and thus known or suspected to be toxic and/or 
hazardous. These Draft Hazard Assessment Guidelines contain guidance 
for both the screening and hazard assessments of chemicals and are 
available for review in the docket associated with this rulemaking. 
This draft document was distributed at a public meeting on May 29, 
1992. A final version of these guidelines has not yet been developed. 
Requests for further information about these draft guidelines should be 
addressed to the person identified under ``FOR FURTHER INFORMATION 
CONTACT.''
    Based on the results of this screen, the chemicals were 
preliminarily placed in one of three screening categories defined in 
the Draft Hazard Assessment Guidelines: ``sufficient;'' ``may be 
sufficient;'' or ``insufficient.'' EPA received comment in response to 
the Draft Hazard Assessment Guidelines that objected to the Agency's 
use of the terms ``sufficient,'' ``may be sufficient,'' and 
``insufficient'' as titles for the toxicity screening categories. The 
commenter claimed that these terms are appropriate only for the results 
of a hazard assessment. The commenter stated that these terms should 
not be used for screening categories because the toxicity screen only 
identifies chemicals for further consideration. EPA agrees that the 
screening categories only reflect a preliminary determination on each 
chemical, and therefore, to avoid further confusion, will refer to the 
screening categories as ``high priority,'' ``medium priority,'' and 
``low priority'' to reflect the difference between a toxicity screen 
and a hazard assessment. These terms will be used throughout this 
document in reference to the toxicity screening categories. Chemicals 
that were categorized as ``low priority'' during the screening process 
were not considered further as candidates for addition to the EPCRA 
section 313 list in this rulemaking.
    2. Production volume screen. EPCRA section 313(f) establishes 
reporting thresholds related to the amount of a chemical that is 
manufactured, processed, or otherwise used. [The EPCRA section 313 
manufacture (includes import) and processing thresholds are 25,000 
pounds per facility per year. The otherwise use threshold is 10,000 
pounds per facility per year]. EPA anticipates that the addition of 
chemicals manufactured, imported, processed, or used in quantities less 
than the EPCRA section 313 volume thresholds would not result in the 
submission of TRI reports. Thus, EPA elected to initially focus its 
attention on chemicals likely to yield reports. Accordingly, EPA also 
screened potential candidates for the likelihood of meeting the EPCRA 
section 313 volume thresholds. Chemicals for which there were no data 
to indicate that the chemical is likely to meet or exceed the EPCRA 
section 313 volume thresholds were not considered further as possible 
candidates for addition to the section 313 list at this time.
    Production volume data on each of the chemicals were gathered 
primarily from two sources: (1) The TSCA Chemical Update System (1990); 
and (2) the FIFRA Section 7 Tracking System. On June 12, 1986 (51 FR 
21438), EPA promulgated a rule pursuant to section 8(a) of TSCA which 
required manufacturers and importers to report every 4 years, subject 
to certain threshold production quantities and other exclusions, the 
quantities of chemicals they produced (40 CFR part 710). Among the 
exceptions to the inventory update rule (IUR) reporting were polymers, 
biological products, inorganic substances, and chemicals produced at 
less than 10,000 pounds, all with certain limitations. Data from the 
IUR is maintained in EPA's TSCA Chemical Update System (CUS).
    Section 7 of FIFRA provides the Agency with annual production 
information on registered pesticides. EPA regulations implementing 
FIFRA section 7 (40 CFR part 167) require all manufacturers of 
pesticidal products (which includes formulated pesticides, active 
ingredients, and devices) to submit an annual report detailing the 
amount of each type of pesticidal product manufactured, sold and 
distributed during the past year, and estimated to be manufactured, 
imported, and processed during the current year (40 CFR 167.85).
    For industrial inorganic compounds not subject to FIFRA or 
available on CUS, information from the public literature was used, 
supplemented with information from companies.
    3. Hazard evaluation. EPA conducted a hazard evaluation for each of 
the addition candidates that resulted from the above analyses and 
determined based on the weight-of-the evidence if there was sufficient 
evidence to establish that the candidate chemical met the statutory 
criteria for addition to EPCRA section 313. To make this determination, 
EPA senior scientists reviewed readily available toxicity information 
on each chemical for each of the following effect areas: acute human 
health effects; cancer; other chronic human effects; and environmental 
effects. In addition, EPA reviewed, where appropriate, information on 
the environmental fate of the chemical.
    The hazard assessment was conducted in accordance with relevant EPA 
guidelines for each adverse human health or environmental effect (e.g., 
the appropriate guidelines for hazard evaluation of chemical 
carcinogens and for the type of evidence required to substantiate a 
determination of carcinogenicity are the Guidelines for Carcinogen Risk 
Assessment (Ref. 2)). The guidelines that were used for each effect are 
Agency guidelines that are identified in the Draft Hazard Assessment 
Guidelines (Ref. 6). During this assessment the severity and 
significance of the effects induced by the chemical, the dose level 
causing the effect, and the quality and quantity of the available data, 
including the nature of the data (e.g., human epidemiological, 
laboratory animal, field or workplace studies) and confidence level in 
the existing data base, were all considered. Where a careful review of 
the scientific data for a particular chemical results in a high level 
of confidence that the chemical causes an adverse effect at relatively 
low dose levels, EPA believes that this evidence is sufficient for 
listing the chemical under section 313. On the other hand, where a 
review of the scientific data indicates that the chemical will cause 
various adverse effects at moderate dose levels, EPA believes, based on 
the total weight-of-the-evidence, that there is sufficient evidence for 
listing the chemical under EPCRA section 313.
    EPA also conducted an analysis of exposure for each chemical or 
chemical category proposed for listing under EPCRA section 313(d)(2)(A) 
(i.e., based on adverse acute human health effects), and, where 
appropriate, under section 313(d)(2)(C) (i.e., based on adverse 
ecological effects). For chemicals listed under EPCRA section 
313(d)(2)(A), this analysis included estimated concentrations of the 
chemical at or beyond the facility site boundary through the use of 
estimated releases and modelling techniques. EPA requests comment on 
its approach in considering exposure as a part of its evaluation of 
these chemicals under sections 313(d)(2)(A) and (C).
    Based on this analysis for each of the chemicals proposed for 
listing, EPA determined that one or more of the statutory criteria were 
met. A discussion of EPA's interpretation of the EPCRA section 313 
criteria is given in Unit III. of this preamble. A discussion of the 
evidence supporting EPA's proposal to add each of the chemicals to 
EPCRA section 313 is presented in Unit IV. of this preamble and in the 
record supporting this proposed rule.
    4. Other considerations. EPA excluded certain chemicals and 
chemical categories from consideration for proposed listing under EPCRA 
section 313 in this rulemaking for a number of reasons. Some chemicals 
were identified only as environmental degradation products rather than 
chemicals that are manufactured, processed, or otherwise used by a 
facility. These chemicals will only be present in the environment as a 
result of the release into the environment of precursor chemicals. If 
the degradation product meets the toxicity criteria of EPCRA section 
313, the precursor chemical may be considered for listing on EPCRA 
section 313. The degradation product would not be considered for 
listing on EPCRA section 313 because a facility subject to EPCRA 
section 313 is only required to file a TRI report for a chemical that 
it manufactures, processes, or otherwise uses, within the facility 
boundaries. Therefore, EPA does not believe that it is appropriate to 
consider listing such chemicals at this time.
    Some of the lists reviewed by EPA included listings that 
represented waste streams from particular processes. These waste 
streams, such as coke oven emissions, are not discrete chemicals or 
chemical categories, but contain a wide range of chemicals, many of 
which are currently listed individually on EPCRA section 313. The focus 
of this rulemaking is on the addition of specific chemicals and 
chemical categories and, as such, EPA believes that these waste streams 
are inappropriate for listing under EPCRA section 313 at this time.
    EPA also excluded chemicals whose only identified toxicity concern 
was a result of their status as a volatile organic compound (VOC). VOCs 
contribute to the formation of tropospheric ozone which causes a number 
of health-related and environmental problems. EPA continues to believe 
that VOCs meet the listing criteria of EPCRA section 313. However, EPA 
intends to address the issue of how VOCs should be listed on EPCRA 
section 313 separately. Therefore, chemicals whose only identified 
toxicity concern is due to their status as VOCs were excluded from 
consideration at this time.
    EPA also identified chemicals that are routinely manufactured, 
processed, or otherwise used at levels far below the reporting 
thresholds of EPCRA section 313. These chemicals are not expected to 
ever be manufactured, processed, or otherwise used in quantities at or 
above these reporting thresholds. In this proposed rulemaking, EPA is 
attempting to add chemicals to EPCRA section 313 that are manufactured, 
processed, or otherwise used in quantities greater than the EPCRA 
section 313 volume thresholds and thus would result in the submission 
of TRI reports. Consequently, chemicals that are manufactured, 
processed, or otherwise used in quantities less than the EPCRA section 
313 volume thresholds were excluded from further consideration at this 
time, because no reports would be filed under EPCRA section 313 for 
such chemicals.
    Some of the chemicals that are manufactured, processed, or 
otherwise used below the EPCRA section 313 activity thresholds, 
particularly those chemicals that are manufactured in trace amounts in 
waste streams, are highly toxic at very low dose levels and have 
physical, chemical, or biological properties that make the chemicals 
persist for extended periods in the environment, and bioaccumulate 
through the food chain. Persistent bioaccumulative toxic chemicals, 
such as dioxins, are of particular concern in ecosystems such as the 
Great Lakes Basin due to the long retention time of the individual 
lakes and the cycling of the chemical from one component of the 
ecosystem to another. EPA may reconsider in the future the issue of 
listing such chemicals in a manner which would result in the submission 
of TRI reports. EPA requests comment on the following: Is it 
appropriate to list such chemicals on EPCRA section 313? If EPA were to 
add this type of chemical to EPCRA section 313, what modifications to 
EPCRA section 313, such as lowering the reporting thresholds and 
modifying the de minimis in mixture exemptions (40 CFR part 372.38), 
would be required to insure that release and transfer information would 
be collected?

III. EPCRA Section 313 Statutory Criteria

    EPCRA section 313(d)(2) sets out criteria for adding chemicals to 
the list of chemicals subject to reporting under section 313(a). For a 
chemical (or category of chemicals) to be added to the EPCRA section 
313(c) list of toxic chemicals, the Administrator must determine 
whether, in her judgement, there is sufficient evidence to establish 
any one of the following:
    (A) The chemical is known to cause or can reasonably be anticipated 
to cause significant adverse acute human health effects at 
concentration levels that are reasonably likely to exist beyond 
facility site boundaries as a result of continuous, or frequently 
recurring, releases.
    (B) The chemical is known to cause or can reasonably be anticipated 
to cause in humans--
    (i) cancer or teratogenic effects, or
    (ii) serious or irreversible--
    (I) reproductive dysfunctions,
    (II) neurological disorders,
    (III) heritable genetic mutations, or
    (IV) other chronic health effects.
    (C) The chemical is known to cause or can reasonably be anticipated 
to cause, because of--
    (i) its toxicity,
    (ii) its toxicity and persistence in the environment, or
    (iii) its toxicity and tendency to bioaccumulate in the 
environment, a significant adverse effect on the environment of 
sufficient seriousness, in the judgement of the Administrator, to 
warrant reporting under this section.
    To remove a chemical from the section 313(c) list, the 
Administrator must determine that there is not sufficient evidence to 
establish any of the criteria described above as required by EPCRA 
section 313(d)(3). Thus, the criteria for listing or delisting a 
chemical are identical. However, whereas EPA can add a chemical if only 
one of the criteria is met, it can only delete a chemical if none of 
the criteria are met.
    To ascertain whether there is sufficient or insufficient evidence 
to determine that the statutory criteria are met for listing a 
chemical, EPA conducts a hazard assessment on the chemical and 
determines based on the weight-of-the-evidence, whether the chemical 
can reasonably be anticipated to cause any of the adverse effects 
specified in EPCRA section 313(d)(2). The hazard analysis is described 
above in Unit II.B.3. of this preamble. EPA's interpretation of the 
specific statutory criteria follows.
    1. Section 313(d)(2)(A) (acute human health effects). To determine 
whether the section 313(d)(2)(A) ``acute human health effects'' 
criterion is met, EPA must examine the adverse effects associated with 
the chemical, the ``concentration levels'' which would cause acute 
human health effects, and the likelihood of such levels existing 
``beyond facility site boundaries as a result of continuous, or 
frequently recurring, releases.'' Such a determination may include, 
among other factors, consideration of production processes, workplace 
procedures, pollution controls, and the volume and pattern of 
production, use, and release, as well as other chemical-specific 
factors. EPA believes that to make the section 313(d)(2)(A) 
determination it must demonstrate that a chemical can reasonably be 
anticipated to be released in quantities that result in concentration 
levels, or within a reasonable margin of exposure of the concentration 
levels, that would be expected to cause acute human health effects 
beyond the facility site boundary. The margin of exposure applied is 
dependent upon the type of hazard data (e.g., data in animals versus 
human) and the confidence in this hazard data base for acute effects 
(e.g., sufficiency of the hazard data). However, EPA is not required to 
make a facility-specific finding, nor is it necessary for EPA to 
demonstrate that these concentration levels or effects occur at or near 
any particular facility (Ref. 1). Furthermore, ``EPA may, but is not 
required to, conduct new studies or risk assessments or perform site-
specific analyses to establish actual ambient concentrations or to 
document adverse effects at any particular location'' (Ref. 1). Nor is 
EPA limited to considering concentration levels and potential acute 
human health effects at the ``fenceline.'' Rather, the phrase ``beyond 
facility site boundaries'' reflects Congress' recognition that the 
``highest concentration to which persons outside the site boundary may 
be exposed'' could occur at ``any point outside the boundaries of the 
site on which the facility is located,'' including, for example, where 
an air emissions plume cools and settles to the ground (Ref. 1). 
Therefore, EPA believes that to make a finding under EPCRA section 
313(d)(2)(A), the Agency may estimate concentrations at or beyond the 
facility site boundary through the use of estimated releases and 
modelling techniques. The term ``continuous or frequently recurring 
releases'' is included only to distinguish routine releases that are a 
normal consequence of the operation of a facility from the episodic and 
accidental releases that are subject to EPCRA section 304 (Ref. 1). As 
such, EPA believes that episodic and accidental releases are not 
pertinent in a determination that a chemical meets the section 
313(d)(2)(A) criterion.
    2. Section 313(d)(2)(B) (chronic human health effects). In contrast 
to the section 313(d)(2)(A) criterion, section 313(d)(2)(B) does not 
require consideration of either the nature and frequency of releases or 
concentration levels at facility site boundaries. Rather, section 
313(d)(2)(B) is focused solely on whether the chemical is known or can 
reasonably be anticipated to cause cancer, teratogenicity, or other 
serious or irreversible chronic human health effects. Consequently, EPA 
believes that it is sufficient to consider only the toxicity of the 
subject chemical to make the section 313(d)(2)(B) determination.
    3. Section 313(d)(2)(C) (environmental effects). The section 
313(d)(2)(C) criterion requires EPA to consider a chemical's potential 
to cause significant adverse effects on the environment. The statute 
directs EPA to base its determination on a consideration of the 
toxicity of the chemical, either alone or in combination with the 
persistence of the chemical or the potential for the chemical to 
bioaccumulate. Congress intended that EPA consider a broad range of 
environmental effects when making a determination under section 
313(d)(2)(C).

    In determining what constitutes a significant adverse effect on 
the environment...the Administrator should consider the extent to 
which the toxic chemical causes or can reasonably be anticipated to 
cause any of the following adverse reactions, even if restricted to 
the immediate vicinity adjacent to the site: (1) Gradual or sudden 
changes in the composition of animal life or plant life, including 
fungal or microbial organisms in an area. (2) Abnormal number of 
deaths of organisms (e.g. fish kills). (3) Reduction of the 
reproductive success or the vigor of a species. (4) Reduction in 
agricultural productivity, whether crops or livestock. (5) 
Alterations in the behavior or distribution of a species. (6) Long 
lasting or irreversible contamination of components of the physical 
environment, especially in the case of groundwater, and surface 
water and soil resources that have limited self-cleansing capability 
(Ref. 1).

    EPA believes that the environmental effects criterion inherently 
contains a limited exposure component because of the statutory 
requirement for EPA to find a ``significant adverse effect on the 
environment of sufficient seriousness, in the judgment of the 
Administrator, to warrant reporting'' under EPCRA section 313. Unlike 
section 313(d)(2)(B), where EPA only has to determine whether certain 
kinds of effects are ``known or reasonably anticipated'' to occur, 
section 313(d)(2)(C) requires EPA to find the effect to be of 
sufficient seriousness to warrant reporting, which implies the 
possibility that under certain circumstances, a chemical that could 
theoretically cause a significant adverse effect on the environment is 
unlikely to cause one of a magnitude to warrant listing.
    The extent to which exposure is factored into EPA's determination 
depends upon the inherent toxicity of a chemical, and a variety of 
other chemical-specific characteristics. EPA believes that when a 
chemical is inherently extremely toxic, that is, it is toxic at very 
low dose levels, an exposure assessment is not necessary because even 
minimal releases of such a chemical may reasonably be anticipated to 
result in significant adverse environmental effects. In such cases, EPA 
could rely on toxicity alone under section 313(d)(2)(C)(i) as a basis 
for listing.
    However, for chemicals that exhibit adverse effects upon the 
environment solely based on toxicity at moderately low doses, EPA 
believes that consideration of potential exposure is warranted because 
minimal releases may not result in significant adverse effects upon the 
environment. These exposure considerations may include, among other 
factors, pollution controls, the volume and pattern of production, use, 
and release, environmental fate, as well as other chemical-specific 
factors, and the use of estimated releases and modelling techniques.
    EPCRA sections 313(d)(2)(C)(ii) and (iii) allow EPA to consider the 
impacts of other characteristics of a chemical. Where a chemical 
exhibits significant adverse effects in the environment based on 
toxicity and persistence or toxicity and bioaccumulation at very low to 
moderately low dose levels, EPA believes that exposure considerations 
are not required in addition to those considerations implicit in 
evaluation of the chemical's potential for persistence and 
bioaccumulation. This is because even minimal releases of the chemical 
may result in elevated concentrations in the environment or in an 
organism that can reasonably be anticipated to result in significant 
adverse effects. This reflects the increased likelihood that there will 
be exposure to a chemical that persists due to its longer residence 
time in the environment. Repeated minimal releases of a persistent 
chemical may result in elevated concentrations in the environment. For 
a chemical that bioaccumulates, even low levels of the chemical in the 
environment may result in increased concentrations in an organism. 
Therefore, evaluation of a chemical's persistence or bioaccumulation 
potential may be considered the functional equivalent of an exposure 
analysis.
    In addition, for chemicals which induce well-established adverse 
effects, e.g. chlorofluorocarbons, which cause stratospheric ozone 
depletion, EPA believes that an exposure assessment is unnecessary. EPA 
believes that these chemicals typically do not affect solely one or two 
species but rather affect changes across a whole ecosystem. EPA 
believes that these effects are of sufficient seriousness that 
additional exposure considerations are not warranted because of the 
scope of their impact and the well-documented evidence supporting the 
adverse effects. EPA requests comment on its approach for considering 
exposure as a part of its evaluation for listing of these chemicals 
under section 313(d)(2)(C).
    In Unit IV.B. of this preamble, EPA identifies each of the 
chemicals proposed for addition to EPCRA section 313 and the specific 
statutory criteria upon which the proposed addition is based.

IV. EPA's Technical Review

A. Introduction

    Data on the chemicals and chemical categories were reviewed for 
evidence indicating adverse acute and chronic toxicity, 
carcinogenicity, mutagenicity, developmental and reproductive effects, 
neurotoxicity, and environmental effects. Information on the 
environmental fate was also reviewed.
    For each chemical proposed for addition to EPCRA section 313 in 
this rulemaking, EPA conducted an extensive hazard assessment, and, 
where appropriate, an analysis of exposure, to determine whether the 
chemical met one or more of the EPCRA section 313(d)(2) listing 
criteria. This hazard assessment is discussed in detail in Unit II.B.3 
of this preamble. Only after this careful review was a final 
determination made as to whether one of the EPCRA section 313(d)(2) 
listing criteria was met for each individual chemical or chemical 
category proposed for listing below. EPA need only show that one of the 
listing criteria is met in order to list a chemical or chemical 
category under EPCRA section 313. The information summarized below for 
each chemical or chemical category represents the key data elements 
that lead EPA to believe that there is sufficient evidence to establish 
that one of the section 313(d)(2) listing criteria is met. A more 
extensive review of the existing data base for each chemical or 
chemical category proposed for listing, which reflects the entire 
weight-of-the-evidence considered by EPA, is contained in following 
support documents: Support Document for the Addition of Chemicals from 
Federal Insecticide, Fungicide, Rodenticide Act (FIFRA) Active 
Ingredients to EPCRA Section 313 (Ref 3); Physical Properties and 
Environmental Fate of Some TRI Expansion Chemicals (Ref. 5); Support 
Document for the Addition of Chemicals from Section 112(b) of the Clean 
Air Act Amendments and Chlorinated Paraffins to EPCRA Section 313 (Ref. 
7); and Support Document for the Health and Ecological Toxicity Review 
of TRI Expansion Chemicals (Ref. 8). These support documents contain a 
complete list of the references (which can be found in the public 
record for this proposed rulemaking) that were used in support of these 
proposed additions.
    A list of the 313 chemicals and chemical categories and their 
Chemical Abstract Service (CAS) number, where appropriate, follows.

    1. Abamectin (Avermectin B1) (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'-(1-methylethyl)-6-(methylthio)-
1,3,5,triazine- 2,4 diamine) (CAS No. 000834-12-8)
    10. Amitraz (CAS No. 033089-61-1)
    11. Anilazine (4,6-Dichloro-N-(2-chlorophenyl)-1,3,5-triazin-2-
amine) (CAS No. 000101-05-3)
    12. Atrazine (6-Chloro-N-ethyl-N'-(1-methylethyl)-
1,3,5,triazine-2,4-diamine) (CAS No. 001912-24-9)
    13. Bendiocarb (2,2-Dimethyl-1,3-benzodioxol-4-ol 
methylcarbamate) (CAS No. 022781-23-3)
    14. Benfluralin (N-Butyl-N-ethyl-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-(1-methylpropyl)-2,4-(1H,3H)- 
pyrimidinedione) (CAS No. 000314-40-9)
    22. Bromacil lithium salt (2,4-(1H,3H)-Pyrimidinedione, 5-bromo-
6-methyl-3-(1-methylpropyl), lithium salt) (CAS No. 053404-19-6)
    23. Bromine (CAS No. 007726-95-6)
    24. 1-Bromo-1-(bromomethyl)-1,3-propanedicarbonitrile (CAS No. 
035691-65-7)
    25. 2-Bromo-2-nitropropane-1,3-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-methylpropyl)carbamothioic 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-1,3-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. 1-(3-Chloroallyl)-3,5,7-triaza-1-azoniaadamantane chloride 
(CAS No. 004080-31-3)
    43. p-Chloroaniline (CAS No. 000106-47-8)
    44. 5-Chloro-2-(2,4-dichlorophenoxy)phenol (CAS No. 003380-34-5)
    45. 3-Chloro-2-methyl-1-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-1,3,5-
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-
dimethylcyclopropanecarboxylic acid, cyano(4-fluoro-3-
phenoxyphenyl)methyl ester) (CAS No. 068359-37-5)
    59. Cyhalothrin (3-(2-Chloro-3,3,3-trifluoro-1-propenyl)-2,2- 
dimethylcyclopropanecarboxylic acid cyano(3-phenoxyphenyl)methyl 
ester) (CAS No. 068085-85-8)
    60. Cyromazine (N-Cyclopropyl-1,3,5-triazine-2,4,6-triamine) 
(CAS No. 066215-27-8)
    61. Dazomet (Tetrahydro-3,5-dimethyl-2H-1,3,5-thiadiazine-2-
thione) (CAS No. 000533-74-4)
    62. Dazomet, sodium salt (2H-1,3,5-Thiadiazine-2-thione, 
tetrahydro-3,5-dimethyl-, ion(1-), 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)
    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-ethylhexyl ester (CAS No. 001928-43-4)
    69. 2,4-D 2-ethyl-4-methylpentyl 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-methyoxybenzoic 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'-Dichlorobenzidine sulfate (CAS No. 064969-34-2)
    76. trans-1,4-Dichloro-2-butene (CAS No. 000110-57-6)
    77. Dichloromethylphenylsilane (CAS No. 000149-74-6)
    78. Dichlorophene (2,2'-Methylenebis(4-chlorophenol) (CAS No. 
000097-23-4)
    79. trans-1,3-Dichloropropene (CAS No. 010061-02-6)
    80. Diclofop methyl (2-[4-(2,4-Dichlorophenoxy) 
phenoxy]propanoic acid, methyl ester) (CAS No. 051338-27-3)
    81. Dicyclopentadiene (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 dihydrochloride (o-Dianisidine 
dihydrochloride) (CAS No. 020325-40-0)
    88. 3,3'-Dimethoxybenzidine hydrochloride (o-Dianisidine 
hydrochloride) (CAS No. 111984-09-9)
    89. Dimethylamine (CAS No. 000124-40-3)
    90. Dimethylamine dicamba (CAS No. 002300-66-5)
    91. 3,3'-Dimethylbenzidine dihydrochloride (o-Tolidine 
dihydrochloride) (CAS No. 000612-82-8)
    92. 3,3'-Dimethylbenzidine dihydrofluoride (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-Dimethylformamide (CAS No. 000068-12-2)
    96. 2,6-Dimethylphenol (CAS No. 000576-26-1)
    97. Dinocap (CAS No. 039300-45-3)
    98. Dinoseb (CAS No. 000088-85-7)
    99. Diphenamid (CAS No. 000957-51-7)
    100. Diphenylamine (CAS No. 000122-39-4)
    101. Dipotassium endothall (7-Oxabicyclo(2.2.1)heptane-2,3-
dicarboxylic acid, dipotassium salt) (CAS No. 002164-07-0)
    102. Dipropyl isocinchomeronate (CAS No. 000136-45-8)
    103. Disodium cyanodithioimidocarbonate (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 monoacetate) (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)propanoic acid, 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-(1-methylethyl)benzeneacetic 
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]-phenoxy]propanoic 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-1,6-diisocyanate (CAS No. 000822-60-0)
    133. n-Hexane (CAS No. 000110-54-3)
    134. Hexazinone (CAS No. 051235-04-2)
    135. Hydramethylnon (Tetrahydro-5,5-dimethyl-
2(1H)pyrimidinone[3-[4-(trifluoromethyl)phenyl]-1-[2-
[4(trifluoromethyl) phenyl]ethenyl]-2 propenylidene]hydrazone) (CAS 
No. 067485-29-4)
    136--151. Hydrochlorofluorocarbons, specifically:
    136. Dichloropentafluoropropane (CAS No. 127564-92-5)
    137. 1,3-Dichloro-1,1,2,3,3-pentafluoropropane (HCFC-225ea) (CAS 
No. 136013-79-1)
    138. 2,2-Dichloro-1,1,1,3,3-pentafluoropropane (HCFC-225aa) (CAS 
No. 128903-21-9)
    139. 1,1-Dichloro-1,2,3,3,3-pentafluoropropane (HCFC-225eb) (CAS 
No. 111512-56-2)
    140. 1,1-Dichloro-1,2,2,3,3-pentafluoropropane (HCFC-225cc) (CAS 
No. 13474-88-9)
    141. 1,3-Dichloro-1,1,2,2,3-pentafluoropropane (HCFC-225cb) (CAS 
No. 000507-55-1)
    142. 1,2-Dichloro-1,1,3,3,3-pentafluoropropane (HCFC-225da) (CAS 
No. 000431-86-7)
    143. 3,3-Dichloro-1,1,1,2,2-pentafluoropropane (HCFC-225ca) (CAS 
No. 000422-56-0)
    144. 2,3-Dichloro-1,1,1,2,3-pentafluoropropane (HCFC-225ba) (CAS 
No. 000422-48-0)
    145. 1,2-Dichloro-1,1,2,3,3-pentafluoropropane (HCFC-225bb) (CAS 
No. 000422-44-6)
    146. Dichlorofluoromethane (HCFC-21) (CAS No. 000075-43-4)
    147. 1,1,1,2-Tetrachloro-2-fluoroethane (HCFC-121a) (CAS No. 
000354-11-0)
    148. 1,1,2,2-Tetrachloro-1-fluoroethane (HCFC-121) (CAS No. 
000354-14- 3)
    149. 1,2-Dichloro-1,1-difluoroethane (HCFC-132b) (CAS No. 
001649-08-7)
    150. 2-Chloro-1,1,1-trifluoroethane (HCFC-133a) (CAS No. 000075-
88-7)
    151. 3-Chloro-1,1,1-trifluoropropane (HCFC-253fb) (CAS No. 
000460-35-5)
    152. Imazalil (1-[2-(2,4-Dichlorophenyl)-2-(2-
propenyloxy)ethyl]1H-imidazole) (CAS No. 035554-44-0)
    153. 3-Iodo-2-propynyl butylcarbamate (CAS No. 055406-53-6)
    154. Iprodione (3-(3,5-Dichlorophenyl)-N-(1-methylethyl)-2,4-
dioxo-1-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[(1-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-1-methyl-2-oxoethyl ester) (CAS No. 077501-63-4)
    161. Linuron (CAS No. 000330-55-2)
    162. Lithium carbonate (CAS No. 000554-13-2)
    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-1,2,4-
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. 1,1-Methylene bis(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 (1H-Azepine-1-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)-1H-
1,2,4-triazole-1-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)phenyl]-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-[2,4-Dichloro-5-(1-methylethoxy)phenyl]-5(1,1-
dimethylethyl)-1,3,4-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-(1-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-methyl-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[1,2,3-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-chlorophenyl)-O-ethyl-S-propyl 
phosphorothioate) (CAS No. 041198-08-7)
    255. Prometryn (N,N'-Bis(1-methylethyl)-6-methylthio-1,3,5-
triazine-2,4-diamine) (CAS No. 007287-19-6)
    256. Propachlor (2-Chloro-N-(1-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 (1-[2-(2,4-Dichlorophenyl)-4-propyl-1,3-
dioxolan-2-yl]-methyl-1H-1,2,4,-triazole) (CAS No. 060207-90-1)
    262. Quizalofop-ethyl (2-[4-[(6-Chloro-2-quinoxalinyl) 
oxy]phenoxy] propanoic acid ethyl ester) (CAS No. 076578-14-8)
    263. Resmethrin ([5-(Phenylmethyl)-3-furanyl]methyl 2,2-
dimethyl-3-(2-methyl-1-propenyl) cyclopropanecarboxylate]) (CAS No. 
010453-86-8)
    264. Sethoxydim (2-[1-(Ethoxyimino)butyl]-5-
[2(ethylthio)propyl]-3-hydroxyl-2-cyclohexen-1-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)
    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-phenylphenoxide (CAS No. 000132-27-4)
    275. Sodium 2-pyridinethiol-1-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-
(methylthio)phenyl]phosphorodithioic acid S- propyl ester) (CAS No. 
035400-43-2)
    281. Tebuthiuron (N-[5-(1,1-Dimethylethyl)-1,3,4-thiadiazol-2-
yl)- N,N'-dimethylurea) (CAS No. 034014-18-1)
    282. Tefluthrin (CAS No. 079538-32-2)
    283. Temephos (CAS No. 003383-96-8)
    284. Terbacil (5-Chloro-3-(1,1-dimethylethyl)-6-methyl- 2,4-
(1H,3H)-pyrimidinedione) (CAS No. 005902-51-2)
    285. Tetracycline hydrochloride (CAS No. 000064-75-5)
    286. Tetramethrin (2,2-Dimethyl-3-(2-methyl-1-propenyl) 
cyclopropanecarboxylic acid (1,3,4,5,6,7-hexahydro-1,3-dioxo-2H-
isoindol-2-yl)methyl ester) (CAS No. 007696-12-0)
    287. Tetrasodium ethylenediaminetetraacetate (CAS No. 000064-02-
8)
    288. Thiabendazole (2-(4-Thiazolyl)-1H-benzimidazole) (CAS No. 
000148-79-8)
    289. Thiabendazole, hypophosphite salt (2-(4-Thiazolyl) 
benzimidazole, hypophosphite salt) (CAS No. 028558-32-9)
    290. Thiobencarb (Carbamic acid, diethylthio-, S-(p-
chlorobenzyl)) (CAS No. 028249-77-6)
    291. Thiodicarb (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. Thiosemicarbazide (CAS No. 000079-19-6)
    295. Triadimefon (1-(4-Chlorophenoxy)-3,3-dimethyl-1-(1H-1,2,4-
triazol-1-yl)-2-butanone) (CAS No. 043121-43-3)
    296. Triallate (CAS No. 002303-17-5)
    297. Tribenuron methyl (2-(((((4-Methoxy-6-methyl-1,3,5-triazin-
2-yl)-methylamino)carbonyl)amino)sulfonyl)-, methyl ester) (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-Tributyltrithiophosphate (DEF) (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 B1) (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 LC50 of 9.6 parts per billion (ppb), a rainbow trout 96-hour 
LC50 of 3.6 ppb, and a daphnid 48-hour LC50 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 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. Alachlor (CAS No. 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-1 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 LC50 of 50 ppb for bluegill 
and a measured 48-hour LC50 of 70 ppb for daphnid. In addition, 
the measured 48-hour EC50 for daphnid is 51 ppb. Measured 
terrestrial acute toxicity data for wildlife include an oral LD50 
for female mallard ducks of 3.4 milligram per kilogram (mg/kg) and an 
oral LD50 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-Allethrin [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'-(1-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 EC50 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 days 
1 and 2). The NOAEL in this study was 0.25 mg/kg/day and the oral RfD 
derived from the NOAEL was 0.0025 mg/kg/day. These findings were 
supported by 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)-1,3,5-triazin-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 LC50 of 0.27 ppb and an oyster 96-hour 
EC50 (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'-(1-methylethyl)-1,3,5,-triazine-
2,4-diamine) (CAS No. 001912-24-9) (FIFRA 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-1,3-benzodioxol-4-ol methylcarbamate) 
(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 EC50 of 6.7 ppb and a daphnid 48-hour EC50 of 29.2 ppb. 
Avian acute toxicity values include a mallard duck LD50 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 doses. NOEL values based on the appearance of 
tremors (often transient) ranged from 1 to 2.67 mg/kg/day. The oral RfD 
for bifenthrin was based on a 1year beagle dog feeding study, in which 
the LOEL, based on tremors observed during weeks 15 to 29, was 3.0 mg/
kg/day and the NOEL was 1.5 mg/kg/day. The RfD based on this NOEL was 
0.015 mg/kg/day.
    In a rat teratology study, an increased incidence of hydroureter 
(without hydronephrosis) was noted in fetuses at 2 mg/kg/day (LOEL). 
The NOEL was 1 mg/kg/day.
    EPA believes that there is sufficient evidence for listing 
bifenthrin on EPCRA section 313 pursuant to EPCRA section 313(d)(2)(B) 
based on the available neurological and developmental toxicity data.
    Aquatic acute toxicity values for bifenthrin include a bluegill 96-
hour LC50 of 0.35 ppb, a rainbow trout 96-hour LC50 of 0.15 
ppb, a sheepshead minnow LC50 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).
    In 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 LC50 of 7.6 ppb, a rainbow trout 96-hour 
LC50 6.9 ppb, a measured fathead minnow 96-hour LC50 of 2.7 
ppb, and a daphnid 48-hour LC50 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-(1-methylpropyl)-2,4-(1H,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-(1H,3H)-pyrimidinedione, 5-bromo-6-
methyl-3-(1-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.
    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. 1-Bromo-1-(bromomethyl)-1,3-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-1-(bromomethyl)-1,3-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 ppm (150 mg/kg/day) there was 
decreased 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-
1-(bromomethyl)-1,3-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-1,3-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-1,3-diol. In an acute 
oral study in mice, the LD50 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-1,3-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 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. 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 LD50 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 
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 Zymbal's 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.I. 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 LC50 for rainbow trout of 60 ppb and a 96-hour measured 
LC50 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 LC50 for bluegill of 80 ppb. In addition, the 
measured 48-hour EC50 for daphnids is 35 ppb. Measured terrestrial 
acute toxicity data for wildlife include an oral LD50 for mallard 
ducks of 0.397 mg/kg for females and 0.480 mg/kg for males and an oral 
LD50 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 believes 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 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-phenyl-1,4-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 established 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-1,3-dithiolo[4,5-b]quinoxalin-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. Chlorimuron 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: CxH2x-y+2Cly 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 (LC50s 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 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-1-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 1-(3-chloroallyl)-
3,5,7-triaza-1-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 1-(3-chloroallyl)-3,5,7-triaza-1-azoniaadamantane 
chloride on EPCRA section 313 pursuant to EPCRA section 313(d)(2)(B) 
based on the available chronic toxicity data for 1-(3-chloroallyl)-
3,5,7-triaza-1-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-dichlorophenoxy)phenol (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-1-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-1-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-1-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 LC50 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 LC50 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 LD50 is 
51.3 mg/kg.
    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 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, 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-
pyridyl)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 LD50 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 LC50 of 1.11 ppb and a rainbow trout 96-hour 
LC50 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-1,3,5-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.
    In 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 triazine-type herbicide. In a three-generation 
reproduction study in Long-Evans rats, F3b 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 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 on the chronic neurological, hepatic, renal, 
myocardial, and reproductive toxicity data for this chemical.
    58. Cyfluthrin (3-(2,2-Dichloroethenyl)-2,2-
dimethylcyclopropanecarboxylic acid, cyano(4-fluoro-3-
phenoxyphenyl)methyl ester) (CAS No. 068359-37-5) (FIFRA AI) (Ref. 3). 
In a 14-day rat study, oral administration of 60 mg/kg/day produced 
tremors, uncoordinated gait, salivation, slight brain hemorrhages, 
necrosis of the skeletal muscle fibers, and death. The NOEL was not 
defined. In another study, salivation, straddled gait, axonal 
degeneration of sciatic nerve, microtubular dilation, and mitochondria 
degeneration in the sciatic and femoral nerves were observed in rats 
administered 80 mg/kg/day orally for 5 days and 40 mg/kg/day for the 
following 9 days. No NOEL was established.
    Liver and adrenal weight increases were observed in rats orally 
administered 40 to 80 mg/kg/day for 28 days. The highest dose of 80 mg/
kg/day was reduced to 40 mg/kg/day. The NOEL was 20 mg/kg/day. Liver 
weight changes and urobilinogen and ketone bodies in the urine were 
observed in rats fed 15 mg/kg/day for 28 days. No NOEL was established. 
In a 28-day mouse feeding study, increased liver weight was observed at 
50 mg/kg/day (LOEL). The NOEL was 15 mg/kg/day. Inflammatory foci in 
the kidneys of females were observed at 7.5 mg/kg/day in a 2-year rat 
feeding study. The NOEL was 2.5 mg/kg/day. Based on the NOEL of the 
study, an oral RfD of 0.025 mg/kg/day was determined. Increased 
alkaline phosphatase activity was observed in males at 7.5 mg/kg/day in 
a 23-month mouse feeding study.
    EPA believes that there is sufficient evidence for listing 
cyfluthrin on EPCRA section 313 pursuant to EPCRA section 313(d)(2)(B) 
based on the available neurological, hepatic, and renal toxicity data.
    Aquatic acute toxicity values for cyfluthrin include a rainbow 
trout 96-hour LC50 of 0.68 ppb, a bluegill 96-hour LC50 of 
1.5 ppb, and a daphnid 48-hour EC50 of 0.14 ppb. EPA believes that 
there is sufficient evidence for listing cyfluthrin on EPCRA section 
313 pursuant to EPCRA section 313(d)(2)(C) based on the available 
environmental toxicity data.
    59. Cyhalothrin (3-(2-chloro-3,3,3-trifluoro-1-propenyl)-2,2-
dimethylcyclopropanecarboxylic acid cyano(3-phenoxyphenyl)methyl ester) 
(CAS No. 068085-85-8) (FIFRA AI) (Ref. 3). Cyhalothrin administered 
orally (in capsules) to dogs at 10 mg/kg/day for 26 weeks produced 
occasional disturbances of the nervous system (unsteadiness and/or 
muscular trembling). The NOEL for these effects was not defined. In a 
1-year dog study, ataxia, muscle tremors, and convulsions were observed 
following oral administration at 3.5 mg/kg/day. Abnormal gait and 
convulsions were observed at 0.5 mg/kg/day. The LOEL of the study was 
0.5 mg/kg/day and the NOEL was 0.1 mg/kg/day. EPA believes that there 
is sufficient evidence for listing cyhalothrin on EPCRA section 313 
pursuant to EPCRA section 313(d)(2)(B) based on the available 
neurological toxicity data.
    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, an 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-1,3,5-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-1,3,5-
thiadiazine-2-thione, ion(1-), 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 
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 acid, dazomet.
    63. 2,4-DB (CAS No. 000094-82-6) (FIFRA SR) (Ref. 8). 2,4-DB (4-
(2,4-dichlorophenoxy)butanoic 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 preimplantation 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) based 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. EPA 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 LC50 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 LC50 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 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 
LC50 for rainbow trout of 90 ppb and a daphnid 96-hour LC50 
of 0.90 ppb. In addition, measured terrestrial wildlife acute toxicity 
data for diazinon include an oral LD50 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 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 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-1,4-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 LC50 in rats was 86 ppm (0.44 mg/L). EPA's exposure 
analysis indicates that trans-1,4-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 LC50 value for 
dichloromethylphenylsilane is 0.17 mg/L. EPA's exposure analysis 
indicates 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 LC50 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-1,3-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 cis isomer, 45 percent trans isomer, 1 percent epichlorhydrin) 
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 bronchioalveolar 
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-1,3-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. Diclofop methyl (2-[4-(2,4-dichlorophenoxy) phenoxy]propanoic 
acid, 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 lipid 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 LD50 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 chemical.
    82. Diethatyl 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 LC50 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 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-1,4-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-1 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 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 
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 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 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 carcinogenicity 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 
burns and the vapor is harmful to humans. The 2-hour mouse inhalation 
LC50 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 
LC50 for rainbow trout is 15 ppb and the LC50 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 F1b, F2a, and F3a pups. The 
F1b 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 or 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 LC50 of 88 ppb. EPA 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 the 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 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 F2b and F3a 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 
EC50 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) based 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 LC50 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 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 EC50 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-dichlorophenoxy)propionic 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 LD50 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 LC50 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 
LC50 of 7.5 ppb, a shrimp 96-hour LC50 of 13 ppb, and a 
daphnid 48-hour EC50 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 LD50 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 
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 LD50 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 chemical.
    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 LD50 values for the redwinged blackbird and 
the starling are 1.78 mg/kg and 4.22 mg/kg, respectively. In addition, 
the measured oral LD50 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 bilirubin, 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 LC50 of 1.7 ppb, a fathead minnow 96-hour 
LC50 of 1.9 ppb, a daphnid 48-hour EC50 of 3.1 ppb, a 
bluegill sunfish 96-hour of LC50 of 4.8 ppb, and a sheepshead 
minnow 96-hour LC50 of 20.8 ppb. Avian acute toxicity values 
include a quail oral LD50 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 F2a 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 EC50 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) based on the available environmental 
toxicity data.
    119. Fenoxycarb (2-(4-phenoxyphenoxy)ethyl]carbamic acid ethyl 
ester) (CAS No. 072490-01-8) (FIFRA 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 ataxia, 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 LC50 of 2.3 ppb, a bluegill 96-hour LC50 of 2.2 
ppb, a sheepshead minnow 96-hour LC50 of 3.1 ppb, and a daphnid 
48-hour EC50 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, the 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 LC50 of 0.62 ppb for immobilization. Acute toxicity values 
for other non-standard aquatic invertebrates range from a 48-hour 
EC50 of 0.024 ppb for brown shrimp to a 96-hour EC50 of 110 
ppb for scud. Avian acute toxicity values include a male mallard duck 
oral LD50 of 5.94 mg/kg, a male bobwhite quail LD50 of 4 mg/
kg, and a mourning dove oral LD50 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-alpha-(1-methylethyl)benzeneacetic 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 LD50 dose of 70.2 mg/kg. The oral mouse 
LD50 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 mg/
kg.
    In 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 LC50 of 0.26 ppb, a fathead minnow 96-hour 
LC50 of 0.33 ppb, a rainbow trout 96-hour LC50 of 1.2 ppb, an 
Atlantic salmon 96-hour LC50 of 1.2 ppb, and a sheepshead minnow 
96-hour LC50 of 4.4 ppb. In addition, the 48-hour LC50 for 
daphnids is 0.05 ppb. EPA believes that there is sufficient evidence 
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 LD50 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 
LC50 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 EC50 of greater than 2.8 ppb, a bluegill 
sunfish 96-hour LC50 of greater than 3.2 ppb, and a rainbow trout 
96-hour LC50 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 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 EC50 of 0.40 ppb, a bluegill sunfish 96-hour LC50 of 0.9 
ppb, a rainbow trout 96-hour LC50 of 2.9 ppb, and a sheepshead 
minnow 96-hour LC50 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-1 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 LC50 of 39 ppb for rainbow trout, and a measured 96-hour 
LC50 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 
methylsulfonyl)-2-nitrobenzamide) (CAS No. 072178-02-0) (FIFRA AI) 
(Ref. 3). Decreased plasma cholesterol and triglycerides and increased 
liver weights (reversible at 7 days post-treatment) were observed at 50 
mg/kg/day (only dose tested) when administered in the diet of rats for 
4 weeks. In a 90-day rat study, dietary administration of 5 mg/kg/day 
(LOEL) produced alterations in lipid metabolism and increases in liver 
weight. The NOEL was 0.25 mg/kg/day. In a 26-week dog study, dietary 
administration of 25 mg/kg/day (LOEL) produced alterations in lipid 
metabolism and liver changes (changes not defined). The NOEL was 1 mg/
kg/day. Liver toxicity (increased liver masses, discolored hepatocytes, 
and pigmented Kupffer cells) was observed in a 2-year rat feeding study 
at 50 mg/kg/day (LOEL). The NOEL was 5 mg/kg/day. Metabolism studies 
have shown that fomesafen accumulates in the liver. EPA believes that 
there is sufficient evidence for listing fomesafen on EPCRA section 313 
pursuant to EPCRA section 313(d)(2)(B) based on the available hepatic 
toxicity data for this chemical.
    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 EC50 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-1,6-diisocyanate or Diisocyanates category (CAS 
No. 000822-60-0) (CAA HAP) (Ref. 7). Hexamethylene-1,6-diisocyanate 
(HDI) is extremely toxic via the inhalation route. The rat LC50 
for HDI ranges from 56 (385 mg/m3) to 45 ppm (310 mg/m3). The 
mouse LC50 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-1,6-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 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 
are 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:

    1,3-Bis(methylisocyanate)cyclohexane (CAS No. 038661-72-2)
    1,4-Bis(methylisocyanate)cyclohexane (CAS No. 010347-54-3)
    1,4-Cyclohexane diisocyanate (CAS No. 002556-36-7)
    Diethyldiisocyanatobenzene (CAS No. 134190-37-7)
    4,4'-Diisocyanatodiphenyl ether (CAS No. 004128-73-8)
    2,4'-Diisocyanatodiphenyl sulfide (CAS No. 075790-87-3)
    3,3'-Dimethoxybenzidine-4,4'-diisocyanate (CAS No. 000091-93-0)
    3,3'-Dimethyl-4,4'-diphenylene diisocyanate (CAS No. 000091-97-4)
    3,3'-Dimethyldiphenylmethane-4,4'-diisocyanate (CAS No. 000139-25-
3)
    Hexamethylene-1,6-diisocyanate (CAS No. 000822-06-0)
    Isophorone diisocyanate (CAS No. 004098-71-0)
    4-Methyldiphenylmethane-3,4-diisocyanate (CAS No. 075790-84-0)
    1,1-Methylene bis(4-isocyanatocyclohexane) (CAS No. 005124-30-1)
    1,5-Naphthalene diisocyanate (CAS No. 003173-72-6)
    1,3-Phenylene diisocyanate (CAS No. 000123-61-5)
    1,4-Phenylene diisocyanate (CAS No. 000104-49-4)
    Polymeric diphenylmethane diisocyanate (CAS No. 009016-87-9)
    2,2,4-Trimethylhexamethylene diisocyanate (CAS No. 016938-22-0)
    2,4,4-Trimethylhexamethylene diisocyanate (CAS No. 015646-96-5)
    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 
EC50 of 7 ppb for S. capricornutum. 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(1H)-pyrimidinone[3-
[4- (trifluoromethyl)phenyl]-1-[2-[4(trifluoromethyl) phenyl]ethenyl]-
2-propenylidene]hydrazone) (CAS No. 067485-29-4) (FIFRA AI) (Ref. 3). 
In a 90-day dog feeding study, testicular atrophy was observed at 6 mg/
kg/day (LOEL). The NOEL was 3 mg/kg/day. In a 90-day rat study, dietary 
administration of 5 mg/kg/day (LOEL) produced testicular atrophy. The 
NOEL was 2.5 mg/kg/day. Dietary administration of 6.5 mg/kg/day for 18 
months produced testicular lesions in mice. The NOEL was 2.75 mg/kg/
day. In a 2-year rat study, dietary administration of 5 mg/kg/day 
produced decreased testicular weight and testicular atrophy. The NOEL 
was 2.5 mg/kg/day. In a 3-generation rat reproduction study, oral 
administration of 5 mg/kg/day produced male infertility. The NOEL was 
2.5 mg/kg/day.
    Decreased fetal weight was observed in the offspring of rats 
administered 30 mg/kg/day (LOEL). The NOEL was 10 mg/kg/day. Increased 
post implantation loss and decreased fetal viability were observed in 
the offspring of rabbits administered 15 mg/kg/day (LOEL). The NOEL was 
5 mg/kg/day. Vertebral anomalies were seen in the offspring of rabbits 
administered 10 mg/kg/day (LOEL). The NOEL was 5 mg/kg/day.
    Dietary administration of 1 mg/kg/day (LOEL) for 6 months to dogs 
produced increased absolute and relative liver weights. The NOEL was 
0.33 mg/kg/day. Based on the NOEL of the study, an oral RfD of 0.0003 
mg/kg/day was derived.
    EPA believes that there is sufficient evidence for listing 
hydramethylnon on EPCRA section 313 pursuant to EPCRA section 
313(d)(2)(B) based on the available reproductive, developmental, and 
hepatic toxicity data for this chemical.
    The 96-hour LC50 in the Chanel Catfish was 90 ppb. 
Bioaccumulation factors in bluegill sunfish are 1300 for the whole 
fish, 780 for the fillet, and 1900 for viscera. EPA believes that there 
is sufficient evidence for listing hydramethylon on EPCRA section 313 
pursuant to EPCRA section 313(d)(2)(C) based on the available 
environmental toxicity data and the potential for bioaccumulation.
    136. Hydrochlorofluorocarbons (CAA OD) (Ref. 8). 
Hydrochlorofluorocarbons are known to release chlorine radicals into 
the stratosphere. Chlorine radicals act as catalysts to reduce the net 
amount of stratospheric ozone.
    Stratospheric ozone shields the earth from ultraviolet-B (UV-B) 
radiation (i.e., 290 to 320 nanometers). Decreases in total column 
ozone will increase the percentage of UV-B radiation, especially at its 
most harmful wavelengths, reaching the earth's surface.
    Exposure to UV-B radiation has been implicated by laboratory and 
epidemiologic studies as a cause of two types of nonmelanoma skin 
cancers: squamous cell cancer and basal cell cancer. Studies predict 
that for every 1 percent increase in UV-B radiation, nonmelanoma skin 
cancer cases would increase by about 1 to 3 percent.
    Recent epidemiological studies, including large case control 
studies, suggest that UV-B radiation plays an important role in causing 
malignant melanoma skin cancer. Recent studies predict that for each 1 
percent change in UV-B intensity, the incidence of melanoma could 
increase from 0.5 to 1 percent.
    Studies have demonstrated that UV-B radiation can suppress the 
immune response system in animals, and, possibly, in humans. Increases 
in exposure to UV-B radiation are likely to increase the incidence of 
cataracts and could adversely affect the retina.
    Aquatic organisms, particularly phytoplankton, zooplankton, and the 
larvae of many fishes, appear to be susceptible to harm from increased 
exposure to UV-B radiation because they spend at least part of their 
time at or near the surface of waters they inhabit.
    Increased UV-B penetration has been shown to result in adverse 
impacts on plants. Field studies on soybeans suggest that yield 
reductions could occur in some cultivars of soybeans, while evidence 
from laboratory studies suggest that two out of three cultivars are 
sensitive to UV-B.
    Because this increased UV-B radiation can be reasonably anticipated 
to lead to cancer and other chronic human health effects and 
significant adverse environmental effects, EPA believes there is 
sufficient evidence for listing the following HCFCs that are 
commercially viable on EPCRA section 313 pursuant to EPCRA sections 
313(d)(2)(B) and (C). EPA is proposing that the following HCFCs be 
added individually to EPCRA section 313:
    Dichloropentafluoropropane (CAS No. 127564-92-5)
    1,3-Dichloro-1,1,2,3,3-pentafluoropropane (HCFC-225ea) (CAS No. 
136013-79-1)
    2,2-Dichloro-1,1,1,3,3-pentafluoropropane (HCFC-225aa) (CAS No. 
128903-21-9)
    1,1-Dichloro-1,2,3,3,3-pentafluoropropane (HCFC-225eb) (CAS No. 
111512-56-2)
    1,1-Dichloro-1,2,2,3,3-pentafluoropropane (HCFC-225cc) (CAS No. 
13474-88-9)
    1,3-Dichloro-1,1,2,2,3-pentafluoropropane (HCFC-225cb) (CAS No. 
000507-55-1)
    1,2-Dichloro-1,1,3,3,3-pentafluoropropane (HCFC-225da) (CAS No. 
000431-86-7)
    3,3-Dichloro-1,1,1,2,2-pentafluoropropane (HCFC-225ca) (CAS No. 
000422-56-0)
    2,3-Dichloro-1,1,1,2,3-pentafluoropropane (HCFC-225ba) (CAS No. 
000422-48-0)
    1,2-Dichloro-1,1,2,3,3-pentafluoropropane (HCFC-225bb) (CAS No. 
000422-44-6)
    Dichlorofluoromethane (HCFC-21) (CAS No. 000075-43-4)
    1,1,1,2-Tetrachloro-2-fluoroethane (HCFC-121a) (CAS No. 000354-11-
0)
    1,1,2,2-Tetrachloro-1-fluoroethane (HCFC-121) (CAS No. 000354-14-3)
    1,2-Dichloro-1,1-difluoroethane (HCFC-132b) (CAS No. 001649-08-7)
    2-Chloro-1,1,1-trifluoroethane (HCFC-133a) (CAS No. 000075-88-7)
    3-Chloro-1,1,1-trifluoropropane (HCFC-253fb) (CAS No. 000460-35-5).
    137. Imazalil (1-[2-(2,4-dichlorophenyl)-2-(2-propenyloxy)ethyl]-
1H-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-(1-methylethyl)-2,4-dioxo-
1-imidazolidinecarboxamide) (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 
EC50 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 LD50 is 25 mg/kg and the rat 
inhalation LC50 value is 0.044 mg/L. The 4-hour inhalation 
LC100 in mice is 0.007 mg/L. The rabbit oral LD50 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 LC50 of 12 ppb for bluegills and a 24-hour 
LC50 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[(1-methylethyl) amino] 
phosphinothioyl] oxy] benzoic 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 EC50 of 1.6 ppb and a mysid 96-hour EC50 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 LC50 value of isophorone diisocyanate in 
rats is 0.123 mg/L. The rat and mouse 3-hour inhalation RD50 (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-1-methyl-2-oxoethyl ester) (CAS No. 077501-63-4) (FIFRA AI) 
(Ref. 3). Lactofen meets the criteria of an EPA Group B2 compound, 
i.e., a probable human carcinogen. This conclusion was based on an 
increased incidence of hepatocellular carcinomas in males and combined 
incidence of hepatocellular adenomas and carcinomas in both sexes of 
CD-1 mice following dietary administration of lactofen. In CD rats, 
there was increased incidence of liver neoplastic nodules in both 
sexes. Four structurally similar chemicals, acifluorfen, nitrofen, 
oxyfluorfen, and fomesafen, all produced hepatocellular tumors in 
rodents.
    Results of several subchronic and chronic studies indicated the 
liver and kidney as target organs for lactofen. Increased absolute and 
relative liver weight and hepatocytomegaly (the LOEL was 1.5 mg/kg/day; 
the NOEL was not determined) were observed in male mice fed lactofen 
for 78 weeks. At 37.5 mg/kg/day, there was also an increased incidence 
of cataracts and renal pigmentation. Based on the LOEL, an oral RfD of 
0.002 mg/kg/day was derived. Renal dysfunction and decreased hemoglobin 
and hematocrit levels and red blood cell counts (the LOEL was 25/75 mg/
kg/day; the NOEL was 5 mg/kg/day) were observed in a 1-year feeding 
study in dogs. Increased renal and hepatic pigmentation (the LOEL was 
50 mg/kg/day; the NOEL was 25 mg/kg/day) were noted in a 2-year feeding 
study in rats. In a 90-day mouse study, increased alkaline phosphatase, 
serum glutamate oxaloacetate transaminase (SGOT), and serum gleutanic 
pyruvic transaminase (SGPT) activities, increased liver weight, hepatic 
necrosis, biliary hyperplasia, decreased hematocrit and hemoglobin 
levels and red blood cell counts, extramedullary hematopoiesis, and 
kidney nephrosis and fibrosis (the LOEL was 26 mg/kg/day; the NOEL was 
not determined) were seen. Decreased hemoglobin and hematocrit levels, 
decreased red blood cell counts, and brown pigment in the kidney and 
liver (the LOEL was 50 mg/kg/day) were noted in a 90-day feeding study 
in rats.
    EPA believes that there is sufficient evidence for listing lactofen 
on EPCRA section 313 pursuant to EPCRA section 313(d)(2)(B) based on 
the available carcinogenicity data and hepatic, renal, and 
hematological toxicity data for this chemical.
    146. Linuron (CAS No. 000330-55-2) (FIFRA SR) (Ref. 8). The 
appearance of sulfhemoglobin 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 LC50 of 68 ppb for rainbow trout, a 96-hour LC50 of 51 
ppb for sheepshead minnow, and a 96-hour LC50 of 76 ppb for lake 
trout. In addition, the measured 48-hour EC50 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 
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 (MBT) (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 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-dichlorophenyl)-4-methyl-1,2,4-
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(d)(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 
LD50 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-methylphenoxy) 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 LC50 value for 1,1-
methylenebis(4-isocyanatocyclohexane) is 0.21 mg/L. The 3-hour mouse 
inhalation RD50 (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 1,1-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(thiocyanate) 
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 LD50 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 LC50 of 130 ppb for 
bluegills, and a daphnid 48-hour LC50 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 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.
    162. 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 LD50 values are reported to be 6.01 mg/kg and 18 mg/kg, 
respectively. The rat and mouse 4-hour inhalation LC50 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 
hepatotoxicity, 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 EC50 of 0.14 ppb for daphnids and a 96-hour LC50 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 F1 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 (EBDC) 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.
    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 the 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 ppm (2.5 mg/kg/day). In a 2-year rat feeding 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 mevinphos include a 96-hour 
LC50 of 70 ppb for bluegills, and a 96-hour LC50 of 0.16 ppb 
for daphnids. Measured acute avian toxicity data include a pheasant 
oral LD50 of 1.37 mg/kg, a mallard duck oral LD50 of 4.63 mg/
kg, and a sharp-tailed grouse oral LD50 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 (1H-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 EC50 
of 90 ppb and a 10-day EC50 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)-1H-1,2,4-
triazole-1-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 toxicity 
data for ethylenethiourea, a metabolite and degradation product of 
nabam.
    173. Naled (CAS 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 
EC50 of 0.35 ppb for daphnids and a 96-hour LC50 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 in 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 in 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 believes 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 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-Nitroaniline (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). In 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. Norflurazon (4-Chloro-5-(methylamino)-2-
[3(trifluoromethyl)phenyl]-3(2H)-pyridazinone) (CAS No. 027314-13-2) 
(FIFRA AI) (Ref. 3). Congestion of the liver, hepatocyte swelling and 
increased liver weights, and increase in colloid vacuole in the thyroid 
were observed in dogs fed 450 ppm (10.25 mg/kg/day) norflurazon for 6 
months. The NOEL was 150 ppm (3.75 mg/kg/day). An oral RfD of 0.04 mg/
kg/day has been determined. Increased relative liver weight and 
hypertrophy of the thyroid with depletion of colloid were seen in rats 
fed 2,500 ppm (125 mg/kg/day) norflurazon for 90 days. The NOEL was 500 
ppm (25 mg/kg/day). Hepatic hyperplasia and hypertrophy and increased 
relative liver weight were noted in a 28-day feeding study in rats. The 
LOEL was 1,000 ppm (50 mg/kg/day) and the NOEL was 500 ppm (25 mg/kg/
day). Increased relative liver weight and diffuse and smooth granular 
livers were seen in a 28-day feeding study in mice. The LOEL was 2,520 
ppm (328 mg/kg/day) and the NOEL was 420 ppm (55 mg/kg/day). EPA 
believes that there is sufficient evidence for listing norflurazon on 
EPCRA section 313 pursuant to EPCRA section 313(d)(2)(B) based on the 
available hepatic and thyroid toxicity data.
    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 mg/kg/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 the available hepatic and hematological toxicity 
data for this chemical.
    182. Oxydemeton methyl (S-(2-(Ethylsulfinyl)ethyl) 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 F0 and F1 
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-(1-methylethoxy)phenyl]5- (1,1-
dimethylethyl)-1,3,4-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 
LC50 of 80 ppb for striped bass, a 96-hour LC50 of 30 ppb for 
channel catfish, and a 96-hour LC50 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 LD50 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-(1-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. 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.
    Intraperitoneal 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) 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 LD50 and 4-hour rat inhalation 
LC50 values for perchloromethyl mercaptan are 8.26 mg/kg and 0.26 
mg/L, respectively. The 2-hour mouse inhalation LC50 value is 
reported to be 0.296 mg/L. In an eye irritation test, 50 micrograms 
(g) (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-
dimethylcyclopropanecarboxylic acid, (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 liver 
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 LC50 of 3.5 ppb, a rainbow trout 96-hour measured 
LC50 of 0.62 ppb, a bluegill 96-hour LC50 of 2.52 ppb, an 
Atlantic silverside 96-hour measured LC50 2.2 ppb, and a daphnid 
48-hour LC50 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 
LC50 of 700 ppb for daphnids. The measured 28-day LC50 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-phenoxyphenyl)methyl 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 LC50 of 16.7 ppb and a goldfish 48-hour LC50 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 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 LC50 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 
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 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 
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/m3) and 
a LOAEL of 110 mg/m3 (80 ppm; HEC is 2.4 mg/m3). 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 LC50 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.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. 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 RfD 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 LC50 of 3.4 ppb for rainbow trout and a 96-hour LC50 
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-dimethyl 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.
    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, nitroarenes, 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 promotors, 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 carcinogenicity 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 (1,2,3-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(j)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.
    l. Dibenzo(a,h)pyrene (CAS No. 000189-64-0). Dibenzo(a,h)pyrene is 
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. Dibenzo(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-
Dibenzo(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-Methylchrysene (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[1,2,3-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 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 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 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] amino]sulfonyl] benzoate) (CAS No. 
086209-51-0) (FIFRA AI) (Ref. 3). In a 90-day dog feeding study, 
reduced thyroid weights accompanied by colloid depletion and 
parafollicular hyperplasia and anemia were observed at the LOEL of 25 
mg/kg/day. The NOEL was 0.625 mg/kg/day. In a 1-year dog study, dietary 
administration of 250/125 mg/kg/day (LOEL: the dose was changed after 
week 10 in the study) produced thyroid hyperplasia, anemia, increased 
platelet levels, vacuolar changes, and increased absolute and relative 
liver weights. The NOEL was 25 mg/kg/day. In an 18-month study in mice, 
dietary administration of 1.7 mg/kg/day produced increased absolute and 
relative liver weights in females. No NOEL was established. Based on 
this study, an oral RfD of 0.006 mg/kg/day was derived. In a 2-year 
mouse study, increases in absolute and relative liver weights were 
observed at 408 mg/kg/day in males and 1.7 mg/kg/day in females. The 
systemic LOEL and NOEL in males was 408 mg/kg/day and 40.2 mg/kg/day, 
respectively. The systemic LOEL in females was 1.7 mg/kg/day and a NOEL 
could not be established. EPA believes that there is sufficient 
evidence for listing primisulfuron on EPCRA section 313 pursuant to 
EPCRA section 313(d)(2)(B) based on the available thyroid and liver 
toxicity data for this chemical.
    Plant toxicity values include a duckweed 14-day EC50 of 0.27 
ppb and an algae 7-day EC50 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(1-methylethyl)-6-methylthio-1,3,5-
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-(1-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-dichlorophenyl)propanamide) (CAS No. 000709-
98-8) (FIFRA AI) (Ref. 3). Results of several subchronic and chronic 
toxicity studies indicated the 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 SGOT 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 LC50 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; RCRA APP8; 
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] oxy]-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.
    Red blood 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 (1-[2-(2,4-dichlorophenyl)-4-propyl-1,3-
dioxolan-2-yl]- methyl-1H-1,2,4,-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 SGOT 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) oxy]phenoxy] 
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 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]methyl 2,2-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 LC50 of 0.275 ppb (89 percent a.i.), a bluegill 
sunfish 96-hour LC50 of 0.750 ppb (89 percent a.i.), a lake trout 
96-hour LC50 of 1.7 ppb (84.5 percent a.i.), and a fathead minnow 
96-hour LC50 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-[1-(ethoxyimino)butyl]-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 SGOT 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 SGOT, 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 
g/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.
    227. Sodium dimethyldithiocarbamate (CAS No. 000128-04-1) (FIFRA 
AI) (Ref. 3). By analogy to potassium dimethyldithiocarbamate, 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 sternebrae, 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, gavage administration of sodium fluoroacetate (0.02 mg/kg/day) 
resulted in decreased testis weight and altered spermatogenesis in 
males (the NOAEL was 0.05 mg/kg/day). In addition, increased heart 
weight was noted in females and males administered 0.20 mg/kg/day of 
sodium fluoroacetate. The increase in heart weight, however, was only 
accompanied by subacute, minimal inflammation (not dose-related). Also, 
fluorocitrate levels were significantly increased after 4 weeks in 
males administered 0.50 mg/kg/day and after 13 weeks in both male and 
female rats administered 0.20 or 0.50 mg/kg/day. The testicular and 
cardiac effects were reported to be consistent with those noted in the 
literature.
    A case study reported a deliberate ingestion of an unspecified dose 
of sodium fluroacetate by a healthy female. The woman experienced 
nausea, vomiting, and abdominal pain 30 minutes after ingestion, with 
subsequent seizures occurring 60 minutes after the initial onset of 
symptoms. Neurological examination after 2 weeks revealed severe 
cerebellar dysfunction. By 18 months, memory disturbances and 
depressive behavior persisted. Inhalation exposure to unspecified 
levels of sodium fluoroacetate caused salivation, loss of speech, 
violent convulsions, and coma in a male worker. The patient ultimately 
recovered. Neurological effects have also been reported in rats in a 
13-week oral study. Four of 20 female rats treated with 0.50 mg/kg/day 
(the highest dose tested) exhibited convulsions at day 79, with no 
recurrences for the remainder of the study. An estimated lethal dose of 
sodium fluoroacetate in humans ranges from 5 to 10 mg/kg.
    EPA believes that there is sufficient evidence for listing sodium 
fluoroacetate on EPCRA section 313 pursuant to EPCRA section 
313(d)(2)(B) based on the neurologic, reproductive, and myocardial 
toxicity data for this chemical.
    Measured oral LD50 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 LD50 of 0.22 
to 0.44 mg/kg for mule deer, an oral LD50 of 1.41 mg/kg for male 
ferrets, and an oral LD50 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 LC50 of 100 ppb for bluegill and a 96-hour measured 
LC50 of 80 ppb for fathead minnow. In addition, the 96-hour 
measured LC50 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 LC50 of 55 ppb, a bluegill 96-hour 
LC50 of 44 ppb, a fathead minnow 96-hour LC50 of 20 ppb, and 
a shrimp 96-hour LC50 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 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-1-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-1-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.
    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 
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/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 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 LD50 is between 745 mg/kg and 994 mg/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 
LC50 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-(1,1-Dimethylethyl)-1,3,4-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 
cell, lymphocyte, and neutrophil counts in males and females. The NOEL 
for females was 5 mg/kg/day. Increased absolute and relative liver 
weights were observed at 5 mg/kg/day in males, thus no NOEL could be 
established for males. Dietary administration of 10 mg/kg/day (LOEL) 
for 3 months to rats produced increased absolute liver weights, 
decreased bilirubin levels, and hepatocellular hypertrophy. The NOEL 
was 5 mg/kg/day. In a 6-month dog study, dietary administration of 10 
mg/kg/day (LOEL) produced hepatotoxicity (effects not reported). The 
NOEL was 1 mg/kg/day. In a 2-year mouse study, dietary administration 
of 13.5 mg/kg/day produced liver necrosis. The NOEL was 3.4 mg/kg/day.
    EPA believes that there is sufficient evidence for listing 
tefluthrin on EPCRA section 313 pursuant to EPCRA section 313(d)(2)(B) 
based on the available developmental, neurological, hepatic, and 
hematological toxicity data for this chemical.
    Aquatic acute toxicity values for tefluthrin include a rainbow 
trout 96-hour LC50 of 0.06 ppb, a bluegill 96-hour LC50 of 
0.13 ppb, a sheepshead minnow 96-hour LC50 of 0.13 ppb, a daphnid 
48-hour EC50 of 0.07 ppb, and a mysid 96-hour EC50 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-(1,1-dimethylethyl)-6-methyl- 2,4-
(1H,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 (1,3,4,5,6,7-hexahydro-1,3-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 LD50 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 
LD50 was greater than 2,500 mg/kg. Tremors, ataxia, dyspnea, 
gastointestinal hypermotility, and diarrhea were observed in rats and 
mice administered tetramethrin subcutaneously or intraperitonealy. The 
LD50 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 LC50 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)-1H-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 LC50 of 560 ppb, a daphnid 48-hour EC50 of 0.31 
ppb, and a mysid 96-hour LC50 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 LC50 of 560 ppb, a daphnid 48-hour 
EC50 of 0.31 ppb, and a mysid 96-hour LC50 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 
LC50 of 760 ppb, a striped bass 96-hour LC50 of 760 ppb, a 
rainbow trout 96-hour LC50 of 790 ppb, and a green algae 72-hour 
EC50 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 LC50 of 1.47 ppm , a rainbow trout 96-hour LC50 of 2.65 
ppm, a sheepshead minnow 96-hour LC50 of 530 ppb, a daphnid 48-
hour EC50 of 27 ppb, a mysid 96-hour LC50 of 29.3 ppb, an 
eastern oyster 96-hour LC50 of 1.0 ppb, and an algae 96-hour 
EC50 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)] 
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/kg/day.
    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 LD50s 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 LD50 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 (1-(4-chlorophenoxy)-3,3-dimethyl-1-(1H-1,2,4-
triazol-1-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 study. 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 nonneoplastic 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-1,3,5-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 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.
    256. Tributyltin fluoride (CAS No. 001983-10-4) (FIFRA AI) (Ref. 
3). Aquatic acute toxicity values for tributyltin fluoride include a 
bleak fish 96-hour LC50 of 2.3 ppb, an algae 72-hour EC50 of 
9.3 ppb, and a Harpacticoid copepod 96-hour LC50 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 resorptions 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.
    258. S,S,S-Tributyltrithiophosphate (DEF) (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 LC50 of 
660 ppb (0.660 ppm) and a bluegill 96-hour LC50 of 620 ppb (0.620 
ppm). The measured log Kow 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 LC50 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 LC50 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 
LC50 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 the most sensitive effects of 1,2,3-
trichloropropane.
    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/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/m3. 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 LC50 for carp of 55 ppb and a 72-hour EC50 
(growth) for marine green algae of 0.92 ppb. In addition, the measured 
aquatic toxicity information indicates a freshwater green algae 8-day 
EC50 (growth) of 2 ppb. EPA believes that there is sufficient 
evidence for listing triphenyltin chloride on EPCRA section 313 
pursuant to EPCRA section 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 LC50 of 5.4 ppb, a bluegill 96-
hour LC50 of 23 ppb, a rainbow trout 96-hour LC50 of 15 ppb, 
and a marine green algae 72-hour LC50 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/m3 
(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 in 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. Other 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. In 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 
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; isophorone diisocyanate; 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.

VIII. 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 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 Sec. 372.65 by adding chemicals to paragraph (a) 
alphabetically, to paragraph (b) by CAS no. sequence, and to paragraph 
(c) by alphabetically adding four categories to read as follows:


Sec. 372.65  Chemicals and chemical categories to which the part 
applies.

      *  *  *  *  *
    (a)  *  *  *

------------------------------------------------------------------------
                                                              Effective 
            Chemical Name                    CAS No.             Date   
------------------------------------------------------------------------
Abamectin [Avermectin B1]              71751-41-2                 1/1/95
Acephate (Acetylphosphoramidothioic    30560-19-1                 1/1/95
 acid O,S-dimethyl ester)                                               
                                                                        
                                 *******                                
Acifluorfen, sodium salt [5-(2-Chloro- 62476-59-9                 1/1/95
 4-(triflouromethyl)phenoxy)-2-nitro-                                   
 benzoic acid, sodium salt]                                             
                                                                        
                                 *******                                
Alachlor                               15972-60-8                 1/1/95
Aldicarb                               116-06-3                   1/1/95
                                                                        
                                 *******                                
d-trans-Allethrin [d-trans-            28057-48-9                 1/1/95
 Chrysanthemic acid of d-allethrone]                                    
Allylamine                             107-11-9                   1/1/95
                                                                        
                                 *******                                
Aluminum phosphide                     20859-73-8                 1/1/95
Ametryn (N-Ethyl-N'-(1-methylethyl)-6- 834-12-8                   1/1/95
 (methylthio)-1,3,5,-triazine-2,4-                                      
 diamine)                                                               
                                                                        
                                 *******                                
Amitraz                                33089-61-1                 1/1/95
                                                                        
                                 *******                                
Anilazine [4,6-dichloro-N-(2-          101-05-3                   1/1/95
 chlorophenyl)-1,3,5-triazin-2-amine]                                   
                                                                        
                                 *******                                
Atrazine (6-Chloro-N-ethyl-N'-(1-      1912-24-9                  1/1/95
 methylethyl)-1,3,5,-triazine-2,4-                                      
 diamine)                                                               
                                                                        
                                 *******                                
Bendiocarb [2,2-Dimethyl-1,3-          22781-23-3                 1/1/95
 benzodioxol-4-ol methylcarbamate]                                      
Benfluralin (N-Butyl-N-ethyl-2,6-      1861-40-1                  1/1/95
 dinitro-4-                                                             
 (trifluoromethyl)benzenamine)                                          
Benomyl                                17804-35-2                 1/1/95
                                                                        
                                 *******                                
o-Benzyl-p-chlorophenol                120-32-1                   1/1/95
                                                                        
                                 *******                                
Bifenthrin                             82657-04-3                 1/1/95
                                                                        
                                 *******                                
Bis(tributylin) oxide                  56-35-9                    1/1/95
Boron trichloride                      10294-34-5                 1/1/95
Boron trifluoride                      7637-07-2                  1/1/95
Bromacil (5-Bromo-6-methyl-3-(1-       314-40-9                   1/1/95
 methylpropyl)-2,4-(1H,3H)-                                             
 pyrimidinedione)                                                       
Bromacil, lithium salt [2,4-(1H,3H)-   53404-19-6                 1/1/95
 Pyrimidinedione, 5-bromo-6-methyl-3-                                   
 (1-methylpropyl), lithium salt]                                        
Bromine                                7726-95-6                  1/1/95
1-Bromo-1-(bromomethyl)-1,3-           35691-65-7                 1/1/95
 propanedicarbonitrile                                                  
                                                                        
                                 *******                                
2-Bromo-2-nitropropane-1,3-diol        52-51-7                    1/1/95
 (Bronopol)                                                             
                                                                        
                                 *******                                
Bromoxynil (3,5-Dibromo-4-             1689-84-5                  1/1/95
 hydroxybenzonitrile)                                                   
Bromoxynil octanoate (Octanoic acid,   1689-99-2                  1/1/95
 2,6-dibromo-4-cyanophenyl ester)                                       
Brucine                                357-57-3                   1/1/95
                                                                        
                                 *******                                
Butylate (Bis-2-                       2008-41-5                  1/1/95
 methylpropyl)carbamothioic acid S-                                     
 ethyl ester)                                                           
Butylated hydroxyanisole               25013-16-5                 1/1/95
                                                                        
                                 *******                                
C.I. Acid Red 114                      6459-94-5                  1/1/95
                                                                        
                                 *******                                
C.I. Direct Blue 218                   28407-37-6                 1/1/95
                                                                        
                                 *******                                
Calcium hypochlorite                   7778-54-3                  1/1/95
Caprolactam                            105-60-2                   1/1/95
                                                                        
                                 *******                                
Carbofuran                             1563-66-2                  1/1/95
                                                                        
                                 *******                                
Carbon monoxide                        630-08-0                   1/1/95
                                                                        
                                 *******                                
Carboxin (5,6-Dihydro-2-methyl-N-      5234-68-4                  1/1/95
 phenyl-1,4-oxathiin-3-carboxamide)                                     
                                                                        
                                 *******                                
Chinomethionat [6-Methyl-1,3-          2439-01-2                  1/1/95
 dithiolo[4,5-b]quinoxalin-2-one]                                       
                                                                        
                                 *******                                
Chlorendic acid                        115-28-6                   1/1/95
Chlorimuron ethyl [Ethyl-2-[[[(4-      90982-32-4                 1/1/95
 chloro-6-methoxyprimidin-2-yl)-                                        
 carbonyl]-amino]sulfonyl]benzoate]                                     
                                                                        
                                 *******                                
1-(3-Chloroallyl)-3,5,7-triaza-1-      4080-31-3                  1/1/95
 azoniaadamantane chloride                                              
p-Chloroaniline                        106-47-8                   1/1/95
                                                                        
                                 *******                                
5-Chloro-2-(2,4-                       3380-34-5                  1/1/95
 dichlorophenoxy)phenol                                                 
                                                                        
                                 *******                                
3-Chloro-2-methyl-1-propene            563-47-3                   1/1/95
p-Chlorophenyl isocyanate              104-12-1                   1/1/95
Chloropicrin                           76-06-2                    1/1/95
                                                                        
                                 *******                                
3-Chloropropionitrile                  542-76-7                   1/1/95
                                                                        
                                 *******                                
p-Chloro-o-toluidine                   95-69-2                    1/1/95
2-Chloro-1,1,1-trifluoro-ethane (HCFC- 75-88-7                    1/1/95
 133a)                                                                  
Chlorotrifluoromethane (CFC-13)        75-72-9                    1/1/95
3-Chloro-1,1,1-trifluoro-propane       460-35-5                   1/1/95
 (HCFC-253fb)                                                           
Chlorpyrifos methyl [O,O-dimethyl-O-   5598-13-0                  1/1/95
 (3,5,6-trichloro-2-                                                    
 pyridyl)phosphorothioate                                               
Chlorsulfuron [2-chloro-N-[[4-methoxy- 64902-72-3                 1/1/95
 6-methyl-1,3,5-triazin-2-                                              
 yl)amino]carbonyl]benzenesulfonamide                                   
 ]                                                                      
                                                                        
                                 *******                                
Clomazone [2-[(2-Chlorophenyl)methyl]- 81777-89-1                 1/1/95
 4,4-dimethyl-3-isoxazolidinone]                                        
Crotonaldehyde                         4170-30-3                  1/1/95
Cyanazine                              21725-46-2                 1/1/95
                                                                        
                                 *******                                
Cycloate                               1134-23-2                  1/1/95
                                                                        
                                 *******                                
Cyclohexanol                           108-93-0                   1/1/95
Cyfluthrin [3-(2,2-Dichloroethenyl)-   68359-37-5                 1/1/95
 2,2-dimethylcyclopropanecarboxylic                                     
 acid, cyano(4-fluoro-3-                                                
 phenoxyphenyl)methyl ester]                                            
Cyhalothrin [3-(2-Chloro-3,3,3-        68085-85-8                 1/1/95
 trifluoro-1-propenyl)-2,2-                                             
 dimethylcyclopropanecarboxylic acid                                    
 cyano(3-phenoxyphenyl)methyl ester]                                    
Cyromazine [N-Cyclopropyl-1,3,5-       66215-27-8                 1/1/95
 triazine-2,4,6-triamine]                                               
                                                                        
                                 *******                                
Dazomet(Tetrahydro-3,5-dimethyl-2H-    533-74-4                   1/1/95
 1,3,5-thiadiazine-2-thione)                                            
Dazomet, sodium salt [Tetrahydro-3,5-  53404-60-7                 1/1/95
 dimethyl-2H-1,3,5-thiadiazine-2-                                       
 thione, ion(1-), sodium]                                               
2,4,-DB                                94-82-6                    1/1/95
2,4-D butoxyethyl ester                1929-73-3                  1/1/95
2,4-D butyl ester                      94-80-4                    1/1/95
2,4-D chlorocrotyl ester               2971-38-2                  1/1/95
                                                                        
                                 *******                                
Desmedipham                            13684-56-5                 1/1/95
2,4-D 2-ethylhexyl ester               1928-43-4                  1/1/95
2,4-D 2-ethyl-4-methylpentyl ester     53404-37-8                 1/1/95
                                                                        
                                 *******                                
Diazinon                               333-41-5                   1/1/95
                                                                        
                                 *******                                
2,2-Dibromo-3-nitrilopropionamide      10222-01-2                 1/1/95
                                                                        
                                 *******                                
Dicamba (3,6-Dichloro-2-               1918-00-9                  1/1/95
 methyoxybenzoic acid)                                                  
Dichloran [2,6-Dichloro-4-             99-30-9                    1/1/95
 nitroaniline]                                                          
                                                                        
                                 *******                                
3,3'-Dichlorobenzidine                 612-83-9                   1/1/95
 dihydrochloride                                                        
3,3'-Dichlorobenzidine sulfate         64969-34-2                 1/1/95
                                                                        
                                 *******                                
trans-1,4-Dichloro-2-butene            110-57-6                   1/1/95
1,2-Dichloro-1,1-difluoroethane (HCFC- 1649-08-7                  1/1/95
 132b)                                                                  
                                                                        
                                 *******                                
Dichlorofluoromethane (HCFC-21)        75-43-4                    1/1/95
                                                                        
                                 *******                                
Dichloromethylphenylsilane             149-74-6                   1/1/95
Dichloropentafluoropropane             127564-92-5                1/1/95
1,1-dichloro-1,2,2,3,3-                13474-88-9                 1/1/95
 pentafluoropropane (HCFC-225cc)                                        
1,1-dichloro-1,2,3,3,3-                111512-56-2                1/1/95
 pentafluoropropane (HCFC-225eb)                                        
1,2-dichloro-1,1,2,3,3-                422-44-6                   1/1/95
 pentafluoropropane (HCFC-225bb)                                        
1,2-dichloro-1,1,3,3,3-                431-86-7                   1/1/95
 pentafluoropropane (HCFC-225da)                                        
1,3-dichloro-1,1,2,2,3-                507-55-1                   1/1/95
 pentafluoropropane (HCFC-225cb)                                        
1,3-dichloro-1,1,2,3,3-                136013-79-1                1/1/95
 pentafluoropropane (HCFC-225ea)                                        
2,2-dichloro-1,1,1,3,3-                128903-21-9                1/1/95
 pentafluoropropane (HCFC-225aa)                                        
2,3-dichloro-1,1,1,2,3-                422-48-0                   1/1/95
 pentafluoropropane (HCFC-225ba)                                        
3,3-dichloro-1,1,1,2,2-                422-56-0                   1/1/95
 pentafluoropropane (HCFC-225ca)                                        
Dichlorophene [ 2,2'-Methylene-bis(4-  97-23-4                    1/1/95
 chlorophenol)]                                                         
                                                                        
                                 *******                                
trans-1,3-Dichloropropene              10061-02-6                 1/1/95
                                                                        
                                 *******                                
Diclofop methyl [2-[4-(2,4-            51338-27-3                 1/1/95
 Dichlorophenoxy)phenoxy]propanoic                                      
 acid, methyl ester]                                                    
                                                                        
                                 *******                                
Dicyclopentadiene                      77-73-6                    1/1/95
                                                                        
                                 *******                                
Diethatyl ethyl                        38727-55-8                 1/1/95
                                                                        
                                 *******                                
Diflubenzuron                          35367-38-5                 1/1/95
Diglycidyl resorcinol ether            101-90-6                   1/1/95
Dimethipin [2,3,-Dihydro-5,6-dimethyl- 55290-64-7                 1/1/95
 1,4-dithiin-1,1,4,4-tetraoxide]                                        
Dimethoate                             60-51-5                    1/1/95
                                                                        
                                 *******                                
3,3'-Dimethoxybenzidine                20325-40-0                 1/1/95
 dihydrochloride (o-Dianisidine                                         
 dihydrochloride)                                                       
3,3'-Dimethoxybenzidine hydrochloride  111984-09-9                1/1/95
 (o-Dianisidine hydrochloride)                                          
Dimethylamine                          124-40-3                   1/1/95
Dimethylamine dicamba                  2300-66-5                  1/1/95
                                                                        
                                 *******                                
3,3'-Dimethylbenzidine                 612-82-8                   1/1/95
 dihydrochloride (o-Tolidine                                            
 dihydrochloride)                                                       
3,3'-Dimethylbenzidine                 41766-75-0                 1/1/95
 dihydrofluoride (o-Tolidine                                            
 dihydrofluoride)                                                       
                                                                        
                                 *******                                
Dimethyl chlorothiophosphate           2524-03-0                  1/1/95
Dimethyldichlorosilane                 75-78-5                    1/1/95
N,N-Dimethylformamide                  68-12-2                    1/1/95
                                                                        
                                 *******                                
2,6-Dimethylphenol                     576-26-1                   1/1/95
                                                                        
                                 *******                                
Dinocap                                39300-45-3                 1/1/95
Dinoseb                                88-85-7                    1/1/95
                                                                        
                                 *******                                
Diphenamid                             957-51-7                   1/1/95
Diphenylamine                          122-39-4                   1/1/95
                                                                        
                                 *******                                
Dipotassium endothall [7-              2164-07-0                  1/1/95
 Oxabicyclo(2.2.1)heptane-2,3-                                          
 dicarboxylic acid, dipotassium salt]                                   
Dipropyl isocinchomeronate             136-45-8                   1/1/95
Disodium cyanodithioimidocarbonate     138-93-2                   1/1/95
2,4-D isopropyl ester                  94-11-1                    1/1/95
2,4-Dithiobiuret                       541-53-7                   1/1/95
Dithiopyr [2-(Difluoromethyl)-4-(2-    97886-45-8                 1/1/95
 methylpropyl)-6-(trifluoromethyl)-                                     
 3,5-pyridinedicarbothioic acid S,S-                                    
 dimethyl ester]                                                        
Diuron                                 330-54-1                   1/1/95
2,4-D 2-octyl ester                    1917-97-1                  1/1/95
Dodine [Dodecylguanidine monoacetate]  2439-10-3                  1/1/95
2,4,-DP                                120-36-5                   1/1/95
2,4-D propylene glycol butyl ether     1320-18-9                  1/1/95
 ester                                                                  
2,4-D sodium salt                      2702-72-9                  1/1/95
                                                                        
                                 *******                                
Ethoprop [Phosphorodithioic acid O-    13194-48-4                 1/1/95
 ethyl S,S-dipropyl ester]                                              
                                                                        
                                 *******                                
Ethyl dipropylthiocarbamate [EPTC]     759-94-4                   1/1/95
                                                                        
                                 *******                                
Famphur                                52-85-7                    1/1/95
Fenarimol [.alpha.-(2-Chlorophenyl)-   60168-88-9                 1/1/95
 .alpha.-4-chlorophenyl)-5-                                             
 pyrimidinemethanol]                                                    
Fenbutatin oxide (Hexakis(2-methyl-2-  13356-08-6                 1/1/95
 phenyl-propyl)distannoxane)                                            
Fenoxaprop ethyl [2-(4-((6-Chloro-2-   66441-23-4                 1/1/95
 benzoxazolylen)oxy)phenoxy)propanoic                                   
 acid,ethyl ester]                                                      
Fenoxycarb [2-(4-                      72490-01-8                 1/1/95
 Phenoxyphenoxy)ethyl]carbamic acid                                     
 ethyl ester]                                                           
Fenpropathrin [2,2,3,3-                39515-41-8                 1/1/95
 Tetramethylcyclopropane carboxylic                                     
 acid cyano(3-phenoxy-phenyl)methyl                                     
 ester]                                                                 
Fenthion [O,O-Dimethyl O-[3-methyl-4-  55-38-9                    1/1/95
 (methylthio)phenyl]ester,                                              
 phosphorothioic acid]                                                  
Fenvalerate [4-Chloro-alpha-(1-        51630-58-1                 1/1/95
 methylethyl)benzeneacetic acid                                         
 cyano(3-phenoxyphenyl)methyl ester]                                    
Ferbam [Tris(dimethylcarbamo-          14484-64-1                 1/1/95
 dithioato-S,S')iron]                                                   
Fluazifop-butyl [2-[4-[[5-             69806-50-4                 1/1/95
 (Trifluoromethyl)-2-pyridinyl]oxy]-                                    
 phenoxy]propanoic acid, butyl ester]                                   
Flumetralin [2-Chloro-N-(2,6-dinitro-  62924-70-3                 1/1/95
 4-(trifluoromethyl)phenyl)-N-ethyl-6-                                  
 fluorobenzenemethanamine]                                              
                                                                        
                                 *******                                
Fluorine                               7782-41-4                  1/1/95
Fluorouracil (5-Fluorouracil)          51-21-8                    1/1/95
Fluvalinate [N-[2-Chloro-4-            69409-94-5                 1/1/95
 (trifluoromethyl)phenyl]-DL-                                           
 valine(+)-cyano (3-                                                    
 phenoxyphenyl)methyl ester]                                            
Folpet                                 133-07-3                   1/1/95
Fomesafen [5-(2-Chloro-4-              72178-02-0                 1/1/95
 (trifluoromethyl)phenoxy)-N-                                           
 methylsulfonyl)-2-nitrobenzamide]                                      
                                                                        
                                 *******                                
alpha-Hexachlorocyclohexane            319-84-6                   1/1/95
                                                                        
                                 *******                                
Hexamethylene-1,6-diisocyanate         822-60-0                   1/1/95
                                                                        
                                 *******                                
n-Hexane                               110-54-3                   1/1/95
Hexazinone                             51235-04-2                 1/1/95
Hydramethylnon [Tetrahydro-5,5-        67485-29-4                 1/1/95
 dimethyl-2(1H)-pyrimidinone[3-[4-                                      
 (trifluoromethyl)phenyl]-1-[2-[4-                                      
 (trifluoromethyl)phenyl]ethenyl]-2-                                    
 propenylidene]hydrazone]                                               
                                                                        
                                 *******                                
Imazalil [1-[2-(2,4-Dichlorophenyl)-2- 35554-44-0                 1/1/95
 (2-propenyloxy)ethyl]-1H-imidazole]                                    
3-Iodo-2-propynyl butylcarbamate       55406-53-6                 1/1/95
Iprodione [3-(3,5-Dichlorophenyl)-N-   36734-19-7                 1/1/95
 (1-methylethyl)-2,4-dioxo-1-                                           
 imidazolidinecarboxamide]                                              
Iron pentacarbonyl                     13463-40-6                 1/1/95
                                                                        
                                 *******                                
Isodrin                                465-73-6                   1/1/95
Isofenphos [2-[[Ethoxyl[(1-            25311-71-1                 1/1/95
 methylethyl)amino]phosphinothioyl]ox                                   
 y]benzoic acid 1-methylethyl ester]                                    
Isophorone                             78-59-1                    1/1/95
Isophorone diisocyanate                4098-71-9                  1/1/95
                                                                        
                                 *******                                
Lactofen [5-(2-Chloro-4-               77501-63-4                 1/1/95
 (trifluoromethyl)phenoxy)-2-nitro-2-                                   
 ethoxy-1- methyl-2-oxoethyl ester]                                     
                                                                        
                                 *******                                
Linuron                                330-55-2                   1/1/95
Lithium carbonate                      554-13-2                   1/1/95
Malathion                              121-75-5                   1/1/95
                                                                        
                                 *******                                
Mecoprop                               93-65-2                    1/1/95
2-Mercaptobenzothiazole (MBT)          149-30-4                   1/1/95
                                                                        
                                 *******                                
Merphos                                150-50-5                   1/1/95
Metham sodium (Sodium                  137-42-8                   1/1/95
 methyldithiocarbamate)                                                 
                                                                        
                                 *******                                
Methazole [2-(3,4-Dichlorophenyl)-4-   20354-26-1                 1/1/95
 methyl-1,2,4-oxadiazolidine-3,5-                                       
 dione]                                                                 
Methiocarb                             2032-65-7                  1/1/95
Methoxone (4-Chloro-2-methylphenoxy)   94-74-6                    1/1/95
 acetic acid (MCPA))                                                    
Methoxone-sodium salt ((4-chloro-2-    3653-48-3                  1/1/95
 methylphenoxy) acetate sodium salt)                                    
                                                                        
                                 *******                                
1,1'-Methylene bis(4-                  5124-30-1                  1/1/95
 isocyanatocyclohexane)                                                 
                                                                        
                                 *******                                
Methylene bis(thiocyanate)             6317-18-6                  1/1/95
                                                                        
                                 *******                                
Methyl isothiocyanate                  556-61-6                   1/1/95
 [Isothiocyanatomethane]                                                
2-Methyllactonitrile                   75-86-5                    1/1/95
                                                                        
                                 *******                                
N-Methylolacrylamide                   924-42-5                   1/1/95
Methyl parathion                       298-00-0                   1/1/95
N-Methyl-2-pyrrolidone                 872-50-4                   1/1/95
Methyltrichlorosilane                  75-79-6                    1/1/95
Metiram                                9006-42-2                  1/1/95
Metribuzin                             21087-64-5                 1/1/95
Mevinphos                              7786-34-7                  1/1/95
                                                                        
                                 *******                                
Molinate (1H-Azepine-1-carbothioic     2212-67-1                  1/1/95
 acid, hexahydro-S-ethyl ester)                                         
                                                                        
                                 *******                                
Monuron                                150-68-5                   1/1/95
                                                                        
                                 *******                                
Myclobutanil [.alpha.-Butyl-.alpha.-   88671-89-0                 1/1/95
 (4-chlorophenyl)-1H-1,2,4-triazole-1-                                  
 propanenitrile]                                                        
Nabam                                  142-59-6                   1/1/95
Naled                                  300-76-5                   1/1/95
                                                                        
                                 *******                                
Nitrapyrin (2-Chloro-6-                1929-82-4                  1/1/95
 (trichloromethyl) pyridine)                                            
Nitrate ion                            14797-55-8                 1/1/95
                                                                        
                                 *******                                
Nitric oxide                           10102-43-9                 1/1/95
                                                                        
                                 *******                                
p-Nitroaniline                         100-01-6                   1/1/95
                                                                        
                                 *******                                
Nitrogen dioxide                       10102-44-0                 1/1/95
                                                                        
                                 *******                                
Norflurazon [4-Chloro-5-(methylamino)- 27314-13-2                 1/1/95
 2-[3-(trifluoromethyl)phenyl]-3(2H)-                                   
 pyridazinone]                                                          
                                                                        
                                 *******                                
Oryzalin [4-(Dipropylamino)-3,5-       19044-88-3                 1/1/95
 dinitrobenzenesulfonamide]                                             
                                                                        
                                 *******                                
Oxydemeton methyl [S-(2-               301-12-2                   1/1/95
 (ethylsulfinyl)ethyl) o,o-dimethyl                                     
 ester phosphorothioic acid]                                            
Oxydiazon [3-[2,4-Dichloro-5-(1-       19666-30-9                 1/1/95
 methylethoxy)phenyl]-5-(1,1-                                           
 dimethylethyl)-1,3,4-oxadiazol-2(3H)-                                  
 one]                                                                   
Oxyfluorfen                            42874-03-3                 1/1/95
Ozone                                  10028-15-6                 1/1/95
Paraquat dichloride                    1910-42-5                  1/1/95
                                                                        
                                 *******                                
Pebulate [Butylethylcarbamothioic      1114-71-2                  1/1/95
 acid S-propyl ester]                                                   
Pendimethalin [N-(1-Ethylpropyl)-3,4-  40487-42-1                 1/1/95
 dimethyl-2,6-dinitrobenzenamine]                                       
                                                                        
                                 *******                                
Pentobarbital sodium                   57-33-0                    1/1/95
                                                                        
                                 *******                                
Perchloromethyl mercaptan              594-42-3                   1/1/95
Permethrin [3-(2,2-Dichloroethenyl)-   52645-53-1                 1/1/95
 2,2-dimethylcyclopropanecarboxylic                                     
 acid, (3-phenoxyphenyl)methyl ester]                                   
Phenanthrene                           85-01-8                    1/1/95
                                                                        
                                 *******                                
Phenothrin [2,2-Dimethyl-3-(2-methyl-  26002-80-2                 1/1/95
 1-propenyl)cyclopropanecarboxylic                                      
 acid (3-phenoxyphenyl)methyl ester]                                    
1,2-Phenylenediamine                   95-54-5                    1/1/95
1,3-Phenylenediamine                   108-45-2                   1/1/95
1,2-Phenylenediamine dihydrochloride   615-28-1                   1/1/95
1,4-Phenylenediamine dihydrochloride   624-18-0                   1/1/95
                                                                        
                                 *******                                
Phenytoin                              57-41-0                    1/1/95
                                                                        
                                 *******                                
Phosphine                              7803-51-2                  1/1/95
                                                                        
                                 *******                                
Phosphorous oxychloride                10025-87-3                 1/1/95
Phosphorous pentachloride              10026-13-8                 1/1/95
Phosphorous pentasulfide               1314-80-3                  1/1/95
Phosphorous pentoxide                  1314-56-3                  1/1/95
                                                                        
                                 *******                                
Picloram                               1918-02-1                  1/1/95
                                                                        
                                 *******                                
Piperonyl butoxide                     51-03-6                    1/1/95
Pirimiphos methyl [O-(2-               29232-93-7                 1/1/95
 (Diethylamino)-6-methyl-4-                                             
 pyrimidinyl)-O,O-                                                      
 dimethylphosphorothioate]                                              
                                                                        
                                 *******                                
Potassium bromate                      7758-01-2                  1/1/95
Potassium dimethyldithiocarbamate      128-03-0                   1/1/95
Potassium N-methyldithiocarbamate      137-41-7                   1/1/95
Primisulfuron [Methyl 2-[[[[[4,6-      86209-51-0                 1/1/95
 bis(difluoromethoxy)-2-pyrimidinyl]-                                   
 amino]carbonyl]amino]sulfonyl]benzoa                                   
 te]                                                                    
Profenofos [O-(4-Bromo-2-              41198-08-7                 1/1/95
 chlorophenyl)-O-ethyl-S-propyl                                         
 phosphorothioate]                                                      
Prometryn [N,N'-Bis(1-methylethyl)-6-  7287-19-6                  1/1/95
 methylthio-1,3,5-triazine-2,4-                                         
 diamine]                                                               
Propachlor [2-Chloro-N-(1-             1918-16-7                  1/1/95
 methylethyl)-N-phenylacetamide]                                        
                                                                        
                                 *******                                
Propanil [N-(3,4-                      709-98-8                   1/1/95
 Dichlorophenyl)propanamide]                                            
Propargite                             2312-35-8                  1/1/95
Propargyl alcohol                      107-19-7                   1/1/95
Propetamphos [3-                       31218-83-4                 1/1/95
 [[(Ethylamino)methoxyphosphinothioyl                                   
 ]oxy]-2-butenoic acid, 1-methylethyl                                   
 ester]                                                                 
Propiconazole [1-[2-(2,4-              60207-90-1                 1/1/95
 Dichlorophenyl)-4-propyl-1,3-                                          
 dioxolan-2-yl]- methyl-1H-1,2,4,-                                      
 triazole]                                                              
                                                                        
                                 *******                                
Quizalofop-ethyl [2-[4-[(6-Chloro-2-   76578-14-8                 1/1/95
 quinoxalinyl)oxy]phenoxy]propanoic                                     
 acid ethyl ester]                                                      
Resmethrin [[5-(Phenylmethyl)-3-       10453-86-8                 1/1/95
 furanyl]methyl 2,2-dimethyl-3-(2-                                      
 methyl-1-                                                              
 propenyl)cyclopropanecarboxylate]]                                     
                                                                        
                                 *******                                
Sethoxydim [2-[1-(Ethoxyimino)butyl]-  74051-80-2                 1/1/95
 5-[2-(ethylthio)propyl]-3-hydroxy-2-                                   
 cyclohexen-1-one]                                                      
                                                                        
                                 *******                                
Simazine                               122-34-9                   1/1/95
Sodium azide                           26628-22-8                 1/1/95
Sodium chlorite                        7758-19-2                  1/1/95
Sodium dicamba [3,6-Dichloro-2-        1982-69-0                  1/1/95
 methoxybenzoic acid, sodium salt]                                      
Sodium dimethyldithiocarbamate         128-04-1                   1/1/95
Sodium fluoroacetate                   62-74-8                    1/1/95
Sodium hypochlorite                    7681-52-9                  1/1/95
Sodium nitrite                         7632-00-0                  1/1/95
Sodium pentachlorophenate              131-52-2                         
Sodium o-phenylphenoxide               132-27-4                   1/1/95
Sodium 2-pyridinethiol-1-oxide         15922-78-8                 1/1/95
                                                                        
                                 *******                                
Sulfur dioxide                         7446-09-5                  1/1/95
                                                                        
                                 *******                                
Sulfur trioxide                        7446-11-9                  1/1/95
Sulfuryl fluoride [Vikane]             2699-79-8                  1/1/95
Sulprofos [O-Ethyl O-[4-               35400-43-2                 1/1/95
 (methylthio)phenyl]phosphorodithioic                                   
 acid S-propyl ester]                                                   
Tebuthiuron [N-[5-(1,1-Dimethylethyl)- 34014-18-1                 1/1/95
 1,3,4-thiadiazol-2-yl)-N,N'-                                           
 dimethylurea]                                                          
Tefluthrin                             79538-32-2                 1/1/95
Temephos                               3383-96-8                  1/1/95
Terbacil [5-Chloro-3-(1,1-             5902-51-2                  1/1/95
 dimethylethyl)-6-methyl-2,4(1H,3H)-                                    
 pyrimidinedione]                                                       
                                                                        
                                 *******                                
1,1,1,2-Tetrachloro-2-fluoroethane     354-11-0                   1/1/95
 (HCFC-121a)                                                            
1,1,2,2-Tetrachloro-1-fluoroethane     354-14-3                   1/1/95
 (HCFC-121)                                                             
                                                                        
                                 *******                                
Tetracycline hydrochloride             64-75-5                    1/1/95
Tetramethrin [2,2-Dimethyl-3-(2-       7696-12-0                  1/1/95
 methyl-1-                                                              
 propenyl)cyclopropanecarboxylic acid                                   
 (1,3,4,5,6,7-hexahydro-1,3-dioxo-2H-                                   
 isoindol-2-yl)methyl ester]                                            
Tetrasodium                            64-02-8                    1/1/95
 ethylenediaminetetraacetate                                            
                                                                        
                                 *******                                
Thiabendazole [2-(4-Thiazolyl)-1H-     148-79-8                   1/1/95
 benzimidazole]                                                         
Thiabendazole, hypophosphite salt [2-  28558-32-9                 1/1/95
 (4-Thiazolyl)benzimidazole,                                            
 hypophosphite salt]                                                    
                                                                        
                                 *******                                
Thiobencarb [Carbamic acid,            28249-77-6                 1/1/95
 diethylthio-, s-(p-chlorobenzyl)]                                      
                                                                        
                                 *******                                
Thiodicarb                             59669-26-0                 1/1/95
Thiophanate ethyl [[1,2-               23564-06-9                 1/1/95
 Phenylenebis(iminocarbonothioyl)]bis                                   
 carbamic acid diethyl ester]                                           
Thiophanate-methyl                     23564-05-8                 1/1/95
Thiosemicarbazide                      79-19-6                    1/1/95
                                                                        
                                 *******                                
Triadimefon [1-(4-Chlorophenoxy)-3,3-  43121-43-3                 1/1/95
 dimethyl-1-(1H-1,2,4-triazol-1-yl)-2-                                  
 butanone]                                                              
Triallate                              2303-17-5                  1/1/95
                                                                        
                                 *******                                
Tribenuron methyl [2-(((((4-Methoxy-6- 101200-48-0                1/1/95
 methyl-1,3,5-triazin-2-yl)-                                            
 methylamino)carbonyl)amino)sulfonyl)-                                  
 , methyl ester]                                                        
Tributyltin fluoride                   1983-10-4                  1/1/95
Tributyltin methacrylate               2155-70-6                  1/1/95
S,S,S-Tributyltrithiophosphate (DEF)   78-48-8                    1/1/95
                                                                        
                                 *******                                
Trichloroacetyl chloride               76-02-8                    1/1/95
                                                                        
                                 *******                                
Trichloroethylsilane                   115-21-9                   1/1/95
                                                                        
                                 *******                                
Trichlorophenylsilane                  98-13-5                          
1,2,3-Trichloropropane                 96-18-4                    1/1/95
Triclopyr, triethylammonium salt       57213-69-1                 1/1/95
Triethylamine                          121-44-8                   1/1/95
Triforine [N,N'-[1,4-Piperazinediyl-   26644-46-2                 1/1/95
 bis(2,2,2-trichloroethylidene)]                                        
 bisformamide]                                                          
                                                                        
                                 *******                                
Trimethylchlorosilane                  75-77-4                    1/1/95
2,3,5-Trimethylphenyl methylcarbamate  2655-15-4                  1/1/95
Triphenyltin chloride                  639-58-7                   1/1/95
Triphenyltin hydroxide                 76-87-9                    1/1/95
                                                                        
                                 *******                                
Vanadium pentoxide                     1314-62-1                  1/1/95
Vinclozolin [3-(3,5-Dichlorophenyl)-5- 50471-44-8                 1/1/95
 ethenyl-5-methyl-2,4-                                                  
 oxazolidinedione]                                                      
                                                                        
                                 *******                                
------------------------------------------------------------------------

    (b)  *  *  *

------------------------------------------------------------------------
                                                              Effective 
       CAS No.                    Chemical Name                  Date   
------------------------------------------------------------------------
                                                                        
                                 *******                                
51-03-6               Piperonyl butoxide                          1/1/95
51-21-8               Fluorouracil (5-Fluorouracil)               1/1/95
                                                                        
                                 *******                                
52-51-7               2-Bromo-2-nitropropane-1,3-diol             1/1/95
                       (Bronopol)                                       
                                                                        
                                 *******                                
52-85-7               Famphur                                     1/1/95
                                                                        
                                 *******                                
55-38-9               Fenthion [O,O-Dimethyl O-[3-methyl-4-       1/1/95
                       (methylthio)phenyl] ester,                       
                       phosphorothioic acid]                            
                                                                        
                                 *******                                
56-35-9               Bis(tributyltin) oxide                      1/1/95
                                                                        
                                 *******                                
57-33-0               Pentobarbital sodium                        1/1/95
57-41-0               Phenytoin                                   1/1/95
                                                                        
                                 *******                                
60-51-5               Dimethoate                                  1/1/95
                                                                        
                                 *******                                
62-74-8               Sodium fluoroacetate                        1/1/95
                                                                        
                                 *******                                
64-02-8               Tetrasodium                                 1/1/95
                       ethylenediaminetetraacetate                      
                                                                        
                                 *******                                
64-75-5               Tetracycline hydrochloride                  1/1/95
                                                                        
                                 *******                                
68-12-2               N,N-Dimethylformamide                       1/1/95
                                                                        
                                 *******                                
75-43-4               Dichlorofluoromethane (HCFC-21)             1/1/95
                                                                        
                                 *******                                
75-72-9               Chlorotrifluoromethane (CFC-13)             1/1/95
75-77-4               Trimethylchlorosilane                       1/1/95
75-78-5               Dimethyldichlorosilane                      1/1/95
75-79-6               Methyltrichlorosilane                       1/1/95
75-86-5               2-Methyllactonitrile                        1/1/95
75-88-7               2-Chloro-1,1,1-trifluoroethane (HCFC-       1/1/95
                       133a)                                            
76-02-8               Trichloroacetyl chloride                    1/1/95
76-06-2               Chloropicrin                                1/1/95
                                                                        
                                 *******                                
76-87-9               Triphenyltin hydroxide                      1/1/95
                                                                        
                                 *******                                
77-73-6               Dicyclopentadiene                           1/1/95
                                                                        
                                 *******                                
78-48-8               S,S,S-Tributyltrithiophosphate (DEF)        1/1/95
78-59-1               Isophorone                                  1/1/95
                                                                        
                                 *******                                
79-19-6               Thiosemicarbazide                           1/1/95
                                                                        
                                 *******                                
85-01-8               Phenanthrene                                1/1/95
                                                                        
                                 *******                                
88-85-7               Dinoseb                                     1/1/95
                                                                        
                                 *******                                
93-65-2               Mecoprop                                    1/1/95
94-11-1               2,4-D isopropyl ester                       1/1/95
                                                                        
                                 *******                                
94-74-6               Methoxone (4-Chloro-2-methylphenoxy)        1/1/95
                       acetic acid (MCPA)                               
                                                                        
                                 *******                                
94-80-4               2,4-D butyl ester                           1/1/95
94-82-6               2,4-DB                                      1/1/95
                                                                        
                                 *******                                
95-54-5               1,2-Phenylenediamine                        1/1/95
                                                                        
                                 *******                                
95-69-2               p-Chloro-o-toluidine                        1/1/95
                                                                        
                                 *******                                
96-18-4               1,2,3-Trichloropropane                      1/1/95
                                                                        
                                 *******                                
97-23-4               Dichlorophene [ 2,2'-Methylene-bis(4-       1/1/95
                       chlorophenol)]                                   
                                                                        
                                 *******                                
98-13-5               Trichlorophenylsilane                       1/1/95
                                                                        
                                 *******                                
99-30-9               Dichloran [2,6-Dichloro-4-                  1/1/95
                       nitroaniline]                                    
                                                                        
                                 *******                                
100-01-6              p-Nitroaniline                              1/1/95
                                                                        
                                 *******                                
101-05-3              Anilazine [4,6-dichloro-N-(2-               1/1/95
                       chlorophenyl)-1,3,5-triazin-2-amine]             
                                                                        
                                 *******                                
101-90-6              Diglycidyl resorcinol ether                 1/1/95
                                                                        
                                 *******                                
104-12-1              p-Chlorophenyl isocyanate                   1/1/95
                                                                        
                                 *******                                
105-60-2              Caprolactam                                 1/1/95
                                                                        
                                 *******                                
106-47-8              p-Chloroaniline                             1/1/95
                                                                        
                                 *******                                
107-11-9              Allylamine                                  1/1/95
                                                                        
                                 *******                                
107-19-7              Propargyl alcohol                           1/1/95
                                                                        
                                 *******                                
108-45-2              1,3-Phenylenediamine                        1/1/95
                                                                        
                                 *******                                
108-93-0              Cyclohexanol                                1/1/95
                                                                        
                                 *******                                
110-54-3              n-Hexane                                    1/1/95
110-57-6              trans-1,4-Dichloro-2-butene                 1/1/95
                                                                        
                                 *******                                
115-21-9              Trichloroethylsilane                        1/1/95
115-28-6              Chlorendic acid                             1/1/95
                                                                        
                                 *******                                
116-06-3              Aldicarb                                    1/1/95
                                                                        
                                 *******                                
120-32-1              o-Benzyl-p-chlorophenol                     1/1/95
120-36-5              2,4-DP                                      1/1/95
                                                                        
                                 *******                                
121-44-8              Triethylamine                               1/1/95
                                                                        
                                 *******                                
121-75-5              Malathion                                   1/1/95
122-34-9              Simazine                                    1/1/95
122-39-4              Diphenylamine                               1/1/95
                                                                        
                                 *******                                
124-40-3              Dimethylamine                               1/1/95
                                                                        
                                 *******                                
128-03-0              Potassium dimethyldithiocarbamate           1/1/95
128-04-1              Sodium dimethyldithiocarbamate              1/1/95
                                                                        
                                 *******                                
131-52-2              Sodium pentachlorophenate                   1/1/95
132-27-4              Sodium o-phenylphenoxide                    1/1/95
                                                                        
                                 *******                                
133-07-3              Folpet                                      1/1/95
                                                                        
                                 *******                                
136-45-8              Dipropyl isocinchomeronate                  1/1/95
137-41-7              Potassium n-methyldithiocarbamate           1/1/95
137-42-8              Metham Sodium                               1/1/95
138-93-2              Disodium cyanodithioimidocarbonate          1/1/95
                                                                        
                                 *******                                
142-59-6              Nabam                                       1/1/95
148-79-8              Thiabendazole [2-(4-Thiazolyl)-1H-          1/1/95
                       benzimidazole]                                   
149-30-4              2-Mercaptobenzothiazole                     1/1/95
149-74-6              Dichloromethylphenylsilane                  1/1/95
150-50-5              Merphos                                     1/1/95
150-68-5              Monuron                                     1/1/95
                                                                        
                                 *******                                
298-00-0              Methyl parathion                            1/1/95
300-76-5              Naled                                       1/1/95
301-12-2              Oxydemeton methyl [s-(2-                    1/1/95
                       (Ethylsulfinyl)ethyl)o,o-dimethyl                
                       ester phosphorothioic acid]                      
                                                                        
                                 *******                                
314-40-9              Bromacil (5-Bromo-6-methyl-3-(1-            1/1/95
                       methylpropyl)-2,4-(1H,3H)-                       
                       pyrimidinedione)                                 
319-84-6              alpha-Hexachlorocyclohexane                 1/1/95
330-54-1              Diuron                                      1/1/95
330-55-2              Linuron                                     1/1/95
333-41-5              Diazinon                                    1/1/95
                                                                        
                                 *******                                
354-11-0              1,1,1,2-Tetrachloro-2-fluoroethane          1/1/95
                       (HCFC-121a)                                      
354-14-3              1,1,2,2-Tetrachloro-1-fluoroethane          1/1/95
                       (HCFC-121)                                       
357-57-3              Brucine                                     1/1/95
422-44-6              1,2-dichloro-1,1,2,3,3-                     1/1/95
                       pentafluoropropane (HCFC-225bb)                  
422-48-0              2,3-dichloro-1,1,1,2,3-                     1/1/95
                       pentafluoropropane (HCFC-225ba)                  
422-56-0              3,3-dichloro-1,1,1,2,2-                     1/1/95
                       pentafluoropropane (HCFC-225ca)                  
431-86-7              1,2-dichloro-1,1,3,3,3-                     1/1/95
                       pentafluoropropane (HCFC-225da)                  
460-35-5              3-chloro-1,1,1-trifluoropropane (HCFC-      1/1/95
                       253fb)                                           
                                                                        
                                 *******                                
465-73-6              Isodrin                                     1/1/95
                                                                        
                                 *******                                
507-55-1              1,3-dichloro-1,1,2,2,3-                     1/1/95
                       pentafluoropropane (HCFC-225cb)                  
                                                                        
                                 *******                                
533-74-4              Dazomet (Tetrahydro-3,5-dimethyl-2H-        1/1/95
                       1,3,5-thiadiazine-2-thione)                      
                                                                        
                                 *******                                
541-53-7              2,4-Dithiobiuret                            1/1/95
                                                                        
                                 *******                                
542-76-7              3-Chloropropionitrile                       1/1/95
                                                                        
                                 *******                                
554-13-2              Lithium carbonate                           1/1/95
556-61-6              Methyl isothiocyanate                       1/1/95
                       [Isothiocyanatomethane]                          
563-47-3              3-Chloro-2-methyl-1-propene                 1/1/95
                                                                        
                                 *******                                
576-26-1              2,6-Dimethylphenol                          1/1/95
                                                                        
                                 *******                                
594-42-3              Perchloromethyl mercaptan                   1/1/95
                                                                        
                                 *******                                
612-82-8              3,3'-Dimethylbenzidine                      1/1/95
                       dihydrochloride (o-Tolidine                      
                       dihydrochloride)                                 
612-83-9              3,3'-Dichlorobenzidine                      1/1/95
                       dihydrochloride                                  
                                                                        
                                 *******                                
615-28-1              1,2-Phenylenediamine dihydrochloride        1/1/95
                                                                        
                                 *******                                
624-18-0              1,4-Phenylenediamine dihydrochloride        1/1/95
                                                                        
                                 *******                                
630-08-0              Carbon monoxide                             1/1/95
                                                                        
                                 *******                                
639-58-7              Triphenyltin chloride                       1/1/95
                                                                        
                                 *******                                
709-98-8              Propanil [N-(3,4-                           1/1/95
                       Dichlorophenyl)propanamide]                      
                                                                        
                                 *******                                
759-94-4              Ethyl dipropylthiocarbamate (EPTC)          1/1/95
822-60-0              Hexamethylene-1,6-diisocyanate              1/1/95
834-12-8              Ametryn (N-Ethyl-N'-(1-methylethyl)-6-      1/1/95
                       (methylthio)-1,3,5,-triazine-2,4-                
                       diamine)                                         
872-50-4              N-Methyl-2-pyrrolidone                      1/1/95
                                                                        
                                 *******                                
924-42-5              N-Methylolacrylamide                        1/1/95
957-51-7              Diphenamid                                  1/1/95
                                                                        
                                 *******                                
1114-71-2             Pebulate [Butylethylcarbamo-thioic          1/1/95
                       acid S-propyl ester]                             
                                                                        
                                 *******                                
1134-23-2             Cycloate                                    1/1/95
                                                                        
                                 *******                                
1314-56-3             Phosphorous pentoxide                       1/1/95
1314-62-1             Vanadium pentoxide                          1/1/95
1314-80-3             Phosphorous pentasulfide                    1/1/95
                                                                        
                                 *******                                
1320-18-9             2,4-D propylene glycol butyl ether          1/1/95
                       ester                                            
                                                                        
                                 *******                                
1563-66-2             Carbofuran                                  1/1/95
1649-08-7             1,2-dichloro-1,1-difluoroethane (HCFC-      1/1/95
                       132b)                                            
1689-84-5             Bromoxynil (3,5-Dibromo-4-                  1/1/95
                       hydroxybenzonitrile)                             
1689-99-2             Bromoxynil octanoate (Octanoic acid,        1/1/95
                       2,6-dibromo-4-cyanophenyl ester)                 
                                                                        
                                 *******                                
1861-40-1             Benfluralin(N-Butyl-N-ethyl-2,6-            1/1/95
                       dinitro-4-                                       
                       (trifluoromethyl)benzenamine)                    
                                                                        
                                 *******                                
1910-42-5             Paraquat dichloride                         1/1/95
1912-24-9             Atrazine (6-Chloro-N-ethyl-N'-(1-           1/1/95
                       methylethyl)-1,3,5,-triazine-2,4-                
                       diamine)                                         
1917-97-1             2,4-D 2-octyl ester                         1/1/95
1918-00-9             Dicamba (3,6-Dichloro-2-                    1/1/95
                       methyoxybenzoic acid)                            
1918-02-1             Picloram                                    1/1/95
1918-16-7             Propachlor [2-Chloro-N-(1-                  1/1/95
                       methylethyl)-N-phenylacetamide]                  
1928-43-4             2,4-D 2-ethylhexyl ester                    1/1/95
1929-73-3             2,4-D butoxyethyl ester                     1/1/95
1929-82-4             Nitrapyrin (2-Chloro-6-                     1/1/95
                       (trichloromethyl)pyridine)                       
                                                                        
                                 *******                                
1982-69-0             Sodium dicamba [3,6-Dichloro-2-             1/1/95
                       methoxybenzoic acid, sodium salt]                
1983-10-4             Tributyltin fluoride                        1/1/95
2008-41-5             Butylate (Bis-2-methylpropyl)               1/1/95
                       carbamothioic acid S-ethyl ester)                
2032-65-7             Methiocarb                                  1/1/95
2155-70-6             Tributyltin methacrylate                    1/1/95
2164-07-0             Dipotassium endothall [7-                   1/1/95
                       Oxabicyclo(2.2.1)heptane-2,3-                    
                       dicarboxylic acid, dipotassium salt]             
                                                                        
                                 *******                                
2212-67-1             Molinate (1H-Azepine-1-carbothioic          1/1/95
                       acid, hexahydro-S-ethyl ester)                   
                                                                        
                                 *******                                
2300-66-5             Dimethylamine dicamba                       1/1/95
                                                                        
                                 *******                                
2303-17-5             Triallate                                   1/1/95
2312-35-8             Propargite                                  1/1/95
2439-01-2             Chinomethionat [6-Methyl-1,3-               1/1/95
                       dithiolo[4,5-b]quinoxalin-2-one]                 
2439-10-3             Dodine [Dodecylguanidine monoacetate]       1/1/95
2524-03-0             Dimethyl chlorothiophosphate                1/1/95
                                                                        
                                 *******                                
2655-15-4             2,3,5-Trimethylphenyl methylcarbamate       1/1/95
2699-79-8             Sulfuryl Fluoride [Vikane]                  1/1/95
2702-72-9             2,4-D sodium salt                           1/1/95
                                                                        
                                 *******                                
2971-38-2             2,4-D chlorocrotyl ester                    1/1/95
                                                                        
                                 *******                                
3380-34-5             5-Chloro-2-(2,4-                            1/1/95
                       dichlorophenoxy)phenol                           
3383-96-8             Temephos                                    1/1/95
3653-48-3             Methoxone - sodium salt (4-Chloro-2-        1/1/95
                       methylphenoxy acetate sodium salt)               
                                                                        
                                 *******                                
4080-31-3             1-(3-Chloroallyl)-3,5,7-triaza-1-           1/1/95
                       azoniaadamantane chloride                        
4098-71-9             Isophorone diisocyanate                     1/1/95
4170-30-3             Crotonaldehyde                              1/1/95
                                                                        
                                 *******                                
5124-30-1             1,1'-Methylene bis(4-                       1/1/95
                       isocyanatocyclohexane)                           
5234-68-4             Carboxin (5,6-Dihydro-2-methyl-N-           1/1/95
                       phenyl-1,4-oxathiin-3-carboxamide)               
5598-13-0             Chlorpyrifos methyl [O,O-dimethyl-O-        1/1/95
                       (3,5,6-trichloro-2-                              
                       pyridyl)phosphorothioate]                        
5902-51-2             Terbacil [5-Chloro-3-(1,1-                  1/1/95
                       dimethylethyl)-6-methyl-2,4-(1H,3H)-             
                       pyrimidinedione]                                 
6317-18-6             Methylene bis(thiocyanate)                  1/1/95
6459-94-5             C.I. Acid Red 114                           1/1/95
                                                                        
                                 *******                                
7287-19-6             Prometryn [N,N'-Bis(1-methylethyl)-6-       1/1/95
                       methylthio-1,3,5-triazine-2,4-                   
                       diamine]                                         
                                                                        
                                 *******                                
7446-09-5             Sulfur dioxide                              1/1/95
7446-11-9             Sulfur trioxide                             1/1/95
                                                                        
                                 *******                                
7632-00-0             Sodium nitrite                              1/1/95
7637-07-2             Boron trifluoride                           1/1/95
                                                                        
                                 *******                                
7681-52-9             Sodium hypochlorite                         1/1/95
7696-12-0             Tetramethrin [2,2-Dimethyl-3-(2-            1/1/95
                       methyl-1-propenyl)cyclopropane-                  
                       carboxylic acid (1,3,4,5,6,7-                    
                       hexahydro-1,3-dioxo-2H-isoindol-2-               
                       yl)methyl ester]                                 
                                                                        
                                 *******                                
7726-95-6             Bromine                                     1/1/95
7758-01-2             Potassium bromate                           1/1/95
7758-19-2             Sodium chlorite                             1/1/95
7778-54-3             Calcium hypochlorite                        1/1/95
7782-41-4             Fluorine                                    1/1/95
                                                                        
                                 *******                                
7786-34-7             Mevinphos                                   1/1/95
7803-51-2             Phosphine                                   1/1/95
                                                                        
                                 *******                                
9006-42-2             Metiram                                     1/1/95
10025-87-3            Phosphorous oxychloride                     1/1/95
10026-13-8            Phosphorous pentachloride                   1/1/95
10028-15-6            Ozone                                       1/1/95
                                                                        
                                 *******                                
10061-02-6            trans-1,3-Dichloropropene                   1/1/95
10222-01-2            2,2-Dibromo-3-nitrilopropionamide           1/1/95
10102-43-9            Nitric oxide                                1/1/95
10102-44-0            Nitrogen dioxide                            1/1/95
10294-34-5            Boron trichloride                           1/1/95
10453-86-8            Resmethrin [[5-(Phenylmethyl)-3-            1/1/95
                       furanyl]methyl 2,2-dimethyl-3-(2-                
                       methyl-1-                                        
                       propenyl)cyclopropanecarboxylate]]               
                                                                        
                                 *******                                
13194-48-4            Ethoprop [Phosphorodithioic acid O-         1/1/95
                       ethyl S,S-dipropyl ester]                        
13356-08-6            Fenbutatin oxide (hexakis(2-methyl-2-       1/1/95
                       phenylpropyl)distannoxane)                       
13463-40-6            Iron pentacarbonyl                          1/1/95
13474-88-9            1,1-Dichloro-1,2,2,3,3-                     1/1/95
                       pentafluoropropane (HCFC-225cc)                  
13684-56-5            Desmedipham                                 1/1/95
14484-64-1            Ferbam [Tris(dimethylcarbamo-               1/1/95
                       dithioato-S,S')iron]                             
14797-55-8            Nitrate ion                                 1/1/95
15922-78-8            Sodium 2-pyridinethiol-1-oxide              1/1/95
15972-60-8            Alachlor                                    1/1/95
                                                                        
                                 *******                                
17804-35-2            Benomyl                                     1/1/95
19044-88-3            Oryzalin [4-(Dipropylamino)-3,5-            1/1/95
                       dinitrobenzene-sulfonamide]                      
19666-30-9            Oxydiazon [3-[2,4-Dichloro-5-(1-            1/1/95
                       methylethoxy)phenyl]-5-(1,1-                     
                       dimethylethyl)-1,3,4-oxadiazol-2(3H)-            
                       one]                                             
20325-40-0            3,3'-Dimethoxybenzidine                     1/1/95
                       dihydrochloride (Dianisidine                     
                       dihydrochloride)                                 
20354-26-1            Methazole [2-(3,4-Dichlorophenyl)-4-        1/1/95
                       methyl-1,2,4-oxadiazolidine-3,5-                 
                       dione]                                           
                                                                        
                                 *******                                
20859-73-8            Aluminum phosphide                          1/1/95
21087-64-9            Metribuzin                                  1/1/95
21725-46-2            Cyanazine                                   1/1/95
22781-23-3            Bendiocarb [2,2-Dimethyl-1,3-               1/1/95
                       benzodioxol-4-ol methylcarbamate]                
23564-05-8            Thiophanate methyl                          1/1/95
23564-06-9            Thiophanate ethyl [[1,2-                    1/1/95
                       Phenylenebis(iminocarbonothioyl)]bis             
                       carbamic acid diethyl ester]                     
25013-16-5            Butylated hydroxyanisole                    1/1/95
25311-71-1            Isofenphos [2-[[Ethoxyl[(1-                 1/1/95
                       methylethyl)amino]phosphinothioyl]ox             
                       y]benzoic acid 1-methylethyl ester]              
26002-80-2            Phenothrin [2,2-Dimethyl-3-(2-methyl-       1/1/95
                       1-propenyl)cyclopropanecarboxylic                
                       acid (3-phenoxyphenyl)methyl ester]              
                                                                        
                                 *******                                
26628-22-8            Sodium azide                                1/1/95
26644-46-2            Triforine [N,N'-[1,4-                       1/1/95
                       Piperazinediylbis(2,2,2-                         
                       trichloroethylidene)] bisformamide]              
27314-13-2            Norflurazon [4-Chloro-5-(methylamino)-      1/1/95
                       2-[3-(trifluoromethyl)phenyl]- 3(2H)-            
                       pyridazinone]                                    
28057-48-9            d-trans-Allethrin [d-trans-                 1/1/95
                       Chrysanthemic acid of d-allethrone]              
28249-77-6            Thiobencarb [Carbamic acid,                 1/1/95
                       diethylthio-, s-(p-chlorobenzyl)]                
28407-37-6            C.I. Direct Blue 218                        1/1/95
28558-32-9            Thiabendazole, hypophosphite salt [2-       1/1/95
                       (4-Thiazolyl)benzimidazole,                      
                       hypophosphite salt]                              
29232-93-7            Pirimiphos methyl [O-(2-                    1/1/95
                       (Diethylamino)-6-methyl-4-                       
                       pyrimidinyl)-O,O-dimethyl                        
                       phosphorothioate]                                
30560-19-1            Acephate (Acetylphosphoramidothioic         1/1/95
                       acid O,S-dimethyl ester)                         
31218-83-4            Propetamphos [3-                            1/1/95
                       [[(Ethylamino)methoxyphosphino-                  
                       thioyl]oxy]-2-butenoic acid, 1-                  
                       methylethyl ester]                               
33089-61-1            Amitraz                                     1/1/95
34014-18-1            Terbuthiuron [N-[5-(1,1-                    1/1/95
                       Dimethylethyl)-1,3,4-thiadiazol-2-               
                       yl)-N,N'- dimethylurea]                          
35367-38-5            Diflubenzuron                               1/1/95
35400-43-2            Sulprofos [O-Ethyl O-[4-                    1/1/95
                       (methylthio)phenyl]phosphorodithioic             
                       acid S-propyl ester]                             
35554-44-0            Imazalil [1-[2-(2,4-Dichlorophenyl)-2-      1/1/95
                       (2-propenyloxy)ethyl]-1H-imidazole]              
35691-65-7            1-Bromo-1-(bromomethyl)-1,3-                1/1/95
                       propanedicarbonitrile                            
36734-19-7            Iprodione [3-(3,5-Dichlorophenyl)-N-        1/1/95
                       (1-methylethyl)-2,4-dioxo-1-                     
                       imidazolidine-carboxamide]                       
38727-55-8            Diethatyl ethyl                             1/1/95
                                                                        
                                 *******                                
39300-45-3            Dinocap                                     1/1/95
39515-41-8            Fenpropathrin [2,2,3,3-                     1/1/95
                       Tetramethylcyclopropane carboxylic               
                       acid cyano(3-phenoxyphenyl)methyl                
                       ester]                                           
40487-42-1            Pendimethalin [N-(1-Ethylpropyl)-3,4-       1/1/95
                       dimethyl-2,6-dinitrobenzen-amine]                
41198-08-7            Profenofos [O-(4-Bromo-2-                   1/1/95
                       chlorophenyl)-O-ethyl-S-propyl                   
                       phosphorothioate]                                
41766-75-0            3,3'-Dimethylbenzidine                      1/1/95
                       dihydrofluoride (ortho-Tolidine                  
                       dihydrofluoride)                                 
42874-03-3            Oxyfluorfen                                 1/1/95
43121-43-3            Triadimefon [1-(4-Chlorophenoxy)-3,3-       1/1/95
                       dimethyl-1-(1H-1,2,4-triazol-1-yl)-2-            
                       butanone]                                        
50471-44-8            Vinclozolin [3-(3,5-Dichlorophenyl)-5-      1/1/95
                       ethenyl-5-methyl-2,4-                            
                       oxazolidinedione]                                
51235-04-2            Hexazinone                                  1/1/95
51338-27-3            Diclofop methyl [2-[4-(2,4-                 1/1/95
                       Dichlorophenoxy)phenoxy]propanoic                
                       acid, methyl ester]                              
51630-58-1            Fenvalerate                                 1/1/95
52645-53-1            Permethrin [3-(2,2-Dichloroethenyl)-        1/1/95
                       2,2-dimethylcyclopropanecarboxylic               
                       acid, (3-phenoxyphenyl)methyl ester]             
53404-19-6            Bromacil, lithium salt [2,4-(1H,3H)-        1/1/95
                       Pyrimidinedione, 5-bromo-6-methyl-3-             
                       (1-methylpropyl), lithium salt]                  
53404-37-8            2,4-D 2-ethyl-4-methylpentyl ester          1/1/95
53404-60-7            Dazomet, sodium salt [Tetrahydro-3,5-       1/1/95
                       dimethyl-2H-1,3,5-thiadiazine-2-                 
                       thione, ion(1-), sodium]                         
55290-64-7            Dimethipin [2,3,-Dihydro-5,6-dimethyl-      1/1/95
                       1,4-dithiin 1,1,4,4-tetraoxide]                  
55406-53-6            3-Iodo-2-propynyl butylcarbamate            1/1/95
57213-69-1            Triclopyr, triethylammonium salt            1/1/95
59669-26-0            Thiodicarb                                  1/1/95
60168-88-9            Fenarimol [.alpha.-(2-Chlorophenyl)-        1/1/95
                       .alpha.-4-chlorophenyl)-5-pyrimidine-            
                        methanol]                                       
60207-90-1            Propiconazole [1-[2-(2,4-                   1/1/95
                       Dichlorophenyl)-4-propyl-1,3-                    
                       dioxolan-2-yl]-methyl-1H-1,2,4,-                 
                       triazole]                                        
62476-59-9            Acifluorfen, sodium salt [5-(2-Chloro-      1/1/95
                       4-(triflouromethyl)phenoxy)-2-nitro-             
                       benzoic acid, sodium salt]                       
62924-70-3            Flumetralin [2-Chloro-N-(2,6-dinitro-       1/1/95
                       4-(trifluoromethyl)-phenyl)-N-ethyl-             
                       6-fluorobenzenemethanamine]                      
64902-72-3            Chlorsulfuron [2-chloro-N-[[4-methoxy-      1/1/95
                       6-methyl-1,3,5-triazin-2-yl)amino]               
                       carbonyl]benzenesulfonamide]                     
64969-34-2            3,3'-Dichlorobenzidine.sulfate              1/1/95
66215-27-8            Cyromazine [N-Cyclopropyl-1,3,5-            1/1/95
                       triazine-2,4,6-triamine]                         
66441-23-4            Fenoxaprop ethyl [2-(4-((6-Chloro-2-        1/1/95
                       benzoxazolylen)oxy)phenoxy)                      
                       propanoic acid, ethyl ester]                     
67485-29-4            Hydramethylnon [Tetrahydro-5,5-             1/1/95
                       dimethyl-2(1H)-pyrimidinone[3-[4-                
                       (trifluoromethyl)phenyl]-1-[2-[4-                
                       (trifluoromethyl)phenyl]ethenyl]-2-              
                       propenylidene]hydrazone]                         
68085-85-8            Cyhalothrin [3-(2-Chloro-3,3,3-             1/1/95
                       trifluoro-1-propenyl)-2,2-                       
                       dimethylcyclopropanecarboxylic acid              
                       cyano(3-phenoxyphenyl)methyl ester]              
68359-37-5            Cyfluthrin [3-(2,2-Dichloro-ethenyl)-       1/1/95
                       2,2-dimethylcyclo-propanecarboxylic              
                       acid, cyano(4-fluoro-3-                          
                       phenoxyphenyl)methyl ester]                      
69409-94-5            Fluvalinate [N-[2-Chloro-4-                 1/1/95
                       (trifluoromethyl)phenyl]-DL-                     
                       valine(+)-cyano(3-                               
                       phenoxyphenyl)methylester]                       
69806-50-4            Fluazifop-butyl [2-[4-[[5-                  1/1/95
                       (Trifluoromethyl)-2-pyridinyl]oxy]-              
                       phenoxy]propanoic acid, butyl ester]             
71751-41-2            Abamectin [Avermectin B1]                   1/1/95
72178-02-0            Fomesafen [5-(2-Chloro-4-                   1/1/95
                       (trifluoromethyl)phenoxy)-N-                     
                       methylsulfonyl)-2- nitrobenzamide]               
72490-01-8            Fenoxycarb [2-(4-                           1/1/95
                       Phenoxyphenoxy)ethyl]carbamic acid               
                       ethyl ester]                                     
74051-80-2            Sethoxydim [2-[1-(Ethoxyimino)butyl]-       1/1/95
                       5-[2-(ethylthio)propyl]-3-hydroxy-2-             
                       cyclohexen-1-one]                                
76578-14-8            Quizalofop-ethyl [2-[4-[(6-Chloro-2-        1/1/95
                       quinoxalinyl)oxy]phenoxy] propanoic              
                       acid ethyl ester]                                
77501-63-4            Lactofen [5-(2-Chloro-4-                    1/1/95
                       (trifluoromethyl)phenoxy)-2-nitro-2-             
                       ethoxy-1-methyl-2-oxoethyl ester]                
79538-32-2            Tefluthrin                                        
81777-89-1            Clomazone [2-[(2-Chlorophenyl)methyl]-      1/1/95
                       4,4-dimethyl-3-isoxazolidinone]                  
82657-04-3            Bifenthrin                                  1/1/95
86209-51-0            Primisulfuron [Methyl 2-[[[[[4,6-           1/1/95
                       bis(difluoromethoxy)-2-pyrimidinyl]-             
                       amino]carbonyl]amino]sulfonyl]benzoa             
                       te]                                              
88671-89-0            Myclobutanil [.alpha.-Butyl-.alpha.-        1/1/95
                       (4-chlorophenyl)-1H-1,2,4-triazole-              
                       1-propanenitrile]                                
90982-32-4            Chlorimuron ethyl [Ethyl-2-[[[(4-           1/1/95
                       chloro-6-methoxyprimidin-2-yl)-                  
                       carbonyl]-amino]sulfonyl]benzoate]               
97886-45-8            Dithiopyr [2-(Difluoromethyl)-4-(2-         1/1/95
                       methylpropyl)-6-(trifluoro-methyl)-              
                       3,5-pyridinedicarbothioic acid S,S-              
                       dimethyl ester]                                  
101200-48-0           Tribenuron methyl [2-(((((4-Methoxy-6-      1/1/95
                       methyl-1,3,5-triazin-2-yl)-                      
                       methylamino)carbonyl)amino)sulfonyl)-            
                       , methyl ester]                                  
111512-56-2           1,1-dichloro-1,2,3,3,3-                     1/1/95
                       pentafluoropropane (HCFC-225eb)                  
111984-09-9           3,3'-Dimethoxybenzidine hydrochloride       1/1/95
                       (Dianisidine dihydrochloride)                    
127564-92-5           Dichloropentafluoropropane                  1/1/95
128903-21-9           2,2-Dichloro-1,1,1,3,3-                     1/1/95
                       pentafluoropropane (HCFC-225aa)                  
136013-79-1           1,3-Dichloro-1,1,2,3,3-                     1/1/95
                       pentafluoropropane (HCFC-225ea)                  
------------------------------------------------------------------------

    (c)  *  *  *

------------------------------------------------------------------------
                                                              Effective 
                       Category Name                             Date   
------------------------------------------------------------------------
                                                                        
                                 *******                                
Chlorinated paraffins: Includes those chemicals defined by              
 the following formula:                                           1/1/95
    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.              1/1/95
                                                                        
                                 *******                                
Nicotine and salts                                                1/1/95
                                                                        
                                 *******                                
Polycyclic Aromatic Compounds (PACs): (This category                    
 includes only those chemicals listed below)                      1/1/95
  00056-55-3 Benz(a)anthracene                                          
  00218-01-9 Benzo(a)phenanthrene                                       
  00050-32-8 Benzo(a)pyrene                                             
  00205-99-2 Benzo(b)fluoranthene                                       
  00205-82-3 Benzo(j)fluoranthene                                       
  00207-08-9 Benzo(k)fluoranthene                                       
  00189-55-9 Benzo(rst)pentaphene                                       
  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 Dibenz(a,j)anthracene                                      
  00053-70-3 Dibenzo(a,h)anthracene                                     
  05385-75-1 Dibenzo(a,e)fluoranthene                                   
  00192-65-4 Dibenzo(a,e)pyrene                                         
  00189-64-0 Dibenzo(a,h)pyrene                                         
  00191-30-0 Dibenzo(a,l)pyrene                                         
  00194-59-2 7H-Dibenzo(c,g)carbazole                                   
  00057-97-6 7,12-Dimethylbenz(a)anthracene                             
  00193-39-5 Indeno[1,2,3-cd]pyrene                                     
  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 6560-50-F