[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 sitespecific 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 dallethrone] (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]-DLvaline(+)- 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-dimethyl2(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-nitro2-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)-1H1,2,4-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-2Hisoindol-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-(pchlorobenzyl)) (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-triazin2-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 LC<INF>50 of 9.6 parts per billion (ppb), a rainbow trout 96-hour 

LC<INF>50 of 3.6 ppb, and a daphnid 48-hour LC<INF>50 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 

F<INF>2 adult males and F<INF>3 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 doserelated, 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 LC<INF>50 of 50 ppb for bluegill 

and a measured 48-hour LC<INF>50 of 70 ppb for daphnid. In addition, 

the measured 48-hour EC<INF>50 for daphnid is 51 ppb. Measured 

terrestrial acute toxicity data for wildlife include an oral LD<INF>50 

for female mallard ducks of 3.4 milligram per kilogram (mg/kg) and an 

oral LD<INF>50 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 EC<INF>50 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 LC<INF>50 of 0.27 ppb and an oyster 96-hour 

EC<INF>50 (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,-triazine2,4-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 EC<INF>50 of 6.7 ppb and a daphnid 48-hour EC<INF>50 of 29.2 ppb. 

Avian acute toxicity values include a mallard duck LD<INF>50 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 LC<INF>50 of 0.35 ppb, a rainbow trout 96-hour LC<INF>50 of 0.15 

ppb, a sheepshead minnow LC<INF>50 of 17.5 ppb, and a daphnid 48-hour 

EC<INF>50 of 1.6 ppb. EPA believes that there is sufficient evidence 

for listing bifenthrin on EPCRA section 313 pursuant to EPCRA section 

313(d)(2)(C) based on the available environmental toxicity data.

 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 LC<INF>50 of 7.6 ppb, a rainbow trout 96-hour 

LC<INF>50 6.9 ppb, a measured fathead minnow 96-hour LC<INF>50 of 2.7 

ppb, and a daphnid 48-hour LC<INF>50 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-bromo1-(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 LD<INF>50 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 LD<INF>50 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 LC<INF>50 for rainbow trout of 60 ppb and a 96-hour measured 

LC<INF>50 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 threegeneration 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 LC<INF>50 for bluegill of 80 ppb. In addition, the 

measured 48-hour EC<INF>50 for daphnids is 35 ppb. Measured terrestrial 

acute toxicity data for wildlife include an oral LD<INF>50 for mallard 

ducks of 0.397 mg/kg for females and 0.480 mg/kg for males and an oral 

LD<INF>50 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: C<INF>xH<INF>2x-y+2Cl<INF>y where x ranges from 10 

to 30 and y ranges from 3 to 26. Both 58 percent-chlorinated, shortchain (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 (LC<INF>50s 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 LC<INF>50 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 LC<INF>50 of 16.5 ppb, a bluegill 96-hour LC<INF>50 of 

105 ppb, and a 48-hour EC<INF>50 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 LD<INF>50 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 longterm 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 (CFC13) 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 LD<INF>50 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 LC<INF>50 of 1.11 ppb and a rainbow trout 96-hour 

LC<INF>50 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-triazin2-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, betaunsaturated 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, F<INF>3b 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 LC<INF>50 of 0.68 ppb, a bluegill 96-hour LC<INF>50 of 

1.5 ppb, and a daphnid 48-hour EC<INF>50 of 0.14 ppb. EPA believes that 

there is sufficient evidence for listing cyfluthrin on EPCRA section 

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

environmental toxicity data.

 59. Cyhalothrin (3-(2-chloro-3,3,3-trifluoro-1-propenyl)-2,2-

dimethylcyclopropanecarboxylic acid cyano(3-phenoxyphenyl)methyl ester) 

(CAS No. 068085-85-8) (FIFRA AI) (Ref. 3). Cyhalothrin administered 

orally (in capsules) to dogs at 10 mg/kg/day for 26 weeks produced 

occasional disturbances of the nervous system (unsteadiness and/or 

muscular trembling). The NOEL for these effects was not defined. In a 

1-year dog study, ataxia, muscle tremors, and convulsions were observed 

following oral administration at 3.5 mg/kg/day. Abnormal gait and 

convulsions were observed at 0.5 mg/kg/day. The LOEL of the study was 

0.5 mg/kg/day and the NOEL was 0.1 mg/kg/day. EPA believes that there 

is sufficient evidence for listing cyhalothrin on EPCRA section 313 

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

neurological toxicity data.

 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-dichlorophenoxytype 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-dichlorophenoxytype 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-dichlorophenoxytype 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 LC<INF>50 of 8.8 ppm for bluegill. In addition, 2,4-D 

isooctyl esters are expected to bioaccumulate based on the estimated 

log K<INF>ow 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 LC<INF>50 of 8.8 ppm for bluegill. In addition, 2,4-D isooctyl 

esters are expected to bioaccumulate based on the estimated log 

K<INF>ow 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 

LC<INF>50 for rainbow trout of 90 ppb and a daphnid 96-hour LC<INF>50 

of 0.90 ppb. In addition, measured terrestrial wildlife acute toxicity 

data for diazinon include an oral LD<INF>50 for male mallard ducks of 

3.54 mg/kg and an oral LD<INF>50 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 (odichlorobenzidine) 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 (odichlorobenzidine) 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 LC<INF>50 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 LC<INF>50 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 LC<INF>50 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 glutamicpyruvic 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 LD<INF>50 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 LC<INF>50 of 4.55 ppb for daphnids. EPA believes that there is 

sufficient evidence for listing diflubenzuron on EPCRA section 313 

pursuant to EPCRA section 313(d)(2)(C) based on the environmental 

toxicity data for this chemical.

 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 

LC<INF>50 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,Ndimethylformamide 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 

LC<INF>50 for rainbow trout is 15 ppb and the LC<INF>50 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 F<INF>1b, F<INF>2a, and F<INF>3a pups. The 

F<INF>1b 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 LC<INF>50 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 F<INF>2b and F<INF>3a 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 

EC<INF>50 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 LC<INF>50 of 8.8 ppm for bluegill. In addition, 2,4-D 

isooctyl esters are expected to bioaccumulate based on the estimated 

log K<INF>ow 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 EC<INF>50 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 postimplantation 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 LD<INF>50 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 LC<INF>50 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 

LC<INF>50 of 7.5 ppb, a shrimp 96-hour LC<INF>50 of 13 ppb, and a 

daphnid 48-hour EC<INF>50 of 93 ppb. Avian acute and dietary toxicity 

data include a ring-necked pheasant 14-day LD<INF>50 of 4.2 mg/kg and a 

mallard duck 14-day LD<INF>50 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-lethalconcentration values are 0.2 mg/L and 0.4 mg/L, respectively. 

Somnolence and salivation were observed in exposed animals. The dermal 

rabbit LD<INF>50 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 LD<INF>50 values for the redwinged blackbird and 

the starling are 1.78 mg/kg and 4.22 mg/kg, respectively. In addition, 

the measured oral LD<INF>50 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 LC<INF>50 of 1.7 ppb, a fathead minnow 96-hour 

LC<INF>50 of 1.9 ppb, a daphnid 48-hour EC<INF>50 of 3.1 ppb, a 

bluegill sunfish 96-hour of LC<INF>50 of 4.8 ppb, and a sheepshead 

minnow 96-hour LC<INF>50 of 20.8 ppb. Avian acute toxicity values 

include a quail oral LD<INF>50 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 F<INF>2a and F<INF>2b 

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 EC<INF>50 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 LC<INF>50 of 2.3 ppb, a bluegill 96-hour LC<INF>50 of 2.2 

ppb, a sheepshead minnow 96-hour LC<INF>50 of 3.1 ppb, and a daphnid 

48-hour EC<INF>50 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 LC<INF>50 of 0.62 ppb for immobilization. Acute toxicity values 

for other non-standard aquatic invertebrates range from a 48-hour 

EC<INF>50 of 0.024 ppb for brown shrimp to a 96-hour EC<INF>50 of 110 

ppb for scud. Avian acute toxicity values include a male mallard duck 

oral LD<INF>50 of 5.94 mg/kg, a male bobwhite quail LD<INF>50 of 4 mg/

kg, and a mourning dove oral LD<INF>50 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 LD<INF>50 dose of 70.2 mg/kg. The oral mouse 

LD<INF>50 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 LC<INF>50 of 0.26 ppb, a fathead minnow 96-hour 

LC<INF>50 of 0.33 ppb, a rainbow trout 96-hour LC<INF>50 of 1.2 ppb, an 

Atlantic salmon 96-hour LC<INF>50 of 1.2 ppb, and a sheepshead minnow 

96-hour LC<INF>50 of 4.4 ppb. In addition, the 48-hour LC<INF>50 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 LD<INF>50 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 

LC<INF>50 of 90 ppb, a 96-hour LC<INF>50 of 52 ppb for the eastern 

oyster, and a guppy 96-hour LC<INF>50 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 EC<INF>50 of greater than 2.8 ppb, a bluegill 

sunfish 96-hour LC<INF>50 of greater than 3.2 ppb, and a rainbow trout 

96-hour LC<INF>50 of greater than 3.2 ppb. EPA believes that there is 

sufficient evidence for listing flumetralin on EPCRA section 313 

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

environmental toxicity data for this chemical.

 126. Fluorine (CAS No. 007782-41-4) (CERCLA; EPCRA EHS; RCRA APP8; 

RCRA P) (Ref. 8). Inhalation of fluorine causes initial coughing, 

choking and chills, which is followed 1 or 2 days later with pulmonary 

edema. Fluorine has a strong caustic action on mucous membranes, eyes 

and skin. In human volunteers exposed to 100 ppm (0.16 mg/L) for 30 

seconds, much irritation to the nose and eyes was reported. In acute

inhalation studies in animals, lethality occurs at a fairly uniform 

level and is the result of pulmonary edema. Following 1 hour exposures 

in mice, rats or guinea pigs, the inhalation LC<INF>50 values ranged 

from 150 to 185 ppm (0.23 to 0.29 mg/L). The LC<INF>50 for rabbits 

following a 30-minute exposure was 270 ppm (0.42 mg/L). EPA's exposure 

analysis indicates that fluorine concentrations are likely to exist 

beyond facility site boundaries, as a result of continuous, or 

frequently recurring releases, at levels that can reasonably be 

anticipated to cause significant adverse acute human health effects. 

EPA believes that there is sufficient evidence for listing fluorine on 

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

available acute toxicity and exposure data for this chemical.
 127. Fluorouracil (5-Fluorouracil) (CAS No. 000051-21-8) (CAL; 

EPCRA EHS) (Ref. 8). A major use of fluorouracil is in the palliative 

treatment of carcinoma of the colon, rectum, breast, stomach, and 

pancreas that is not amenable to surgery or irradiation. The major 

toxic effects of fluorouracil are on the normal, rapidly proliferating 

tissues particularly of the bone marrow and lining of the 

gastrointestinal tract. Leukopenia, predominantly of the 

granulocytopenic type, thrombocytopenia, and anemia occur commonly with 

intravenous fluorouracil therapy at doses ranging from 6 to 12 mg/kg. 

Pancytopenia and agranulocytosis also have occurred.

 Developmental abnormalities or other effects on newborns were 

reported in offspring of women receiving 150 or 240 mg/kg fluorouracil 

intravenously during weeks 11 to 14 or 20 to 31 of pregnancy. In 

addition, maternal toxicity to the reproductive organs, toxicity to the 

fetus, and developmental abnormalities have been reported in mice, 

rats, and hamsters receiving oral, intraperitoneal, or intramuscular 

doses of fluorouracil ranging from 10 to 700 mg/kg.

 Chronic neurotoxic effects were noted in dogs fed fluorouracil at a 

dietary dose of 2 mg/kg/day for 6 months. In this study, animals were 

examined at the end of 3 months and 6 months. At the end of the 

experiment, or at death, the brain was removed and examined (only one 

dog survived the entire 6-month period). Histological sections of the 

brain showed the presence large multiple monolocular vacuoles in the 

wall of the fornix of the third ventricle.

 EPA believes that there is sufficient evidence for listing 

fluorouracil on EPCRA section 313 pursuant to EPCRA section 

313(d)(2)(B) based on the toxicity of this substance to bone marrow, 

and on the developmental and chronic neurotoxicity data for this 

chemical.

 128. Fluvalinate (N-[2-chloro-4-(trifluoromethyl)phenyl]DLvaline(+)- cyano (3-phenoxyphenyl)methyl ester) (CAS No. 069409-94-5) 

(FIFRA AI) (Ref. 3). Delayed ossification and decreased weight and 

length of fetuses were observed in offspring of rats orally 

administered 50 mg/kg/day (LOEL) on days 6 to 15 of gestation. The NOEL 

was 10 mg/kg/day. These effects were observed at doses that produced 

maternal toxicity. Curved tibia and fibula were observed in the 

offspring of rabbits orally administered 125 mg/kg/day (LOEL). The NOEL 

was 25 mg/kg/day. In a 2-generation reproduction study, a decrease in 

pup weight and growth were observed in offspring of rats orally 

administered 5 mg/kg/day (LOEL). The NOEL was 1 mg/kg/day. 

Significantly decreased weight and survival were observed in offspring 

of rats orally administered 25 mg/kg/day.
 In a range finding study, dietary administration of 50 mg/kg/day 

for 30 days produced skin lesions in rats. The NOEL was not determined. 

A 2-year rat feeding study was terminated at 64 weeks due to dermal 

lesions produced in animals at 15 mg/kg/day. The NOEL was 2 mg/kg/day. 

Dietary administration of 10 mg/kg/day (LOEL for effect) to mice for 2 

years produced scabbing and dermal abrasion. No NOEL for these effects 

was established. An increase in plantar ulcers was observed in rats fed 

2.5 mg/kg/day (LOEL) for 2 years. The NOEL was 1 mg/kg/day. Decreases 

in body weight gain were also observed in this study. Based on the NOEL 

of the study, an oral RfD of 0.01 mg/kg/day was derived. In a 2-

generation rat reproduction study, dietary administration of 5 mg/kg/

day produced decreased body weight gain and skin lesions in parents and 

offspring.

 Dietary administration of 2.5 mg/kg/day to rats for 13 weeks 

produced anemia in blood parameters (decreased hematocrit, hemaglobin, 

and red blood cells). The NOEL was 1.0 mg/kg/day. Dietary 

administration of 30 mg/kg/day (LOEL) to rats for 3 months produced 

decreased hemoglobin, hematocrit, and red blood cell count in rats. The 

NOEL was 3 mg/kg/day.

 EPA believes that there is sufficient evidence for listing 

fluvinate on EPCRA section 313 pursuant to EPCRA section 313(d)(2)(B) 

based on the available developmental, dermal, and hematological 

toxicity data for this chemical.

 Aquatic acute toxicity values for fluvalinate include a daphnid 48-

hour EC<INF>50 of 0.40 ppb, a bluegill sunfish 96-hour LC<INF>50 of 0.9 

ppb, a rainbow trout 96-hour LC<INF>50 of 2.9 ppb, and a sheepshead 

minnow 96-hour LC<INF>50 of 10.8 ppb. EPA believes that there is 

sufficient evidence for listing fluvinate on EPCRA section 313 pursuant 

to EPCRA section 313(d)(2)(C) based on the available environmental 

toxicity data for this chemical.

 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 LC<INF>50 of 39 ppb for rainbow trout, and a measured 96-hour 

LC<INF>50 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. alphaHexachlorocyclohexane 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 alphahexachlorocyclohexane include a 48-hour EC<INF>50 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 alphahexachlorocyclohexane 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 LC<INF>50 

for HDI ranges from 56 (385 mg/m<SUP>3) to 45 ppm (310 mg/m<SUP>3). The 
mouse LC<INF>50 for HDI is 4 ppm (30 mg/m<SUP>3). HDI also induces 

irritation of the upper respiratory tract in mice after acute exposure. 

The mouse LOAEL was 0.062 ppm (0.43 mg/m<SUP>3) 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/m<SUP>3, 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 isocyanatesensitized 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/m<SUP>3 (58 ppm, LOAEL(ADJ) of 73 

mg/m<SUP>3) was established for these electrophysiological alterations 

in humans. The alterations observed are consistent with n-hexaneinduced 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 

EC<INF>50 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 LC<INF>50 in the Chanel Catfish was 90 ppb. 

Bioaccumulation factors in bluegill sunfish are 1300 for the whole 

fish, 780 for the fillet, and 1900 for viscera. EPA believes that there 

is sufficient evidence for listing hydramethylon on EPCRA section 313 

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

environmental toxicity data and the potential for bioaccumulation.

 136. Hydrochlorofluorocarbons (CAA OD) (Ref. 8). 

Hydrochlorofluorocarbons are known to release chlorine radicals into 

the stratosphere. Chlorine radicals act as catalysts to reduce the net 
amount of stratospheric ozone.

 Stratospheric ozone shields the earth from ultraviolet-B (UV-B) 

radiation (i.e., 290 to 320 nanometers). Decreases in total column 

ozone will increase the percentage of UV-B radiation, especially at its 

most harmful wavelengths, reaching the earth's surface.

 Exposure to UV-B radiation has been implicated by laboratory and 

epidemiologic studies as a cause of two types of nonmelanoma skin 

cancers: squamous cell cancer and basal cell cancer. Studies predict 

that for every 1 percent increase in UV-B radiation, nonmelanoma skin 

cancer cases would increase by about 1 to 3 percent.

 Recent epidemiological studies, including large case control 

studies, suggest that UV-B radiation plays an important role in causing 

malignant melanoma skin cancer. Recent studies predict that for each 1 

percent change in UV-B intensity, the incidence of melanoma could 

increase from 0.5 to 1 percent.

 Studies have demonstrated that UV-B radiation can suppress the 

immune response system in animals, and, possibly, in humans. Increases 

in exposure to UV-B radiation are likely to increase the incidence of 

cataracts and could adversely affect the retina.

 Aquatic organisms, particularly phytoplankton, zooplankton, and the 

larvae of many fishes, appear to be susceptible to harm from increased 

exposure to UV-B radiation because they spend at least part of their 

time at or near the surface of waters they inhabit.

 Increased UV-B penetration has been shown to result in adverse 

impacts on plants. Field studies on soybeans suggest that yield 

reductions could occur in some cultivars of soybeans, while evidence 

from laboratory studies suggest that two out of three cultivars are 

sensitive to UV-B.

 Because this increased UV-B radiation can be reasonably anticipated 

to lead to cancer and other chronic human health effects and 

significant adverse environmental effects, EPA believes there is 

sufficient evidence for listing the following HCFCs that are 

commercially viable on EPCRA section 313 pursuant to EPCRA sections 

313(d)(2)(B) and (C). EPA is proposing that the following HCFCs be 

added individually to EPCRA section 313:

 Dichloropentafluoropropane (CAS No. 127564-92-5)

 1,3-Dichloro-1,1,2,3,3-pentafluoropropane (HCFC-225ea) (CAS No. 

136013-79-1)

 2,2-Dichloro-1,1,1,3,3-pentafluoropropane (HCFC-225aa) (CAS No. 

128903-21-9)

 1,1-Dichloro-1,2,3,3,3-pentafluoropropane (HCFC-225eb) (CAS No. 

111512-56-2)
 1,1-Dichloro-1,2,2,3,3-pentafluoropropane (HCFC-225cc) (CAS No. 

13474-88-9)

 1,3-Dichloro-1,1,2,2,3-pentafluoropropane (HCFC-225cb) (CAS No. 

000507-55-1)

 1,2-Dichloro-1,1,3,3,3-pentafluoropropane (HCFC-225da) (CAS No. 

000431-86-7)

 3,3-Dichloro-1,1,1,2,2-pentafluoropropane (HCFC-225ca) (CAS No. 

000422-56-0)

 2,3-Dichloro-1,1,1,2,3-pentafluoropropane (HCFC-225ba) (CAS No. 

000422-48-0)

 1,2-Dichloro-1,1,2,3,3-pentafluoropropane (HCFC-225bb) (CAS No. 

000422-44-6)

 Dichlorofluoromethane (HCFC-21) (CAS No. 000075-43-4)

 1,1,1,2-Tetrachloro-2-fluoroethane (HCFC-121a) (CAS No. 000354-11-

0)

 1,1,2,2-Tetrachloro-1-fluoroethane (HCFC-121) (CAS No. 000354-14-3)

 1,2-Dichloro-1,1-difluoroethane (HCFC-132b) (CAS No. 001649-08-7)

 2-Chloro-1,1,1-trifluoroethane (HCFC-133a) (CAS No. 000075-88-7)

 3-Chloro-1,1,1-trifluoropropane (HCFC-253fb) (CAS No. 000460-35-5).

 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-dioxo1-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 

EC<INF>50 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 LD<INF>50 is 25 mg/kg and the rat 

inhalation LC<INF>50 value is 0.044 mg/L. The 4-hour inhalation 

LC<INF>100 in mice is 0.007 mg/L. The rabbit oral LD<INF>50 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 LC<INF>50 of 12 ppb for bluegills and a 24-hour 

LC<INF>50 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 EC<INF>50 of 1.6 ppb and a mysid 96-hour EC<INF>50 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 LC<INF>50 value of isophorone diisocyanate in 

rats is 0.123 mg/L. The rat and mouse 3-hour inhalation RD<INF>50 (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 LC<INF>50 of 68 ppb for rainbow trout, a 96-hour LC<INF>50 of 51 

ppb for sheepshead minnow, and a 96-hour LC<INF>50 of 76 ppb for lake 

trout. In addition, the measured 48-hour EC<INF>50 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 timeweighted 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 

LD<INF>50 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 LC<INF>50 value for 1,1-

methylenebis(4-isocyanatocyclohexane) is 0.21 mg/L. The 3-hour mouse 

inhalation RD<INF>50 (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 LD<INF>50 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 LC<INF>50 of 94 ppb, a 96-hour LC<INF>50 of 130 ppb for 

bluegills, and a daphnid 48-hour LC<INF>50 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 LD<INF>50 values are reported to be 6.01 mg/kg and 18 mg/kg, 

respectively. The rat and mouse 4-hour inhalation LC<INF>50 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 EC<INF>50 of 0.14 ppb for daphnids and a 96-hour LC<INF>50 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 F<INF>1 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 Nmethylpyrrolidone 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 LC<INF>50 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 

LC<INF>50 of 70 ppb for bluegills, and a 96-hour LC<INF>50 of 0.16 ppb 

for daphnids. Measured acute avian toxicity data include a pheasant 

oral LD<INF>50 of 1.37 mg/kg, a mallard duck oral LD<INF>50 of 4.63 mg/

kg, and a sharp-tailed grouse oral LD<INF>50 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 EC<INF>50 

of 90 ppb and a 10-day EC<INF>50 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 

EC<INF>50 of 0.35 ppb for daphnids and a 96-hour LC<INF>50 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 (NO<INF>3<SUP>-). 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 F<SUP>0 and F<SUP>1 

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 K<INF>ow is 

6.1. EPA believes that there is sufficient evidence for listing 

oxyfluorfen on EPCRA section 313 pursuant to EPCRA section 313(d)(2)(C) 

based on the environmental toxicity data and potential for 

bioaccumulation for this chemical.

 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 

LC<INF>50 of 80 ppb for striped bass, a 96-hour LC<INF>50 of 30 ppb for 

channel catfish, and a 96-hour LC<INF>50 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 LD<INF>50 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 LD<INF>50 and 4-hour rat inhalation 

LC<INF>50 values for perchloromethyl mercaptan are 8.26 mg/kg and 0.26 

mg/L, respectively. The 2-hour mouse inhalation LC<INF>50 value is 

reported to be 0.296 mg/L. In an eye irritation test, 50 micrograms 

(<greek-m>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 LC<INF>50 of 3.5 ppb, a rainbow trout 96-hour measured 

LC<INF>50 of 0.62 ppb, a bluegill 96-hour LC<INF>50 of 2.52 ppb, an 

Atlantic silverside 96-hour measured LC<INF>50 2.2 ppb, and a daphnid 

48-hour LC<INF>50 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 

LC<INF>50 of 700 ppb for daphnids. The measured 28-day LC<INF>50 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 LC<INF>50 of 16.7 ppb and a goldfish 48-hour LC<INF>50 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 LC<INF>50 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 LC<INF>50 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/m<SUP>3 

(30.5 ppm; Human Equivalent Concentration (HEC) is 0.93 mg/m<SUP>3) and 

a LOAEL of 110 mg/m<SUP>3 (80 ppm; HEC is 2.4 mg/m<SUP>3). 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 LC<INF>50 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 LC<INF>50 of 3.4 ppb for rainbow trout and a 96-hour LC<INF>50 

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 mouseskin 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). 7HDibenzo(c,g)carbazole is classified as a Group 2B compound by IARC, 

i.e., the compound is a possible human carcinogen. 7HDibenzo(c,g)carbazole has been shown to be carcinogenic in animals. EPA 

believes that there is sufficient evidence for listing 7Hdibenzo(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 EC<INF>50 of 0.27 

ppb and an algae 7-day EC<INF>50 of 24 ppb. EPA believes that there is 

sufficient evidence for listing primisulfuron on EPCRA section 313 

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

environmental toxicity data for this chemical.

 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 LC<INF>50 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 LC<INF>50 of 0.275 ppb (89 percent a.i.), a bluegill 

sunfish 96-hour LC<INF>50 of 0.750 ppb (89 percent a.i.), a lake trout 

96-hour LC<INF>50 of 1.7 ppb (84.5 percent a.i.), and a fathead minnow 

96-hour LC<INF>50 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 

<greek-m>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 LD<INF>50 values of fluoroacetate in the house 

sparrow, redwinged blackbird, starling and golden eagle are 3.0, 4.22, 

2.37, and 1.25 to 5 mg/kg, respectively. In addition, measured acute 

toxicity data for mammalian wildlife include an oral LD<INF>50 of 0.22 

to 0.44 mg/kg for mule deer, an oral LD<INF>50 of 1.41 mg/kg for male 

ferrets, and an oral LD<INF>50 of 0.5 to 1.0 mg/kg for bears. EPA 

believes that there is sufficient evidence for listing sodium 

fluoroacetate on EPCRA section 313 pursuant to EPCRA section 

313(d)(2)(C) based on the environmental toxicity data for this 

chemical.

 229. Sodium hypochlorite (CAS No. 007681-52-9) (CERCLA) (Ref. 8). 

Aquatic acute toxicity data for sodium hypochlorite include a 96-hour 

measured LC<INF>50 of 100 ppb for bluegill and a 96-hour measured 

LC<INF>50 of 80 ppb for fathead minnow. In addition, the 96-hour 

measured LC<INF>50 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 LC<INF>50 of 55 ppb, a bluegill 96-hour 

LC<INF>50 of 44 ppb, a fathead minnow 96-hour LC<INF>50 of 20 ppb, and 

a shrimp 96-hour LC<INF>50 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 manmade 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/m<SUP>3 

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/m<SUP>3 may act 

synergistically with copollutants such as ozone, NO<INF>2, 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/m<SUP>3 

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/m<SUP>3 may act 

synergistically with copollutants such as ozone, NO<INF>2, 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 LD<INF>50 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 

LC<INF>50 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 LC<INF>50 of 0.06 ppb, a bluegill 96-hour LC<INF>50 of 

0.13 ppb, a sheepshead minnow 96-hour LC<INF>50 of 0.13 ppb, a daphnid 

48-hour EC<INF>50 of 0.07 ppb, and a mysid 96-hour EC<INF>50 of 0.053 

ppb. EPA believes that there is sufficient evidence for listing 

teflurin on EPCRA section 313 pursuant to EPCRA section 313(d)(2)(C) 

based on the available environmental toxicity data for this chemical.

 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 sunexposed 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-Hisoindol-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 LD<INF>50 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 

LD<INF>50 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 

LD<INF>50 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 LC<INF>50 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 LC<INF>50 of 560 ppb, a daphnid 48-hour EC<INF>50 of 0.31 

ppb, and a mysid 96-hour LC<INF>50 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 LC<INF>50 of 560 ppb, a daphnid 48-hour 

EC<INF>50 of 0.31 ppb, and a mysid 96-hour LC<INF>50 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 

LC<INF>50 of 760 ppb, a striped bass 96-hour LC<INF>50 of 760 ppb, a 

rainbow trout 96-hour LC<INF>50 of 790 ppb, and a green algae 72-hour 

EC<INF>50 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 LC<INF>50 of 1.47 ppm , a rainbow trout 96-hour LC<INF>50 of 2.65 

ppm, a sheepshead minnow 96-hour LC<INF>50 of 530 ppb, a daphnid 48-

hour EC<INF>50 of 27 ppb, a mysid 96-hour LC<INF>50 of 29.3 ppb, an 

eastern oyster 96-hour LC<INF>50 of 1.0 ppb, and an algae 96-hour 

EC<INF>50 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 thiophanatemethyl. 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 LD<INF>50s 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 LD<INF>50 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. Ninetyday feeding studies in rats (10 mg/kg/day) and dogs (5 mg/kg/day) 

showed no treatment related adverse effects except for increased liverto-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 LC<INF>50 of 2.3 ppb, an algae 72-hour EC<INF>50 of 

9.3 ppb, and a Harpacticoid copepod 96-hour LC<INF>50 of 0.8 ppb. EPA 

believes that there is sufficient evidence for listing tributyltin 

fluoride on EPCRA section 313 pursuant to EPCRA section 313(d)(2)(C) 

based on the available environmental toxicity data.

 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,Stributyltrithiophosphate include a rainbow trout 96-hour LC<INF>50 of 

660 ppb (0.660 ppm) and a bluegill 96-hour LC<INF>50 of 620 ppb (0.620 

ppm). The measured log K<INF>ow 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 LC<INF>50 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 LC<INF>50 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 

LC<INF>50 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/m<SUP>3 

with a range of 4 to 24 mg/m<SUP>3. 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-shortterm 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 LC<INF>50 for carp of 55 ppb and a 72-hour EC<INF>50 

(growth) for marine green algae of 0.92 ppb. In addition, the measured 

aquatic toxicity information indicates a freshwater green algae 8-day 

EC<INF>50 (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 LC<INF>50 of 5.4 ppb, a bluegill 96-

hour LC<INF>50 of 23 ppb, a rainbow trout 96-hour LC<INF>50 of 15 ppb, 

and a marine green algae 72-hour LC<INF>50 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/m<SUP>3 (0.0005 mg/L) for a 

period of up to 2 weeks developed respiratory symptoms that persisted 

for nearly 2 weeks after removal from exposure. Inhalation of 

unspecified levels of vanadium pentoxide for 1 to 5 years produced 

asthma in 3 of 20 workers. Mice and rats exposed to 1 to 3 mg/m<SUP>3 

(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: hexamethylene1,6-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-nitrobenzoic acid, sodium salt] 

 

 ******* 

Alachlor 15972-60-8 1/1/95

Aldicarb 116-06-3 1/1/95

 

 ******* 

d-trans-Allethrin [d-trans- 28057-48-9 1/1/95

Chrysanthemic acid of d-allethrone] 

Allylamine 107-11-9 1/1/95

 

 ******* 

Aluminum phosphide 20859-73-8 1/1/95

Ametryn (N-Ethyl-N'-(1-methylethyl)-6- 834-12-8 1/1/95

(methylthio)-1,3,5,-triazine-2,4- 

diamine) 

 

 ******* 

Amitraz 33089-61-1 1/1/95

 

 ******* 

Anilazine [4,6-dichloro-N-(2- 101-05-3 1/1/95

chlorophenyl)-1,3,5-triazin-2-amine] 

 

 ******* 

Atrazine (6-Chloro-N-ethyl-N'-(1- 1912-24-9 1/1/95

methylethyl)-1,3,5,-triazine-2,4- 

diamine) 

 

 ******* 

Bendiocarb [2,2-Dimethyl-1,3- 22781-23-3 1/1/95
benzodioxol-4-ol methylcarbamate] 

Benfluralin (N-Butyl-N-ethyl-2,6- 1861-40-1 1/1/95

dinitro-4- 

(trifluoromethyl)benzenamine) 

Benomyl 17804-35-2 1/1/95

 

 ******* 

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 Sethyl 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,Sdimethyl 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]-DLvaline(+)-cyano (3- 

phenoxyphenyl)methyl ester] 

Folpet 133-07-3 1/1/95

Fomesafen [5-(2-Chloro-4- 72178-02-0 1/1/95

(trifluoromethyl)phenoxy)-Nmethylsulfonyl)-2-nitrobenzamide] 

 

 ******* 

alpha-Hexachlorocyclohexane 319-84-6 1/1/95

 

 ******* 

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,Odimethylphosphorothioate] 

 

 ******* 

Potassium bromate 7758-01-2 1/1/95

Potassium dimethyldithiocarbamate 128-03-0 1/1/95

Potassium N-methyldithiocarbamate 137-41-7 1/1/95

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-2Hisoindol-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

 

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Nicotine and salts 1/1/95
 

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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 

 

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Strychnine and salts 1/1/95

 

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[FR Doc. 94-753 Filed 1-11-94; 3:34 pm]

BILLING CODE 6560-50-F