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

SUMMARY: EPA is proposing to add 313 chemicals and chemical categories

to the list of toxic chemicals required to be reported on under section

313 of the Emergency Planning and Community Right-to-Know Act of 1986

and section 6607 of the Pollution Prevention Act of 1990. The proposed

addition of these chemicals and chemical categories is based on their

acute human health effects, carcinogenicity or other chronic human

health effects, and/or their environmental effects. EPA believes that

these chemicals and chemical categories meet the EPCRA section

313(d)(2) criteria for addition to the list of toxic chemicals.

DATES: Written comment on this proposed rule must be received on or

before April 12, 1994. The public meeting will take place on March 2,

1994, at 1 p.m. and adjourn by 5 p.m.

ADDRESSES: Written comments should be submitted in triplicate to: OPPT

Docket Clerk, TSCA Document Receipt Office (7407), Office of Pollution

Prevention and Toxics, Environmental Protection Agency, Rm. E-G99, 401

M St., SW., Washington, DC 20460. Comments containing information

claimed as confidential must be clearly marked as confidential business

information (CBI). If CBI is claimed, three additional sanitized copies

must also be submitted. Nonconfidential versions of comments on this

proposed rule will be placed in the rulemaking record and will be

available for public inspection. Comments should include the docket

control number for this proposal, OPPTS-400082. Unit VI. of this

preamble contains additional information on submitting comments

containing information claimed as CBI.

The public meeting will be held at the: Environmental Protection

Agency, Auditorium, Education Center, 401 M St., SW., Washington, DC.

FOR FURTHER INFORMATION CONTACT: Maria J. Doa, Emergency Planning and

Community Right-to-Know Information Hotline, Environmental Protection

Agency, Mail Stop 5101, 401 M St., SW., Washington, DC 20460, Toll

free: 800-535-0202 or Toll free TDD: 800-553-7672, Attention: Docket

Number OPPTS-400082.

SUPPLEMENTARY INFORMATION:

I. Introduction

A. Statutory Authority

This proposed rule is issued under sections 313(d) and (e)(1) of

the Emergency Planning and Community Right-to-Know Act of 1986 (EPCRA),

42 U.S.C. 11023. EPCRA is also referred to as Title III of the

Superfund Amendments and Reauthorization Act of 1986.

B. Background

Section 313 of EPCRA requires certain facilities manufacturing,

processing, or otherwise using listed toxic chemicals to report their

environmental releases of such chemicals annually. Beginning with the

1991 reporting year, such facilities also must report pollution

prevention and recycling data for such chemicals, pursuant to section

6607 of the Pollution Prevention Act, 42 U.S.C. 13106. When enacted,

section 313 established an initial list of toxic chemicals that was

comprised of more than 300 chemicals and 20 chemical categories.

Section 313(d) authorizes EPA to add chemicals to or delete chemicals

from the list, and sets forth criteria for these actions. Under section

313(e), any person may petition EPA to add chemicals to or delete

chemicals from the list. EPA has added to and deleted chemicals from

the original statutory list.

EPA issued a statement of petition policy and guidance in the

Federal Register of February 4, 1987 (52 FR 3479), to provide guidance

regarding the recommended content and format for submitting petitions.

EPA must respond to petitions within 180 days either by initiating a

rulemaking or by publishing an explanation of why the petition is

denied. On May 23, 1991 (56 FR 23703), EPA issued guidance regarding

the recommended content of petitions to delete individual members of

the section 313 metal compound categories.

II. Explanation for Expansion of the EPCRA Section 313 Chemical

List

A. General Rationale

The Toxics Release Inventory (TRI), through the public access

provisions of EPCRA, has proven to be one of the most powerful forces

in empowering the Federal government, State governments, industry,

environmental groups, and the general public, to fully participate in

an informed dialogue about the environmental impacts of toxic chemicals

in the United States.

A major section of EPCRA, which Congress passed in 1986, resulted

in the creation of the Toxics Release Inventory. TRI is a publicly

available data base that provides quantitative information on toxic

chemical releases, transfers, recycling, and disposal. With the

collection of this information for the first time in 1987, came the

ability for the public, government, and the regulated community to

understand the magnitude of chemical emissions in the United States; to

compare chemical releases and transfers of chemical wastes among

States, industries, facilities, and environmental media; and perhaps

most importantly, to assess the need to reduce and where possible,

eliminate these releases and transfers. TRI enables all interested in

environmental progress to establish credible baselines, to set

realistic goals, and to measure progress over time, in meeting those

goals. The TRI system has become a neutral yardstick by which progress

can be measured by all interested parties.

The original list of chemicals for which reporting was required

consisted of 320 chemicals and chemical categories. The list was a

combination of the Maryland Chemical Inventory Report List of Toxic or

Hazardous Substances and the New Jersey Environmental Hazardous

Substance List. The combination of these two lists provided a sound and

logical starting point for the national TRI program. Recognizing

however that the list would need to be a dynamic one, EPCRA

specifically authorizes additions to and deletions from the list. To

date, EPA has added 16 chemicals to the list and has deleted 12

chemicals from the list.

With 5 years experience behind the program, EPA, other federal

agencies, Congress, and the public have recognized the need to expand

the TRI list beyond the original chemicals and chemical categories and

beyond the relatively limited reporting universe. (Currently reporting

is only required from facilities that fall within the manufacturing

Standard Industrial Classification (SIC) codes 20 through 39 that meet

certain thresholds).

While the data on the chemicals that are covered have allowed the

public and private sectors to be informed and involved in environmental

decisionmaking as they never were before, it has become increasingly

evident to those same constituents that they have access to information

on a relatively small number of important chemicals. Congress has

echoed this recognition in the Right-to-Know More bills that were put

forward in the 102nd Congress. EPA and State regulatory agencies have

integrated TRI information as a critical component in their

environmental decisionmaking and in many cases are constrained by the

lack of similar information on chemicals of concern not covered by the

TRI. While the TRI has been successful in focusing attention on the

initial list of chemicals and in many cases fostering emissions

reductions and prevention activities, that same focus has highlighted

the need to expand beyond that initial list and to include additional

chemicals that exhibit similar toxicity characteristics. This proposal

is one of the first in a series of actions that EPA plans to use to

expand the coverage of the TRI. This first phase will focus on adding

chemicals, followed by a second phase that will identify additional

facilities for inclusion. EPA is considering a third phase, which would

look at modification of the data elements currently required by TRI.

In conjunction with these expansion activities EPA has been

considering whether other adjustments are needed in the scope of the

TRI program. EPA received petitions from the Small Business

Administration and the American Feed Industry Association seeking an

exemption for ``small sources'' (i.e, those facilities that file TRI

forms with zero or small release estimates). EPA previously put those

petitions out for public comment and, on review, believes there is

substantial merit to the general concerns raised in the petitions.

The Agency's plan for proceeding on the small source issue would

include the following steps. EPA is examining four options for

establishing a small release exemption from the TRI reporting

obligation: Cutoffs at zero, 500 pounds, 1,000 pounds, and 5,000

pounds. EPA will provide the public with a report on these four options

by the end of January. This analysis will consider what data might not

be available at both the national and community level, and the cost

savings to the government and to industry of the four exemption levels.

EPA plans to hold a public meeting in February for discussion of the

report. Based on this feedback, EPA will then design a regulatory

strategy that will align the small source issue with final action on

today's proposal. The Agency's objective will be to minimize

unnecessary data collection and reporting by facilities, including for

the chemicals identified in today's proposal.

B. Development of the Chemical Addition Candidates

As a starting point for screening candidates for addition to the

toxic chemical list under EPCRA section 313, EPA chose to examine the

lists of chemicals regulated or identified, as of concern, under

various environmental statutes including: (1) Section 112(b) of the

Clean Air Act (CAA) as amended in 1990 (Hazardous Air Pollutants); (2)

section 602(b) of the CAA (Class II ozone depleting substances); (3)

section 307(a) of the Clean Water Act (CWA) (Priority Pollutant List);

(4) Federal Insecticide, Fungicide, and Rodenticide Act (FIFRA) Active

Ingredients, including Special Review, Canceled/Denied or Suspended,

and Restricted Use Pesticides; (5) section 302 of EPCRA (Extremely

Hazardous Substances); (6) section 102 of the Comprehensive

Environmental Response, Compensation, and Liability Act (CERCLA); (7)

section 3001 of the Resource Conservation and Recovery Act (RCRA) and

chemicals listed at 40 CFR 261.33(e) and (f) and Appendix VIII; (8)

section 1412 of the Safe Drinking Water Act as amended; (9) certain

chemicals subject to the Toxics Substance Control Act (Existing

Chemicals); and (10) the State of California Safe Drinking Water and

Toxic Enforcement Act of 1986 (Proposition 65) (List of Chemicals Known

to the State to Cause Reproductive Toxicity).

In addition, EPA considered chemicals designated as possible,

probable, or known carcinogens in the Monographs of the International

Agency for Research on Cancer (IARC) and the 6th Annual Report on

Carcinogens of the National Toxicology Program (NTP), U.S. Department

of Health and Human Services (DHHS).

From this initial group of substances, EPA excluded chemicals that

are already listed on section 313 or are already reportable under one

of the EPCRA section 313 categories. For example, ``cyanide, total'' is

listed under section 307(a) of the CWA. This listing is considered to

be a subset of the EPCRA section 313 cyanide compounds category and the

hydrogen cyanide listing. EPA decided not to propose listing these

types of chemicals separately because they are already reportable under

one of the existing section 313 categories. To prioritize chemicals for

possible addition to EPCRA section 313, EPA applied a human health and

ecotoxicity screen and a production volume screen, which are described

below. The results of the toxicity screen for a subset of these

chemicals were presented at a public meeting on May 29, 1992 (Ref. 4).

Other chemicals were also removed from consideration for this

rulemaking because they are the subjects of two recently published

EPCRA petition responses. On March 4, 1992, EPA received a petition

from Governor Mario M. Cuomo of New York and the Natural Resources

Defense Council (NRDC) to add 80 chemicals and 2 chemical categories to

the list of toxic chemicals under section 313 of EPCRA. All of these

chemicals and chemical categories appear on the RCRA list of hazardous

wastes under 40 CFR 261.33(f) and as such are a subset of the chemicals

screened by EPA. EPA responded to the petition in a proposed rulemaking

on September 8, 1992 (57 FR 41020) and in a final rule adding 22

chemicals on November 30, 1993 (58 FR 63500).

On December 3, 1991, EPA received a petition from the NRDC, Friends

of the Earth, and the Environmental Defense Fund to add

hydrochlorofluorocarbons (HCFCs) to the list of toxic chemicals under

section 313 of EPCRA. The HCFCs are listed under section 602(b) of the

CAA as Class II ozone depleting substances and as such are a subset of

the chemicals screened by EPA. EPA responded to the petition in a

proposed rulemaking on June 24, 1992 (57 FR 28159) and in a final rule

adding 11 HCFCs on November 30, 1993 (58 FR 63496). An additional 16

HCFCs not added to the TRI list by the November 30, 1993 final rule are

proposed for addition in this rulemaking (See Unit IV.B.135. of this

preamble).

1. Toxicity screen. A toxicity screen is a limited review of

readily available toxicity data (e.g., information in data bases and

other secondary sources) that is used for a preliminary categorization

of a chemical during the process of selecting candidates for possible

listing under EPCRA section 313. The toxicity screen is used to

identify chemicals for further consideration and does not reflect a

final determination for listing a chemical under EPCRA section 313.

Such a determination can only be made after a hazard assessment is

conducted (See Unit II.B.3. of this preamble). The chemicals identified

above were screened for four general effect categories: Acute human

health effects, cancer, other chronic human health effects, and

ecological effects.

The screening criteria associated with each of the effect areas

used in the toxicity screen are discussed in detail in the Revised

Draft Hazard Assessment Guidelines for Listing Chemicals on the Toxic

Release Inventory (Draft Hazard Assessment Guidelines), (Ref. 6). The

numerical screening values reflected in the Draft Hazard Assessment

Guidelines were developed to capture, in the ``sufficient for listing''

screening category, the majority of chemicals already listed on various

CERCLA and EPCRA lists, and thus known or suspected to be toxic and/or

hazardous. These Draft Hazard Assessment Guidelines contain guidance

for both the screening and hazard assessments of chemicals and are

available for review in the docket associated with this rulemaking.

This draft document was distributed at a public meeting on May 29,

1992. A final version of these guidelines has not yet been developed.

Requests for further information about these draft guidelines should be

addressed to the person identified under ``FOR FURTHER INFORMATION

CONTACT.''

Based on the results of this screen, the chemicals were

preliminarily placed in one of three screening categories defined in

the Draft Hazard Assessment Guidelines: ``sufficient;'' ``may be

sufficient;'' or ``insufficient.'' EPA received comment in response to

the Draft Hazard Assessment Guidelines that objected to the Agency's

use of the terms ``sufficient,'' ``may be sufficient,'' and

``insufficient'' as titles for the toxicity screening categories. The

commenter claimed that these terms are appropriate only for the results

of a hazard assessment. The commenter stated that these terms should

not be used for screening categories because the toxicity screen only

identifies chemicals for further consideration. EPA agrees that the

screening categories only reflect a preliminary determination on each

chemical, and therefore, to avoid further confusion, will refer to the

screening categories as ``high priority,'' ``medium priority,'' and

``low priority'' to reflect the difference between a toxicity screen

and a hazard assessment. These terms will be used throughout this

document in reference to the toxicity screening categories. Chemicals

that were categorized as ``low priority'' during the screening process

were not considered further as candidates for addition to the EPCRA

section 313 list in this rulemaking.

2. Production volume screen. EPCRA section 313(f) establishes

reporting thresholds related to the amount of a chemical that is

manufactured, processed, or otherwise used. [The EPCRA section 313

manufacture (includes import) and processing thresholds are 25,000

pounds per facility per year. The otherwise use threshold is 10,000

pounds per facility per year]. EPA anticipates that the addition of

chemicals manufactured, imported, processed, or used in quantities less

than the EPCRA section 313 volume thresholds would not result in the

submission of TRI reports. Thus, EPA elected to initially focus its

attention on chemicals likely to yield reports. Accordingly, EPA also

screened potential candidates for the likelihood of meeting the EPCRA

section 313 volume thresholds. Chemicals for which there were no data

to indicate that the chemical is likely to meet or exceed the EPCRA

section 313 volume thresholds were not considered further as possible

candidates for addition to the section 313 list at this time.

Production volume data on each of the chemicals were gathered

primarily from two sources: (1) The TSCA Chemical Update System (1990);

and (2) the FIFRA Section 7 Tracking System. On June 12, 1986 (51 FR

21438), EPA promulgated a rule pursuant to section 8(a) of TSCA which

required manufacturers and importers to report every 4 years, subject

to certain threshold production quantities and other exclusions, the

quantities of chemicals they produced (40 CFR part 710). Among the

exceptions to the inventory update rule (IUR) reporting were polymers,

biological products, inorganic substances, and chemicals produced at

less than 10,000 pounds, all with certain limitations. Data from the

IUR is maintained in EPA's TSCA Chemical Update System (CUS).

Section 7 of FIFRA provides the Agency with annual production

information on registered pesticides. EPA regulations implementing

FIFRA section 7 (40 CFR part 167) require all manufacturers of

pesticidal products (which includes formulated pesticides, active

ingredients, and devices) to submit an annual report detailing the

amount of each type of pesticidal product manufactured, sold and

distributed during the past year, and estimated to be manufactured,

imported, and processed during the current year (40 CFR 167.85).

For industrial inorganic compounds not subject to FIFRA or

available on CUS, information from the public literature was used,

supplemented with information from companies.

3. Hazard evaluation. EPA conducted a hazard evaluation for each of

the addition candidates that resulted from the above analyses and

determined based on the weight-of-the evidence if there was sufficient

evidence to establish that the candidate chemical met the statutory

criteria for addition to EPCRA section 313. To make this determination,

EPA senior scientists reviewed readily available toxicity information

on each chemical for each of the following effect areas: acute human

health effects; cancer; other chronic human effects; and environmental

effects. In addition, EPA reviewed, where appropriate, information on

the environmental fate of the chemical.

The hazard assessment was conducted in accordance with relevant EPA

guidelines for each adverse human health or environmental effect (e.g.,

the appropriate guidelines for hazard evaluation of chemical

carcinogens and for the type of evidence required to substantiate a

determination of carcinogenicity are the Guidelines for Carcinogen Risk

Assessment (Ref. 2)). The guidelines that were used for each effect are

Agency guidelines that are identified in the Draft Hazard Assessment

Guidelines (Ref. 6). During this assessment the severity and

significance of the effects induced by the chemical, the dose level

causing the effect, and the quality and quantity of the available data,

including the nature of the data (e.g., human epidemiological,

laboratory animal, field or workplace studies) and confidence level in

the existing data base, were all considered. Where a careful review of

the scientific data for a particular chemical results in a high level

of confidence that the chemical causes an adverse effect at relatively

low dose levels, EPA believes that this evidence is sufficient for

listing the chemical under section 313. On the other hand, where a

review of the scientific data indicates that the chemical will cause

various adverse effects at moderate dose levels, EPA believes, based on

the total weight-of-the-evidence, that there is sufficient evidence for

listing the chemical under EPCRA section 313.

EPA also conducted an analysis of exposure for each chemical or

chemical category proposed for listing under EPCRA section 313(d)(2)(A)

(i.e., based on adverse acute human health effects), and, where

appropriate, under section 313(d)(2)(C) (i.e., based on adverse

ecological effects). For chemicals listed under EPCRA section

313(d)(2)(A), this analysis included estimated concentrations of the

chemical at or beyond the facility site boundary through the use of

estimated releases and modelling techniques. EPA requests comment on

its approach in considering exposure as a part of its evaluation of

these chemicals under sections 313(d)(2)(A) and (C).

Based on this analysis for each of the chemicals proposed for

listing, EPA determined that one or more of the statutory criteria were

met. A discussion of EPA's interpretation of the EPCRA section 313

criteria is given in Unit III. of this preamble. A discussion of the

evidence supporting EPA's proposal to add each of the chemicals to

EPCRA section 313 is presented in Unit IV. of this preamble and in the

record supporting this proposed rule.

4. Other considerations. EPA excluded certain chemicals and

chemical categories from consideration for proposed listing under EPCRA

section 313 in this rulemaking for a number of reasons. Some chemicals

were identified only as environmental degradation products rather than

chemicals that are manufactured, processed, or otherwise used by a

facility. These chemicals will only be present in the environment as a

result of the release into the environment of precursor chemicals. If

the degradation product meets the toxicity criteria of EPCRA section

313, the precursor chemical may be considered for listing on EPCRA

section 313. The degradation product would not be considered for

listing on EPCRA section 313 because a facility subject to EPCRA

section 313 is only required to file a TRI report for a chemical that

it manufactures, processes, or otherwise uses, within the facility

boundaries. Therefore, EPA does not believe that it is appropriate to

consider listing such chemicals at this time.

Some of the lists reviewed by EPA included listings that

represented waste streams from particular processes. These waste

streams, such as coke oven emissions, are not discrete chemicals or

chemical categories, but contain a wide range of chemicals, many of

which are currently listed individually on EPCRA section 313. The focus

of this rulemaking is on the addition of specific chemicals and

chemical categories and, as such, EPA believes that these waste streams

are inappropriate for listing under EPCRA section 313 at this time.

EPA also excluded chemicals whose only identified toxicity concern

was a result of their status as a volatile organic compound (VOC). VOCs

contribute to the formation of tropospheric ozone which causes a number

of health-related and environmental problems. EPA continues to believe

that VOCs meet the listing criteria of EPCRA section 313. However, EPA

intends to address the issue of how VOCs should be listed on EPCRA

section 313 separately. Therefore, chemicals whose only identified

toxicity concern is due to their status as VOCs were excluded from

consideration at this time.

EPA also identified chemicals that are routinely manufactured,

processed, or otherwise used at levels far below the reporting

thresholds of EPCRA section 313. These chemicals are not expected to

ever be manufactured, processed, or otherwise used in quantities at or

above these reporting thresholds. In this proposed rulemaking, EPA is

attempting to add chemicals to EPCRA section 313 that are manufactured,

processed, or otherwise used in quantities greater than the EPCRA

section 313 volume thresholds and thus would result in the submission

of TRI reports. Consequently, chemicals that are manufactured,

processed, or otherwise used in quantities less than the EPCRA section

313 volume thresholds were excluded from further consideration at this

time, because no reports would be filed under EPCRA section 313 for

such chemicals.

Some of the chemicals that are manufactured, processed, or

otherwise used below the EPCRA section 313 activity thresholds,

particularly those chemicals that are manufactured in trace amounts in

waste streams, are highly toxic at very low dose levels and have

physical, chemical, or biological properties that make the chemicals

persist for extended periods in the environment, and bioaccumulate

through the food chain. Persistent bioaccumulative toxic chemicals,

such as dioxins, are of particular concern in ecosystems such as the

Great Lakes Basin due to the long retention time of the individual

lakes and the cycling of the chemical from one component of the

ecosystem to another. EPA may reconsider in the future the issue of

listing such chemicals in a manner which would result in the submission

of TRI reports. EPA requests comment on the following: Is it

appropriate to list such chemicals on EPCRA section 313? If EPA were to

add this type of chemical to EPCRA section 313, what modifications to

EPCRA section 313, such as lowering the reporting thresholds and

modifying the de minimis in mixture exemptions (40 CFR part 372.38),

would be required to insure that release and transfer information would

be collected?

III. EPCRA Section 313 Statutory Criteria

EPCRA section 313(d)(2) sets out criteria for adding chemicals to

the list of chemicals subject to reporting under section 313(a). For a

chemical (or category of chemicals) to be added to the EPCRA section

313(c) list of toxic chemicals, the Administrator must determine

whether, in her judgement, there is sufficient evidence to establish

any one of the following:

(A) The chemical is known to cause or can reasonably be anticipated

to cause significant adverse acute human health effects at

concentration levels that are reasonably likely to exist beyond

facility site boundaries as a result of continuous, or frequently

recurring, releases.

(B) The chemical is known to cause or can reasonably be anticipated

to cause in humans--

(i) cancer or teratogenic effects, or

(ii) serious or irreversible--

(I) reproductive dysfunctions,

(II) neurological disorders,

(III) heritable genetic mutations, or

(IV) other chronic health effects.

(C) The chemical is known to cause or can reasonably be anticipated

to cause, because of--

(i) its toxicity,

(ii) its toxicity and persistence in the environment, or

(iii) its toxicity and tendency to bioaccumulate in the

environment, a significant adverse effect on the environment of

sufficient seriousness, in the judgement of the Administrator, to

warrant reporting under this section.

To remove a chemical from the section 313(c) list, the

Administrator must determine that there is not sufficient evidence to

establish any of the criteria described above as required by EPCRA

section 313(d)(3). Thus, the criteria for listing or delisting a

chemical are identical. However, whereas EPA can add a chemical if only

one of the criteria is met, it can only delete a chemical if none of

the criteria are met.

To ascertain whether there is sufficient or insufficient evidence

to determine that the statutory criteria are met for listing a

chemical, EPA conducts a hazard assessment on the chemical and

determines based on the weight-of-the-evidence, whether the chemical

can reasonably be anticipated to cause any of the adverse effects

specified in EPCRA section 313(d)(2). The hazard analysis is described

above in Unit II.B.3. of this preamble. EPA's interpretation of the

specific statutory criteria follows.

1. Section 313(d)(2)(A) (acute human health effects). To determine

whether the section 313(d)(2)(A) ``acute human health effects''

criterion is met, EPA must examine the adverse effects associated with

the chemical, the ``concentration levels'' which would cause acute

human health effects, and the likelihood of such levels existing

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

frequently recurring, releases.'' Such a determination may include,

among other factors, consideration of production processes, workplace

procedures, pollution controls, and the volume and pattern of

production, use, and release, as well as other chemical-specific

factors. EPA believes that to make the section 313(d)(2)(A)

determination it must demonstrate that a chemical can reasonably be

anticipated to be released in quantities that result in concentration

levels, or within a reasonable margin of exposure of the concentration

levels, that would be expected to cause acute human health effects

beyond the facility site boundary. The margin of exposure applied is

dependent upon the type of hazard data (e.g., data in animals versus

human) and the confidence in this hazard data base for acute effects

(e.g., sufficiency of the hazard data). However, EPA is not required to

make a facility-specific finding, nor is it necessary for EPA to

demonstrate that these concentration levels or effects occur at or near

any particular facility (Ref. 1). Furthermore, ``EPA may, but is not

required to, conduct new studies or risk assessments or perform site-

specific analyses to establish actual ambient concentrations or to

document adverse effects at any particular location'' (Ref. 1). Nor is

EPA limited to considering concentration levels and potential acute

human health effects at the ``fenceline.'' Rather, the phrase ``beyond

facility site boundaries'' reflects Congress' recognition that the

``highest concentration to which persons outside the site boundary may

be exposed'' could occur at ``any point outside the boundaries of the

site on which the facility is located,'' including, for example, where

an air emissions plume cools and settles to the ground (Ref. 1).

Therefore, EPA believes that to make a finding under EPCRA section

313(d)(2)(A), the Agency may estimate concentrations at or beyond the

facility site boundary through the use of estimated releases and

modelling techniques. The term ``continuous or frequently recurring

releases'' is included only to distinguish routine releases that are a

normal consequence of the operation of a facility from the episodic and

accidental releases that are subject to EPCRA section 304 (Ref. 1). As

such, EPA believes that episodic and accidental releases are not

pertinent in a determination that a chemical meets the section

313(d)(2)(A) criterion.

2. Section 313(d)(2)(B) (chronic human health effects). In contrast

to the section 313(d)(2)(A) criterion, section 313(d)(2)(B) does not

require consideration of either the nature and frequency of releases or

concentration levels at facility site boundaries. Rather, section

313(d)(2)(B) is focused solely on whether the chemical is known or can

reasonably be anticipated to cause cancer, teratogenicity, or other

serious or irreversible chronic human health effects. Consequently, EPA

believes that it is sufficient to consider only the toxicity of the

subject chemical to make the section 313(d)(2)(B) determination.

3. Section 313(d)(2)(C) (environmental effects). The section

313(d)(2)(C) criterion requires EPA to consider a chemical's potential

to cause significant adverse effects on the environment. The statute

directs EPA to base its determination on a consideration of the

toxicity of the chemical, either alone or in combination with the

persistence of the chemical or the potential for the chemical to

bioaccumulate. Congress intended that EPA consider a broad range of

environmental effects when making a determination under section

313(d)(2)(C).

In determining what constitutes a significant adverse effect on

the environment...the Administrator should consider the extent to

which the toxic chemical causes or can reasonably be anticipated to

cause any of the following adverse reactions, even if restricted to

the immediate vicinity adjacent to the site: (1) Gradual or sudden

changes in the composition of animal life or plant life, including

fungal or microbial organisms in an area. (2) Abnormal number of

deaths of organisms (e.g. fish kills). (3) Reduction of the

reproductive success or the vigor of a species. (4) Reduction in

agricultural productivity, whether crops or livestock. (5)

Alterations in the behavior or distribution of a species. (6) Long

lasting or irreversible contamination of components of the physical

environment, especially in the case of groundwater, and surface

water and soil resources that have limited self-cleansing capability

(Ref. 1).

EPA believes that the environmental effects criterion inherently

contains a limited exposure component because of the statutory

requirement for EPA to find a ``significant adverse effect on the

environment of sufficient seriousness, in the judgment of the

Administrator, to warrant reporting'' under EPCRA section 313. Unlike

section 313(d)(2)(B), where EPA only has to determine whether certain

kinds of effects are ``known or reasonably anticipated'' to occur,

section 313(d)(2)(C) requires EPA to find the effect to be of

sufficient seriousness to warrant reporting, which implies the

possibility that under certain circumstances, a chemical that could

theoretically cause a significant adverse effect on the environment is

unlikely to cause one of a magnitude to warrant listing.

The extent to which exposure is factored into EPA's determination

depends upon the inherent toxicity of a chemical, and a variety of

other chemical-specific characteristics. EPA believes that when a

chemical is inherently extremely toxic, that is, it is toxic at very

low dose levels, an exposure assessment is not necessary because even

minimal releases of such a chemical may reasonably be anticipated to

result in significant adverse environmental effects. In such cases, EPA

could rely on toxicity alone under section 313(d)(2)(C)(i) as a basis

for listing.

However, for chemicals that exhibit adverse effects upon the

environment solely based on toxicity at moderately low doses, EPA

believes that consideration of potential exposure is warranted because

minimal releases may not result in significant adverse effects upon the

environment. These exposure considerations may include, among other

factors, pollution controls, the volume and pattern of production, use,

and release, environmental fate, as well as other chemical-specific

factors, and the use of estimated releases and modelling techniques.

EPCRA sections 313(d)(2)(C)(ii) and (iii) allow EPA to consider the

impacts of other characteristics of a chemical. Where a chemical

exhibits significant adverse effects in the environment based on

toxicity and persistence or toxicity and bioaccumulation at very low to

moderately low dose levels, EPA believes that exposure considerations

are not required in addition to those considerations implicit in

evaluation of the chemical's potential for persistence and

bioaccumulation. This is because even minimal releases of the chemical

may result in elevated concentrations in the environment or in an

organism that can reasonably be anticipated to result in significant

adverse effects. This reflects the increased likelihood that there will

be exposure to a chemical that persists due to its longer residence

time in the environment. Repeated minimal releases of a persistent

chemical may result in elevated concentrations in the environment. For

a chemical that bioaccumulates, even low levels of the chemical in the

environment may result in increased concentrations in an organism.

Therefore, evaluation of a chemical's persistence or bioaccumulation

potential may be considered the functional equivalent of an exposure

analysis.

In addition, for chemicals which induce well-established adverse

effects, e.g. chlorofluorocarbons, which cause stratospheric ozone

depletion, EPA believes that an exposure assessment is unnecessary. EPA

believes that these chemicals typically do not affect solely one or two

species but rather affect changes across a whole ecosystem. EPA

believes that these effects are of sufficient seriousness that

additional exposure considerations are not warranted because of the

scope of their impact and the well-documented evidence supporting the

adverse effects. EPA requests comment on its approach for considering

exposure as a part of its evaluation for listing of these chemicals

under section 313(d)(2)(C).

In Unit IV.B. of this preamble, EPA identifies each of the

chemicals proposed for addition to EPCRA section 313 and the specific

statutory criteria upon which the proposed addition is based.

IV. EPA's Technical Review

A. Introduction

Data on the chemicals and chemical categories were reviewed for

evidence indicating adverse acute and chronic toxicity,

carcinogenicity, mutagenicity, developmental and reproductive effects,

neurotoxicity, and environmental effects. Information on the

environmental fate was also reviewed.

For each chemical proposed for addition to EPCRA section 313 in

this rulemaking, EPA conducted an extensive hazard assessment, and,

where appropriate, an analysis of exposure, to determine whether the

chemical met one or more of the EPCRA section 313(d)(2) listing

criteria. This hazard assessment is discussed in detail in Unit II.B.3

of this preamble. Only after this careful review was a final

determination made as to whether one of the EPCRA section 313(d)(2)

listing criteria was met for each individual chemical or chemical

category proposed for listing below. EPA need only show that one of the

listing criteria is met in order to list a chemical or chemical

category under EPCRA section 313. The information summarized below for

each chemical or chemical category represents the key data elements

that lead EPA to believe that there is sufficient evidence to establish

that one of the section 313(d)(2) listing criteria is met. A more

extensive review of the existing data base for each chemical or

chemical category proposed for listing, which reflects the entire

weight-of-the-evidence considered by EPA, is contained in following

support documents: Support Document for the Addition of Chemicals from

Federal Insecticide, Fungicide, Rodenticide Act (FIFRA) Active

Ingredients to EPCRA Section 313 (Ref 3); Physical Properties and

Environmental Fate of Some TRI Expansion Chemicals (Ref. 5); Support

Document for the Addition of Chemicals from Section 112(b) of the Clean

Air Act Amendments and Chlorinated Paraffins to EPCRA Section 313 (Ref.

7); and Support Document for the Health and Ecological Toxicity Review

of TRI Expansion Chemicals (Ref. 8). These support documents contain a

complete list of the references (which can be found in the public

record for this proposed rulemaking) that were used in support of these

proposed additions.

A list of the 313 chemicals and chemical categories and their

Chemical Abstract Service (CAS) number, where appropriate, follows.

1. Abamectin (Avermectin B1) (CAS No. 071751-41-2)

2. Acephate (Acetylphosphoramidothioic acid O,S-dimethyl ester)

(CAS No. 030560-19-1)

3. Acifluorfen sodium salt (5-(2-Chloro-4-

(triflouromethyl)phenoxy)-2-nitro-benzoic acid, sodium salt) (CAS

No. 062476-59-9)

4. Alachlor (CAS No. 015972-60-8)

5. Aldicarb (CAS No. 000116-06-3)

6. d-trans-Allethrin [d-trans-Chrysanthemic acid of d-

allethrone] (CAS No. 028057-48-9)

7. Allylamine (CAS No. 000107-11-9)

8. Aluminum phosphide (CAS No. 020859-73-8)

9. Ametryn (N-Ethyl-N'-(1-methylethyl)-6-(methylthio)-

1,3,5,triazine- 2,4 diamine) (CAS No. 000834-12-8)

10. Amitraz (CAS No. 033089-61-1)

11. Anilazine (4,6-Dichloro-N-(2-chlorophenyl)-1,3,5-triazin-2-

amine) (CAS No. 000101-05-3)

12. Atrazine (6-Chloro-N-ethyl-N'-(1-methylethyl)-

1,3,5,triazine-2,4-diamine) (CAS No. 001912-24-9)

13. Bendiocarb (2,2-Dimethyl-1,3-benzodioxol-4-ol

methylcarbamate) (CAS No. 022781-23-3)

14. Benfluralin (N-Butyl-N-ethyl-2,6-dinitro-4-(trifluoromethyl)

benzenamine) (CAS No. 001861-40-1)

15. Benomyl (CAS No. 017804-35-2)

16. o-Benzyl-p-chlorophenol (CAS No. 000120-32-1)

17. Bifenthrin (CAS No. 082657-04-3)

18. Bis(tributyltin) oxide (CAS No. 000056-35-9)

19. Boron trichloride (CAS No. 010294-34-5)

20. Boron trifluoride (CAS No. 007637-07-2)

21. Bromacil (5-Bromo-6-methyl-3-(1-methylpropyl)-2,4-(1H,3H)-

pyrimidinedione) (CAS No. 000314-40-9)

22. Bromacil lithium salt (2,4-(1H,3H)-Pyrimidinedione, 5-bromo-

6-methyl-3-(1-methylpropyl), lithium salt) (CAS No. 053404-19-6)

23. Bromine (CAS No. 007726-95-6)

24. 1-Bromo-1-(bromomethyl)-1,3-propanedicarbonitrile (CAS No.

035691-65-7)

25. 2-Bromo-2-nitropropane-1,3-diol (Bronopol) (CAS No. 000052-

51-7)

26. Bromoxynil (3,5-Dibromo-4-hydroxybenzonitrile) (CAS No.

001689-84-5)

27. Bromoxynil octanoate (Octanoic acid, 2,6-dibromo-4-

cyanophenyl ester) (CAS No. 001689-99-2)

28. Brucine (CAS No. 000357-57-3)

29. Butylate (Bis-2-methylpropyl)carbamothioic acid S-ethyl

ester) (CAS No. 002008-41-5)

30. Butylated hydroxyanisole (CAS No. 025013-16-5)

31. C.I. Acid Red 114 (CAS No. 006459-94-5)

32. C.I. Direct Blue 218 (CAS No. 028407-37-6)

33. Calcium hypochlorite (CAS No. 007778-54-3)

34. Caprolactam (CAS No. 000105-60-2)

35. Carbofuran (CAS No. 001563-66-2)

36. Carbon monoxide (CAS No. 000630-08-0)

37. Carboxin (5,6-Dihydro-2-methyl-N-phenyl-1,4-oxathiin-3-

carboxamide) (CAS No. 005234-68-4)

38. Chinomethionat (6-Methyl-1,3-dithiolo[4,5-b]quinoxalin-2-

one) (CAS No. 002439-01-2)

39. Chlorendic acid (CAS No. 000115-28-6)

40. Chlorimuron ethyl (Ethyl-2-[[[(4-chloro-6-methoxyprimidin-2-

yl)-carbonyl]-amino]sulfonyl]benzoate) (CAS No. 090982-32-4)

41. Chlorinated paraffins

42. 1-(3-Chloroallyl)-3,5,7-triaza-1-azoniaadamantane chloride

(CAS No. 004080-31-3)

43. p-Chloroaniline (CAS No. 000106-47-8)

44. 5-Chloro-2-(2,4-dichlorophenoxy)phenol (CAS No. 003380-34-5)

45. 3-Chloro-2-methyl-1-propene (CAS No. 000563-47-3)

46. p-Chlorophenyl isocyanate (CAS No. 000104-12-1)

47. Chloropicrin (CAS No. 000076-06-2)

48. 3-Chloropropionitrile (CAS No. 000542-76-7)

49. p-Chloro-o-toluidine (CAS No. 000095-69-2)

50. Chlorotrifluoromethane (CFC-13) (CAS No. 000075-72-9)

51. Chlorpyrifos methyl (O,O-Dimethyl-O-(3,5,6-trichloro-2-

pyridyl)phosphorothioate) (CAS No. 005598-13-0)

52. Chlorsulfuron (2-Chloro-N-[[(4-methoxy-6-methyl-1,3,5-

triazin-2-yl)amino]carbonyl]benzenesulfonamide) (CAS No. 064902-72-

3)

53. Clomazone (2-[(2-Chlorophenyl)methyl]-4,4-dimethyl-3-

isoxazolidinone) (CAS No. 081777-89-1)

54. Crotonaldehyde (CAS No. 004170-30-3)

55. Cyanazine (CAS No. 021725-46-2)

56. Cycloate (CAS No. 001134-23-2)

57. Cyclohexanol (CAS No. 000108-93-0)

58. Cyfluthrin (3-(2,2-Dichloroethenyl)-2,2-

dimethylcyclopropanecarboxylic acid, cyano(4-fluoro-3-

phenoxyphenyl)methyl ester) (CAS No. 068359-37-5)

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

dimethylcyclopropanecarboxylic acid cyano(3-phenoxyphenyl)methyl

ester) (CAS No. 068085-85-8)

60. Cyromazine (N-Cyclopropyl-1,3,5-triazine-2,4,6-triamine)

(CAS No. 066215-27-8)

61. Dazomet (Tetrahydro-3,5-dimethyl-2H-1,3,5-thiadiazine-2-

thione) (CAS No. 000533-74-4)

62. Dazomet, sodium salt (2H-1,3,5-Thiadiazine-2-thione,

tetrahydro-3,5-dimethyl-, ion(1-), sodium) (CAS No. 053404-60-7)

63. 2,4-DB (CAS No. 000094-82-6)

64. 2,4-D butoxyethyl ester (CAS No. 001929-73-3)

65. 2,4-D butyl ester (CAS No. 000094-80-4)

66. 2,4-D chlorocrotyl ester (CAS No. 002971-38-2)

67. Desmedipham (CAS No. 013684-56-5)

68. 2,4-D 2-ethylhexyl ester (CAS No. 001928-43-4)

69. 2,4-D 2-ethyl-4-methylpentyl ester (CAS No. 053404-37-8)

70. Diazinon (CAS No. 000333-41-5)

71. 2,2-Dibromo-3-nitrilopropionamide (CAS No. 010222-01-2)

72. Dicamba (3,6-Dichloro-2-methyoxybenzoic acid) (CAS No.

001918-00-9)

73. Dichloran (2,6-Dichloro-4-nitroaniline) (CAS No. 000099-30-

9)

74. 3,3'-Dichlorobenzidine dihydrochloride (CAS No. 000612-83-9)

75. 3,3'-Dichlorobenzidine sulfate (CAS No. 064969-34-2)

76. trans-1,4-Dichloro-2-butene (CAS No. 000110-57-6)

77. Dichloromethylphenylsilane (CAS No. 000149-74-6)

78. Dichlorophene (2,2'-Methylenebis(4-chlorophenol) (CAS No.

000097-23-4)

79. trans-1,3-Dichloropropene (CAS No. 010061-02-6)

80. Diclofop methyl (2-[4-(2,4-Dichlorophenoxy)

phenoxy]propanoic acid, methyl ester) (CAS No. 051338-27-3)

81. Dicyclopentadiene (CAS No. 000077-73-6)

82. Diethatyl ethyl (CAS No. 038727-55-8)

83. Diflubenzuron (CAS No. 035367-38-5)

84. Diglycidyl resorcinol ether (CAS No. 000101-90-6)

85. Dimethipin (2,3,-Dihydro-5,6-dimethyl-1,4-dithiin 1,1,4,4-

tetraoxide) (CAS No. 055290-64-7)

86. Dimethoate (CAS No. 000060-51-5)

87. 3,3'-Dimethoxybenzidine dihydrochloride (o-Dianisidine

dihydrochloride) (CAS No. 020325-40-0)

88. 3,3'-Dimethoxybenzidine hydrochloride (o-Dianisidine

hydrochloride) (CAS No. 111984-09-9)

89. Dimethylamine (CAS No. 000124-40-3)

90. Dimethylamine dicamba (CAS No. 002300-66-5)

91. 3,3'-Dimethylbenzidine dihydrochloride (o-Tolidine

dihydrochloride) (CAS No. 000612-82-8)

92. 3,3'-Dimethylbenzidine dihydrofluoride (o-Tolidine

dihydrofluoride) (CAS No. 041766-75-0)

93. Dimethyl chlorothiophosphate (CAS. No. 002524-03-0)

94. Dimethyldichlorosilane (CAS No. 000075-78-5)

95. N,N-Dimethylformamide (CAS No. 000068-12-2)

96. 2,6-Dimethylphenol (CAS No. 000576-26-1)

97. Dinocap (CAS No. 039300-45-3)

98. Dinoseb (CAS No. 000088-85-7)

99. Diphenamid (CAS No. 000957-51-7)

100. Diphenylamine (CAS No. 000122-39-4)

101. Dipotassium endothall (7-Oxabicyclo(2.2.1)heptane-2,3-

dicarboxylic acid, dipotassium salt) (CAS No. 002164-07-0)

102. Dipropyl isocinchomeronate (CAS No. 000136-45-8)

103. Disodium cyanodithioimidocarbonate (CAS No. 000138-93-2)

104. 2,4-D isopropyl ester (CAS No. 000094-11-1)

105. 2,4-Dithiobiuret (CAS No. 000541-53-7)

106. Dithiopyr (2-(Difluoromethyl)-4-(2-methylpropyl)-6-

(trifluoromethyl)-3,5-pyridinedicarbothioic acid S,S-dimethyl ester)

(CAS No. 097886-45-8)

107. Diuron (CAS No. 000330-54-1)

108. 2,4-D 2-octyl ester (CAS No. 001917-97-1)

109. Dodine (Dodecylguanidine monoacetate) (CAS No. 002439-10-3)

110. 2,4-DP (Dichlorprop) (CAS No. 000120-36-5)

111. 2,4-D propylene glycol butyl ether ester (CAS No. 001320-

18-9)

112. 2,4-D sodium salt (CAS No. 002702-72-9)

113. Ethoprop (Phosphorodithioic acid O-ethyl S,S-dipropyl

ester) (CAS No. 013194-48-4)

114. Ethyl dipropylthiocarbamate (EPTC) (CAS No. 000759-94-4)

115. Famphur (CAS No. 000052-85-7)

116. Fenarimol (.alpha.-(2-Chlorophenyl)-.alpha.-4-

chlorophenyl)-5-pyrimidinemethanol) (CAS No. 060168-88-9)

117. Fenbutatin oxide (hexakis(2-methyl-2-

phenylpropyl)distannoxane) (CAS No. 013356-08-6)

118. Fenoxaprop ethyl (2-(4-((6-Chloro-2

benzoxazolylen)oxy)phenoxy)propanoic acid, ethyl ester) (CAS No.

066441-23-4)

119. Fenoxycarb (2-(4-Phenoxyphenoxy)ethyl]carbamic acid ethyl

ester) (CAS No. 072490-01-8)

120. Fenpropathrin (2,2,3,3-Tetramethylcyclopropane carboxylic

acid cyano(3-phenoxyphenyl)methyl ester) (CAS No. 039515-41-8)

121. Fenthion (O,O-Dimethyl O-[3-methyl-4-(methylthio) phenyl]

ester, phosphorothioic acid) (CAS No. 000055-38-9)

122. Fenvalerate (4-Chloro-alpha-(1-methylethyl)benzeneacetic

acid cyano(3-phenoxyphenyl)methyl ester) (CAS No. 051630-58-1)

123. Ferbam (Tris(dimethylcarbamodithioato-S,S')iron) (CAS No.

014484-64-1)

124. Fluazifop butyl (2-[4-[[5-(Trifluoromethyl)-2-

pyridinyl]oxy]-phenoxy]propanoic acid, butyl ester) (CAS No. 069806-

50-4)

125. Flumetralin (2-Chloro-N-(2,6-dinitro-4-

(trifluoromethyl)phenyl)-N-ethyl-6-fluorobenzenemethanamine) (CAS

No. 062924-70-3)

126. Fluorine (CAS No. 007782-41-4)

127. Fluorouracil (5-Fluorouracil) (CAS No. 000051-21-8)

128. Fluvalinate (N-[2-Chloro-4-(trifluoromethyl)phenyl]-DL-

valine(+)- cyano (3-phenoxyphenyl)methyl ester) (CAS No. 069409-94-

5)

129. Folpet (CAS No. 000133-07-3)

130. Fomesafen (5-(2-Chloro-4-(trifluoromethyl)phenoxy)-N

methylsulfonyl)-2-nitrobenzamide) (CAS No. 072178-02-0)

131. alpha-Hexachlorocyclohexane (CAS NO. 000319-84-6)

132. Hexamethylene-1,6-diisocyanate (CAS No. 000822-60-0)

133. n-Hexane (CAS No. 000110-54-3)

134. Hexazinone (CAS No. 051235-04-2)

135. Hydramethylnon (Tetrahydro-5,5-dimethyl-

2(1H)pyrimidinone[3-[4-(trifluoromethyl)phenyl]-1-[2-

[4(trifluoromethyl) phenyl]ethenyl]-2 propenylidene]hydrazone) (CAS

No. 067485-29-4)

136--151. Hydrochlorofluorocarbons, specifically:

136. Dichloropentafluoropropane (CAS No. 127564-92-5)

137. 1,3-Dichloro-1,1,2,3,3-pentafluoropropane (HCFC-225ea) (CAS

No. 136013-79-1)

138. 2,2-Dichloro-1,1,1,3,3-pentafluoropropane (HCFC-225aa) (CAS

No. 128903-21-9)

139. 1,1-Dichloro-1,2,3,3,3-pentafluoropropane (HCFC-225eb) (CAS

No. 111512-56-2)

140. 1,1-Dichloro-1,2,2,3,3-pentafluoropropane (HCFC-225cc) (CAS

No. 13474-88-9)

141. 1,3-Dichloro-1,1,2,2,3-pentafluoropropane (HCFC-225cb) (CAS

No. 000507-55-1)

142. 1,2-Dichloro-1,1,3,3,3-pentafluoropropane (HCFC-225da) (CAS

No. 000431-86-7)

143. 3,3-Dichloro-1,1,1,2,2-pentafluoropropane (HCFC-225ca) (CAS

No. 000422-56-0)

144. 2,3-Dichloro-1,1,1,2,3-pentafluoropropane (HCFC-225ba) (CAS

No. 000422-48-0)

145. 1,2-Dichloro-1,1,2,3,3-pentafluoropropane (HCFC-225bb) (CAS

No. 000422-44-6)

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

147. 1,1,1,2-Tetrachloro-2-fluoroethane (HCFC-121a) (CAS No.

000354-11-0)

148. 1,1,2,2-Tetrachloro-1-fluoroethane (HCFC-121) (CAS No.

000354-14- 3)

149. 1,2-Dichloro-1,1-difluoroethane (HCFC-132b) (CAS No.

001649-08-7)

150. 2-Chloro-1,1,1-trifluoroethane (HCFC-133a) (CAS No. 000075-

88-7)

151. 3-Chloro-1,1,1-trifluoropropane (HCFC-253fb) (CAS No.

000460-35-5)

152. Imazalil (1-[2-(2,4-Dichlorophenyl)-2-(2-

propenyloxy)ethyl]1H-imidazole) (CAS No. 035554-44-0)

153. 3-Iodo-2-propynyl butylcarbamate (CAS No. 055406-53-6)

154. Iprodione (3-(3,5-Dichlorophenyl)-N-(1-methylethyl)-2,4-

dioxo-1-imidazolidinecarboxamide) (CAS No. 036734-19-7)

155. Iron pentacarbonyl (CAS No. 013463-40-6)

156. Isodrin (CAS No. 000465-73-6)

157. Isofenphos (2-[[Ethoxyl[(1-methylethyl)

amino]phosphinothioyl]oxy]benzoic acid 1-methylethyl ester) (CAS No.

025311-71-1)

158. Isophorone (CAS No. 000078-59-1)

159. Isophorone diisocyanate (CAS No. 004098-71-9)

160. Lactofen (5-(2-Chloro-4-(trifluoromethyl)phenoxy)-2-nitro-

2-ethoxy-1-methyl-2-oxoethyl ester) (CAS No. 077501-63-4)

161. Linuron (CAS No. 000330-55-2)

162. Lithium carbonate (CAS No. 000554-13-2)

163. Malathion (CAS No. 000121-75-5)

164. Man-made mineral fibers

165. Mecoprop (CAS No. 000093-65-2)

166. 2-Mercaptobenzothiazole (MBT) (CAS No. 000149-30-4)

167. Merphos (CAS No. 000150-50-5)

168. Metham sodium (Sodium methyldithiocarbamate) (CAS No.

000137-42-8)

169. Methazole (2-(3,4-Dichlorophenyl)-4-methyl-1,2,4-

oxadiazolidine-3,5-dione) (CAS No. 020354-26-1)

170. Methiocarb (CAS No. 002032-65-7)

171. Methoxone ((4-Chloro-2-methylphenoxy) acetic acid) (MCPA)

(CAS No. 000094-74-6)

172. Methoxone sodium salt ((4-Chloro-2-methylphenoxy) acetate

sodium salt) (CAS No. 003653-48-3)

173. 1,1-Methylene bis(4-isocyanatocyclohexane) (CAS No. 005124-

30-1)

174. Methylene bis(thiocyanate) (CAS No. 006317-18-6)

175. Methyl isothiocyanate (CAS No. 00556-61-6)

176. 2-Methyllactonitrile (CAS No. 000075-86-5)

177. N-Methylolacrylamide (CAS No. 000924-42-5)

178. Methyl parathion (CAS No. 000298-00-0)

179. N-Methyl-2-pyrrolidone (CAS No. 000872-50-4)

180. Methyltrichlorosilane (CAS No. 000075-79-6)

181. Metiram (CAS No. 009006-42-2)

182. Metribuzin (CAS No. 021087-64-5)

183. Mevinphos (CAS No. 007786-34-7)

184. Molinate (1H-Azepine-1-carbothioic acid, hexahydro-S-ethyl

ester) (CAS No. 002212-67-1)

185. Monuron (CAS No. 000150-68-5)

186. Myclobutanil (.alpha.-Butyl-.alpha.-(4-chlorophenyl)-1H-

1,2,4-triazole-1-propanenitrile) (CAS No. 088671-89-0)

187. Nabam (CAS No. 000142-59-6)

188. Naled (CAS No. 000300-76-5)

189. Nicotine and salts

190. Nitrapyrin (2-Chloro-6-(trichloromethyl) pyridine) (CAS No.

001929-82-4)

191. Nitrate ion (CAS No. 014797-55-8)

192. Nitric oxide (CAS No. 010102-43-9)

193. p-Nitroaniline (CAS No. 000100-01-6)

194. Nitrogen dioxide (CAS No. 010102-44-0)

195. Norflurazon (4-Chloro-5-(methylamino)-2-

[3(trifluoromethyl)phenyl]-3(2H)-pyridazinone) (CAS No. 027314-13-2)

196. Oryzalin (4-(Dipropylamino)-3,5-dinitrobenzenesulfonamide)

(CAS No. 019044-88-3)

197. Oxydemeton methyl (S-(2-(Ethylsulfinyl)ethyl) O,O-dimethyl

ester phosphorothioic acid) (CAS No. 000301-12-2)

198. Oxydiazon (3-[2,4-Dichloro-5-(1-methylethoxy)phenyl]-5(1,1-

dimethylethyl)-1,3,4-oxadiazol-2(3H)-one) (CAS No. 019666-30-9)

199. Oxyfluorfen (CAS No. 042874-03-3)

200. Ozone (CAS No. 010028-15-6)

201. Paraquat dichloride (CAS No. 001910-42-5)

202. Pebulate (Butylethylcarbamothioic acid S-propyl ester) (CAS

No. 001114-71-2)

203. Pendimethalin (N-(1-Ethylpropyl)-3,4-dimethyl-2,6-

dinitrobenzenamine) (CAS No. 040487-42-1)

204. Pentobarbital sodium (CAS No. 000057-33-0)

205. Perchloromethyl mercaptan (CAS No. 000594-42-3)

206. Permethrin (3-(2,2-Dichloroethenyl)-2,2-

dimethylcyclopropanecarboxylic acid, (3-phenoxyphenyl)methyl ester)

(CAS No. 052645-53-1)

207. Phenanthrene (CAS No. 000085-01-8)

208. Phenothrin (2,2-Dimethyl-3-(2-methyl-1-propenyl)

cyclopropanecarboxylic acid (3-phenoxyphenyl)methyl ester) (CAS No.

026002-80-2)

209. 1,2-Phenylenediamine (CAS No. 000095-54-5)

210. 1,3-Phenylenediamine (CAS No. 000108-45-2)

211. 1,2-Phenylenediamine dihydrochloride (CAS No. 000615-28-1)

212. 1,4-Phenylenediamine dihydrochloride (CAS No. 000624-18-0)

213. Phenytoin (CAS No. 000057-41-0)

214. Phosphine (CAS No. 007803-51-2)

215. Phosphorus oxychloride (CAS No. 010025-87-3)

216. Phosphorus pentachloride (CAS No. 010026-13-8)

217. Phosphorus pentasulfide (CAS No. 001314-80-3)

218. Phosphorus pentoxide (CAS No. 001314-56-3)

219. Picloram (CAS No. 001918-02-1)

220. Piperonyl butoxide (CAS No. 000051-03-6)

221. Pirimiphos methyl (O-(2-(Diethylamino)-6-methyl-4-

pyrimidinyl)-O,O-dimethyl phosphorothioate) (CAS No. 029232-93-7)

222-- 249. Polycyclic aromatic compounds (PACs) including:

222. Benz(a)anthracene (CAS No. 000056-55-3)

223. Benzo(a)phenanthrene (CAS No. 000218-01-9)

224. Benzo(a)pyrene (CAS No. 000050-32-8)

225. Benzo(b)fluoranthene (CAS No. 000205-99-2)

226. Benzo(j)fluoranthene (CAS No. 000205-82-3)

227. Benzo(k)fluoranthene (CAS No. 000207-08-9)

228. Benzo(rst)pentaphene (CAS No. 000189-55-9)

229. Carbazole (CAS No. 000086-74-8)

230. Cyclopenta(cd)pyrene (CAS No. 027208-37-3)

231. Dibenz(a,h)acridine (CAS No. 000226-36-8)

232. Dibenz(a,j)acridine (CAS No. 000224-42-0)

233. Dibenz(a,c)anthracene (CAS No. 000215-58-7)

234. Dibenz(a,j)anthracene (CAS No. 000224-41-9)

235. Dibenzo(a,h)anthracene (CAS No. 000053-70-3)

236. Dibenzo(a,e)fluoranthene (CAS No. 005385-75-1)

237. Dibenzo(a,e)pyrene (CAS No. 000192-65-4)

238. Dibenzo(a,h)pyrene (CAS No. 000189-64-0)

239. Dibenzo(a,l)pyrene (CAS No. 000191-30-0)

240. 7H-Dibenzo(c,g)carbazole (CAS No. 000194-59-2)

241. 7,12-Dimethylbenz(a)anthracene (CAS No. 000057-976)

242. Indeno[1,2,3-cd]pyrene (CAS No. 000193-39-5)

243. 2-Methylchrysene (CAS No. 003351-32-4)

244. 3-Methylchrysene (CAS No. 003351-31-3)

245. 4-Methylchrysene (CAS No. 003351-30-2)

246. 5-Methylchrysene (CAS No. 003697-24-3)

247. 6-Methylchrysene (CAS No. 001705-85-7)

248. 2-Methylfluoranthene (CAS No. 033543-31-6)

249. 1-Nitropyrene (CAS No. 005522-43-0)

250. Potassium bromate (CAS No. 007758-01-2)

251. Potassium dimethyldithiocarbamate (CAS No. 000128-03-0)

252. Potassium N-methyldithiocarbamate (CAS No. 000137-41-7)

253. Primisulfuron (Methyl 2-[[[[[4,6-bis(difluoromethoxy)-

2pyrimidinyl]-amino]carbonyl]amino]sulfonyl]benzoate) (CAS No.

086209-51-0)

254. Profenofos (O-(4-Bromo-2-chlorophenyl)-O-ethyl-S-propyl

phosphorothioate) (CAS No. 041198-08-7)

255. Prometryn (N,N'-Bis(1-methylethyl)-6-methylthio-1,3,5-

triazine-2,4-diamine) (CAS No. 007287-19-6)

256. Propachlor (2-Chloro-N-(1-methylethyl)-N-phenylacetamide)

(CAS No. 001918-16-7)

257. Propanil (N-(3,4-Dichlorophenyl)propanamide) (CAS No.

000709-98-8)

258. Propargite (CAS No. 002312-35-8)

259. Propargyl alcohol (CAS No. 000107-19-7)

260. Propetamphos (3-[(Ethylamino)methoxyphosphinothioyl]oxy]-2-

butenoic acid, 1-methylethyl ester) (CAS No. 031218-83-4)

261. Propiconazole (1-[2-(2,4-Dichlorophenyl)-4-propyl-1,3-

dioxolan-2-yl]-methyl-1H-1,2,4,-triazole) (CAS No. 060207-90-1)

262. Quizalofop-ethyl (2-[4-[(6-Chloro-2-quinoxalinyl)

oxy]phenoxy] propanoic acid ethyl ester) (CAS No. 076578-14-8)

263. Resmethrin ([5-(Phenylmethyl)-3-furanyl]methyl 2,2-

dimethyl-3-(2-methyl-1-propenyl) cyclopropanecarboxylate]) (CAS No.

010453-86-8)

264. Sethoxydim (2-[1-(Ethoxyimino)butyl]-5-

[2(ethylthio)propyl]-3-hydroxyl-2-cyclohexen-1-one) (CAS No.074051-

80-2)

265. Simazine (CAS No. 000122-34-9)

266. Sodium azide (CAS No. 026628-22-8)

267. Sodium chlorite (CAS No. 007758-19-2)

268. Sodium dicamba (3,6-Dichloro-2-methoxybenzoic acid, sodium

salt) (CAS No. 001982-69-0)

269. Sodium dimethyldithiocarbamate (CAS No. 000128-04-1)

270. Sodium fluoroacetate (CAS. No. 000062-74-8)

271. Sodium hypochlorite (CAS No. 007681-52-9)

272. Sodium nitrite (CAS No. 007632-00-0)

273. Sodium pentachlorophenate (CAS No. 000131-52-2)

274. Sodium o-phenylphenoxide (CAS No. 000132-27-4)

275. Sodium 2-pyridinethiol-1-oxide (CAS No. 015922-78-8)

276. Strychnine and salts

277. Sulfur dioxide (CAS No. 007446-09-5)

278. Sulfur trioxide (CAS No. 007446-11-9)

279. Sulfuryl fluoride (Vikane) (CAS No. 002699-79-8)

280. Sulprofos (O-Ethyl O-[4-

(methylthio)phenyl]phosphorodithioic acid S- propyl ester) (CAS No.

035400-43-2)

281. Tebuthiuron (N-[5-(1,1-Dimethylethyl)-1,3,4-thiadiazol-2-

yl)- N,N'-dimethylurea) (CAS No. 034014-18-1)

282. Tefluthrin (CAS No. 079538-32-2)

283. Temephos (CAS No. 003383-96-8)

284. Terbacil (5-Chloro-3-(1,1-dimethylethyl)-6-methyl- 2,4-

(1H,3H)-pyrimidinedione) (CAS No. 005902-51-2)

285. Tetracycline hydrochloride (CAS No. 000064-75-5)

286. Tetramethrin (2,2-Dimethyl-3-(2-methyl-1-propenyl)

cyclopropanecarboxylic acid (1,3,4,5,6,7-hexahydro-1,3-dioxo-2H-

isoindol-2-yl)methyl ester) (CAS No. 007696-12-0)

287. Tetrasodium ethylenediaminetetraacetate (CAS No. 000064-02-

8)

288. Thiabendazole (2-(4-Thiazolyl)-1H-benzimidazole) (CAS No.

000148-79-8)

289. Thiabendazole, hypophosphite salt (2-(4-Thiazolyl)

benzimidazole, hypophosphite salt) (CAS No. 028558-32-9)

290. Thiobencarb (Carbamic acid, diethylthio-, S-(p-

chlorobenzyl)) (CAS No. 028249-77-6)

291. Thiodicarb (CAS No. 059669-26-0)

292. Thiophanate ethyl ([1,2-Phenylenebis (iminocarbonothioyl)]

biscarbamic acid diethyl ester) (CAS No. 023564-06-9)

293. Thiophanate-methyl (CAS No. 023564-05-8)

294. Thiosemicarbazide (CAS No. 000079-19-6)

295. Triadimefon (1-(4-Chlorophenoxy)-3,3-dimethyl-1-(1H-1,2,4-

triazol-1-yl)-2-butanone) (CAS No. 043121-43-3)

296. Triallate (CAS No. 002303-17-5)

297. Tribenuron methyl (2-(((((4-Methoxy-6-methyl-1,3,5-triazin-

2-yl)-methylamino)carbonyl)amino)sulfonyl)-, methyl ester) (CAS No.

101200-48-0)

298. Tributyltin fluoride (CAS No. 001983-10-4)

299. Tributyltin methacrylate (CAS No. 002155-70-6)

300. S,S,S-Tributyltrithiophosphate (DEF) (CAS No. 000078-48-8)

301. Trichloroacetyl chloride (CAS No. 000076-02-8)

302. Trichloroethylsilane (CAS No. 000115-21-9)

303. Trichlorophenylsilane (CAS No. 000098-13-5)

304. 1,2,3-Trichloropropane (CAS No. 000096-18-4)

305. Triclopyr triethylammonium salt (CAS No. 057213-69-1)

306. Triethylamine (CAS No. 000121-44-8)

307. Triforine (N,N'-[1,4-Piperazinediylbis(2,2,2-

trichloroethylidene)] bisformamide) (CAS No. 026644-46-2)

308. Trimethylchlorosilane (CAS No. 000075-77-4)

309. 2,3,5-Trimethylphenyl methylcarbamate (CAS No. 002655-15-4)

310. Triphenyltin chloride (CAS No. 000639-58-7)

311. Triphenyltin hydroxide (CAS No. 000076-87-9)

312. Vanadium pentoxide (CAS No. 001314-62-1)

313. Vinclozolin (3-(3,5-Dichlorophenyl)-5-ethenyl-5-methyl-2,4-

oxazolidinedione) (CAS No. 050471-44-8)

A limited discussion of the health and environmental effects

associated with each of the 313 chemicals and chemical categories is

provided below in Unit IV.B. of this preamble. Each chemical is

identified by chemical name, CAS No., and the list(s) from which the

chemical originated. These lists are designated as follows:

CAA HAP: Clean Air Act section 112(b) ``Hazardous Air

Pollutants.''

CAA OD: Clean Air Act section 602(b) Class II ozone depleters.

CAL: State of California Safe Drinking Water and Toxic

Enforcement Act of 1986 (Proposition 65) ``List of Chemicals Known

to the State to Cause Reproductive Toxicity.''

CERCLA: Comprehensive Environmental Response, Compensation, and

Liability Act section 102.

CWA PPL: Clean Water Act section 307(a) ``Priority Pollutant

List.''

EPCRA EHS: EPCRA section 302 ``Extremely Hazardous Substances.''

FIFRA AI: Federal Insecticide, Fungicide, and Rodenticide Act

(FIFRA) ``Active Ingredients.''

FIFRA SR: FIFRA ``Special Review, Canceled/Denied or Suspended,

and Restricted Use Pesticides.''

IARC: Monographs of the International Agency for Research on

Cancer.

NTP: The 6th Annual Report on Carcinogens of the National

Toxicology Program.

RCRA APP8: Resource Conservation and Recovery Act (RCRA)

Chemicals listed at 40 CFR part 261 Appendix VIII.

RCRA P: RCRA Chemicals listed at 40 CFR part 261.33(e).

SDWA: Safe Drinking Water Act section 1412.

TSCA: Toxic Substances Control Act ``Existing Chemicals.''

EPA requests comment on the sufficiency of the evidence for each of

the chemicals proposed for addition. In addition, EPA requests comment

on any issues that may be specific to any of the individual chemicals

or chemical categories. For example, should chemicals be listed on

EPCRA section 313 that meet the EPCRA section 313 criteria but whose

only use is as a drug product.

B. Chemicals Proposed for Addition to EPCRA Section 313

1. Abamectin (avermectin B1) (CAS No. 071751-41-2) (FIFRA AI) (Ref.

3). This compound induces developmental toxicity in several species

with the mouse being the most sensitive species. Increased retinal

folds in weanlings, decreased viability and lactation indices, and

decreased body weight were noted in a two-generation rat reproduction

study. The lowest-observed-effect level (LOEL) was 0.4 milligram per

kilogram per day (mg/kg/day) and the no-observed-effect level (NOEL)

was 0.12 mg/kg/day. Based on the NOEL, EPA derived a reference dose

(RfD) of 0.0004 mg/kg/day. EPA believes that there is sufficient

evidence for listing abamectin on EPCRA section 313 pursuant to EPCRA

section 313(d)(2)(B) based on the available developmental toxicity

data.

Aquatic acute toxicity values for abamectin include a bluegill 96-

hour LC50 of 9.6 parts per billion (ppb), a rainbow trout 96-hour

LC50 of 3.6 ppb, and a daphnid 48-hour LC50 of 0.34 ppb. EPA

believes that there is sufficient evidence for listing abamectin on

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

available environmental toxicity data.

2. Acephate (acetylphosphoramidothioic acid O,S-dimethyl ester)

(CAS No. 030560-19-1) (FIFRA AI) (Ref. 3). In a 28-month feeding study

in rats, inhibition of brain, plasma, and red blood cell cholinesterase

activities was observed at 50 parts per million (ppm) (2.5 mg/kg/day).

The NOEL for this study was 5 ppm (0.25 mg/kg/day). Similar findings

were noted in a 2-year feeding study in dogs. The LOEL for this study

was 100 ppm (2.5 mg/kg/day) and the NOEL was 30 ppm (0.75 mg/kg/day).

EPA believes that there is sufficient evidence for listing acephate on

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

available neurotoxicity data for this chemical.

3. Acifluorfen sodium salt (5-(2-chloro-4-

(triflouromethyl)phenoxy)-2-nitro-benzoic acid, sodium salt) (CAS No.

062476-59-9) (FIFRA AI) (Ref. 3). Acifluorfen is classified as a Group

B2 compound, i.e., the chemical is a probable human carcinogen.

Acifluorfen produced an increased incidence of combined malignant and

benign liver tumors in two different strains of mice. The compound also

displayed positive mutagenic activity in several non-mammalian test

systems, and is structurally similar to four other diphenyl ether

herbicide compounds which caused increased incidences of liver tumors

in two different strains of mice. EPA believes that there is sufficient

evidence for listing acifluorfen sodium salt on EPCRA section 313

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

carcinogenicity data.

4. Alachlor (CAS No. 015972-60-8) (FIFRA SR) (Ref. 8). Alachlor is

an aniline-type herbicide. Dose-related hemolytic anemia with

reductions in red blood cell counts, hematocrit and hemoglobin, as well

as hemosiderosis in the liver, spleen and kidney occurred in male dogs

orally exposed to alachlor for 1-year. The LOEL based on these effects

was 3.0 mg/kg/day, and the NOEL was 1.0 mg/kg/day. Effects in female

dogs in the same study were not demonstrated as clearly as in males but

were considered suggestive of anemia. EPA derived an oral RfD of 0.01

mg/kg/day from this study.

In a three-generation reproduction study in rats, chronic nephritis

and increased relative and absolute kidney weights were reported in

F2 adult males and F3 pups. The LOEL was 10 mg/kg/day, and

the NOEL was 3 mg/kg/day. Rabbits (Dutch Belted strain) that received

alachlor via oral gavage during gestation days 6 to 27 had an increased

rate of preimplantation loss (49 percent) and offspring with increased

incidences of developmental malformations including major vessel

variations, presacral vertebrae, and rudimentary and full 13th ribs.

The increased incidence of rudimentary and full 13th ribs was dose-

related, and a lowest-observed-adverse-effect level (LOAEL) of 10 mg/

kg/day was determined based on this effect. The no-observed-adverse

effect level (NOAEL) was not determined.

EPA has classified alachlor as a category Group B2 compound, i.e.,

the chemical is a probable human carcinogen. In a 2-year rat feeding

study with Long-Evans rats, there were increased incidences of nasal

turbinate tumors, malignant stomach tumors and thyroid follicular

adenomas and carcinomas in both sexes at doses greater than or equal to

42 mg/kg/day. In an 18-month study in female CD-1 mice, bronchiolar

tumors occurred at an increased incidence at 200 mg/kg/day.

EPA believes that there is sufficient evidence for listing alachlor

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

the chronic toxicity and carcinogenicity data for this chemical.

5. Aldicarb (CAS No. 000116-06-3) (CERCLA; EPCRA EHS; FIFRA SR;

RCRA APP8; RCRA P) (Ref. 8). Aquatic acute toxicity test data for

aldicarb include a measured 96-hour LC50 of 50 ppb for bluegill

and a measured 48-hour LC50 of 70 ppb for daphnid. In addition,

the measured 48-hour EC50 for daphnid is 51 ppb. Measured

terrestrial acute toxicity data for wildlife include an oral LD50

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

oral LD50 for California quail of 2.58 mg/kg in males and 4.67 mg/

kg in females. EPA believes that there is sufficient evidence for

listing aldicarb on EPCRA section 313 pursuant to EPCRA section

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

chemical.

6. d-trans-Allethrin [d-trans-Chrysanthemic acid of dallethrone]

(CAS No. 028057-48-9) (FIFRA AI) (Ref. 3). Centrilobular hydropic

degeneration of the liver (LOEL was 1,000 ppm or 25 mg/kg/day; the NOEL

was 200 ppm or 5 mg/kg/day) was seen in dogs fed allethrin for 3

months. Increases in serum liver enzymes in female rats and increased

liver weights in male and female rats (the LOEL was 250 mg/kg/day; the

NOEL was 1,500 ppm or 75 mg/kg/day) were observed in rats fed allethrin

for 3 months. Histopathology data were not presented in this study.

Taken together, the results of these studies indicate hepatotoxic

potential for d-trans-allethrin. EPA believes that there is sufficient

evidence for listing d-trans-allethrin on EPCRA section 313 pursuant to

EPCRA section 313(d)(2)(B) based on the available hepatic toxicity

data.

7. Allylamine (CAS No. 000107-11-9) (EPCRA EHS) (Ref. 8). Repeated

inhalation exposure to 5 ppm (0.011 mg/L) allylamine for 50 exposures

of 7 hours caused liver and renal damage and myocarditis in rats.

Congestion of the liver and kidney was observed in rats, rabbits, and

dogs exposed to 5 or 20 ppm (0.011 or 0.044 milligram per liter (mg/L))

allylamine for 8 hours/day, 5 days/week, for 1-year. EPA believes that

there is sufficient evidence for listing allylamine on EPCRA section

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

and nephrotoxicity data for this chemical.

8. Aluminum phosphide (CAS No. 020859-73-8) (CERCLA; EPCRA EHS;

RCRA APP8; RCRA P) (Ref. 8). The median lethal dose of aluminum

phosphide in humans is 20 mg/kg. The acute inhalation toxicity of

aluminum phosphide is attributed to phosphine gas resulting from

decomposition of aluminum phosphide on contact with moisture in the

air. Symptoms of phosphine poisoning include restlessness, headache,

dizziness, fatigue, chest tightness, nausea, vomiting, lethargy,

stupor, coma, convulsions, lowered blood pressure, pulmonary edema and

respiratory failure; disorders of the kidney, liver, heart and brain

can also occur. In female CFT-Wistar rats exposed to phosphine gas

generated from aluminum phosphide pellets in distilled water, 100

percent mortality was observed after a 6-hour exposure to 40 ppm (0.1

mg/L), and exposure to 20 to 40 ppm (0.05 to 0.1 mg/L) for 6 hours

resulted in 33 percent mortality. Symptoms of toxicity reported in

these animals included dyspnea, loss of muscular coordination,

polyuria, and paralysis.

EPA's exposure analysis indicates that aluminum phosphide

concentrations are likely to exist beyond facility site boundaries, as

a result of continuous, or frequently recurring releases, at levels

that can reasonably be anticipated to cause significant adverse acute

human health effects. EPA believes that there is sufficient evidence

for listing aluminum phosphide on EPCRA section 313 pursuant to EPCRA

section 313(d)(2)(A) based on the available acute toxicity and exposure

data for this chemical.

9. Ametryn (N-Ethyl-N'-(1-methylethyl)-6-(methylthio)1,3,5,-

triazine- 2,4-diamine) (CAS No. 000834-12-8) (FIFRA AI) (Ref. 3). Fatty

degeneration of the liver was observed in rats administered 100 mg/kg/

day ametryn by gavage, 6 days per week for 13 weeks. The NOEL was 10

mg/kg/day (8.6 mg/kg/day adjusted for duration). In another study,

hepatic effects (severe vascular congestion, centrilobular liver

necrosis and fatty degeneration of individual liver cells) were

observed in rats that died following gavage administration of 500 mg/

kg/day ametryn for 6 days per week for 28 days. The NOEL was 250 mg/kg/

day. EPA believes that there is sufficient evidence for listing ametryn

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

the available hepatotoxicity data for this chemical.

The 72-hour EC50 for green algae is 14 ppb. Ametryn is a

herbicide and may be expected to affect nontarget plants such as algae.

EPA believes that there is sufficient evidence for listing ametryn on

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

available environmental toxicity data for this chemical.

10. Amitraz (CAS No. 033089-61-1) (FIFRA SR) (Ref. 8). Amitraz is

an aniline-type insecticide. In a 2-year beagle dog feeding study,

effects noted at the LOAEL dose (1.0 mg/kg/day) at various times during

the study included significantly increased mean blood glucose

concentration, slight hypothermia, and slight central nervous system

depression (the latter effect occurred immediately after dosing on days

1 and 2). The NOAEL in this study was 0.25 mg/kg/day and the oral RfD

derived from the NOAEL was 0.0025 mg/kg/day. These findings were

supported by similar results obtained in a 90-day feeding study in

dogs. In studies with rats or mice exposed to amitraz from 90 days to 2

years, LOAELs less than or equal to 12 mg/kg/day were derived based on

effects that included decreased body weight gain and changes in organ

(brain or heart) weight (the NOELs were less than or equal to 3 mg/kg/

day).

A three-generation reproduction study in rats demonstrated

decreased litter size and increased mortality during suckling. The

fetotoxic LOAEL in this study was 5 mg/kg/day and the NOAEL was 1.6 mg/

kg/day. In a teratology study in rabbits, a fetotoxicity LOAEL of 5 mg/

kg/day and NOAEL of 1 mg/kg/day were based on the incidences of cleft

palate and meningocoele associated with small ears and displaced toes.

EPA believes that there is sufficient evidence for listing amitraz

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

the chronic toxicity and developmental toxicity data for this chemical.

11. Anilazine (4,6-dichloro-N-(2-chlorophenyl)-1,3,5-triazin-2-

amine) (CAS No. 000101-05-3) (FIFRA AI) (Ref. 3). When anilazine was

administered to rats, maternal reproductive parameters were not

affected. The systemic maternal NOEL was 150 mg/kg and the LOEL was 500

mg/kg, based on decreased body weight gain. The developmental NOEL was

1,500 mg/kg, which was the highest dose tested. In rabbits, the

maternal toxicity NOEL was 15 mg/kg and the LOEL was 40 mg/kg, based on

increased mortalities and decreased body weight gain (also decreased

percentage of pregnant does at 75 mg/kg). The developmental NOEL was 40

mg/kg and the LOEL was 75 mg/kg, based on increased fetal mortality,

decreased fetal weight, and increased postimplantation loss and

inhibited ossification (phalanges). EPA believes that there is

sufficient evidence for listing anilazine on EPCRA section 313 pursuant

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

toxicity data.

Aquatic acute toxicity values for anilazine include a scud

(Gammarus) 96-hour LC50 of 0.27 ppb and an oyster 96-hour

EC50 (growth) of 46 ppb. EPA believes that there is sufficient

evidence for listing anilazine on EPCRA section 313 pursuant to EPCRA

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

data.

12. Atrazine (6-chloro-N-ethyl-N'-(1-methylethyl)-1,3,5,-triazine-

2,4-diamine) (CAS No. 001912-24-9) (FIFRA AI) (Ref. 3). Based on

sufficient evidence of carcinogenicity in animals, the International

Agency for Research on Cancer (IARC) has classified atrazine as a Group

2B compound; i.e., the chemical is possibly carcinogenic to humans.

Administration of atrazine to Sprague Dawley rats was associated with

an increased incidence of mammary gland fibroadenomas and

adenocarcinomas in female rats. A hormonal mechanism may be involved in

the induction of mammary tumors by atrazine. Therefore there is

sufficient evidence for listing atrazine on EPCRA section 313 pursuant

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

data for this chemical.

13. Bendiocarb (2,2-dimethyl-1,3-benzodioxol-4-ol methylcarbamate)

(CAS No. 022781-23-3) (FIFRA AI) (Ref. 3). Depressed blood

cholinesterase levels were reported in numerous species. In a

developmental toxicity study in rats, cholinergic signs were observed

in maternal animals at 4 mg/kg/day (LOEL). The maternal NOEL was 1 mg/

kg/day; no adverse effects were observed in fetuses. A LOEL of 2.5 mg/

kg/day for cholinesterase inhibition was reported in dogs in a 4-month

dietary study. The NOEL was 0.5 mg/kg/day. Decreases in cholinesterase

activity were observed in female rats fed 20, 30, or 40 mg/kg/day for

28 days. No NOEL was established in this study. However, no details

regarding clinical signs or histopathological changes in neural tissue

were reported. EPA believes that there is sufficient evidence for

listing bendiocarb on EPCRA section 313 pursuant to EPCRA section

313(d)(2)(B) based on the available neurological toxicity data for this

chemical.

Aquatic acute toxicity values for bendiocarb include a mysid 96-

hour EC50 of 6.7 ppb and a daphnid 48-hour EC50 of 29.2 ppb.

Avian acute toxicity values include a mallard duck LD50 of 3.1 mg/

kg. EPA believes that there is sufficient evidence for listing

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

based on the available environmental toxicity data.

14. Benfluralin (N-butyl-N-ethyl-2,6-dinitro-4(trifluoromethyl)

benzenamine) (CAS No. 001861-40-1) (FIFRA AI) (Ref. 3). Increased

relative liver weights, decreased red blood cell counts and decreased

hematocrit and hemoglobin levels were observed in dogs orally

administered benfluralin at a dose of 125 mg/kg/day for 2 years. The

NOAEL was 25 mg/kg/day. Based on the NOAEL, EPA has established an oral

RfD of 0.003 mg/kg/day. EPA believes that there is sufficient evidence

for listing benfluralin on EPCRA section 313 pursuant to EPCRA section

313(d)(2)(B) based on the available hematological toxicity data for

this chemical.

15. Benomyl (CAS No. 017804-35-2) (CAL; FIFRA SR) (Ref. 8). In a

three-generation study in rats, a dietary level of 25 mg/kg/day of

benomyl resulted in decreased weanling weights. The no-effect level was

5 mg/kg/day. Microphthalmia (the LOEL was 62.5 mg/kg/day; the NOEL was

30 mg/kg/day) was reported in a rat developmental toxicity study.

Decreased fetal weight (the LOEL was 62.5 mg/kg/day; the NOEL was 30

mg/kg/day) was observed in another rat developmental toxicity study.

The developmental effects were observed at doses that were not toxic to

the maternal animal. Anomalies consisting of supra occipital scars,

subnormal vertebral centrum, supernumary ribs, and cleft palate were

reported in an oral developmental toxicity study in mice (the LOEL was

100 mg/kg/day; the NOEL was 50 mg/kg/day). An increase in the incidence

of anomalies including encephalocele, hydrocephalus, microphthalmia,

and anophthalmia was noted following administration of benomyl to rats

by intubation during the first 20 days of pregnancy at doses of 125,

250, and 500 mg/kg. The developmental effects were always associated

with death and were considered to be the cause of death. EPA believes

that there is sufficient evidence for listing benomyl on EPCRA section

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

toxicity data for this chemical.

16. o-Benzyl-p-chlorophenol (CAS No. 000120-32-1) (FIFRA AI) (Ref.

3). In a 16-day oral rat study, dose-related increases in liver and

kidney weights (absolute and relative) and nephrosis were observed at a

dose level of greater than or equal to 62.5 mg/kg/day. A NOEL was not

established. When the compound was administered by gavage for 13 weeks,

rats developed multifocal dilation of renal tubules and increased liver

weights (16 percent) at 240 mg/kg/day. The NOEL was 120 mg/kg/day. In a

90-day oral study, mice receiving 30 mg/kg/day developed kidney

lesions. Increased liver weights were also noted. No NOEL was

established in this study. EPA believes that there is sufficient

evidence for listing o-benzyl-p-chlorophenol on EPCRA section 313

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

and renal toxicity data for this chemical.

17. Bifenthrin (CAS No. 082657-04-3) (FIFRA AI) (Ref. 3). Tremors

or head and forelimb twitching were noted in dogs, rats and rabbits

exposed to various doses. NOEL values based on the appearance of

tremors (often transient) ranged from 1 to 2.67 mg/kg/day. The oral RfD

for bifenthrin was based on a 1year beagle dog feeding study, in which

the LOEL, based on tremors observed during weeks 15 to 29, was 3.0 mg/

kg/day and the NOEL was 1.5 mg/kg/day. The RfD based on this NOEL was

0.015 mg/kg/day.

In a rat teratology study, an increased incidence of hydroureter

(without hydronephrosis) was noted in fetuses at 2 mg/kg/day (LOEL).

The NOEL was 1 mg/kg/day.

EPA believes that there is sufficient evidence for listing

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

based on the available neurological and developmental toxicity data.

Aquatic acute toxicity values for bifenthrin include a bluegill 96-

hour LC50 of 0.35 ppb, a rainbow trout 96-hour LC50 of 0.15

ppb, a sheepshead minnow LC50 of 17.5 ppb, and a daphnid 48-hour

EC50 of 1.6 ppb. EPA believes that there is sufficient evidence

for listing bifenthrin on EPCRA section 313 pursuant to EPCRA section

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

18. Bis(tributyltin) oxide (CAS No. 000056-35-9) (FIFRA AI) (Ref.

3). Adverse effects on the immune system were reported in rats exposed

to various doses of bis(tributyltin) oxide for a duration as short as 4

weeks. SPF-derived Wistar rats were fed the compound for 17 months. In

this study, a LOEL of 0.25 mg/kg/day and a NOEL of 0.025 mg/kg/day were

based on immunotoxicity manifested as decreased resistance to

Trichinella spiralis, reduced natural killer (NK) cell activity in the

spleen and reduced macrophage function. The RfD derived from this NOEL

was 0.00003 mg/kg/day. Similar immunological effects were reported in

4- and 6-week rat feeding studies with 20 and 80 ppm (1 and 4 mg/kg/

day; the LOEL was 1 mg/kg/day).

In rats that received dietary levels (of a range of doses that

included 50 mg/kg/day) for 106 weeks, kidney function was decreased and

serum levels of alanine aminotransferase, aspartate aminotransferase

and alkaline phosphatase were increased. At the end of the 2-year

study, nephrosis and vacuolization and pigmentation of the proximal

tubular epithelium were reported in animals administered 50 mg/kg/day.

On the basis of marginal effects at 5 mg/kg/day (LOEL), a NOEL of 0.5

mg/kg/day was established.

EPA believes that there is sufficient evidence for listing

bis(tributyltin) oxide on EPCRA section 313 pursuant to EPCRA section

313(d)(2)(B) based on the available immunological and renal toxicity

data.

Aquatic acute toxicity values for bis(tributyltin) oxide include a

bluegill 96-hour LC50 of 7.6 ppb, a rainbow trout 96-hour

LC50 6.9 ppb, a measured fathead minnow 96-hour LC50 of 2.7

ppb, and a daphnid 48-hour LC50 of 1.67 ppb. EPA believes that

there is sufficient evidence for listing bis(tributyltin) oxide on

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

available environmental toxicity data.

19. Boron trichloride (CAS No. 010294-34-5) (EPCRA EHS) (Ref. 8).

Boron trichloride is corrosive to the skin and mucosal tissue due to

its rapid hydrolysis to hydrochloric acid and boric acid, the former

acid being the corrosive species. Single, relatively large doses of

boron administered through any route affects the central nervous system

causing depressed circulation, diarrhea, vomiting, shock, and coma. The

kidneys are the most severely affected organ. Symptoms of acute

irritation of the upper airways were observed in humans at exposure

levels of greater than or equal to 0.004 mg/L. Inhalation of 0.48 mg/L

of boron trichloride proved fatal to certain laboratory animals.

Inhalation of 0.096 mg/L of boron trichloride for 7 hours produced

adverse effects on the respiratory tract, and weight loss.

EPA's exposure analysis indicates that boron trichloride

concentrations are likely to exist beyond facility site boundaries, as

a result of continuous, or frequently recurring releases, at levels

that can reasonably be anticipated to cause significant adverse acute

human health effects. EPA believes that there is sufficient evidence

for listing boron trichloride on EPCRA section 313 pursuant to EPCRA

section 313(d)(2)(A) based on the available acute toxicity and exposure

data for this chemical.

20. Boron trifluoride (CAS No. 007637-07-2) (EPCRA EHS) (Ref. 8).

Boron trifluoride is a colorless gas that is corrosive to tissues due

to its rapid hydrolysis to hydrofluoric acid and boric acid. The

principal acute effect in animals is irritation of the mucous membranes

of the respiratory tract and eyes; post mortem examination also

revealed pneumonia and degenerative changes in renal tubules. The

kidneys are most severely affected because boric acid concentrates in

this organ. Exposure of six animal species to 0.28 mg/L of boron

trifluoride for 4 to 7 hours a day, 5 days a week killed all animals

within 30 days. Rats, rabbits, and guinea pigs were exposed to boron

trifluoride via inhalation. Guinea pigs died of respiratory failure

after being exposed to 0.036 mg/L for 19 days; rats experienced

fluorosis of the teeth at this concentration. All three species were

minimally affected at 0.004 mg/L. In a 2-week rat inhalation study, all

animals died after 6 daily exposures to 0.18 mg/L. Rats exposed to

0.024 mg/L showed signs of respiratory irritation, increased lung

weights, and depressed liver weights. Rats exposed to 0.17 mg/L of

boron trifluoride 6 hours/day, 5 days a week for 13 weeks developed

necrosis of the proximal tubular epithelium of the kidneys. Guinea pigs

exposed to 0.035 mg/L, 7 hours/day, 5 days a week for 3 months

developed severe pneumonitis and pulmonary changes indicating chemical

irritation.

EPA believes that there is sufficient evidence for listing boron

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

on the available chronic toxicity data for this chemical.

21. Bromacil (5-bromo-6-methyl-3-(1-methylpropyl)-2,4-(1H,3H)-

pyrimidinedione) (CAS No. 000314-40-9) (FIFRA AI) (Ref. 3). Increased

thyroid activity was seen in male and female rats fed 5,000 ppm (250

mg/kg/day) bromacil for 90 days. In a 2-year dietary study, thyroid

hyperplasia was seen in female rats fed 1,250 ppm (62.5 mg/kg/day).

Thyroid follicular adenoma was observed in one female. EPA believes

that there is sufficient evidence for listing bromacil on EPCRA section

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

thyroid toxicity data for this chemical.

22. Bromacil lithium salt (2,4-(1H,3H)-pyrimidinedione, 5-bromo-6-

methyl-3-(1-methylpropyl), lithium salt) (CAS No. 05340419-6) (FIFRA

AI) (Ref. 3). Bromacil lithium salt will dissociate into bromacil,

which is soluble in aqueous systems and lithium ion. Defects of the

palate, eye, and external ear were reported in the offspring of rats

administered 50 mg lithium chloride intraperitoneally on gestation days

1, 4, 7, and 9 followed by 20 mg/day until day 17. Cleft palates were

also observed in mouse fetuses when mothers were gavaged with 300 to

465 mg/kg/day lithium carbonate on gestation day 6 to 15. An increase

in Ebstein's anomaly was reported among offspring of women taking

lithium; cardiovascular defects were found in 212 offspring exposed in

utero to lithium therapy.

Increased thyroid activity was seen in male and female rats fed

5,000 ppm (250 mg/kg/day) bromacil for 90 days. In a 2-year dietary

study, thyroid hyperplasia was seen in female rats fed 1,250 ppm (62.5

mg/kg/day). Thyroid follicular adenoma was observed in one female.

EPA believes that there is sufficient evidence for listing bromacil

lithium salt on EPCRA section 313 pursuant to EPCRA section

313(d)(2)(B) based on the available developmental and thyroid toxicity

data.

23. Bromine (CAS No. 007726-95-6) (EPCRA EHS) (Ref. 8). Rats fed

bromine at a dose of 0.01 mg/kg/day for 6 months experienced changes in

their reflexes and blood indexes. Rats, mice, and rabbits inhaling

0.001 mg/kg/day for 4 months developed functional abnormalities of the

respiratory, nervous, and endocrine systems. Data on the acute and

chronic effects of bromine in humans are limited. Bromine is very

corrosive to the eyes, skin, and mucous membranes in either the liquid

or vapor form. A concentration of 10 ppm of bromine in air is

intolerable in humans, and can cause severe irritation of the upper

respiratory tract. Other clinical symptoms include neurologic,

dermatologic, and gastrointestinal effects. The maximum concentration

allowable in humans for a 0.5 to 1-hour exposure to bromine is 4 ppm.

Bromine can cause lacrimation at concentrations less than 1 ppm.

Chronic exposure to bromine (estimated concentration at 0.6 ppm) can

result in eye irritation, upper respiratory irritation, coughing, and

headache. Neurological symptoms have also been reported following

chronic exposure to bromine.

EPA believes that there is sufficient evidence for listing bromine

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

the available chronic toxicity data for this chemical.

24. 1-Bromo-1-(bromomethyl)-1,3-propanedicarbonitrile (CAS No.

035691-65-7) (FIFRA AI) (Ref. 3). In a 3-month dietary study where rats

were administered 83.5, 500, and 3,000 ppm (4, 25, and 150 mg/kg/day)

1-bromo-1-(bromomethyl)-1,3-propanedicarbonitrile, a NOEL of 83.5 ppm

(4 mg/kg/day) and a LOEL of 500 ppm (25 mg/kg/day) were established

(based on neonatal splenic hematopoiesis, decreased parental body

weight and food consumption, increased male urinary epithelial cells,

amorphous casts, and crystals). At 3,000 ppm (150 mg/kg/day) there was

decreased lactase dehydrogenase, increased total cholesterol, total

protein, and albumin, elevated female organ-to-body weight ratio for

thyroid, liver, spleen, ovaries, and pituitary. In a 13-week dietary

study in beagle dogs (administered 167, 1,000, and 4,000 ppm; 4, 25,

and 100 mg/kg/day) the LOEL was greater than 167 ppm (4 mg/kg/day)

(increased male thyroid and female ovary organ to body weight ratio).

At 1,000 ppm (25 mg/kg/day), the same signs were seen as at 167 ppm (4

mg/kg/day), plus diarrhea and increased organ to body weight ratio of

thyroid, heart, liver, and adrenals. At 4,000 ppm (100 mg/kg/day),

emesis and ataxia in males, decreased body weight gain/food

consumption, decreased hematocrit, hemoglobin, immature red blood

cells, and alkaline phosphatase, extramedullary hematopoiesis in the

liver and spleen, thyroid enlargement with follicular cell hyperplasia,

increased organ to body weight ratios for thyroid, adrenals, liver and

spleen were seen. In a 13-week dietary study where beagle dogs were

administered 167 ppm (4 mg/kg/day), thyroid stimulating hormone (TSH)-

stimulated T3 and T4 increased in both sexes. Thyroids were enlarged

(both sexes) with absolute weights and organ to body weight ratios

increased in females.

EPA believes that there is sufficient evidence for listing 1-bromo-

1-(bromomethyl)-1,3-propanedicarbonitrile on EPCRA section 313 pursuant

to EPCRA section 313(d)(2)(B) based on the available toxicity data for

this chemical.

25. 2-Bromo-2-nitropropane-1,3-diol (bronopol) (CAS No. 000052-51-

7) (FIFRA AI) (Ref. 3). Severe irritation was reported in the

gastrointestinal tracts of rats, mice or dogs administered single or

multiple oral doses of 2-bromo-2-nitropropane-1,3-diol. In an acute

oral study in mice, the LD50 of 374 mg/kg resulted in ulceration

of the stomach and duodenum, thickening of the intestinal wall, and

adhesions of the stomach to the liver. Severe gastric irritation was

reported in dogs administered a single oral dose of 250 mg/kg. The NOEL

was 100 mg/kg. Superficial ulceration with epithelial hyperplasia and

hyperkeratosis, and congested vessels in the gastrointestinal mucosa,

was observed in rats fed 80 mg/kg/day (LOEL) in their diet for 13

weeks. The NOEL was 20 mg/kg/day. Vomiting was noted in dogs fed 20 mg/

kg/day in their diet for 13 weeks. The NOEL in this study was 8 mg/kg/

day. In addition, blood was noted in the urine of these dogs.

Mortality, irritation of the gastrointestinal tract, ulceration and

stomach lesions were reported in a 2-year dietary study in rats fed 40

mg/kg/day. The NOEL was 10 mg/kg/day. EPA believes that there is

sufficient evidence for listing 2-bromo-2-nitropropane-1,3-diol on

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

available toxicity data.

26. Bromoxynil (3,5-dibromo-4-hydroxybenzonitrile) (CAS No. 001689-

84-5) (FIFRA AI) (Ref. 3). Developmental effects (hydrocephalus,

microphthalmia, anophthalmia and severe defects in ossification of the

skull) were observed in rabbits administered 60 mg/kg/day bromoxynil by

gavage. The NOEL was 30 mg/kg/day. Developmental toxicity (increases in

all forms of supernumerary ribs) was also observed in rats at 5 mg/kg/

day. The NOEL was 1.5 mg/kg/day. The maternal LOEL (based on body

weight loss) was 30 mg/kg/day. Several other developmental studies

indicate potential developmental toxicity of bromoxynil. EPA believes

that there is sufficient evidence for listing bromoxynil on EPCRA

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

available developmental toxicity data for this chemical.

27. Bromoxynil octanoate (octanoic acid, 2,6-dibromo-4-cyanophenyl

ester) (CAS No. 001689-99-2) (FIFRA AI) (Ref. 3). Bromoxynil octanoate

hydrolyzes to yield bromoxynil and octanol. In a dermal developmental

toxicity study, bromoxynil octanoate was developmentally toxic to rat

fetuses (increased incidences of supernumerary ribs) at 15 mg/kg/day

(LOEL). The NOEL was 10 mg/kg/day. The maternal LOEL for decreased body

weight gain was 20 mg/kg/day. The NOEL was 15 mg/kg/day. Developmental

effects (hydrocephalus, microphthalmia, anophthalmia and severe defects

in ossification of the skull) were observed in rabbits administered 60

mg/kg/day bromoxynil by gavage. The NOEL was 30 mg/kg/day.

Developmental toxicity (increases in all forms of supernumerary ribs)

was also observed in rats at 5 mg/kg/day. The NOEL was 1.5 mg/kg/day.

The maternal LOEL (based on body weight loss) was 30 mg/kg/day. EPA

believes that there is sufficient evidence for listing bromoxynil

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

based on the available developmental toxicity data for bromoxynil and

bromoxynil octanoate.

28. Brucine (CAS No. 000357-57-3) (CERCLA; RCRA APP8; RCRA P) (Ref.

8). Brucine is an alkaloid similar in structure to strychnine. It is

capable of causing death or permanent injury due to exposures in normal

use. In humans, brucine can cause central and peripheral paralysis,

convulsions, and respiratory failure. A potentially lethal oral dose in

small children is 5 to 10 mg. The lethal oral dose for an adult may be

as low as 30 mg. The acute oral LD50 in rabbits is 4 mg/kg.

EPA's exposure analysis indicates that brucine concentrations are

likely to exist beyond facility site boundaries, as a result of

continuous, or frequently recurring releases, at levels that can

reasonably be anticipated to cause significant adverse acute human

health effects. EPA believes that there is sufficient evidence for

listing brucine on EPCRA section 313 pursuant to EPCRA section

313(d)(2)(A) based on the available acute toxicity and exposure data

for this chemical.

29. Butylate (Bis-2-methylpropyl)carbamothioic acid S-ethyl ester)

(CAS No. 002008-41-5) (FIFRA AI) (Ref. 3). In a 2-year feeding study in

mice, hepatic (cellular infiltrates, focal necrosis) and renal effects

(amyloidosis, chronic nephritis, lymphocytic foci) were observed at 80

mg/kg/day. The NOEL was 20 mg/kg/day. In a separate study, liver

pericholangitis was observed in rats fed 180 mg/kg/day for 56 weeks.

The NOEL was 30 mg/kg/day. An increased relative liver weight was

observed in male dogs fed 25 mg/kg/day for 1-year. The NOEL was 5 mg/

kg/day. Based on the NOEL, EPA has established a chronic oral RfD of

0.05 mg/kg/day. EPA believes that there is sufficient evidence for

listing butylate on EPCRA section 313 pursuant to EPCRA section

313(d)(2)(B) based on the available hepatic and renal toxicity data for

this chemical.

30. Butylated hydroxyanisole (CAS No. 025013-16-5) (CAL; IARC; NTP)

(Ref. 8). Butylated hydroxyanisole is classified by IARC as a Group 2B

compound; i.e., the chemical is possibly carcinogenic to humans.

Butylated hydroxyanisole has been shown to induce gastrointestinal

tumors in rats and hamsters. EPA believes that there is sufficient

evidence for listing butylated hydroxyanisole on EPCRA section 313

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

data for this chemical.

31. C.I. Acid Red 114 (CAS No. 006459-94-5) (TSCA) (Ref. 8). In a

2-year bioassay conducted by the National Toxicology Program (NTP) in

which F344 rats were exposed to C.I. Acid Red 114 via drinking water,

hepatocellular carcinomas of the liver, tumors of the skin, and

adenomas or carcinomas in the Zymbal's gland of both sexes were

observed. In the same study, female rats also had increased incidences

of adenoma or carcinoma in the clitoral gland, and squamous cell

papilloma or carcinoma in the oral cavity. The exposure concentrations

in this study ranged from 70 to 300 ppm (9.8 to 42 mg/kg/day) for males

and from 150 to 600 ppm (21 to 84 mg/kg/day) for females. EPA believes

that there is sufficient evidence for listing C.I. Acid Red 114 on

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

carcinogenicity data for this chemical.

32. C.I. Direct Blue 218 (CAS No. 028407-37-6) (NTP) (Ref. 8). In

an NTP bioassay, there was clear evidence of carcinogenicity of C.I.

Direct Blue 218 in male and female B6C3F1 mice based on significantly

increased incidence of hepatocellular adenomas and carcinomas. In a 2-

year NTP feeding study in rats, there was some evidence of

carcinogenicity in male F344 rats based on a significant increase in

the incidence of squamous cell papillomas of the pharynx in the high

dose group (500 mg/kg/day). EPA believes that there is sufficient

evidence for listing C.I. Direct Blue 218 on EPCRA section 313 pursuant

to EPCRA section 313(d)(2)(B) based on the carcinogenicity data for

this chemical.

33. Calcium hypochlorite (CAS No. 007778-54-3) (CERCLA) (Ref. 8).

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

measured LC50 for rainbow trout of 60 ppb and a 96-hour measured

LC50 for the Atlantic silverside of 37 ppb. EPA believes that

there is sufficient evidence for listing calcium hypochlorite on EPCRA

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

available ecotoxicity data for this chemical.

34. Caprolactam (CAS No. 000105-60-2) (CAA HAP) (Ref. 7). Rats were

administered caprolactam by oral gavage at doses of 0, 100, 500, and

1,000 mg/kg/day on gestation days 6 through 20. This resulted in a

LOAEL of 1,000 mg/kg/day and a NOAEL of 500 mg/kg/day for fetal

resorption. Rabbits were administered caprolactam by oral gavage at

doses of 0, 50, 150, and 250 mg/kg/day on gestation days 6 through 28.

This resulted in a LOAEL of 150 mg/kg/day for maternal and fetal body

weight depression. In addition, a slight increase in the severity of

spontaneous nephropathy (10,000 ppm) was observed in male rats of the

first parental generation fed 10,000 ppm of caprolactam in a three-

generation reproductive study, resulting in a NOAEL of 1,000 ppm (50

mg/kg/day). Mean body weights and food consumption were reduced in both

parental generations at 5,000 and 10,000 ppm. Body weights of offspring

were also reduced at these dietary concentrations (the LOAEL was 250

mg/kg/day). EPA believes that there is sufficient evidence for listing

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

based on the available developmental toxicity data for this chemical.

35. Carbofuran (CAS No. 001563-66-2) (CERCLA; EPCRA EHS; FIFRA SR)

(Ref. 8). Aquatic acute toxicity test data for carbofuran include a

measured 96-hour LC50 for bluegill of 80 ppb. In addition, the

measured 48-hour EC50 for daphnids is 35 ppb. Measured terrestrial

acute toxicity data for wildlife include an oral LD50 for mallard

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

LD50 for female ring-necked pheasants of 4.15 mg/kg. EPA believes

that there is sufficient evidence for listing carbofuran on EPCRA

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

environmental toxicity data for this chemical.

36. Carbon monoxide (CAS No. 000630-08-0) (CAL) (Ref. 8).

Cardiovascular (e.g., electrocardiograph changes, atrial fibrillation,

ventricular arrhythmias) and neurological (e.g., headache, dizziness,

convulsions, and coma) effects were reported in humans exposed to

carbon monoxide. In humans, histological effects in the brain include

extensive demyelination of white matter, and necrosis. Neuropsychiatric

disorders have also been reported. Persistant electrocardiograph

changes, and degeneration of myocardial muscle fibers, hemorrhage and

necrosis were observed following inhalation exposure of dogs to 100 ppm

(0.11 mg/L) carbon monoxide, 5.5 hours/day, 6 days/week, for 11 weeks.

Some of the dogs showed disturbances in gait and in postural and

position reflexes. The toxicity of carbon monoxide results from its

combination with hemoglobin in the blood to form carboxyhemoglobin

which is a poor oxygen carrier. Thus, oxygen delivery by the blood is

severely compromised, which leads to tissue hypoxia and possibly tissue

poisoning, resulting in the toxic effects (including death) known for

this substance.

Infants born to women who survive acute exposure to high

concentrations of carbon monoxide during pregnancy often display

neurological sequelae and gross brain damage. Exposure of pregnant rats

to 150 ppm (0.17 mg/L) carbon monoxide caused reduced pup growth rate,

and altered behavior (poor performance on negative geotaxis and homing

tests) in pups.

EPA believes that there is sufficient evidence for listing carbon

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

based on the available chronic neurological, myocardial, and

developmental toxicity data for this chemical.

Carbon monoxide is regulated under Title I of the CAA (Provisions

for Attainment and Maintenance of National Ambient Air Quality

Standards). In addition to this proposal to add carbon monoxide to

EPCRA section 313, in Units IV.B.179. and 235, EPA is proposing to add

two other chemicals, nitrogen dioxide and sulfur dioxide, that are

regulated under Title I of the CAA. Sulfur dioxide is also regulated

under Title IV of the CAA (Acid Deposition Control). Extensive data,

which are highly technical, are collected on these chemicals as

required by the CAA. EPA requests comment on the following: (1) Is the

information collected under the CAA sufficient for public right-to-know

purposes; and (2) suggestions on how the data collected on these

chemicals pursuant to CAA Titles I and IV could be used to meet the

purposes of EPCRA section 313.

37. Carboxin (5,6-dihydro-2-methyl-N-phenyl-1,4-oxathiin-3-

carboxamide) (CAS No. 005234-68-4) (FIFRA AI) (Ref. 3). Decreased body

weight gain and food consumption, increased mortality, and reduced

kidney, heart and spleen weights were observed in rats fed 600 ppm (30

mg/kg/day) carboxin for 2 years. The NOEL is 200 ppm (10 mg/kg/day). A

similar NOEL was established in a three-generation rat reproduction

study. Based on the NOEL, EPA established an oral RfD of 0.01 mg/kg/

day. In a 90-day feeding study in rats, degeneration of the kidneys was

seen at 600 ppm (30 mg/kg/day). The NOEL was 10 mg/kg/day. EPA believes

that there is sufficient evidence for listing carboxin on EPCRA section

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

toxicity data for this chemical.

38. Chinomethionat (6-methyl-1,3-dithiolo[4,5-b]quinoxalin-2-one)

(CAS No. 002439-01-2) (FIFRA AI) (Ref. 3). Increases in liver weight,

liver protein, and both total liver and microsomal RNA levels, as well

as inhibition of mixed-function oxidase enzymes (e.g., N-demethylase,

cytochrome P-450) were noted in rats administered 75 mg/kg/day by oral

gavage for 4 days or in female rats administered 75 mg/kg/day in their

diet for 21 days. Liver enlargement was reported in rats fed 10 mg/kg/

day in their diet for 35 days. The increase in liver size was

attributed to increased cellular protein and an increase in water

content. Rats exposed orally to 2,700 mg/kg for 90 days (30 mg/kg/day)

had changes in liver weight and effects on the hepatic microsomal

oxidases as well as weight loss or decreased body weight gain. In a 1-

year dog study, the NOEL was established at 0.6 mg/kg/day for the test

material in the diet. The LOEL was 1.9 mg/kg/day as indicated by extra

medullary hematopoietic nodules in the liver.

In a developmental toxicity study in rats, increased resorption and

decreased fetal weight were reported at 37.5 mg/kg/day (the highest

dose tested). The NOEL was 12.5 mg/kg/day. In another developmental

study in rats given 30 mg/kg/day in carboxy methyl cellulose by gavage

from gestation day 6 to 20, cleft palate, anasarca and micrognathia was

observed.

EPA believes that there is sufficient evidence for listing

chinomethionat on EPCRA section 313 pursuant to EPCRA section

313(d)(2)(B) based on the available hepatic and developmental toxicity

data.

39. Chlorendic acid (CAS No. 000115-28-6) (NTP) (Ref. 8). Based on

sufficient evidence of carcinogenicity in animals IARC classified

chlorendic acid as a Group 2B compound; i.e., it is possibly

carcinogenic in humans. In an NTP bioassay, there was clear evidence of

liver carcinogenicity in both rats and mice. EPA believes that there is

sufficient evidence for listing chlorendic acid on EPCRA section 313

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

data for this chemical.

40. Chlorimuron ethyl (ethyl-2-[[[(4-chloro-6-methoxyprimidin-2-

yl)-carbonyl]-amino]sulfonyl]benzoate) (CAS No. 090982-32-4) (FIFRA AI)

(Ref. 3). In a 1-year dog study, dietary administration of 37.5 mg/kg/

day (LOEL) produced an increase in white blood cells in both sexes, a

decrease in red blood cells, hematocrit, and hemoglobin in females, and

an increase in alkaline phosphatase in males. The NOEL was 6.25 mg/kg/

day. Based on the NOEL, an oral RfD of 0.02 mg/kg/day was derived. This

study was given a high confidence rating. In a 2-year rat feeding

study, changes in hematology parameters were observed at the LOEL of

125 mg/kg/day. The NOEL was 12.5 mg/kg/day. In an 18-month mouse

feeding study, centrilobular hepatocellular hypertrophy was observed at

90 days at 187.5 mg/kg/day (LOEL). The NOEL was 18.75 mg/kg/day. EPA

believes that there is sufficient evidence for listing chlorimuron

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

on the available hematological toxicity data.

41. Chlorinated paraffins category (CAA HAP) (Ref. 7). Chlorinated

paraffins are defined as mixtures of linear saturated chlorinated

hydrocarbons obtained through the partial chlorination of paraffin,

olefin, or acetylene feedstocks which have an average chain length of

10 to 30 carbon atoms and contain average chlorine levels ranging from

40 to 70 percent by weight. Chlorinated paraffins can be described by

the general formula: CxH2x-y+2Cly where x ranges from 10

to 30 and y ranges from 3 to 26. Both 58 percent-chlorinated, short-

chain (10 to 12 carbons) and 43 percent-chlorinated, long-chain (22 to

26 carbons) chlorinated paraffins were tested in rats and mice by

gavage in a 2-year bioassay. The 58 percent-chlorinated, short-chain

(10 to 12 carbons) chlorinated paraffins were carcinogenic in rats and

mice: dosed male and female mice showed increased incidences of liver

tumors, dosed male rats had increased incidences of kidney tubular cell

hyperplasia and adenomas or adenocarcinomas (combined), and dosed

female rats and mice showed increased thyroid gland follicular cell

neoplasms, indicating an EPA Group B2 classification, i.e., a probable

human carcinogen. The 43 percent-chlorinated, long-chain (22 to 26

carbons) chlorinated paraffins were carcinogenic in male mice showing

an increased incidence of malignant lymphomas, and marginal increase in

hepatocellular neoplasms in female mice and adrenal gland

pheochromocytomas in female rats, indicating an EPA Group B2 category

classification, i.e., the chemical is a probable human carcinogen. EPA

believes that there is sufficient evidence for listing chlorinated

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

based on the available carcinogenicity data for these chemicals.

The following ecotoxicity data (LC50s followed by experiment

duration in parenthesis) have been reported for short chain (10 to 13

carbons) and intermediate chlorination (59 percent chlorine)

chlorinated paraffins: daphnid, 46 ppb (48-hour); mysid shrimp, 14 ppb

(96-hour); marine algae, 42 ppb (96-hour); daphnid, 2 ppb and 9 ppb

(21-day chronic study); and midge, 78 ppb (49-day chronic study).

Ranges of chronic toxicity values are as follow: Freshwater

invertebrates, 2 to 162 ppb; freshwater fish, 3 to 17.2 ppb; marine

invertebrates, 2.4 to 24 ppb; and marine fish, 2.4 ppb to 620.5 ppm.

Chlorinated paraffins are persistent with a half-life of greater than

30 days in the environment. EPA believes that there is sufficient

evidence for listing the category chlorinated paraffins on EPCRA

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

available ecotoxicity data for these chemicals and their persistence in

the environment.

EPCRA section 313 requires threshold determinations for chemical

categories to be based on the total of all chemicals in the category

manufactured, processed, or otherwise used. For example, a facility

that manufactures three members of a chemical category would count the

total amount of all three chemicals manufactured towards the

manufacturing threshold for that category. When filing reports for

chemical categories the releases are determined in the same manner as

the thresholds. One report if filed for the category and all releases

are reported on this form.

42. 1-(3-Chloroallyl)-3,5,7-triaza-1-azoniaadamantane chloride (CAS

No. 004080-31-3) (FIFRA AI) (Ref. 3). Decrease in heart weight,

obliterative vasculitis, and perivasculitis of the hepatic blood

vessels were observed in dogs orally administered 1-(3-chloroallyl)-

3,5,7-triaza-1-azoniaadamantane for 90 days. The NOEL was 7.5 mg/kg/

day; the LOEL was 15 mg/kg/day. EPA believes that there is sufficient

evidence for listing 1-(3-chloroallyl)-3,5,7-triaza-1-azoniaadamantane

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

based on the available chronic toxicity data for 1-(3-chloroallyl)-

3,5,7-triaza-1-azoniaadamantane.

43. p-Chloroaniline (CAS No. 000106-47-8) (CERCLA; RCRA APP8; RCRA

P) (Ref. 8). In a 78-week study in which rats were fed p-chloroaniline,

non-neoplastic proliferative lesions of the splenic capsule (focal

fibrosis with subcapsular mesenchymal proliferation) were observed. The

LOAEL was 12.5 mg/kg/day (the lowest dose tested) and the RfD derived

from this data is 0.004 mg/kg/day. EPA believes that there is

sufficient evidence for listing p-chloroaniline on EPCRA section 313

pursuant to section 313(d) (2)(B) based on the chronic toxicity data

for this chemical.

44. 5-Chloro-2-(2,4-dichlorophenoxy)phenol (CAS No. 003380-34-5)

(FIFRA AI) (Ref. 3). In a 3-month dog feeding study, decreased red

blood cell and hemoglobin values, increased serum alkaline phosphatase,

jaundice, and increased liver weight were observed at 25 mg/kg/day

(LOEL). No NOEL could be established. In another 3-month dog feeding

study, the LOEL of 25 mg/kg/day produced morphologic changes in the

liver (focal acidophilic granular degeneration of cytoplasm). The NOEL

was 12.5 mg/kg/day. In a 3-month rat feeding study, 125 mg/kg/day

(LOEL) produced increased liver weights in males. The NOEL was 50 mg/

kg/day. At 150 mg/kg/day (LOEL), decrease in triglycerides, increase in

creatinine, decrease in red blood cells, increase in spleen and heart

weight, and cytomegaly were observed in another 3-month rat feeding

study (NOEL was 50 mg/kg/day). In a 2-year study, dietary

administration of 15 mg/kg/day produced decreases in red blood cells,

hemoglobin concentration, and hematocrit as well as hepatic necrosis in

males. At 50 mg/kg/day, there were decreases in red blood cells in

females. EPA believes that there is sufficient evidence for listing 5-

chloro-2-(2,4-dichlorophenoxy)phenol on EPCRA section 313 pursuant to

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

toxicity data for this chemical.

45. 3-Chloro-2-methyl-1-propene (CAS No. 000563-47-3) (NTP) (Ref.

8). In an NTP gavage bioassay there was clear evidence of

carcinogenicity from 3-chloro-2-methyl-1-propene in rats and mice. The

substance induced adrenal cortex, testicular and gastrointestinal

tumors in rats and adrenal cortex and gastrointestinal tumors in mice.

EPA believes that there is sufficient evidence for listing 3-chloro-2-

methyl-1-propene on EPCRA section 313 pursuant to EPCRA section

313(d)(2)(B) based on the carcinogenicity data for this chemical.

46. p-Chlorophenyl isocyanate (CAS No. 000104-12-1) (TSCA) (Ref.

8). p-Chlorophenyl isocyanate is very lethal following inhalation. The

4-hour mouse inhalation LC50 value is 0.053 mg/L. In addition,

isocyanates as a class are generally severe skin, eye, and respiratory

irritants following acute exposure.

EPA's exposure analysis indicates that p-chlorophenyl isocyanate

concentrations are likely to exist beyond facility site boundaries, as

a result of continuous, or frequently recurring releases, at levels

that can reasonably be anticipated to cause significant adverse acute

human health effects. EPA believes that there is sufficient evidence

for listing p-chlorophenyl isocyanate on EPCRA section 313 pursuant to

EPCRA section 313(d)(2)(A) based on the available acute toxicity and

exposure data for this chemical.

47. Chloropicrin (CAS No. 000076-06-2) (FIFRA AI) (Ref. 3).

Measured aquatic acute toxicity data for chloropicrin include a rainbow

trout 96-hour LC50 of 16.5 ppb, a bluegill 96-hour LC50 of

105 ppb, and a 48-hour EC50 of 80 ppb. EPA believes that there is

sufficient evidence for listing chloropicrin on EPCRA section 313

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

environmental toxicity data for this chemical.

48. 3-Chloropropionitrile (CAS No. 000542-76-7) (CERCLA; EPCRA EHS;

RCRA APP8; RCRA P) (Ref. 8). 3-Chloropropionitrile is metabolized by

hepatic cytochrome P450 enzymes to release cyanide. The substance is

readily absorbed both dermally and orally. The mouse oral LD50 is

51.3 mg/kg.

EPA's exposure analysis indicates that 3-chloropropionitrile

concentrations are likely to exist beyond facility site boundaries, as

a result of continuous, or frequently recurring releases, at levels

that can reasonably be anticipated to cause significant adverse acute

human health effects. EPA believes that there is sufficient evidence

for listing 3-chloropropionitrile on EPCRA section 313 pursuant to

EPCRA section 313(d)(2)(A) based on the available acute toxicity and

exposure data for this chemical.

49. p-Chloro-o-toluidine (CAS No. 000095-69-2) (IARC; NTP) (Ref.

8). p-Chloro-o-toluidine is classified as a Group B2 carcinogen by EPA;

i.e., the compound is a probable human carcinogen. It is classified as

a Group 2B carcinogen by IARC; i.e., a possible human carcinogen.

Epidemiology studies are inadequate in evaluating the carcinogenic

potential of 4-chloro-o-toluidine hydrochloride in humans. In a long-

term feeding study by NCI, p-chloro-o-toluidine hydrochloride induced

hemangiomas, hemangiosarcomas, and vascular tumors in mice. An increase

in the incidence of pituitary chromophobe adenomas was observed in

female rats following dietary administration. EPA believes that there

is sufficient evidence for listing p-chloro-o-toluidine on EPCRA

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

available carcinogenicity data for this chemical.

50. Chlorotrifluoromethane (CFC-13) (CAS No. 000075-72-9) (CAA OD)

(Ref. 8). Chlorofluorocarbons, including chlorotrifluoromethane (CFC-

13) are known to release chlorine radicals into the stratosphere.

Chlorine radicals act as catalysts to reduce the net amount of

stratospheric ozone.

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

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

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

most harmful wavelengths, reaching the earth's surface.

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

epidemiologic studies as a cause of two types of nonmelanoma skin

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

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

cancer cases would increase by about 1 to 3 percent.

Recent epidemiological studies, including large case control

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

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

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

increase from 0.5 to 1 percent.

Studies have demonstrated that UV-B radiation can suppress the

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

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

cataracts and could adversely affect the retina.

Aquatic organisms, particularly phytoplankton, zooplankton, and the

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

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

time at or near the surface of waters they inhabit.

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

impacts on plants. Field studies on soybeans suggest that yield

reductions could occur in some cultivars of soybeans, while evidence

from laboratory studies suggest that two out of three cultivars are

sensitive to UV-B. Because this increased UV-B radiation can be

reasonably anticipated to lead to cancer and other chronic human health

effects and significant adverse environmental effects, there is

sufficient evidence for listing chlorotrifluoromethane (CFC-13) on

EPCRA section 313 pursuant to EPCRA sections 313(d)(2)(B) and (C).

51. Chlorpyrifos methyl (O,O-dimethyl-O-(3,5,6-trichloro-2-

pyridyl)phosphorothioate) (CAS No. 005598-13-0) (FIFRA AI) (Ref. 3).

Humans experienced a 10 percent reduction in plasma cholinesterase

activity after 10 dermal exposures to 10 mg/kg/day and a 47 percent

reduction after 4 dermal exposures to 25 mg/kg/day (exposures were for

12 hours per day). Rabbits experienced a 97 to 100 percent reduction in

plasma cholinesterase activity after 5 dermal exposures to 10 mg/kg/day

for 12 hours a day or 2 dermal exposures to 25 mg/kg/day for 12 hours a

day. In a 2-year rat feeding study, red blood cell and plasma

cholinesterase inhibition were observed at 1 mg/kg/day (LOEL). The NOEL

was 0.1 mg/kg/day. In a 2-year dog feeding study, plasma cholinesterase

inhibition was observed at 1 mg/kg/day (LOEL). The NOEL was 0.1 mg/kg/

day. The oral rat LD50 is between 1,159 mg/kg and 3,833 mg/kg.

Lethargy, ataxia, diarrhea, salivation, and tremors were observed in

these studies. EPA believes that there is sufficient evidence for

listing chlorpyrifos methyl on EPCRA section 313 pursuant to EPCRA

section 313(d)(2)(B) based on the available neurological toxicity data.

Aquatic acute toxicity values for chlorpyrifos methyl include a

daphnid 48-hour LC50 of 1.11 ppb and a rainbow trout 96-hour

LC50 of 12.6 ppb. EPA believes that there is sufficient evidence

for listing chlorpyrifos methyl on EPCRA section 313 pursuant to EPCRA

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

data.

52. Chlorsulfuron (2-chloro-N-[[(4-methoxy-6-methyl-1,3,5-triazin-

2-yl)amino]carbonyl]benzenesulfonamide) (CAS No. 064902-72-3) (FIFRA

AI) (Ref. 3). In a rabbit developmental study, an increased incidence

of fetal resorptions was observed at the LOEL of 75 mg/kg/day. The NOEL

was 25 mg/kg/day.

In a 3-generation rat reproduction study, a decrease in fertility

index was observed at 125 mg/kg/day (LOEL). The NOEL was 25 mg/kg/day.

EPA believes that there is sufficient evidence for listing

chlorsulfuron on EPCRA section 313 pursuant to EPCRA section

313(d)(2)(B) based on the available developmental and reproductive

toxicity data for this chemical.

53. Clomazone (2-[(2-chlorophenyl)methyl]-4,4-dimethyl-3-

isoxazolidinone) (CAS No. 081777-89-1) (FIFRA AI) (Ref. 3). In a 90-day

dog feeding study, increased cholesterol and increased absolute and

relative liver weights were observed at 62.5 mg/kg/day (LOEL). The NOEL

was 12.5 mg/kg/day. Dietary administration of 62.5 mg/kg/day (LOEL) to

dogs for 1-year also produced increased cholesterol and increased liver

weights. The NOEL was 12.5 mg/kg/day. In a 90-day mouse feeding study,

megalocytosis of the liver cells was seen at 2.6 mg/kg/day (LOEL). No

NOEL was established. In a 2-year rat feeding study, elevated

cholesterol levels and liver-to-body weight ratios were observed at

21.5 mg/kg/day (LOEL). The NOEL was 4.3 mg/kg/day. Dietary

administration of 62.5 mg/kg/day (LOEL) to dogs for 1-year increased

cholesterol and liver weights. The NOEL was 12.5 mg/kg/day.

In a two-generation reproduction study, decreased pup viability,

reduced survival, decreased body weight, and nonfunctional limbs were

observed in the offspring of rats that were orally administered 50 mg/

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

EPA believes that there is sufficient evidence for listing

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

based on the available hepatic and developmental toxicity data.

54. Crotonaldehyde (CAS No. 004170-30-3) (RCRA APP8) (Ref. 8).

Crotonaldehyde has been tested for carcinogenicity in one animal study.

When crotonaldehyde was administered to male F344 rats at 0, 42, or 421

mg/L for 113 weeks, there was a statistically significant increase in

the incidence of hepatocellular neoplasms (benign and malignant

combined) in the low dose group. The lack of tumorigenic effects at the

high-dose group is believed to be due to the hepatotoxicity observed in

this group. At high dose, crotonaldehyde is cytotoxic; cells died

before neoplasms are manifested. Crotonaldehyde and other alpha, beta-

unsaturated carbonyls are chemically reactive compounds which can

readily react with cellular macromolecules such as DNA and proteins.

Mutagenicity studies in a slightly modified preincubation Ames test

have clearly shown that crotonaldehyde is mutagenic. EPA believes that

there is sufficient evidence for listing crotonaldehyde on EPCRA

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

available carcinogenicity and mutagenicity data for this chemical.

55. Cyanazine (CAS No. 021725-46-2) (CAL; FIFRA SR) (Ref. 8).

Cyanazine is a triazine-type herbicide. In a three-generation

reproduction study in Long-Evans rats, F3b female weanlings had

increased relative brain weights and decreased relative kidney weights.

The LOAEL was 4.05 mg/kg/day and the NOAEL was 1.35 mg/kg/day. In

rabbits that received cyanazine in gelatin capsules during gestation

days 6 to 18, there was increased postimplantation loss, decreased

litter size, and alterations in ossification. In addition, there were

increased malformations in the offspring, including anophthalmia/

microphthalmia, dilated brain ventricles, dome cranium and

thoracoschisis (the LOAEL was 2 mg/kg/day; the NOAEL was 1 mg/kg/day).

Similar developmental effects were reported in Fischer 344 rats

administered cyanazine during gestation days 6 to 15 (the LOAEL was 25

mg/kg/day; the NOAEL 5 was mg/kg/day). EPA believes that there is

sufficient evidence for listing cyanazine on EPCRA section 313 pursuant

to EPCRA section 313(d)(2)(B) based on the developmental toxicity data

for this chemical.

56. Cycloate (CAS No. 001134-23-2) (FIFRA AI) (Ref. 3). Cycloate, a

carbamate pesticide, is a cholinesterase inhibitor. Symptoms of

poisoning include salivation, lacrimation, convulsions, and death.

Depressed plasma cholinesterase was observed in a 9-week rat inhalation

study at 0.0025 mg/L. The NOEL was less than 0.0025 mg/L. Decreased

serum cholinesterase (in males and females) and Wallerian degeneration

of nerve fibers in spinal cord and sciatic nerve (females) were

observed at 0.12 mg/L in a 10-week rat inhalation study (cholinesterase

NOEL is 0.012 mg/L). In both inhalation studies, animals were exposed

for 6 hours/day, 5 days/week. Plasma, red blood cell, and brain

cholinesterase inhibition was reported in rats fed 8 mg/kg/day for 2

years. The NOEL was less than 8 mg/kg/day. Dose-related neuropathy and

muscle myopathy were observed. In a 2-year rat feeding study, distended

myelin sheath demyelination and nerve fiber loss occurred at 3 mg/kg/

day (LOEL). The NOEL was 0.5 mg/kg/day.

Decreased weight and survival were observed in the offspring of

rats orally administered 24 mg/kg/day (LOEL) and 72 mg/kg/day of

cycloate, respectively (duration and frequency of dosing not reported).

The reproductive NOEL was 8 mg/kg/day. Decreased pup weight was

observed at 20 mg/kg/day and decreased pup survival was observed at 50

mg/kg/day in a 2-generation rat reproduction study. The NOEL values for

these endpoints were 2.5 mg/kg/day and 20 mg/kg/day, respectively.

EPA believes that there is sufficient evidence for listing cycloate

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

the available neurological and developmental toxicity data.

57. Cyclohexanol (CAS No. 000108-93-0) (TSCA) (Ref. 8). Four

rabbits exposed to 997 ppm (4 mg/L) for 11 days (6 hours/day, 5 days/

week) and a rabbit receiving dermal applications of approximately 2,500

mg/kg/day for 10 days (1 hour/day) developed tremors, central nervous

system depression, lethargy or hypothermia.

Microscopic or degenerative changes were observed in the livers and

kidneys of rabbits inhaling 145 ppm (0.59 mg/L) of cyclohexanol for 50

days (6 hours/day, 5 days/week), or repeated doses at 272 ppm (1.1 mg/

L). In addition, degenerative myocardial effects were observed at this

exposure level. Repeated inhalation exposure to higher doses (997 to

1,229 ppm; 4 to 5 mg/L) in rabbits resulted in degenerative changes in

the brain and heart as well as liver and kidneys.

Reproductive effects including testicular atrophy, loss of Type A

spermatogonia, spermatocytes and spermatozoa, ``shrinkage'' of

seminiferous tubules and Leydig cells, reductions in RNA protein,

sialic acid, and glycogen in testes, epididymis and seminal vesicles

and increased testicular cholesterol and alkaline phosphatase were

observed in male rats or gerbils exposed to 15 mg/kg of cyclohexanol

for 21 to 37 days. These changes were accompanied with decreased

fertility, and occurred at exposure levels which had no effect on the

liver or kidney.

EPA believes that there is sufficient evidence for listing

cyclohexanol on EPCRA section 313 pursuant to EPCRA section

313(d)(2)(B) based on the chronic neurological, hepatic, renal,

myocardial, and reproductive toxicity data for this chemical.

58. Cyfluthrin (3-(2,2-Dichloroethenyl)-2,2-

dimethylcyclopropanecarboxylic acid, cyano(4-fluoro-3-

phenoxyphenyl)methyl ester) (CAS No. 068359-37-5) (FIFRA AI) (Ref. 3).

In a 14-day rat study, oral administration of 60 mg/kg/day produced

tremors, uncoordinated gait, salivation, slight brain hemorrhages,

necrosis of the skeletal muscle fibers, and death. The NOEL was not

defined. In another study, salivation, straddled gait, axonal

degeneration of sciatic nerve, microtubular dilation, and mitochondria

degeneration in the sciatic and femoral nerves were observed in rats

administered 80 mg/kg/day orally for 5 days and 40 mg/kg/day for the

following 9 days. No NOEL was established.

Liver and adrenal weight increases were observed in rats orally

administered 40 to 80 mg/kg/day for 28 days. The highest dose of 80 mg/

kg/day was reduced to 40 mg/kg/day. The NOEL was 20 mg/kg/day. Liver

weight changes and urobilinogen and ketone bodies in the urine were

observed in rats fed 15 mg/kg/day for 28 days. No NOEL was established.

In a 28-day mouse feeding study, increased liver weight was observed at

50 mg/kg/day (LOEL). The NOEL was 15 mg/kg/day. Inflammatory foci in

the kidneys of females were observed at 7.5 mg/kg/day in a 2-year rat

feeding study. The NOEL was 2.5 mg/kg/day. Based on the NOEL of the

study, an oral RfD of 0.025 mg/kg/day was determined. Increased

alkaline phosphatase activity was observed in males at 7.5 mg/kg/day in

a 23-month mouse feeding study.

EPA believes that there is sufficient evidence for listing

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

based on the available neurological, hepatic, and renal toxicity data.

Aquatic acute toxicity values for cyfluthrin include a rainbow

trout 96-hour LC50 of 0.68 ppb, a bluegill 96-hour LC50 of

1.5 ppb, and a daphnid 48-hour EC50 of 0.14 ppb. EPA believes that

there is sufficient evidence for listing cyfluthrin on EPCRA section

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

environmental toxicity data.

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

dimethylcyclopropanecarboxylic acid cyano(3-phenoxyphenyl)methyl ester)

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

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

occasional disturbances of the nervous system (unsteadiness and/or

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

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

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

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

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

is sufficient evidence for listing cyhalothrin on EPCRA section 313

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

neurological toxicity data.

60. Cyromazine (N-cyclopropyl-1,3,5-triazine-2,4,6-triamine) (CAS

No. 066215-27-8) (FIFRA AI) (Ref. 3). In a 6-month dog feeding study,

7.5 mg/kg/day (LOEL) produced changes in hematocrit and hemoglobin

levels. The NOEL was 0.75 mg/kg/day. Based on the NOEL, an oral RfD of

0.0075 mg/kg/day was derived. In a 90-day dog feeding study, the LOEL

of 25 mg/kg/day produced an increase in relative liver weights in

males. The NOEL was 7.5 mg/kg/day. In a 90-day rat feeding study, the

LOEL of 15 mg/kg/day produced a decrease in relative liver weights in

males. The NOEL was 1.5 mg/kg/day. EPA believes that there is

sufficient evidence for listing cyromazine on EPCRA section 313

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

hematological toxicity data.

61. Dazomet (tetrahydro-3,5-dimethyl-2H-1,3,5-thiadiazine-2-thione)

(CAS No. 000533-74-4) (FIFRA AI) (Ref. 3). Animals fed dazomet at a

dietary dose of 40 ppm for 2 years showed focal necrosis and fatty

metamorphosis of the liver. Rats fed 30.3 mg/kg/day experienced

decreased weight gain and changes in liver weight. Renal focal tubular

necrosis was seen in rats fed 10 ppm (0.5 mg/kg/day) for 2 years. EPA

believes that there is sufficient evidence for listing dazomet on EPCRA

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

available hepatic and renal toxicity data for this chemical.

62. Dazomet sodium salt (tetrahydro-3,5-dimethyl-2H-1,3,5-

thiadiazine-2-thione, ion(1-), sodium) (CAS No. 053404-60-7) (FIFRA AI)

(Ref. 3). The available toxicity data is on dazomet. Rats fed 80 ppm

for 2 years (4 mg/kg/day) showed focal necrosis and fatty metamorphosis

of the liver. Rats fed 30.3 mg/kg/day experienced decreased weight gain

and changes in liver weight. Renal focal tubular necrosis was seen in

rats fed 10 ppm (0.5 mg/kg/day) for 2 years. EPA believes that there is

sufficient evidence for listing dazomet sodium on EPCRA section 313

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

toxicity data for its free acid, dazomet.

63. 2,4-DB (CAS No. 000094-82-6) (FIFRA SR) (Ref. 8). 2,4-DB (4-

(2,4-dichlorophenoxy)butanoic acid) is a 2,4-dichlorophenoxy-type

herbicide. In a study involving beagle dogs fed a diet containing 2,4-

DB for 90 days, a LOAEL of 25 mg/kg/day was determined, based on

internal hemorrhaging and mortality observed during the first 3 to 9

weeks of treatment. The NOAEL in this study was 8 mg/kg/day. At this

dose level, slight increases in liver weights were observed, but

unaccompanied by any gross or histopathologic lesions. EPA has derived

an oral RfD of 0.008 mg/kg/day from the LOAEL. In a subchronic rat

feeding study, the LOAEL and NOAEL values determined were higher (the

LOAEL was approximately 80 to 100 mg/kg/day; the NOAEL was

approximately 25 to 30 mg/kg/day), and were based on severe liver and

kidney damage.

In the above-mentioned subchronic (90-day) dog feeding study, it

was observed that the animals exposed to doses of 2,4-DB at 25 mg/kg/

day (the LOAEL) and higher exhibited aspermatogenesis within the first

3 to 9 weeks of treatment. The offspring of rats orally exposed to 17

mg/kg of 2,4-DB during days 1 to 7 of gestation developed

abnormalities. There was also an increase in stillbirths at this dose

level. In a separate study, offspring of rats orally exposed to 416 mg/

kg on days 5 or 9 of gestation exhibited increased preimplantation loss

and/or developmental toxicity.

EPA believes that there is sufficient evidence for listing 2,4-DB

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

the hepatic, reproductive, and developmental toxicity data for this

chemical.

64. 2,4-D butoxyethyl ester (CAS No. 001929-73-3) (CERCLA; FIFRA

AI; IARC) (Ref. 8). 2,4-D butoxyethyl ester is a 2,4-dichlorophenoxy-

type herbicide. In mammals, the butoxyethyl ester of 2,4-D is

hydrolyzed to yield the free acid, 2,4-D. Therefore, the toxicity of

2,4-D butoxyethyl ester is expected to be similar to that of 2,4-D, in

which the kidney, liver, and nervous system are the primary targets of

injury. EPA believes that there is sufficient evidence for listing 2,4-

D butoxyethyl ester on EPCRA section 313 pursuant to EPCRA section

313(d)(2)(B) based on the known chronic effects of its metabolite 2,4-

D.

65. 2,4-D butyl ester (CAS No. 000094-80-4) (CERCLA; FIFRA AI;

IARC) (Ref. 8). 2,4-D butyl ester is a 2,4-dichlorophenoxytype

herbicide. In mammals, the butyl ester of 2,4-D is hydrolyzed to yield

the free acid, 2,4-D. Therefore, the toxicity of 2,4-D butyl ester is

expected to be similar to that of 2,4-D, in which the kidney, liver,

and nervous system are the primary targets of injury. EPA believes that

there is sufficient evidence for listing 2,4-D butyl ester on EPCRA

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

toxic effects of its metabolite 2,4-D.

66. 2,4-D chlorocrotyl ester (CAS No. 002971-38-2) (CERCLA; FIFRA

AI; IARC) (Ref. 8). 2,4-D chlorocrotyl ester is a 2,4-dichlorophenoxy-

type herbicide. In mammals, the chlorocrotyl ester of 2,4-D is

hydrolyzed to yield the free acid, 2,4-D. Therefore, the toxicity of

2,4-D chlorocrotyl ester is expected to be similar to that of 2,4-D, in

which the kidney, liver and nervous system are the primary targets of

injury. EPA believes that there is sufficient evidence for listing 2,4-

D chlorocrotyl ester on EPCRA section 313 pursuant to EPCRA section

313(d)(2)(B) based on the known toxic effects of its metabolite 2,4-D.

67. Desmedipham (CAS No. 013684-56-5) (FIFRA AI) (Ref. 3). In a 90-

day dog study, groups of four beagles/sex were fed diets containing 0

to 5.24 mg/kg/day. This caused increased methemoglobin at 5.24 mg/kg/

day (LOEL). EPA believes that there is sufficient evidence for listing

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

based on the available hematological toxicity data.

68. 2,4-D 2-ethylhexyl ester (CAS No. 001928-43-4) (CERCLA; FIFRA

AI; IARC) (Ref. 8). 2,4-D 2-ethylhexyl ester is a 2,4-dichlorophenoxy-

type herbicide. The 2-ethylhexyl moiety contains eight carbons and,

therefore, is an isooctyl group. Developmental toxicity following

maternal exposure to 2,4-D isooctyl esters has been demonstrated in the

rat and mouse. Fetotoxicity occurred in offspring of rats exposed to

528 mg/kg during gestation days 8 through 11. Rats orally exposed to

doses as low as 302 mg/kg during gestation days 9 through 12 had

musculoskeletal abnormalities. Exposure to a lower dose (188 mg/kg) for

a longer period during gestation (days 6 through 15) caused

developmental effects on homeostasis and effects on newborn growth

statistics. In mice, 438 mg/kg administered orally during gestation

days 8 to 12 also caused effects on newborn growth statistics.

EPA believes that there is sufficient evidence for listing 2,4-D 2-

ethylhexyl ester on EPCRA section 313 pursuant to EPCRA section

313(d)(2)(B) based on the developmental toxicity data for 2,4-D

isooctyl esters, and on the toxic effects of its metabolite 2,4-D.

The aquatic acute toxicity data for 2,4-D isooctyl esters include a

measured 48-hour LC50 of 8.8 ppm for bluegill. In addition, 2,4-D

isooctyl esters are expected to bioaccumulate based on the estimated

log Kow of 6.6. EPA believes that there is sufficient evidence for

listing 2,4-D 2-ethylhexyl ester on EPCRA section 313 pursuant to EPCRA

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

and the potential for bioaccumulation.

69. 2,4-D 2-ethyl-4-methylpentyl ester (CAS No. 053404-37-8)

(CERCLA; FIFRA AI; IARC) (Ref. 8). 2,4-D 2-ethyl-4-methylpentyl ester

is a 2,4-dichlorophenoxy-type herbicide. The 2-ethyl-4-methylpentyl

ester moiety contains eight carbons and, therefore, is an isooctyl

group. Developmental toxicity following maternal exposure to 2,4-D

isooctyl esters has been demonstrated in the rat and mouse.

Fetotoxicity occurred in offspring of rats exposed to 528 mg/kg during

gestation days 8 through 11. Rats orally exposed to doses as low as 302

mg/kg during gestation days 9 through 12 had musculoskeletal

abnormalities. Exposure to a lower dose (188 mg/kg) for a longer period

during gestation (days 6 through 15) caused developmental effects on

homeostasis and effects on newborn growth statistics. In mice, 438 mg/

kg administered orally during gestation days 8 through 12 also caused

effects on newborn growth statistics.

EPA believes that there is sufficient evidence for listing 2,4-D 2-

ethyl-4-methylpentyl ester on EPCRA section 313 pursuant to EPCRA

section 313(d)(2)(B) based on the developmental toxicity data for 2,4-D

isooctyl esters, the toxic effects of its metabolite 2,4-D. The aquatic

acute toxicity data for 2,4-D isooctyl esters include a measured 48-

hour LC50 of 8.8 ppm for bluegill. In addition, 2,4-D isooctyl

esters are expected to bioaccumulate based on the estimated log

Kow of 6.6. EPA believes that there is sufficient evidence for

listing 2,4-D 2-ethyl-4-methylpentyl ester on EPCRA section 313

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

environmental toxicity data and the potential for bioaccumulation.

70. Diazinon (CAS No. 000333-41-5) (CERCLA; FIFRA SR) (Ref. 8).

Diazinon, an organophosphate insecticide, causes plasma cholinesterase

inhibition and central nervous system depression. Significant

inhibition of plasma cholinesterase was observed in two men

administered five doses of 0.025 mg/kg/day. Diazinon administered to

men at doses of 0.05 mg/kg/day for 28 days caused a 35 to 40 percent

reduction in plasma cholinesterase. A NOEL for cholinesterase

inhibition of 0.02 mg/kg/day was identified from several controlled

studies in humans. Clinical symptoms of diazinon poisoning include

headache, nausea, sweating, vomiting, and diarrhea all of which are

indicative of neurotoxicity. Plasma cholinesterase inhibition (93

percent) and red blood cell inhibition (90 percent) occurred in monkeys

orally exposed to diazinon in doses of 5 mg/kg/day for 52 weeks. The

NOEL for inhibition of cholinesterase in this study was 0.05 mg/kg/day

and the LOEL was 0.5 mg/kg/day.

Urogenital defects in the offspring of female rats orally

administered diazinon at doses of 26.4 mg/kg on days 12 to 15 of

gestation has been reported. Diazinon also induced musculoskeletal

abnormalities in offspring when administered orally to mothers at doses

of 45 mg/kg on days 8 to 12 of gestation. Post-implantation mortality

was increased in female rats administered 63.5 mg/kg on day 10 of

gestation. Similar reproductive and developmental effects were observed

in mice. Oral administration of 3.96 mg/kg of diazinon (days 1 to 22 of

gestation) caused decreased litter size and delayed behavioral effects

in the newborn. Doses of 0.210 mg/kg and 3.78 mg/kg administered orally

on days 1 to 21 of gestation caused abnormalities in the immune and

reticuloendothelial system and biochemical and metabolic abnormalities

of the offspring, respectively.

EPA believes that there is sufficient evidence for listing diazinon

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

the developmental and chronic neurotoxicity data for this chemical.

Measured aquatic acute toxicity data for diazinon include a 96-hour

LC50 for rainbow trout of 90 ppb and a daphnid 96-hour LC50

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

data for diazinon include an oral LD50 for male mallard ducks of

3.54 mg/kg and an oral LD50 for male pheasants of 4.33 mg/kg. EPA

believes that there is sufficient evidence for listing diazinon on

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

environmental toxicity data for this chemical.

71. 2,2-Dibromo-3-nitrilopropionamide (CAS No. 010222-01-2) (FIFRA

AI) (Ref. 3). Oral administration of 50 mg/kg/day (LOEL) to rats for 4

weeks produced dyspnea and weight loss. The NOEL was 25 mg/kg/day. Oral

administration of 30 mg/kg/day to rats for 13 weeks produced dyspnea.

The NOEL was 13 mg/kg/day. These data may be indicative of direct

effects of the compound on the respiratory system. EPA believes that

there is sufficient evidence for listing 2,2-dibromo-3-

nitrilopropionamide on EPCRA section 313 pursuant to EPCRA section

313(d)(2)(B) based on the available chronic respiratory data.

72. Dicamba (3,6-Dichloro-2-methyoxybenzoic acid) (CAS No. 001918-

00-9) (FIFRA AI) (Ref. 3). Decreased fetal body weights and increased

post-implantation loss was observed in the offspring of rabbits

receiving 10 mg/kg/day of dicamba on days 6 through 18 of gestation.

The LOEL was 10 mg/kg/day and NOEL was 3 mg/kg/day. Based on the NOEL,

EPA derived an oral RfD value of 0.03 mg/kg/day. In a separate study,

disorders of oxidative phosphorylation and focal necrosis in the heart

were observed in newborn rats following transplacental exposure to

dicamba. In a developmental toxicity study, an increase in skeletal

malformations was seen in the offspring of rats orally administered 64

mg/kg/day on days 6 through 19 of gestation. EPA believes that there is

sufficient evidence for listing dicamba on EPCRA section 313 pursuant

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

toxicity data for this chemical.

73. Dichloran (2,6-Dichloro-4-nitroaniline) (CAS No. 000099-30-9)

(FIFRA AI) (Ref. 3). Dichloran, an aniline, is a potential inducer of

methemoglobinemia. Either single or repeated oral doses of dichloran

produced enlarged livers and induction of microsomal enzymes in the

rat. Dogs fed 21 mg/kg/day had increases in serum transaminases. In

Rhesus monkeys, where dichloran does not induce hepatic enzymes, 160

mg/kg/day for 3 months caused hepatic centrilobular fatty infiltration

and death. Inhalation exposure to 0.17 mg/L produced elevated

cholesterol levels and increased liver weight in a 3-month rabbit study

and increased liver weight in a 21-day rat study. In a 2-year mouse

study, dietary administration of 102.7 mg/kg/day (LOEL) produced

centrilobular hepatocyte enlargement, focal necrosis, acute

inflammatory cell infiltration, vacuolization of centrilobular

hepatocytes, increased weight of the liver and increased incidence of

erythropoiesis in males. The NOEL was 30 mg/kg/day. EPA believes that

there is sufficient evidence for listing dichloran on EPCRA section 313

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

toxicity data.

74. 3,3'-Dichlorobenzidine dihydrochloride (CAS No. 000612-83-9)

(TSCA) (Ref. 8). IARC has classified 3,3'dichlorobenzidine (o-

dichlorobenzidine) as a group 2B compound, i.e. this chemical is

possibly carcinogenic in humans. IARC uses the generic name 3,3'-

dichlorobenzidine interchangeably with 3,3'-dichlorobenzidine

dihydrochloride. The dihydrochloride salt of 3,3'-dichlorobenzidine is

expected to be equally as toxic as the free base (3,3'-

dichlorobenzidine). EPA believes that there is sufficient evidence for

listing 3,3'-dichlorobenzidine dihydrochloride on EPCRA section 313

pursuant to EPCRA section 313(d)(2)(B) based on its potential to cause

cancer in humans.

75. 3,3'-Dichlorobenzidine sulfate (CAS No. 064969-34-2) (TSCA)

(Ref. 8). IARC has classified 3,3'-dichlorobenzidine (o-

dichlorobenzidine) as a group 2B compound, i.e. this chemical is

possibly carcinogenic in humans. The sulfate salt of

3,3'dichlorobenzidine is expected to be equally as toxic as the free

base (3,3'-dichlorobenzidine). EPA believes that there is sufficient

evidence for listing 3,3'-dichlorobenzidine sulfate on EPCRA section

313 pursuant to EPCRA section 313(d)(2)(B) based on its potential to

cause cancer in humans.

76. trans-1,4-Dichloro-2-butene (CAS No. 000110-57-6) (EPCRA EHS)

(Ref. 8). Mortality in two of six rats was observed following

inhalational exposure to 62 ppm (0.34 mg/L) for 4 hours. An acute

inhalation LC50 in rats was 86 ppm (0.44 mg/L). EPA's exposure

analysis indicates that trans-1,4-dichloro-2-butene concentrations are

likely to exist beyond facility site boundaries, as a result of

continuous, or frequently recurring releases, at levels that can

reasonably be anticipated to cause significant adverse acute human

health effects. EPA believes that there is sufficient evidence for

listing trans-1,4-dichloro-2-butene on EPCRA section 313 pursuant to

EPCRA section 313(d)(2)(A) based on the available acute toxicity and

exposure data for this chemical.

77. Dichloromethylphenylsilane (CAS No. 000149-74-6) (EPCRA EHS)

(Ref. 8). As a class, chlorinated silanes are very corrosive to the

skin and mucous membranes and liberate hydrochloric acid in the

presence of water. The 2-hour mouse inhalation LC50 value for

dichloromethylphenylsilane is 0.17 mg/L. EPA's exposure analysis

indicates that dichloromethylphenylsilane concentrations are likely to

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

frequently recurring releases, at levels that can reasonably be

anticipated to cause significant adverse acute human health effects.

EPA believes that there is sufficient evidence for listing

dichloromethylphenylsilane on EPCRA section 313 pursuant to EPCRA

section 313(d)(2)(A) based on the available acute toxicity and exposure

data for this chemical.

78. Dichlorophene (2,2'-methylenebis(4-chlorophenol) (CAS No.

000097-23-4) (FIFRA AI) (Ref. 3). Increased incidence of microphthalmia

was observed in the offspring of rats administered 25 mg/kg/day

(teratogenic LOEL). The NOEL was 5.0 mg/kg/day. A dose of 75 mg/kg/day

(fetotoxic LOEL) produced delayed ossification of vertebral centra and

sternaebrae, reduced body weight and length, and increased resorptions

in rat fetuses. The fetotoxic NOEL was 5.0 mg/kg/day. No other

developmental studies were available. EPA believes that there is

sufficient evidence for listing dichlorophene on EPCRA section 313

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

developmental toxicity data.

Aquatic acute toxicity values for dichlorophene include a measured

48-hour LC50 of 50 ppb for Spicodioptomus (calanoid copipod). EPA

believes that there is sufficient evidence for listing dichlorophene on

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

available environmental toxicity data.

79. trans-1,3-Dichloropropene (CAS No. 010061-02-6) (CERCLA; CWA

PPL) (Ref. 8). Clinical reports have documented the occurrence of

histiocytic lymphoma in two firemen and acute myelomonocytic leukemia

in a farmer exposed accidently to 1,3-dichloropropene. Information on

the isomer or isomer mixture (i.e., trans/cis isomers) was not

specified. The lymphoma and leukemia were refractory to treatment, and

all three men died. There is evidence that 1,3-dichloropropene may

cause cancer in rats and mice after oral exposure. In a 2-year gavage

study, rats treated with 25 or 50 mg/kg/day 1,3-dichloropropene (53

percent cis isomer, 45 percent trans isomer, 1 percent epichlorhydrin)

developed squamous cell papillomas and carcinomas of the forestomach.

Male rats also developed neoplastic nodules of the liver. Female mice

that received 50 or 100 mg/kg/day developed squamous cell papillomas

and carcinomas of the forestomach, transitional cell carcinomas of the

urinary bladder, and an increased incidence of alveolar/bronchiolar

adenomas. A statistically significant increase in bronchioalveolar

adenomas was noted in male mice exposed to 60 ppm (272 mg/L) 1,3-

dichloropropene vapors (50 percent cis isomer, 43 percent trans

isomer). This benign lung tumor was not seen in female mice or in male

or female rats. IARC assigned 1,3-dichloropropene to Group 2B, i.e.,

possibly carcinogenic in humans. EPA believes that there is sufficient

evidence for listing trans-1,3-dichloropropene on EPCRA section 313

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

carcinogenicity data for 1,3-dichloropropene (unspecified isomer).

80. Diclofop methyl (2-[4-(2,4-dichlorophenoxy) phenoxy]propanoic

acid, methyl ester) (CAS No. 051338-27-3) (FIFRA AI) (Ref. 3). In a rat

teratology study, increased resorptions, reduced body weights, and

dilation of the renal pelvis or distension of the ureter in offspring

were reported in rats fed 1.6 mg/kg/day (LOEL). The NOEL was 0.5 mg/kg/

day. Increased pup mortality was observed at 5 mg/kg/day (LOEL) in a 3-

generation rat reproduction study. The NOEL was 1.5 mg/kg/day.

In a 30-day rat feeding study, increased relative heart, liver, and

kidney weights were observed at the LOEL of 4 mg/kg/day. No NOEL was

established. Jaundice, increased bilirubin, increased serum glutamic-

pyruvic transaminase and serum glutamic-oxaloacetic transaminase, and

increased liver and kidney weights were observed in a 30-day dog

feeding study at 50 mg/kg/day. The NOEL was 12.5 mg/kg/day. In a 90-day

rat feeding study, elevated liver weights and centrilobular enlargement

of hepatic cells were observed at 4 mg/kg/day. The NOEL was 1.6 mg/kg/

day. Dogs fed 6.25 mg/kg/day for 90 days had increased lipid content

and focal changes in the renal cortex. The NOEL was 2 mg/kg/day. EPA

believes that there is sufficient evidence for listing diclofop methyl

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

the available developmental, hepatic, and renal toxicity data.

81. Dicyclopentadiene (CAS No. 000077-73-6) (TSCA) (Ref. 8).

Convulsions were reported in rats or mice following inhalation of

dicyclopentadiene at dosage levels of 332 or 145 ppm (1.8 or 0.78 mg/

L), respectively, for 1 or 2 days. The reported acute oral LD50 in

rats is 353 mg/kg. Animals at this dose level had convulsions and

muscle weakness. In a 90-day inhalation study in dogs, neurotoxic

symptoms observed included diarrhea, excessive salivation and lack of

control of hind quarters. The NOAEL in this study was 8.9 ppm (0.048

mg/L); no LOEL was reported. EPA believes that there is sufficient

evidence for listing dicyclopentadiene on EPCRA section 313 pursuant to

EPCRA section 313(d)(2)(B) based on the chronic neurotoxicity data for

this chemical.

82. Diethatyl ethyl (CAS No. 038727-55-8) (FIFRA AI) (Ref. 3). In a

2-year study, groups of six beagles/sex were given doses orally from 0

to 31.25 mg/kg/day. The lowest dose (0.25 mg/kg/day) produced a

positive Coombs test. EPA believes that there is sufficient evidence

for listing diethatyl ethyl on EPCRA section 313 pursuant to EPCRA

section 313(d)(2)(B) based on the available hematological toxicity data

for this chemical.

83. Diflubenzuron (CAS No. 035367-38-5) (FIFRA SR) (Ref. 8). In a

2-year study in which beagle dogs received diflubenzuron daily in

gelatin capsules, the LOAEL for increases in sulfhemoglobin and

methemoglobin was 10 mg/kg/day and the NOAEL was 2 mg/kg/day. EPA has

derived an oral RfD of 0.02 mg/kg/day for this chemical from this

study. Similar effects were noted in two separate 2-year rat feeding

studies (the LOAEL was 7.8 to 8 mg/kg/day; the NOAEL was 2 mg/kg/day),

and in a lifetime oral study in mice (the LOAEL was 12 mg/kg/day; the

NOAEL was 2.4 mg/kg/day). EPA believes that there is sufficient

evidence for listing diflubenzuron on EPCRA section 313 pursuant to

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

toxicity data.

Measured aquatic acute toxicity data for diflubenzuron include a

48-hour LC50 of 4.55 ppb for daphnids. EPA believes that there is

sufficient evidence for listing diflubenzuron on EPCRA section 313

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

toxicity data for this chemical.

84. Diglycidyl resorcinol ether (CAS No. 000101-90-6) (IARC; NTP)

(Ref. 8). Diglycidyl resorcinol ether is classified by IARC as a Group

2B compound, i.e., it is possibly carcinogenic in humans. In an NTP

bioassay, rats orally administered 12 mg/kg of diglycidyl resorcinol

ether 5 days a week for 103 weeks developed squamous cell papillomas

and squamous cell carcinomas of the stomach. Mice orally administered

50 mg/kg 5 days a week for 103 weeks developed squamous cell carcinomas

and squamous cell papillomas of the stomach. Mice orally administered

70.5 mg/kg/day of diglycidyl resorcinol ether for 2 years developed

blood lymphomas and Hodgkin's disease. Mice receiving dermal

applications of diglycidyl resorcinol ether for 1-year developed skin

tumors. EPA believes that there is sufficient evidence for listing

diglycidyl resorcinol ether on EPCRA section 313 pursuant to EPCRA

section 313(d)(2)(B) based on the carcinogenicity data for this

chemical.

85. Dimethipin (2,3,-Dihydro-5,6-dimethyl-1,4-dithiin 1,1,4,4-

tetraoxide) (CAS No. 055290-64-7) (FIFRA AI) (Ref. 3). In a 1-year dog

feeding study, decreased erythrocyte, hemoglobin, and hematocrit levels

as well as increased platelet levels were observed at 75 mg/kg/day. The

LOEL for systemic toxicity based on decreased body weight was 7.5 mg/

kg/day. No NOEL could be established. In a 2-year rat feeding study,

increased absolute and relative liver weights were observed at 10 mg/

kg/day (LOEL). The NOEL was 2 mg/kg/day. Based on the NOEL in the

study, EPA established an oral RfD of 0.02 mg/kg/day. EPA believes that

there is sufficient evidence for listing dimethipin on EPCRA section

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

hematological and hepatic toxicity data.

86. Dimethoate (CAS No. 000060-51-5) (CERCLA; EPCRA EHS; FIFRA SR;

RCRA APP8; RCRA P) (Ref. 8). Dimethoate is an organophosphate

insecticide. In humans, dimethoate causes typical symptoms of

cholinesterase inhibition (sweating, diarrhea, salivation, headache,

difficulty in breathing, etc.). In a controlled human study, subjects

were administered dimethoate for 57 days. Whole blood and erythrocyte

cholinesterase inhibition was observed from day 20 on. The NOEL was

0.202 mg/kg/day, and the LOEL was 0.434 mg/kg/day. In another study in

which humans were administered dimethoate for 57 days, the NOEL for

cholinesterase inhibition was 15 mg/day (0.2 mg/kg based on a 70 kg

person). The LOEL was not specified. Cholinergic symptoms reflective of

cholinesterase inhibition following dimethoate administration have also

been observed in laboratory animals. A 2-year feeding study in rats

determined the NOEL and LOEL for plasma and brain cholinesterase

inhibition to be 0.05 and 0.5 mg/kg/day, respectively.

Dimethoate was tested for developmental effects in Wistar rats.

Cygon 4E (47.3 percent dimethoate, 52.7 percent unspecified

constituents) was administered to pregnant females on days 6 to 15 of

gestation. The NOEL for developmental effects was 6 mg/kg/day. At a

LOEL of 12 mg/kg/day, an increase in the incidence of wavy ribs was

observed in the fetuses. An increase in offspring mortality occurred in

a five-generation chronic feeding study (actual doses were 9.5 to 10.5

mg/kg/day) in male and female CD-1 mice. At 12 mg/kg/day (120 mg/kg,

gestation days 6 to 15), musculoskeletal abnormalities were observed in

the rat offspring. EPA believes that there is sufficient evidence for

listing dimethoate on EPCRA section 313 pursuant to EPCRA section

313(d)(2)(B) based on the available developmental and neurotoxicity

data for this chemical.

87. 3,3'-Dimethoxybenzidine dihydrochloride (o-Dianisidine

dihydrochloride) (CAS No. 020325-40-0) (TSCA) (Ref. 8). IARC has

classified 3,3'-dimethoxybenzidine (o-dianisidine) as a Group 2B

compound, i.e., this chemical is possibly carcinogenic. In an NTP

carcinogenicity bioassay, increases in neoplasms of the skin, oral

cavity, large intestine, liver, uterus, and cervix were noted in rats

administered this chemical in drinking water at dose levels of 6, 12,

or 21 mg/kg/day in males and 7, 14, or 23 mg/kg/day in females. The

dihydrochloride salt of o-dianisidine is expected to be equally as

toxic as the free base (o-dianisidine). EPA believes that there is

sufficient evidence for listing 3,3'-dimethoxybenzidine dihydrochloride

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

its potential to cause cancer in humans.

88. 3,3'-Dimethoxybenzidine hydrochloride (o-Dianisidine

hydrochloride) (CAS No. 111984-09-9) (TSCA) (Ref. 8). IARC has

classified 3,3'-dimethoxybenzidine (o-dianisidine) as a Group 2B

compound, i.e., this chemical is possibly carcinogenic. In an NTP

carcino

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