Technical Background Document To Support Rulemaking Pursuant To Cercla Section 102 Volume 3 (Proposed Rulemaking) A Report To Releases Control Branch Office Of Research And Development And To Emergency Response Division Office Of Solid Waste And Emer


TECHNICAL BACKGROUND DOCUMENT
TO SUPPORT RULEMAKING
PURSUANT TO CERCLA SECTION 102
VOLUME 3
(PROPOSED RULEMAKING)
A Report to
RELEASES CONTROL BRANCH
OFFICE OF RESEARCH AND DEVELOPMENT
And to
EMERGENCY RESPONSE DIVISION
OFFICE OF SOLID WASTE AND EMERGENCY RESPONSE
U.S. ENVIRONMENTAL PROTECTION AGENCY
Under
Contract No. 68-03-3182
Prepared by
ENVIRONMENTAL MONITORING & SERVICES, INC.
A WHOLLY OWNED SUBSIDIARY OF COMBUSTION ENGINEERING, INC.
CAMARILLO, CALIFORNIA 93010
December 1986

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TECHNICAL BACKGROUND DOCUHENT
TO SUPPORT RULEMAKING
PURSUANT TO CERCLA SECTION 102
VOLUME 3
(PROPOSED RULEMAKING)
A Report to
RELEASES CONTROL BRANCH
OFFICE OF RESEARCH AND DEVELOPMENT
And to
EMERGENCY RESPONSE DIVISION
OFFICE OF SOLID WASTE AND EMERGENCY RESPONSE
U.S. ENVIRONMENTAL PROTECTION AGENCY
Under
Contract No. 68-03-3182
Prepared by
ENVIRONMENTAL MONITORING & SERVICES, INC.
A WHOLLY OWNED SUBSIDIARY OF COMBUSTION ENGINEERING, INC.
CAMARILLO, CALIFORNIA 93010
December 1986

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ii

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FOREWORD
This draft report is being submitted to the Releases Control Branch,
Office of Research and Development, Edison, Nev Jersey, and the Emergency
Response Division of the Office of Emergency and Remedial Response,
Office of Solid Vaste and Emergency Response, of the U.S. Environmental
Protection Agency (EPA). The purpose of this report is to provide the
technical basis for adjusting the statutory reportable quantities (RQs)
of a third group of hazardous substances defined in CERCLA Section
101 (14) for vhich no final adjusted RQs have been promulgated in either
the April 4, 1985 final rule (50 FR 13456-13513) or in the final rule
published on September 29, 1986 (51 FR 34534-34549).
This report was prepared by the technical staff of Environmental
Monitoring and Services, Inc. (EHSI), a wholly owned subsidiary of
Combustion Engineering. Principal authors are Mr. Steven C. Gibson,
Mr. Gregory R. Ricci, Mr. Jeffrey S. Gift, Dr. Bartholomew L. Tuffly,
Mr. Franz J. Burmann, Mr. James M. Conis, Ms. Kathleen Doehrer, and
Ms. tfilraa Seltzer.
The guidance of many members of the EPA staff was provided not only in a
continuous fashion, but also in special working group meetings and by
written and oral comments on the various drafts. The assistance of Dr.
K. Jack Kooyoomjian, Senior Project Officer, Mr. John Riley, Chief,
Response Standards and Criteria Branch, and Ms. Ivette Ortiz, Chemical
Engineer, all of the Emergency Response Division, was especially helpful.
Valuable guidance was also provided by several members of the Agency's
Carcinogen Assessment Group (CAG), including Dr. James Cogliano,
Dr. Aparna Koppikar, Dr. Robert McGaughy, and Dr. Villiam Farland. The
EPA Project Officer is Mr. Richard Field of the Releases Control Branch,
Edison, New Jersey.
iii

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The support and helpful suggestions of Mr. James Janis, Mr. George
Lowden, Mr. James Bunting, Mr. Andrew Siegel, and other staff members of
ICF, Inc., subcontractor to Environmental Monitoring and Services, Inc.,
are acknowledged.
iv

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CONTENTS
PAGE
Foreword			ill
Executive Summary 	ES-1
Section 1. Introduction 	1-1
Background 	1-1
Regulatory Status ofRQ Adjustments 	1-3
Hethod of RQ Adjustment 	1-3
The CERCLA Potential Carcinogens 	1-5
Summary o£ RQ Adjustments	1-6
Organization o£ this Report 	1-8
Section 2. Methodology for Assessment of Potential Carcinogens
and RQ Adjustment 			2-1
General Methodology for RQ Adjustments 	2-1
Primary Criteria 	2-1
Secondary Criteria (BHP) 	2-2
Methodology for Identifying Hazardous
Substances Subject to Assessment for
Potential Carcinogenicity	.	2-3
Methodology for Ranking Potential Carcinogens ..2-5
Veight of Evidence—The Qualitative
Phase 	2-6
Potency Factor—The Quantitative Phase ....2-9
Assignment of Potency Group 		 2-10
Hazard Ranking 	2-10
Sample Hazard Ranking for Chloroform 	2-12
Veight-of-Evidence Determination for
Chloroform 			2-12
Potency Factor Determination for
Chloroform 	2-12
Hazard Ranking of Chloroform	2-14
RQ Assignment Based on Hazard Ranking	2-14
The Three-Tier System for Ranking the
Potential Carcinogens 	2-14
Alternate Methodologies Considered for
Ranking Potential Carcinogens			2-17
Alternate Methodology 1 - Clustering
Potency Factors 	2-18
Alternate Methodology 2 - Clustering
Potency Factors with Adminsitrative
Overlays 	2-19
Alternate Methodology 3 - Ranking Only
Known Human Carcinogens 	2-19
Hazard Ranking Methodology Changes 	2-20
V

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CONTENTS (Continued)
Section 3. Results 	3-1
Results of the Methodology Used to
Identify Potential Carcinogens	3-1
Substances Identified as Potential
Carcinogens and Addressed in the NPRM	3-35
Substances Not Identified as Potential
Carcinogens 			3-35
Adjustment of RQs for the 273 Hazardous
Substances 	3-37
Results of the CAG Ranking Methodology	3-37
RQs for Potential Carcinogens for Vhich
Potency Factors Cannot be Calculated 	3-38
RQs for Organic Arsenic Compounds 	3-39
RQ for 3,3'-Dichlorobenzidine 	3-39
RQsfor Beryllium and Beryllium Salts 	3-40
RQ for PCBs 	3-40
Status of Hazardous Substances Designated
Under the CVA Section 311 	3-43
RQs for F- and K- Hazardous Waste Streams 	3-45
RQs for Unlisted Hazardous Wastes 	3-47
RQ Adjustments Based on BHP 	3-48
Section 4. Data Tables for Hazardous Substances 	4-1
Section 5. Quality Assurance 	5-1
The Chemical Profiles 	5-1
Quality Assurance of the Chemical Profiles	5-2
CAG Review 	5-3
Potency and Hazard Ranking Verification 	5-3
Section 6. References 	6-1
Appendix A. Methodology for Evaluating Potential Carcinogenicity in
Support of Reportable Quantity Adjustments Pursuant to
CERCLA Section 102 	A-l
Appendix B. Evaluation of the Potential Carcinogenicity of
Chloroform in Support of Reportable Quantity
Adjustments Pursuant to CERCLA Section 102 	B-l
Appendix C. Data for Evaluation of Biodegradation, Hydrolysis
and Photolysis (BHP) 	C-l
Appendix D. Derivation of the Multistage Model 		.D-l
Appendix E. A Comparison of Chronic Toxicity and Potential
Carcinogenicity as Primary Criteria 	E-l
Appendix F. Evaluation of the 100-Pound RQ Cap for Potential
Carcinogens Using Air Dispersion Modeling 	F-l
vi

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TABLES
TABLE NO.	PAGE
1-1	Regulatory Status of RQ Adjustments 	1-4
2-1	Bazard Ranking Scheme for Potential
Carcinogens 	.2-11
3-1	List of Hazardous Substances and Reportable
Quantities 	3-2
3-2	Aquatic Toxicity Data for PCBs 	3-42
3-3	List of CERCLA Bioaccumulative Insoluble
Sinkers (BIS) 	3-44
3-4	Final Candidate List for Upward RQ
Adjustments Based on Other Factors (BHP) 	3-49
4-1	Data for the NPRM Hazardous Substances 	.4-3
FIGURES
FIGURE NO.	PAGE
2-1	Illustrative Categorization of Evidence
Based on Animal and Human Data 	2-7
vii

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EXECUTIVE SUMMARY
Sections 103(a) and 103(b) of the Comprehensive Environmental Response,
Compensation, and Liability Act of 1980 (CERCLA), as amended, require
that persons in charge of vessels or facilities from which a hazardous
substance has been released in quantities that are equal to or greater
than its reportable quantity (RQ) immediately notify the National
Response Center of the release. Section 102(b) of CERCLA establishes RQs
for releases of designated hazardous substances at one pound except those
for which RQs were established pursuant to Section 311(b)(4) of the Clean
Water Act (CWA).
Section 102(a) authorizes the Administrator of the U.S. Environmental
Protection Agency (EPA) to adjust RQs for hazardous substances and to
designate as hazardous substances those substances which, when released
into the environment, may present substantial danger to the public health
or welfare or the environment. A final rule published on April 4, 1985
(50 FR 13456) adjusted reportable quantities for 340 hazardous
substances. In a Notice of Proposed Rulemaking (NPRM) also published on
April 4, 1985, the Agency proposed adjusted RQs for 105 additional
hazardous substances (50 FR 13514). A final rule published on September
29, 1986 (51 FR 34534) finalized RQ adjustments for 102 of these 105
hazardous substances.^ Currently there are 717 CERCLA hazardous
substances.
Technical background for the previous adjustment of the statutory RQs of
442 hazardous substances may be found in two documents: "Technical
As noted in that final rule, the Agency decided to retain the
statutory one-pound RQs for lead, pentachloroethane, and methyl
chloride, pending analysis of their potential carcinogenicity.
ES-1

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Background Document to Support Rulemaking Pursuant to CERCLA Section 102,
Volume 1," March 1985 and "Technical Background Document to Support
Rulemaking Pursuant to CERCLA Section 102, Volume 2," August 1986. Both
of these documents are available in the public docket for RQ rulemaking.
This report provides the technical background required for adjusting the
statutory reportable quantities (RQs) for an additional 273 hazardous
substances (including 78 hazardous waste streams) of the remaining 275
hazardous substances designated pursuant to CERCLA, which have not yet
had final adjusted RQs promulgated. The Environmental Protection Agency
(EPA or the "Agency") has identified most of these hazardous substances
as potential carcinogens and analysis of their carcinogenic properties is
complete. This report contains the details of the methodology the Agency
proposes to use to adjust RQs on the basis of potential carcinogenicity.
Most of the 273 hazardous substances have proposed adjusted RQs based on
their potential carcinogenicity.
This report does not address the two remaining hazardous substances (lead
and methyl isocyanate) for which final adjusted RQs have yet to be
promulgated. As noted in the September 29, 1986 final rule (51 FR 34534)
the Agency decided to retain the statutory 1-pound RQ for lead pending
analysis of its potential carcinogenicity. The RQ for lead will be
adjusted in a future rulemaking. As noted in the April 4, 1985 final
rule (50 FR 13456) the Agency decided to retain the statutory 1-pound RQ
for methyl isocyanate (MIC) pending further analysis of its acute
inhalation toxicity characteristics. The RQ for methyl isocyanate may be
adjusted in a future rulemaking.
This technical report also does not address the 1-pound statutory RQ for
2
radionuclides. Radionuclides are hazardous substances under CERCLA
2
Radionuclides are not counted among the 717 CERCLA hazardous substances
because they are listed as a broad, generic category, encompassing
hundreds of separate substances.
ES-2

-------
because they are designated as a hazardous air pollutant under Section
112 of the Clean Air Act (CAA). In the preambles to the May 25, 1983
NPRM and the April 4, 1985 final rule, the Agency recognized that the
statutory RQ of one pound may not be appropriate for radionuclides, but
deferred regulatory action to adjust this RQ until the Agency's analysis
of radionuclides was completed. The statutory 1-pound RQ for
radionuclides is proposed for adjustment in a separate NPRM. The
Agency's preferred methodology for adjusting the statutory 1-pound RQ of
radionuclides is discussed in a draft report entitled "Technical
Background Document to Support Proposed Rulemaking Pursuant to Section
102 of the Comprehensive Environmental Response, Compensation, and
Liability Act: Radionuclides," December 1986.
The Agency's selected RQ adjustment methodology first assigns primary
criteria RQs on the basis of aquatic toxicity, mammalian toxicity (oral,
dermal, and inhalation), ignitability, reactivity, chronic toxicity and
potential carcinogenicity. The primary criteria RQ for each hazardous
substance is the lowest value derived from the applicable primary
criteria. The Agency then evaluates each hazardous substance according
to another set of criteria consisting of biodegradation, hydrolysis, or
photolysis (BHP). The primary criteria RQ is then raised one level if
this analysis indicates that the hazardous substance naturally degrades
by one or more of the BHP processes into less hazardous products when
released into the environment. If the degradation products are more
hazardous than the parent hazardous substance, the RQ is adjusted on the
basis of the degradation products, and an upward adjustment on the basis
of BHP is not made.
SUMMARY OF RQ ADJUSTMENTS
The table belov summarizes the proposed RQ adjustments for the 273
hazardous substances for which technical background is provided in this
draft report. The number of hazardous substances is given for each of the
five RQ categories. The proposed RQs lower the statutory RQs of 56
ES-3

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hazardous substances, raise the statutory RQs of 123 hazardous
substances, and leave the statutory RQs of 94 hazardous substances
unchanged.
3
No. of Hazardous Substances With Specified RQs
RQ (Pounds)	Statutory RQ	Proposed RQ
1	212	124
10	12	105
100	6	41
1000	25	1
5000	JL8	2
Total:	273	273
3
This summary of proposed RQ adjustments does not include the 1-pound
statutory RQs for lead or methyl isocyanate (MIC) since these hazardous
substances are being further assessed for their toxicity
characteristics.
ES-4

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SECTION 1
INTRODUCTION
BACKGROUND
Sections 103(a) and 103(b) of the Comprehensive Environmental Response,
Compensation, and Liability Act of 1980 (CERCLA), as amended, require
that persons in charge of vessels or facilities from which a hazardous
substance has been released in quantities that are equal to or greater
than its reportable quantity (RQ) immediately notify the National
Response Center of the release. Section 102(b) of CERCLA establishes RQs
for releases of designated hazardous substances at one pound except those
for which RQs were established pursuant to Section 311(b)(4) of the Clean
Water Act (CVA).
Section 102(a) authorizes the Administrator of the U.S. Environmental
Protection Agency (EPA) to adjust RQs for hazardous substances and to
designate as hazardous substances those substances which, when released
into the environment, may present substantial danger to the public health
or welfare or the environment. A final rule published on April 4, 1985
(50 FR 13456) adjusted reportable quantities for 340 hazardous
substances. In a Notice of Proposed Rulemaking (NPRM) also published on
April 4, 1985, the Agency proposed adjusted RQs for 105 additional
hazardous substances (50 FR 13514). A final rule published on September
29, 1986 (51 FR 34534) finalized RQ adjustments for 102 of these 105
4
hazardous substances. Currently there are 717 CERCLA hazardous
As noted in that final rule, the Agency decided to retain the
statutory 1-pound RQs for lead, pentachloroethane, and methyl chloride,
pending analysis of their potential carcinogenicity. The RQs for
methyl chloride and pentachloroethane are reproposed for adjustment in
the rulemaking which this technical background document supports.
1-1

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substances.^
Technical background for the previous adjustment of the statutory RQs of
442 hazardous substances may be found in tvo documents: "Technical
Background Document to Support Rulemaking Pursuant to CERCLA Section 102,
Volume 1," March 1985 and "Technical Background Document to Support
Rulemaking Pursuant to CERCLA Section 102, Volume 2," August 1986. Both
of these documents are available in the public docket for RQ rulemaking.
This report provides the technical background required for adjusting the
statutory reportable quantities (RQs) for an additional 273 hazardous
substances (including 78 hazardous waste streams) of the remaining 275
hazardous substances designated pursuant to CERCLA, which have not yet
had final adjusted RQs promulgated. The Environmental Protection Agency
(EPA or the "Agency") has identified most of these hazardous substances
as potential carcinogens and analysis of their carcinogenic properties is
complete. This report contains the details of the methodology the Agency
proposes to use to adjust RQs on the basis of potential carcinogenicity.
Most of the 273 hazardous substances have proposed adjusted RQs based on
their potential carcinogenicity.
This report does not address the two remaining hazardous substances (lead
and methyl isocyanate) for which final adjusted RQs have yet to be
promulgated. As noted in the September 29, 1986 final rule (51 FR 34534)
the Agency decided to retain the statutory 1-pound RQ for lead pending
analysis of its potential carcinogenicity. The RQ for lead will be
adjusted in a future rulemaking. As noted in the April 4, 1985 final
rule (50 FR 13456) the Agency decided to retain the statutory one-pound
^ Since the April 4, 1985 final rule, 19 additional hazardous substances
have been listed under section 101(14): waste streams F020, F021, F022,
F023, F026, F027, and F028 under section 3001 of RCRA (50 FR 1978);
waste streams Kill, K112, K113, K114, K115, and K116 under section 3001
of RCRA (50 FR 42936); o-toluidine and p-toluidine under section 3001
of RCRA (50 FR 42936); waste streams K117, K118, and K136 under section
3001 of RCRAT51 FR 5327); and 2-ethoxyethanol under section 3001 of
RCRA (51 FR 6537).
1-2

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RQ for methyl isocyanate (MIC) pending further analysis of its acute
toxicity characteristics. The RQ for methyl isocyanate may be adjusted
in a future rulemaking.
This technical report also does not address the 1-pound statutory RQ for
radionuclides.^ Radionuclides are hazardous substances under CERCLA
because they are designated as a hazardous air pollutant under Section
112 of the Clean Air Act (CAA). In the preambles to the May 25, 1983
NPRM and the April 4, 1985 final rule, the Agency recognized that the
statutory RQ of one pound may not be appropriate for radionuclides, but
deferred regulatory action to adjust this RQ until the Agency's analysis
of radionuclides vas completed. The statutory 1-pound RQ for
radionuclides is proposed for adjustment in a separate NPRM. The
Agency's preferred methodology for adjusting the statutory 1-pound RQ of
radionuclides is discussed in a draft report entitled "Technical
Background Document to Support Proposed Rulemaking Pursuant to Section
102 of the Comprehensive Environmental Response, Compensation, and
Liability Act: Radionuclides," December 1986.
Regulatory Status of RQ Adjustments
Table 1-1 summarizes the regulatory status of the 717 CERCLA hazardous
substances currently designated pursuant to CERCLA Section 101(14)
relative to the adjustment of their statutory RQs.
Method of RQ Adjustment
RQs are adjusted using a methodology that assigns primary criteria RQ
values based on the following intrinsic properties of each hazardous
substance: aquatic toxicity, mammalian toxicity (oral, dermal, and
Radionuclides are not counted among the 717 CERCLA hazardous
substances because they are listed as a broad, generic category
encompassing hundreds of separate substances.
1-3

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Table 1-1
BEGULATOBY STATUS OF BQ ADJUSTMENTS
Ho. of CEBCLA Hazardous
No. of CEBCLA Hazardous	Ho. of CEBCLA Hazardous	Substances Addressed in this
Substances with Final Adjusted Substances with Final Adjusted Technical Background Document
BQs Promulgated on April 4, 1985 BQs Promulgated on Sept. 29, 1986 Proposed	Statutory
(SO FB 13456-13513)	(51 PB 34534-34549)"	Adjusted BQs	BQS	Total
Individual CEBCLA
Hazardous Substances
319
95
19 S
611
CEBCLA Hazardous
Substances that are P-
and K-Waste Streaas
Designated Pursuant to
Section 3001 of BCBA
21
78
106
TOTAL:
340*
102
273	2
= 275
717"
a BQ adjustaents for these hazardous substances were proposed in an NPBM published on April 4, 1985 (50 FB 13514-13522).
b The technical background which supports the final adjusted BQs for these CEBCLA hazardous substances is contained in:
Technical Background Document to Support Bulenaking Pursuant to CEBCLA Section 102, Volume 1, March 1985.
c The technical background which supports the final adjusted BQs for these CEBCLA hazardous substances is contained in:
"Technical Background Document to Support Bulemaking Pursuant to CEBCLA Section 102, Volume 2, August, 1986." Since
publication of the HPBH lead metal will retain its statutory 1-pound BQ until adjusted in a future rulemaking, and the
adjusted BQs for methyl chloride and pentachloroethane are proposed in the rulemaking which this technical background
document supports.
d Includes the seven dioxin-contaiaing waste streams (F020, F021, F022, F023, F026, F027, and F028) added to the list of
BCBA hazardous wastes on January 14, 1985 (50 FB 1978-2006), siz waste streams (Kill, K112, K113, K114, K115, and K116)
added to the list of BCBA hazardous wastes on October 23, 1985 (50 FB 42936-42943), and three waste streaas (K117, K118
and K136) added to the list of BCEA wastes on February 13, 1986 (51 FB 5327-5331).
• Methyl isocyanate (MIC) and lead aetal.
f Total number of CEBCLA hazardous substances designated pursuant to CEBCLA Section 101(14) to date, excluding the generi
listing of radionuclides which is the subject of a separate rulemaking.

-------
inhalation), ignitability, reactivity, chronic toxicity, and potential
carcinogenicity. The primary criteria RQ for each hazardous substance is
the lowest value derived from the applicable primary criteria. The
Agency then evaluates each hazardous substance according to another set
of criteria consisting of the natural degradative processes of
biodegradation, hydrolysis, or photolysis (BHP). The primary criteria RQ
is then raised one level if this analysis indicates that the hazardous
substance naturally degrades by one or more of the BHP processes into
less hazardous products when released into the environment. However, if a
hazardous substance is found to be bioaccumulative, environmentally
persistent, highly reactive or degradable to more hazardous products, it
is not eligible for a one-level RQ increase on the basis of BHP. If
degradation of a hazardous substance produces a more hazardous product,
not only is an upward BHP adjustment not made, but the RQ adjustment is
based on the more hazardous product rather than on the less hazardous
parent substance, and the RQ lowered.
The CERCLA Potential Carcinogens
Prior to publication of the May 25, 1983 NPRM leading to the promulgation
of a final rule for adjusting the RQs of 340 hazardous substances (50 FR
13456, April 4, 1985), the Agency identified a large number of CERCLA
hazardous substances as potential carcinogens. The methodology used by
the Agency for identifying potential carcinogens was described in the May
25, 1983, NPRM and in the document "Technical Background Document to
Support the Notice of Proposed Rulemaking Pursuant to CERCLA Section
102(b)," May 1983, which was included as part of the public docket.
Briefly, the methodology for identifying potential carcinogens from among
the CERCLA hazardous substances consists of reviewing four sources of
human epidemiologic and/or animal bioassay data on hazardous substances
that suggest possible carcinogenic effect. These sources are: (1) the
Annual Reports on Carcinogens of the National Toxicology Program, U.S.
Department of Health and Human Services (DHHS); (2) the Monographs of the
1-5

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International Agency for Research on Cancer (IARC); (3) final Agency
determinations published in the Federal Register identifying substances
as potential carcinogens; and (4) ongoing determinations by the Agency's
Office of Health and Environmental Assessment that substances may be
potential carcinogens, based on either published or unpublished data. The
Agency compared the list of substances derived from these four sources
with the list of the 717 CERCLA hazardous substances to determine which
hazardous substances should be evaluated for potential carcinogenicity.
In its evaluation of CERCLA hazardous substances that were identified as
potential carcinogens, the Agency initially employed a ranking
methodology that used a veight-of-evidence evaluation scheme developed by
the IARC. EPA subsequently developed its own veight-of-evidence scheme,
which the Agency used in conjunction with potency factors, to obtain
hazard rankings for CERCLA hazardous substances that are potential
carcinogens. The new methodology is summarized in the EPA's Carcinogen
Assessment Group (CAG) report entitled "Methodology for Evaluating
Potential Carcinogenicity in Support of Reportable Quantity Adjustments
Pursuant to CERCLA Section 102," 0HEA-C-073, December, 1986. This report
is reproduced here as Appendix A. The methodology is also described in
this technical background document.
The EPA decided to use its own veight-of-evidence scheme because it
refines the IARC approach and has had extensive peer review, both within
and outside the Agency. The methodology was presented in the Federal
Register on November 23, 1984 in a notice entitled "Proposed Guidelines
for Carcinogen Risk Assessment" (49 FR 46294-46301). The guidelines were
finalized on September 24, 1986 (51 FR 33992-34003).
SUMMARY OF RQ ADJUSTMENTS
The table belov summarizes the proposed RQ adjustments for the 273
hazardous substances for which technical background is provided in this
1-6

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draft report. The number of hazardous substances is given for each of the
five RQ categories. The proposed RQs lover the statutory RQs of 56
hazardous substances, raise the statutory RQs of 123 hazardous
substances, and leave the statutory RQs of 94 hazardous substances
unchanged.
No. of Hazardous Substances With Specified RQs^
RQ (Pounds)	Statutory RQ	Proposed RQ
1	212	124
10	12	105
100	6	41
1000	25	1
5000	_18	2
Total	273	273
There are 195 individual hazardous substances that are having their
statutory RQs proposed for adjustment in the NPRM which this technical
background document supports. Ninety of these hazardous substances have
been evaluated for chronic toxicity by the Environmental Criteria and
Assessment Office (ECA0) in Cincinnati, Ohio, a branch of the EPA's
Office of Health and Environmental Assessment (0HEA). In addition, 191
of these hazardous substances have been evaluated for potential
carcinogenicity by the EPA's CAG, which is also a part of 0HEA. The 195
This summary of proposed RQ adjustments does not include the
1-pound statutory RQs for lead or methyl isocyanate (MIC) since these
hazardous substances are being further assessed for their toxicity
characteristics.
1-7

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individual hazardous substances which were evaluated by ECAO and CAG are
identified in Table 4-1 of Section 4 in the column labelled "Chronic
Toxicity/Carcinogen," along with the results of each evaluation. The
results of the CAG's evaluation show that 184 of the 191 individual
hazardous substances were able to be ranked as potential carcinogens
using the Agency's ranking methodology. Most of these have been assigned
RQ values based on potential carcinogenicity. However, in some cases,
another primary criterion (i.e., aquatic toxicity, mammalian toxicity,
chronic toxicity, ignitability, or reactivity) results in assignment of a
lover RQ to the hazardous substance than would have resulted from the
potential carcinogenicity ranking. The basis for the proposed adjusted
RQs of the 195 individual hazardous substances is as follows: 136 on the
basis of potential carcinogenicity alone, 22 on the basis of potential
carcinogenicity and at least one other primary criterion, 31 on the basis
of primary criteria other than potential carcinogenicity, and 6 on the
basis of BHP.
ORGANIZATION OF THIS REPORT
Section 2 of this report contains a discussion of the scientific and
technical methodology used for adjusting the statutory RQs of the CERCLA
hazardous substances. In addition, Section 2 contains a discussion of
the methodology used by CAG to identify and rank potential carcinogens.
It also contains a discussion of the alternative methods the Agency has
considered for ranking potential carcinogens and a discussion of the
differences between chronic toxicity and potential carcinogenicity as
primary RQ adjustment criteria.
Section 3 presents the results of applying the primary and secondary RQ
adjustment criteria, including the primary criterion of potential
carcinogenicity, to the CERCLA hazardous substances addressed in this
report. Table 3-1 includes the list of the 275 hazardous substances
("List of Hazardous Substances and Reportable Quantities"), their
regulatory synonyms, their statutory RQs and proposed adjusted RQs for
273 of them.
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Section 4 provides the data which support the proposed adjusted RQs
presented in Table 3-10. Section 5 describes the Agency's quality
assurance program for ensuring the validity of the data associated with
the potential carcinogens. Appendix A contains a report prepared by the
Agency's CAG entitled "Methodology for Evaluating Potential
Carcinogenicity in Support of Reportable Quantity Adjustments Pursuant to
CERCLA Section 102", 0HEA-C-073, December 1986, which provides a complete
description of the ranking methodology for potential carcinogens.
Appendix A also contains a summary table of the hazard rankings developed
for the 191 potential carcinogens. In the CAG report (Appendix A),
reference is made to the chemical profiles which describe the derivation
of the hazard rankings assigned to the potential carcinogens. These
chemical profiles are a part of the CAG report, but they are not included
here for the sake of brevity. The chemical profiles for each potential
carcinogen can be found in the public docket. For illustrative purposes,
Appendix B contains a sample chemical profile for the hazardous substance
chloroform. Appendix C, entitled "Data for Evaluation of Biodegradation,
Hydrolysis, and Photolysis (BHP)," contains the data used for RQ
adjustment based on the secondary criteria. Appendix D provides a
derivation of the multistage model that is used to calculate potency
factors for the CERCLA potential carcinogens. Appendix E provides a
discussion of the differences between chronic toxicity and potential
carcinogenicity as primary RQ adjustment criteria. Finally, Appendix F
provides a description of the air dispersion model the Agency used, in
part, to determine the appropriate RQ levels to assign potential
carcinogens.
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SECTION 2
METHODOLOGY FOR ASSESSMENT OF POTENTIAL CARCINOGENS AND RQ ADJUSTMENT
This section describes the methodology the Agency uses to adjust the
statutory RQs of the CERCLA hazardous substances and the methodology the
Agency is proposing to use for identifying and ranking CERCLA hazardous
substances for potential carcinogenicity. The general methodology used
for adjusting RQs has been discussed in detail in the report "Technical
Background Document to Support Rulemaking Pursuant to CERCLA Section 102,
Volume 1," March 1985, and is summarized in the paragraphs that follow.
Also included in this section is a description of a sample hazard ranking
for the hazardous substance chloroform, the Agency's rationale for using
a three-tier instead of a five-tier system for ranking the potential
carcinogens, and a brief discussion of the alternate methodologies that
were considered but rejected for ranking the potential carcinogens.
GENERAL METHODOLOGY FOR RQ ADJUSTMENT
Primary Criteria
The RQ adjustment methodology is one with which the regulated community
is familiar and is based, in part, on the methodology used to establish
RQs pursuant to Section 311 of the Clean Water Act (CVA). The
methodology begins with an evaluation of six intrinsic physical,
chemical, and toxicological properties associated with each hazardous
substance. The intrinsic properties evaluated, called primary criteria,
are: aquatic toxicity, mammalian toxicity (oral, dermal, and inhalation),
ignitability, reactivity, chronic toxicity, and potential
carcinogenicity.
The Agency ranks each intrinsic property, except potential
carcinogenicity, on a five-tier scale, associating a specific range of
values on each scale with a particular RQ value. This five-tier scale
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uses the five RQ levels of 1, 10, 100, 1000, and 5000 pounds, which were
originally established pursuant to Section 311 of the CWA (see AO CFR
Part 117 and 44 FR 50766). For hazardous substances evaluated for
potential carcinogenicity, each substance is assigned a hazard ranking of
"high," "medium," or "low." These hazard rankings correspond with RQ
levels of 1, 10 and 100 pounds, respectively. Each hazardous substance
receives several tentative RQ values based on its particular
O
properties. The lowest of all of the tentative RQs becomes the
primary criteria RQ for that hazardous substance. For example, if a
substance is evaluated for aquatic toxicity and mammalian toxicity, and
RQs of 100 pounds and 1000 pounds are set for aquatic toxicity and
mammalian toxicity, respectively, the 100-pound value will be the
applicable primary criteria RQ. Thus, the overall methodology for
adjusting RQs consists of associating the intrinsic properties of the
hazardous substances with the RQ levels and selecting the lowest level to
arrive at the primary criteria RQ.
Secondary Criteria (BHP)
Upon completion of the evaluation and the establishment of a primary
criteria RQ, other factors may then be applied. The other factors are
the natural degradative processes of biodegradation, hydrolysis, and
photolysis (BHP). The rationale for applying BHP is that certain
hazardous substances, when released into the environment, may quickly
degrade through one or more of these processes into less hazardous or
innocuous products. If such is determined to be the case, the applicable
g
If available evidence shows that a substance undergoes biodegradation,
hydrolysis, or photolysis to form a more hazardous reaction product,
the primary criteria are applied to the more hazardous product rather
than to the original substance to determine the tentative RQ values for
the original substance. For example, substances known to generate
hydrofluoric acid, hydrogen sulfide, or phosphine upon hydrolysis are
assigned primary criteria RQs on the basis of these more hazardous
degradation products.
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primary criteria RQ is subsequently adjusted upward one RQ level. This
adjustment reflects the Agency's judgment that the danger posed by the
release of certain hazardous substances may be reduced by these
degradative processes. The upward adjustment for potential carcinogens
is restricted, however, such that if a potential carcinogen's primary
criteria RQ is 100 pounds, it cannot be raised to 1000 pounds. A
100-pound maximum RQ value is maintained for all potential carcinogens.
If a hazardous substance is found to be bioaccumulative, environmentally
persistent, highly reactive or degradable to more hazardous products, it
is not eligible for a one-level RQ increase on the basis of BHP. If
degradation of a hazardous substance produces a more hazardous product,
not only is upward BHP adjustment not made, but the RQ adjustment is
based on the product rather than on the less hazardous parent substance,
and the RQ could be lowered.
METHODOLOGY FOR IDENTIFYING HAZARDOUS SUBSTANCES SUBJECT TO ASSESSMENT
FOR POTENTIAL CARCINOGENICITY
In order to identify those CERCLA hazardous substances that may be
potential carcinogens, EPA reviewed four sources of human epidemiologic
and/or animal bioassay data (as of November 1986) on hazardous substances
that suggest possible carcinogenic effect. These sources are:
1. The Annual Reports on Carcinogens of the National Toxicology
Program, U.S. Department of Health and Human Services (DHHS):
o "First Annual Report on Carcinogens." This report was issued
in July 1980 by the Department of Health and Human Services
(DHHS). It was prepared by the National Toxicology Program,
U.S. Public Health Services. It lists 26 substances, classes
of substances, processes, and byproducts which "have been
reviewed by panels of international experts and initially
found to be associated with the induction of cancer in man."
This report was mandated under an amendment to Section
301(b)(4) of the Public Health Service Act, Public Law 96-622,
signed November 8, 1978.
o "Second Annual Report on Carcinogens." This report (December
1981) was also issued by DHHS as required by the Public Health
Service Act (see above). It lists 88 substances, classes of
substances, processes, and byproducts which are "known human
carcinogens and substances which may reasonably be anticipated
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to cause cancer in humans." All but one of the substances
listed in the First Annual Report vere repeated in this Second
Report. (The one substance dropped, chloroamphenicol, is not
on the CERCLA Section 101(14) list.)
o "Third Annual Report on Carcinogens" Summary. NTP 82-830.
This report (September 1983) is the third in the series by the
DHHS, as required by the Public Health Services Act. It lists
28 substances not identified in the two prior reports, which
are "known carcinogens" or "which may reasonably be anticipat-
ed to be carcinogens."
o "Fourth Annual Report on Carcinogens" Summary. NTP 85-002.
This report (1985) is the fourth in the series by the DHHS, as
required by the Public Health Services Act. It lists 32
substances not identified in the three previous reports, which
are "known carcinogens" or "which may reasonably be
anticipated to be carcinogens."
2.	The Monographs of the International Agency for Research on Cancer
(IARC):
o "Monographs Supplement 1. Chemicals and Industrial Processes
Associated with Cancer in Humans." This report was issued
September, 1979 by the International Agency for Research on
Cancer (IARC). It encompasses the results of a special working
group established to re-evaluate all prior IARC assessments to
determine where studies identifying carcinogens met IARC's
newer evaluation criteria. The report lists 142 substances
and classes of substances for which there is "sufficient
evidence of carcinogenicity in experimental animals."
o "Monographs Supplement 4. Chemicals, Industrial Processes and
Industries Associated with Cancer in Humans." This report was
issued in 1982 by the IARC and is essentially an updated
version of Monographs Supplement 1. This report lists 175
substances and classes of substances for which there is
"sufficient evidence of carcinogenicity in experimental
animals." It further evaluates the risk to humans for a total
of 154 chemicals, processes or industries.
3.	Final Agency determinations published in the Federal Register
identifying substances as potential carcinogens; and
4. Ongoing determinations by the Agency's Office of Health and
Environmental Assessment that substances may be potential
carcinogens, based on either published or unpublished data.
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The above lists were compared with the list of 717 CERCLA hazardous
substances to determine which hazardous substances should be evaluated
for potential carcinogenicity.
Sources 3 and 4 listed above have recently been added to supplement the
Agency's screening criteria for identifying potential carcinogens. The
Agency is currently in the process of screening for potential
carcinogenicity the hazardous substances that received adjusted RQs in
the April 4, 1985 final rule and the September 29, 1986 final rule. Any
hazardous substance identified as a potential carcinogen will receive a
hazard ranking as a result of this review for potential carcinogenicity,
as described below, and, if appropriate, may have its RQ readjusted on
that basis in a future rulemaking.
METHODOLOGY FOR RANKING POTENTIAL CARCINOGENS
The Agency's Carcinogen Assessment Group (CAG) has developed a unique
method for ranking CERCLA hazardous substances on the basis of their
potential carcinogenicity. The methodology is neither a risk assessment
nor an absolute measure of harm. It is simply a method for sorting a
list of potentially carcinogenic substances into levels of relative
potential carcinogenicity, which may then be equated to RQ levels for
notification purposes. Once notification is made, the federal On-Scene
Coordinator (OSC) vill perform a risk assessment and assess the need for
a federal response to the release.
The Agency's ranking procedure examines all information available in the
scientific literature on known and potential human carcinogens, and
applies this information in a two-phase process. The first phase is
qualitative, wherein the reliability of the available data is evaluated
through use of the CAG classification system for weight of evidence, as
presented in the Agency's Guidelines for Carcinogen Risk Assessment (51
FR 33992, September 24, 1986). The second phase is quantitative, and is
designed to determine how potent a potential carcinogen may be. This
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second phase allows potential carcinogens to be compared on a numerical
basis by identifying those hazardous substances inducing cancer at the
lowest doses (i.e., the most potent substances). These two factors are
then combined to form a final hazard ranking for each CERCLA hazardous
substance that was evaluated. A detailed description of the CAG
methodology is given in Appendix A. The following is a brief description
of the methodology.
Weight of Evidence—The Qualitative Phase
In order to evaluate the quality and reliability of the available data
during the qualitative phase, the Agency evaluates data from human
epidemiology studies and from experimental animal bioassay and in vitro
studies to arrive at a weight of evidence to determine the probability of
a substance being a potential human carcinogen. The guidelines used for
the weight of evidence follow the Guidelines for Carcinogen Risk
Assessment (51 FR 33992) published on September 24, 1986. This
procedure determines the quality of the human and animal data. Using
these data, the substance is classified into one of six groups (A, Bl,
B2, C, D, or E) as shown in Figure 2-1, and described below.
Group A: Carcinogenic to Humans—
This group is used only when there is "sufficient" evidence from
epidemiologic studies to support a causal association between exposure to
the agent(s) and cancer. (See Appendix A for definitions of the terms
"sufficient," "limited," "inadequate," "no data," and "no evidence.")
Group B: Probably Carcinogenic to Humans—
This group includes agents for which the weight of evidence of human
carcinogenicity, based on epidemiologic studies, is limited and also
includes agents for which the weight of evidence of carcinogenicity,
based on animal studies, is sufficient. The group is divided into two
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Figure 2-1
ILLUSTRATIVE'CATEGORIZATION OF EVIDENCE BASED ON ANIMAL AND HUMAN DATA 9
Human
Evidence
Animal Evidence
No No
Sufficient Limited Inadequate Data Evidence
Sufficient
A
A
A
A
A
Limited
B1
B1
B1
B1
B1
Inadequate
B2
C
D
D
D
No Data
B2
C
D
D
E
No Evidence
B2
C
D
D
E
9
The above assignments are presented £or illustrative purposes. There
may be instances in the classification of both animal and human data
indicating that different categorizations than those given in the table
should be assigned. Furthermore, these assignments are tentative and may
be modified by ancillary evidence. In this regard all relevant
information should be evaluated to determine if the designation of the
overall weight of evidence needs to be modified. Relevant factors to be
included along with the tumor data from human and animal studies include
structure-activity relationships, short-term test findings, results of
appropriate physiological, biochemical and toxicological observations,
and comparative metabolism and pharmacokinetic studies. The nature of
these findings may cause an adjustment of the overall categorization of
the weight of evidence.
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subgroups, B1 and B2. Group B1 is usually reserved for agents for which
there is limited evidence of carcinogencity from epidemiologic studies.
It is reasonable, for practical purposes, to regard an agent for which
there is sufficient evidence of carcinogenicity in animals as if it
presented a carcinogenic risk to humans. Therefore, agents for which
there is sufficient evidence from animal studies and for which there are
inadequate evidence or no data from epidemiologic studies would usually
be categorized under Group B2.
Group C: Possibly Carcinogenic to Humans—
This group is used for agents with limited evidence of carcinogenicity in
animals in the absence of human data. It includes a wide variety of
evidence such as: (a) a malignant tumor response in a single
well-conducted experiment that does not meet conditions for sufficient
evidence; (b) tumor responses of marginal statistical significance in
studies having inadequate design or reporting; (c) benign but not
malignant tumors with an agent showing no response in a variety of
short-term tests for mutagenicity; and (d) responses of marginal
statistical significance in a tissue known to have a high or variable
background rate.
Group D: Not Classifiable as to Human Carcinogenicity—
This group is generally used for agents with inadequate human and animal
evidence of carcinogenicity or for which no data are available.
Group E: Evidence of Non-Carcinogenicity for Humans—
This group is used for agents that show no evidence for carcinogenicity
in at least two adequate animal tests in different species or in both
adequate epidemiologic and animal studies. The designation of an agent
as being in Group E is based on the available evidence and should not be
interpreted as a definitive conclusion that the agent will not be a
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carcinogen under any circumstance. Group D and E substances are not
considered to be "potential carcinogens" for purposes o£ the proposed
rulemaking which this technical background document supports. For
purposes of this proposed rule, the term "potential carcinogens" refers
to all hazardous substances assigned to Group A, B, or C under the
Agency's weight of evidence methodology. Hazardous substances ranked in
Group D and E depend on other primary criteria for RQ adjustment.
Potency Factor— The Quantitative Phase
In the quantitative phase, in order to compare carcinogenic potencies,
the Agency's linearized multistage model is fit to the dose-response
data. The point on this extrapolated line associated with a lifetime
cancer risk of 10% is then determined, and the estimated dose (ED^q) at
this point is used to calculate a potency factor "F" where F = 1/ED^q.
The units of ED^q are mg/kg/day. Appendix D describes the mathematics
involved in this determination in more detail.
It should be understood that the calculation results in a numerical value
to be used only for ranking a hazardous substance for purposes of
determining RQs. The use of a 10% lifetime risk has the advantage of
being within the experimental range and does not require additional
extrapolation to estimate carcinogenic responses at low environmental
levels.
Whenever there is usable information on the absorption, distribution,
metabolism, or excretion of the hazardous substance, the potency factor
is adjusted to reflect this information. For example, if the effective
dose to the target organ in an animal, due to any of these four factors,
is known to be a fraction of the administered dose, then the effective
dose is used to estimate the potency factor. However, in the absence of
information on differences in absorption, distribution, metabolism or
excretion between animals and humans, no such adjustments are made.
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Assignment of Potency Group
Based on its calculated potency factor, each potential carcinogen is
ranked and classified into one of three potency groups (Group 1, 2, or 3)
as shovn below:
Those potential carcinogens with relatively high potencies are classified
in Group 1, while other potential carcinogens with medium and low
potencies are placed into Groups 2 and 3, respectively.
Hazard Ranking
The final step in the ranking procedure is to combine both the
qualitative weight-of-evidence group and the quantitative potency group
factors into a matrix to yield a relative hazard ranking for each
substance. The three relative ranking groups are identified as "high,"
"medium," or "low," and are determined as shown in Table 2-1. Depending
on whether a substance falls into Potency Groups 1, 2, or 3, a respective
hazard ranking of high, medium, or "low" is assigned to Group B
carcinogens. Hazard rankings are one level higher ( high, high, or
medium respectively) for Group A carcinogens. This increased concern is
justified because there is direct human evidence that Group A substances
Potency Group
Potency Factor Range
1
2
3
F > 100
F = 1 to 100
F < 1
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Table 2-1
HAZARD RANKING SCHEME FOR POTENTIAL CARCINOGENS
Potency Group
Weight-of-Evidence
Group	
F > 100
1-100
3
F < 1
A
B
Carcinogenic to Humans
Probablg Carcinogenic to
Humans
Possibly Carcinogenic to
Humans
Not Classifiable as to
Human Carcinogenicity
Evidence of Noncarcino-
genicity for Humans
High
High
Medium
High
Medium
Low
No hazard ranking.
No hazard ranking.
Medium
Low
Low
10
Includes veight-of-evidence groups Bj and B^-
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cause cancer. Hazard rankings are one level lower (medium, low, or low
respectively) for Group C carcinogens. This reduced concern is justified
because the evidence implicating Group C substances either is
unreplicated or is of marginal biological or statistical significance.
SAMPLE HAZARD RANKING FOR CHLOROFORM
The following example shows how the hazard ranking for chloroform was
derived. The complete set of data on chloroform is contained in Appendix
B.
Veight-of-Evidence Determination for Chloroform
The document entitled "Evaluation of the Potential Carcinogenicity of
Chloroform in Support of Reportable Quantity Adjustments Pursuant to
CERCLA Section 102" (a copy of which is provided in Appendix B)
summarizes the animal studies which provide sufficient evidence that
chloroform causes cancer in animals. These studies indicate that cancers
develop in rats and mice when they are given chloroform orally. The
review also describes why human studies provide inadequate evidence that
chloroform causes cancer in humans. Based on the cited data of
sufficient animal and inadequate human evidence, chloroform is classified
as weight-of-evidence Group B2 (see Figure 2-1).
Potency Factor Determination for Chloroform
The experimental doses of chloroform were given only 5 days per week
during the study and were administered for only 546 days, while the study
lasted for 650 days. Thus, the experimental doses must be corrected to
normalize the discontinuous dose to the daily dose by multiplying them by
^ j!|yg and 65Q jays' ^his gives the transformed doses, which are
reproduced below, along with the associated tumor responses:
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Experimental
Animal Dose
(mg/kg/day)
Transformed Dose
(mg/kg/day)
Tumor Response
(Animals with Tumors/
Total Animals)
0
0.0
0/20
238
143
36/45
477
288
39/41
Equation 3 of Appendix D, repeated belov, provides the basis for
estimating the potency factor, l/ED^:
2	k
A(d)= 1-exp [-(q^d +	)] , where
A(d) represents the extra risk over background at a dose rate d. The
GLOBAL 82 computer program described in Appendix D uses the above dose
response data to solve this equation for the q coefficients (Crump,
1982):
qa = 0.10866 x 10"1
q2 = 0.0
Using these coefficients^ the dose (d), which corresponds to an
additional risk level of A(d) = 0.1, is 9.6276 (mg/kg/day). This can be
verified by substituting the above values for q and d in Eq.(3) from
Appendix 0, as shovn above. Thus,
A(d) = 1 - exp [-0.10866 x 10"1 x 9.6276]
= 1 - exp [-0.10461]
= 0.1
Only one coefficent, q^, is derived for two data points. More data
points vould allow for the computation of more coefficients (q«>
q^> etc.) to fit the model to the data.
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Because d in this case is equivalent to the ED^q,	the animal	potency
factor is the reciprocal of this dose: F	= 1/9.6276	= 0.104
(mg/kg/d)~*. The human potency factor is	calculated	as 1.97
(mg/kg/d)~* by correcting for life span and weight	differences	between
rats and humans, as described in Appendix A.
A potency factor of 1.97 places chloroform into Potency Group 2, since it
lies between 1 and 100 which defines the range of potency factors for
Potency Group 2.
Hazard Ranking of Chloroform
Table 2-1 shows that combining the veight-of-evidence Group B2 of
chloroform with its Potency Group 2 produces a hazard ranking of
medium.
RQ ASSIGNMENT BASED ON HAZARD RANKING
It should be noted that the CAG's carcinogen ranking scheme does not in
itself yield an RQ. Rather, it ranks a hazardous substance's
carcinogenic potential as high, medium, or low. RQ levels have been
assigned to these three relative rankings as follows:
Hazard Rank	RQ (Pounds)
High	1
Medium	10
Low	100
1000
5000
THE THREE-TIER SYSTEM FOR RANKING THE POTENTIAL CARCINOGENS
In deciding whether to use five or fewer levels for assigning adjusted
RQs to potential carcinogens, the Agency has examined the special
properties associated with these substances, used an Agency air
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dispersion model to analyze the risks posed by their release, and
evaluated them in light of the Agency's chronic toxicity methodology. The
Agency decided not to use the two highest RQ levels for potential
carcinogens for several reasons. First, cancer can be considered to be a
chronic health effect. EPA therefore believes that reference to the
Agency's chronic toxicity methodology is appropriate in assigning RQs to
potential carcinogens. (See Appendix E for a comparison of chronic
toxicity and potential carcinogenicity as primary RQ adjustment
criteria.) Under the chronic toxicity methodology, each substance is
assigned two rating values, one based on the dose that causes a
particular effect, and the other based on the nature and severity of the
toxic effect. The dose ratings range from 1 to 10, with 10 representing
the most toxic substances. The effect rating values also range from 1 to
10, with 10 representing the most severe effect. The product of the dose
and effect ratings for each substance yields a composite ranking score
between 1 and 100. (See "Technical Background Document to Support
Rulemaking Pursuant to CERCLA Section 102, Volume 1", March 1985, for
details of the methodology for adjusting RQs based on chronic toxicity.
This report is available for inspection at Room LG, U.S. Environmental
Protection Agency, 401 H. Street, S.V., Washington D.C. 20460). Because
cancer is a life-threatening or life-shortening effect, the effect rating
for cancer would be 10 if cancer were ranked on the chronic toxicity
scale. Therefore, the composite score for any potential carcinogen would
be at least 10. A composite score of 10 corresponds to an RQ of 1000
pounds. Thus, a 5000-pound RQ for a potential carcinogen would be
inappropriate based on the Agency's chronic toxicity scale. The Agency
therefore has decided not to assign a 5000-pound RQ to potential
carcinogens.
In addition, application of an air dispersion model developed by the
Agency shows that substantial cancer risks can result from releases of
1000 pounds or more of moderate to weak potential carcinogens. The
results of the Agency's evaluation using the air dispersion model
indicate that reporting levels of 100 pounds or less for potential
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carcinogens are necessary to protect public health from releases of these
potential carcinogens. The air dispersion model is based on a plausible
but conservative exposure scenario that includes the following release
conditions: (1) the substance is a stable gas, volatile liquid, or
aerosol that remains suspended in the air long enough to reach the point
of exposure; (2) the duration of exposure is 24 hours; (3) the release
occurs under stable (class D) meteorological conditions (one meter per
second wind speed); and (4) exposure occurs 30 meters downwind from the
point of release. For a more detailed discussion of the Agency's air
dispersion model and the assumptions on vhich it is based, see Appendix
F.
The Agency is aware that it has rejected the use of scenarios for RQ
adjustment purposes in previous RQ rulemakings (see 50 FR 13467, April 4,
1985). Several important characteristics specific to cancer, however,
justify the Agency's use of a scenario to focus on the appropriate RQ
levels assigned to potential carcinogens. First, threshold levels of
exposure below which a potential carcinogen does not present some risk of
cancer have not been demonstrated. Thus, a release of any quantity of a
potential carcinogen may increase the risk of cancer in the exposed
population. This is in contrast with other toxic effects for which
thresholds can be demonstrated. Second, because cancer risks are
considered to be cumulative, a number of small releases can be as serious
as one large release. Doses that have been shown to cause cancer are
generally lower than the lowest dose which induces a chronic effect. The
linear non-threshold mechanisms of carcinogenesis contained in the
Agency's Guidelines for Carcinogen Risk Assessment (51 FR 33992-34003,
September 24, 1986) suggest that appropriately designed studies could
demonstrate onset of cancer at even lower doses. For these reasons,
together with the fact that cancer is an extremely serious health effect
and has a latent period that does not allow direct observation of
carcinogenic risks from substances newly released into the environment,
the Agency has decided to calculate the appropriate maximum RQ level for
potential carcinogens using a model that is based on conservative
assumptions.
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Establishing maximum notification levels for potential carcinogens below
those for substances that cause other health and environmental effects
follows the precedent set by past Agency rulemaking action. For example,
the Agency has published water quality criteria which recommend
acceptable intake levels for potential carcinogens that are almost
uniformly several orders of magnitude lower than the water quality
criteria for other health and environmental effects (see Water Quality
Criteria Documents; Availability, November 28, 1980, 45 FR 79318). The
criteria are almost invariably below 1 ug/L when based on cancer and
above 1 ug/L when based on other toxic effects. The Agency's proposal of
a three-tier system with a 100-pound maximum RQ for potential carcinogens
reflects a recognition by EPA of the need to be conservative with respect
to adjusting the RQs of potential carcinogens due to the unique risks
afforded to public health and the environment by release of these
substances.
ALTERNATE METHODOLOGIES CONSIDERED FOR RANKING POTENTIAL CARCINOGENS
The Agency considered a number of alternative methods for assigning
hazard rankings and RQs to the CERCLA potential carcinogens. Many of
these alternate methodologies were suggested by the external reviewers
who reviewed initial drafts of this report and initial drafts of Appendix
A ("Methodology for Evaluating Potential Carcinogenicity in Support of
Reportable Quantity Adjustments Pursuant to CERCLA Section 102"). Most
commenters agreed with the need to consider the potential carcinogenicity
of the CERCLA hazardous substances when adjusting RQs. However, several
of these same commenters suggested alternative ways for ranking the
potential carcinogens according to the weight of evidence and potency of
the substances. These alternative methods are described briefly below,
along with the Agency's reasons for not using them.
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Alternate Methodology 1 - Clustering Potency Factors
One commenter suggested using only the potency of the potential
carcinogens for hazard ranking purposes, by analyzing the distribution of
the potency factors from all of the potential carcinogens, grouping them
using standard statistical techniques, and assigning hazard rankings to
the groups.
The commenter suggested that after calculating the potency factors for
all of the potential carcinogens, the mean log potency (the average of
all of the logarithms of .the potency factors) be calculated, along with
the standard deviation. The frequency of the potencies could then be
plotted against the log potency to provide a histogram from which RQs
could be derived. One method of deriving RQs provides for assigning
100-pound RQs to the potential carcinogens with potencies within plus or
minus one standard deviation of the mean. Since 67 2/3% of the potential
carcinogens will have potency factors within plus or minus one standard
deviation of the mean potency factor, 2/3 of the potential carcinogens
would have their RQs set at 100 pounds. Potential carcinogens with
potencies between plus one and plus two standard deviations from the mean
would be assigned RQs of 10 pounds, and potential carcinogens at the
other end of the frequency distribution curve (i.e., a potency factor
between minus one and minus two standard deviations of the mean), would
have RQs of 1000 pounds. Finally, all substances with potencies
exceeding plus two standard deviations (the most potent carcinogens)
would be assigned 1-pound RQs. Those potential carcinogens having
potency factors less than minus two standard deviations would be assigned
RQs of 5000 pounds.
The Agency rejected this methodology because it ignores the experimental
evidence that a hazardous substance causes cancer. The risk, assessment
guidelines used by both IARC and the Agency use the weight-of-evidence
analysis as a prime criterion for evaluating the risk of potential
2-18

-------
carcinogens, and the Agency has therefore chosen not to use potency alone
to assign RQs. In addition, it allows potential carcinogens to have RQs
of 1000 and 5000 pounds (e.g., epichlorohydrin, and 1,4-dioxane), which
the Agency considers too high to adequately protect human health,
welfare, and the environment.
Alternate Methodology 2 - Clustering Potency Factors with Administrative
Overlays
Alternate Methodology 1, described above, was rejected because it fails
to consider weight of evidence. A variation of Methodology 1 was
considered, however, in which the weight of evidence was overlayed to
arrive at RQs. Using this method, all potential carcinogens which the CAG
has evaluated as weight-of-evidence Group A (i.e., that group of
potential carcinogens for which there is sufficient epidemiological
evidence to classify the substance as a human carcinogen) would be
lowered one RQ level from the level assigned using the clustering
analysis described in Alternate Methodology 1. For example, if a
substance had a potency factor within one standard deviation of the mean,
its RQ would be 100 pounds. If that substance was also classified as a
Group A substance, its RQ would be lowered one RQ level to 10 pounds.
This overlay is similar to the Agency's decision to base an adjusted RQ
on a substance's more hazardous degradation product rather than on the
parent substance, when degradation to this more hazardous product occurs.
This methodology was ultimately rejected by the Agency because it still
allows potential carcinogens to have RQs of 1000 and 5000 pounds, which
the Agency has considered unacceptable for protection of human health,
welfare, and the environment.
Alternate Methodology 3 - Ranking Only Known Human Carcinogens
A third alternate methodology which was considered for assigning hazard
rankings and RQs to the potential carcinogens was to administratively
place all Group A substances (i.e., those which are known human
2-19

-------
carcinogens) in the "high" category, regardless of the potency of the
carcinogen, and assign these Group A substances a 1-pound RQ.
This methodology was eventually rejected because it would not materially
reduce the risks to human health. In addition, even though
epidemiological experiments show a substance to be a potential human
carcinogen, if the bioassay data clearly show that the potency of that
carcinogen is low, reporting such low releases would not likely result in
a federal response. For example, benzene is assigned to
weight-of-evidence Group A but it has a very low potency (F = 0.27). A
release of 1 pound of benzene would not likely result in a federal
response action, since it is such a weak carcinogen, even though benzene
is a known human carcinogen.
HAZARD RANKING HETH000L0GY CHANGES
In its evaluation of CERCLA hazardous substances that are potential
carcinogens, the Agency initially employed a ranking methodology that
used a weight-of-evidence scheme developed by the International Agency
for Research on Cancer (IARC). EPA subsequently developed its own
weight-of-evidence scheme, which the Agency used in conjunction with
potency factors to obtain hazard rankings for potential carcinogens.
EPA decided to use the new weight-of-evidence scheme because the new
methodology refines the IARC approach and has had extensive peer review
both within and outside the Agency. In order to distinguish more
accurately those substances for which there is limited evidence of
carcinogenicity, but not enough evidence to satisfy Group B requirements,
EPA divided IARC Group 3 (insufficient evidence of human carcinogenicity)
into Group C (possible human carcinogen) and Group D (not classifiable
for carcinogenicity). The new EPA methodology allows Group C substances
to be assigned RQs based on potential carcinogenicity. IARC Group 3
substances could not be so assigned.
2-20

-------
In addition, the Agency's methodology considers certain benign tumor
data, as veil as malignant tumor data, when appropriate, and pooling of
significantly elevated tumor sites and types. Because the RQ adjustment
process for potential carcinogens was initiated while the Guidelines for
Carcinogen Risk Assessment (51 FR 33992-34003, September 24, 1986) were
still being developed, potency factors for some CERCLA potential
carcinogens may not at present fully reflect the position set forth in
the guidelines regarding consideration of benign tumors and pooling of
tumor sites and types. The Agency is in the process of verifying that
all potency factor calculations are in accordance with the guidelines.
The Agency expects that few, if any, of the substances still undergoing
verification will have proposed RQs altered as a result of this review,
since the ranges of potency factors assigned to the three potency groups
are broad and a large change in potency factor would generally be
required for a substance to change potency groups. The list of
substances subject to verification is available for review in the public
docket. This verification process will be completed during the comment
period and the resulting chemical profiles and adjusted RQs will be
available in the public docket for public review and comment. In
addition, the Agency has completed a separate primary review of the RQ
profiles for each of the 191 individual hazardous substances that have
been evaluated for potential carcinogenicity. Currently, the Agency is
conducting a secondary level of review of these profiles. The Agency
expects that this secondary review will be completed during the public
comment period.
2-21

-------
SECTION 3
RESULTS
This section summarizes the results obtained after applying the RQ
adjustment methodology to 273 of the remaining 275 hazardous substances
12
addressed in this report . Table 3-1 lists each CERCLA hazardous
substance along with its statutory and proposed RQ. The table is
arranged alphabetically and identifies by numerical code in the Statutory
Code column the statutory source for the designation of each hazardous
substance under CERCLA Section 101(14). The codes are explained in
footnotes to the table. In addition, since many hazardous substances are
regulated under more than one statute and may be identified by different
names in the different statutes, all the names under vhich a hazardous
substance are listed pursuant to any statute or implementing regulation
are listed alphabetically and their synonyms are included in the
Regulatory Synonyms column. Each hazardous substance is uniquely
identified by its Chemical Abstracts Service Registry Number (CASRN).
Table 3-1 also provides the RCRA waste number (vhere applicable).
RESULTS OF THE METHODOLOGY USED TO IDENTIFY POTENTIAL CARCINOGENS
This section of the report presents the results of applying the
methodology that vas used to identify potential carcinogens from among
the CERCLA hazardous substances, as described in Section 2.
12
The two substances whose RQs are not adjusted in the rulemaking which
this technical background document supports are being evaluated as
follows: methyl isocyanate on the basis of inhalation toxicity; and
lead on the basis of potential carcinogenicity. The statutory
one-pound RQs for methyl isocyanate and lead will be retained, pending
completion of the Agency's analysis of their toxicity or potential
carcinogenicity.
3-1

-------
TABLE 3-1
LIST OF HAZARDOUS SUBSTANCES AND REPORTABLE QUANTITIES
Hazardous Substance
1
1
1
1
| CASRN
Regulatory Synonyms
1 HQ
Statutory 	
|BCRA
jWaste
Code tjllumber
	 Proposed RQ 	
Category| Pounds(Kg)
Acetaldehyde, tnchloro-
1
| 75876
I
Chloral

1 1*
4
U034
1
O I
1
5000 (2270)
Acetamide, N-(4-ethoxyphenyl)-
1
| 62442
|
Phenacetln

1 1*
4
U187
1
B |
100 (45.4)
Acetamide, H-fluoran-2-yl-
| 53963
1
2-Acetylaminofluorene

1 1*
4
U005
[
A |
I
10
(4.54)
Acetic acid, lead salt
1
| 301042
I
Lead acetate

|5000
1.4
U144
1
A |
i
10
(4.54)
2-Acetylaminofluorene
1
| 53963
1
Acetamide, H-fluoren-2-yl-

1 1*
4
U005
1
A I
i
10
(4.54)
Acrylomtnle
1
t 107131
2-Propenenitrile

|100
1,2,4
11009
1
A I
1
10
(4.54)
Alanine, 3-(p-bis(2-chloroethy1)amino]phenyl—,L-
1
| 148623
1
Helphalan

1 1*
4
U150
1
X 1
i
1
(0.454)
Aldrin
1
| 309002
1
I
1,2,3,4,10-10-Uexachloro-l,4,4a,5,6,8a-bexahydro-l,
4:5,8-endo,exo-dimethanonaphthalene
| 1
1,2,4
P004
1
X 1
1
1
1
(0.454)
2-Amino-l-methylbenzene
| 95534
1
o-Toluidine

1 1*
4
U328
1
B |
I
100 (45.4)
4-Amino-l-methylbeneene
1
| 106490
1
p-Toluidine

1 1*
4
U353
1
B |
1
100 (45.4)
Amitrole
1
| 61625
I
111-1,2,4-Triazol-3-amine

1 1*
4
U011
1
A |
i
10
(4.54)
Ammonium bichromate
1
| 7789095
I


|1000
1

1
x I
¦
1
(0.454)
Ammonium chromate
1
| 778(1989
¦


|1000
1

1
X 1
¦
1
(0.454)
Aroclor 1016
1
112674112
l
Polychlorinated Biphenyls
(PCBsl
1 10
1.2

1
X 1
1
1
(0.454)
Aroclor 1221
1
|111042B2
i
Polychlorinated Biphenyls
(PCBsl
1 10
1.2

1
X 1
1
1
(0.454)
Aroclor 1232
1
|11141165
1
Polychlorinated Biphenyls
(PCBs)
1 10
1.2

1
X 1
1
1
(0.454)
Aroclor 1242
1
(53469219
1
Polychlorinated Biphenyls
(PCBs)
1 10
1.2

1
X 1
1
1
(0.454)
Aroclor 1248
1
|12672296
I
Polychlorinated Biphenyls
(PCBs(
1 10
1.2

1
X 1
1
1
(0.4S4)
Aroclor 1254
1
|11097691
Polychlorinated Biphenyls
(PCBs)
1 10
1,2

1
X 1
1
(0.454)
MOTE: ALL COMMENTS/NOTES ABE LOCATED AT THE END OF THIS TABLE

-------
LIST OP HAZARDOUS SUBSTANCES ADD BEPOHTABLE QUANTITIES - Continued
Hazardous Substance
| CASBN
Regulatory Synonyms
1
1
1
1 HQ
Statutory 	
|HCBA
(Waste
Cod- "t jtluabar
	 Proposed KQ 	
Category| Pounds(Kg)
Aroclor 1260
111096825
Polychlorinated Biphenyls (PCBs)
1
1
|
1,2

1
X 1
1
1 (0.454)
Arsenic ft
| 7410382

1
1 I6
1
2,3

1
X 1
1
1 (0.454)
Arsenic acid
| 1327522
| 7778394

1
1 1*
1
1
4
P010
1
X 1
1
1 (0.454)
Arsenic disulfide
| 1303328

1
|5000
i
1

1
* 1
1 (0.454)
Arsenic!Ill) oxide
| 1327533
Arsenic trioxide
1
|5000
¦
1.4
P012
1
* 1
1
1 (0.454)
Arsenic(V) oxide
| 1303282
Arsenic pentoxide
1
|5000
1
1,4
P011
I
X 1
1
1 (0.454)
Arsenic pentoxide
| 1303282
Arsenic(V) oxide
1
|5000
>
1,4
von
1
x 1
1
1 (0.454)
Arsenic trichloride
| 7784341

1
|5000
i
1

1
X 1
t
1 (0.454)
Arsenic tnoxide
| 1327533
Arsenic(III) oxide
I
|5000
¦
1,4
M12
1
X 1
¦
1 (0.454)
Arsenic trisulfide
| 1303339

1
|5000
i
1

1
X |
¦
1 (0.454)
Arsine, diethyl-
| 692422
Olethylarsine
1
1
¦
4
P038
1
X 1
1
1 (0.454)
Asbestos 1"tt
| 1332214

1
1 1A
¦
2,3

1
X 1
1
1 (0.454)
Auramine
| 492808
Benzenaaine, 4,4'-carbonimidoyIbis (N,N—dimethyl—
1
1 1*
i
4
U014
1
B |
a
100 (45.41
Azaserine
| 115026
L-Serine, diazoaeetata (aster)
1
1 *•
i
4
U015
1
& 1
i
10 (4.54)
Azindine
| 151564
Ethylenimine
1
1 **
¦
4
P054
1
* |
i
1 (0.454)
Azirino(2*,3':3,4)pyrrolo(l,2-a)indole-4,7-dion*,6
amino-8- ((
-------
LIST or HAZARDOUS SUBSTANCES ADD REPORTABLE QUANTITIES - Continued
UaucdouD Substance
1
1
1
1
| CASBB
Regulatory Synonyms
1
1
1
1 BQ
Statutory 	
|ECHA
IHaste
Code < |Number
	 Proposed BQ 	
Category| Founds(Kg)
3,4-Banzacndine
•
j 22551*
1
Benz[c)acridine
1
1 1*
4
U016
1
A I
10 (4.54)
Benz[a)anthracene
1
| 56553
i
1
Benzo(a]anthracene
1,2-Bonzanthracene
1
j 1*
1
|
2,4
uoia
1
A |
1
i
10 <4.54)
1,2-Benzanthracene
1
| 56553
1
i
Benz[a]anthracene
Banzo(a]anthracene
1
1 **
1
i
2,4
uoia
1
A |
1
1
10 (4.54)
1,2-Benzanthracene, 7,12-dimethyl-
| 57976
|
7,12-Dioethylbenz(a|anthracene
1
1 1*
i
4
U094
1
X |
1
1 (0.454)
Benzenamine, 4,4'-carbonlmidoylbis (H.N-dimethyl-
| 492008
1
Auraoine
1
i
¦
4
U014
1
B |
1
100 (45.4)
Benzenasune, 4-chloro-2-aatfayl-l hydrochloride
1
| 3X65933
j
4-Qiloro-o-toluidine, hydrochloride
i
1 i*
i
4
V049
1
B |
1
100 (45.4)
Benzenamine, H,N-diDathyl.-4-vbanyLaEO-
| 60117
Dime thylaminoazobensene
i
1
¦
4
IT093
1
* 1
1
1 (0.454)
Barzanamine, 4,4'-oethylenebis(2—chloro-
1
| 101144
4,4*-Hethylenebia(2-chloroaniline)
l
1
i
4
U158
1
A |
1
10 (4.54)
Benzenamine, 2-oethyl-, hydrochloride
1
| 636215
j
o-Toluidine hydrochloride
l
1 i*
¦
4
U222
1
B 1
1
100 (45.4)
Benzenamine, 2-methyl-S-nitro-
1
| 99558
I
5-Hitro-o-toluidine
l
1 i*
¦
4
U1S1
1
B I
i
100 (45.4)
Banzena
1
| 71432
i

1
jiooo
1
1,2,3.4
U019
1
A |
i
10 (4.54)
Benzene, chloromethyl-
1
| 100447
I
Benzyl chloride
|100
1
1,4
P028
1
B I
a
100 (45.4)
Benzene, hexachloro—
1
| 118741
I
Hexachlorobenzene
1
1 1*
1
2,4
U127
1
A |
i
10 (4*54)
Benzene, l-methyl-2,4—dinitro-
1
| 121142
l
2,4-Oiu trotoluene
1
(1000
1
1,2,4
U105
1
A |
i
10 (4.54)
Benzene, l-oethyl-2,6—danitro-
1
| 606202
¦
2,6-Dimtrotoluene
1
|1000
I
1.2,4
0106
1
B 1
i
100 (45.4)
Bonzono , 1,2-methylenedioicy-4-allyl-
1
| 94597
Safrole
1
1 **
1
4
U203
1
B I
1
100 (45.4)
Benzene, 1,2-methylenedioKy—4-propenyl-
1
| 120S81
1
Isosafrole
1
1 J*
1
4
U141
1
B |
1
100 (45.4)
Benzene, 1,2-oethylenediO)iy-4-prapyl-
1
| 94566
i
Dihydrosafrole
1
1 1*
1
4
U090
1
A |
a
10 (4.54)
Benzene, pentachloromtro-
1
| 82688
Pentachloronitrobenzene
1
1 1*
4
U185
1
8 I
100 (45.4)
NOTE: ALL COMMENTS/NOTES ARE LOCATED AT THE END OF THIS TABLE
-------
LIST OF HAZARDOUS SUBSTANCES AND REPORTABLE QUANTITIES - Continued
Hazardous Substance
CAS8H
Regulatory Synonyms
I
1
1
1 >Q
Statutory 	
|BCBA
| Waste
Codat jKuicber
	 Proposed HQ 	
Category| founds(Kg)
Benzene, (trichloromethyl)-
98071
Benzotricblorida
1
1
1
4
U023
1
* 1
1 (0.454)
Benzeneacatic acid, 4-chloro-alpha-(4-chlorophanyl)
-alpha-hydroxy-,ethyl ester
510156
Ethyl 4,4'-dlchlorobenEilata
1
1 1*
i
i
4
U03S
1
A |
1
¦
10 (4.54)
1,2-Benzanedicarborylic acid, (bis(2-ethylhexyl)]
ester
U7B17
Bis(2-ethylhery1) phthalate
1
1
i
¦
2,4
U028
1
B |
i
¦
100 (45.4)
Bensidin*
93815
(l,l'-Biphenyl)-4,4'diaaino
i
i
¦
2,4
U021
1
X |
1 (0.454)
l,2-Benzisothia8olin-3-one,l,l-dioxide, and salts
81072
Saccharin and salts
¦
j i*
¦
4
U202
1
B |
i
100 (45.4)
Benzo(a)anthracene
56553
Bens(a)anthracene
1,2-Banzanthracena
i
i i*
i
¦
2.4
U01S
1
* 1
i
¦
10 (4.54)
Benzo(b1fluoranthene
205992

1
i
¦
2

1
X 1
i
1 (0.454)
Benzo(k>fluoranthane
207089

i
i i*
¦
2

1
D |
1
5000 (2270)
Benzo(a]pyrene
50328
3,4-Benzopyrene
i
i
¦
2,4
U022
1
X 1
1
1 (0.454)
3,4-Benzopyrene
50328
BenzolaJpyrene
¦
i i*
¦
2,4
U022
1
* 1
1 (0.454)
Benzotnchlonde
98077
Benzan*, (trichloromethyl )-
i
1
¦
4
<1023
1
X 1
1
1 (0.454)
1,2-Benzphenanthrene
218019
Qirysene
i
i i*
i
2,4
U050
1
A |
I
10 (4.54)
Benzyl chloride
100447
Benzene, chloronethyl-
i
|100
1
1.4
P028
1
B |
i
100 (45.4)
Beryllium tt
7440117
Beryllium dust ^
1
1 1*
1
2,3,4
P015
1
A |
i
10 (4.54)
Beryllium chloride
7787475

1
|5000
¦
1

1
X |
1 (0.454)
Beryllium dust tt
7440417
Beryllium tt
1
1 1*
l
2,3,4
P015
1
A |
i
10 (4.54)
Beryllium fluoride
7787497

1
|5000
i
1

1
X 1
1
1 (0.454)
Beryllium nitrate
13597994
7787555

1
|5000
1
1

1
X 1
1
1 (0.454)
MOTE: ALL OQMKENTS/NOTES ARC LOCATED AT THE END OF THIS TABLE
-------
LIST OF HAZARDOUS SUBSTANCES AND REPORTABLE QUANTITIES - Continued
Hazardous Substance
CASHN
Bequlatory Synonyms
1
1
1
1 8Q
Statutory 	
| |BC8A
j jwaste
j Codel" j Number
	 Proposed HQ 	
Category 1 Pounds(Kg)
alpha - BHC
319846

»
1 1*
1
| 2

1
A |
1
10 (4.54)
beta - BHC
319857

1
1 1 *
|
| 2

1
X {
i
1 (0.454)
gaum* - BHC
58899
Hexachlorocyclohexane (gamma isomer)
Lindane
1
1 1
1
1
1 1.2,4
Ul 29
1
X I
1
1
1 <0.454)
2,2'-Bio*irane
1464535
1,2:3,4-Diepoxybutana
1
1 1'
|
1 4
U085
1
A |
1
10 (4.54)
(l,l'-Biphenyl)-4,4'diamine
92815
Benxidine
1
1 1*
1
1 2,4
11021
1
X |
i
1 (0.454)
(1,l'-Biphanyl)-4,4•diamine,1,3'dichloro-
91941
3,3'-Dichlorobenzidine
1
1 I*
|
I 2,4
U073
1
X 1
1
1 (0.454)
(1,l'-Biphanyl)-4,4'diamine,3,3'dimethoxy-
119904
3,3'-Dimothoxybenzidine
1
1 1*
I
1 4
mm
1
B |
i
100 (45.4)
(X,1'Biphenyl 1-4,4'-diamine,3,3'-dimethyl-
119931
3,3'-Dime thylbenzidine
1
1 1*
1
1 4
U095
1
B |
1
100 (45.4)
Bi s (2-chloroethy 1) ethe tr
111444
Dichloroethyl ether
Ethane, l,l'-oxyt>is(2-chloro-
1
I 1*
1
1
1 2,4
ITO2S
I
A |
1
1
10 (4.54)
Bis(chloromethyl) ether
542881
Methane, oxybis(chloro-
1
1 1*
1
1 4
P016
1
A |
j
10 (4.54)
Bis(2-ethyllwxyl) phthalate
111811
1,2-Bensenedicarboxylic acid, [bis(2-ethylhexyl))
ester
1
1 1*
1
1 2,4
ff02B
1
B |
1
I
100 (45.4)
1,3-Butadiene, 1,1,2,3,4,4-hexachloro-
87683
Hexachlorobutadiene
1
1 1*
1 2,4
U12B
1
* 1
1
1 (0.454)
1-Butanamin*, N-butyl-H-mtroso-
924163
H-Hitrosodi-n-butylamina
1
1 1*
I
1 4
0172
1
A |
1
10 (4.54)
Butanoic acid, 4-(bis(2-chloroethyl| aminoJbenxene-
305033
Chlorambucil
1
1 1*
1
1 4
0035
1
A |
i
10 (4.54)
Cacodylic acid
75605
ttydroxydiaethylarsine oxide
1
| 1»
1
1 4
0136
1
* |
1
1 (0.454)
Cadmium ft
1440439

1
1 1'
¦
| 2

1
A |
i
10 (4.54)
Cadmium acetate
543908

1
jioo
¦
| 1

1
A |
i
10 (4.54)
Cadmium bromide
7189426

1
jioo
| 1

1
A |
10 (4.54)
NOTE: ALL COHHEWTS/NOTES ABE LOCATED AT THE END OF THIS TABLE
-------
LIST OF HAZARDOUS SUBSTANCES ABD REPORTABLE QUANTITIES - Contiauftd
Hazardous Substance
1
1
1
1
| CAS EH
Regulatory Synonyms
HQ
Statutory 	
|ECBA
, 1 Waste
Code T|Number
	 Proposed BQ 	
Category| Pounds(Kg)
Cadmium chloride
1
110108642
l

100
1

a i
10 (4.54)
Calcium arsenate
1
| 7718441
¦

1000
1

X j
1 (0.454)
Calcium araenito
1
|52740166
I

1000
1

X 1
1 (0.454)
Calcium chronate
1
113765190
I
Chromic acid, calcium salt
1000
1.4
U032
X 1
1 (0.454)
Camphene, octachloro-
<
| 8001352
j
Toaaphene
1
1,2,4
P123
X |
1 (0.454)
Carbamic acid, ethyl aster
| 51796
I
Ethyl carbamate (Urethan)
1*
4
U238
B 1
100 (45.4)
Carbamic acid, methylnitroso-, ethyl ester
1
| 615512
i
N-Nitroso-W-oethylurethane
1*
4
U178
X j
1 (0.454)
Carbamide, H-othyl-S-nitroso-
| 759739
j
H-Hi troso-N-ethy1urea
1*
4
11176
A |
10 (4.54)
Carbamide, H-methy1-H—nitroao—
1
| 684935
1
B-tlitroso-N-methylurea
1*
4
U177
X |
1 (0.454)
Carbamide, thlo—
1
| 62566
¦
Thiourea
1*
4
U219
A 1
10 (4.54)
Carbamoyl chloride, dimethyl-
1
| 79447
i
Dioethylcarbaooyl chloride
1»
4
U097
* 1
1 (0.454)
Carbon tetrachloride
| 56215
¦
Kethane, tetrachloro-
5000
1.2.4
V211
A |
10 (4.54)
Oiloral
| 75876
I
Acetaldehyde, tnchloro—
1*
4
U034
D 1
5000 (2270)
Chlorambucil
1
| 305033
t
Butanoic acid, 4-{bis(2-chloroethyl) aminoIbenzene-
1*
4
U035
A 1
10 (4.54)
Chlordane
f
j 57749
1
1
i
Chlordana, technical
4,7-Methanoindan, 1,2,4,5,6,7,8,8-octachloro-3a,4,
7,7a-tetrahydro-
1
1.2,4
U0J6
X |
1 (0.4S4)
Chlordane, technical
| 57749
1
1
i
Cblordane
4,7-Methanoindan, 1,2,4,5,6,7,8,8-octachloro-3a,4,
7,7a-tetrahydro-
1
1.2,4
U036
* 1
1 (0.454)
Chlornaphasine
1
| 494031
2-Haphthylamine, H,B-bls<2-chloroethyl)-
1*
4
U026
B |
100 (45.4)
NOTE: ALL COKHENTS/tiOTES ARE LOCATED AT THE END OP THIS TABLE
-------
LIST OP HAZARDOUS SUBSTANCES AND REPORTABLE QUANTITIES - Continued
Hazardous substance
1
1
1
1
| CASED
Regulatory synonyms
1
1
1
1 HQ
Statutory 	
|KCRA
j Wast*
Code + j Number
	 Proposed RQ 	
Category | Pounds (Kg)
1-Chio ro—2,3—epoxypropano
1
j 106898
1
1
Epicblorohydrin
Oxirini, 2-(chloromethyl)-
1
|1000
1
1
1,4
U041
1
B |
1
1
100 (45.4)
Chlorofora
| 67663
i
Hathana, trichloro-
1
|5000
1
1,2.4
U044
1
A |
1
10 (4.54)
Chloromethyl methyl ether
1
j 107302
I
Methane, chloromethoxy-
1
1 1*
|
4
U046
1
A |
I
10 (4.54)
4-Chloro-o-toluidine, hydrochloride
1
| 3165933
i
Benxenaiune, 4-chloro-2-methyl-, hydrochloride
1
1
1
4
U049
1
B |
1
100 (45.4)
Chronuc acid
1
111115745
| 7733945
1

1
j 1000
]
1
1

1
* |
1
¦
1 (0.454)
Chromic acid, calcium salt
113765190
i
Calciua chronate
1
jiooo
1
1,4
U032
1
* I
i
1 (0.454)
Chromium 1"^°
1
j 7440473
¦

1
1
¦
2

1
X 1
1
1 (0.454)
chcyseno
1
| 218019
l
1,2-BaaKphenanthten«
1
| 1*
l
2,4
uoso
1
A 1
1
10 (4.54)
COKE OVEN EMISSIONS
1
| N.A.
¦

1
1 1*
i
3

1
x 1
1
1 (0.454)
Creosote
1
| 6001589

I
1 1*
i
4
0051
1
X 1
1
1 (0.454)
Cupric acetoarsenite
1
11200203a
1

1
|100
1
1

1
X 1
1
1 (0.454)
1,3-Cyclopentadiene, 1,2,3,4,5,5—hoxachloro—
| 77474
I
Beiachlorocyclopentadian*
1
1 1
1
1,2,4
U130
1
A |
1
10 (4.54)
Cyclophosphamide
1
| 50180
1
|
2H-1,3,2-oxazaphosphorine,2-{bis(2-chloroethyl)
amino ] tet rahydro-2-oxide
I
1 1*
1
1
4
UOSS
1
A |
1
1
10 (4.54)
Daunonycin
(20830813
1
1
1
i
5, 12-Naphthncenadione, (SS-cis)-8-ac»tyl-10-{3-
aiuno-2,3,6-t rideoxy-alpha-L-lyxo-haxopyranoayl)
oxyl 1-7,8,9,10-t«ttahydt»-<, 8,11-trihydrory-l-
oethoxy-
I
1 1*
1
1
1
1
4
U059
1
A |
1
1
1
1
10 (4.54)
DDD
1
| 72540
1
1
¦
Dichlorodiphenyl dichlocoethane
TDE
4,4'-DDD
1
1 1
1
1
1
1,2,4
11060
1
X |
t
1
I
1 (0.454)
4,4'-DDD
1
| 72540
i
i
DDD
Dlchlorodi phenyl dichloroethana
TDE
1
1 1
1
1
1,2,4
U060
1
X |
I
•
1 (0.454)
NOTE: ALL COMMENTS/NOTES ARE LOCATED AT THE END OP THIS TABLE
-------
LIST or HAZARDOUS SUBSTANCES AND BEfQRTABLE QUANTITIES - Continued
Hazardous Substance
CASBH
Regulatory Synonyms
1
1
t
1 BQ
Statutory 	
| |RCRA
j jWaste
j Code 1" 'Number
	 Proposed BQ 	
Category| Pounds(Kg)
DOE
72559
4,4'-DEE
1
1 1*
1
| 2

1
* 1
1 (0.454)
4,4'-DDE
72559
DDE
1
1 I'
1
| 2

1
X 1
1 (0.454)
DOT
50293
Dlchlorodiphenyl trichloroethane
4,4'-DDT
1
| 1
1
|
1 1.2,4
U061
1
X 1
1
1
1 (0.454)
4,4'-DDT
50293
DDT
Dlchlorodiphenyl trichloroethane
1
| 1
1
1
1 1.2.4
U061
1
X 1
1
1
1 (0.454)
Decachlocooctahydro-1,3,4—tootheno—2H—cyclobuta [c, d|
—pentalan-2—on®
143500
Kepone
1
j 1
1
1
1 1.4
Ul 42
1
x 1
1
1
1 (0.454)
Diallate
2303164
S-(2,3-Oichloroallyl) diisopropylthiocarbamate
1
i i*
•
1 4
U062
1
B I
I
100 (45.4)
Diamine
302012
Hydrazine
i
1 1*
1
1 4
U133
1
* |
¦
1 (0.454)
Di aminotolusne
95407
496*720
623405
2537645B
Toluenediamine
1
1
1
1
1
•
1 4
U221
1
A |
1
1
1
i
10 (4.54)
Dibenz|a,hianthracene
53703
Dibenso[a,h)anthracene
1,2:5,6-Dibenzanthracene
1
1 1*
i
*
1 2,4
U063
i
x i
t
1 (0.454)
1,2:5,6-Dibonianthracene
53703
Dibenz[a,h)anthracene
Dibenso(a,h)anthracene
1
I
i
i
1 2.4
U063
i
* 1
1
1 (0.454)
Dibenzo[a.b]anthracene
53703
Dibensfa,hIanthracene
1,2:5,6-Dibenzanthracene
1
1 1*
i
¦
i 2,4
U063
1
* 1
1
1
1 (0.454)
1,2:7,B-Dibencopyrene
189559
Dibenz[a,ilpyrene
i
i i*
¦
1 4
U064
1
A |
I
10 (4.54)
Dibanz(&,i|pyrene
189559
1,2:7,8-Dibeniopyr ene
i
i i*
¦
1 4
U064
1
A I
i
10 (4.54)
1,2-Dlbrooo-J-chloiopropane
96128
Propane, 1,2-dibroao-3-chloro-
i
i i*
¦
1 4
U066
1
A I
1
10 (4.54)
S—(2,3-Dichloroallyl) diisopropylthiocarbamate
2303164
Diallate
i
i i*
1 4
U062
1
8 1
100 (45.4)
NOTE: ALL CQKMEOTS/SOTES ARE LOCATED AT THE END OP THIS TABLE
-------
LIST OP HAZARDOUS SUBSTANCES AND REPORTABLE QUANTITIES - Continued
Hazardous Substance
1
1
1
1
| CASRN
Regulatory Synonyms
1 RQ
Statutory 	
|BCBA
j Waste
Code T|Kuober
	 Proposed RQ 	
Category| Pounds(Kg)
3,3•-Dichlorobenzidine
1
| 91941
i
(1,1'-Biphenyl)-4,4' diamine,3,3' dichloro-
1 1*
2.4
U073
1
x 1
1 (0.454)
Dichlorodiphenyl dichloroethane
1
| 72S4S
t
1
I
DDD
THE
4,4'-DDD
| 1
1,2,4
(1060
1
x 1
1
I
1
1 (0.454)
Dichlorodiphenyl tnchloroethane
1
| 50293
1
i
DDT
4,4'-DDT
| 1
1,2,4
11061
1
x I
1
1
1 (0.454)
1,2-Dichloroatbane
1
| 107062
1
i
Ethane, 1,2-dichloro-
Ethylens di chloride
|5000
1,2,4
U077
1
B |
i
«
100 (45.4)
1,1-Dichloroathylene
| 75354
1
1
Ethane, 1,1-dichloro-
Vinylidena chloride
|5000
1,2,4
U078
1
B |
i
¦
100 (45.4)
Dichloroethyl ether
1
| 111444
1
Bis(2-chloroethyl) ethar
Ethane, l,l'-oxybia[2-chLaco-
j p
2,4
11025
i
A I
1
1
10 (4.54]
DichLocophanylacsine
1
j 696286
i
Phonyl dichloroarsine
1 11
4
P036
1
X 1
1
1 (0.454)
Dialdrin
1
| 60571
1
I
l,2,3,4,10,10-Hexachloro-6,7-epoxy-l,4,4a,5,6,7,8,
8a-octahydro-endo, exo-1,4:5, 8-din»thanonaphtha lane
| 1
1,2,4
P037
1
X i
1
1
1 (0.454)
1,2:3,4-Diapoxybutane
l
| 1464535
j
2,2'-Bioxirane
1 1*
4
inas
1
A I
j
10 (4.54)
Diethylarsine
| 692422
I
Arsine, diethyl-
1 1*
4
P03S
1
X I
1
1 (0.454)
1,4-Diethylene dioxide
1
j 123911
I
1,4-Dlozane
1
4
inoa
1
B I
¦
100 (45.4)
H,N'-Diethylhydraslne
1
| 1615801
|
Hydrazine, 1,2—diethyl-
1 l'
4
U086
1
A I
1
10 (4.54)
Diethylstilbestrol
| 56531
i
4,4'-Stilbenediol, alpha,alpha'-diethyl-
t 1*
4
U089
1
X I
j
1 (0.454)
Dihydcosafrola
| 945S6
I
Benzene, 1,2—methylenedioxy-4—propyl-
1
4
U090
1
A I
|
10 (4.54)
3,3' -Dimethoxybenzidine
1
| 119904
j
(1,1'-Biphenyl(-4,4'diamine,3,3'dimethoxy-
1 1*
4
U091
1
B |
|
100 (45.4)
Dioethylaminoacobenzene
| 60117
Banzenamine, N, H—dioothyl-4-phanylaio-
1 1*
4
U093
1
2 I
1 (0.454)
MOTE: ALL COMMENTS/NOTES ARE LOCATED AT THE END OF THIS TABLE
-------
LIST OF HAZAHDOUS SUBSTANCES AMD REPORTABLE QUANTITIES - Continued
Hazardous Substance
\
1
1
1
| CASBN
Regulatory Synonyms
1
1
1
I BQ
Statutory 	
|BCBA
jWaste
Coda t jttunber
	 Proposed BQ 	
Category| Founds(Kg)
7,12-Dlmothyibans(a]anthracene
1
| 57916
1,2-Banianthracene, 7,12—dimethy1-
1
1
4
U094
1
X 1
1
1 <0.454)
3,3'-Dimethylbenxidine
j 119937
I
(1,1' Bipheny 1 >-4,4' —diamine ,3,3' -dime thyl-
1
|
4
U095
1
B |
1
100 (45.4)
Dimethylcarbaaoyl chloride
| 19447
1
Carbamoyl chloride, dimethyl-
1
1 1*
1
4
U097
1
X 1
1
1 (0.454)
1, 1-Dimethylhydraiine
1
j 57147
|
Hydra tine, 1,1-dime thy 1-
1
1 1*
1
4
U098
1
A |
1
10 (4.54)
1,2-Dimethylhydraiine
| 540738
Hydraclne, 1,2-ditaathyl-
1
1 f
1
4
U099
1
* 1
1 (0.454)
Dioethylnitros&mine
| 62759
I
B-Hitrosodimethylamina
1
1 1«
2.4
P082
1
A |
1
10 (4.54)
Dimethyl sulfate
| 77781
i
Sulfuric acid, dimethyl aster
1
1 1*
1
4
U103
1
B 1
1
100 (45.4)
Dinitrotoluene
1
125321146
i

1
|1000
1
1.2

1
A |
1
10 (4.54)
3,4-Oimtrotoluene
1
610399

1
1
1


1
1
i

2,4-Dinit rotoluene
121142
Benzene, l-mathyl-2,4-dinitro-
1
|1000
1
1,2,4
U105
1
A |
I
10 (4.54)
2,6-Dinit rotoluene
1
j 606202
1
Benzene, 1-me thy1-2,6—dimt ro—
1
|1000
1
1.2,4
U106
1
B I
1
100 (45.4)
1,4-Dioxane
| 123911
1,4-Diethylane dioxide
1
1 1*
1
4
uioa
1
fi |
i
100 (45.4)
1,2-Diphenylhydrasine
1
122667
Hydrazine, 1, 2 ^<11 phenyl—
1
1 1*
1
2.4
U109
1
A |
1
10 (4.54)
Di-n-propylnitrosamine
| 621647
N-Hitro3odi-n-propylamine
1
1 1*
1
2.4
uiii
1
A |
1
10 (4.54)
Epichlorohydrin
106898
|
oxirana, 2-(chloronathyl)-
l-Chloro-2,3-apoxypropana
1
|1000
1
1
1.4
U041
1
B |
1
t
100 (45.4)
Ethanamine, H—ethyl-tJ-nitroso-
| 55185
H-tiitrosodiethy lamina
1
1 1*
1
4
U174
1
x I
1
1 (0.454)
Ethane, 1,2—dibroao-
| 106934
Ethylene dibromida
1
|1000
1
1.4
U0S7
1
X 1
1
1 (0.454)
Ethane, 1,2—dichloro-
107062
¦
Ethylene dichlonda
1,2-Dichloroethane
1
|5000
1
1
1,2,4
U077
1
B |
1
¦
100 (45.4)
Ethane, 1,1,1,2,2,2-hexachloro-
i
| 67721
Hexachlorosthone
1
1
2,4
U131
i
B 1
100 (45.4)
NOTE: ALL OKMEHTS/MOTES ARE LOCATED AT THE END 0? THIS TABLE
-------
LIST or HAZARDOUS SUBSTANCES AND BEPOBXABLE QUANTITIES - Continued
Hazardous substance
1
1
1
1
| CASHN
Regulatory synonyms
Bfl
Statutory 	
IBCBA
| Waste
code "t" j number
	 Proposed HQ 	
Category| Pounds(Kg)
Ethane, 1,1'—oxybis(2-chloro-
1
| 111444
1
1
Bis(2-chloroethyl) ether
Dichloroethyl ether
1*
2,4
U02S
1
A I
1
10 (4.54)
Ethana, pentachloro—
| 76017
1
Pentachloroethane
1*
4
1/184
1
A |
1
10 (4.54)
Ethane, 1,1,1,2-tetrachloro-
1
j 630206
i
1,1,1,2-Tet rachloroethane
1«
4
U208
1
B 1
I
100 (45.4)
Ethano, 1,1,2,2-tetrachloro-
1
| 79345
i
1,1,2,2-Tetrachloroethane
1*
2,4
U209
1
B |
¦
100 (45.4)
Ethanethioaaide
1
| 62555
i
Thioacetamide
1*
4
U21S
1
A 1
I
10 (4.54)
Ethana, 1,1,2-tclchloco-
1
| 79005
a
1,1,2-Trichloroethane
1*
2,4
U221
1
& 1
i
100 (45.4)
Ethanol , 2,2'Hnltrosoiaino)bis-
1
| 1116547
i
H-Nitroaodiethanolamina
1*
4
U173
1
* I
1
1 (0.454)
Ethenamine, B-mathyl-H-nitroso-
1
| 4549400
l
N-Nitroaoaothylvinylamine
1*
4
P0S4
1
A |
i
10 (4.54)
Ethane, chloro-
1
j 75014
i
Vinyl chloride
1*
2,3,4
U043
1
A 1
i
10 (4.54)
Ethene, 1,1-dichloro-
1
| 75354
1
i
Vinylidene chloride
1,l-Oichloroethylene
5000
1,2,4
U07S
1
a |
1
i
100 (45.4)
Ethene, 1,1,2,2-tetrachloro-
| 127184
1
1
1
Perchloroethylene
Tetrachloroethene
Tetrachloroethylene
1*
2,4
U210
i
B 1
1
1
i
100 (45.4)
2-Ethoxyathanol
1
| 110*05
1
Ethylene glycol monoethyl ether
1»
4
U359
1
C |
1
1000 (454)
Ethyl carbaoate (Urethan)
| 51796
i
Carbaaic acid, ethyl ester
1«
4
U238
\
B |
1
100 (45.4)
Ethyl 4,4'-dichlorobenzilate
1
| 510156
1
l
Benzeneacetic acid, 4-chloro-alpha-(4-chlorophenyl)
-alpha-hydroxy-,ethyl eater
1*
4
U038
1
A 1
1
1
10 (4.54)
Ethylene dibroiude
1
| 106934
¦
Ethane, 1,2—dibromo-
1000
1,4
U067
I
* |
i
1 (0.454)
Ethylene dichlonda
1
| 107062
1
i
Etfaane, 1,2—dichloro-
1,2-Dicbloroethane
5000
1.2,4
U077
1
d 1
1
¦
100 (45.4)
Ethylene glycol monoethyl ether
1
| 110805
2-Ethoxyethanol
1«
4
U359
i
C 1
1000 (454)
NOTE: ALL COMMENTS/NOTES ARE LOCATED AT THE EHD OF THIS TABLE
-------
LIST or HAZARDOUS SUBSTANCES AND HETOKTABL£ QUANTITIES - Continued
Hazardous Substance
CASBH
Regulatory Synonyns
BQ
Statutory 	
|BCRA
|Waste
Code t|Number
	 Proposed BQ 	
Category| Pounds(Kg)
Ethyleno oxide
15218
Oxlran*
1*
4
U115
1
A I
I
10 (4.54)
Ethylenethiourea
96457
2-lmidasolidinethione

4
U116
1
A |
1
10 (4.54)
Ethylenimine
151564
Axiridine
1*
4
P0S4
1
X I
i
1 (0.454)
Ethyl methanesultonate
62500
Hathanesulfonic acid, ethyl ester
11
4
U119
1
* 1
i
1 (0.454)
Formaldehyde
50000
Methylene oxide
1000
1.4
III 2 2
1
B |
1
100 (45.4)
D-Glucopyranoae, 2-deoxy-2-(3-oethyl-3-
nitrosoureido)-
18883664
St reptoxotocin
x*
4
U206
1
X |
1
1
1 (0.454)
Glycidylaldehyde
765344
1-Propanal, 2,3-epoxy-

4
U126
1
A |
I
10 (4.54)
Guanidine, H—nitroso-N-methyl-W-ni tro-
70257
H-Methyl-N'-nitro-N-nitrosoguanidine
X *
4
U163
1
A |
1
10 (4.54)
Heptachlor
76448
4,7-Methano-lH-indene,1,4,5,6,7,8,8-heptachloro-3a,
4,7,7a-tetrahydro-
1
1.2,4
F059
X 1
1
1
1 (0.454)
Heptachlor ipoudt
1024S73


2

1
X 1
1
1 (0.454)
Hexachlorobenzene
118741
Bensene, hexachloro-

2,4
U127
1
A 1
1
10 (4.54)
Hexachlorobutadiene
87683
1,3-Butadiene, 1,1,2,3,4,4-hexachloro-
It
2,4
U128
1
X 1
1
1 (0.454)
Hexachlorocyclohexane (gamma isomer)
58899
gauma - BUC
Lindane
1
1.2,4
U129
1
s 1
1
1 (0.454)
Hexachlorocyclopentadiene
77474
1,3-Cyclopentadiene, 1,2,3,4,5,5-hexachloro-
1
1.2.4
U130
1
A I
10 (4.54)
I,2,3,4,10,lO-Hexachloro-6,7-epoxy-l,4,4a,5,6,7,8,
8a-octahydro-endo, exo-1,4:5, S-diaetbanonaphthalene
60571
Dleldxin
1
1.2.4
P037
1
X 1
1
1
1 (0.454)
Haxachloroethane
67721
Ethane, 1,1,1,2,2,2-hexachloro-

2.4
U131
1
B I
1
100 (45.4)
1,2,3,4,10-10-Hexachloro-l,4,4a,5,9,Ba-hexahydro-1,
4:5,8-enda,exo-diaethsnonaphthalene
309002
Aldrin
1
1.2.4
P004
1
X 1
1
1 (0.454)
Hydrazine
302012
Diamine

4
U133
1
x I
1 (0.454)
NOTE: ALL CQ?«HE»rS/NOTES ABE LOCATED AT THE END OF THIS TABLE
-------
LIST OF HAZARDOUS SUBSTANCES AND BEFOBSABLB QUANTITIES - Continued
Hazardous Substance
1
1
1
1
| OkSBH
Regulatory Synonyms
EQ
Statutory 	
|RCRA
| Waste
Coda T |Number
	 Proposed BQ 	
Category! Pounds (Kg)
Hydrazine, 1,2-diethyl-
1
| 1615801
1
N,H'-Diathylhydrazine
1"
1
4 | U086
1
i
A 1
1
10 (4.54)
Hydrazine, 1,1-dinwthyl-
| 57147
1
•
s
M
4
$
£
»—~
8
H
Q
1
H
1»
1
4 | U098
1
1
A |
1
10 <4-54]
Hydrazina, 1,2-dnaathyl-
| 540730
j
1,2-Dimathylhydi:azine
1*
1
4 j U099
i
1
X |
1
1 (0.454)
Hydrazine, 1,2-diphenyl-
| 122667
j
1,2-Diphanylhydrasina
1*
1
2,4 I in09
1
1
A |
1
10 (4.54)
HydroxydiJMtbylarsme oxide
| 75605
j
Cacodylic acid
1*
1
4 | U136
i
1
X J
1
1 (0.4S4)
2-Inidazolidinathione
| 96457
Ethylenethiourea
1*
1
4 j U116
1
A |
1
10 (4.54)
Indeno|l,2,3—cd|pyrene
J
| 193395
¦
l,10-(l,2-Phenylene)pyrane
1*
1
2,4 j in.37
1
1
B |
I
100 (45.4)
Isocyanic acid. Bethy1 ester
| 624639
j
Methyl isocyonata
1*
1
4 | F064
1
1
X 1
1
111 (0.454)
Isosaftola
| 120581
j
Benzene, 1,2-methylenedioxy-4-propenyl-
1*
1
4 | U141
I
1
B |
1
100 (45.4)
Kepona
| 143500
j
Decachlorooctahydro—1,3,4-mattaeno-2H-cyelobutatc,d]
-pentalen-2-one
1
1
1,4 j U142
1
¦
1
X 1
1
1
1 (0.454)
Lasiocarpina
1
| 303344
i

1 *
4 | U143
¦
1
A |
i
10 (4.54)
Lead
7439921
¦

1 *
2 J
|
1
X |
i
It (0.454)
Lead acetata
i
| 301042
i
Acetic acid, lead salt
5000
1
1,4 | U144
1
1
A |
i
10 (4.54)
Lead arsenate
1
| 7134409
| 7645252
|10102484

sooo
1
1 1
1
1
1
X |
1
1
¦
1 (0.454)
Lead phosphate
1
| 7446277
|
Phosphoric acid, lead salt
1*
1
4 I U145
1
i
A 1
I
10 (4.54)
Lead aubacatata
1
| 1335326

1*
1
4 I Ul 4 6
1
1
B 1
I
100 (45.4)
Lindane
1
50899
i
I
gaaaa - BHC
Hexachlorocyclohexana (gamma isomer)
1
1
1,2,4 | UI29
1
I
I
X |
1
¦
1 (0.454)
Lithium chcoaata
1143073S8

1000
I
1 1
1
x 1
1 (0.454)
MOTE. MX COMHEHTS/NOTES ARE LOCATED AT THE EHD OF THIS TABLE
-------
LIST OF HAZABDOUS SUBSTANCES AND HEPOHTABLE QUANTITIES - Continued
Hazardous substance
CASRH
Regulatory synonyms
1 bq
Statutory 	
|RC8A
jwast*
Coda T| Number
	 Proposed BQ 	
Category| Pounds < Kg)
Melphalan
148823
Alanine, 3-[p-bis(2-chloro«thyl)aai no|phenyl-,L-
F 1*
4
in so
1
X I
1
1 (0.454)
Methane, chloro-
7487}
Methyl chloride
1 1*
2,4
U045
1
B 1
|
100 (45.4)
Methana, chloronethoKy-
107302
Chloromathyl methyl ether
1 1*
4
U046
f
A |
1
10 (4.54)
Methane, iodo-
74884
Ma thy1 iodide
1 1*
4
U138
1
B |
1
100 (45.4)
Ma thane, orybia(chloro-
542881
Bis(chloromathyl) ether
1 1*
4
P016
1
A 1
i
10 (4.54)
Hethane, tetrachloro-
56235
Carbon tetrachloride
|5000
1,2,4
U211
1
A |
i
10 (4.54)
Methana, trichloro-
67663
Chloroform
|5000
1,2,4
U04«
1
A 1
I
10 (4.54)
Methanesulfonic acid, ethyl ester
62500
Ethyl Beth anasulfonate
1 1*
4
U119
1
X |
I
1 (0.454)
4,7-Methano-lH—ind&no,1,4,5,6,7,8,8-taeptachloco-3a,
4,7,7a-tetrahydro-
76448
Heptachlor
| 1
1,2,4
P059
1
X 1
1
1
1 (0.454)
4,7-Methanoindan, 1,2,4,5,6,7,3,8-octachloro-3a,4,
7,7a-te t rahydro-
57749
Chlordane
Chlocdane, technical
| 1
1,2.4
U036
1
X 1
1
1
1 (0.454)
Methyl chloride
74873
Methane, cbloro-
i 1*
2,4
U045
1
B |
1
100 (45.4)
2-Methylazindine
75558
1,2-Propylenimine
1 1*
4
P067
1
A |
1
10 (4.54)
1-Methylcholanthrene
56495
BensIjlaceanthrylene, 1,2—dihydro—3-mothyl-
1
4
U157
i
A |
1
10 (4*54)
4,4'-Methylenebis(2-chloroanilino)
101144
BenEenaaice, 4,4'-«ethylenebis(2-chlaro-
1 1*
4
U158
1
A |
1
10 (4.54)
Methylene oxide
50000
Pornaldahyda
|1000
1.4
(1122
1
B |
1
100 (45.4)
Methyl iodide
74884
Methane, lodo-
1 1*
4
U138
1
B |
I
100 (45.4)
Methyl laocyanate
624839
Isocyanic acid, methyl ester
1 1*
4
P064
1
X |
1
111 (0.454)
N-Methy1-N'-oit ro-tf-nit rosoguanidina
70257
Guanidine, N-nitraso-N-aethyl-N'-nitro-
1 1*
4
Ul 6 3
1
A |
1
10 (4.54)
Methylthiouracil
56042
4(1H)-Pyrimidinone, 2,3—dihydro—6-mathyl-2-thioxo-
1 1*
4
U164
1
A |
10 (4.54)
NOTE: ALL COMMENTS/NOTES ABE LOCATED AT THE END OF THIS TABLE
-------
LIST 07 HAZARDOUS SUBSTANCES AND REPORTABLE QUANTITIES - Continued
Hazardous Substance
CASRN
Regulatory synonyms
RQ
Statutory 	
|HCRA
jwaste
code + jnumber
	 Proposed BQ 	
Category| Pounds(Kg)
Mitomycin C
50077
Azirino< 2',3':3,4)pyrrolo(1,2-a)indole-4,7-dione,6-
araino-6- (((aminocarbonyl)ory)methyl|-l,la,2,8,8a,
8b-hexahydro-8a-oethoxy-5-aethyl-
1*
4
U010
A i
10 (4.54)
5,12-Naphthacenedione, (SS-cis)-8-acetyl-10-(3-
amino-2,3,6-tndeoxy-alpha-L-lyxo-hexopyranosyl}
oxyl ]-7,6,9,10-tetrahydro-<,8, 11-tnhydroxy-l-
methoxy-
20830813
Daunomycin
1*
4
U059
A I
10 (4.54)
2,7-Naphthalenedisulfomc acid,3,3'-[ (3,3'—
dimethyl-< 1,1 '-bipheny1 )-4,4 '-diy 1 )-bis (azo) )bls< 5-
amino-4-bydroxy l-tetrasodiuai salt
72571
Trypan blue
I*
4
U236
A |
10 (4.54)
1-Naphthylamina
134327
alpha-Naphthylaouna
1*
4
U167
B 1
100 (45.4)
2-Naphthylanine
91S98
beta-Naphthylaoin*
1*
4
U168
A I
10 (4.54)
a lpha-Naphthylaoine
134327
1-Naphthylamina
1»
4
U167
B 1
100 (45.4)
beta-Naphtbylamlne
91598
2-Haphthylanine
1*
4
U168
A 1
10 (4.54)
2-Naphthylaoina, H,N-bis(2-chloroethy 1)-
494031
Chlomaphazine
1*
4
U026
B I
100 (45.4)
Nickel ff
7440020

1*
2

* 1
1 (0.454)
Nickel nmmoniua sulfate
15699180

5000
1

B 1
100 (45.4)
Nickel carbony1
13463393
Nickel tetracarbonyl
1*
4
P073
A I
10 14.54)
Nickel chloride
7718549
37211055

5000
1

B I
100 (45.4)
Nickel cyanide
557197
Nickel(II) cyanide
I*
4
P074
A I
10 (4.54)
Nickel(II) cyanide
557197
Nickel cyanide
1*
4
P074
A I
10 (4.54)
Nickel hydroxide
12054487

1000
1

A 1
10 (4.54)
Nickel nitrate
14216752

5000
1

B I
100 (45.4)
NOTE: ALL COMMENTS/NOTES ABE LOCATED AT THE END OF THIS TABIC
-------
LIST OF HAZARDOUS SUBSTANCES AND REPORTABLE QUANTITIES - Continued
Hazardous Substance
1
1
1
1
| CASBN
Regulatory Synonyms
1
1
1
1 BQ
Statutory 	
|BCBA
jWaste
Coda t|Number
	 Proposed BQ 	
Category| Pounds(Kg)
Nickel sulfate
1
| 7786814
I

1
|5000
1
1

1
B 1
1
100 (45.4)
Nickel tatcacarbonyl
1
113463393
i
Nickel carbonyl
1
1 1*
1
4
P073
1
A |
1
10 (4.54)
2-Nitropropana
1
| 79469
j
Propane, 2-nitco—
1
1 1'
1
4
U171
1
A |
1
10 <4.54)
N-Nitrosodi-n-butylaoine
| 924163
¦
1-Butanamino, H-butyl-H-nitroao-
1
1 1*
|
4
U172
1
A 1
1
10 (4.54)
N-Nitrosodiethanolaaine
| 1116547
i
Ethanol, 2,2'-(nltrosolnino)bis-
1
1 1*
1
4
U173
1
* 1
i
1 (0.454)
N-Nitrosodiethylanina
1
| 55185
Ethanamina, H-ethyl-N-nitroso-
1
1 1*
1
4
U174
1
X 1
1
1 (0.454)
tt-Hit rosodlmethylaBlne
| 62759
j
Dinnthylnitrosamne
1
1 1*
a
2,4
P082
1
A |
1
10 (4.54)
K-Nltrosodl-n-propylamine
| 621647
j
Di-a-propylnitrosasune
1
11*
I
2,4
uiii
I
A |
10 (4.54)
N-Nitroso-R-athylurea
| 759739
Carbamide, H-athyl-N-nittoso-
1
11*
1
4
U176
1
A |
1
10 (4.54)
N-Nltroso-H-oethylurea
1
| 6S4935
Carbaiu.de, H-methyl-H-nitroso-
1
i i*
1
4
in 77
1
X |
1
1 (0.454)
N-Nlt roao-B-iae thy lur ethane
| 615532
Carbaaic acid, mathylmtroso-, athyl ester
1
i i*
1
4
U178
1
X 1
a
1 (0.454)
N-Nitrosooethylvinylamine
1
| 4549400
Ethenanina, H-methyl-M-ni t roso-
1
i i*
1
4
poai
1
A 1
1
10 (4.54)
N-Nltrosopipendina
1
| 100754
i
Pyridine, hexahydro-N-oitroso-
1
i i*
1
4
U179
I
A |
1
10 (4.54)
N-Nitrosopyrrolidine
| 930552
I
Pyrrole, tetrahydro-N-nitroso-
1
i i*
1
4
UlflO
1
* |
1
1 (0.454)
5-Nltro-o-toluidine
1
| 99558
¦
Benzenaaine, 2—me thy1-5—nit ro-
1
i i*
a
4
U1B1
1
B |
i
100 (45.4)
1,2-0*athiolane, 2,2-dioxida
| 1120714
i
1,3-Propane sultona
1
1 i*
I
4
U193
1
A |
1
10 (4.54)
2H-1,3,2-Oxaiaphosphorine,2-(bis<2-chloroethyl)
amino]tetrahydro-2-oxide
1
| 50180
1
|
Cyclophosphamide
1
1 i*
l
I
4
U058
1
A |
1
1
10 (4.54)
Oxirane
| 75218
¦
Ethylene oxida
1
l
i
4
U115
1
A |
i
10 (4.54)
Oxirane, 2—(chloromethyl)-
1
| 106898
1
Epichlorobydnn
1—Chloro—2,3—epoxypropana
1
|1000
1
1,4
U041
1
B |
1
100 (45.4)
NOTE: ALL CCHKENTS/BOTES ABE LOCATED AT THE END OF THIS TABLE
-------
LIST OP HAZARDOUS SUBSTANCES AND REPORTABLE QUANTITIES - Continued
Hazardous Substance
CASBH
Regulatory Synonyms
HQ
Statutory 	
|BCRA
jwaata
Coda + j number
	 Proposed RQ 	
Category| Pounds(Kg)
Parathion
56382
Phosphorothioic acid, 0,0-diethyl o-(p-nitrophenyl)
•star
1
1.4
F0S9
1
A I
1
1
10 (4.54)
Pentachloroathane
76017
Ethane, pontachloro-
1*
4
U184
1
A |
1
10 (4.54)
Pentachloronitrobenxene
82688
Benzena, pentachloromtro-
1*
4
U185
1
B |
1
100 (4S.4)
Pentachlorophenol
87865
Phenol, pentachloro-
10
1,2,4
U242
1
A |
1
10 (4.54)
Perchloroethylene
127114
Ethena, 1,1,2,2-tetrachloro-
Tetrachloroethene
Tetrachloroathylana
1«
2,4
U210
1
B |
1
1
1
100 (45.4)
Phenacetin
62442
Acetaoide, N-(4-«thoxyphany11-
1»
4
in. 8 7
1
B t
1
100 (45.4)
Phenol, pentachloro-
87865
Pentachlorophenol
10
1,2,4
U242
1
A |
i
10 (4.54)
Phenol, 2,4,5-tnchloro-
95954
2,4,5-Trichlorophenol
10
1.4
U230
I
A |
1
10 (4.54)
Phonol, 2,4,6-trichloro-
88062
2,4,6-Trichlorophenol
10
1,2,4
U231
1
A |
>
10 (4.54)
Phenyl dichloroarsine
696286
Dichloropbenylarsine
1*
4
P036
1
X |
1
1 (0.454)
1,10-41,2-Phonyleno)pyrena
193395
Indeno(1,2,3—cdjpyrena
1*
2,4
U137
1
B |
1
100 (45.4)
Phosphoric acid, lead salt
7446277
Lead phosphate
1»
4
0145
1
A |
1
10 (4.54)
Phosphorothioic acid, 0,0-diathyl O-(p-nitrophenyl)
aster
56382
Parathion
1
1,4
P089
1
A |
1
¦
10 (4.54)
Polychlorinatad Biphenyls (PCBs)
1336363
Aroclors
10
1.2

i
X 1
1
1 (0.454)
Polychlorinatad Biphenyls (PCBs)
12674112
Aroclor 1016
10
1.2

1
X 1
1
1 (0.454)
Polychlorinatad Biphenyls (PCBs)
11104282
Aroclor 1221
10
1.2

1
* 1
1
1 (0.4S4)
Polychlorinatad Biphenyls (PCBs)
11141165
Aroclor 1232
10
1,2

1
X 1
1
1 (0.454)
Polychlorinatad Biphenyls (PCBs)
53469219
Aroclor 1242
10
1.2

1
X 1
1 (0.454)
NOTE: ALL COMMENTS/NOTES ABE LOCATED AT THE END OF THIS TABLE
-------
LIST OF HAZARDOUS SUBSTANCES AND REPORTABLE QUANTITIES - Continued
Ibntdous Substance
| CASEH
Ragulatory Synonyms
1
1
1
1 RQ
Statutory —
I&CBA
JWaste
CodaT (Number
	 Proposed KQ 	
Category| Pounds(Kg)
Polychlorinated Biphenyls (PCBa)
|126722»6
Aroclor 1248
1
1 10
1
1,2

1
X I
1
1
(0.454)
Polychlorinated Biphanyla (PCBa)
111097691
Aroclor 1254
1
1 10
1
1,2

1
z 1
1
(0.454)
Polychlorinated Biphenyls (PCBs)
|11096825
Aroclor 1260
1
1 1°
1
1.2

1
X I
1
1
(0.454)
Potassium arsenate
| 7784410

1
|1000
1
1

1
* 1
1
(0.454)
Potassium arsenite
|10124502

1
|1000
1
1

1
X 1
1
(0.454)
PotassiuD bichromate
| 7778509

I
|1000
1
1

1
* 1
1
1
(0.454)
Potassium chromata
| 7789006

1
jiooo
1
1

1
X I
i
1
(0.454)
1-Propanal, 2,3—e poxy-
| 765344
Glycidylaldahyde
1
1 X*
1
4
U126
1
A |
¦
10
(4.54)
Propane, l,2-dibroao-3-chloco-
| 96128
1,2-Dibroao-3-chloropropane
1
1 X*
1
4
U066
1
A |
1
10
(4.54)
Propane, 2-aitro-
| 79469
2-cu.tropropane
1
1 1*
1
4
11171
1
A |
i
10
(4.54)
1,3-Propane sultone
| 1120714
1,2-Oxathiolane, 2,2-dioiide
1
1 X*
1
4
U193
1
A |
i
10
(4.54)
1-Propanol, 1,3-dibromo-, phosphate (3:1)
| 126727
Tns<2,3—dibromopropyl) phosphate
1
1 X*
1
4
U235
1
A |
1
10
14.54)
2-Propenenltrile
| 107131
Acrylonitrile
|100
1
1.2,4
U009
I
A |
I
10
(4.54)
1,2-Propylaniaine
| 7S558
2-Mathylaiiridina
J
1 X*
I
4
P067
1
A |
i
10
(4.54)
Pyridine, bexahydro-B-nitroso—
| 100754
N-Hitrosopipendine
1
1 X*
1
4
U179
1
A |
i
10
(4.54)
4 (1H )-Py rialdinono, 2,3-dihydro-6-aethyl-2-thioxo-
J 56042
Katbyltbiouracil
1
1 X*
1
4
U164
1
A |
i
10
(4.54)
Pyrrole, tatrahydro-B-aitroso-
| 930552
B-ttitrosopyrrolidina
1
1 X*
1
4
U180
1
X |
i
1
(0.454)
BAOIOHUCLIDES
| H.A.

1
1 x*
1
3

1
X j
i
1§ (0.454)
Saccharin and salts
| 81072
l,2-Bensisothiazolm-3-one,l,l-dioxide, and salts
1
1 X*
1
4
U202
1
B |
i
100 (45.4)
Safrole
| 94597
BenEene, l,2-asttaylenedioKy-4-allyl-
1
1 !•
4
U203
i
B I
100 (45.4)
NOTE: ALL COHHENTS/WJTES ABE LOCATED AT THE END OP THIS TABLE
-------
LIST OF HAZARDOUS SUBSTANCES AND BEFOBXABLE QUANTITIES - Continued
Hazardous Substance
1
1
1
1
| CASKH
Regulatory Synonyms
1
1
1
1 «Q
Statutory 	
|BCBA
j Waste
Code 1" |Number
	 Proposed RQ 	
Category | Pounds(Kg)
Selenium disulfide
1
| 7486564
1
Sulfur selenide
1
1 1*
1
4
V205
A
1
| 10 (4.54)
1
L-Serme, diazoacetate (ester)
1
| 115026
i
Azaserine
1
I 1*
4
U015
A
1
j 10 <4.54)
i
Sodium arsenate
1
| 7631892
i

1
jlOGO
i
1

X
1
| 1 (0.454)
i
Sodium arsenite
1
| 7784465
i

1
|1000
1
1

X
1
| 1 <0.454)
Sodiua bichromate
1
|10588019
i

1
(1000
1
1

X
1
| 1 (0.454)
¦
Sodium chronate
1
| 7775113
i

1
|1000
1
1

X
1
| 1 (0.454)
¦
4,4'-StiltHmediol, alpha,alpha'-dietbyl-
1
| 56S31
i
Diethylstilbestrol
1
1 1*
1
4
U089
X
1
| 1 (0.4541
1
Streptozotocin
i
110883664
1
I
D-Glucopyranose, 2-deoxy-2-(3-methyl-3-
mtrosoureldo 1-
1
1 1*
1
1
4
U206
X
1
j 1 (0.454)
1
I
StrontiujB chromate
\
| 7769062
i

1
|1000
1
1

X
1
{ 1 <0.454)
i
Sulfur selenide
1
| 7406564
i
Selemum disulfide
1
1 !•
1
4
U205
K
1
| 10 (4.54)
¦
sulfuric acid, dimethyl ester
1
| 77701
i
Dimethyl sulfate
1
1 1*
1
4
til 03
B
1
j 100 (45.4)
i
TDE
1
| 72548
1
1
DDD
Dichlorodiphenyl dichloroethane
4,4'—DDD
1
1 1
1
1
1
1,2,4
U060
X
1
j 1 (0.454)
I
1
i
2,3,1,8-Totrachlorodlbenro-p—diojcin 
-------
LIST OF HAZARDOUS SUBSTANCES AND REPORTABLE QUANTITIES - Continued
Hazardous Substance
1
1
1
1
| CASRN
Regulatory Synonym
i
i
i
1 RQ
Statutory 	
l&CRA
j Waste
Coda '|dumber
	 Proposed RQ 	
Category| Pounds(Kg)
Thiodcet amide
1
| 62555
i
Ethanethioamide
1
1 1*
i
4
| U218
1
A I
10 (4.54)
Thiourea
1
| 62566
I
Carbaaide, thio-
1
1 1*
i
4
| U219
1
A |
*
10 (4.54)
Toluenedi amine
1
| 95807
j 496720
j 823405
125376458
I
Diaainotoluane
1
1 1*
1
1
1
i
4
| U221
1
A |
i
i
I
i
10 (4.54)
o-Toluidine
1
j 95534
i
2-Amino-l-methy lbenzen®
1
1 1*
¦
4
| U328
1
B |
i
100 (45.4)
p-Toluidine
1
| 106490
l
4-Amino-l-«thylbanzen®
1
1
¦
4
| U353
1
B |
¦
100 (45.4)
o—Toluidine hydrochloride
1
| 636215
l
Banzenaaine, 2-methyl-, hydrochloride
1
1 1*
i
4
| U222
1
B |
1
100 (45.4)
Toxaphene
1
j 8001352
I
Canphane, octachloro-
1
| 1
¦
1,2,4
| P123
1
X |
I
1 (0.454)
1H-1,2,4-Triazol-3-aiune
1
| 61825
Anitrole
1
1 1*
i
4
| U011
1
A |
i
10 (4.54)
1,1,2-Trichloroethane
1
| 79005
*
Ethane, 1,1,2-trichloro-
1
1 l*
i
2.4
| U227
1
B |
i
100 (45.4)
Trichloroethene
1
j 79016
i
Trichloroethylene
1
|1000
1
1,2,4
| U228
1
B |
1
100 (45.4)
Trichloroethylene
1
j 79016
i
Trichloroethene
1
|1000
I
1,2,4
| U228
1
B |
i
100 (45.4)
Trichlorophenol
1
|25167822
i

1
1 10
I
1

1
A |
i
10 (4.54)
2,3,4-Tnchlorophenol
1
|15950660
l

1
1
1


1
1
i

2,3, 5-Tnchlorophenol
1
| 933788
1

1
1
1


1
1
i

2,3,6-Trichlorophenol
1
j 933755
I

1
1
1


1
1
i

2,4,S-Tnchlorophenol
1
j 95954
i
Phenol ,2,4,5-trichloro-
1
1 10
1
1.4
| U230
1
A |
i
10 (4.54)
2,4,6-Trichlorophenol
1
| 88062
1
Phenol,2,4,6-trichloro-
1
1 10
1
1,2,4
| U231
1
A |
i
10 (4.54)
3,4,5-Trichlorophenol
1
| 609198

1
1


1
1

NOTE: ALL COMMENTS/NOTES ARE LOCATED AT THE END OF THIS TABLE
-------
LIST or HAZARDOUS SUBSTANCES AND REPORTABLE QUANTITIES - Continued
Hazardous Substance
1
1
1
1
| CASBH
Regulatory Synonyms
1 BQ
Statutory 	
|RCBA
j Waste
Code tJSunfaar
	 Proposed BQ 	
Category| Pounds(Kg)
2,4,5-Trichlorophenol
1
| 95954
1
Phenol, 2,4,5-tnchloro—
1
1,4
in 30
1
A I
|
10 (4.54)
2,4,6-Trichlo rophonol
1
| 88062
¦
Phenol, 2,4,6-tnchloro-
1
1,2,4
U231
1
A |
I
10 (4.54)
Tns(2,3-dibrooopropyl) phosphate
| 126727
1
1-Propanol, 2,3-dlbromo-, phosphate (3:1)
1 1*
4
U235
1
A |
i
10 (4.54)
Trypan blue
| 72571
1
1
1
2,7-Naphthalenedisulfonic acid,3,3'-[(3,3*-
dioethyl-(l,l'-biphenyl)-4,4'-diyl)-bis(azo)[bis(5
-amino—4-hydroxy)-tot rasodiuja salt
1 1*
4
U23S
1
A |
1
1
i
10 (4.54)
Unlisted Hazardous Wastes
1
| N.A.
i




1
1
i

<3>aracteristic of EP Toxicity
1
i
1




1
i
¦

Arsenic
1
| 0.A.
i

1 1*
4
D004
i
* i
¦
1 (0.454)
Cadmium
1
\ 8.A.
¦


4
DO 06
i
A |
i
10 (4.54)
Chromium (VI)
1
| S.A.
i

1 1*
4
D007
I
* I
I
1 (0.454)
Lead
1
1 s.a.
i

1 1*
2.4
DOOB
1
B |
¦
100 (45.4)
Lindane
1
| 0.A.
¦

1 1*
1.4
P013
1
* I
¦
1 (0.454)
Toxaphene
1
j H.A.
t

1 1*
1.4
0015
1
* I
1
1 (0.454)
Uracil, 5-{bis(2-chloroethyl1amino 1-
A
Ul
Uracil sustard
1 1*
4
U237
1
A I
I
10 (4.54)
Uracil mustard
| 66751
i
Uracil, 5-
-------
LIST or HAZARDOUS SUBSTANCES AND REPORTABLE QUANTITIES - Continued

1
1

1
Statutory 	



1

1

RCBA



1

1

Waste
	 Proposed BQ 	
tUxardous substance j
CASRN |
Regulatory Synonyns
I bq
Code t
Number
Category|
Pounds(Kg)
F001 |
1
1

1
1 1®
4
F001
1
A I
10 (4.54)
The following spent haloganated solvents used in j
1

1


1

decreasing end sludges from the recovery of these j
1

1


1

solvents in degreasing operations: j
1

1


1

(a) Tetrachloroethylene j
127184|

1 1*
2,4
U210
B |
100 (45.4)
(b) Trichloroethylene j
79016 j

j 1000
1.2.4
U228
B j
100 (45.4)
(c) Methylene chloride j
75092 j

1 1*
4

C j
1000 (454)
(d) 1,1,1-Trichloroethane j
71556j

1 1*
2,4

c I
1000 (454)
(e) carbon tetrachloride j
56235|

15000
1.2,4
U211
A
10 (4.54)
it) chlorinated fluorocarbons j
N.A. j
i

1 I6
4

» 1
1
5000 (2270)
F002 |
1
1

1
1 **
4
F002
1
B |
100 (45.4)
The following spent halogenated solvents and the j
1

i


i

still bottoas froa the recovery of these solvents: j
1

i


i

(a) Tetrachloroethylene j
127184|

i i*
2.4
U210
B 1
100 (45.4)
(b) Methylene chloride j
75092|

i **
4

c
1000 (454)
(c) Trichloroethylene |
79016 j

j 1000
1.2.4
U228
B j
100 (45.4)
(d) 1,1,1-Trichloroethane j
71556|

1
2.4

c I
1000 (454)
(e) Chlorobenzene j
108907|

|100


B
100 (45.4)
(f) l,l,2-Trichloro-l,2,2-trifluoroethane j
76131|

1 1*
4

D
5000 (2270)
(g) o-Dichlorobensene |
95501|

100


B
100 (45.4)
(h) Trichlorofluorooethane j
75694|
I

1 1*
1
4

•> i
|
5000 (2270)
F006 |
1
1

1
1 1*
4
F00S
1
Z 1
1 (0.454)
Wastewater treatment sludges froa electroplating j
1

1


1

operations except froa the following processes: (1)|
1

1


1

sulfuric acid anodizing of aluainua; (2) tin j
1

1


1

plating on carbon steel; (3) zinc plating (segre- |
1

1


1

gated basis) on carbon steel; (4) aluainua or line-|
1

1


1

aluainua plating on carbon steel; (5) cleaning/ j
1

1


1

stripping associated with tin, sine and aluainua j
1

1


1

plating on carbon steel; and (6) chemical etching j
1

1


1

and Billing of aluainua. j
1

1


1

NOTE: ALL COMMENTS/NOTES ARE LOCATED AT THE END OF THIS TABLE
-------
LIST OF HAZARDOUS SUBSTANCES AND REPORTABLE QUANTITIES - Continued
1 1
1 1
1 1
1 1
Hazardous Substance | CASBN |
Regulatory Synonyms
1
1
1
I BQ
Statutory 	
|ECBA
|Haate
Code T j number
	 Proposed BQ 	
Category| Pounds(Kg)
1 1
F019 | j
Wastewater treatnent sludges from the chemical | j
conversion coating of aluminum. | |
I i

1
1 1*
1
1
1
1
4 | P019
1
1
1
X | 1 (0.454)
1
1
1
1 1
P020 | |
Wastes (except wastewater and spent carbon froa | |
hydrogen chloride purification) froa the production! |
or manufacturing use (as a reactant, chemical in- j j
termediate, or component in a formulating process) j j
of tri- or tatrachlorophenol, or of intermediates j j
used to produce their pesticide derivatives. (Ihisj j
listing does not include wastes froa the production! 1
of Hexachlorophene from highly purified 2,4,5- | j
trichlorophenol.). | |
I i

1
1
1
1
1
1
1
1
1
1
1
1
1
4 j F020
i
i
i
i
i
i
i
i
i
1
1
X 1 1 (0.454)
i
i
i
i
i
i
i
i
i
i
1 1
F021 | |
Wastes (except wastewater and spent carbon froa | |
hydrogen chloride purification) froa the production! j
or manufacturing use (as a reactant, cheaical In- j j
termediate, or component in a formulating process) j j
of pentachlorophenol, or of intermediates used to j j
produce its derivatives. j j
I i

1
1
1
1
1
1
1
1
1
1
4 | P021
i
i
i
i
i
i
i
1
X | 1 <0.454)
i
i
i
i
i
i
i
1 1
F022 j j
Wastes (except wastewater and spent carbon froa j j
hydrogen chloride purification) froa the j j
or manufacturing use (as a reactant, cheaical in- j j
termediate, or component in a formulating process) j j
of tetra-, penta-, or hexachlorobenzenes under) j j
alkaline conditions. j j
¦ i

1
1
1
1
1
1
1
1
1
1
4 | P022
i
i
i
i
i
i
¦
1
X | 1 (0.454)
i
i
i
i
i
i
¦
1 1
P023 | |
Wastes (except wastewater and spent carbon froa j j
hydrogen chloride purification) froa the production! j
of materials on equipment previously used for the j j
production or aanufacturing use (as a reactant, j j
chemical intermediate, or component in a formula- j j
ting process) of tri- and tetrachlorophenols. j j
(This listing does not include wastes from j j
equipment used only for the production or use of j j
Hexachlorophene from highly purified 2,4,5- j j
trichlorophenol.). j j

1
1
i
i
i
i
i
i
i
i
i
i
1
4 j F023
i
i
i
i
i
i
i
i
i
i
i
X 1 1 (0.454)
1
1
1
1
1
1
1
1
1
1
NOTE: ALL COMMENTS/ROTES ARE LOCATED AT THE BID OF THIS TABLE
-------
LIST OP HAZARDOUS SUBSTANCES AND REPORTABLE QUANTITIES - Continued
1 1
1 1
1 I
1 1
Hazardous Substance | CASBN |
Regulatory Synonyms
1
1
1
1 BQ
Statutory 	
|BCHA
j Waste
Code T jnumber
	 Proposed BQ 	
Category) Pounds(Kg)
1 1
F024 | |
Wastes, Including but not limitad to, distillation j |
residues, heavy ends, tars, and reactor cleanout ( |
wastes, Croa the production at chlorinated | |
aliphatic hydrocarbons, having carbon content from | |
one to five, utilising (roe radical catalysed j |
processes. (This listing does not include light | |
ends, spent filters and filter aids, spent | |
dessicants(sic), wastewater, wastewater treatment | |
sludges, spent catalysts, and wastes listed in j j
Section 261.32.). j j
I i

1
1 1*
1
1
1
1
1
1
1
1
1
1
1
1
4 | F024
1
1
1
1
1
1
1
1
1
1
1
1
X 1 1 (0.454)
1
1
1
1
1
1
1
1
1
1
1 I
F026 | I
Wastes (except wastewater and spent carbon froa j |
hydrogen chloride purification) from the j |
production of aaterials on equipment previously | |
used for the manufacturing use (as a reactant, | |
chemical intermediate, or component in a | |
formulating process) of tetra-, penta-, or | |
hexachlorobenzene under alkaline conditions. | |
I i

1
1
1
1
1
1
1
1
1
|
1
4 | P026
i
i
i
i
i
i
i
¦
1
X | I (0.454)
i
i
i
i
i
i
i
i
1 1
F027 | |
Discarded unused formulations containing tri-, j j
tetra-, or pentachlorophenol or discarded unused j |
formulations containing compounds derived froa j |
these chlorophenols. (This listing does not includej j
formulations containing Hexachlorophene synthesized | |
from prepurified 2,4,5-tnchlorophenol as the sole j |
component.). | |
i |

1
1 1*
i
i
i
i
i
i
i
1
1
4 j F027
i
i
i
i
i
i
i
I
i
X 1 1 (0.454)
1
1
1
1
1
1
1
1 1
F028 | |
Residues resulting from the incineration or thermalj |
treatment of soil contaminated with EPA Hazardous | |
Waste Nos. F020, F021, F022, F023, F026, and F027. j j

1
1 1'
i
i
i
1
4 | F028
i
i
i
1
X I 1 <0.454)
i
i
i
NOTE; ALL COMMENTS/BOTES ARE LOCATED AT THE END 07 THIS TABLE
-------
LIST OP HAZARDOUS SUBSTANCES AND REPORTABLE QUANTITIES - Continued
1 1
1 1
1 1
1 1
Hazardous Substance | CASRN |
Regulatory Synonyms
1
1
1
1 BQ
Statutory 	
| |BCBA
j jWaste
j Code 1* jsuaber
	 Proposed BQ 	
Category| Pounds(Kg)
1 1
K001 | |
Bottom sediment sludge from the treatment of | |
wastewaters from wood preserving processes that use| |
creosote and/or pentachlorophenol. | |
i i

1
1 1*
1
1
1
|
1 1
| 4 | K001
1 1
1 1
1 1
¦ |
1
* I
1
1
1
1
1 (0.454)
1 1
K002 | |
Wastewater treatment sludge from the production of | |
chrome yellow and orange pigments. | |
1 i

1
1 1*
1
1
I
| 4 | K002
1 1
1 1
| |
1
X |
1
1
1
1 (0.454)
1 1
K003 | |
Wastewater treatment sludge from the production of j j
molybdate orange pigments. | |
i i

1
1 1*
1
1
|
| 4 | K003
1 1
1 1
i I
1
* 1
1
1
1
1 (0.454)
1 1
K004 | |
Wastewater treatment sludge from the production of | |
zinc yellow pigments. | |
I i

1
1 1*
1
1
1
1 1
| 4 | K004
1 1
1 1
1
1
z 1
1
1
1
1 (0.454)
1 1
K005 | |
Wastewater treatment sludge from the production of | |
chrome green pigments. | |
i !

1
1 1*
1
1
|
| 4 | K005
1 1
1 1
¦ |
1
X 1
1
1
1
1 (0.454)
1 1
K006 | |
Wastewater treatment sludge from the production of | |
chrome oxide green pigments (anhydrous and | |
hydrated). j j
I i

1
1 1*
1
1
1
|
| 4 | K006
1 1
1 1
1 1
j |
1
X 1
1
1
1
1
1 (0.454)
1 1
K007 | |
Wastewater treatment sludge from the production of | |
iron blue pigments. | |
I i

1
1 1*
1
1
1
| 4 | K007
1 1
1 1
¦ |
1
X 1
1
1
1
1 (0.454)
1 1
K008 | |
Oven residue from the production of chroma oxide | |
green pigments. | |

1
1 1*
1
1
| 4 | K008
1 1
1 1
1
X 1
1
1
1 (0.454)
NOTE: ALL COMMENTS/NOTES ARE LOCATED AT THE END OF THIS TABLE
-------
LIST OF HAZARDOUS SUBSTANCES AND REPORTABLE QUANTITIES - Continued
Haiardous Substance
1 1
1 1
1 1
1 1
| CASRH |
Regulatory Synonyas
1
1
1
I BQ
Statutory 	
| |HCE&
j j Waste
j Code T jNumber
	 Proposed BQ 	
Category| Pounds(Kg)
K009
Distillation bottoms froa tha production of
acetaldehyde froa ethylene.
1 1
1 1
1 1
1 1
1 1

1
1 1*
1
1
1
1 4
K009
1
A I
1
1
|
10 (4.54)
K010
Distillation sida cuts from tha production of
acetaldehyde froa ethylene.
1 1
1 1
1 1
1 1
1 1

1
1 **
1
1
I
| 4
K010
1
A |
1
1
1
10 (4.54)
K011
Bottom straaa froa tha wastewater stripper in tha
production of acrylonitrila.
1 1
1 1
1 1
1 1
I 1

1
1 1*
1
1
1 4
K011
1
A |
i
i
1
10 (4.54)
K013
Bottom straaa froa tha acetonitrile column in tha
production of acrylonitrila.
1 1
1 1
1 1
1 1
1 1

1
1 1*
i
i
I
1 4
K013
1
A |
i
i
1
10 (4.54)
K015
Still bottoas froa the distillation of benzyl
chloride.
1 1
1 1
1 1
1 1
1 I

1
1 1*
i
i
i
1 4
K015
1
X |
i
i
1 (0.454)
K016
Heavy ends or distillation residues froa tha
production of carbon tetrachloride.
1 1
1 1
1 1
1 1
| |

1
1 **
i
i
a
1 4
KOlfi
i
x i
i
i
1 (0.454)
K017
Heavy ends (still bottoms) froa the purification
column in tha production of epichlorohydrin.
1 1
1 1
1 1
1 1
I I

1
1 1*
i
i
I
1 4
K017
1
A 1
i
i
i
10 (4.54)
K016
Heavy ends froa the fractionation column in ethyl
chloride production.
1 1
1 1
1 1
1 1
1 1

1
1
i
i
¦
1 4
K018
1
X |
i
i
i
1 (0.454)
K019
Heavy ends froa tha distillation of ethylene
dichloride in ethylene dichloride production.
1 1
1 1
1 1
1 1

i
i i*
i
i
1 4
K019
1
A |
i
i
10 (4.54)
NOTE: ALL COMMENTS/NOTES ARE LOCATED AT THE END OF THIS TABLE
-------
LIST 07 HAZARDOUS SUBSTAHCES AMD REPORTABLE QUANTITIES - Continued
1 1
1 1
1 1
1 1
Hazardous Substance | CASHH |
Regulatory Synonyms
1
1
1
1 HQ
Statutory 	
|RCBA
.(Waste
Code TjHuiber
	 Proposed BQ 	
Category| Pounds(Kg)
1 1
K020 | |
Heavy ends from the distillation of vinyl chloride | |
in vinyl chloride monomer production. (Components j j
of this waste are identical with those of K019, j j
immediately preceding.) j j
j j

1
1 1*
1
1
1
1
1
1
4 | K020
1
1
1
1
I
1
A |
1
1
1
1
1
10 (4.54)
K021 | |
Aqueous spent antimony catalyst waste from j j
fluoromethanes production. | j
i i

1
1
1
1
1
4 | K021
i
i
1
1
A |
i
i
1
10 (4.54)
1 1
K022 | |
Distillation bottom tars from the production of j j
phenol/acetone from cumene. j j
I i

1
1 I'
1
1
1
4 | K022
i
i
i
1
X |
i
i
I
1 (0.454)
1 1
K025 j j
Distillation bottoms from the production of j j
nitrobenzene by the nitration of benzene. j j
i i

1
1
i
i
•
i
4 | K02S
1
1
|
1
A |
i
i
10 (4.54)
1 1
K027 j |
Centrifuge and distillation residues from toluene j j
diisocyanat* production. j j
1 i

i
i i*
i
i
i
1
4 | K027
1
1
I
i
A I
1
1
1
10 (4.54)
1 1
K028 j j
Spent catalyst from the hydrochlorinator reactor inj |
the production of 1,1,1-trichloroethane. j j
i i

1
1 1*
i
i
i
1
4 | £028
i
i
i
1
A |
i
i
i
10 (4.54)
1 1
K029 | |
Waste from the product steam stripper in the j j
production of 1,1,1- trichloroethane. j j
¦ i

1
1 1*
i
i
i
1
4 | K029
i
i
i
1
A |
I
\
i
10 (4.54)
1 1
K030 j j
Column bottoms or heavy ends from the combined j j
production of trichloroethylene and j j
perchloroethylene. j j

i
11*
i
i
i
i
4 | K030
1
1
1
t
* I
i
i
i
1 (0.454)
NOTE: ALL COMMENTS/NOTES ABE LOCATED AT THE END OF THIS TABLE
-------
LIST or HAZARDOUS SUBSTANCES AND REPORTABLE QUANTITIES - Continued
1 1
1 1
1 1
i 1
• Hazardous Substance | CASBH |
Regulatory Synonyas
1
1
1
1 HQ
Statutory 	
|BCRA
,| Waste
Coda ' jNumber
	 Proposed BQ 	
Category| Pounds(Kg)
1 1
K031 | j
By-product salts generated in the production of | j
MSMA and cacodylic acid. j |
1 |

1
i i»
i
i
I
1
4 | K031
1
1
1
1
X | 1 (0.454)
1
1
1
1 1
K032 j j
Wastewater treataant sludge from the production of j j
chlordane. j j
¦ i

1
1 14
i
i
¦
1
4 | K032
i
i
i
1
A | 10 (4.54)
i
i
i
1 1
K033 | j
Wastewater and scrub water froa the chloriaation of| |
cyclopentadiena in the production of chlordana. | |
1 i

1
1 1*
i
i
i
1
4 j K033
i
i
i
1
A | 10 (4.54)
i
i
i
1 1
K034 | |
Filter solids froa the filtration of j j
hexachlorocyclopantadiene in the production of j j
chlordane. j j
I i

1
1
i
i
i
¦
1
4 | K034
i
i
i
i
1
A | 10 <4.54)
i
i
i
1 1
K03S | |
Wastewater treataant sludges generated in the | |
production of craosota. j j
¦

1
1 1*
i
i
1
1
4 j K035
i
i
¦
1
Z 1 1 (0.454)
1
1
1
K036 | |
Wastewater froa the washing and stripping of j j
phorate production. | }
j |

1
1 1*
i
i
l
i
4 | K038
1
1
I
1
A | 10 (4.54)
i
i
i
K040 | |
Wastewater treatment sludge froa the production of j j
phorate. (Components of this waste are identical j j
with those of K03B, above.) | j
¦ i

1
1
i
i
i
¦
1
4 | K040
1
1
1
1
1
A J 10 (4.54)
1
1
1
|
1 1
K041 | j
Wastewater treatment sludge froa the production of j j
toxaphene. | |

1
1
i
i
1
4 | K041
i
i
1
X | 1 (0.454)
1
1
NOTE: ALL COHMENTS/BOTES ARE LOCATED AT THE EKD OF THIS TABLE
-------
LIST or HAZARDOUS SUBSTANCES AND REPORTABLE QUANTITIES - Continued
Hazardous Substance
1 1
1 1
1 1
1 1
| CASRN |
Regulatory Synonyms
1
1
1
1 BQ
Statutory 	
|RCBA
| Waste
Code i'lHunfaar
	 Proposed BQ 	
Category| Pounds(Kg)
K042
Heavy enda or distillation residues from the
distillation of tetrachlorobenzane in the
production of 2,4,5-T.
1 1
1 1
1 1
1 1
1 1
| 1

1
1
1
1
1
|
1
4 | K042
1
1
1
1
1
A |
1
1
1
1
10 (4.54)
K043
2,6-Dichlorophenol waste from the production of
2,4-D.
1 1
1 1
1 1
1 1
1 1

1
1 1*
1
1
|
1
4 | K043
1
1
1
A |
1
1
1
10 (4.54)
K04S
Dissolved air flotation (DAP) float froa the
petroleum refining industry.
1 1
1 1
1 1
1 1
1 1

1
1
1
1
1
1
4 | E048
1
1
¦
1
X 1
1
1
1
1 (0.454)
K049
Slop oil emulsion solids from the petroleum
refining industry.
1 1
1 1
1 1
1 1
1 1

1
1 1*
1
1
1
4 | K049
1
1
1
1
x 1
1
1
1
1 (0.454)
K050
Heat exchanger bundle cleaning sludge from the
petroleum refining industry.
1 1
1 1
1 1
1 1
I 1

1
1
1
1
I
1
4 j K050
i
i
¦
1
X 1
1
1
1
1 (0.454)
K051
API separator sludge from the petroleum refining
industry.
1 1
1 1
1 1
1 1
1 1

1
1 1*
1
1
1
i
4 | K051
1
1
i
1
X 1
1
1
1
1 (0.454)
K060
Ammonia still lias sludge from coking operations.
1 1
1 1
1 1
1 1

1
1 1*
1
1
1
4 | K060
1
i
1
X 1
1
1
1 (0.454)
K061
Emission control dust/sludge froa the primary
production of steel in electric furnaces.
1 1
1 1
1 1
1 1
| I

1
1 1*
1
1
4 | K061
1
1
1
1
X 1
1
1
1 (0.454)
K062
Spent pickle liquor from steel finishing
operations.
1 1
1 1
1 1
1 1

1
1 1*
1
1
1
4 | K062
i
i
1
X 1
1
1
1 (0.454)
NOTE: ALL COMMENTS/NOTES ARE LOCATED AT THE END OF THIS TABLE
-------
LIST or HAZARDOUS SUBSTANCES AND REPORTABLE QUANTITIES - Continued
1 1
1 1
1 1
1 1
Hazardous Substance | CASRH |
Bogulatory Synonyas
1
1
1
1 HQ
Statutory 	
|BCBA
i Waste
Code T jnumber
	 Proposed BQ 	
Category| Pounds(Kg)
1 1
K069 I |
Emission control dust/sludge from secondary lead | |
smelting. | |
j j

1
1 1*
1
1
1
1
4 | K069
1
1
I
1
X | 1 (0.454)
1
1
I
K07J | |
Chlorinated hydrocarbon waste from the purification) |
step of the diaphragm cell process using graphite | |
anodes in chlorine production. | |
I i

1 1*
1
1
1
1
4 | K073
1
1
1
|
A | 10 (4.54)
1
1
1
|
1 1
K084 | |
Wastewater treatment sludges generated during the | |
production of veterinary pharmaceuticals froa | |
arsenic or organo-arsenic compounds. | |
i i

1
1
i
i
i
i
4 | K084
1
1
1
X | 1 (0.454)
1
1
1
I
1 1
K08S | |
Distillation or fractionation coluan bottoas froa | |
the production of chlorobenzenes. | |
i i

1
1 1*
i
i
i
4 | K085
1
1
|
A | 10 (4.54)
1
1
1
1 1
K086 | |
Solvent washes and sludges, caustic washes and | |
sludges, or water washes and sludges froa cleaning | |
tubs and equipment used in the formulation of ink | |
froa pigments, driers, soaps, and stabilisers | |
containing chroaiua and lead. | |
i i

i
j i*
i
i
i
i
i
i
4 | K086
1
1
1
1
1
|
X | 1 (0.454)
1
1
1
1
1
I
1 1
K095 | |
Distillation bottoas from the production of 1,1,1- | |
trichloroethane. | |
i i

i
i i*
i
i
¦
4 | K095
1
1
i
1
B | 100 (45.4)
i
i
1
1 1
K096 | |
Heavy ends froa the heavy ends column froa the | |
production of 1,1,1-trichloroethane. | |
i i

i
i i*
i
i
i
1
4 | K096
1
1
|
1
A | 10 <4-54)
i
i
i
1 1
K097 | |
Vacuum stripper discharge from the chlordane | |
chlonnator in the production of chlordane. | |

i
i i*
i
i
4 | K097
1
1
X 1 1 (0.454)
1
1
NOTE: ALL COMMENTS/NOTES ARE LOCATED AT THE END OF THIS TABLE
-------
LIST OP HAZARDOUS SUBSTANCES AND REPORTABLE QUANTITIES - Continued
1 1
t 1
i 1
1 1
Hazardous Substance | CASBN |
Regulatory Synonyms
1
1
1
I BO
Statutory 	
|HCRA
jWaste
Code TjNumber
	 Proposed RQ 	
Category| Pounds(Kg)
1 1
K098 | |
untreated process wastewater fron the production ofj j
toxaphene. j j
I |

1
1 1*
1
1
1
1
4 j K098
1
1
|
1
X 1 1 (0.454)
1
1
1
1 1
K099 | |
untreated wastewater from the production of 2,4,-D.j j
i i

1
1 1*
1
I
1
4 j K099
i
i
1
A | 10 (4.54)
i
i
1 1
K100 j j
Waste leaching solution from acid leaching of | |
emission control dust/sludge froa secondary lead j j
smelting. (Components of this waste are identical j j
with those of K069.) j j
i i

1
1
1
1
1
1
1
1
4 | K100
i
i
i
i
¦
1
2C j 1 (0.454)
i
i
i
i
¦
1 1
K101 j j
Distillation tar residues froa the distillation of j j
aniline-based compounds in the production of j j
veterinary pharmaceuticals froa arsenic or organo- | |
arsenic compounds. | |
¦ i

1
1
1
1
1
1
1
i
4 | K101
1
1
1
1
1
i
X | 1 (0.454)
1
1
1
1
a
1 1
K102 j j
Residue froa the use of activated carbon for j j
decolonzation in the production of veterinary | j
pharmaceuticals fron arsenic or organo-arsenic j j
compounds j j
1 i

1
1 1#
1
1
1
1
1
1
4 j K102
i
i
i
i
i
1
X j 1 <0.454)
i
i
i
i
1
1 1
K104 j |
Combined wastewater streams generated froa j j
nitrobenzene/aniline chlorobensenes. j j
i i

1
1 I'
1
1
|
1
4 j K104
i
i
i
1
h | 10 (4.54)
i
i
i
1 1
K10S j j
Separated aqueous stream froa the reactor product | j
washing step in the production of chlorobensenes. j j
¦ i

1
1 I'
1
1
J
1
4 | K105
i
i
i
1
h | 10 (4.54)
i
i
i
1 1
Kill | |
Product washwaters fron the production of j j
dimtrotoluene via nitration of toluene. | j

1
1
1
1
1
4 | Kill
i
i
I
A | 10 (4.54)
1
1
MOTE: ALL COMMENTS/NOTES ARE LOCATED AT THE END OP THIS TABLE
-------
LIST OF HAZARDOUS SUBSTANCES AND REPORTABLE QUANTITIES - Contimiad
1 1
1 1
1 1
1 1
H&mardous Substance | CASK) |
Regulatory Synonyms
1
1
1
1 «J
Statutory 	
| |HCBA
j i Waste
| Code ¦'jsuBber
	 Proposed BQ 	
Category| Pounds(Kg)
1 1
K112 j |
Reaction by-product water from the drying colum inj j
the production of toluenediaiune via hydrogenation j j
of dinitrotoluene. j j
i i

1
1 1*
1
1
1
I
1 1
| 4 | K112
1 1
1 1
1 1
| 1
1
A | 10 (4.54)
1
1
1
1 1
K113 | |
Condensed liquid light ends fron the purification j j
of toluenediaain* in the production of j j
toluenediamine via hydrogenation of dinitrotoluene.j j
¦ i

1
1 1*
1
1
1
1
1 1
| 4 | K113
1 1
1 1
1 1
1 1
1
A | 10 (4.54)
1
1
1
|
1 1
K114 j j
Vicinals from the purification of toluenodiamine inj |
the production of toluenediaiune via hydrogenation j j
of dinitrotoluene. j |
i i

1
1 1*
1
1
1
1
1 1
| 4 j K114
1 1
1 1
1 1
1 I
1
A | 10 (4.54)
i
i
i
1 1
K115 | j
Heavy ends from the purification of toluenediaaine j j
in the production of toluenediaiune via | |
hydrogenation of dinitrotoluene. | |
I i

1
1 1"
1
1
1
1
1 1
| 4 | KU5
1 1
1 1
1 1
1 1
i
A | 10 (4.54)
1
1
1
|
1 1
K116 j |
Organic condensate froa the solvent recovery column| |
in the production of toluene diisocyanate via j j
phosgenation of toluenediamine. | |
I i

1
1 1*
I
1
1
I
1 1
| 4 j Kll6
i i
i i
i i
i i
1
A | 10 (4.54)
1
1
1
|
1 1
K117 | |
Wastewater froa the reaction vent gas scrubber in j j
the production of ethylene bronide via broaination j j
of ethene. j |
i i

1
1 1*
1
1
1
|
i i
| 4 | K117
1 1
1 1
1 1
1 |
1
X | 1 (0.454)
1
1
1
|
1 1
K118 | |
Spent absorbent solids froo purification of j j
ethylene dibromide in the production of ethylene j j
dibronide. j j

1
1 1*
1
1
1
1 1
| 4 | K11S
1 1
1 1
1 1
1
X | 1 (0.454)
1
1
1
NOTE: ALL COMMENTS/NOTES ARE LOCATED AT THE BHD OF THIS TABLE
-------
LIST OF HAZARDOUS SUBSTANCES AND REPORTABLE QUANTITIES - Continued
Hazardous Substance
1 1
1 1
1 1
1 1
| CASBN |
Regulatory Synonyms
1 1
|	 Statutory 	1
1 1 IHCBA |
| | |waste |	 Proposed BQ 	
j BQ j Code tjsumber|Category| Pounds(Kg)
K136
still bottoms from the purification of ethylene
dibromide in the production of ethylene dlbrostide
via bromination of ethene.
1 1
1 1
1 1
1 1
1 1

till 1
| 1* I 4 j K136 j X | 1 (0.454)
1 1 1 1 1
1 1 1 1 1
1 1 1 1 1
t - indicates the statutory source as defined by 1, 2, 3, or 4 below
+ + - Ho reporting of releases of this hazardous substance is required if the diameter of the pieces of the solid metal released is equal to or exceeds
100 micrometers (0.004 inches).
u> ttt - The HQ for asbestos is limited to friable forms only.
1 - indicates that the statutory source for designation of this hazardous substance under CEBCLA is CWA Section 311(b)(4)
¦t- 2 - indicates that the statutory source for designation of this hazardous substance under CEHCLA is CWA Section 307(a)
3	- indicates that the statutory source for designation of this hazardous substance under CERCLA is CAA Section 112
4	- indicates that the statutory source for designation of this hazardous substance under CERCLA is RCRA Section 3001
1* - indicates that the 1-pound BQ is a CEBCLA statutory BQ
• - indicates that the BQ is subject to change when the assessment of potential carcinogenicity and/or chronic toxicity is completed,
ttt - The Agency nay adjust the BQ for methyl isocyanate in a future rulemaking; until then the statutory 1-pound RQ applies.
§ - The Agency nay adjust the BQ for radionuclides in a future rulemaking; until then the statutory BQ applies.
-------
Substances Identified as Potential Carcinogens and Addressed in the NPRM
A total of 191 hazardous substances were identified from among the 611
individual CERCLA hazardous substances as potential carcinogens. These
191 potential carcinogens vere submitted to the CAG for a detailed
potential carcinogenicity ranking and are having adjusted RQs proposed in
the NPRM for vhich this report provides the technical background. Some
of these hazardous substances are not specifically mentioned in the
sources cited in the preceding section entitled "METHODOLOGY FOR
IDENTIFYING HAZARDOUS SUBSTANCES SUBJECT TO ASSESSMENT FOR POTENTIAL
CARCINOGENICITY," but vere identified because they are members of some
particular class of chemical compounds with known potential for
carcinogenicity. For instance, the "First Annual Report on Carcinogens"
lists "arsenic and arsenic compounds," "cadmium and cadmium compounds,"
"nickel and nickel compounds," "chromium and chromium compounds," and
"soots, tars, and carbon black," the latter with the active agents
identified as "polycyclic aromatic hydrocarbons." As a result, all CERCLA
Section 101(14) hazardous substances which are members of these classes
were submitted to the CAG for review and detailed assessment.
Substances Not Identified as Potential Carcinogens
For 414 individual hazardous substances and 28 waste streams, criteria
other than potential carcinogenicity are used to adjust their RQs since
they were not identified as potential carcinogens (or, in the case of
wastes, do not contain constituents that vere identified as potential
carcinogens). Final RQs for 340 of these appear in the final rule
published on April 4, 1985 (50 FR 13456-13513). Final RQs for an
additional 102 appear in the final rule published on September 29, 1986
(51 FR 34534-34549).
Within the 273 hazardous substances (195 individual hazardous substances
and 78 hazardous waste streams) addressed in this report, there are four
hazardous substances that were not evaluated for the primary RQ
3-35
-------
adjustment criterion of potential carcinogenicity. They are chloral,
parathion, hexachlorocyclopentadiene, and 2-ethoxyethanol. The proposed
RQs for these four hazardous substances are based on primary criteria
other than potential carcinogenicity.
Chloral originally vas identified as a potential carcinogen because it
vas thought to hydrolyze to chloroform, a potential carcinogen. The May
25, 1983 NPRM (48 FR 23552-23602) indicated that chloral was to be
assessed for potential carcinogenicity based on its potentially
carcinogenic reaction product, chloroform. However, one comment received
in response to the May 25, 1983 NPRM pointed out that chloral does not
readily hydrolyze. The Agency concurs, and the adjusted RQ of chloral is
being reproposed (5000 pounds), based on evaluation of the primary
criteria for chloral itself, not on an evaluation of the primary criteria
of its hydrolysis products.
Parathion and hexachlorocyclopentadiene have not been identified as
potential carcinogens for RQ adjustment purposes. The RQs for both
substances are being reproposed from the 1-pound RQs proposed in the
May 25, 1983 NPRM for both substances on the basis of the primary RQ
adjustment criterion of aquatic toxicity. A comment received on the May
25, 1983 NPRM cited more recent aquatic toxicity data using preferred
species. This new aquatic toxicity data supports a proposed 10-pound RQ
for parathion. Since publication of the May 25, 1983 NPRM, the Agency has
also obtained additional data on the degradation of
hexachlorocyclopentadiene in the environment. These additional data
support raising the previously proposed 1-pound RQ for
hexachlorocyclopentadiene to 10 pounds based on the secondary criteria of
BHP.
Finally, 2-ethoxyethanol also has not been identified as a potential
carcinogen and its proposed 1000-pound RQ is based on the primary RQ
adjustment criterion of chronic toxicity. After the most recent
rulemaking proposing RQ adjustments (50 FR 13514, April 4, 1985),
3-36
-------
2-ethoxyethanol was added to the list of CERCLA hazardous substances as a
result of its listing as a hazardous waste under Section 3001 of RCRA (51
FR 6537-6542, February 25, 1986). Therefore, the proposed RQ adjustment
for 2-ethoxyethanol is included in the proposed rule which this technical
background document supports.
Two substances (pentachloroethane and methyl chloride) for which adjusted
RQs originally were proposed in the April 4, 1985 NPRM (50 FR 13514) have
their RQs reproposed for adjustment in the proposed rule. As noted in
the September 29, 1986 final rule (51 FR 34534), the statutory one-pound
RQs for these two substances were retained, pending analysis of their
potential carcinogenicity. That analysis is now complete and the
proposed RQ for methyl chloride is 100 pounds based on ignitability and
potential carcinogenicity. Pentachloroethane was evaluated for potential
carcinogenicity, but received a lower RQ of 10 pounds based on aquatic
toxicity. Therefore, the proposed RQ for pentachloroethane is 10 pounds
based on aquatic toxicity.
ADJUSTMENT OF RQS FOR THE 273 HAZARDOUS SUBSTANCES
Results of the CAG Ranking Methodology
The detailed results of the CAG's assessment of 191 CERCLA hazardous
substances for potential carcinogenicity appear in the summary table in
Appendix A. The available data allow the assignment of a high, medium,
or low rank to 184 of the hazardous substances. Seven hazardous
substances identified with a footnote of "None require that primary
criteria other than potential carcinogenicity be used as a basis for
hazard ranking. A detailed breakdown of the CAG hazard rankings and
footnotes is shown below:
3-37
-------
Number of
Hazardous Substances
Hazard Ranking
or Footnote
62
High
77
Medium
45
Low ,
7
"None
151

RQs for Potential Carcinogens for Which Potency Factors Cannot be
Calculated
For 22 of the 191 individual hazardous substances identified as potential
carcinogens, there is either sufficient or limited data shoving them
to have a potential carcinogenic effect, but not enough quantitative
information about the associated dose to allow a potency factor to be
estimated. (These substances are identified with the footnotes "a",
"ab", or "p" in the table in Appendix A.)
In the case vhere available data are inadequate for estimation of a
potency factor, the Agency has identified two possible alternatives:
1.	If the best available data suggest that the substance is a
possible strong carcinogen, but there is no basis for assigning a
specific ED^q dose (i.e., all treated animals at every
experimental dose developed tumors), then the substance can Be
administratively assigned to the highest potency group (i.e.,
Potency Group 1).
2.	If the best available data are inadequate for calculating a
potency factor and no quantitative inferences can be made (i.e.,
in animal studies where control groups were not used or the
number of animals treated was not specified), then the substance
can be assigned a mid-range potency factor. This has the result
of placing these substances into Potency Group 2.
Hazard rankings can then be assigned by following the standard procedure
of combining the weight-of-evidence group with the assigned potency
group.
This methodology assigns a high hazard ranking to four potential
carcinogens, a medium hazard ranking to 14 potential carcinogens, and a
low hazard ranking to four potential carcinogens.
3-38
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Asbestos has been identified as a known human carcinogen (weight-of-
evidence Group A). However, exposure to asbestos is measured by
calculating the size and number o£ airborne fibers, and not by the
standard method of measuring exposure to potential carcinogens based on
weight, volume, or concentration. Therefore, a numerical potency factor
based on weight cannot be calculated for asbestos to achieve a direct
potency ranking. Thus, EPA has administratively assigned a median or
mid-range potency (Potency Group 2) to asbestos. Using the Agency's
matrix for ranking potential carcinogens, a substance such as asbestos,
in weight-of-evidence Group A and Potency Group 2, receives a high
hazard ranking and a 1-pound RQ.
RQs for Organic Arsenic Compounds
Three organic arsenic compounds appear on the CERCLA Section 101(14)
list: cacodylic acid, dichlorophenylarsine, and diethylarsine. The CAG
found no qualitative or quantitative evidence demonstrating that these
substances themselves cause cancer and which would allow them to be
ranked as potential carcinogens. However, because each of these three
hazardous substances can and will degrade to inorganic arsenic oxides
(which are potential carcinogens) when released to the environment, the
Agency has decided to propose a 1-pound RQ for each substance, based on
the RQs for arsenic oxides. This assignment is consistent with the fate
of the organic arsenic compounds, and follows the Agency's methodology of
considering, for purposes of RQ adjustment, chemical reactions of
hazardous substances once they are released into the environment and
basing the RQ of a substance on its more hazardous degradation products.
RQ for 3,3'-Dichlorobenzidine
The CAG methodology ranks 3,3'-dichlorobenzidine as medium, leading to
an RQ assignment of 10 pounds. However, in reviewing substances for BHP
adjustment, it was found that 3,3'-dichlorobenzidine is subject to rapid
photolysis if released into the environment, yielding benzidine itself as
one of the photolysis products. The proposed RQ for
3-39
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3,3'-dichlorobenzidine was reduced to be equivalent to that of benzidine
which is ranked high by the CAG, and assigned a 1-pound RQ.
RQs for Beryllium and Beryllium Salts
The proposed adjusted RQ for beryllium metal is based on human
occupational studies that yield a potency factor of between 1 and 100,
which, along with a weight-of-evidence ranking of B2, yields a hazard
ranking of medium and an RQ of 10 pounds. Every soluble beryllium
compound that has been tested, including beryllium sulfate, beryllium
fluoride, beryllium oxide, and beryllium phosphate has been shown to be
carcinogenic. It is therefore considered likely that all soluble forms
of beryllium are carcinogenic in animals. The potency factor for all
soluble forms of beryllium is based on beryllium sulfate exposure in
rats, which produces a potency factor of over 19,000 and a 1-pound RQ.
Because all soluble forms of beryllium exhibit similar carcinogenic
response, the Agency has chosen to use the same data to adjust the
statutory RQs of beryllium chloride, beryllium fluoride, and beryllium
nitrate to one pound.
RQ for PCBs
In the May 25, 1983 NPRM (48 FR 23552), the Agency proposed to lower the
RQ for PCBs from the statutory level of 10 pounds (established on the
basis of aquatic toxicity data under Section 311 of the CVA) to one
pound, on the basis of other aquatic toxicity data. EPA received 28
comment letters containing 66 total comments, all of which objected to
the proposed 1-pound RQ for PCBs. The Agency stated in the April 4, 1985
final rule that it was evaluating PCBs for potential carcinogenicity and
would retain the 10-pound statutory RQ until that analysis was completed.
The Agency's analysis of PCBs for potential carcinogenicity is now
complete, and that analysis has yielded a hazard ranking of medium,
corresponding to a 10-pound RQ. However, based on a re-examination of
all of the comments received on the appropriate RQ for PCBs in response
to the May 25, 1983 proposal and a re-evaluation of all available aquatic
3-40
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toxicity data concerning PCBs, the Agency has decided to repropose a
1-pound RQ for PCBs based on aquatic toxicity.
The Agency's current methodology for adjusting RQs based on aquatic
toxicity favors use of data from tests using adult life stages. However,
use of data from tests using juvenile or younger life stages is
appropriate for adjusting the RQ for PCBs because PCBs bioaccumulate, are
insoluble, and sink in water. Because of the combined effect of these
chemical and physical properties, PCBs pose a particular threat to
benthic organisms (including the early life stages of many aquatic
species). The Agency used early life stage data to support the original
proposed 1-pound RQ for PCBs in the Nay 25, 1983 NPRM. As mentioned
earlier, the EPA received extensive comments opposing a 1-pound RQ for
PCBs. None of these comments, however, objected to the Agency's reliance
on early life stage data. In addition, use of such data is entirely
consistent with and in fact, is mandated by the EPA's 1985 Guidelines for
Deriving Numerical National Water Quality Criteria for the Protection of
Aquatic Organisms and Their Uses.
In contrast to the aquatic toxicity data derived from tests using early
life stages which supports a 1-pound RQ for PCBs, available data from
tests using adult life stages support a 10-pound RQ for PCBs. These data
are presented in Table 3-2.
The Agency has decided that where both early life stage and adult life
stage data are available for substances that are bioaccumulative
insoluble sinkers, the early life stage data will be preferred because
3-41
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Table 3-2
AQUATIC TOXICITY DATA FOR PCBs
PCB Isomer
Aroclor 1254
Aroclor 1242*
Aroclor 1242*
Capacitor 21**
Capacitor 21**
Capacitor 21**
Aroclor 1016^
Aroclor 1242^
Aroclor 1248^
Aroclor 1254^
Aroclor 1260^
LC50
Test Species	(ppm)
Fathead Minnow	0.008
Fathead Minnov	0.015
Fathead Minnov	0.3
Largemouth Bass	0.002
Rainbow Trout	0.002
Redear Sunfish	0.019
Bluegill	0.46
Bluegill	0.125
Bluegill	0.69
Bluegill	2.7
Bluegill	0.4
Age
Newly Hatched
Newly Hatched
Fingerling
Newly Hatched
Newly Hatched
Newly Hatched
Fingerling
Fingerling
Fingerling
Fingerling
Fingerling
RQ
Based on Aquatic
Toxicity (pounds)
1
1
10
1
1
1
10
10
10
100
10
From Ambient Water Quality Criteria for Polychlorinated Biphenyls, U.S.
EPA, 1980 (EPA 440/5-80-068).
2
From Handbook of Acute Toxicity of Chemicals to Fish and Aquatic
Invertebrates, Fish and Wildlife Service, Department of the Interior, Report
137, 1980.
* A PCB containing 21% chlorine.
3-42
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this approach is consistent with the Agency's 1985 National Water Quality
Guidelines mentioned above. Table 3-3 provides a list of other hazardous
substances which are bioaccumulative insoluble sinkers. The Agency is in
the process of reviewing the aquatic toxicity data Cor the hazardous
substances listed in Table 3-3 and may readjust their RQs in a future
rulemaking action.
Status of Hazardous Substances Designated Under the CVA Section 311
The April 4, 1985 final rule (50 FR 13456) amended 40 CFR 117.3 to make
RQs adjusted under CERCLA the applicable RQs for notification of
discharges of hazardous substances pursuant to CVA Section 311. Thus,
the RQ adjustments proposed in the rulemaking which this technical
background document supports will, when finalized, apply to both CERCLA
and CVA Section 311 RQs.
Of the 195 individual hazardous substances assigned proposed RQs in the
NPRM associated with this technical background document, 63 were
originally listed as hazardous substances and assigned RQs under Section
311 of the CVA (40 CFR Parts 116 and 117). The proposed RQs lower the
statutory CVA RQs of 49 of these substances, raise the statutory RQs of
two of the substances, and leave the RQs of 12 of the substances at the
statutory level.
RQs under both CERCLA and the CVA are set forth in Table 3-1. Vhere
there is a release of a hazardous substance of an RQ into navigable
waters a single report to the National Response Center by the person in
charge will satisfy the notification requirements of both statutes. For
further discussion of the relationship between CERCLA RQs and CVA Section
311 RQs, see the May 25, 1983 proposed rule preamble at 48 FR 23569, and
the April 4, 1985 final rule preamble at 50 FR 13473.
3-43
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TABLE 3-3
LIST OF CERCLA 3IOACCUMULATIVE INSOLUBLE SINKERS (BIS)
Aldrin
Antimony
Antimony potassium tartrate
Antimony tribromide
Antimony trichloride
Antimony trioxide
Aroclor 1016
Aroclor 1221
Aroclor 1232
Aroclor 1242
Aroclor 1248
Aroclor 1254
Aroclor 1260
Arsenic
Arsenic disulfide
Arsenic trisulfide
alpha-BHC
beta-BHC
gamma-BHC
Bromoform
Brucine
Colbaltous sulfonate
Copper
Copper cyanide
Cupric oxalate
Cupric tartrate
ODD
DDE
DDT
Dichlorobenzene (mixed)
1.2-Dichlorobenzene
1.3-Dichlorobenzene
3,3'-Dichlorobenzidine
Dichloropropane
1,3-Dichloropropene
2,3-Dichloropropene
Dieldrin
1,2-Diphenylhydrazine
Endrin
Endrin aldehyde
Epichlorohydrin
Heptachlor
Hexachlorobutadiene
Hexachlorohexahydro-endo,
endo-dime thanonap thalene
Lead
Lead arsenate
Lead chloride
Lead fluoride
Lead iodide
Lead phosphate
Lead stearate
Lead sulfate
Lead sulfide
Lead thiocyanate
Mercuric sulfate
Mercuric thiocyanate
Mercury
Mercury fulminate
Mexacarbate
Parathion
PCBs
Pentachlorophenol
Selenium
TCDD
Toxaphene
1,2,4-Trichlorobenzene
Vanadium pentoxide
Source: Melvold, et al., 1985
3-44
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RQs for the F- and K- Hazardous Waste Streams
Hazardous waste streams, as defined in the Resource Conservation and
Recovery Act (RCRA, also called the Solid Waste Disposal Act of 1976)
regulations (40 CFR Parts 261.31 and 261.32), are commonly called the
"F-" and "K-" hazardous waste streams. These letters refer to the
prefixes used in the identifying hazardous waste number assigned by the
EPA. A total of 78 such waste streams are assigned proposed adjusted RQs
in this additional group of 273 hazardous substances. The procedure for
assigning RQs to hazardous wastes is based on analysis of constituents as
described below.
The F- waste streams (with the exception of F001 though F005) are
hazardous wastes from nonspecific sources (e.g., F019 is wastewater
treatment sludges from the chemical conversion coating of aluminum). The
K- hazardous waste streams are hazardous wastes from specific sources
(e.g., K.087 is decanter tank car sludge from coking operations). In
order to assign proposed RQs to these waste streams, each hazardous
constituent is examined. The next step is to identify the RQ associated
with each hazardous constituent and then assign an RQ to each waste
stream. The waste stream RQ is the lowest RQ associated with the
individual hazardous constituents of the waste stream.
Under 40 CFR 302.6, if a person in charge knows of the percentage
composition of a waste stream, the CWA mixture rule may be applied to the
RCRA F- and K- waste streams (all of which tend to be mixtures, except
for the waste streams F001 through F005). The CWA mixture rule provides
that "[d]ischarges of mixtures and solutions are subject to [regulation]
only where a component hazardous substance of the mixture or solution is
discharged in a quantity equal to or greater than its RQ "(44 FR 50767,
August 29, 1979). If the concentrations of the constituents are unknown,
the RQ of the waste stream applies. However, CERCLA itself does not
impose any testing requirements.
3-45
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The RCRA waste streams F001 through F005 are collective listings (e.g.,
five solvents which are hazardous wastes are listed collectively under
F005). RQs are assigned to these waste streams using the following
procedure. RQs are first assigned to each individual solvent (or
constituent) as described above. Then, a generic RQ is assigned to the
several hazardous wastes equal to the lowest RQ assigned to any of these
individual solvents. If the releaser is unsure which solvent he has
released, or if he has released a mixture of solvents, he must use the
generic RQ to determine whether notification is necessary. If the
releaser knows which solvent has been released, he can use the RQ
assigned to that particular solvent.
RQ adjustments are being proposed for 12 of the F- list hazardous waste
streams and 66 of the R- list hazardous waste streams. The statutory RQ
for these 78 hazardous wastes is currently 1 pound. The proposed
adjustments leave the RQs of 44 hazardous waste streams at 1 pound, raise
the RQs of 33 to 10 pounds, and raise the RQs of one hazardous waste
stream to 100 pounds.
The proposed adjusted RQs for waste streams K112 and K113 are 10 pounds
based on the proposed RQ for the component toluenediamine. Each of these
waste streams also contain the hazardous substances o-toluidine,
p-toluidine and aniline as components. o-Toluidine and p-toluidine have
proposed RQs of 100 pounds, and aniline has a final adjusted RQ of 5000
pounds (see 50 FR 13456-13513). The Agency is in the process of
evaluating the potential carcinogenicity of aniline. However, even if
aniline is found to have a high hazard ranking and is assigned a
1-pound RQ based on the primary RQ adjustment critiera, the RQ would be
raised one level to 10 pounds based on the secondary RQ adjustment
criteria of BHP since aniline biodegrades in the environment. Therefore,
regardless of the outcome of the assessment of aniline for potential
carcinogenicity, the proposed RQs of waste streams K112 and K113 would
remain at 10 pounds.
3-46
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RQs for Unlisted Hazardous Wastes
The Characteristic of Extraction Procedure (EP) Toxicity was designed to
identify wastes that would be likely to contribute to contamination of
groundwater by leaching from landfills. There are 14 constituents for
which the EP toxicity characteristic can be determined, as listed in the
RCRA regulation, 40 CFR Section 261.24. Six of these are specific
compounds and eight, while nominally listed as metals, must actually be
determined on the basis of some soluble compound of the metals. A
detailed discussion of the assignment of RQs based on the Characteristic
of EP Toxicity is given in the "Technical Background Document to Support
Rulemaking Pursuant to CERCLA Section 102, Volume 1," March 1985.
The NPRM which this technical background document supports proposes
adjusted RQs for six of the constituents used to determine the RCRA
characteristic of EP toxicity for unlisted hazardous wastes. These six
constituents have been assigned proposed RQs as follows: 1 pound for
arsenic and chromium and 10 pounds for cadmium, all on the basis of
potential carcinogenicity; 100 pounds for lead on the basis of chronic
toxicity; and 1 pound for lindane and toxaphene on the basis of aquatic
toxicity. The proposed RQ applies to the unlisted waste itself, not
merely to the toxic constituent. The RQ for the metal constituents is
based on the RQ for soluble metal salts, and not the metal itself.
The Agency has proposed a new procedure for determining the hazardous
characteristics of unlisted hazardous wastes (51 FR 21648-21693, June 13,
1986). This new procedure is called the Toxicity Characteristic Leaching
Procedure (TCLP). The Agency will incorporate any new constituents
specified by the TCLP procedure into Table 302.4 in 40 CFR Part 302 when
the TCLP procedure is promulgated.
3-47
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RQ Adjustments Based on BHP
As discussed in Section 2, hazardous substances are eligible for a
one-level RQ increase on the basis of BHP. Appendix C summarizes the
results of the review of candidate hazardous substances Cor BHP
adjustment. It lists the biodegradation, hydrolysis and photolysis data
that are available, identifies those hazardous substances rejected on the
basis of bioaccumulation, persistence, high reactivity, or hazardous
degradation products, and indicates those hazardous substances for which
no data or insufficient information are available to make an evaluation.
Table 3-4 presents six final candidates for which sufficient data are
available to justify an upward RQ adjustment (one level) on the basis of
one or more of the BHP processes. Also shown in the table are the
original primary criteria RQ assignments and the basis on which those
assignments were made. The BHP adjustment made to
hexachlorocyclopentadiene affects the adjusted RQs of waste streams K032,
K033, and K034, because hexachlorocyclopentadiene is the only constituent
of these waste streams.
In some cases, the processes of BHP may result in the formation of other
hazardous substances which potentially could lead to increased danger to
public health, welfare, and the environment after a release has occurred.
The Agency has taken this into account whenever such hazardous
degradation products are known to be produced. In particular, when
assessing reactivity during the primary criteria analysis, hazardous
substances which can hydrolyze to yield hydrofluoric acid, hydrogen
sulfide, or phosphine have been assigned reactivity RQs on the basis of
these hazardous products.
In this current group of 273 hazardous substances, one potential
carcinogen, sulfur selenide, hydrolyzes to form two hazardous reaction
products, hydrogen sulfide and selenium dioxide. The RQ for hydrogen
3-48
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Table 3-4
FINAL CANDIDATE LIST FOR UPWARD RQ ADJUSTMENTS BASED ON
OTHER FACTORS (BHP)
Primary	Proposed
Basis for Adjustment Criteria RQ	RQ
Hazardous Substance	B* H* P*	(Pounds) Basis (Pounds)
Bis(chloromethyl) ether
X

1
CARC
10
Chloromethyl methyl ether
X

1
CARC
10
Dimethyl sulfate
X

10
CARC
100
Formaldehyde X


10
CARC
100
Hexachlorocyclopentadiene

X
1
AQTX
10
2-Naphthylamine X


1
CARC
10
NOTES:
*B - refers	to biodegradation.
*H - refers	to hydrolysis.
*P - refers	to photolysis.
ABBREVIATIONS:
CARC - Potential carcinogenicity
AQTX - Aquatic toxicity
3-49
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sulfide is 100 pounds and the RQ for selenium dioxide is 10 pounds.
Therefore, a 10-pound RQ is proposed for sulfur selenide, based on the
lowest RQ of its two reaction products. Another potential carcinogen,
3,3'-dichlorobenzidine, is subject to rapid photolysis if released into
the environment, yielding benzidine as one of the photolysis products.
Therefore, although the CAG methodology yields a medium ranking
(10-pound RQ) for 3,3'-dichlorobenzidine, the Agency is proposing a
1-pound RQ for this hazardous substance based on the "high" hazard
ranking (1-pound RQ) for its photolysis product, benzidine.
3-50
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SECTION 4
DATA TABLES FOR HAZARDOUS SUBSTANCES
Detailed tables shoving the primary criteria data, the proposed RQs and
the basis for the proposed RQs are presented in Table 4-1. The tables
include data on aquatic toxicity, mammalian toxicity (oral, dermal, and
inhalation), chronic toxicity, potential carcinogenicity, ignitability,
and reactivity upon which the choice of the proposed RQ is based.
Data entered in the Aquatic Toxicity, Mammalian Toxicity, Chronic
Toxicity/Carcinogen, and Ignitability/Reactivity columns are followed by
a letter (X, A, B, C, or D) indicating the RQ level corresponding to that
particular data point (e.g., 1, 10, 100, 1000 or 5000 pounds,
respectively). The numerical value corresponding to the lowest level so
identified is given in the proposed RQ column.
All notes listed in the table are located at the end of this section, and
all abbreviations used are discussed there at some length. For those not
concerned with the complete development of the data presented in Table
4-1, the most common abbreviations are as follows:
(X),(A), - RQ Categories 1, 10, 100, 1000, and 5000 pounds,
(B),(C), respectively
(D)
311	- The RQ was established on the basis of aquatic
toxicity under the regulations from Section 311
of the CVA.
AQTX - Aquatic toxicity (other than a CVA Section 311
assignment).
T(orl) - Mammalian toxicity (oral)
T(ihl) - Mammalian toxicity (inhalation)
4-1
-------
T(skn)	- Majmnalian toxicity (skin, or dermal)
CT or CTX - Chronic toxicity
CARC	- Potential carcinogenicity
F	- Plash point (°P)
B	- Boiling Point (°F)
I	- Ignilability
R	- Reactivity
CS	- The RQ was assigned on the basis of chemical
similarity to another hazardous substance, in the
absence of data for the primary criteria.
Max	- Maximum possible RQ assignment
BHP	- Biodegradation, hydrolysis, or photolysis
LD^0	- The lowest reported dose which has caused death
LC^0	- The lowest reported concentration which has
caused death
CARC=b - Other primary criteria must be used as a basis for
hazard ranking. (See footnote nb" in the summary
table in Appendix A.)
CARCoLOV - The substance received a potential carcinogenicity
ranking of "low," which corresponds to an RQ of 100
pounds for this primary criterion.
CARC=MED - The substance received a potential carcinogenicity
ranking of "medium," which corresponds to an RQ of
10 pounds for this primary criterion.
CARCbHIGH - The substance received a potential carcinogenicity
ranking of "high," which corresponds to an RQ of
1 pound for this primary criterion.
4-2
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TABLE 4-1
QUA FOB THE NPRM HAZARDOUS SUBSTANCES
Hazardoua Substance (Note 1)
j CAS an
Aquatic
Toxicity
(Hot* 2)
1
1
1
1
| Mammalian Toxicity (Note 3)
i
| Chronic
j Toxicity/
|Carcinogen
j (Note 4)
Ignitability/
Beactivity
(Note 5)
311
BQ
(Note 6)
Proposed
BQ
(Note 7)
Baals for
Proposed
BQ
(Not* 8)
(Comments
Acetaldehyde, trichloro-
| 15676

1
|Rbt-orl:480(D)
|
1
|cr=i.D.
1


5000
T(ocl)

|9
Acetaaide, H-|4-ethoxypheny1)-
| 62442

1
|Rat-orl:1650(D)
i
1
|CARC=LOW
1
SOLID

100
CABC


Acetaaide, N-fluoren-2-yl-
| 53963

1
|ttua-ocl:1020(D)
i
1
| CAROMED
1
SOLID

10
CARC


Acatic acid, lead salt
J 301042
500-100(D)
1
|Dog-orl LDlo:300(D)
|Dog-orl:30032
¦
8=171
F=32 (C)
100
10
CABC

in
Alanine, 3-|p-bis<2-chloroethyl)amino|
phenyl-, L-
| 148823

\
i
i
•
1
|CAHCsUIGH
1
i
SOLID

1
CABC


Aldrin
| 309002
<0.1U>
i
|Rat-orl:39(C)
i
1
|CARC=HIGH
1
SOLID
i
1
311,CABC
110
2-Amino-l-methylbonzene
| 95534

1
|Rbt-skn:3250(D)
|Kua-orl:520(D)
|Bat-orl:670(O)
|Rbt-orl:840(D)
|Bat-orl:940(D)
I
1
(CABCoLOW
1
1
1
1
I
B=392 (D|
F-189

100
CABC

|12
4-Amino-l-oathylbenzene
| 106490

1
|Kus-orl:330(D)
|Hat-orl:650(D)
1
1
|CARC=LCW
i
¦
B=392 (D|

100
CABC


Amitrole
| 61625

1
|Rat-orl: 1100 {D)
i
|CARC=HED
i
SOLID

10
CABC


Annuo muni bichromate
| 7789095
lOO-lO(C)
1
i
i
i
1
|CAHC=HIGH
|CT=I.D.
i
SOLID
1000
1
CABC

{10
Ammonium chrornate
| 7788989
lOO-lO(C)
1
i
i
1
|CABC=UIGH
i
SOLID
1000
1
CABC


Aroclor 1016
112674112
(0.1ID
1
i
i
1
|CARC=MED
1

10
1
AQTX

1"
Aroclor 1221
|11104282
<0.1(1)
1
|Rat-orl;3980(D)
i
1
|CAKC=MED
i

10
1
AQrra

ii3
Aroclor 1232
111141165
<0.1U)
1
|Rat-orl:4470(D)
1
|CABC=HED

10
1
AQTX

1"
Note: All comments/notes are located at the end
of this table.
-------
DATA FOB THE NVRM HAZARDOUS SUBSTANCES - Continuad
Hazardous Substance (Note 1)
I
I
I
I
| CASBN
Aquatic
Toxicity
(Hot* 2)
1
1
1
1
| Mammalian Toxicity (Not* 3)
i
| Chronic
j Toxicity/
j Carcinogen
| (Note 4)
Ignitability/
Reactivity
(Hot* 5)
311
RQ
(Not* 6)
Proposed
RQ
(Not* 7)
Basis for
Proposed
RQ
(Not* 8)
|Comaents
Aroclor 1242
I
153469219
I
<0.1(X>
1
|Bat-orl:4250(D)
|
1
|CAHC=MED
1

10
1
AQTX
|13
Aroclor 1248
1
112672296
I
<0.1U)
1
|Rat-orl:ll gn/kg(D)
a
1
|CARC=MED
1

10
1
AQTX
113
Aroclor 1254
1
|11097691
1
<0.1(X)
1
|&at-orl :1010 mq/kq{t>)
i
1
|CARC=MED
1

10
1
AfflX
1*3
Aroclor 1260
1
111096825
¦
<0.1(X)
1
|Bat-orl:1315(D)
¦
1
| CAROMED
i

10
1
AQTX
113
Arsenic 1"+
1
| 7440382
1
I

1
1
1
1
1
|CARC=HIGH
|CT=I.D.
i
SOLID

1
CABC
110
Arsenic acid
1
| 1327522
j 7778394
I

1
|&ftt-orl:48(C)
i
i
1
|CAHC=HIGH
|CT=1B(C)
I
SOLID

1
CARC
114
Arsenic disulfide
1
| 1303328
1
1
500-100(0)
1
i
i
a
1
|CARC°HIGH
|CT=I.D.
I
SOLID
5000
1
CABC
110
Arsenic)III) oxide
1
| 1327533
1
1
10-1(B)
1
|MAn-orl;l(8)
|BAt-orl:20(C)
a
1
|CAHC=HIGH
|CT=41 (A)
i
SOLID
5000
1
CARC
110
Arsemc(V) oxide
1
| 1303282
1
I
lO-l(B)
1
|Bat-ori:B(B)
i
1
1
|CAHC=HIGH
|CT=«19(C)
1
SOLID
5000
1
CARC
110
Arsenic pentoxide
| 1303282
1
|
lO-l(B)
1
|EAt-ori:8(B)
1
I
1
|CAEC=aiGH
|CT=19(C)
1
SOLID
5000
1
CARC
jio
Arsenic trichloride
| 7784341
1
I
10—1(B)
1
|Mus-ihl LClo:338/10M(C)
1
1
1
|CARC=HIGH
|CT=39(B)
i
B:NH) (D)
5000
1
CARC
Us
Arsenic trioxide
| 1327533
1
1
lO-l(B)
1
|Man-orl:l(B)
|RAt—orl:20(C)
¦
1
|CAEC=HIGH
|CT=41 (A)
1
SOLID
5000
1
CARC
110
Arsenic trisulflde
1
| 1303339
1
I
500-100(0)
1
i
i
I
1
|CABC=HIGH
|CT=>35(B)
1
SOLID
5000
1
CARC
110
Arsine, diethyl-
1
| 692422
1
i

1
i
i
¦
1
|CAEC=b
|CT=I.D.
i
PYRO (A)

1
CARC
116,17
Asbestos fi (-
1
| 1332214
1

1
i
i
1
|CARO=HIGH
|CT=>79(A»
SOLID

1
CARC

Bote: All cooments/hotes are located at the end
of this table.
-------
DATA FOB THE NPRM HAZARDOUS SUBSTANCES - Continued
Hazardous Substance (Note 1) |
CAS EN j
Aquatic
Toxicity
(Note 2)
1
1
1
1
| Mammalian Toxicity (Not* 3)
i
| Chronic
j Toxicity/
|Carcinogen
j (Note 4)
Ignitability/
Reactivity
(Note 5)
311
BQ
(Not* 6)
Proposed
BQ
(Not* 7)
1
Basis for |
Proposed j
BQ |
(Bote 8) |Comments
Auramne |
4928081

1
1
I
1
JCAEOLOW
1
SOLID

100
1
CABC |
1
Azasenne |
115026|

1
|Rat-orl:170(D)
a
1
|CARC<=MED
i
SOLID

10
1
CABC |10
i
Azindine j
151S64|

1
|Rat-ihl LClo:25/8H(B)
|Rat-orl:15(C)
1
1
|CARC°UIGH
|CT=I.D.
1
Req. stab.
(B)

1
1
CABC |
1
¦
Azirino(2*,3':3,4)pyrrolo(l,2-a)indole-|
4,7-dione,6-a»ino-8- [((aoinocarbonyl) j
oxy(methyl|-1,la,2,8,8a,8b-hoxahydro- j
8a-methoxy-5-Bethyl- j
50077|

1
|Eat-orl:14(C)
1
1
1
«
1
|CARC=MED
1
1
1
1
SOLID

10
1
CARC |18
i
i
i
I
Benz|)|aceanthrylene, 1,2-dihydro-J- j
methyl- j
56495|

1
1
1
i
1
|CARC=MED
1
1
SOLID

10
1
CABC |
i
¦
Benz|c]acridine |
225514|

1
1
i
1
| CAROMED
I
SOLID

10
i
CABC |
¦
3,4-Benzacndine |
225514|

1
i
1
|CARC=HED
1
SOLID

10
1
CABC |
i
Banz(a|anthracene j
56553|

1
i
i
i
1
|CABC=MED
|CT=«r.D.
1
SOLID

10
1
CABC |
1
1,2-Benzanthracene j
56551|

1
i
i
i
1
|CABC=MED
ICTal.D.
1
SOLID

10
1
CABC |
1
|
1,2-Benzanthracene, 7,12-dimethyl- j
57976|

1
|&At-ori:32?(D)
i
1
ICAEC^UIGU
I
SOLID

1
1
CARC |
t
Benzenanine, 4,4'-carbonioidoylbis (N, j
B-dimethyl- j
492808|

1
i
i
¦
1
|CARCa|£M
1
1
SOLID

100
1
CABC |
1
|
Benzenanine, 4-chloro-2-oethyl-, j
hydrochloride |
3165933|

i
|Mus-orl:560(D)
|Rat-orl:680(D)
|Mus-orl:700(D)
|Bat-orl:720(D)
I
1
|CARC=L0W
1
1
1
I
SOLID

100
1
CABC |
1
1
1
|
Benzenamine, N,N-dinethyl-4-phenylazo- |
60117|

1
|Rat-orl:200(D)
1
1
|CAHC=HIGH
1
SOLID

1
1
CABC |
Benzenamine, 4,4'-methylenebis(2- |
chloro- |
101144|

1
i
i
1
fCA&C^MED
i
SOLID

10
1
CARC |
1
Note: All comments/notes are located at the end of this table.
-------
DATA FOB THE NPBH HAZARDOUS SUBSTANCES - Continued
Hazardous Substance (Note 1)
CASBN
Aquatic
Toxicity
(Note 2)
1
1
1
1
| Mammalian Toxicity (Note 3)
i
| Chronic
j Toxicity/
|Carcinogen
| (Note 4)
Ignitability/
Reactivity
(Note 5)
311
HQ
(Note
1
1
|Proposed
1 BQ
6)j (Note 7)
Basis (or
Proposed
BQ
(Note 8)
|Comments
Benzenaoine, 2-methyl-, hydrochloride
636215

1
|Bat-orl:2951(D)
1
1
|CABC° LOW
1
SOLID

1
|100
1
CABC

Benzenamine, 2-oethyl-S-nitro-
99558

1
|Bat-orl:574(D)
i
1
|CAROLOW
1
F-315

1
|100
1
CABC

Benzene
71432
lO-l(B)
1
|Bat-lhl:10,000/7H(D)
|Bat-orl:3800(D)
1
l
| CAROMED
|CT=17(C)
I
B=176
P=12 (C)
1000
1
110
1
1
CABC

Benxene, chlorooethyl-
100447
lO-l(B)
1
|Bat-orl:1231(D)
|Rat-ihl:1S0/2H(C)
1
1
I
1
(CAROLOW
1
1
1
1
B»354
P°153 (Max)
Beq. stab.
(B)
100
1
jioo
1
1
1
1
CABC,B,311
118,19
Benzene, hexachloro-
118741

1
|Bat-orl:10.000(D)
1
l
1
| CAROMED
|CT=>29.5(B)
1
SOLID

110
1
1
CABC
|10
Benzene, l-nethyl-2,4-dinitro-
121142
100-10(C)
1
|Rat-orl:268(D)
1
I
1
| CAROMED
|CT=32(B)
i
B=>576
Fo404 (Max)
1000
110
1
1
CABC

Benzane, l-oethyl-2,6-dinitro-
606202
100-10(C)
1
|Rat-orl:177(D)
1
1
1
| CAROLOW
|CT=> 30(B)
1
SOLID
1000
1
|100
1
1
CABC.CTX
118
Benzene, 1, 2-o>ethylenedioxy-4-allyl-
94597

1
|R&t-orl:1950(D)
i
1
| CAROLOW
1
F<=>212

1
jioo
1
CABC

Benzene, 1,2-methylenadioxy-4-proponyl-
120581

1
|&*t-orl:1340(D)
i
1
|CARCsUM
1


1
|100
1
CABC

Benzene, 1,2-nethylenedioxy-4-propyl-
94586

1
(Rat-orl;2260(D)
i
1
{CAROMED
1


1
110
1
CABC

Benzene, pentachloronitro-
82688

1
|Rat-orl:1650(D)
i
i
1
| CAROLOW
|CT=10.4(C)
I
SOLID

1
|100
1
1
CABC

Benzene, (trichloromethyl)-
98077

1
|Bat-ihl:125/4H(C)
¦
1
|CAROHIGH
1
F=260

I
II
1
CABC

Benzeneacetic acid, 4-chloro-alpha-(4-
chlorophenyl)-alpha-hydroxy-,ethyl
ester
S10156

1
|Bat-orl:700(D)
1
1
I
1
| CAROMED
1
1
I
SOLID

110
1
1
1
CABC

1,2-Benzenedicarboxylic acid, (bis(2-
ethylhexyl|| ester
1X7817

1
|Rat-orl:31 Dg/kg(D)
i
1
| CAROLOW
i
Fo420

1
|100
1
CABC
110
Note: All comments/notes are located at the end
of this table.
-------
DATA FOR THE NPRM HAZARDOUS SUBSTANCES * Continued
Hazardous Substance (Note 1)
CASBH
Aquatic
Toxicity
(Note 2)
1
1
1
1
| Mammalian Toxicity (Nota 3)
1
| Chronic
j Toxicity/
jCarcinogen
| (Nota 4)
Iqnitability/
Reactivity
(Note 5)
311
BQ
(Nota 6)
Proposed
BQ
(Nota 7)
Basis Cor
Proposed
BQ
(Nota 8)
|Comments
Benzidina
9287S
lO-l(B)
1
|Bat-orl:309(D)
1
1
1
ICABOHIGH
|CT=28(B)
1
SOLID

1
CAHC

1,2-Benzisothiazolin-3-one,1,1-dioxide,
and salts
81072

1
1
1
1
1
|CAR OVM
i
I
SOLID

100
CARC

Benzo|a)anthracene
56553

1
1
1
1
1
|CARC=MED
IOI.D.
1
SOLID

10
CARC

Benzo|b|fluoranthena
205992

1
1
1
1
1
|CARC=UIGH
|CT»I.D.
I


1
CARC

Benzo(k)fluoranthena
207089

1
1
1
1
|CARC=b
i


5000
HAX
14 4
Benzol aIpyrene
50328

1
1
1
1
1
|CARC=HIGH
|CTV46(A)
I
SOUD

1
CAHC

3,4-Benzopyreno
50328

1
1
1
1
1
|CARC=HIGU
|CT="46(A)
I
SOLID

1
CAHC

Benzotrichlorida
98077

1
|Rat-ihl:125/4H(C)
i
1
|CAfiC=HIGH
I
F=260

1
CARC

1,2-Benzphenanthrene
218019

1
i
i
i
1
|CARC=MED
|CT=I.D.
1
SOLID

IP
CARC
118
Benzyl chloride
100447
lO-l(B)
1
|Bat-orl:123KD)
|Rat-lhl:150/2H(C)
1
1
1
1
(CAROLCM
1
1
1
¦
B=354
P=»153 (Hax)
Req. stab.
(B)
100
100
CAHC,H,311
118(19
Beryllium t1"
7440417
100-10(C)
1
1
1
1
i
|CARC=MED
|CT=I.D.
i
SOLID

10
CARC

Beryllium chloride
7787475
100-10(C)
1
|Rat-orl:86(C)
i
i
1
| CARO=HIGH
|CT=46.7(A)
i
R:NH3 (D)
5000
1
CARC
120
Beryllium dust +1"
7440417
100-10(C)
1
i
i
i
1
|CAfiC=HED
|CT=I.D.
i
SOLID

10
CARC

Beryllium fluoride
7787497
500-100(D)
1
|Rat—orl:98(C)
1
1
|CAHC=HIGH
|CT=49.6(A)
SOLID
5000
1
CARC

Note: All comments/notes are located at the end of this table
-------
DMA FOR THE HPRM HAZARDOUS SUBSTANCES - Continued
Hazardous Substance (Note 1)
| CASRN
Aquatic
Toxicity
(Not* 2)
Mammalian Toxicity (Note 3)
1
| Chronic
j Toxicity/
jCarcinogen
j (Note 4)
Ignitabillty/
Reactivity
(Note 5)
311
RQ
(Note 6)
Proposed
BQ
(Not* 7)
Basis for
Proposed
RQ
(Note 8)
|Comments
Beryllium nitrate
113597994
j 7781553
500-100(D)

1
|CARC=HIGH
|CT=44(A)
|
SOLID
5000
1
CARC

alpha - BHC
| 319646

Rat-orl:177(D)
1
|CARC=MED
i


10
CAHC

beta - BHC
| 319857

Bat-orl:6000(D)
1
\ChBOUM
1


1
CS
121
gamma - BHC
| S8899
<0.1(X)
Bat-skn:500(D)
Rat-orl:76(C)
1
| CAROMED
1
i
SOLID
1
1
311
110
2,2'-Bioxirane
| 1464535

Rat-orl:78(C)
Rat-lhl:90/4H(C)
1
| CAROMED
i
1


10
CARC

(l,l'-Biphenyl)-4,4'diamine
| 92875
lO-l(B)
Rat-orl:309(D)
1
|CABC=HIGH
|CTs28(B)
1
SOLID

1
CARC

(1,l'-Biphenyl(-4,4'diamine,3,3'
dl chloro-
| 91941

Rat-orl LDlo:4740 mg/kg(D)
1
| CAROMED
jcTal.D.
i
SOLID

1
CARC.CS
|10,22
ll, 1 '-Biphenyl )-4,4'diamine,3,3'
dinethoxy-
| 119904

Rat-orl:1920(D)
1
|CAROL0W
1
1
SOLID

100
CARC

(1,1'Biphenyl)-4,4'-diamine,3,3
dimethyl-
| 119937

Rat-orl:404(D)
1
|CAROLQW
1
1
SOLID

100
CARC

Bia(2-chloroethyl) ether
| 111444
1000-100(D)
Rat-lhl:1000/4 5M
Rat-orl:75(C)
1
| CAROMED
1
¦
P-131 (D)

10
CARC

Bis(chloromethyl) ether
| S428B1

Rat-orl:210(D)
Rat-lhl:7/7U(B)
i
|CARC=HIGH
|CT=>I.D.
I


10
BHP
123
Bis(2-ethylhexyl) phthalate
| 117817

Rot-orl:31 gg/kglD)
1
|CARC°L0W
1
F=420

100
CARC
110
1,3-Butadiene, 1,1,2,3,4,4-hexachloro-
| 87683
<0.1(X)
Rat-orl:90(C)
1
|CABC=UJW
|CT=10.3(C)
i


1
MJTX
iio
1-Butanamine, N-butyl-N-nitroso-
| 924163

Rat-orl:1200(D)
1
|CAHC=KED
1


10
CARC

Butanoic acid, 4-(bis(2-chloroethyl)
amino Jbenzene-
| 305033


1
|CARC=MED
1
SOLID

10
CARC
| IB
Note: All comments/tootes are located at the end
of this table.
-------
DATA FOB THE NPRM HAZARDOUS SUBSTANCES - Continued
Hazardous Substance (Note 1)
1
1
1
1
| CASBN
Aquatic
Toxicity
(Note 2)
1
1
1
1
| Mammalian Toxicity (Note 3)
i
| Chronic
| Toxicity/
|Carcinogen
j (Note 4)
Ignitability/
Beactivity
(Note 5)
311
HQ
(Note 6)
Proposed
BQ
(Note 7)
Basis for
Proposed
BQ
(Note 8)
ICommsnts
Cacodylic acid
1
| 75605
1

1
|Bat-orl:700(D)
1
1
|CARC=b
1
SOLID

1
CARC
116
Cadmium tt
1
| 7440439
i
i

1
|Rat-orl:22S{D)
i
i
1
|CARC=MED
|CT=>I.D.
1
SOLID

10
CARC
110
Cadmium acetate
1
| 543908
i
I
lO-l(B)
1
i
i
1
1
| CAROMED
|CT=41(A)
1
SOLID
100
10
CARC.CTX
|10
Cadmium broside
1
| 7169426
i
l
10-1(B)
1
i
i
1
1
|CARC=HED
|CT=41(A)
a
SOLID
100
10
CABC.CTX
110
Cadmium chloride
1
|10106642
i
i
1.94(B)
1
|BAt-orl:66(C)
i
a
1
|CABC=MED
|CT=»42 (A)
1
SOLID
100
10
CARC, era
110
Calcium arsenate
1
| 7776441
i
i
100-10(C)
1
|Bat-orl:20(C)
i
1
1
|CABC=UIGH
|CT°33.1(B)
1
SOLID
1000
1
CARC
110
Calcium arsenite
i
|52140166
1
I
40(C)
1
i
i
i
1
|CARC=UIGH
|CT»39(B)
1
SOLID
1000
1
CARC
iio
Calcium chrooate
1
113765190
1
I
28(C)
1
i
i
i
1
|CARC=HIGU
|CT=29(B)
i
SOLID
1000
1
CAHC
110
Caophene, octachloro-
1
| 8001352
1
1
I
<0.1(JC|
i
|Dog-orl:15(C)
jaat-orl:40(C)
|Rat-skn:600(D)
1
1
|CA&C=HED
1
1
I
SOLID
1
1
311
jio
Carbaoic acid, ethyl ester
| S1796
j

1
|Mus-orl: 2500(D)
i
1
|CABC=L0W
I
SOLID

100
CARC

Carbamic acid, oethylmtroso-, ethyl
ester
| 615532
1
i

1
|Rat-orl:160(D)
i
¦
1
|CARC=HIGH
l
¦
SOLID

1
CARC

Carbamide, H-ethyl-N-nitroso-
1
| 759739
I

1
|Rat-orl:300(D|
I
i
|CARC=HED
¦
SOLID

10
CARC

Carbaolde, N-oathyl-H-nitroso-
1
| 684935
1

1
|Bat-orl:110{D)
i
1
|CARC=HIGH
1
SOLID

1
CARC

Carbamide, thio-
1
| 62566
i

1
|Bat-orl; 125(D)
i
1
|CARC=HED
i
SOLID

10
CARC

Catbaooyl chloride, dimethyl-
1
| 79447

1
|Rat-orl;1000(0)
1
| CARC=HIGH


1
CARC

Note: All comments/notes are located at the end
of this table-
-------
DATA FOB TOE NFRH HAZARDOUS SUBSTANCES - Continued
Hazardous Substance (Note 1)
I
I
I
I
| CASBN
Aquatic
Toxicity
(Not* 2)
Mammalian Toxicity (Note 3)
1
| Chronic
j Toxicity/
|Carcinogen
j (Note 4)
Ignitability/
Reactivity
(Note 5)
311
HQ
(Note 6)
Proposed
HQ
(Note 7)
Basis (or
Proposed
BQ
(Note 8)
jComments
Carbon tetrachloride
I
| 56235
I
I
100-10(C)
Bat-orl:2800(D)
Bat-ihl:4000/4H
1
|CARC=MED
|CT=>25.3(D)
a

5000
10
CABC

Chloral
I
| 75876
|

Bbt-orl:480(D)
1
|CT=I.D.
1


5000
T(orl)
|9
Chlorambucil
| 305033
i


1
|CABC=MED
¦
SOLID

10
CARC
118
Chlordano
1
| 57749
1
i
<0.1(X)
Rbt-orl:100(C)
Rat-skn:700(D)
1
|CABCsKED
1
1
SOLID
1
1
311
110
Chlordane, technical
1
| 57749
1
I
<0.1(X)
Rbt-orl:100(C)
Rat-skn:700(D)
1
| CAROMED
1
1
SOLID
1
1
311
|10
Chlomaphasine
1
| 494031
1


1
|CAR&>IXJW
1
SOLID

100
CARC
118
1—Oiloro-2,3-epoxypropane
1
| 106898
1
1
i
100-10(C)
Rat-ihl LClo:2S0 ppn/4H(C)
Rat-skn LOlo:1000(D)
Rat-orl:90(C)
1
|CABOLOW
|CT=26(B)
1
1
B=239
F=91 (C)
1000
100
CARC,era

Chloroforn
| 67663
1
i
100-10IC)
Rat-orl:800(D)
Rat-ihl:8000/4HID)
1
|CARC=MED
1
1

5000
10
CARC

Chloronethyl methyl ether
1
| 107302
1
I
1000-100(D)
Rat-ihl:S5/7H(C)
Rat-orl:817(D)
1
|CABC=HIGH
jcT=30.4(B)
I


19
BHP
|23
4-Chloro-o-toluidine, hydrochloride
1
| 3165933
1
1
1
|

Kus-orl:560(D)
Rat-orl:680(D)
Hus-orl:700(D)
Rat-orl:720(D)
1
|CABC°L0W
1
1
1
i
SOLID

100
CARC

Chromic acid
1
111115745
| 7738945
1
i
100-10(C|

1
|CARG=H1GH
jcT°31.2(B)
1
I
Strong oxi.
(A)
SOLID
1000
1
CARC
|10,24
Chrome acid, calcium salt
1
113765190
1
i
28(C)

1
|CARC=HIGH
|CT=29(B)
I
SOLID
1000
1
CARC
110
Chromium +t
1
| 7440473
1


1
|CARC=HIGH
|CT=>1 .D.
SOLID

1
CARC
|10
Bote: All comments/notes are located at the end of this table.
-------
DATA FOR THE HPBM HAZARDOUS SUBSTANCES - Continued
Hazardous Substance (Note 1)
1
1
1
1
| CASBN
Aquatic
Toxicity
(Hot* 2)
1
1
1
1
| Mammalian Tonicity (Note 3)
1
| Chronic
| Toxicity/
|Ca rcinogen
| (Not* 4)
Ignitability/
Reactivity
(Note 5)
311
BQ
(Bote 6)
Proposed
BQ
(Note 7)
Basis for
Proposed
BQ
(Note 8)
|Comaents
Chcysene
1
| 214019
1
I

1
1
1
1
1
|CABC=MED
|CT=I.D.
|
SOLID

10
CABC
|18
COKE OVEN EMISSIONS
1
| H.A.
i
1

1
1
1
1
1
|CARC=HIGH
|CT=>46 (A)
1


1
CARC
125
Creosote
1
| 8001569
i
i
10—1(B)
1
|Rat—orl:725(D)
i
i
1
|CARC=HIGH
|CT=>1.0
i
F=16S

1
CARC
|26
Cupric acetoarsenite
1
I1200203B
i
l
10-1(B)
1
|Eat-orl:22(C)
1
¦
1
|CAHC=HIGH
|CT=»I .D.
1
SOLID
100
1
CARC
110
1,3-Cyclopentadiene, 1,2,3,4,5,5-
hexachloro-
1
| 77474
i
¦
<0.1|X)
1
|R*t-orl:113(D)
|Bbt-skn:430(D)
I
1
|CT»62
-------
DATA FOB THE HFHM HAZARDOUS SUBSTANCES - Continued
Hazardous Substance (Not* 1)
1
1
1
1
| CASRN
Aquatic
Toxicity
(Note 2)
1
1
1
1
| Mammallan Toxicity (Not* 3)
1
| Chronic
| Toxicity/
jCarcinogen
j (Note 4)
Ignitability/
Beactivity
(Bote 5)
311
HQ
(Not* 6)
Proposed
HQ
(Note 7)
1
Basis tor |
Proposed |
RQ I
(Note 8) |Comments
Decacblorooctahydro-1,3,4-aetheno-2H-
cyclobuta(c,d|-pentalen-2-one
1
| 143500
1
1
i
<0.1(X)
1
|Bbt-skn:345(D)
|Bbt-orl:65(C)
|Bat-orl:95(C)
I
1
|CABC=tf£D
1
1
1
SOLID
1
1
1
311 110
1
1
1
Diallate
1
| 2303164
I

1
|Bat-orl:395(OI
1
1
|CARC=LOW
1
SOLID

100
1
CAHC |
1
Diamine
1
| 302012
1
i

1
|Hus-ihl:252/4H(C)
i
I
1
|CARC=HIGH
1
1
Spont. ign.
(A)

1
1
CARC |
1
1
Diaminotoluene
1
| 95807
| 496720
| 823405
135376458
i

1
|Rat-orl:260(D)
i
i
i
a
1
|CABC=HED
1
1
1
|
SOLID

10
1
CARC |
1
1
1
i
Dibenz(a,h]anth r acen*
1
| 53703
1
1

1
i
i
i
1
|CARC«tiIGH
|CT=I.D.
1
SOLID

1
1
CARC |
i
i
1,2:5,6-Dibenzantbracen*
1
| 53703
i
i

1
i
i
i
1
|CARC=HIGH
ICTal.D.
i
SOLID

1
1
CARC |
i
i
Dlbenzo(a,b|anth racene
1
| 53703
i
i

1
i
i
i
1
|CARCMUGH
|CT=I.D.
1
SOLID

1
1
CARC |
I
1
1,2:7,8-Dibenzopyrene
1
| 169559

1
i
I
1
|CARC=MED
1
SOLID

10
1
CARC |18
1
Dibenz|a,iJpyrene
!
| 159559
i

1
i
I
1
|CABO=*tED
1
SOLID

10
1
CARC |16
1
l,2-Dlbromo-3-chloropropane
1
| 96126
1
i

1
|Bat-ihl:103/SH
-------
DATA FOR THE NPRM HAZARDOUS SUBSTANCES - Continued
Hazardous Substance (Note X)
1
1
1
1
| CASRH
Aquatic
Toxicity
(Hota 2)
Mammalian Toxicity (Note 3)
1
| chronic
| Toxicity/
|Carcinogen
j (Hot# 4)
Ignitability/
Beactivity
(Note 5)
311
BQ
(Note 6)
Proposed
RQ
(Hot* 7)
Basis (or
Proposed
RQ
(Note 8)
| Comments
1,2-Dichloroethane
1
| 107062
1
1
1
1000-100(D)
Bat-lhl LClo:1000 ppm/4H(D)
Mus-orl LDlo:600(D)
Rat-orl:670(D)
1
|CABCoLOW
|CT=18.4
1
1
B=183
F°56 (C)
5000
100
CARC

1,1-Dichloroethylene
1
| 75354
i
i
i
1000-100(D)
Mus-lhl LC50:98 ppV22H(C)
Bat-lhl:10,000/24HID)
Bat-orl:200(D)
1
|CARC=L0W
|CT=19(C)
1
1
B=99
F=0 (B)
5000
100
CABC.I
|27
Dichloroethyl other
1
| 111444
i
i
1000-100(D)
Rat-lhl:1000/45M
Rat-orl:75(C)
1
|CARC=MED
1
i
F»131 (D)

10
CARC

Dichlorophenylarsine
1
j 696286
i
i
i

Rbt-skn:0.5(B)
Rat-skn:16(C)
Cp9-skn:4(B)
1
|CARC=b
|CT=I.D.
1
I


1
CARC
116
Dieldnn
| 60571
i
<0.1(X)
Rat-orl:46(C)
1
| CARCsHIGH
1
SOLID
1
1
311,CARC
110
1,2:3,4-Diepoxybutana
1
| 1464535
1
¦

Rat-orl:78(C)
Bat-lhl:90/4H(C)
1
|CARC=KED
1
I


10
CARC

Diethylarsine
| 692422
1
I


1
|CABC=b
|CT=.I.D.
I
PYRO (A)

1
CARC
116,17
1,4-Diethylene dioxide
1
| 123911
i
¦
1000—100
-------
DATA FOR THE NPBM HAZARDOUS SUBSTANCES - Continued
Hazardous Substance (Not* 1)
1
1
1
1
| CASBN
Aquatic
Toxicity
(Not* 2)
Mammalian Toxicity (Note 3)
1
| Qironic
| Toxicity/
|carcinogen
| (Not* 4)
Ignitability/
Reactivity
(Not* 5)
311
HQ
(Not* 6)
Proposed
HQ
(Not* 7)
1
Basis for |
Proposed |
BQ I
(Not* 8) |Comments
Dimethylcarbamoyl chloride
1
| 79447
1

Rat-orl:1000|D)
1
| CARC=HIGH
1


1
1
CARC |
1
X,1-Dimethylhydrasine
1
| 57147
i
1

Rat-lhl:252/4H(C)
1
|CARC=MED
i
I
Spont. ign.
(A)

10
1
I.CARC |
1
1
1,2-Dimethylhydraxine
| 540738
1
i

Rat-orl:100(C)
Rat-ihl:280/4H(C)
1
|CARC=HIGH
i
1


1
1
CARC |
1
1
Dimethylni trosaain*
| 62759
1
1

Bat-lhl LC50:78/4H(C)
Hat-orl:26(C)
1
|CARC=MED
1
1


10
1
CARC |
1
i
Dimethyl sulfate
1
j 77701
i
i
100-10(C)
Bat-ihl LClo:32/4H(B)
Bat-orl:440(D)
1
|CARC=MED
1
1
F-182

100
1
BHP |16,23
i
i
Dinitrotoluene
1
125321146
i
i
100-10214
F=54 (C)

100
1
CARC |
i
I
1,2-Diphenylhydrazine
1
j 122667
1
a
l-O.1(A)
Rat-orl:301(D)
i
|CAHC=MED
|CT=>28(B)
i
SOLID

10
1
A0ra,CARC |10,28
i
I
Di-n-propy lni t rosamne
1
| 621647
j

Rat-orl:480(D)
1
| CAROMED
1


10
1
CARC |18
I
Epichlorohydnn
| 106898
1
1
¦
lOO-lO(C)
Rat-ihl LClo:250 ppm/4H(C)
Rat-skn LDlo:1000(D)
Rat-orl:90(C)
1
|CARC°LCW
|CT=26(B)
1
I
B=239
F=91 (C)
1000
100
1
CARC,CTX |
I
i
i
Ethanauine, N-ethyl-N-mtroso-
i
| 55185

Rat-orl:280(D)
1
|CARC=HIGH


1
1
CARC |
Note: All comments/notes are located at the end of this table.
-------
DATA FOB THE NPRM HAZARDOUS SUBSTANCES - Continued
Hazardous Substance (Note 1)
1
1
1
1
| CASBH
Aquatic
Toxicity
(Not* 2)
Mammalian Toxicity (Not* 3)
1
| Chronic
j Toxicity/
|Carcinogen
j (Note 4)
Iqnitability/
Reactivity
(Not* 5)
311
RQ
(Not* 6)
Proposed
BQ
(Not* 7)
1
Basis for |
Proposed |
BQ |
(Not* 8) jComments
Ethane,
1, 2-dibroao-
1
| 106934
1
1
|
100-10(C)
Rat-orl:108(D)
Kat-ihl:400/2H(C)
Kbt-orl:55(C)
1
|CARC=HIGH
1
1
i

1000
1
1
CARC |
1
1
Ethane,
1,2-dichloro-
1
| 107062
i
i
i
1000-100(D)
Rat-ihl LClo:1000 ppm/4H(D)
Kua-orl LDlo:600(D)
Bat-orl:670(D)
1
|CABC=LOW
|CT=.H.4(C)
1
i
B=»183
F=56 (C)
5000
100
1
CARC |
1
1
Ethane,

1
| 67121
i
1
10-1(B)
Rat-orl:6000(D>
1
|CAROl£M
|CT=15.2(C)
i
SOLID

100
1
Affix,CARC |
1
|
Ethane,
1,1'-oxybis|2-chloro-
1
| 111444
i
i
1000—100(D)
Rat-lhl:1000/45M
Rat-orl:75(C)
1
| CAROMED
1
i
P°131 (D)

10
1
CARC |
1
Ethane,
1,1,1,2-tetrachloro-
1
| 630206
i
I


1
|CAROL0W
|CT=I.D.
1


100
1
CARC |
1
i
Ethane,
1,1,2,2-tetrachloro-
1
j 79345
i
i
lO-l(B)
Rat-lhl LClo:1000/4H(D)
Doq-orl LDlo:300(D)
1
|CARO»LOW
|CT=17.5(C)
1


100
i
AQTX,CARC |10
1
1
Ethane,
1,1,2-trichloro-
i
| 79005
1
¦
100-10(C)
Bat-ihl LClo:500/8U(D)
Bat-orl:1140(D)
1
|CAROL0W
|CT=I.D.
i


100
1
CARC |
i
Ethane,
pentachloro—
1
| 7601?
1
I
<1(A)
Doq-orl:5000(D|
1
| CARD? LOW
|CT=I.D.
i


10
i
AQTX |
1
Ethanethioaaide
1
| 62555
I

Bat-orl:200(D)
1
| CAROMED
i
SOLID

10
1
CARC |
Ethanol
2,2'-(nitrosoimino)bis-
1
| 1116547
I

Rat-orl:7500(D)
1
| CARC=HXGH
i


1
1
CARC |
Ethenamine, N-nathyl-N-nitroso-
1
| 4549400
1

Rat-orl:24(C)
1
| CAROMED
1


10
1
CARC |18
Ethene,
chloro-
1
| 75014
1
1
1000(D)
Gpg-ihl LClo:20/30M(B)
Rat-orl:500(D)
1
(CAROMED
|CT=20(C)
1
B=7
F=GAS (B)

10
1
CARC |29
1
Ethene,
1,1-dichloro-
| 75354
1
1
i
1000—100(D)
Mus-lhl LC50:98 ppo/22H(C)
Rat-lhl:10,000/24HID)
Rat-orl:200(D)
1
|CAROLCM
|CT=19(C)
1
i
B=99
F=0 (B)
5000
100
1
CARC,I |27
1
1
Ethene,
1,1,2,2-tetrachloro-
1
| 127184
1
100-10(C)
Bat-lhl LClo:4000/4H(D)
Kus-orl:8100|D)
1
|CAROLOW
|CT=10(C)


100
1
CARC |
1
Note: All comments/notes are located at the end of this table.
-------
DATA FOB THE HP KM HAZARDOUS SUBSTANCES - Continued
Hazardous Substance (Note 1)
ctsm
Aquatic
Toxicity
(Hot* 2)
Mammalian Toxicity (Hota 3)
chrome
Toxicity/
Carcinogen
(Hot* 4)
Xgnitability/
Reactivity
(Bote St
311
RQ
(Hot* 6)
Proposed
BO
(Mote 7)
Basis for
Proposed
BQ
(Mote 8)
Comments
2-Ethoxyethano1
Ethyl carbonate (Urethan)
Ethyl 4,4'-dichlorobenzilate
Ethylene dibromide
Ethylene dichlorida
Ethylene glycol nonoethyl ether
Ethylene oxide
Ethylenethiourea
Ethylemaine
Ethyl methonesulfonate
Formaldehyde
D-Glucopyranose, 2-deoxy-2-(3-methy1-3-
m trosoureido)-
110805
51796
510156
106934
107062
110805
75218
96457
151S64
62500
50000
18683664
100—1000(D)
100-10(C)
1000-100 (D)
100—1000(D)
100-10(0)
100-10(C)
Bat-ihl LClo:4000 pp^/4H(D)
Rat-orl:3000(D)
Rbt-orl .-3100(D)
Bbt-skn:3500(D)
Mus-orl:4300(D)
Hus-orl:2500(D)
Rat-orl:700(D)
Rat-orl:10B(D)
Bat—ihl:400/2HIC)
Rbt-orl:55(C)
Rat-ibl LClo:1000 ppo/4H(D>
Hus-orl LDlo:600(D)
Bat-orl:670(D)
Rat-ihl LClo:4000 ppm/4H(D|
Eat-otl:3000(D)
Bbt-orl:3100(D)
Rbt-skn:3500(D)
Mus-orl:4300(D)
Rat-«rl:72(C)
Bat-orl:1832(D)
Bat-ihl LClo:25/8H(B)
Kat-orl:15(C)
Bat-ihl LClo:250 pps*/4H(C)
Bbt-skn:270(D)
Rat-orl:800(D)
Kus—orl:264(D)
CT=13.6(C)
CARC=LOW
CAROMED
CARCcHIGH
CABC°UM
CT°18.4(C)
cr=i3.6(c)
CAEC=MED
CARC=HED
CARCeHIGH
CT=I.D.
CARC=HIGH
CAKC=MED
CT=39(B)
CARO=UIGU
B»135 (D)
F=223
SOLID
SOLID
B»1B3
r-S6 (C)
B=>135 (D)
P°223
B=51
r=<0 (B)
SOLID
Seq. stab.
|B>
B=-3
F=GAS (B)
SOLID
1000
5000
1000
1000
100
10
1
100
1000
10
10
1
1
100
CTX
CARC
CARC
CARC
CARC
CTX
CARC
CARC
CARC
CARC
HHP
CARC
23
Note: All comments/notes are located at the end of this table.
-------
DATA FOR THE HFRM HAZARDOUS SUBSTANCES - Continued
Hazardous Substance (Not* 1)
CASRN
Aquatic
Toxicity
(Nota 2)
1
1
1
1
| Mammalian Toxicity (Nota 3)
1
| Chronic
j Toxicity/
{carcinogen
j (Nota 4)
Ignitability/
Baactlvity
(Nota 5)
311
RQ
(Nota 6)
Proposed
RQ
(Nota 7)
Basis Cor
Proposed
RQ
(Nota 8)
|Comments
Glycidylaldehyde
765344

1
|Rat-orl:50(C)
|
1
|CABOMED
I



10
CABC

Guam dine, N-ni t roso-N-oe thy 1-N' -ni t ro-
70257

1
|Rat-orl:90(C)
i
1
|CARC=MED
i
SOLID


10
CARC

Heptachlor
76448
<0.1(X)
1
|Rat-skn:119(D)
jRat—orl:40
i



1
AQTX.
jio
Hexachlorocyclohexane (gamma isomer I
58899
<0.1(X)
I
|Rat-skn:500(D)
|Rat—orl:76(C)
1
1
|CARC=MED
1
I
SOLID

1
1
311
i io
Haxachlorocyclopentadiena
77474

1
|Rat-orl:113(D)
|Rbt-akn:430(D)
1
|CT=62(A)
1
I
SOLID

1
10
BliP
110 ,23
1,2,3,4,10,l0-Hexachloro-6,1—epoxy-1,4,
48,5,6,7,8,fla-octahydro-endo,exo-1,4:
5,8-dimethanonaphthalene
60571
<0.1(Xt
1
|Rat—orl:46(C)
1
1
I
1
|CARC=HIGH
i
i
i
SOLID

1
1
311,CABC
110
Hexachloroethane
67721
10-1(8)
1
|Rat—orl:6000{D)
i
i
1
|CAR C=»LOW
|CT=15.2(C)
i
SOLID


100
AQIX.CARC

1,2,3,4,10-10-Hexachloro-l,4,4a,5,8,8a-
hexahydro-1,4:5,8-ando,exo-
dimethanonaphthalene
309002
<0.1(X)
1
|Rat-orl:39(C)
i
i
1
1
|CARC=HIGH
i
i
1
SOLID

1
1
311,CARC
|10
Hydrazine
302012

1
|Mus-ihl:2S2/4H(C)
i
i
1
|CARC=HIGH
i
i
Spont.
(A)
ign.

1
CARC

Hydrazine, 1,2-diathyl-
1615801

1
i
1
1
|CARC=HED
i



10
CABC
118
Hydrazine, 1,1-dioethyl-
57147

1
|Rat-ihl:252/4H(C)
i
¦
1
|CARC=HED
i
1
Spont.
(A)
ign.

10
I.CARC

Hydrazine, 1,2—dimethy1-
540738

¦
|Bat-orl:100(C)
|Rat—ihl:280/4H(C)
1
|CARC=HIGH
i



1
CARC

Noto. All comsents/Qotes are located at the er.a o/ 2 s tab.:
-------
DATA FOB THE NPRM HAZARDOUS SUBSTANCES - Continued
Hazardous Substance (Note 1)
1
1
1
1
| CASBH
Aquatic
Toxicity
(Note 2)
1
1
1
1
| Mammalian Toxicity (Hote 3)
i
| Chronic
| Toxicity/
(Carcinogen
j (Note 4|
Ignitability/
Reactivity
(Not* 5)
311
BQ
(Note 6)
Proposed
BQ
(Note 7)
Basis Cor
Proposed
BQ
(Note 8)
|Cooments
Hydrazine, 1,2-diphenyl-
1
j 122667
1
|
1-0.1(A)
1
|Rat-orl:301(0)
1
1
1
|CAKC=MED
|CT=28(B)
|
SOLID

10
AOnC.CABC
110,24
Hydroxydinethylarsina oxide
1
| 75605
a

1
|Eat-otl:700(D>
1
1
|CARC=b
I
SOLID

1
CAfiC
116
2-Iaidazolidinethione
| 96457
*

1
|Rat-orl:1832(D)
i
1
|CARC«HED
1
SOLID

10
CARC

Indeno(1,2,J-cd|pyrene
1
j 193395
1
¦

1
1
1
i
1
|CAROL0W
ICTal.D.
I
SOLID

100
CAHC
|1S
Isocyanic acid, methyl aster
1
| 624839
i
i

1
ihl:5/4H(B)
jaat-orl:71(C)
i
1
1
1
I
B=102
F°19 (C(

ltl
STAT

Isosafrole
1
| 120581
i

1
|EUt-orl:1340(D)
j
1
|CARCaLW
i


100
CARC

Kepone
1
j 143500
1
1
l
<0.1|X)
|Hbt-skn:345
I
SOLID

10
CAR C

Lead subacetate
1
| 1335326
1
I

1
i
i
1
1
ICABCoLCH
|CT°33(B)
I


100
CARC,CTX

Lindane
1
| 58699
1
<0.1(X)
1
|Rat-skn;500JD)
|Hat-orl:76(C)
1
|CABC=MED
1
SOLID
1
1
311
(10
Hote: All cososents/tiotes are located at tho and of this table.
-------
DATA FOR THE NFRM HAZARDOUS SUBSTANCES - Continued
Hazardous Substance (Note 1)
1
1
1
1
| CASBH
Aquatic
Toxicity
(Note 2)
Hamuli an Toxicity (Note 3)
1
| Chronic
j Toxicity/
|Carcinogen
1 (Note 4)
Ignitability/
Reactivity
(Note 5)
311
HQ
(Note 6)
Proposed
RQ
(Note 7)
Basis Cor
Proposed
HQ
(Note 8)
(Comments
Lithium chrornate
1
11430735S
1
100-10(C)

1
|CARC=UIGH
|CT=I.D.
I
SOLID
1000
1
CABC
|10
Melphalan
1
j 146823
i


1
|CARC=HIGH
1
SOLID

1
CABC

Methane, chloro-
1
| 74873
1
I
1000(D)
Hat-lhl:152000 ag/n3/30H(D)
Mus-ihl:3146/7H(D)
1
|CARC°UM
|CT»20(C)
1
B=»-ll
F=
-------
DMA FOB THE NPRH HAZARDOUS SUBSTANCES - Continued
Hazardous Substance (Note 1)
| CASBH
Aquatic
Toxicity
(Note 2)
1
1
1
1
| Mammalian Toxicity (Note 3)
i
| Chronic
| Toxicity/
jCarcinogen
1 (Note 4)
Ignitability/
Reactivity
(Note 5)
311
RQ
(Note 6)
Proposed
RQ
(Note 7)
Basis for
Proposed
BQ
(Note 6)
|Comments
Methyl iodide
| 74664

1
|Rat-orl:150(D)
|
1
ICAROUM


100
CARC
| IB
Methyl isocyanate
| 624639

1
|JUt-ihl:5/4H(B)
|Rat-orl:71(C)
i
1
1
1
1
B=102
F=19 (C)

lift
STAT

N-Methy1-N'-nitro-tt-oitrosoguanidine
| 70257

I
|Rat-orl:90(C)
j
1
|CARO=MED
l
SOLID

10
CARC

Methylthiouracil
| 56042

1
|Rbt-orl:2500(D)
a
1
| CAROMED
i
SOLID

10
CARC

Mitomycin C
| S0077

1
|!Ut-orl;14(C)
i
i
| CAROMED
1
SOLID

10
CARC
| IB
5,12-Naphthacenedione, (8S-cis)-8-
acety1-10-(3-aaino-2,1,6-t ndeoxy-
alpha-L-lyxo-hexopyranosyl)oxyl|-7,8,9,
10-tetrahydro-6,8,11-trihydroxy-l-
methoxy-
120810813

1
i
i
i
i
i
i
1
| CAROMED
i
i
i
i
|
SOLID

10
CARC
118
2,7-Naphthalenedlsulfonic acid,3,3'-
((3,3'-diDothyl-(l,l'-biph«nyl)-4,4'-
diyl)-bls(ozo)|bis(5-amino-4-hydroxy)-
tetrasodiun salt
| 72571

1
i
i
i
i
i
1
(CAROMED
I
i
i
i
SOLID

10
CARC

1-Naphthylamina
| 134327
lO-l(B)
1
|fiat-orl:779(D)
I
1
|CARC=b
i
SOLID

lpo
AOTX

2-Naphthylamne
| 91598
10—1(B)
1
|fiat-orl;727(D)
¦
1
|CAROtiIGH
1
SOLID

10
BHP
123
alpha-Naphthylaoine
| 134327
lO-l(B)
1
|KUt-orl :77949( A)
B=110
P=-4 (C)

10
CARC,era

Note: All comaents/notes are located at the end of this table.
-------
DATA FOB THE HP KM HAZARDOUS SUBSTANCES - Continued
Hazardous Substance (Not* 1)
1
1
1
1
| CASSH
Aquatic
Toxicity
(Note 2)
| Mammalian Toxicity (Note 3)
1
| Oironic
j Toxicity/
j Carcinogen
i (Note 4)
Ignitability/
Reactivity
(Bote 5)
311
RQ
(Note 6)
Proposed
BQ
(Note 7)
1
Basis tor |
Proposed j
BQ |
(Note 8) |Comments
Nickel chlorida
1
| 7716549
|37211055
|
500-100(0)
|Bat-orl:105(D)
1
|CAROLOW
|CT=40(B)
1
SOLID
5000
100
1
CARC.CH |
1
Nickel cyanide
| 557197
i
¦
1-0.1(A)

1
|CAROLGW
|CT»49(A)
I
SOLID

10
1
AQTO,CTX 131
i
i
Nickel(II) cyanide
| 557197
1
i
1-0.1(A)

1
|CAROUM
|CT»49(A)
i
SOLID

10
1
wamc.cTx |3i
1
1
Nickel hydroxide
|12054487
1
¦
100-10(C)

1
|CAROLCM
|CT»50(A)
i
SOLID
1000
10
1
CTX |
i
1
Nickel nitrate
|14216752
1
I
500-100(D)

1
|CAROL0W
|CT°38(B)
1
SOLID
5000
100
1
CAEC,CTX |
i
i
Nickel sulfate
1
| 7766814
i
1
500-100(D)

1
|CAROLOW
|CT=.39(B)
1
SOLID
5000
100
i
CARC.CIX |
1
a
Nickel tetracarbonyl
|13461393
1
1
100-10(C)
|Bat-ihl LClo:35/30M(B)
1
| CAROMED
|CT=49(A)
i
B=110
P=-4 (C|

10
1
CABC,CTX |
i
1
2-Nitropropane
| 79469
i
1

|Rat-lhl:400/6H(C)
|Bat-orl:500(D)
1
| CAROMED
1
1
B=248
P=75 (C)

10
1
CABC |
i
i
M-N11 rosodi-n-butylaaine
| 924163
j

|Kat-orl:1200(D)
1
| CAROMED
1


10
1
CABC |
i
N-Nitrosodiethanolanine
| 1116547
¦

|Bat-orl:7500(O)
1
|CAEOHIGH
1


1
1
CABC |
i
N-Nitrosodiethylanine
1
| 55165
j

|Rat-orl:280(D)
1
|CAROHIGH
|


1
1
CABC |
1
N-Nitrosodimethylamine
| 62759
1
¦

|Bat-lhl LCS0:78/4H(C)
|Bat-orl:26(C)
1
| CAROMED
1
1


10
1
CABC |
1
I
N-Nit rosodi-n-propy1amine
| 621647
¦

|Rat-orl:480(D)
1
| CAROMED
1


10
1
CABC |18
a
N-Nitroso-N-ethylurea
| 759739
I

|Rat-orl:300(D)
1
| CAROMED
1
SOLID

10
1
CABC |
i
N-Nitroso-N-Dethylurea
1
| 664935
i

|Rat-orl:110(D)
1
ICAROHIGH
1
SOLID

1
1
CABC |
i
N-Nitroso-N-oethylurethane
1
| 615532

|Rat-orl:180(D)
1
ICAROHIGH
SOLID

1
1
CABC |
Note: Ml consents/notes are located at the and
of this table.
-------
DATA FOB THE HPRM HAZARDOUS SUBSTANCES - Continued
Hazardous substanca |Nota 1)
1
1
1
1
| CASBB
Aquatic
Toxicity
(Nota 2)
| Mammalian Toxicity (Hot* J)
1
| CJironic
j Toxicity/
|Carcinoqan
| (Nota 4)
Ignitability/
Baactivity
(Hota 5)
111
BQ
(Nota
1
1
|Propos*d
j HQ
6)| (Nota 71
1
Basis for |
Proposed |
BQ |
(Nota 8) )Comments
H-Ni c rosooethyl vinylaaina
1
| 4549*00
|

|Bat—orl:24(C)
1
|CAHC=MED
1


1
110
1
1
CABC 118
1
H-Hit rosopipa r idina
| 100754
i

|Bat-orl:200(0)
1
|CABC=ttED
1
SOLID

1
110
1
1
CABC |
1
N-Nitrosopyrrolidina
| 930552
I

|Hat—orl:900(D)
1
|CARCaUIGH
¦
SOLID

I
II
1
1
CARC |
¦
5-Nic ro-o-toluidina
1
| 99558
I

|Rat-orl:51«(D)
1
ICARCaLOM
I
P=31S

1
|100
1
1
CARC |
¦
1,2-Oxathiolane, 2,2-diaxida
1
| 1120114
l

jlfeis-skn: 1000(D)
1
jCAACsMED
i
SOLID

1
iio
1
1
CARC |
2K-1,J,2-Oxasaphosphorina,2-Ibis(2-
chloroethyl|amino|tatrahydro-2-oxida
1
| 50180
1
i

|Bat-orl:94(C)
1
|CARCsHED
1
i
SOLID

1
110
1
1
1
CABC |
1
i
On cans
| 75218
1
¦
100-10(C)
|Bat-orl:72(C)
1
| CAROMED
1
1
B=51
F=<0 (B)

1
|10
1
1
1
CARC |
i
i
Oxirane, 2-(chloronetbyl)-
| 106898
1
1
1
100-10IC)
|Kat-ihl LClo:250 ppa/4H(C)
|Hat-okn LDlo:1000(D)
|Hat-orl:90(C)
1
|CARC®LOW
|CT=26(B>
1
I
B=239
F=91 (C)
1000
1
|100
1
1
1
i
CABC,CIX 1
1
1
Parathion
1
| 56)62
i
i
t
0.4(A)
|Bat-ihl LClo:10/2H(B)
|Bat—orl:2(B)
|Bat-skn:6.8(C|
1
|CT»32I.D.
I


1
110
1
1
1
AQTIX |
1
1
Pentachloromtrobencana
1
| 8366ft
i
i

|Bat-orl:1650(D)
1
|CABC=»LCW
|CT=«10.420(c)
1
SOLID
10
1
110
1
1
1
311 |10
1
1
Not a: All coaments/notes an located at the and of this table.
-------
DATA FOB THE NPHM HAZARDOUS SUBSTANCES - Contlnuad
Hazardous Substance (Hots 1)
CASES
Aquatic
Toxicity
(dot* 2)
1
1
1
1
| Mammalian Toxicity (Mote 3)
1
| Q>ronic
j Toxicity/
|Carcinogen
| (Bote 4)
Ignitability/
Reactivity
(Note 5)
311
BQ
(Note 6)
Proposed
BQ
(Note 7)
Basis Cor
Proposed
BQ
(Hot* 8)
|Comments
Phenol, 2,4,5-tnchloro-
95954
1-0.1(A)
1
|Bat-orl:820(D)
1
1
1
|CAROb
|CT-1J(C)
|
SOLID
10
10
311


Phenol, 2,4,6-tnchloro-
88062
1-0.1(A)
1
|Bat-orI:620(D)
i
a
1
|CAKOL0W
|CT=>I.D.
a
SOLID
10
10
311


Phenyl dichloroarsina
69(286

1
|Bbt-8kn;0.S(B)
|Bat-skn:16
|CT=>I.D.
1
a


1
CABC

116
1,10-(1,2-Phenylene)pyrene
193395

1
I
I
I
1
|CABOL0W
|CT=I.D.
I
SOLID

100
CABC

i is
Phosphoric acid, lead salt
7446277

I
I
I
¦
1
|CARO=MED
|CT=»33(B>
a
SOLID

10
CABC

116
Phosphorothloic acid, 0,0-diethyl 0-(p-
nitrophenyl) ester
56382
0.4(A)
i
|Rat-lhl LClo:10/2H(B)
|Rat-orl:2(B)
|Bat-skn:6.8(C)
1
1
|CTa32(B)
1
1
i

1
10
311

132
Polychlorinated Biphenyls (PCBs)
1336363
<0.1(X)
1
1
1
•
|CARC=MED
¦

10
1
AffTX

110
Polychlorinated Biphenyls (PCBs)
12674112
<0.1U)
1
1
a
1
| CAROMED
¦

10
1
AQTX

I"
Polychlorinated Biphenyls (PCBs)
11104282
<0.1(X)
1
|Rat-orl:3960(D)
a
1
| CAROMED
I

10
1
AffIX

113
Polychlorinated Biphenyls (PCBs)
11141165
<0.1(X)
1
|Rat-orl;4470(D)
i
1
| CAROMED
¦

10
1
AfflX

113
Polychlorinated Biphenyls (PCBs)
53469219
<0.1(X)
1
|IUt-orl:4250(D)
a
1
| CAROMED
¦

10
1
AffIX

|13
Polychlorinated Biphenyls (PCBs)
12672296
<0.1(X)
1
|RAt-orl:ll gVkg(D)
i
1
| CAROMED
¦

10
1
AfflX

113
Polychlorinated Biphenyls (PCBs)
11097691
<0.1(X)
1
|Rat-orl:l0lQ ng/k^D)
a
1
| CAROMED
1

10
1
AfflZ

|13
Polychlorinated Biphenyls (PCBs)
1109682S
<0.1(X)
1
|Rat-orl:131S(D)
I
1
| CAROMED
1

10
1
AffTX

113
Potassium arsenate
7784410
100-10(C)
1
i
i
¦
1
|CARC=UIGH
|CT=16(C>
1
SOLID
1000
1
CABC


Potassium arsemte
10124502
lOO-lO(C)
I
|Bat-orl:14(C)
|Bat-skn:150(C)
1
|CABC°UIGH
|CTb41(A)
SOLID
1000
1
CABC

110
Note: All comients/notes are located at the and
of this table.
-------
DMA FOB THE NFBM HAZARDOUS SUBSTANCES - Continued
Haiardous Substance (Not* 1)
CASHH
Aquatic
Toxicity
(Note 2)
1
1
1
1
| Mammalian Toxicity (Mote 3)
1
| Chronic
j Toxicity/
|Carcinogen
| (Note 4)
Ignitabillty/
Reactivity
(Note 5)
311
BQ
(Note 6)
Proposed
RQ
(Note 7)
Basis Cor
Proposed
BQ
(Note 8)
|Comments
Potassium bichromate
7775509
100-10
1
|Dog-orl LDlo:2829(D)
1
1
1
|CARC=HIGH
|CT=I.D.
¦
SOLID
1000
1
CABC
jlO
Potassium chrornate
7789006
lOO-lO(C)
1
1
1
1
1
|CAHC=HIGH
ICToI.D.
¦
SOLID
1000
1
CARC
110
1-Propanal, 2,3-epoxy-
765344

1
|Rat—orl:50(C)
l
1
|CAHC=MED
¦


10
CABC

Propane, 1,2-dibrono-3-chloro-
96126

1
|Hat-ibl;103/6H{C)
|Rdt-orl:170(D)
i
1
|CAEC=MED
1
1


10
CABC

Progane, 2-nitro-
79469

1
|Rat-ihl:400/6H(C)
jfUt-orl:5G0(D)
1
1
|CAHG=MED
1
1
B=>248
F=75 |C»

10
CARC

1,3-Propane sultone
1120714

1
|Kus-skn:1000(D)
i
1
|CARC=MED
1
SOLID

10
CARC

1-Propanol, 2,3-dibromo-, phosphate (3
:1)
126727

1
|!Ut-orl: 1010(D)
i
1
|CAROMED
1


10
CARC

2-Propenemtnle
107131
lO-l(B)
i
|Rat-lhl:500/4H(D)
|Rat-orl:82(C)
I
1
|CARC=MED
|CT=30(B)
1
B=171
F=32 (C)
100
10
CARC
1"
1,2-Propylenimine
75558

1
|Rat-orl:19(C)
i
1
|CARC=>ttED
I


10
CARC

Pyridine, hexahydro-ti-nitroso-
100754

1
|IUt-orl:200(D)
I
1
|CARC=MED
1
SOLID

10
CARC

4(lH)-Pynmidinone, 2,3-dihydro-6-
nethyl-2-thioxo-
56042

1
l&bt-orl:2500(D)
i
i
1
|CARC=MED
1
I
SOLID

10
CARC

Pyrrole, tetrahydro-B-nitroso-
930552

1
|Hat-orl:900(D)
i
1
(CARCoHIGH
1
SOLID

1
CARC

BADIONUCLIDES
a.A.

1
i
i
1
1
I


1§
STAT
| <' 3 3
Saccharin and salts
81072

1
i
¦
1
|CAEC=LOW
1
SOLID

100
CABC

Safrole
94597

i
|Bat—orl:1950(D)
I
1
|CAHC=U3W
1
F=212

100
CABC

Selenium disulfide
7488564

1
|Bat-orl:138(D)
1
1
|CAHC=LOW
|CT=I.D.
B:Se02 (A)

10
R

Mote: All coau&ents/notes are located At the end
of thia table.
-------
QKTA FOH THE NPBH HAZARDOUS SUBSTANCES - Continued
Hazardous Substance (Not* 1)
1
1
1
1
| CASBH
Aquatic
Toxicity
(Hote 2)
1
1
1
1
j Mammalian Toxicity (Note 3)
i
| Chronic
j Toxicity/
|Carcinogen
1 (Note 4)
Ignitability/
Baactivity
(Note 5)
311
BQ
(Note 6)
Proposed
BQ
(Note 7)
Basis tor
Proposed
BQ
(Note 6)
|Comments
L-Serine, diaxoacetate (aster)
1
| 115026

1
|Rat-orl:170(D)
|
1
|CABC°MED
1
SOLID

10
CABC
118
Sodium arsenate
1
j 7631692
i
i
100-10(C)
1
|Rbt-orl LDlo:12.5(C)
i
i
1
|CARC°HIGH
|CT=16(C)
1
SOLID
1000
1
CABC
110
Sodiua arsenite
1
j 7764465
i
i
100-101C)
1
|Rat-skn:150(D)
|Rat-orl:41(C)
a
1
|CABC°HIGH
|CT»41(A)
1
SOLID
1000
1
CABC
110
Sodiua bichroaate
1
110568019
i
i
100-10IC)
1
|R4t-orl:50(C)
i
i
1
ICABOHIGH
|CT=>I.D.
1
SOLID
1000
1
CABC
j 10
Sodiua chroaate
1
| 7775113
i
i
100-10(C)
1
i
i
a
1
|CABC=HIGH
|CT=I.D.
1
SOLID
1000
1
CABC
110
4,4'-Stilbenediol, alpha,alpha'-
diethyl-
1
| 56531
1
I

1
|Kus-orl:2500(D)
i
1
1
|CAHC=UIGH
1
1
SOLID

1
CABC

Streptozotocin
1
|16063664
|

1
|Kus-orl:264(D)
1
1
|CABO°HIGH
i
SOLID

1
CABC

Strontium chroaate
| 7769062
I
100-10(C)
1
i
a
1
|CABO=HIGH
1
SOLID
1000
1
CABC
|10
Sulfur selemde
1
| 1466564
1

1
|Rat-orl:138(D)
i
i
1
|CABO>UM
|CT»I.D.
1
B:Se02 (A)

10
B

Sulfuric acid, dimethyl ester
1
| 77781
i
i
lOO-lO(C)
1
|&At-ihl LClo:32/4H(B)
jtUt-orl: 440(D)
¦
1
|CA£OH£D
1
1
P°162

100
BHP
|16,23
THE
1
| 72546
i
i
<0.1(X>
i
|Bat-orl:113(D)
jsbt-skn:1200(D)
¦
1
|CABOMED
1
1
SOLID
1
1
311
110
2,3,7,8-Tetrachlorodibenso-p-dioxin
(TCDD)
1
j 1746016
i
i
i
<0.1(X)
1
|Kus-skn LDlo:0.06(A)
|Dog-orl LDlo:3(B)
|Mus-orl:0.114(A)
a
1
|CABOHIGH
1
1
1


1
AQIX.CABC
|10
1,1,1,2-Tet rachlo roethane
1
| 630206
i
i

1
1
1
1
1
|CABC°L0W
|CT=I.D.
1


100
CABC

1,1,2,2-Tetrachloroethane
1
| 79345
i
lO-l(B)
1
|Rat-ihl LClo:1000/4U(D)
|Dog-orl LDlo:300(D)
1
|CABO=LOW
|CT=17.5(C)


100
AQIX.CABC
110
Note: All comments/notes are located at the acc'i of this tibk
-------
DATA FOB THE HFRM HAZARDOUS SUBSTANCES - Continued
Hazardous Substance (Not* 11
1
1
1
1
| CASBH
Aquatic
Toxicity
(Hot* 2)
1
1
1
1
| Hamuli an Toxicity (Hota 3)
1
| Chronic
j Toxicity/
|Carcinogen
I (Not. 4)
Ignitability/
Baactivity
(Not* 5)
311
BQ
(Hot* 6)
Propoaad
BO
(Hot* 7)
1
Basis for |
Proposed |
BQ I
(Not* 8) jcooiments
Tetrachloroethena
1
| 127104
1
1
lOO-lO(C)
1
iBat-ibl l£lo:4000/4H(D)
|Kus-orl:8100(D)
1
1
|CABC°L0W
|CT=10(C)
I


100
1
CARC |
1
1
Tatrachloroathylane
1
j 127184
i
¦
100-10
-------
DATA FOR TOE NFRM HAZARDOUS SUBSTANCES - Continued
Hazardous Substance (Hot* 1)
j CASHH
Aquatic
Toxicity
(Hot* 2)
1
1
1
1
| Hamuli an Toxicity (Mote 3)
i
| Chronic
j Toxicity/
|Carcinogen
1 (ttot* 4)
I^nitability/
Reactivity
(Note 5)
311
BQ
(Note 6)
Proposed
BQ
(Not* 7)
1
Basis for |
Proposed |
BQ |
(Bote 8) jcomments
Trichlorophenol
|2S167822
1-0.1(A)
1
1
1
1
(CABC-LOW
1
SOLID
10
10
1
111 j 34
2,3,4-Trichlorophenol
(15950660

1
1
1
1
1
1



1
1
|
2,3,5-Tnchlorophenol
| 913748

1
\
|
1
1
I



1
1
i
2,3,6-Trichlorophenol
| 931755

1
1
1
1
1
1



1
I
I
2,4, S-Tnchlorophenol
| 95954
1-0.1(A)
1
|R*t-orl:d20(D)
1
a
1
|CABC=to
|CTal3(C)
1
SOLID
10
10
311 |
i
i
2,4,6-Trichlorophenol
| 88062
1-0.1(A)
1
|R*t-orl:820(D)
1
I
1
|CABOLOW
jci^I.D.
¦
SOLID
10
10
311 |
1
3,4,5-Trichiorophenol
| 609198

1
1
i
1
1
1



1
1
1
2,4,5-Tnchlorophenol
| 95954
1-0.1(A)
1
|Rat-orl;820(D)
i
1
1
|CAHC=b
|CT=13(C)
j
SOLID
10
10
311 |
i
1
2,4,6-Tnchlorophenol
| 88062
1-0.1(A)
1
|Rat-orl;820(D)
1
a
1
|CAROL0W
|CT»I«D.
1
SOLID
10
10
311 |
i
¦
Tns(2,3-dibromopropyl) phosphate
| 126727

1
|Ret-orl:1010(D)
1
1
| CAROMED
1


10
1
GARC |
I
Trypan blue
| 72571

1
1
i
1
|CARC°MED
«
SOLID

10
1
CARC |
>
Unlisted Hazardous Wastes
| H.A.

1
1
t
1
1
1



1
1
Characteristic of EP Toxicity


J
1
i
1
1
i



1
i
I
Arsenic
| H.A.

1
1
i
1
J
1


1
1
CARC |
¦
Cadmiua
j H.A.

1
1
1
I
¦


10
1
CARC |
¦
Chroniun(VI)
| H.A.

1
i
I
1
I
1


1
1
CARC |
¦
Lead
j H.A.

1
i
i
1
I
¦


100
1
era |
¦
Lindane
| H.A.

1
i
i
1
•
1

1*
1
311 |
¦
Toxaphene
j H.A.

1
i
1
i

1*
1
1
311 |
Mote; All comments/notes Are located c" enc*
r1" r tabl*
-------
DATA FOR THE NPBM HAZABDOUS SUBSTANCES - Continued
Hazardous Substance (Not# i)
1
1
1
1
| CASBH
Aquatic
Toxicity
(Hot* 2)
1
1
1
1
| NMuliu Toxicity (Not* 3)
1 1
| Chronic |
| Toxicity/jlgnitability/
|Carcinog«n| Reactivity
| (Hot* 4)j (Not* 5)
311
BQ
(Not*
1
1
|Proposed
1 BQ
6)| (Not* 7)
Basis for
Proposed
BQ
(Not* S)
| Comments
Uracil, S-(bis(2-chloroathyl)amino|-
1
| <6751
i

1
|Rat-orl:7.5(B)
1
1
|CARO=MED
j
1
| SOLID
1

1
|10
I
CARC

Uracil mustard
| 66751
i

1
|Rat-orl:7.S(B)
i
1
|CARC=*ED
1
1
| SOLID
I

|10
1
CAfiC

Vinyl chlond*
1
| 75014
1
¦
1000(D)
1
|Gpg-ihl LClo:20/30M(B)
|Rat-orl:500(D)
1
|CAHC=MED
|CT=20(C)
i
1
|B=7
|F=GAS (B)
1

|10
1
1
CARC
129
Vinylidane chloride
1
| 75354
1
1
I
1000-100(D) |Mus-ihl LC50.-98 ppa/22H(C)
|Bat-ihl:10,000/24H(D)
|Rat-orl:200(D)
1
|CABC»U3W
|CT=19(C)
1
1
|B=99
|f=0 (B)
1
5000
1
(100
1
1
CABC.I
127
I
N3
00
Hote: All consents/notes are located at the end of this table.
-------
DATA FOR THE HPRM HAZARDOUS SUBSTANCES - Continued
Hazardous Substance (Note 1)
CASHH
Aquatic
Toxicity
(Note 2)
1
1
1
1
| Mammalian Toxicity (Note 3)
1
| Chronic
| Toxicity/
I Carcinogen
1 (Note 4)
Ignitability/
Reactivity
(Note 3)
311
BQ
(Bote 6)
Proposed
HQ
(Note 7)
Basis for
Proposed
BQ
(Note 8)
|Commenta
F001


1
1
1
1


10
Comp

The following spent halogenated


1
1





solvents used in degreasing and


1
1





sludges froa the recovery of these


1
1





solvents in degreasing operations:


1
1





(a) Tetrachloroethylene
127184
100-10
|Rat—orl:4920(D)
|CARC=LOW
B»188
1000
100
CARC




1
|CT=>20(C)
F=90 (C)




(d) 1,1,1-Tnchloroethane
71S56

1
1


1000
AQTX.CTX

(e) Chlorobenzene
108907

1
1


100
311

(f) 1,1,2-Trichloro-1,2,2-
76131

1
1


5000
Max
|35
tnf luoroe thane


1
1





(g) o-Dichlorobenzene
95501

1
1


100
311

(h) Trichlorof luorooethaiie
75694

1
|
1
|


5000
Max

P006


1
1
1
1


1
Coap

Wastewater treatment sludges fron


1
1





electroplating operations except froa


1
1





the following processes: (1) sulfuric


1
1





acid anodizing of aluainum; (2) tin


1
1





plating on carbon steel; (3) zinc


1
1





plating (segregated basis) on carbon


1
1





steel; (4) aluainum or zinc-aluminua


1
1





plating on carbon steel; (5) cleaning/


1
1





stripping associated with tin, zinc


1
1





and aluainum plating on carbon steel;


1
1





and (6) chemical etching and milling *


1
1





Hote: All comments/notes are located at the end of this table -
VOL 3 (R31B1.HFW/R31B2.HPW/3R31B.HED/RECORD4.THP) 12/26/86 16:14 PAGE 1
-------
DATA FOB THE HPBM HAZARDOUS SUBSTANCES - Continued
Hazardous Substance 
-------
DATA FOB THE HPRH HAZARDOUS SUBSTANCES - Continued
Hazardous Substance (Not* II
CASHiJ
Aquatic
Toxicity
(Hot* 2)
Hamuliin Toxicity (Not* ))
Oiromc
Toxicity/
Carcinogen
(Note 4)
Ignitability/
Beactivity
(Note 5)
311
BQ
(Note 6)
Proposed
BQ
(Mote 7)
Basis for
Proposed
BO
(Note 8)
Comments
2,3,4,6-Tetrachlorophenol
20(C)
SOLID
10
1
1
1
10
T(orl)
T(orl)
Korl)
311
Coop
10
Note: All comments/notes are located at tha end
of thiB table.
-------
DATA FOB THE NPBH HAZARDOUS SUBSTANCES - Continued
Hazardous Substance (Nota 1)
CASBH
Aquatic
Toxicity
(Not* 2)
Hamulian Toxicity (Hot* 31
Chronic
Toxicity/
Circinogen
(Note 4)
Ignitability/
Reactivity
(Hota 5)
311
BQ
(Hota 6)
Proposed
BQ
(Hota 7)
Basis tor
Proposed
BQ
(Hota 8)
Commenta
(a)
(b)
(c)
(d>
(a)

Tetrachlorodibanxo-p—dioxins
2,1,7,8-Tet rachlorodibenzo—p-
dloxin (TCDD)
Pentachlorodibanso-p-dioxins
Heiachlorodibanxo-p-dloxins
1,2,3,7,8,9-
Hexachlorodibenso-p-dioxin
Haxachlorodibenxo-p-dioxin
1,2,3,4,7,8-
tjexachlorodibenxo-p-dioxin
Tatracblorodibeniofurans
2,3,7,8-
Tatrachlorodibenxofuran
Pentachlorodibenxofurans
Hexachlorodibanzofurans
H.A.
1746016
H.A.
H.i.
19408743
34463468
39221286
H.A.
S1207319
H.A.
H.A.
<0.1(X)
F023
Wastaa (except wastewater and spent
carbon froa hydrogen chloride
purification) froa the production of
materials on equipment previously used
for the production or manufacturing
usa (as a raactant, chemical
intermediate, or coaponant in a
formulating process) of tri- and
tetrachlorophenols. (This listing does
not include wastes froa equipment used
only for the production or usa of Hex*
(a) Tetrachlorodibanxo-p-dioxins
2,3,7,8-Tetrachlorodibenso-p-
dioxin (TCDD)
H.A.
1746016
<0.1(X>
fftis-skn LDlo:0.08(A)
Dog-orl LDlo:3(B)
Kus-orl:0.114(A)
Gpg-orl:60 ug/kg(X)
Mus-orl:1250 ug/kg(B)
Gpg-orl:70 ug/kg(X)
Gpg-orl:72.S ug/kg(X)
Hus-orl:825 ug/kg(A)
Gpg-orl:5 ug/kg(X)
Mus-skn LDlo:0.08(A)
Dog-orl LD1g:3(B)
Hus-orl:0.114(A)
CARC=HIGH
AQT2£,CABC
T(orl)
T(orl)
T(orl)
T(orl)
Coop
10
CABOHIGH
AQIX.CARC
10
Nota: All comments/notes ara located at the and of this table-
-------
DMA FOB THE NPBM HAZARDOUS SUBSTANCES - Continued




1
1
1
| Chronic



1
Basis Cor |



Aquatic
1
j Toxicity/
Ignitability/
311
Proposed
Proposed |



Toxicity
1
jCarcinogen
Beactivity
BQ
BQ
BQ I
Hazardous Substance (Bote 1)
j CkSBH
(Hot* 2)
| Mammalian Toxicity (Hot* 3)
| (Mote 4)
(Note S)
(Note 6)
(Koto 7)
(Hot* 8) |Comments
(b)
Fentachlorodibenso-p-dioxins
| B.A.

1
1



1
(c)
Tet rachlorodibanzofurans
j b.a.

1
1



1

2.3,7,8-
|5120?319

|Gpg-orl:S ug/XglX)
1


1
T(orl) |

Tetrachlorodibenzofuran


1
1



1
Id)
Fentachlorodibensofurans
| B.A.

1
1



1
(a)
Tnchlorophenols and their
| B.A.

1
1



1

chlorophenoxy derivative acids.


1
1



1

esters, ethers, aaine and other


1
1



1

salts.


1
1



1

2,4,5-Trichlorophenol
| 95954
1-0.1(A)
|Bat-orl:620(D)
|CABC=b
SOLID
10
10
311 |




1
jcToll(C)



1

2,4,6-Trichlorophenol
I aeos2
1-0.1(A)
|Bat-orl:020(D)
jcAROUM
SOLID
10
10
111 |




1
jcTal.D.



1
(f)
Tetrachlorophenols and their
| B.A.

1
1



1

chlorophenoxy derivative acids,


1
1



1

esters, ethers, aaine and other


1
1



1

salts.


1
t



1

2,3,4,6-Tetrachlorophanol
| 58902
1-0.1(A)
|Rat-orl:140(D)
|CTb32(B)
SOLID

10
AQES |




|Rbt-skn:250(D)
1
1
1



1
1
P024



1
1
1
1


1
1
CO Dp |
Wastes, including but not limited to.


1
1



1
distillation residues, heavy ends.


1
1



1
tars
and reactor cleanout wastes,


1
1



1
from the production of chlorinated


1
1



1
aliphatic hydrocarbons, having carbon


1
1



1
content Iron one to five, utilizing


1
1



1
free radical catalyzed processes.


1
1



1
(This listing does not include light


1
1



1
ends
spent (liters and filter aids.


1
1



1
spent desslcants(sic), wastewater.


1
1



1
wastewater treatment sludges, spent c*


1
1



1
(a)
Chlorooethane
| 74873
1000(D)
|Bat-ibl:152000 Bg/a3/30M(D)
|CAaOLOW
B=-ll

100
I.CABC |




|nis-lhl:3146/7H(D)
jcr»20(c)
K=<1AS (B)


1
Note: All comments/notes are located at the end 01C this table.
-------
DATA FOR THE NPBM HAZARDOUS SUBSTANCES - Continued


1
1


1
| chronic



Basis for



1
Aquatic

j Toxicity/
Ignitability/
311
Proposed
Proposed



1
Toxicity

|Carcinogen
Boactivity
BQ
BQ
BQ

Hazardous Substance (Not* 1)
| CASBH
(Note 2)
Mammalian Toxicity (Not* 3)
j (Bote 4)
(Note 5)
(Hot* 6)
(Hot* 7)
(Note 8)
|Comments
< b
Dichloromethane
| 75092


1


1000
CTX

(cl
Tnchlorome thane
| 67663
100-10(C)
Bat-orl:800(D)
|CABC=MED

5000
10
CARC



1

Bat-lhl:8000/4H(D)
1





18.4(C)
P=56 (C)






1

Rat-orl:670(D)
1





(h|
trans-1,2-Dichloroethylene
| 156605


1


1000
I,CTX

(i)
1,1-Dichloroethylene
| 7S3S4
1000—100(D)
Mus-lhl LC50:98 ppn/22H(C)
|CABOLOW
B=99
5000
100
CARC, I
127


1

Bat-lhl:10,000/24H(D)
|CT=19(C)
F=0 (B)






1

Bat-orl:200(D)
1





(])
1,1,1-Tnchloroethana
| 71556


1


1000
AQTX.CTX

(k)
1,1,2-Trichloroethana
| 79005
100-10(C)
Bat-lhl LClo:500/8H(D)
|CAKC=L0W


100
CABC



1

Bat-orl:1140(D)
|CT=>I.D.





(1)
Tnchloroethylene
| 79016
100-10IC)
Bat-orl:4920(D)
jcABCaLOM
B=188
1000
100
CARC



I


|CT=20(C)
F=90 (C)




In)
1,1,1,2-Tatrachloroethana
| 630206


(CABCoLOW


100
CARC



1


jcr=i.D.





(n)
1,1,2,2-Tetrachloroethane
| 79345
10—1(B)
Bat-lhl LClo:1000/4HID)
jcAROLOW


100
AQfTX.CARC
iio


1

Dog—or1 LOlo:300(D)
|CTal7.5(C)





(o)
Tatrachloroethylene
| 127184
100-10(C)
Bat-ihl LClo:4000/4U(D)
|CARC°L0W


100
CARC



1

Mus-orl:8100(D)
|CTol0(C)






Hexachloroethane
| 67721
10—1(B)
Bat-orl:6000(D)
jcAHC=L£JW
SOLID

100
AQTX,CARC



1


|CT=15.2(C)





(r
Allyl chloride (3-chloropropene)
| 107051


1


1000
311,T(orl),



1


1



T(ihl),1

(s)
Dichloropropane
126638197


1


1000
I,CS

(t)
Dichloropropane
126932238


1


100
AQTX.CTX

Note: All comments/notes are located at the and of this table.
-------
DMCA FOR THE NPRM HAZARDOUS SUBSTANCES - Continued



1
1
1
| Chronic



Basis for



Aquatic
1
j Toxicity/
Ignitability/
311
Proposed
Proposed



Toxicity
1
|Carcinogen
Reactivity
HQ
HQ
RQ

Hazardous Substance (Note 1)
CASHN
(Note 2)
| Mammalian Toxicity (Note 3)
j (Note 4)
(Note 5)
(Note 6)
(Note 7)
(Note 8)
|Comments
(u) 2-Chloro-l,3-butadiene
126998

1
1


1000
AQTX,I
136
(v) Hexachloro-l,3-butadiene
•7683
<0.1(X)
|Bat-orl:90(C)
|CABC°L0W


1
AQTX
110



1
|CT»10.3(C)





(w) Hexachlorocyclopentadiene
77174
<0.1(X)
|Bat-orl:113(D)
|CT«62(A)
SOLID
1
10
BMP
|10,23



|Rbt-skn:430(D)
1





(x) Hexachlorocyclohexane
98B99
<0.1(X)
|Rat-skn:500(D)
| CAROMED
SOLID
1
1
311
110



jaat-orl:76(C)
1





(y) Benzene
71432
10-1(B)
jRat-ihl:10,000/7U(D)
| CAROMED
B-176
1000
10
CARC




|Bat-orl:3800(D)
|Cr»17(C)
P=12 (C)




|z) Oilorobenzene
108907

1
1


100
311

(aa) Dichlorobenzenes
25321226

1
1


100
311

(bb) 1,2,4-Trichlorobenzene
120821

1
1


100
AQTX

(cc) Tetrachlorobenzene
95943

1
1


5000
CIX

(dd) Pentachlorobenzene
608935

1
1


10
AQTX

lee) Hexachlorobenzene
118741

|Bat-orl:10,000(D)
| CAROMED
SOLID

10
CARC
110



1
jcT=29.5(B)





(ff) Toluene
108883

1
1


1000
311,I,CTX

(99) Naphthalene
91203

1
I
1
|


100
AQTX

F026


1
1
1
1


1
Coop

Wastes (except wastewater and spent


1
1





carbon from hydrogen chloride


1
1





purification) from the production of


1
1





materials on equipment previously used


1
1





for the manufacturing use (as a


1
1





reactant, chemical intermediate, or


1
1





component in a formulating process) of


1
1





tetra-, penta-, or hexachlorobenzene


1
1





under alkaline conditions.


1
1





(a) Tetrachlorodibenzo-p-dioxins
H.A.

1
1





2,3,1,fl-Tetrachlorodlbenzo-p-
1746016
<0.1(X)
|Hus-skn U)lo:0.08(A)
|CARC=HIGH


1
AQTX, CARC
110
dioxin (TCDD)


|Dog-orl LDlo:3(B)
1








|Mus-orl:0.114(A)
1





(b) Pentachlorodibenzo-p-dioxins
B.A.

1
1





Note: All comments/notes are located at the end of this tab)".
-------
DATA FOR THE NFHM HAZARDOUS SUBSTANCES - Continued



1
1
| Chronic



1
Basis for |


Aquatic
1
j Toxicity/
Ignitability/
311
Proposed
Proposed |


Toxicity
1
jCarcinogen
Reactivity
BQ
BQ
BQ I
Hazardous Substanc* (Hot* 1)
CASBH
(Not* 2)
| Maternalian Toxicity (Note 3)
j (Note 4)
(Hot* St
(Hot* 6)
(Not* 7)
(Note 8) jComments
(c) Hexachlorodibanso-p-dioxins
H.A.

1




1
1,2,1,7,8,9—
19408743

|Gpg-orl:60 ug/kg(X)



1
T(orl) |
Hexacblorodibenxo-p-dioxin


1




1
Hexachlorodibenxo-p-dioxin
34465468

|Mus-orl:1250 ug/kg(B)



1
T(orll |



|Gpg-orl:70 ug/kg(Xl




1
1,2,3.4,7,8-
39227286

|Gpg-orl:72.5 ug/kg(X)



1
Ttorl) |
Hexachlorodibenzo-p-dioxin


|Mus-orl:825 ug/kg(A)




1
(d) Tetrachlorodibensofurans
H.A.

1




1
2,3,7,8-
S1207319

|Gpg-orl:5 ug/VgOO



1
T(orl) |
Tetrachlorodibenxofuran


1




1
(a) Pentachlorodibansofurans
H.A.

1




1
(f) Hexachlorodlbencofurans
H.A.

1




1
F027


1
1



1
1
Coop |
Discarded unused formulations


1




i
containing tri-, tatra-, or


1




i
pentachlorophenol or discarded unused


1




i
formulations containing compounds


1




i
derived ftorn these chlorophenols.


1




i
(This listing does not include


1




i
formulations containing


1




i
Hexachlorophene synthesized froa


1




i
prepurified 2,4,5-trichlorophenol as


1




i
the sole component.).


1




i
(a) Tetrachlorodibenso-p-dioxins
H.A.

1




i
2,3,7,8-Tatrachlorodlbenzo-p-
1746016
<®.1(X)
|Mus-skn LElo:0.08(A)
jcABOHIGH


1
AQTX.CAHC 110
dioxin (TCDD)


|Dog—a rl U)lo:3(B)




1



|Kus-orl:0.114(A)




1
(b) Pentachlorodibonco-p-dioxins
H.A.

1




1
(c) Hexachlorodibenzo-p—dioxins
H.A.

1




1
1,2,3,7,8,9-
19408743

|Gpg-orl:60 ug/kg(X)



1
T(orl) |
Hexachlorodibenso-p-dioxin


1




1
Hexachlorodibenzo-p-dioxin
34465468

|Hus-orl:1250 ug/kg(B)



1
T(orl) |



|Gpg-orl:70 ug/kg(X)




1
Nota: All comments/notes are located at th« and of this table.
-------
DAXA rOH THE NPBM HAZARDOUS SUBSTANCES - Continued




1
1
1
| Chronic



1
Basis for |



Aquatic
1
| Toxicity/
Ignitability/
311
Proposed
Proposed |



Toxicity
1
|Carcinogen
Beactivity
BQ
BQ
BQ |
Hazardous Substance (Note 1)
CASBH
(Hote 2)
| Mammalian Toxicity (Note 3)
1 (Note 4)
(Note 5)
(Note 6)
(Note 7)
(Hote 8) jComments

1,2,3,4,7,8-
39227286

|Gpg—orl:72.5 ug/kg(X)
1


1
T(orl) |

Hexachlorodibenso-p—dioxin


|Mus-orl:625 ug/kg(A)
1



1
(d)
Tet rachlorodibenzofurans
N.A.

1
1



1

2,3,7,8-
51207319

|Gpg-orl:5 ug/kg(X)
1


1
T(orl) |

Tetrachlorodibenxofuran


1
1



1
(e)
Pentachlorodibenzofurans
N.A.

1
1



1
(f>
Hexachlorodibensofurans
N.A.

1
1



1
<9>
Tnchlorophenols and their
N.A.

1
1



1

chlorophenoxy derivative acids,


1
1



1

esters, ethers, amine and other


1
1



1

salts.


1
1



1

2,4, 5-Tnchlorophenol
9S954
1-0.1(A)
|Bat-orl:820(D)
|CAEC=b
SOLID
10
10
311 |




1
|CT»13(C)



1

2,4,6-Tnchlorophenol
88062
1-0.1(A)
|Bat-orl:820(D)
|CABC°U3W
SOLID
10
10
311 j




1
|CT»I.D.



1
(hi
Tetrachlorophenols and their
N.A.

1
1



1

chlorophenoxy derivative acids,


1
1



1

esters, ethers, amine and other


1
1



1

salts.


1
1



1

2,1,4,6-Tet rachlo rophenol
58902
1-0.1(A)
|Bat-orl:140(D)
|CT=32(B)
SOLID

10
AQTJC |




|Bbt-skn:250(D)
1



1
U)
Pentachlorophenols and their
87865
0.6-0.2(A)
jBat-ska;105(D)
|CABC=b
SOLID
10
10
311 |10

chlorophenoxy derivative acids.


|Rat—lhl:11.7(B)
|CT=20(C)



1

esters, ethers, amine and otther


|Bat-orl:50(C)
1



1

salts


1
I
1
I



1
I
F028



1
1
1
1


1
1
Comp |
Residues resulting (ioi the


1
1



1
incineration or thermal treatment of


1
1



1
soil
contaminated with EPA Hazardous


1
1



1
Waste Nos. F020, F021, F022, F023.


1
1



1
F026
and F027.


1
1



1
(a)
Tetrachlorodibenzo-p—dioxins
N.A.

1
1



1

2,3,7,8-Tet rachlorodibenso-p-
1746016
<0.1(X)
|Mus-skn U>lo:0.08(A)
|CABOHIGH


1
AOIX.CABC 110

dioxin (TCDD)


|Dog-orl L01o:3(B)
1



1




|Kus-orl:0.114(A)
1



1
Note: All conments/notea are located at tbi and of this table.
-------
DATA FOB THE NPRM HAZARDOUS SUBSTANCES - Continued
Haxardous Substance (Hot# 1)
CASBH
Aquatic
Toxicity
(Not* 2)
Mammalian Toxicity (Not* 3)
Chronic
Toxicity/
Carcinogen
(Not* 4)
Ignitability/
Reactivity
(Not* 5)
311
BQ
(Not* 6)
Proposed
BQ
(Not* 7)
Basis for
Proposed
BQ
(Not* 8)
OJ
00
(b)	Pentachlorodibenxo-p-dioxins
(c)	Hexachlorodibenso-p-dioxins
1,2,3,7,8,9-
Hexachlo rodibenro-p-dloxin
HexachlorodibenEo-p-dioxin
1,2,3,4,7,8-
Hexachlorodibenxo-p-dioxin
(d)	Tetrachlorodibenxofurans
2,3,7.8-
Tetrachlorodibenzofuran
(e)	Pentachlorodibenxofurans
(f)	Hexachlorodibenxofurans
(9) Tnchlorophenols and their
chlorophenoxy derivative acids,
esters, ethers, amine and other
salts.
2,4,5-Trichlorophenol
2,4,fi-Trichlorophenol
(h) Tetrachlorophenols and their
chlorophenoxy derivative acids,
asters, ethers, amine and other
salts.
2,3,4,6-Tet rachlorophenol
(1) Pentachlorophenols and their
chlorophenoxy derivative acids,
esters, ethers, anine and other
salts
K001
Bottom sediment sludge from the
treatment of wastewaters from wood
preserving processes that use creosote
and/or pentachlorophenol.
I.A.
N.A.
19408743
34465468
39227286
N.A.
51207319
N.A.
N.A.
H.A.
95954
88062
N.A.
58902
87865
Gpg-orl:60 ug/kg(X)
Kus-orl:1250 ug/kg(B)
Gpg-orl:70 ug/Vg(X)
Gpg-orl:72.5 ug/kg(X)
ttus-orl;825 ug/kg(A)
Gpg-orl:5 ug/kg(X)
1-0.1(A)
1-0.1(A)
1-0.1(A)
0.6-0.2(A)
Bat-orl:820(D)
Rat-orl:820(DI
Rat-orl:140(D)
Bbt-skn:250(D)
Bat-skn:105(D)
Bat-ihl:11.7(B)
Rat-orl:50(C)
CARC=b
CT=13(C)
CARO LOW
CT=I.D.
CT=>32(B)
CAEC=b
CT=20(C)
SOLID
SOLID
SOLID
SOLID
10
10
10
10
10
10
10
T(orl)
T(orl)
T(orl)
T(orl)
311
311
AQfTX
311
Coop
Note: All comments/notes are located at the end of this table.
-------
DATA FOB THE HFBM HAZARDOUS SUBSTANCES - Continued
Hazardous Substance (Not* 1)
CASBN
Aquatic
Toxicity
(Hot* 2)
Mammalian Toxicity (Not* 1)
Chronic
Toxicity/
Carcinogen
(Hot* 4)
Ignitability/
Reactivity
(Not* 5)
311
HQ
(Nota 6)
Proposed
HQ
(Hot* 7)
Basis tor
Proposed
HQ
(Not* 8)
Comments
(a) Pentachlorophenol
(b)	Phenol
(c)	2-Qilorophenol
(d)	p-Qiloro-n-cresol
(e)	2,4-Dinitrophenol
(f)	Tnchlorophenols
(1)	2,4,5-Trichlorophenol
(2)	2,4,6-Trichlorophenol
(9) Tetrachlorophenols
(1) 2,3,4,6-Tetrachlorophenol
Wastewater treatment sludge (roi the
production of chrome yellow and orange
pigments.
87865
108952
95578
59507
51285
H.i.
95954
88062
B.A.
58902
0.6-0.2(A)
-P-
(hi
Creosote
j 80015S9|
I |
1
U)
VO
(1)
dirysene
j 218019|
I I

(})
(k)
Naphthalene
Benzo(b|fluoranthene
| 91203|
j 205992|
¦ j

(1)
(m)
Fluoranthene
Benzo(a)pyrene
| 206440|
| 503281
j j

(n)
Indenol1,2,l-cd|pyrene
| 191395|
j j

(0)
Benz(a)anthracene
| 56553|
1 1


DlbenzI a,h|anthracene
| 53703)
1 1

(q)
(r)
Acenaphthylene
2,4-Dimethylphenol
1 1
| 208968 j
| 105679 j
1 i

K002

1 1
1 1
1—0.1(A)
1-0.1(A)
1-0.1(A)
lO-l(B)
Bat-skn:105(D)
Bat-ihl:11.7(B)
Hat-orl:50(C)
Bat-orl:820(D)
Bat-orl:820(D)
Bat-orl:140(D)
Rbt-skn:250(D)
Bat-orl:725(D)
CABOb
CT=20(C|
SOLID
10
CABC=b
CT*13(C)
CAEC-LOW
CT=I.D.
CT»32(B)
CAEOHIGH
CT>1.0(D)
CABOMED
CT=I.D.
CAEC=HIGH
CT=I.D.
CAEC=HIGH
CT=46( A)
CABOLOW
CT=I.D.
CABOMED
CT=I.D.
CA»C=HI
-------
DATA FOR THE HFBM HAZARDOUS SUBSTANCES - Continued
Haeardous Substance (Hot* 1)
1
1
1
1
| CAS EH
Aquatic
Toxicity
(Note 2)
1
| Chronic
j Toxicity/
|Carcinogen
Mammalian Toxicity (Note 3) j (Mote 4)
Ignitability/
Reactivity
(Note S)
1
1
111 |Proposed
BQ | BQ
(Note 6)j (Note 7)
1
Basis for |
Proposed |
BQ |
(Note S) |Comments
(a)	Hexavalent chroaiua compounds
(b)	Lead compounds
| H.A.
| H.A.
|

1
1
1

|1
jioo
1
CARC |
CTX j
I
KOOJ
Wastewater treatment sludge (coa the
production of molybdate orange
pigments.
(a)	Haxavalent chroaiua compounds
(b)	Lead compounds
1
1
1
1
1
| H.A.
j N.A.
I

1
1
1
1
1
1
1
1

1
|1
1
1
1
U
jioo
1
1
Comp |
1
1
1
CARC |
CTX j
1
K004
Wastewater treatment sludge from the
production of xinc yellow pigments,
(a) Hexavalent chromium compounds
1
1
1
1
| H.A.
1

1
1
1
1
1
I

I
II
1
I
II
1
1
Comp |
1
1
CARC |
1
K005
Wastewater treatment sludge from the
production of chrome green pigments.
(a)	Hexavalent chromium compounds
(b)	Lead compounds
1
1
1
1
| H.A.
j H.A.

1
1
1
1
1
1
1

I
II
1
I
II
|100
1
1
Comp |
•
i
CARC |
CTX j
i
K006
Wastewater treatment sludge from the
production of chrome oxide green
pigments (anhydrous and hydrated).
(a) Hexavalent chromium compounds
1
1
1
1
1
| H.A.
1

1
1
1
1
1
1
1

I
II
1
1
I
II
1
1
Comp |
1
1
1
CARC |
1
K007
Wastewater treatment sludge from the
production of iron blue pigments.
(a)	Cyanides (cooplexed)
(b)	Hexavalent chromium compounds
1
1
1
1
| H.A.
j H.A.
1

1
1
1
1
1
1
1

I
II
1
I
110
II
1
1
Conp |
i
i
311 |31
CARC j
1
KOO!
Oven residue from the production of
chrome oxide green pigments.
1
1
1
1

1
1
1
1

1
jl
1
1
1
Coop |
i
i
Note; All comments/notes are located at the end of this table.
-------
QfhTA roa IKE NPHM HAZARDOUS SUBSTANCES - Continued


1
1

1
1
j Chronic



Basis
for



1
Aquatic
1
j Toxicity/
I gaitability/
111
Proposed
Proposed



1
Toxicity
1
(Carcinogen
Eaactivity
BO
HQ
BQ


Hazardous Substance (tlote 1)
| CASBH
(Note 2)
| Mammalian Toxicity (Note It
j (Hot. 4)
(Bote 3)
(Note 6)
(Hot* 7)
(Note
6)
|Comments
(a I
Hexavalent chromium compounds
| H.A.
1

1
1



I
CARC


K009

1
1

1
1



10
Coop


Distillation bottoms (roa the
1

1







production of acetaldehyds from
1

1







ethylene.
1

\







(a|
Chlorofora
| 67663
100-10(C)
|Bat-orl:800(D)
|CARC=HED

5000
10
CARC




1

j Bat-ihl:8000/4H(D)







(b)
Formaldehyde
| 50000
100-10(C)
jBat-ihl LClo: 250 ppn/4H(C)
|CAHC=MED
B»-3
1000
100
HHP

123


1

|Bbt-skn:270(D)
|Cr»)9(B)
F=GAS (B)







1

|Bat-orl:800(D)








jcAaCoLCW
B»-ll

100
I,CAHC




1

jttus-lhl: 3146/7H(D)
|CT=>20(C)
F=CAS (B)





(e)
Paraldehyde
| 123637

1



1000
I


(f)
Formic acid
j 64186
1

1
a



5000
311


K010

\
1

1
l



10
Coop


Distillation side cuts froa the
1

l







production of acetaldehyde from
1

l







ethylene.
•

1







(a)
Chlorofora
| 67663
100-10(C)
|Hat-orl:S00(D>
jcABOMED

5000
10
CARC




1

|Rat-ihl:B000/4H(D)







(b)
Formaldehyde
| 50000
100-10(0
j Bat-ihl LClo: 250 ppV4H(C>
|CAE&=MED
B—3
1000
lpo
BHF

123


t

jBbt-skn:270(D)
jcT=39(B)
F=GAS (B)







1

|Rat~orl:800(D)







(c)
Methylene chloride
| 7S092

1



1000
CTX


(d)
Methyl chloride
j 74873
1000(Dl
|&at-lhl:152000 mg/m3/}0M20(C)
FcOAS (B)





(e)
Paraldehyde
| 123637

1



1000
I


If)
Formic acid
j 64186

1



5000
311


(9)
Chloroacetaldehyde
| 107200
1

1
1



1000
T(orl)


K011

1
1

1
1



10
Conp


Bottom stream froa the wastewater
1

1







stripper in the production of
1

1







acrylomtrile.
1

1







Note: AI1 comments/notes ere located at ths end of this table.
-------
DMA FOB THE NFHM HAZARDOUS SUBSTANCES - Continued
Hazardous Substance (Not* 1)
CASRH
Aquatic
Toxicity
(Hot* 2)
Mimaliu Toxicity (Nota 1)
chronic
Toxicity/
Carcinogen
(Hot* 4)
Ignitability/
Reactivity
(Hot* 5)
311
BQ
(Hot* 6)
Proposed
RQ
(Hot* 7)
Basis for
Proposed
BQ
(Hot* a)
(a) Acrylomtnl*
(bl Acetonitnl*
(c| Hydrocyanic acid
K013
Bottoa strean (roa th* acetonitrile
column in the production of
acrylonitrile.
(a)	Acrylomtnl*
(b)	Acetonitrile
|c) Hydrocyanic acid
K015
Still bottoms froa th* distillation of
-F- benzyl chloride.
(a) Benzyl chloride
ro
(b) cblorobenzens
Ic) Toluene
(d) Benzotnchloride
K016
Heavy ends or distillation residues
froo the production of carbon
tetrachloride.
(a)	Hexachlorobenzene
(b)	Henachlorobutadiene
(c)	Carbon tetrachloride
107131
750S8
74908
107131
75054
74908
100447
108907
108883
98077
118741
87683
56235
10-1(8)
lO-l(B)
lO-l(B)
<0.1(X)
lOft-lO(C)
Rat—ihl:500/4H(D)
Rat-orl:B2(C)
Bat-ihl:500/4H(D)
Bat-orl:82(C)
Rat—orl:1231(D)
Rat-ihl:1S0/2H(C)
Rat-ihl:125/4H(C)
Rat-orl:10,000(D)
Rat-orl:90(C)
Rat-orl:2800(D)
Rat-ihl:4000/4H
CAROMED
CT=>30(B)
CAROMED
CT=30(B)
B=171
F=I2 (C)
B=171
F=32 (C)
CAROLOW
CARC=HIGH
CARC=HED
CI*>29.5(B)
CAROLOW
CT=10.3(C)
CAROMED
CT=25.3(B)
B=354
F=153 (Max)
Req. stab.
(B)
F=260
SOLID
100
100
100
5000
10
5000
10
10
10
sooo
10
100
100
1000
1
10
1
10
CARC
BHP
311. R
Comp
CARC
BHP
311, R
Comp
CARC,R,311
311
311,1,CH
CARC
Comp
CARC
Affix
CARC
Note: All comments/notes are located at the end of this table.
-------
DATA FOR THE NFBM HAZARDOUS SUBSTANCES - Continued





1
| Chronic



Basis
for




Aquatic

j Toxicity/
Ignitability/
311
Proposed
Proposed




Toxicity

|Carcinogen
Reactivity
HQ
RQ
RQ


Hazardous Substance (dote 1)
j CASBH
(Hot* 21
Hamuli an Toxicity (Note 3)
I (Note 4)
(Note 5)
(Note 6)
(Note 7)
(Note
8)
|Comments
(d)
Hexachloroethane
| 61721
10—1(B)
Rat-orl:6000(D)
|CAROUM
SOLID

100
AQTX.CARC






|CTalS.2(C)






(e)
Pe rchlo roethylene
| 121184
100-10(C)
Bat-lhl LClo:4000/4H(D)
|CARO>UM


100
CARC






Mus-orl:8100(D)
jcTolO(C)
1






K011




1
1


10
Coup


Heavy ends (still bottoms) froa the



1






purification column in the production



1






of epichlorohydrin.



1






(a)
Epichlorohydrin
| 106898
100-10(0)
Bat-ihl L£lo:250 ppa/4H(C)
|CARC=L0W
B=239
1000
100
CARC,era





Rat-skn LDlo:1000(D)
|CT»26(B)
F=91 (C)









Rat-orl:90(C)
1






(b)
Bis(chloromethyl) ether
| 542861

Hat-orl:210(D)
|CARC°HIGH


10
BHP

123




Bat-lhl:1/1H(B)
|CT=I.D.






(c)
Bis(2-chloroethyl) ether
| 111444
1000-100(D)
Bat-ihl:1000/4SM
jcARCcMED
F=131 (D)

10
CARC






Rat-orl:15(C)
1






(d)
Tnchloropropane
| N.A.


1







(1) 1,2,3 Trichloropropaae
j 96184


1


5000
T(orl)

131





1



T(ihl)


!«)
Dichloropropanol
| H.A.


1







(1) n-,2,3 Dichloropropanol
| 616239


1


1000
T(orJ)

138





1
I



T(ihl)


K018




1
1


1
Comp


Heavy ends froa the fractionation



1






column in ethyl chloride production.



1






(a)
1,2-Dichloroetbane
| 101062
1000-100(D)
Bat-lhl LClo:1000 ppn/4H(D)
|CARCoLCW
B=183
5000
100
CARC






Mu-orl LDlo: 600(D)
|CT"18.4(C|
F=56 (C)









Bat-orl:610(D)
1






(b)
Trichloroethylene
| 19016
100-10(C)
Rat-orl:4920(D)
|CARC°L0W
B=>188
1000
100
CARC







|CT=20(C)
F=90 (C)





(c)
Hexachlorobutadlene
| 81683
<0.1(X)
Rat-orl:90(C)
|CAROL0W


1
AQTX

110





|CT»10.3(C)






(d)
Hexachlorobenzene
| 118141

Bat-orl:10,000(D)
icARCsHED
SOLID

10
CARC

j 10





|CT=29.5(B>






Note: All comments/notes are located at the end of this tabic..
-------
DATA FOB THE NPRH HAZARDOUS SUBSTANCES - Continued





1
| Chronic



Basis for




Aquatic

| Toxicity/
Ignitability/
311
Proposed
Proposed




Toxicity

|Carcinogen
Reactivity
RQ
RQ
RQ

Hazardous Substance (Note 1)
CASBH
(Hot* 2)
Mammalian Toxicity (Note 3)
I (Not* 4)
(Note 5)
(Hot* 6)
(Note 7)
(Note 8)
|Conments
K019




1
1


10
Comp

Heavy ends from the distillation of



1





ethylene dichloride in ethylene



1





dichloride production.



1





(a)
Ethylene dichloride
107062
1000-100(D)
Rat-ihl LClo:1000 ppa/4H(D)
| CARLCW
B=183
5000
100
CARC





Kus-orl IDlo:600(D)
|CT°18.4(C)
P=56 (C)








Bat-orl:670(D)
1





lb)
1,1,1-Trichloroethane
71556


1


1000
AQTX.CTX

(c)
1,1,2-Tnchloroethane
79005
100-10(C)
Rat-ihl LClo:500/8H(D)
| CAR0= LCW


100
CARC





Rat-orl:1140(D)
|CT=X.D.





(d)
1,1,1,2-Tetrachloroethana
630206


j CARC« LOW


100
CARC






|CT=I.D.





(e)
1,1,2,2-Tatrachloroethane
79345
10-1(B)
Rat-ihl LClo:1000/4H(D)
|CARC=LOW


100
AQTX.CABC
jio




Dog-orl LDlo:300(D)
|CT=17.5(C)





(f)
Trichloroethylene
79016
100-10IC)
Bat-orl:4920(D)
|CARC=LGW
B=>188
1000
100
CARC






|CT=20|C)
F=90 (C)




(9)
Tetrachloroethylene
127184
100-10(C)
Rat-ihl L£lo:4000/4H(D)
jcAROLOW


100
CARC





Kus-orl:8100(D)
|CT=10(C)





(h)
Carbon tetrachloride
56235
100-10(C)
Bat-orl:28001D)
j CAROMED

SOOO
10
CARC





Rat-ihl:4000/4H
|CT°25.3(B)





(i)
Chloroform
67663
100-10IC)
Rat-orl:800(D)
|CARCaMED

5000
10
CARC





Rat-ihl:8000/4H(D)
1





(]>
Vinyl chloride
75014
1000(D)
Gpg-ihl LClo:20/30M(B)
| CAROMED
B=7

IP
CARC
129




Rat-orl:500(D)
|CT=20(C)
F=GAS (B)




(k)
Vinylidene chloride
75354
1000-100(D)
Mus-lhl L£S0:98 pp^/22H(C)
|CARC=LCW
B=99
SOOO
100
CARC,I
127




Rat-ihl:10,000/24H(D)
|CT°19(C)
F=0 (B)








Bat-orl:200(D)
1
1





K020




1
1


10
Comp
jSEE K019
Heavy ends from the distillation of



1





vinyl chloride in vinyl chloride



1





monomer production. (Components of



1





this
waste are identical with thos* of



1





K019
immediately preceding.)



1





Note: Ail com&ents/notes are located at tho end of this table.
-------
DATA FOB TUB HPRM HAZARDOUS SUBSTANCES - Continued

1
1

1
1
1
| Chronic


1
1
Basis for


1
Aquatic
1
j Toxicity/
Ignitability/
311
|Proposed
Proposed


1
Toxicity
1
jcarcinogen
Reactivity
KQ
1 RQ
HQ

Hazardous Substance (Note 1)
| CASBH
(Hot* 2)
| Mammalian Toxicity (Hot* 31
j (Note 4)
(Note 5)
(Note
6)| (Note 7)
(Note 8)
comments
K021
1
1

1
1
1
1


1
|10
Coap

Aqueous spent antiaony catalyst waste
1

1
1


1


from fluoromethanes production.
1

1
1


1


(a) Antimony trichloride
110025919

1
1


jiooo
311
39
(b) Carbon tetrachloride
| 56235
100-10(C)
|Elat-orl: 2800(D)
| CAROMED

5000
jio
CARC


1

j Rat-lhl:4000/4H
|CT=25.3|B)


1


(c) Chlorofora
j 61661
100-10(C)
|Bat-orl:800(D)
j CAROMED

5000
|10
CAHC


1
|

|Bat-ihl:8000/4H(D)
I
1
|


1
1


K022
1
1

1
1
1
1


I
II


Distillation bottoa tars froa the
1

1
1


1


production of phenol/acetone froa
1

1
1


1


cumene.
1

1
1


1


(a) Phenol
| 108952

1
1


|1000
BHP

(b) Tars (polycyclic aromatic)
| H.A.
1

1
1
1
1


jl
1
CAHC
40
K025
1
1

1
1
1
1


|10
Coup

Distillation bottoms from the
1

1
1


1


production of nitrobenzene by the
1

1
1


1


nitration of benzene.
1

1
1


1


(a) aeta-Dinitrobenzene
| 99650

1
1


|100
CTX

(b) 2,4-Dinitrotoluene
| 121142
100-10(C)
|Bat-orl:268(D)
|CARO=MED
0=516
1000
jio
CARC


1
1

1
1
|CT=.32(B)
1
r=404 (Max)

1
1


K027
1
1

1
1
1
1


1
jio
Coop

Centrifuge and distillation residues
1

1
1


1


from toluene dusocyanate production.
1

1
1


1


(a) Toluene dusocyanate
| 584849

1
1


|100
AQTX>T(lhl)

(b) Toluenediaoine
| 95807
1

|Bat-orl:260(D)
|
|CARC=MED
1
SOLID

jio
1
CARC

K028
1
1

1
1
1
1


1
|10
fnrnp

Spent catalyst from the
1

1
1


1


hydrochlorinator reactor in the
1

1
1


1


production of 1,1,1-trichloroethane.
1

1
1


1


Note: All comments/notes are located at the and of this table.
-------
DATA FOB THE NPRM HAZARDOUS SUBSTANCES - Continued
Hazardous Substance (Not* 1)
CASHH
Aquatic
Toxicity
(Not* 2)
Mammalian Toxicity (Not# 3)
Chronic
Toxicity/
Carcinogen
(Not* 4)
Ignitability/
Reactivity
(Not* 5)
311
RQ
(Not* 6)
Proposad
RQ
(Not* 7)
Basis Cor
Proposad
BQ
(Not* 8)

(b)



20(C)
CAHC=LOW
CT=19(C)
CARC=KED
B=7
P=GAS (B)
B=183
F=>56 (C)
B=7
F=GAS (B)
B=99
P=0 (B)
CARC=MED
CT=.29.5(B)
CAHCaLOW
CT=10.3(C)
CABCsLCW
CT=15.2(C)
CABCsLOH
CT=I.D.
CABOLOW
CT=17.5(C)
SOLID
SOLID
5000
5000
5000
1000
10
10
100
1000
10
100
10
10
1
100
100
100
AQTx.crx
CARC
Comp
CARC
AQTX.CTX
CARC
CARC, I
CARC
Comp
CARC
AQTX
AOTX.CABC
CAHC
AQfTX,CARC
Mote:
All comments/notes are located at the end of this table.
-------
data FOR THE NPRM HAZARDOUS SUBSTANCES - Continued




1
| Oironlc



Basis for



Aquatic

j Toxicity/
Ignitability/
311
Proposed
Proposed



Toxicity

|Carcinogen
Reactivity
BQ
RQ
BQ

Hazardous Substance (Note 1)
CASBH
(Hot* 2)
Kaaoalian Toxicity (Note 3)
j (Dote 4)
(Note 5)
(Note 6)
(Note 7|
(Note 8)
|Comments
(f) Ethylene dichloride
101062
1000-100(0)
Bat-ihl LClo:1000 ppn/4H(D)
|CABC°L£M
B=l«3
sooo
100
CARC




Kus-orl LDlo:600(D)
|CT="18 .4(C)
F=56 (C)







Bat-orl:670(D)
1
I





turn



1
1


1
Coup

By-product salts generated in the



1





production of HSMA and cacodylic acid.



1





(a) Arsenic compounds
H.A.


1
1


1
CABC

K032



1
1


10
Comp

Wastewater treatsent sludge froa the



1





production of cblordane.



1





(a) Hexachlorocyclopentadien*
71474
<0.1(X)
Rat-orl: 111(D)
|CT=62(A)
SOUD
1
10
BHP
|10,23



Bbt-akn:430(D)
1
|





KD33



1
1


10
Tninp

Wastewater and scrub water froa the



1





chlonnation of cyclopentadiene in the



1





production of chlordane.



1





(a) Hexachlorocyclopentadiene
71474
<0.1(Z)
Bat-orl:lll(D)
|CT=62(AI
SOLID
1
10
BHP
110,23



Bbt-skn:430(D)
1





K034



1
1


10
Comp

Filter solids from the filtration of



1





hexachlorocyclopentadiene in the



1





production of chlordane.



1





(a) Hexachlorocyclopentadiene
77474
<0.1UI
Bat-orl:113(D)
|CT=62(A)
SOLID
1
10
BHP
|10,23



Bbt-skn:430(D)
1
1





ICO 15



1
1


1
Comp

Wastewater treatment sludges generated



1





in the production of creosote.



1





(a) Creosote
S0015B9
10-1
-------
DAXA FOB THE HPRM HAZARDOUS SUBSTANCES - Continued





1
1
1
| Chronic



Basis
for





Aquatic
1
| Toxicity/
Ignitability/
311
Proposed
Proposed





Toxicity
1
j Carcinogen
Beactivlty
HQ
BQ
BQ


Hazardous Substance (Hot* 1)

CASHN
(Hote 2)
| Mammalian Toxicity (Note 3)
j (Note 4)
(Note 5)
(Note 6)
(Note 7)
(Bote
8)
|Comments
(b)
Chrysene

218019

1
|CABC=HED
SOLID

10
CABC

11B





1
|CT=I.D.






(c)
Naphthalene

91203

1
1


100
AQTX


Id)
Benzo(b)fluo ranthene

205992

1
| CAftC-HIGH


1
CABC







1
|CT=I.D.






(e)
Fluoranthene

206440

1
1


100
AQIX


(f)
Benzol aIpyrene

50128

1
|CABC=HIGH
SOLID

1
CABC







1
|CT=>46(A)






(9)
Indano(1,2,3-cdIpyrene

19339S

1
|CARC=L0W
SOLID

100
CABC

118





1
|CT°I.D.






(h>
Bens(a(anthracene

56553

1
|CARC=HED
SOLID

10
CABC







1
|CT=>I .D.






(1)
Dibenz(a,h|anthracene

53703

1
|CAHC=HIGJI
SOLID

1
CABC







1
|CT=>I.D.






(a)
Acenaphthylene

208968

1
1
1
|


5000
MAX


K038




1
1
1
1


10
Coup


Wastewater from the washing and



1
1






stripping of phorate production.



1
1






(a)
Phorate

298022

1
1


10
BHP


(b)
Formaldehyde

50000
100-10(C>
|Bat-ihl LClo:2S0 ppV4H(C)
|CARC=HED
B=-3
1000
100
BHP

123





|Bbt-skn:270(D)
|CTa39(B)
F=GAS (B)










|Bat-orl:800(D)
1






(c)
Phosphorodithloic esters

N.A.

1
1


1000
BHP

|41
(d)
Phosphorothioic esters

N.A.

1
1
1
1


1000
BHP

j 40
K040




1
1
1
1


10
Coup

jsEE K038
Wastewater treatment sludge from
the


1
1






production of phorato. (Components of


1
1






this
waste are identical with those of


1
1






K038
above.)



1
I
1
1






K041




1
1
1
1


1
Coop


Wastewater treatment sludge from
the


1
1






production of toxaphene.



1
1






Note. Ail cocuoents/notes are located at the end ol this table.
-------
DMA FOB THE NPBM HAZARDOUS SUBSTANCES - Continued



1
1
j Chronic



Basis for



Aquatic
1
| Toxicity/
Ignitability/
311
Proposed
Proposed



Toxicity
1
jCarcinogen
Beactivity
BQ
BQ
BQ

Hazardous Substance (Note 1)
j CASHN
(Not* 2)
| Mammalian Toxicity (Note 3)
j (Note 4)
(Note 5)
(Note 6)
(Note 7)
(Note 8)
|Comments
(a) Toxaphene
| 8001352
<0.1(X)
|Dog-orl:15(C)
|CARC=MED
SOLID
1
1
311
110



|Bat-orl:40(C)









|Bat-skn:600(D)
I






K042


1
1



10
Comp

Heavy ends or distillation residues


1






from the distillation of


1






tetrachlorobensene in the production


1






of 2,4,5-T.


1






(a) Hexachlorobenzene
| 118741

|Bat-orl:10,000(D)
|CAaC=MED
SOLID

10
CABC
|10



1
|Cr>2».5(B)





(b) orthodichlorobenzene
| 95501

1
1



100
311

K043


1
1



10
Comp

2,6-Dichlorophenol waste froa the


1






production of 2,4-0.


1






(a) 2,4-Dichlorophenol
| 120832

1



100
AQTX

(b) 2,6-Dichlorophenol
| 876S0

1



100
AQTX

(c) 2,4,6-Tnchlorophenol
j 88062
1-0.1(A)
|Bat-orl:820(D)
jcABOLCW
SOLID
10
10
311




1
1
|CT»I.D.





K04B


1
1



1
Coop

Dissolved air flotation (DAT) float


1






from the petroleum refining industry.


1






(a) Hexavalent chromium compounds
j N.A.

1



1
CABC

(b) Lead compounds
j H.A.

1
|



100
era

K049


1
1



1
Comp

Slop oil emulsion solids from the


1






petroleum refining industry.


1






(a) Hexavalent chromium compounds
j H.A.

1



1
CABC

(b) Lead compounds
j H.A.

1
|



100
era

K050


1
1



1
Comp

Heat exchanger bundle cleaning sludge


1






from the petroleum refining industry.


1






Note: All comments/notes are located at the and of this table.
-------
DATA FOR 111E NPRM HAZARDOUS SUBSTANCES - Continued



1
| Chronic



1
Basis for |


Aquatic
j Toxicity/
Ignitability/
311
Proposed
Proposed |


Toxicity
jcarcinogen
Baactivity
RQ
RQ
RQ 1
Hazardous Substance (Not* 1)
j CASEN
(Not* 2)
Mammalian Toxicity (Not* 3) j (Not* 4)
(Not* 5)
(Not* 6)
(Not* 7)
(Not* 8) (Comments
(a) Hexavalent chroaiun compounds
| N.A.

1
1


1
CARC |
j
K051


1
1


1
1
Comp |
API separator sludge troa the


1



1
petroleum refining Industry.


1



1
(a) Hexavalent chromium compounds
| N.A.

1


1
CARC |
(b) Lead compounds
j N.A.

1
1


100
en j
1
K060


1
1


1
1
Comp |
Ammonia still lime sludge from coking


1



1
operations.


1



1
(a) cyanides
| N.A.

1


10
111 131
(b) Phenol compounds
j N.A.

1



1
(1) Phenol
| 108952

1


1000
BHP |
|c) Naphthalene
| 91203

1


100
AQTX |
(d) Arsenic compounds
j N.A.

1
1


1
CARC j
i
K061


1
1


1
1
Comp |
Emission control dust/sludge from the


1



1
primary production of steel in


1



1
electric furnaces.


1



1
(a) Hexavalent chromium compounds
j N.A.

1


1
CARC |
(b) Lead compounds
j N.A.

1


100
CTX j
(c) Cadmium compounds
j N.A.

1
1


IP
CARC j
i
K062


1
1


1
1
Comp |
Spent pickle liquor from steel


1



1
finishing operations.


1



1
(a) Hexavalent chromium compounds
| N.A.

1


1
CARC |
(b) Lead compounds
j N.A.

1
1


100
era j
1
K069


1
1


1
1
Comp |
Emission control dust/sludge from


1



1
secondary lead smelting.


1



1
Note:
All comments/hotes are located at the end of this table.
-------
DMA FOB THE HPHM HAZARDOUS SUBSTANCES - Continued



1
1
1
| Chronic



1
Basis for |


Aquatic
1
j Toxicity/
Ignitability/
111
Proposed
Proposed |


Toxicity
1
|Carcinogen
Beactivity
BQ
BQ
BQ |
Hazardous Substance (Note 1)
CASBH
(Not* 2)
| Mammalian Toxicity IHota 3)
j (Dote 4)
(Note 5)
(Mote 6)
(Hot* 7)
(Hot* 8) |Comments
(a) Hexavalent cbcoaiuo compounds
H.A.

1
1


1
CAHC |
(b) Lead compounds
H.A.

1
1


100
CTX j
(c) Cadmiua compounds
H.A.

1
1
1
1


10
CAHC j
j
K073


1
1
1
1


10
1
Coop |
Chlorinated hydrocarbon waste fro» the


1
1



i
purification step of the diaphraga


1
1



i
cell process using graphite anodes in


1
1



i
chlorine production -


1
1



i
(a) Chlorofora
67663
100-10(C)
|Bat-orl;800(D)
|CARC«HED

5000
10
CAHC |



|Kat-ihl:8000/4U(D)
1



1
lb) Carbon tetrachloride
56235
lOO-lO(C)
|Bat-orl:2800(D)
| CAROMED

5000
10
CAHC |



|Bat-ihl:4000/4H
|CT°i25.3(B)



1
(c) Hexachloroethane
67721
lO-l(B)
jftat-orl: 6000(D)
jcABC=UJW
SOLID

100
AOra.CABC 1



1
|CT=>15.2(C)



1
(d) Trichloroethane
H.A.

1
1



t
<11 1,1,i-Trichloroethane
71556

I
I


1000
Aora.crx t
(2) 1,1,2-Tnchloroethan*
79005
lOO-lO(C)
|Bat-lhl LClo:500/8U(D)
|CAEC=LOW


100
CARC I



|Bat-orl:1140(D)
jcToI.D.



1
(e) Tetrachloroethylene
127104
100-10(C)
|Bat-ihl LClo:4000/4H(D)
|CAHC=L0W


100
CARC |



jlfus-orl :8100(D)
|CT=10
-------
DATA FOB T11E NFBM HAZARDOUS SUBSTANCES - Continued




1
1
1
| Chronic



Basis
for




Aquatic
1
| Tozicity/
Ignitability/
311
Proposed
Proposed




Tozicity
I
|Carcinogen
Beactivity
BQ
RQ
BQ


Hazardous Substance (Note 1)
| CASBN
(Mote 2)
| Mammalian Tozicity (Note 3)
I (Note 4)
(Note 5)
(Not* 6)
(Note 7)
(Note
8)
jComments
(a)
Benzene
| 71432
lO-l(B)
|Bat-lhl:10,000/7H(D)
|CABC=MED
B=176
1000
10
CABC






jBat-orl:3800(D)
|Cr=17(C)
P=12 (C)





(b)
Dichlorobenzenes
| N.A.

1
1







(1) 1,2-Dichlorobenzene
| 9SS01

1
1


100
311



(2) 1,3-Dichlorobsnzene
| 541731

1
1


100
AQTX



(3) 1,4-Dichlorobenzene
j 106467

1
1


100
311


(c)
Tnchlorobenzenes
j 8.A.

1
1







(1) 1.2,4-Tnchlorobenzene
j 120821

1
1


100
AQTX


(d)
Te t rachlorobenzane
j H.A.

1
1







(1) 1,2,4,5-Tetrachlorobenzene
j 95943

1
1


5000
CTX


(e)
Fentachlorobensene
| 608935

1
1


10
AQfIX


If)
Hexachlorobenzene
| 118741

|Bat-orl:10,000(D)
|CARC=HED
SOLID

10
CABC

110




1
|CT=29.5(B)






(9)
Benzyl chloride
| 100447
lO-l(B)
|Bat-orl:1231(D)
jcABOLCW
B=354
100
100
CABC,B,
311
118.19




j Bat-ihl:150/2H(C)
1
F=153 (Has)









1
1
Heq. stab.









1
1
1
I
(B)





K036



1
1
1
1


1
Comp


Solvent washes and sludges, caustic


1
1






washes and sludges, or water washes


1
1






and sludges from cleaning tubs and


1
1






equipment used in the formulation of


1
1






ink
Eron pigments, driers, soaps, and


1
1






stabilizers containing chromium and


1
1






lead
.


1
1






(a)
Lead compounds
j H.A.

1
1


100
CTX


(b>
Hexavalent chromium compounds
j H.A.

1
1
1
1


1
CABC


K095



1
1
1
1


100
Comp


Distillation bottoms from the


1
1






production of 1,1,1-trichloroethane.


1
1






(a)
1,1,2-Trichloroethane
| 79005
100-10(C)
|Rat-ihl LClo:500/8H(D)
|CARC=LOW


100
CABC






jBat-orl:1140(D)
jCTal.D.






Note:
All comments/notes are located at the end of this table.
-------
DATA FOB THE NPBM HAZARDOUS SUBSTANCES - Continued




j Chronic



Basis for



Aquatic

j Toxicity/
Ignitability/
311
Proposed
Proposed



Toxicity

(Carcinogen
Beactivity
BQ
BQ
BQ

Hazardous Substance (Note 1)
j CASHH
(Note 2)
Mammalian Toxicity (Note 3)
j (Note 4)
(Note 5)
(Note 6)
(Note 7)
(Note 8)
|Comments
(b) 1,1,1,2-Tetrachloroethane
| 630206


|CABOUM


100
CABC





|CT=I.D.





(c) 1,1,2,2-Tetrachloroethane
| 79345
10-1(B)
Bat-lhl LClo:1000/4H(D)
jcABOLCM


100
AQTX.CARC
110



Dog-orl LDlo:300(D)
|CT»17.5(C)





K096






10
Comp

Heavy ends from the heavy ends coition









from the production of 1,1,1-









tnchloroethane.









(a) 1,2-0ichloroethane
| 107062
1000—100(D)
Bat-ihl LCloUOOO ppa/4H(D)
jcABOLOW
B=183
5000
100
CABC




Kus-orl LDlo:600(D)
|CT=18.4(C)
P=56 (C)







Bat-orl:670(D)






(b) 1,1,1-Trichloroethane
| 71556





1000
Agra,era

(c) 1,1,2-Trichloroethane
j 79005
100-10(C)
Rat-lhl LClo:500/SH(D)
jcABC°L0W


100
CABC




Bat-orl:1140(D)
|CT=I.D.





K097






1
Coop

Vacuum stripper discharge from the









chlordane chlonnator in the









production of chlordane.









(a) Chlordane
| 57749
<0.1(X)
Bbt-orl:100(C)
(CABOMED
SOLID
1
1
311
110



Bat-skn:700(D)






(b) Heptachlor
| 76440
<0.1(X)
Bat-skn:119(D)
|CABOHIGH
SOLID
1
1
311,CABC
110



Bat-orl:40(C)






K098






1
Comp

Untreated process wastewater froa the









production of toxaphene.









(a) Toxaphene
| 8001352
<0.1(X)
Do9~orl:15(C)
|CABG=MED
SOLID
1
1
311
|10



Bat-orl:40(C)









Bat-skn:600(D)






K099






10
Comp

Untreated wastewater from the









production of 2,4,-0.









Note: All comments/notes ate located at the end of this table
-------
DATA FOB THE NPRH HAZARDOUS SUBSTANCES - Continued



1 1
| | chronic



1
Basis for |


Aquatic
| j Toxicity/
Ignitability/
311
Proposed
Proposed |


Toxicity
I jCarcinogen
Reactivity
80
BO
BQ 1
Hazardous Substance (Bote 1) |
CASRN
(Note 2)
j Mammalian Toxicity (Note 31 j (Note 4)
(Note 5)
(Not* 6)
(Note 7)
(Note 8) (Comments
(a) 2,4-Dichlorophenol |
120832

1 1


100
AQTX |
(b) 2,4,6-Trichloroptaenol j
86062
l-O.l (A)
|Rat—orl:820(D) |CAEC=LOW
SOLID
10
10
311 |



| jcToI.D.
| I



1
1
K100 |


1 1
1 1


1
1
Coap |SEE K069
Waste leaching solution from acid |


1 1



i
leaching of emission control dust/ |


1 1



i
sludge from secondary lead smelting. |


1 1



i
(Components of this waste are identical!


1 1



i
with those of K069.) j


1 1
1 1



i
1
K101 |


1 1
1 1


1
1
Conp |
Distillation tar residues froa the |


1 1



i
distillation of aniline-based j


1 1



i
compounds in the production of |


1 1



i
veterinary pharmaceuticals from |


1 1



i
arsenic or organo-arsenic compounds. |


1 1



i
(a) Arsenic compounds |
H.A.

1 1
I 1


1
CARC |
1
K102 |


1 1
1 1


1
1
Coap |
Residue from the use of activated |


1 1



i
carbon for decolorieation in the |


1 1



i
production of veterinary |


1 1



i
pharmaceuticals froa arsenic or organo |


1 1



i
-arsenic compounds |


1 1



i
(a) Arsenic compounds |
a.A.

1 1
1 1


1
CARC |
|
K104 |


1 1
1 1


10
1
Coap |
Combined wastewater streams generated |


1 1



i
from nitrobenzene/aniline |


1 1



i
chlorobenzenes. |


1 1



i
(a) Benzene |
11412
10-1 IB)
|Bat-lhl:10,000/7H|D) |CAROHED
B=176
1000
10
CARC |



|Hat—orl:3600(D) jcTolKO
F=12 (C>


1
(b) Aniline |
62533
100-10(C}
|Rat-ihl LClo:250/4H(C) j
B=364
1000
SOOOItl
BHF |23



|Hat—orl:440|D) j
F=158 (D)


1
Note. All comments/notes act located at the end of this table.
-------
DATA FOB THE NPRM HAZARDOUS SUBSTANCES - Continued



1
1
1
| Chronic



Basis for



Aquatic
1
j Toxicity/
Ignitability/
311
Proposed
Proposed



Toxicity
1
|Carcinogen
Reactivity
BQ
BQ
BQ

Hatardous Substance (Note 1)
CASBN
(dote 2)
| Mammalian Toxicity (Note 3)
| (Note 4)
(dote 5)
(Note 6)
(Hot* 7)
(Note 8)
|Comments
(c) Diphenylamine
122394

1
1


5000
t(orl)
142
(d) Nitrobenzene
96953

1
1


1000
311

(e) Phanylanediamine (para-isomer)
106503

1
1
1
I


100
AQTX
143
K105


1
1
1
1


10
Coop

Separated aqueous stream froa the


1
1





reactor product washing step in the


1
1





production of chlorobenzenes.


1
1





(a) Benzene
71432
lO-l(B)
|Bat-lhl:10,000/7H(D)
|CARG=MED
B=176
1000
10
CAHC




jsat-orl:3800(D)
|Cltal7(C)
F»12 (C)




(b) Monochlorobenzene
108901

1
1


100
311

(c) Dichlorobenzeaes
N.A.

1
1





(11 1,2-Dlcblorobenzene
95501

1
1


100
311

(2) 1,3-Dlchlorobenzene
541731

1
1


100
AQTX

(3) 1,4-Dichlorobenzene
106467

1
1


100
311

(d) 2,4,6-Tnchlorophenol
66062
1-0.1(A)
|Bat-orl:820(D)
|CABC=LGW
SOLID
10
10
311




1
1
|CT=I.D.
I





Kill


1
1
1
1


10
Conp

Product washwaters froa the production


1
1





of dimtrotoluene via nitration of


1
1





toluene.


1
1





(a) 2,4-Dinitrotoluene
121142
100-10(C)
|Bat-orl:268(D)
|CAHC=MED
B=576
1000
10
CAKC




1
I
|CT=>32(B)
1
F=404 (Max)




K112


1
1
1
1


10
CAHC
1"
Reaction by-product water froa the


1
1





drying coluan in the production of


1
1



'

toluenediamine via hydrogenation of


1
1





dimtrotoluene.


1
1





(a) Toluenediamine
95607

|Bat-orl:260(D)
|CARC=MED
SOLID

10
CABC

(b) o-Toluidine
95534

jltbt-skn: 3250(0)
j CARC= LOW
B=392 (D)

100
CAHC
I"



|Mus-orl:520(D)
1
F=169







|B*t-orl:670(D)
1








|Bbt-orl:640(D)
1








|Bat—orl:940(D)
1





Note: All comments/notes art located at the and of this table.
-------
DATA FOR THE NPRH HAZARDOUS SUBSTANCES - Continued



1
1
1
| Chronic



Basis for



Aquatic
1
j Toxicity/
Ignitability/
311
Proposed
Proposed



Toxicity
1
jcarcinogen
Reactivity
RQ
RQ
RQ

Hazardous Substance (Note 1)
j CASBH
(Note 2)
| Mammalian Toxicity (Note 3)
1 (Note 4)
(Note 5)
(Note 6)
(Note 7)
(Note 8)
|Comments
(c) p-Toluidine
| 106490

|Mus-orl:330(D)
|CARC»L0W
B=>392 (D)

100
CARC




j&at-orl:650(D)
1





(d) Aniline
| 62531
100-10364
1000
5000(11
BHP
123



|Rat-orl:440(D)
1
1
1
F=158 (D)




K113


1
1
1
1


10
CARC
112
Condensed liquid light ends fron the


1
1





purification of toluenediamine in the


1
1





production of toluenediaaine via


1
1





hydrogenation of dimtrotoluene.


1
1





(a) Toluenediamne
| 95807

|Rat-orl:260(D)
| CAROMED
SOLID

10
CARC

(b) o-Toluidine
| 95534

|Rbt-skn:3250(D)
|CABCoLOW
B=392 (D)

100
CARC
|12



|Mus-orl:520(D)
1
F=189







|Rat-orl:670(D)
1








|Rbt-orl:840(D)
1








j&at-orl:940(D)
1





(c) p-Toluidine
| 106490

|Hus-orl:330(D)
| CARC*. LOW
B=392 (D)

100
CARC




|Rat-orl:650(D)
1





(d) Aniline
| 62533
100-10(0)
|Rat-lhl LClo:250/4H(C)
1
B-364
1000
5000(11
BHP
123



|Rat-orl:440(D)
i
1
1
P=158 (D)




K114


1
1
1
1


10
CARC

Vicinals from the purification of


1
1





toluenediamine in the production of


1
1





toluenediamine via hydrogenation of


1
1





dimtrotoluene.


1
1





(a) Toluenediamine
| 95807

|Rat-orl:260(D)
|CARC=MED
SOLID

10
CARC

(b) o-Toluidine
| 95534

|Bbt-skn:3250(D)
|CAHC°LCM
B=392 (D)

100
CARC
U2



|Mus—orl:520(D)
1
F=189







|Rat-orl:670(D)
1








jRbt-orl:640(D)
1








|Bat-orl:940(D)
1





(c) p-Toluidine
| 106490

|Kus-orl:330(D)
|CAKC°L0W
B=>392 (D)

100
CARC




jilat-orl: 650(D)
1





Note: All comments/notes are located at the end of this table.
-------
DMA FOB 111E NPBM HAZARDOUS SUBSTANCES - Continued



1
1
1
| Chronic



1
Basis for |


Aquatic
1
| Toxicity/
Ignitability/
311
Proposed
Proposed j


Toxicity
1
|Carcinogen
Beactivity
BQ
BQ
BQ |
Hazardous Substance (Note 1)
CASBH
(Hot# 2)
| Mammalian Toxicity (Note 3)
| (Note 4)
(Note 5)
(Hot* 6)
(Hota 7)
(Note 8) jcomnents
K115


1
1
1
1


10
1
Conp |
Heavy ends (ran the purification of


1
1



1
toluenediaaine in the production of


1
1



1
toluenediaaine via hydrogenation of


1
1



1
dinitrotoluene.


1
1



1
(a) Toluenediaaine
95807

|Bat-orl:260(D)
1
| CAROMED
1
SOLID

10
CABC |
1
K116


1
1
1
1


10
1
Conp |
Organic condensate froa the solvent


1
1



i
recovery column in the production of


1
1



i
toluene diisocyanate via phosgenatlon


1
1



i
of toluenedianine.


1
1



i
(a) Carbon tetrachloride
56235
100-10(C)
|Bat-orl:2800(D)
|CABC°HED

5000
10
CABC j



|Bat-ihl:4000/4H
|CTb25.3(B)



1
(b) Tetrachloroethylene
127184
100-10(C)
|Bat-ihl LClo:4000/4H(D)
jCARC" LOW


100
CABC |



|KUS—or1:8100(D)
|CT=10(C)



1
(c) Chloroforn
67663
100-10(C)
jBat—orl:800(D)
jcASC^MED

5000
10
CABC |



|Bat-ibl:8000/4H(D)
1



1
(d) Phosgene
75445
500-100(D)
|Kus-ihl L£lo:5/30M(A)
1

5000
10
T(ihl) |



|Kus-lhl LClo:5.1/30M(A)
1



1



jaat-ihl L£lo:50/30M(C)
1



1



|Gpg-ihl IjC1o:7/20M(A)
1



1



|Dog-lhl LClo:80/30M(C)
1



1



|Kus-ihl:5.1/30N( A)
|
I
1



1
K117


1
1
1
1


1
1
Conp |
Wastewater froa the reaction vent gas


1
1



i
scrubber in the production of ethylene


1
1



i
broaide via broaination of ethene.


1
1



i
(a) Ethylene dibromde
106934
100-10(C)
|Bat-orl:108(D)
|CARC=HIGH

1000
1
CABC j



|Bat-lhl:400/2H(C)
1



1



|Rbt-orl:55(C)
I
1
|



1
1
Klia


1
1
1
1


1
1
Conp |
Spent absorbent solids froa


1
1



i
purification of ethylene dibroaide in


1
1



i
the production of ethylene dibroaide.


1
1



i
Note: A11 comments/notes are located at the end of this table.
-------
DATA FOR the NPRM HAZARDOUS SUBSTANCES - Continued



1
1
1 1
| Chronic |


1
Basis for |


Aquatic
I
j Toxicity/jlgnitability/
311
Proposed
Proposed j


Toxicity
1
jcarcinogenj Reactivity
BQ
BQ
BQ |
Hazardous Substance (Note 1)
CASBH
(Note 2)
| Mammalian Toxicity (Note 3)
j (Note 4)j (Note 5)
(Note 6)
(Note 7)
(Note 8) |Comments
(a) Ethylene dibromide
106934
100-10(C)
|Rat-orl:108(D)
|CARC=HIGH |
1000
1
CARC |



j Eat-ihl:400/2H(C)
1 1


1



|Hbt-orl:55(C)
1
1 1
I 1


1
I
K136


1
1
1 1
1 1

1
1
Coop |
Still bottoms from the purification of


1
I 1


1
ethylene dibromide in the production


1
1 1


1
of ethylene dibromide via bromination


1
1 1


1
of ethene.


1
1 1


1
(a) Ethylene dibromide
106934
100-10(C)
|Rat-orl:106(D)
jcAROUIGH |
1000
1
CABC j



|Rat-lhl:400/2H(C)
1 1


1



|Rbt-orl:S5(C|
1 1


1
¦C-
I
Ui i '|- No reporting of releases of this hazardous substance is required if the diameter of the pieces of the solid natal released is equal to or
00	exceeds 100 micrometers (0.004 inches).
t"l"1 - The RQ for asbestos is limited to friable forms only.
I - indicates that the HQ is subject to change when the assessment of potential carcinogenicity and/or chronic toxicity is completed.
II - The Agency may adjust the RQ for methyl isocyanate in a future rulemaking, until then the statutory 1-pound BQ applies.
Ill - The final RQ for aniline was promulgated on April 4, 1985 150 PR 13456-13513). Thl3 RQ is subject to change when the assessment of potential
carcinogenicity is completed.
§ - The Agency may adjust the RQ for radionuclides in a future rulemaking; until then the statutory RQ applies.
-------
NOTES FOR TABLE 4-1
DATA FOR THE NPRM HAZARDOUS SUBSTANCES
NOTE 1: The hazardous substances which appear on this list also appear
in Tables 7-1, 8-1, and 8-2 of the document titled "Technical
Background Document to Support Rulemaking Pursuant to CERCLA
Section 102, Volume 1," March 1985. The statutory sources for the
listing of these hazardous substances as CERCLA Section 101(14)
hazardous substances may also be found in those tables. The
statutory sources are the CVA Section 311(b)(4) (40 CFR Part 117),
the CVA Section 307(a), and the CAA Section 112 (40 CFR Part 61),
and those defined in the RCRA regulations (40 CFR Part 261). A
Chemical Abstract Services Registry Number (CASRN) for each
substance is contained in the adjacent column titled "CASRN."
NOTE 2: Aquatic Toxicity, unless specifically noted otherwise, is
given as the LC-q. LC-0 is that concentration of the material
dissolved in water, in parts per million (ppm) or milligrams/liter
(mg/1) (which is equivalent) that will kill 50% of the test
organism population in 96 hours. Each LC~0 entry is followed by a
letter indicating the RQ to which it corresponds, on the following
scale:
<0.1
0.1-1
1-10
10-100
100-500
RQ (Pounds)
X (1)
A (10)
B (100)
C (1000)
D (5000)
Aquatic toxicity data are taken from the following sources:
A.	The reportable quantities assigned under the CVA Section 311
as given in 40 CFR 117.3 (44 FR 50766-50779, August 29, 1979).
The detailed listing of aquatic toxicities that form the basis
for these assignments is found in report No. EPA 440/9-75/009,
"Supplement to Development Document: Hazardous Substances
Regulations, Section 311 of the Federal Vater Pollution
Control Act as Amended 1972," November 1975 (PB 258514).
B.	"The Registry of the Toxic Effects of Chemical Substances,"
RTECS, accessed as a machine-searchable data base via the
Chemical Information System (CIS). RTECS is available in
hardcopy, the latest being DHHS (NI0SH) Publication
No. 83-107, "1981-1982 Registry of the Toxic Effects of
Chemical Substances," Volumes 1, 2, and 3, U.S. Department of
4-59
-------
Health and Human Services, Public Health Service, Center for
Disease Control, National Institute for Occupational Safety
and Health, June 1983.
A supplement to the 1981-1982 edition of RTECS is available as
DHHS Publication No. 84-101.
RTECS draws its aquatic toxicity data from "Water Quality
Characteristics of Hazardous Materials," by Dr. Roy Hahn, Jr.
and Paul Jensen, Texas A&M University, College Station, TX,
77843, 1974.
C.	Publication 2-A, "Water Quality Criteria," Second Edition,
Jack Edvard McKee and Harold V. Wolf (Editors). State of
California, The Resources Agency of California, State Water
Quality Control Board, 1963.
D.	"Handbook of Environmental Data on Organic Chemicals," Karel
Verschueren, Van Nostrand Reinhold Company, New York, NY,
copyright 1977 by Litton Educational Publishing, Inc.
E.	The "Oil and Hazardous Materials Technical Assistance Data
System" (OHMTADS), accessed as a machine-searchable data base
via the EPA/NIH Chemical Information System (CIS).
F.	The 1980 Ambient Water Quality Criteria Documents for 64 toxic
pollutants or pollutant categories, published pursuant to the
CWA Section 304(a)(1) (45 FR 79318).
G.	"Aquatic Toxicity Testing as Fundament for a Spill Prevention
Program," M. W. Curtis, C. M. Curran, and C. H. Ward reported
in the Proceedings of the 1980 National Conference on Control
of Hazardous Materials Spills. (May 13-15, 1980, Louisville,
Kentucky).
H.	"Handbook of Acute Toxicity of Chemicals to Fish and Aquatic
Invertebrates," W. W.Johnson and M. T. Finley, United States
Department of the Interior Publication No. 137, 1980.
I.	"Acute Toxicity of Priority Pollutants to Bluegill,"
R. J. Buccafusco, et al., Bulletin of Environ. Contam.
Toxicol., V. 26, pp. 446-452, 1981.
NOTE 3: Three types of mammalian toxicity are entered in this column,
depending on the route of administration: oral, dermal (skin
absorption) or inhalation. The details of the entries are as
follows:
A. Oral Toxicity: Unless otherwise identified, entries are those
showing the acute oral lethal dose to 502! of the test animal
population (LD^q) in milligrams per kilogram of body weight
4-60
-------
(rag/kg). Test species are coded using the RTECS convention,
as follows:
Hmn a human
Rat a rat
Mus ° mouse
Gpg > guinea pig
Dog a dog
Rbt a rabbit
Thus the entry "Rat-orl^O" indicates oral LD-q of 60 mg/kg
for rats.
B. Dermal Toxicity; These entries are indicated by the
abbreviation "skn" immediately following the species code, and
are again given as the acu1-® rn	"Migrants per kilogram
given under Oral Toxicity, above. Thus the entry "Rat-skn:60"
indicates dermal LD^q of 60 mg/kg for rats.
C.	Inhalation Toxicity; These entries are indicated by the
abbreviation "ihl" immediately following the species code.
Data are presented in terms of the concentration in air lethal
to 50£ of the test animal population in parts per million
(ppm) (LCcq). The exposure time is also given (H a hours,
M a minutes;, when available. Test species are coded the same
as given under Oral Toxicity, above. Thus the entry
"Rat-ihl:60/4H" indicates an Inhalation LC-q of 60 ppm for
4 hours for rats.
D.	Low Lethal Dose or Low Lethal Concentration; These are shown
by the terms "LDi" or "LC, ". LD7 and LC, are the lowest
doses or concentrations known to ha$e had letRal effect on the
test species. Thus the entry "Rat-ihl LC, :60/4H" indicates
an inhalation LC^q of 60 ppm for 4 hours for°rats.
Note: Human LC, and L0io data are not used, since they
generally represent isolates accidental poisoning incidents.
Toxicity data, unless specifically noted otherwise, have been
obtained from RTECS (see Note 2B, above).
Each toxicity entry is followed by a letter indicating the RQ
to which it corresponds, on the following scales. The RQ
assigned on the basis of acute mammalian toxicity is the
lowest of those based on oral, dermal, and inhalation.
of body weight (mg/kg).
coded the same as
4-61
-------
Oral LD,-n Dermal LOcn
or LD1q	or LDlo
Inhalation LCSf)
or LD1q 3U
RQ (Pounds)
<0.1
0.1-1
1-10
<0.04
0.04-0.4
0.4-4
4-40
40-200
<0.4
0.4-4
4-40
X (1)
10-100
100-500
40-400
400-2000
A (10)
B (100)
C (1000)
D (5000)
NOTE 4:
A.
Entries in this column are several and include the following:
The results of evaluations of chronic toxicity effects carried
out by EPA's ECA0. For chronic toxicity, the entries are
given as a numerical score, followed by an equivalent RQ
designation, as follows:
Chronic Toxicity Score	RQ (Pounds)
The scores are based on a combination of values assigned to
minimum effective doses and severity of the toxic effects, as
described in more detail in the report "Technical Background
Document to Support Rulemaking Pursuant to CERCLA Section 102,
Volume 1," March 1985. An "I.D." appears in this column to
indicate where the data were insufficient to complete an
evaluation of the chronic toxicity of a substance. A "TBA"
appears for those substances that are to be assessed for
chronic toxicity. Until this assessment is complete, the
statutory RQ applies.
The results of evaluations of potential carcinogenicity
carried out by EPA's CAG. The GAG's methodology ranks a
substance's relative carcinogenicity as "high," "medium," or
"low." RQ levels have been assigned to these three relative
rankings as follows:
RQ Category	RQ (Pounds)	Hazard Rank
81 to 100
41 to 80
21 to 40
6 to 20
1 to 5
X (1)
A (10)
B (100)
C (1000)
D (5000)
X
A
B
1
10
100
High
Medium
Low
4-62
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c
D
1000
5000
Other entries in this column include:
CARCsb Other primary criteria must be used as a basis
for hazard ranking.
TBA The substance is to be assessed for its potential
carcinogenicity. Until the assessment is
complete, the statutory RQ applies.
NOTE 5: Entries in this column include the following:
A.	Ignitability! This is judged on combinations of flash point
and boiling point. These are entered in the column as
F = flash point, and B ° boiling point, vith the value
immediately following in degrees Fahrenheit. Materials that
are capable of starting fires without an external source of
ignition are considered to be the most hazardous, and are
coded as follows:
PYR	= Pyrophoric
SPONT. IGN ° Capable of spontaneous ignition
STRONG 0XID. ¦ Strong oxidizer, may cause other materials to
ignite, and sustain their combustion.
The entry "Solid" indicates that the material is solid at room
temperature and not readily ignitable.
B.	Reactivity: Reactivity refers to either a material's reaction
with water, compared with certain reference materials (see
scale given below) or to its ability to undergo self-reaction,
with explosion being the worst case. Certain other types of
reactivity, such as the ability to liberate toxic gases, are
discussed as individual cases in separate notes.
Each ignitability or reactivity entry is followed by a letter
indicating the RQ to which it corresponds, based on the
following scales:
4-63
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REACTIVITY
Ignitability
Starts fires
Reaction with Vater
(Reference Compound) Self-Reaction
F
B
F
B
<100
<100
<100
>100
100-140
Inflames
Extreme reaction
(e.g.,SO2)
High reaction
(e.g., oleum)
Moderate reaction
(e.g.,NH3)
Explosive
May polymerize;
requires stabilizer
May polymerize if
contaminated. No
stabilizer required.
Some chance of
polymerization with
small heat release
RQ (Pounds)
A (10)
B (100)
C (1000)
D (5000)
Data for ignitability and reactivity ratings vere taken from "Fire
Protection Guide on Hazardous Materials," 7th Edition, National
Fire Protection Association, Boston, MA, 1978.
NOTE 6: Entries under this column show the value in pounds that was
assigned as an RQ under the CWA Section 311 (AO CFR Part 117.3,
44 FR 10279-10283, February 16, 1979).
NOTE 7: Entries in this column are the lowest RQs derived from the
individual rankings shown under the Aquatic Toxicity, Mammalian
Toxicity, Chronic Toxicity/Carcinogen and/or Ignitability/Reactiv-
ity columns.
NOTE 8: Entries in this column show the basis on which an RQ has been
proposed, coded as follows:
311
AQTX
T(orl)
T(ihl)
T(skn)
CARC
CTX
The proposed RQ is the same as that established on the
basis of aquatic toxicity under the regulations from
the CVA Section 311.
-	Aquatic toxicity (other than a CVA Section
assignment).
-	Mammalian toxicity (oral)
-	Mammalian toxicity (inhalation)
-	Mammalian toxicity (dermal)
-	Potential carcinogenicity
-	Chronic toxicity
311
4-64
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I	- Ignitablity
R	- Reactivity
CS	- The RQ was assigned on the basis of chemical similarity
to another hazardous substance, in the absence of data
for the primary criteria.
Max - This entry indicates that the rating factors all exceed
the upper limit of the rating scales, and that the
assignment of a 5000-pound RQ has been made on the
basis of this being the largest value possible to
assign.
BHP	- Biodegradation, hydrolysis, or photolysis
NOTE 9: Chloral rapidly hydrates upon ingestion to form chloral
hydrate. The toxicity value shovn is that of the hydrate.
NOTE 10: Evidence found in OHMTADS and/or "Water-Related Environmental
Fate of 129 Priority Pollutants" (EPA-440/4-79-029a) indicates
that this material, or a constituent of this material, is
bioaccumulated to toxic levels in the tissue of aquatic and marine
organisms, and has the potential to concentrate in the food chain.
NOTE 11: Polymerization may occur spontaneously in the absence of
oxygen or on exposure to visible light or excessive heat,
violently in the presence of alkali. Pure acrylonitrile is
subject to self-polymerization with rapid pressure development.
The commercial product requires an inhibitor.
NOTE 12: The hazard ranking for potential carcinogenicity is
established by the EPA's Carcinogen Assessment Group (CAG) and is
shovn in the column "Chronic Toxicity/Carcinogen" (Note 4B). Upon
ingestion, o-toluidine converts to o-toluidine hydrochloride, and
therefore the hazard ranking established by the CAG for
o-toluidine hydrochloride is also used for o-toluidine.
NOTE 13: An RQ level of Category X (1 pound) is proposed for each of
the individual Aroclor compounds, based on the aquatic toxicity
listed for the broad class of PCBs.
NOTE 14: There are tvo arsenic acids, one identified by the
CASRN 7778-39-4, and having synonyms as arsenic acid (H_AsO^),
arsenic acid solution, arsenic acid liquid, and orthoarsenie acid.
The other, vith CASRN 1327-52-2, has the synonyms arsenic acid
liquid and arsenic anhydride. Data on the latter may be found in
OHMTADS, while the toxicity of the former may be found in RTECS.
4-65
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NOTE 15: Arsenic trichloride reacts moderately with water to generate
hydrogen chloride.
NOTE 16: Degradation of this substance could lead to the formation of
trivalent inorganic arsenic compounds, which have been identified
as carcinogens in the "First Annual Report on Carcinogens."
(p.2-3)
NOTE 17: No specific data were found for diethylarsine. However, the
alkyl arsines, as a class, are pyrophoric, and diethylarsine has
an RQ level for ignitability of A (10 pounds). (See also
Note 5.)
NOTE 18: At present, there is either "sufficient" or limited data that
shows these substances to have a carcinogenic effect, but not
enough quantitative information about the associated doses to
allow a Potency Factor to be estimated. The mid-range potency
factor is therefore assigned this substance (Potency Group 2) for
the purpose of determining the hazard ranking.
NOTE 19: Benzyl chloride, if unstablized, readily undergoes a
condensation reaction with liberation of heat and hydrogen
chloride in the presence of copper, aluminum, iron, zinc,
magnesium, tin, and various other metals that act as catalysts.
If the reaction takes place in a container, there is the
possibility of violent rupture of the container.
NOTE 20: Beryllium chloride reacts vigorously with water with the
evolution of heat, forming beryllium oxide and hydrochloric acid
solution.
NOTE 21: An RQ of 1 pound was established for the gamma isomer of
hexachlorocyclohexane, commonly known as Lindane, under the CVA
Section 311. An RQ of 1 pound is proposed for the beta isomer of
hexachlorocyclohexane, based on its similar chemical structure.
NOTE 22: The proposed RQ listed for 3,3'-dichlorobenzidine is based on
the RQ for benzidine, since benzidine is a hazardous degradation
product of 3,3'-dichlorobenzidine.
NOTE 23: The proposed RQ takes into consideration one or more of the
natural degradation processes of biodegradation, hydrolysis, or
photoloysis (BHP). More specifically, the lowest RQ supported by
any of the primary criteria has been adjusted upward one level.
Specific BHP data may be found in Appendix C.
NOTE 24: The RQ level of Category A (10 pounds) for ignitability is
based on the fact that this material is a strong oxidizer and can
readily cause fires.
4-66
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NOTE 25: On September 18, 1984 the Agency announced its decison
(49 FR 36560) to list Coke Oven Emissions as a hazardous air
pollutant under Section 112 of the Clean Air Act. Emission
standards remain to be proposed. As part of EPA's efforts to
determine whether to regulate Coke Oven Emissions under
Section 112, EPA prepared several documents relevant to this
decision. In the final document entitled "Carcinogen Assessment
of Coke Oven Emissions," EPA-600/6-82-003F, February 1984, a
number of potentially carcinogenic substances are identified as
constituents of Coke Oven Emissions, including polycyclic organic
matter (POM) (e.g., benzo(a)pyrene, benzo(b)fluoranthene,
benzo(j)fluoranthene, benzo(b)anthracene, and chrysene), aromatic
compounds (e.g., beta-naphthylamine, benzene), and trace metals
(e.g., arsenic, beryllium, cadmium, chromium, nickel) vhich are of
concern due to their potential carcinogenic effects. Extensive
epidemiological studies of coke oven workers have shown them to be
at an excess risk of mortality from lung cancer, prostate cancer,
and kidney cancer. The Carcinogen Assessment Document concludes
that Coke Oven Emissions are carcinogenic to humans, and the
Science Advisory Board (SAB) unanimously concurred with this
conclusion.
The proposed RQ of one pound shown for Coke Oven Emissions is
based upon the "high" CAG ranking for a common constituent of coke
oven emissions, benzo(a)pyrene, which has produced cancer in a
number of organs of nine animal species by various routes of
administration.
NOTE 26: Coal tar creosote is identified by the CASRN 8001-58-9, and
data presented is for this material. No data were found that
would allow rating of beechwood creosote, CASRN 8021-39-4.
NOTE 27: This material requires an inhibitor to prevent
polymerization.
NOTE 28: Common name for this material is hydrazobenzene.
NOTE 29: Vinyl chloride polymerizes in the presence of air, sunlight,
or heat unless stabilized by inhibitors.
NOTE 30: The R0 for methyl isocyanate remains at its statutory 1-pound
level pending analysis of the Bhopal, India data by the Agency.
The Agency may adjust this statutory RQ in a future rulemaking.
NOTE 31: All cyanides assigned RQs under the CVA Section 311
(40 CFR 117.3, 44 FR 10279-10283, February 16, 1979) were placed
at RQ level A (10 pounds) on the basis of the aquatic toxicity of
the cyanide ion. The same practice is continued here.
4-67
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NOTE 32: New data in the "Handbook, of Acute Toxicity of Chemicals to
Fish and Aquatic Invertebrates," USDOI Publication No. 137,
indicates that the aquatic toxicity of parathion results in an RQ
of ten pounds for aquatic toxicity, versus older data used to
assign a 1-pound RQ under the CWA.
NOTE 33: The Agency is proposing to adjust the statutory 1-pound RQ
for radionuclides in a separate rulemaking action.
NOTE 34: The carcinogenic hazard ranking shown for unspecified
trichlorophenol is based on the ranking shown for the specific
isomer 2,4,6-trichlorophenol.
NOTE 35: A maximum RQ (5000 pounds) is suggested for
1,l,2-trichloro-l,2,2-trifluoroethane on the basis of the
following data:
LDcq Rat = 43,000 mg/kg (oral)
LC^q Rat = 87,000 ppm/6 hours (inhalation)
NOTE 36: An RQ level of C (1000 pounds) is proposed for
2-chloro-l,3-butadiene (chloroprene) on the basis of the following
data:
AQTX (TLm 96) = 10 - 100 ppm
Flash Point = -4°F
Boiling Point = 139°F
NOTE 37: An RQ level of D (5000 pounds) is proposed for
1,2,3-trichloropropane on the basis of the following data:
LDcq Rat = 320 mg/kg (oral)
LC^q Rat = 1000 ppm/4 hours (inhalation)
NOTE 38: An RQ level of C (1000 pounds) is suggested for
2,3-dichloro-n-propanol on the basis of the following data:
LDcn Rat = 90 mg/kg (oral)
LC^q Rat = 500 ppm/4 hours (ihl)
NOTE 39: This is an aqueous waste, and it has been assumed that the
antimony compound in solution is the trichloride.
NOTE 40: The proposed RQ for Tars (polycyclic aromatic) is based on
the lowest RQ assigned to specific polycyclic aromatics (i.e.,
benzo(a)pyrene) on the basis of potential carcinogenicity.
NOTE 41: These esters are assumed to be composed of phorate and/or its
analogues, and accordingly an RQ level will be suggested, based on
the RQ assignment of phorate itself.
4-68
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NOTE 42: An RQ level of D (5000 pounds) is suggested for diphenylamine
on the basis of the following data:
LD^q Gpg = 300 mg/kg (oral)
NOTE 43: An RQ level of B (100 pounds) is suggested for
paraphenylenediamine on the basis of the following data:
TL (48) Goldfish = 5.7 ppra
LD™q Rat = 80 mg/kg (oral)
NOTE 44: No data have been found that permit the ranking of this
hazardous substance. The available data for the acute hazards may
lie above the upper limit for the 5000-pound RQ, but since it is a
designated hazardous substance, the largest assignable RQ is 5000
pounds.
4-69
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SECTION 5
QUALITY ASSURANCE
Due to the amount o£ time elapsed between the original evaluations of the
CERCLA potential carcinogens and the present effort to produce this
report, the Agency has been involved in an- extensive reviev of all
supporting potential carcinogenicity assessment documents. In some cases
this involved updating information, but it was primarily a quality
assurance effort. This section of the technical background document
describes the effort the Agency has conducted to assure that the data,
the calculations, and the veight-of-evidence and potency groups of each
potential carcinogen are technically correct.
THE CHEMICAL PROFILES
Each chemical profile (entitled "Evaluation of the Potential
Carcinogenicity of (substance name) In Support of Reportable Quantity
Adjustments Pursuant to CERCLA Section 102") contains three major
sections: (1) Veight of Evidence - Animal Studies; (2) Veight of Evidence
- Human Studies; and (3) Potency. In addition, the profile contains data
sets from relevant experiments found in the published literature prior to
1983. A summary of each data set or each experiment is presented. The
data set that was chosen for use in calculating the potency factor is
comprised of a minimum of two dose levels and a control on the same
species conducted in an experiment classified as adequate. The data set
normally used was from that experiment with the greatest cancerous
response. For example, if there were data sets in one experiment from tvo
species and both sexes, the potency factor was computed using the results
of tumor response in the sex and species which experienced the greatest
response. Further, if there were data from different adequate
experiments involving mice, rats and hamsters, and it was shown that the
highest tumor response was in male mice, then that was the experiment
used for potency calculations.
5-1
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QUALITY ASSURANCE OF THE CHEMICAL PROFILES
Each chemical profile was carefully reviewed and the veight-of-evidence
grouping was re-evaluated on the basis of the Agency's weight-of-evidence
methodology as discussed in the Agency's Guidelines for Carcinogen Risk
Assessment (51 FR 33992-34003, September 24, 1986). The IARC weight-
of-evidence group classification was then revised to reflect the Agency's
classification system.
In the second phase of the quality assurance effort, the potency factor
data sets were scrutinized. The primary reference containing the data
set used in the potency factor calculations was obtained. All data in
the reference were carefully compared with the table in the profile which
summarized the experiment. The data examined included:
(1)	Dose (including controls)
(2)	Route of administration
(3)	Frequency of dosage
(4)	Duration of treatment
(5)	Duration of study
(6)	Response
(7)	Animal lifespan and weight
From these data, the transformed dose was then recalculated to determine
if all the data in the primary reference had been properly transcribed.
In the third phase of the effort, relevant reports issued by the Agency
such as Health Assessment Documents (HADs), Health and Environmental
Effects Profiles (HEEPs), Health Effects Assessments (HEAs), and Drinking
Vater Criteria Documents (DVCDs), were reviewed. The data used in these
documents were compared to the data in the profile to insure that the
weight-of-evidence grouping and the potency factors for those potential
carcinogens were correctly applied.
5-2
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CAG REVIEW
For each chemical profile, a resolution sheet was prepared vhich
identified discrepancies, if any, in the transcription of the data from
the reference to the profile, the calculations of the transformed dose,
the veight-of-evidence grouping, the potency factor calculations, and
finally, the variances with the HAD, HEEP, and/or HEA reports. The CAG
then resolved these discrepancies.
POTENCY AND HAZARD RANKING VERIFICATION
After the CAG had resolved any discrepancies, the potency factors were
recalculated in accordance with Section 3.2.4 of Appendix A and using the
GLOBAL 82 software. Any variance between the new potency factor and the
previous one was brought to the CAG's attention. It was essential that
detailed attention to the calculations be made to insure the technical
merit of the hazard ranking. The hazard ranking of each potential
carcinogen was then made in accordance with Appendix A. The RQs in Table
3-1 of Section 3 vere derived after the CAG's quality assurance effort.
5-3
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SECTION 6
REFERENCES
Anderson, Elizabeth L. et al., Quantitative Approaches in Use to Assess
Cancer Risk, Risk Analysis, Vol. 3, No. 4, 1983.
Crump, K.S. and W.V. Vatson, GLOBAL 82: A FORTRAN Program to Extrapolate
Dichotomous Animal Carcinogenicity Data to Low Doses, National Institute
of Environmental Health Sciences, Contract No. l-ES-2123 (1982).
Crump, Kenny S., An Improved Procedure for Lov-Dose Carcinogenic Risk
Assessment from Animal Data, Journal of Environmental Pathology and
Oncology, 5-4/5: 339-348, 1984.
Melvold, Robert V. and Steven C. Gibson, Sorbent Handbook for Clean-up
and Control of Liquid Hazardous Substances. Final Report prepared for
JRB Associates under Subcontract No. 2-817-33-956-06-9, under sponsorship
of the U.S. EPA, 1984.
6-1
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Appendix A
METHODOLOGY FOR EVALUATING POTENTIAL CARCINOGENICITY
IN SUPPORT OF REPORTABLE QUANTITY ADJUSTMENTS
PURSUANT TO CERCLA SECTION 102
A-l
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United States
Environmental Protection
Agency
&EPA Research and
Development
METHODOLOGY FOR EVALUATING POTENTIAL
CARCINOGENICITY IN SUPPORT OF REPORTABLE QUANTITY
ADJUSTMENTS PURSUANT TO CERCLA SECTION 102
Prepared for
OFFICE OF EMERGENCY AND REMEDIAL RESPONSE
Prepared by
Carcinogen Assessment Group
Office of Health and
Environmental Assessment
Washington DC 20460
DRAFT: DO NOT QUOTE OR CITE
This document is a preliminary draft. It has not been formally
released by the U.S. Environmental Protection Agency and should not
at this stage be construed to represent Agency policy. It is being
circulated for comments on its technical merit and policy implications.
EXTERNAL REVIEW DRAFT
0HEA-C-073
DECEMBER 1986
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DISCLAIMER
This document is intended for review purposes only
and does not constitute Agency policy. Mention of
trade names or commercial products does not
constitute Agency endorsement or recommendation for
use.
ii
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TABLE OF CONTENTS
CONTRIBUTORS AND REVIEWERS		v
1.	INTRODUCTION		1
1.1	BACKGROUND		1
1.2	METHODOLOGY		3
2.	LITERATURE SEARCH AND INFORMATION SOURCES		5
2.1	SEARCH STRATEGY		5
2.2	SELECTION OF APPROPRIATE STUDIES		7
3.	APPROACH TO DATA EVALUATION		10
3.1	QUALITATIVE PHASE: WEIGHT OF EVIDENCE OF CARCINOGENICITY..	11
3.1.1	Assessment o£ Evidence for
Carcinogenicity from Studies in Humans		11
3.1.2	Assessment of Evidence for
Carcinogenicity from Studies in Experimental
Animals		12
3.1.3	Categorization of Overall Weight of Evidence for
Human Carcinogenicity		14
3.2	QUANTITATIVE PHASE: ESTIMATION OF CARCINOGENIC POTENCY		17
3.2.1	Model Selection for Analysis of Dose Response Data..	17
3.2.2	Selection of Bioassay Response Data to be Used in
the Model to Calculate Potency		19
3.2.3	Adjustment (Transformation) of Dose Data		21
3.2.3.1	Calculation of Dose in mg/kg/day from
Doses Expressed as Dietary
Concentrations		21
3.2.3.2	Calculation of Dose in mg/kg/day from Doses
Expressed as Water Concentrations		22
3.2.3.3	Calculation of Dose in mg/kg/day from
Doses Expressed as Air Concentrations		23
iii
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TABLE OP CONTENTS (Continued)
3.2.3.4	Adjustment for Non-Continuous Exposure		26
3.2.3.5	Adjustment for Absorption, Distribution,
Metabolism and Excretion		26
3.2.4	Calculation of the Human Potency Factor (F)		27
3.2.4.1	Animal Potency		27
3.2.4.2	Adjustment for Less than Lifetime Studies..	29
3.2.4.3	Human Potency (F)		30
3.2.5	Grouping of Chemicals Based on Carcinogenic Potency.	31
3.3 OVERALL HAZARD RANKING BASED ON COMBINED QUALITATIVE AND
QUANTITATIVE ASSESSMENTS		32
3.3.1	Use of Chemical and Environmental Fate and
Transformation Data in Hazard Ranking of Metals and
Their Salts		33
3.3.2	Special Problems in Hazard Ranking of Chemicals
Associated with Multimedia Exposure in Humans		34
4.	SUMMARY		35
5.	REFERENCES		37
APPENDIX - HAZARD RANKING OF POTENTIAL CARCINOGENS		A-l
iv
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CONTRIBUTORS AND REVIEWERS
This document was prepared for the Carcinogen Assessment Group by Messrs.
Jeffery S. Gift, Gregory R. Ricci, Steven C. Gibson, James Conis and Dr.
Bartholomew L. Tuffly, of Environmental Monitoring and Services,
Incorporated (EMSI). Drs. James Cogliano, K. Jack Kooyoomjian and Aparna
Koppikar served as the Technical Project Monitors and Mr. Richard Field
as the Project Officer. The guidance of other members of the EPA staff
vas provided in special working group meetings and via written and oral
comments on various drafts. The assistance of Mr. John Riley and Ms.
Ivette Ortiz of the Emergency Response Division, and Mr. Thomas Gleason
and Dr. Robert McGaughy of the Office of Health and Environmental
Assessment was especially helpful.
An earlier draft of this document was prepared by Messrs. Michael Neal,
Steven Bosch, Joseph Santodonato, John Becker and Bruce Harris of the
Syracuse Research Corporation. Dr. Margaret Chu and Mr. Hugh Spitzer
served as Technical Project Monitors and Mr. John Risher as Project
Officer.
The Carcinogen Assessment Group in the Office of Health and Environmental
Assessment had the primary responsibility for methodology development and
peer review of the hazard ranking of carcinogens. Participating members
are as follows:
v
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Roy E. Albert, M.D.
Steven Bayard, Ph.D.
David L. Bayliss, M.S.
Robert P. Bellies, Ph.D.
Chao V. Chen, Ph.D.
Arthur Chiu, M.D., Ph.D.
Margaret H. L. Chu, Ph.D.
Vincent James Cogliano, Ph.D.
Villiam H. Farland, Ph.D.
Herman J. Gibb, B.S., M.P.H.
Bernard H. Haberman, D.V.M., M.S.R. (deceased)
Charalingayya B. Hiremath, Ph.D.
Janes V. Holder, Ph.D.
Aparna M. Koppikar, M.D., D.P.H., D.I.H.
Robert E. McGaughy, Ph.D.
Jean C. Parker, Ph.D.
Villiam E. Pepelko, Ph.D.
Charles H. Ris, M.S., P.E.
Dharm V. Singh, D.V.M., Ph.D.
Hugh L. Spitzer, B.A.
Todd V. Thorslund, Sc.D.
Additional assistance in the peer review and critique of conclusions,
extrapolations, and data summarization presented in this document was
provided by:
External
Dr. Herbert Cornish
School of Public Health
University of Michigan
Dr. Rolf Hartung
School of Public Health
University of Michigan
Dr. Benjamin Van Duuren
Institute of Environmental Medicine
New York University Medical Center
EPA
Donald Barnes
Office
of
Judy Bellin
Office
of
Barbara Davis
Office
of
Ivette Ortiz
Office
of
Patrick Tobin
Office
of
Pesticides and Toxic Substances
Solid Vaste
Vaste Programs Enforcement
Solid Vaste and Emergency Response
Vater Regulations and Standards
vi
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1. INTRODUCTION
1.1 BACKGROUND
This report describes the technical methodology the Agency has used in
developing a hazard ranking for potential carcinogens in order to adjust
reportable quantities (RQs) under Section 102 of the Comprehensive
Environmental Response, Compensation, and Liability Act of 1980 (CERCLA).
Section 103 of CERCLA requires immediate notification to the National
Response Center by any person in charge of a vessel or facility who
releases an amount of a hazardous substance equal to or greater than its
RQ. Under CERCLA Section 102(b), the RQ of any hazardous substance
designated in Section 101(14) is one pound unless a different RQ has been
established pursuant to Section 311(b)(4) of the Federal Water Pollution
Control Act. Under Section 102(a) these statutory RQs may be adjusted by
regulations establishing different quantities to be reported upon release
of a hazardous substance. Section 102(a) also gives EPA authority to
establish a single RQ for each hazardous substance, regardless of the
environmental medium into which the substance is released.
The RQ adjustment methodology is one vith which the regulated community
is familiar and is based, in part, on the methodology used to establish
RQs pursuant to Section 311 of the Clean Vater Act (CVA). Details of the
methodology are given in the document "Technical Background Document to
Support Rulemaking Pursuant to CERCLA Section 102, Volume 1," March 1985,
and in the final rule published on April 4, 1985 (50 FR 13456-13513).
1
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The methodology begins with an evaluation of the intrinsic physical,
chemical, and toxicological properties associated with each hazardous
substance. The intrinsic properties evaluated, called primary criteria,
are: aquatic toxicity, mammalian toxicity (oral, dermal, and inhalation),
ignitability, reactivity, chronic toxicity, and potential
carcinogenicity. The Agency ranks each intrinsic property (other than
potential carcinogenicity, which is discussed below) on a five-tier
scale, associating a specific range of values on each scale with a
particular RQ value. This five-tier scale uses the RQ levels of 1, 10,
100, 1000, and 5000 pounds, which were originally established pursuant to
the CVA Section 311. Each hazardous substance receives several tentative
RQ values based on its particular properties. The lowest of all of the
tentative RQs becomes the primary criteria RQ for that hazardous
substance. The primary criteria RQ can then be raised by one level using
biodegradability, hydrolysis, and photolysis as secondary criteria.
The Agency has determined that no potential carcinogen shall be assigned
an RQ above 100 pounds. The Agency has always regarded potential
carcinogens with special concern and in its regulatory actions has sought
to minimize carcinogenic risks. This concern is justified by scientific
factors particular to cancer:
1. It has not been demonstrated that there is a threshold level of
exposure below which potential carcinogens do not present some
risk of cancer. Therefore, a release of any amount of a
potential carcinogen represents an increased risk of cancer to
the exposed population. This is in contrast with most other
toxic effects, for which thresholds can be demonstrated.
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2.	Cancer risks are considered to be cumulative. A number of small
releases can be as serious as a single large release.
3.	Cancer is not immediately manifested. There is a latent period
betveen exposure to a carcinogen and the manifestation of cancer
that makes it impossible to directly observe carcinogenic risks
from substances newly released into the environment. This is in
contrast to acute toxic effects, which are more immediately
manifested.
In deciding whether to assign RQs for potential carcinogens at all five
RQ levels, the Agency examined the special properties associated with
these substances, used an EPA air dispersion model to analyze the risks
posed by their release, and evaluated them in light of the Agency's
chronic toxicity methodology. The Agency decided not to use the two
highest RQ levels, 1000 and 5000 pounds, for several reasons, all of
which are explained in the main body of this "Technical Background
Document to Support Rulemaking Pursuant to CERCLA Section 102, Volume 3,"
(U.S. EPA, 1986a).
As a consequence of the Agency's decision to adopt a 100-pound maximum RQ
for potential carcinogens, the Carcinogen Assessment Group (CAG) was
requested to rank potential carcinogens on a three-tier scale (High,
Medium, and Low) that corresponds to RQ levels of 1, 10, and 100 pounds.
1.2 METHODOLOGY
The Carcinogen Assessment Group (CAG) developed a methodology for ranking
potential carcinogens based originally on a combination of the
International Agency for Research on Cancer's (IARC) weight-of-evidence
scheme and the CAG's potency factor. This methodology had been reviewed
3
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and was described in a previous draft of this report. On September 24,
1986, the Agency published its Guidelines for Carcinogen Risk Assessment
(51 FR 33992), which refined the IARC veight-of-evidence criteria. The
EPA Reportable Quantity Work Group determined on June 4, 19B5, that the
ranking methodology should be revised to be consistent with the Agency's
proposed guidelines, and should include the Agency's new
weight-of-evidence criteria. This has been done in this methodology.
The following sections of this report present the objectives and
methodology applied in arriving at a carcinogenic hazard assessment for
each of the hazardous substances under study. The major findings are
summarized in tabular form in a separate, but attached, appendix (Hazard
Ranking of Potential Carcinogens). A more detailed discussion of the
available studies, weight-of-evidence determinations, and potency factor
assignments for each potential carcinogen under study, a copy of the
primary reference used for calculating the potency factor, and a
bibliography of other pertinent references is contained in a profile for
each chemical. The profiles, entitled "Evaluation of Potential
Carcinogenicity of [substance name] in Support of Reportable Quantity
Adjustments Pursuant to CERCLA Section 102," collectively form an
additional appendix to, but are not attached as part of, this methodology
document. The profiles can be accessed separately in the record that
supports CERCLA RQ adjustment rulemakings, which are available from EPA's
document room, LG, 401 H Street, SV, Washington, D.C. 20460.
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2. LITERATURE SEARCH AND INFORMATION SOURCES
2.1 SEARCH STRATEGY
The objective of the information search vas to identify all relevant
published reports concerning the potential carcinogenicity of the
chemicals under study. For the most part, only reports published prior
to 1985 vere considered in this review. Epidemiologic studies and the
published results of controlled investigations with experimental
laboratory animals vere sought from the vorldvide biomedical literature.
In order that the information search be exhaustive, both on-line and
hard-copy sources of bibliographic information vere consulted. A list of
the data bases searched for this project is presented in Table 2-1.
Retrieval of old literature vas accomplished through searches of
hard-copy sources and through researching bibliographies of relevant
publications. Every attempt has been made to rely upon primary
publications as opposed to data summaries or abstracts contained in
secondary sources such as monographs, surveys, review articles, criteria
documents, etc.
Searches vere conducted using specific Chemical Abstracts Service names,
CAS registry numbers, common synonyms, designated substructures, and
key words related to carcinogenicity/mutagenicity vhen appropriate. All
of the chemicals included in the study vere first searched in the
CHEMLINE on-line chemical dictionary to identify proper CAS registry
5
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Table 2-1
SOURCES OF BIBLIOGRAPHIC AND NUMERICAL INFORMATION
FOR SUSPECT CARCINOGENS
On-Line Sources
CHEMLINE (National Library of Medicine)
RTECS (National Library of Medicine)
Toxicology Data Bank (National Library of Medicine)
TOXLINE (National Library of Medicine)
CANCERLINE (National Library of Medicine)
Chemical Abstracts (DIALOG Information Services)
Hard-Copy Sources
"Survey of Compounds Tested for Carcinogenicity," PHS-149 (all volumes)
"International Agency for Research on Cancer—Monographs on the
Evaluation of Carcinogenic Risks of Chemicals to Humans," Volumes 1-29
National Toxicology Program, Carcinogenesis Testing Program, "Chemicals
on Standard Protocol" (as of October 7, 1982)
National Cancer Institute—Technical Report Series
"Genetox Carcinogen List" (as of July 9, 1982)
"TOX-TIPS" (National Library of Medicine)
"Chemical Carcinogens," C.E. Searle (ed.)r ACS Monograph 173, 1976
"Documentation of the Threshold Limit Values for Substances in Workroom
Air," American Conference of Governmental Industrial Hygienists
"Ambient Water Quality Criteria Documents," U.S. EPA, ORD
National Institute for Occupational Safety and Health—Criteria
Documents, Technical Reports, Special Occupational Hazard Reviews,
Current Intelligence Bulletins, Information Profiles on Potential
Occupational Hazards
"Current Contents—Life Sciences," Institute for Scientific Information
6
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numbers and all available synonyms. Online bibliographic data bases were
then searched by developing a list of key words, translating them into
data base specific index terms and searching the file. If the citations
retrieved vere relevant, they were printed. If these results indicated
nev key words, the data base vas searched again.
In most cases, the decision to obtain an article in hard copy was based
upon a review of information contained in abstracts which were obtained
from the on-line computer search. For the sake of completeness, many
articles were obtained in hard copy even if it was not clear from the
title that useful data for assessment of carcinogenic risk would be
contained in the report. Thus, a large body of literature relating to
the chemicals under study was collected, although no attempt was made to
cite all of the articles retrieved.
Only published literature was reviewed for the assessments made in this
report. However, the CAG is now in the process of reviewing unpublished
carcinogenicity study data submitted to the Agency. The summary table
(Hazard Ranking of Potential Carcinogens), which is attached as an
appendix to this report, may be revised upon the completion of that
review.
2.2 SELECTION OF APPROPRIATE STUDIES
It is important to recognize that many published studies may be
acceptable to provide qualitative evidence of carcinogenicity, yet still
may be inappropriate for quantitative estimation of carcinogenic potency.
7
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It is important to consider the relevance of the route of administration
of the test substance in experimental animals to the anticipated route of
exposure in humans. For example, the results of animal studies in vhich
test substances are administered by intravenous or intramuscular
injection may provide strong qualitative evidence of carcinogenic
potential and yet be inappropriate to predict the tumor incidence in
humans resulting from ingestion or inhalation of the substance. The
problem is often compounded by a lack of data concerning the extent of
absorption from different routes of exposure (I.e., oral, inhalation,
dermal contact), thereby leading to inaccurate estimates of actual
absorbed doses.
Before a study can be used to support either a qualitative or
quantitative assessment of carcinogenicity, several criteria should be
met. These general criteria, vhich are applied by reviewers when
evaluating the output of a literature search, are listed below.
Factor:	Experimental Design
Scoring	Elements:
1.	What are the objectives of the study?
2.	Does the design address the issues?
3.	Does the design represent the state-of-the-art?
4.	Are there areas which might produce ambiguous results?
5.	Vere the sampling and handling procedures adequate?
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Factor: Experimental Procedure
Scoring Elements:
1.	Vere standard protocols folloved?
2.	Vere any variations from design noted, explained and/or
considered in reporting results?
3.	Were analytical and quantitative parameters provided?
Factor: Results and Conclusions
Scoring Elements:
1.	Vere sufficient data presented to allow a credible case to be
established?
2.	Vere the results understandable?
3.	Vere results statistically valid?
4.	Vere the investigators' conclusions supported by the results?
5.	Does the paper allow for additional conclusions to be reached
concerning correlation of results with the findings of other
investigators?
A publication need not necessarily be rejected from consideration if all
of the above criteria are not net, although deficiencies in the study
should be indicated by the reviewer if the data are intended to be used
for qualitative and quantitative assessment purposes.
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3. APPROACH TO DATA EVALUATION
Bach primary publication retrieved during the literature search phase of
the project is critically evaluated, both with respect to its relevance
to an assessment of carcinogenicity and to the quality of the reported
data. In developing a hazard ranking methodology, the Agency recognizes
that a distinction must be made between the evaluation of the qualitative
strength of the case that a substance causes cancer, and the quantitative
estimate of the strength of the substance to cause cancer. The
qualitative assessments are expressed as an overall veight of evidence of
the likelihood that the substance is a human carcinogen (see Section
3.1).	The quantitative assessment, on the other hand, is a numerical
estimate of the strength of the substance to cause cancer (see Section
3.2).
Because of the large number of substances to be evaluated, it is
necessary to be as systematic as possible in conducting both the
qualitative and quantitative assessments. A two-phase approach was
developed that would facilitate the grouping of substances based on the
overall weight of evidence of carcinogenicity and on the calculated
carcinogenic potency.
A subsequent quality control review, under the direction of the CAG, has
been conducted to assure that all determinations and study
interpretations within each profile are consistent with qualitative and
quantitative analysis in other Agency risk assessment reports. The risk
assessment reports reviewed were Health Effects Assessments (HEAs),
10
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Health and Environmental Effects Profiles (HEEPs), Health Assessment
Documents (HADs) and Drinking Water Criteria Documents (DWCDs).
3.1 QUALITATIVE PHASE: WEIGHT OF EVIDENCE OF CARCINOGENICITY
The first phase of the CAG ranking procedure is a qualitative evaluation
of the strength of the available data. This evaluation is based on the
Agency's Guidelines for Carcinogen Risk Assessment (51 FR 33992,
September 24, 1986). The remainder of this section paraphrases the
guidelines.
3.1.1 Assessment of Evidence for Carcinogenicity from Studies in Humans
Evidence of carcinogenicity from human studies comes from three main
sources:
•	Case reports of individual cancer patients who were exposed to
the agent(s).
•	Descriptive epidemiologic studies in which the incidence of
cancer in human populations was found to vary in space or time
with exposure to the agent(s).
•	Analytical epidemiologic (case-control and cohort) studies in
vhich individual exposure to the agent(s) was found to be
associated vith an increased risk of cancer.
Three criteria must be met before a causal association can be inferred
between exposure and cancer in humans:
•	There is no identified bias that can explain the association.
•	The possibility of confounding variables has been considered and
ruled out as explaining the association.
11
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• The association is unlikely to be due to chance.
In general, although a single study may be indicative of a cause-effect
relationship, confidence in inferring a causal association is increased
when several independent studies shov the association, when the
association is strong, when there is a dose-response relationship, or
when a reduction in exposure is followed by a reduction in the incidence
of cancer.
The evidence for carcinogenicity* from studies in humans is classified as:
•	Sufficient evidence of carcinogenicity, which indicates that
there is a causal relationship between the agent and human
cancer.
•	Limited evidence of carcinogenicity, which indicates that a
causal interpretation is credible, but that alternative
explanations, such as chance, bias, or confounding, could not
adequately be excluded.
•	Inadequate evidence, which indicates that one of two conditions
prevailed: (a) there were few pertinent data; or (b) the
available studies, while showing evidence of association, did not
exclude chance, bias, or confounding and therefore a causal
interpretation is not credible.
•	No data, which indicates that data are not available.
•	No evidence, which indicates that no association was found
between exposure and an increased risk of cancer in well-designed
and well-conducted independent analytical epidemiologic studies.
3.1.2 Assessment of Evidence for Carcinogenicity from Studies in
Experimental Animals
These assessments are classified into five groups:
* For purposes of public health protection, agents associated with life-
threatening benign tumors in humans are included in the evaluation.
12
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2
•	Sufficient evidence of carcinogenicity, vhich indicates that
there is an increased incidence of malignant tumors or combined
malignant and benign tumors : (a) in multiple species or
strains; (b) in multiple experiments (e.g., with different routes
of unusual degree in a single experiment with regard to high
incidence, unusual site or type of tumor, or early age at onset.
Additional evidence may be provided by data on dose-response
effects, as veil as information from short-term tests or on
chemical structure.
•	Limited evidence of carcinogenicity, vhich means that the data
suggest a carcinogenic effect but are limited because: (a) the
studies involve a single species, strain, or experiment and do
not meet criteria for sufficient evidence (see U.S. EPA, 1986);
(b) the experiments are restricted by adequate dosage levels,
inadequate duration of exposure to the agent, inadequate period
of follov-up, poor survival, too fev animals, or inadequate
reporting; or (c) an increase in the incidence of benign tumors
only.
•	Inadequate evidence, vhich indicates that because of major
qualitative or quantitative limitations, the studies cannot be
interpreted as shoving either the presence or absence of a
carcinogenic effect.
•	No data, vhich indicates that data are not available.
•	No evidence, vhich indicates that there is no increased incidence
of neoplasms in at least tvo veil-designed and vell-conducted
animal studies in different species.
The classifications "sufficient evidence" and "limited evidence" refer
only to the veight of the experimental evidence that these agents are
carcinogenic, and not to the potency of their carcinogenic action.
	2	
An increased incidence of neoplasms that occurs even vith high
spontaneous background incidence (e.g., mouse liver tumors and rat
pituitary tumors in certain strains) generally constitutes "sufficient"
evidence of carcinogenicity, but may be changed to "limited" vhen
varranted by the specific information available on the agent.
3
Benign and malignant tumors vill be combined unless the benign tumors
are not considered to have the potential to progress to the associated
malignancies of the same histogenic origin.
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3.1.3 Categorization of Overall Weight of Evidence for Human
Carcinogenicity
The overall scheme for categorizing the weight of evidence of
carcinogenicity of a chemical for humans uses a three-step process: (1)
the evidence in human studies or animal studies is summarized; (2) these
lines of information are combined to yield a tentative assignment to a
veight-of-evidence category (see Table 3-1); and (3) all relevant
supportive information is evaluated to see if the designation of the
overall weight of evidence needs to be modified. Relevant factors to be
included along with the tumor information from human and animal studies
include structure-activity relationships; short-term test findings;
results of appropriate physiological, biochemical, and toxicological
observations; and comparative metabolism and kinetic studies. The nature
of these findings may cause one to adjust the overall categorization of
the weight of evidence.
The substances are categorized as follows:
Group A—Human Carcinogen
An agent is placed in this group only when there is "sufficient" evidence
from epidemiologic studies to support a causal association between
exposure to the agent(s) and cancer.
Group B—Probable Human Carcinogen
This group includes agents for which the weight of evidence of human
carcinogenicity based on epidemiologic studies is "limited" and also
14
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Table 3-1
TENTATIVE WEIGHT^OF-EVIDENCE BASED ON HUMAN AND ANIMAL EVIDENCE4
Human
Evidence
Animal Evidence
No No
Sufficient Limited Inadequate Data Evidence
Sufficient
A
A
A
A
A
Limited
B1
B1
B1
B1
B1
Inadequate
B2
C
D
D
D
No Data
B2
C
D
D
E
No Evidence
B2
C
D
D
E
4
The above assignments are presented £or Illustrative purposes. There may
be instances in the classification of both animal and human data indicating
that different categorizations than those given in the table should be
assigned. Furthermore, these assignments are tentative and may be modified
by ancillary evidence. All relevant information is evaluated to determine
if the designation of the overall weight of evidence needs to be modified.
Relevant factors to be included along with the tumor data from human and
animal studies include structure-activity relationships, short-term test
findings, results of appropriate physiological, biochemical, and
toxicological observations, and comparative metabolism and kinetic studies.
The nature of these findings may cause an adjustment of the overall
categorization of the weight of evidence.
15
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includes agents for which the veight of evidence of carcinogenicity based
on animal studies is "sufficient." The group is divided into two groups.
Group B1 is usually reserved for agents for which there is "limited"
evidence of carcinogenicity from epidemiologic studies. It is
reasonable, for practical purposes, to regard an agent for which there is
"sufficient" evidence of carcinogenicity in animals as if it presented a
carcinogenic risk to humans. Therefore, agents for which there is
"sufficient" evidence from animal studies and for which there is
"inadequate" evidence or "no data" from epidemiologic studies (human)
would usually be categorized under Group B2.
Group C—Possible Human Carcinogen
This group is used for agents with "limited" evidence of carcinogenicity
in animals in the absence of human data. It includes a wide variety of
evidence, for example: (a) a malignant tumor response in a single,
well-conducted experiment that does not meet conditions for "sufficient"
evidence; (b) tumor responses of marginal, statistical significance in
studies having inadequate design or reporting; (c) benign but not
malignant tumors with an agent showing no response in a variety of
short-term tests for mutagenicity; and (d) responses of marginal
statistical significance in a tissue known to have a high or variable
background rate of cancer.
Group D—Not Classifiable as to Human Carcinogenicity
This group is generally used for agent(s) with "inadequate" human and
animal evidence of carcinogenicity or for which "no data" are available.
16
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Group E—Evidence of Non-Carcinogenicity for Humans
This group is used for agent(s) that show no evidence for carcinogenicity
in at least two adequate animal tests in different species or in both
adequate epidemiologic and animal studies.
The designation of a Group E agent is based on the available evidence and
should not be interpreted as a definitive conclusion that the agent will
not be a carcinogen under any circumstances.
3.2 QUANTITATIVE PHASE: ESTIMATION OF CARCINOGENIC POTENCY
After the qualitative determination that a substance is a potential
carcinogen, a quantitative assessment can usually be performed. Such
quantitative assessments are most useful for: (1) estimating the cancer
risk associated with a particular level of exposure; and (2) making
comparisons among potential carcinogens based on their relative
potencies. This latter application is the objective ofV this methodology.
More specifically, the objective is to group potential carcinogens
according to potency.
3.2.1 Model Selection for Analysis of Dose Response Data
Given the stated objective of grouping potential carcinogens according to
potency, there is a need for consistency and comparability in the
evaluation process. In accordance with the Agency's guidelines and with
17
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Agency practice in numerous risk assessments, the multistage model is
used £or estimating carcinogenic potency. Under the multistage model,
the lifetime probability of developing cancer vith a constant dose (d) is
given by:
P(d) = 1 - exp [-(qo + qjd + ... + dk))
In accordance with the Agency's Guidelines for Carcinogenic Risk
Assessment (U.S. EPA, 1986b), when study results, are such that another
model would provide adequate estimates of carcinogenic potency, the CAG
may choose to use the more appropriate model. Any variance from the
standard multistage model is described in the individual potential
carcinogen profiles.
For reportable quantity adjustments pursuant to CERCLA Section 102, the
potency factor (F) is defined as the reciprocal of the estimated dose in
mg/kg/day, associated with a lifetime cancer risk of 10 percent (ED^q).
The potency factor (F) is used in place of the upper bound on the linear
coefficient (q^*) that CAG normally uses to estimate potency^
because:
1. It can be estimated without the use of many assumptions required
for q-*. This is possible because there is no needg for
extrapolation below the experimentally observable dose range .
The multistage model and q.* are described in more detail in another
Appendix of the U.S. EPA, 1986a Technical Background Document to
Support Rulemaking Pursuant to CERCLA~Section 102, Volume 3.
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2.	It is relatively insensitive to the choice of the dose-response
extrapolation model. Therefore the potency rankings are not
distorted by the selection of any particular dose-response model.
3.	The point estimate of ED.Q, which has some optimal statistical
properties, can be used to calculate F. Therefore, it is not
necessary to use statistical upper bounds, which are needed to
ensure stable estimates of q^*.
The potency factor (F) is used together with the qualitative weight of
evidence of carcinogenicity in ranking the potential carcinogens.
3.2.2 Selection of Bioassay Response Data to be Used in the Model to
Calculate Potency
This section covers the selection of animal study response data for use
in the multistage model and estimation of 1/ED^q. Human epidemiology
data must be reviewed and used on a case-by-case basis. Hence if
epidemiologic studies are selected as suitable for derivation of a
potency estimate, their use is described separately in the individual
potential carcinogen profile. In general, the data selection criteria
are those described in EPA's guidelines (U.S. EPA, 1986b).
The following approach to selecting the data sets for calculating a
potency factor is used where several studies on a particular substance
might involve different animal species, strains, and sexes, at several
doses and by different routes of exposure, and may result in different
tumor sites and types.
6 Extrapolation below the experimentally observable dose range is the
whole purpose of the q.,* estimation. It is done because "risk at low
exposure levels cannot be measured directly either by animal
experiments or by epidemiologic studies" (U.S. EPA, 1986b).
19
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The tumor incidence data are separated according to organ site and tumor
type. All biologically and statistically acceptable data sets are
presented in the potential carcinogen profiles. Because it is possible
that human sensitivity is as high as the most sensitive responding animal
species, in the absence of evidence to the contrary, the biologically
acceptable data set from long-term animal studies shoving the greatest
sensitivity is generally used, with due regard to biological and
statistical considerations.
All assumptions are presented in the profile along with a discussion of
any uncertainties in the extrapolation. Vhere tvo or more significantly
elevated tumor sites or types are observed in the same study,
extrapolations may be conducted on selected sites or types. These
selections are made on biological grounds. To obtain a total estimate of
carcinogenic risk, animals with one or more tumor sites or types shoving
significantly elevated tumor incidence are pooled and used for
extrapolation. The pooled estimates are generally used in preference to
potency estimated based on single sites or types. Quantitative risk
extrapolations are generally not performed on the basis of totals that
include tumor sites without statistically significant elevations.
Benign tumors are generally combined vith malignant tumors for potency
estimates unless the benign tumors are not considered to have the
potential to progress to the associated malignancies of the same
histogenic origin.
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3.2.3 Adjustment (Transformation) of Dose Data
Before a potency factor can be calculated all dose information must be
transformed to standard units of milligram (mg) (substance) per kilogram
(kg) (animal weight) per day, administered over the entire length of the
study. If doses are given in units other than mg/kg/day, or if animals
are dosed in a non-continuous manner, or if the reviewer has evidence
that the absorbed or metabolized dose is significantly less than the
administered dose, then the dose data must be converted to a "transformed
dose."
The next three subsections discuss hov this is done for three exposure
routes: diet, water and air.
3.2.3.1 Calculation of Dose in mg/kg/day from Doses Expressed as Dietary
Concentrations
If the authors provide information on body weight and food consumption,
then the dietary dose (d) is calculated directly. If these data are not
provided, then the dose may be estimated by using standard food
consumption estimates. An empirically-derived food factor (f) is used to
estimate the fraction of body weight that is consumed each day as food:
Species	(f)
Mouse	0.13
Rat	0.05
Human	0.028
In order to obtain the dietary dose (d) from the data given in parts per
million (ppm), the daily experimental dose in ppm is multiplied by (f):
21
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d = ppm x £
Note that ppm in food has units o£ rag toxicant per kg food, and the ratio
(f) has units of kg food per kg body weight per day. Thus the product
has units of mg of toxicant per kg body weight per day.
3.2.3.2 Calculation of Dose in mg/kg/day from Doses Expressed as
Water Concentrations
If the authors provide information on body weight and water consumption,
then the dietary dose (d) is calculated directly. If these data are not
available then (d) may be estimated by using standard water consumption
estimates based on the fraction of the body weight consumed as water per
day (fw). The assumptions and the procedure for making this estimation
are the same as for dietary concentrations (Section 3.2.3.1) but the
following rates for (fw) apply:
Species	fw
House	0.17
Rat	0.078
Human	0.029
The dietary dose (d) in mg/kg/day is calculated by multiplying the daily
dose in ppm by the appropriate (fw):
d s ppm x fw
Note that ppm in water has units of mg toxicant per liter water and that
(fw) has units of liters of water per kg body weight per day. Thus the
product has units of mg toxicant per kg body weight per day.
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3.2.3.3 Calculation of Dose in mg/kg/day from Doses Expressed as
Air Concentrations
When exposure is via inhalation, the calculation of dose can be
considered for tvo cases vhere: 1) the carcinogenic agent is either a
completely vater-soluble gas or an aerosol and is absorbed in proportion
to the amount of air breathed in; and 2) vhere the carcinogen is a poorly
vater-soluble gas that reaches an equilibrium betveen the air breathed
and the body compartments. After equilibrium is reached, the rate of
absorption of these agents is expected to be proportional to the
metabolic rate, vhich is proportional to the rate of oxygen consumption,
vhich in turn is a function of surface area.
For Case 1, agents that are in the form of particulate matter or
virtually completely absorbed gases, such as sulfur dioxide, can
reasonably be expected to be absorbed proportional to the inhalation
rate. The inhalation rate (I) for various species can be calculated from
•>
the observations (FASEB, 1974) that 25-g mice breathe 0.0345 m /day and
3
113-g rats breathe 0.105 m /day. For mice and rats of other veights V
(in kilograms), the surface-area proportionality can be used to find
3
breathing rates in m /day as follows:
For mice, I = 0.0345 (V/0.025) 2/3 m3/day
For rats, I = 0.105 (V/0.113)273 m3/day
3
For humans, the value of 1=20 m /day is adopted as the standard breathing
rate. This is calculated from the observation (ICRP, 1977) that the
23
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7 3	7 3
average breathing rate is 10 cm per 8-hour workday and 2 x 10 cm
in 24 hours.
The empirical factors for the air intake per kg per day, i » I/V, based
upon the previously stated relationships for standard weight animals, are
tabulated as follows:
Species	_V	
Mouse	0.03
Rat	0.35
Human 70
The inhalation dose (d) in mg/kg/day
substance's air concentration (v) by
and the absorption fraction (r):
i = I/V
1.3 •
0.64
0.29
multiplying the
intake factor (i)
is calculated by
the appropriate
d = (v) x (i) x (r)
3	3
Note that (v) has units of mg toxicant per m , (i) has units of m per kg
body weight per day, and (r) is dimensionless. Thus the product has
units of mg toxicant per kg body weight per day.
In the absence of experimental information or a sound theoretical
argument to the contrary, the fraction absorbed (r) is assumed to be the
same for all species and therefore drops out of the calculations.
For Case 2, the dose in mg/day of partially soluble vapors is
2/3
proportional to O2 consumption, which in turn is proportional to V
24
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The dose is also proportional to the solubility of the gas in body
fluids, which can be expressed as an absorption coefficient (r) for the
gas.
2/3
Therefore, expressing the Oj consumption as = k V , vhere (k)
is a constant independent of species, it follows that:
M = (k) V2/3 x (v) x (r)
As with the Case 1, in the absence of experimental information or a sound
theoretical argument to the contrary, the absorption fraction (r) is
assumed to be the same for all species. Therefore, for these substances
a certain concentration in ppm or mg/m in experimental animals is
equivalent to the same concentration in humans. This is supported by the
observation that the minimum alveolar concentration necessary to produce
a given "stage" of anesthesia is similar in man and animals (Dripps et
al., 1977). When the animals are exposed via the oral route and human
exposure is via inhalation or vice-versa, the assumption is made, unless
there is pharmacokinetic evidence to the contrary, that absorption is
equal by either exposure route.
In this case, the dose (d) in mg/kg/day is:
d s M/kg (animal)
For either inhalation case, exposures given in terms of ppm (by volume)
3
in air can be converted to units of mg/m by the following formula:
25
(A-34)
-------
3
rag/m a .041 x molecular veight (gas) x ppm
(Note that 1 milliliter in 1 cubic meter is 1 ppm (by volume); therefore,
0.041 x MV is the veight in milligrams o£ 1 milliliter of a gas.)
3.2.3.4	Adjustment for Non-Continuous Exposure
To this point the dose (d) calculated reflects the daily dose given over
the experimental treatment period. To derive the final "transformed
dose" the dose must be multiplied by the fraction of the study over vhich
the animal was actively dosed. If the animal was dosed continuously over
an entire treatment period (e.g., not 5 times per week or, for inhalation
studies, 6 hours per day) then the transformed dose is:
transformed dose = (d) x ^
Where le => duration of the treatment and Le = duration of the study.
If the animal was dosed for a fraction of a week (e.g., 5/7) or a
fraction of a day (e.g., 6/24), then the transformed dose becomes, for
example:
transformed dose "dx^x^x^
3.2.3.5	Adjustment for Absorption, Distribution, Metabolism and
Excretion
Whenever there is usable information on the absorption, distribution,
metabolism, or excretion of the substance, the potency factor is adjusted
to reflect this information. For example, if the effective dose to the
26
(A-35)
-------
target organ in an animal, due to any of these four factors, is known to
be a fraction of the administered dose, then the effective dose is used
to estimate the potency factor. However, in the absence of information
or differences in absorption, distribution, metabolism or excretion
between animals and humans, no such adjustments are made.
3.2.4 Calculation of the Human Potency Factor (F)
The information needed for calculating a human potency factor (F) can be
found in the profiles entitled "Evaluation of the Potential
Carcinogenicity of [substance name] in Support of Reportable Quantity
Adjustments Pursuant to CERCLA Section 102." A sample potency factor
derivation table from the profile for chloroform is presented in Figure
3-1.
3.2.4.1 Animal Potency
The first step in the derivation of a human potency (F) is the
calculation of the animal potency from the transformed dose and response
(tumor incidence) data.
The animal potency is estimated by fitting a multistage dose-response
model to the transformed dose-response data, as described in EPA's Notice
of Availability of Water Quality Criteria Documents (Federal Register,
November 28, 1980, pp 79318-79379). The mathematical assumptions made
for the model used are described in a separate appendix to the technical
support document (U.S. EPA, 1986) for the reportable quantity rule.
27
(A-36)
-------
Figure 3-1
SAMPLE TABLE FOR THE DERIVATION OF POTENCY FACTOR (F)
Agent: Chloroform
REFERENCE:
NCI (1976)

EXPOSURE ROUTE:
oral (gavage)

SPECIES:
mice

STRAIN:
B6C3F1

SEX:
F

VEHICLE OR PHYSICAL STATE:
corn oil

BODY WEIGHT:
0.03 kga

DURATION OF TREATMENT (le):
546 days

DURATION OF STUDY (Le):
644 - 651 days

LIFESPAN OF ANIMAL:
730 days'3

TARGET ORGAN:
liver

TUMOR TYPE:
hepatocellular carcinoma

EXPERIMENTAL DOSES/EXPOSURE:
477 mg/kg day0 238 mg/kg day0
0 mg/kg day
TRANSFORMED DOSESd


(mg/kg/day):
288 143
0
TUMOR INCIDENCE:
39/41 36/45
0/20
ANIMAL POTENCY FACTOR:
.104

HUMAN POTENCY FACTOR (F)
1.97

^ Reported


Assumed


^ Exposures were 5 days/week.
Duration of study was assumed
to be 647 days.
Transformed doses = le x 5
(days/week).

Li 7


28


(A-37)

-------
For chloroform, the dose causing an increased cancer risk of 10 percent
of the population is calculated to be ED^q = 9*62 mg/kg/day. The animal
potency is the reciprocal of this dose, 0.104 (mg/kg/day)
3.2.4.2 Adjustment for Less Than Lifetime Studies
Under the current procedures used by CAG, the risk levels are derived
only for full lifetime experiments. In dealing with experimental data in
which the observation period (Le) is less than the lifespan (L) of the
experimental animal, the potency factor derived from the experimental
data, which would give a risk estimate over the fraction Le/L of the
3
animal's lifespan, is increased by a factor of (L/Le) to obtain an
estimated potency for full lifetime risk. As explained by the EPA
(1980): "Ve assume that if the average dose (d) is continued, the
age-specific rate of cancer will continue to increase as a constant
function of the background rate. The age-specific rates for humans
increase at least by the second power of the age and often by a
considerably higher power, as demonstrated by Doll (1971). Thus ve would
expect the cumulative tumor rate to increase by at least the third power
of age..."
3
Lifetime Animal Potency = Observed Animal Potency x (L/Le)
This adjustment is conceptually consistent with the proportional hazard
model considered by Crump, et al. (1977).
For chloroform, the lifetime animal potency is:
29
(A-38)
-------
Lifetime Animal Potency = 0.104 x (730/648)^ = 0.149.
3.2.4.3 Human Potency (F)
Finally the potency must be adjusted for humans (if derived from animal
data). The human potency adjustment is made using the following
surface-area correction:
1/3
Human Potency (F) = Lifetime Animal Potency x (70 kg/W )
&
where V is the weight of the animal and 70 kg is the assumed average
weight of humans. This is in accordance with the Agency's cancer
guidelines (U.S. EPA, 1986)8.
For chloroform, the Human Potency (F) is:
Human Potency (F) = 0.149 x (70/0.03)1/3 = 1.97
n	
The Agency's guidelines reflect that animal potency is converted to
human potency by first multiplying the animal ED1Q by the ratio of the
the weight of the animal to the weight of man, ana dividing the entire
ED^q by the ratio of the surface area of the animal to man.
animal ED x /W /W ]	,	v 1/3
10
(Wa/"man)	/ V /V \
Human ED^q = 	 2/3	 = animal ED^q I a/ man J
(\
Then, the reciprocal of the Human ED^q is the adjusted Human Potency
(A-39)
30
-------
3.2.5 Grouping of Chemicals Based on Carcinogenic Potency
After the potency factors are estimated, the substances are placed into
three potency groups. The most potent substances, those with potency
factors above 100, are placed in Potency Group 1, substances with potency
factors between 1 and 100 are placed in Potency Group 2, and substances
with potency factors below 1 are placed in Potency Group 3. The Potency
Group will be used along with the weight-of-evidence group in assigning
tentative RQs for potential carcinogenicity.
In the case where available data are inadequate for estimating a potency
factor, the CAG has identified two possible alternatives:
1.	If the best available data suggest that the substance is a
possible strong carcinogen, but there is no basis for assigning a
specific ED-m dose (i.e., all treated animals at every
experimental aose developed tumors), then the substance is
administratively assigned to the highest potency group (i.e.,
Potency Group 1).
2.	If the best available data are inadequate for calculating a
potency factor and no quantitative inferences can be made (for
example, in animal studies where control groups were not used or
number of animals treated were not specified), then the substance
is assigned to the mid-range potency group (i.e., Potency Group
2).
Hazard rankings can then be assigned by following the standard procedure
for combining the weight-of-evidence group and the assigned potency
group.
31
(A-40)
-------
3.3 OVERALL HAZARD RANKING BASED ON COMBINED QUALITATIVE AND
QUANTITATIVE ASSESSMENTS
The culmination of the hazard ranking process performed in this study	is
accomplished by combining the qualitative veight of evidence	for
carcinogenicity (Section 3.1) with the potency group (Section 3.2)	to
arrive at a final hazard ranking for each substance. Substances	are
ranked as "high," "medium," or "low" hazard according to the following
matrix.
Hazard Ranking Scheme for Reportable Quantities under CERCLA
Potency Group
Weight-of-Evidence
Group
1
2
3
A
High
High
Medium
B
High
Medium
Low
C
Medium
Lov
Low
D
No hazard ranking

E
No hazard ranking

Hazard rankings are based jointly on two factors — weight of evidence
and potency — that the Agency believes are important in describing
carcinogenic hazards. Hazard rankings of high, medium, and low are
assigned so that the hazard ranking increases as either the veight of
evidence or the potency increases.
Depending on whether a substance falls into Potency Groups 1, 1, or 3, a
hazard ranking of high, medium, or low is assigned to Group B
carcinogens. Hazard rankings are one level higher (high, high, or
32
(A-41)
-------
medium) for Group A carcinogens. This increased concern is justified
because there is direct human evidence establishing that Group A
substances cause cancer. Hazard rankings are one level lower (medium,
low, or low) for Group C carcinogens. This reduced concern is justified
because the evidence implicating Group C substances either is
unreplicated or is of marginal biological or statistical significance.
Before settling on these hazard ranking assignments, alternative ranking
schemes were considered. Proposals that all Group A substances be ranked
high or that all Group C substances be ranked low were rejected because
the Agency believes strongly that potency, too, is Important in
describing a carcinogenic hazard. Similarly, a proposal to base hazard
rankings on potency alone was rejected because the Agency believes that
the weight of evidence must be considered as well. It is the Agency's
judgment that the hazard scheme finally selected gives proper
consideration to both weight of evidence and potency.
For substances placed in weight of evidence groups D or E, primary
criteria other than potential carcinogenicity must be used to assign an
adjusted RQ.
3.3.1 Use of Chemical and Environmental Fate and Transformation Data
in Hazard Ranking of Metals and Their Salts
The chemical and environmental specification, oxidation state,
solubility, chemical and environmental fate and half-life, and
disproportionation reactions are important determinants of the toxicity
of inorganic compounds. Furthermore, toxicity data relevant to potential
carcinogenicity and other chronic effects are lacking for many of the
33
(A-42)
-------
metals and their salts. Therefore, in cases where toxicity data are not
available on a particular metal salt, and an evaluation of the above
parameters indicates its convertibility to the toxic (i.e., carcinogenic)
species under realistic human exposure conditions, then an appropriate
hazard ranking assignment will be performed based on this evidence.
3.3.2 Special Problems in Hazard Ranking of Chemicals Associated vith
Multimedia Exposure in Humans
Carcinogenic hazard ranking in the present study must take into account
the potential for multimedia exposure. Thus, all routes of human
exposure (oral, inhalation, and dermal) must be considered in the hazard
ranking scheme. The final hazard ranking is based on the route that
gives the highest potency factor.
34
(A-43)
-------
(A-44)
-------
4. SUMMARY
The Agency's Carcinogen Assessment Group (CAG) has developed a unique
method for ranking CERCLA hazardous substances for potential
carcinogenicity. This methodology is not a risk assessment and it does
not yield an absolute measure of harm. Rather, the methodology simply
represents a means of sorting potentially carcinogenic substances into
categories, vhich may then be equated to RQ levels.
The methodology for ranking potential carcinogens begins by reviewing all
information available in the scientific literature on each substance
identified as a potential carcinogen. This information is then evaluated
using a tvo-stage process. The first stage is a qualitative assessment
of the likelihood that a particular hazardous substance is a human
carcinogen. During this stage, the available data is evaluated using
EPA's weight of evidence classification system, developed in the
September 24, 1986 Guidelines for Carcinogen Risk Assessment (51 FR
33992). The second stage is a quantitative assessment designed to
estimate the relative strength of a hazardous substance to elicit a
carcinogenic response ("potency factor"). The quantitative stage allows
the Agency to rank potential carcinogens on a numerical scale. The
results of the qualitative and quantitative assessments are then combined
to arrive at a hazard ranking for each hazardous substance evaluated for
potential carcinogenicity.
There are two separate appendices to this methodology document. The
first is a summary table of the hazard ranking results. The second
35
(A-45)
-------
consists of all of the individual chemical profiles prepared to support
these results. The profiles are not attached but are available from
EPA's document room, LG, 401 M Street, S.V., Washington, D.C. 20460.
36
(A-46)
-------
5. REFERENCES
Cox, C.R. 1972. Regression Model and Life Tables. J. Roy. Stat. Soc. B.
34: 187.
Crump, K.S., H.A. Guess and K.L. Deal. 1977. Confidence Intervals and
Tests of Hypotheses Concerning Dose-Response Relations Inferred for
Animal Carcinogenicity Data. Biometrics. 33: 437-451.
Doll, R. 1971. Veibull Distribution of Cancer: Implications for Models
of Carcinogenesis. J. Roy. Stat. Soc. A. 13: 133.
Dripps, R.D., J.E. Eckenhoff and L.D. Vanden, 1977. Introduction to
Anesthesia: The Principles of Safe Practice. 5th Ed. Philadelphia, PA:
V.B. Saunders Company, pp. 121-123.
FASEB (Federation of American Societies for Experimental Biology), 1974.
2nd Ed., Vol. III. Altman, P.L.; Dittman, D.S., eds. Bethesda, M.D.
Library of Congress No. 72-87738.
IARC (International Agency for Research on Cancer), 1979. IARC
Monographs on the Evaluation of the Carcinogenic Risk of Chemicals to
Humans. Chemicals and Industrial Processes Associated with Cancer in
Humans. IARC Monograph Supplement 1. Lyon, France, September 1979.
ICRP (International Commission on Radiological Protection), 1977.
Recommendation of the ICRP, Publication No. 26, adopted Jan. 17, 1977.
Oxford, United Kingdom, Pergamon Press.
U.S. Environmental Protection Agency, 1976. Interim Procedures and
Guidelines for Health Risk and Economic Impact Assessments of Suspected
Carcinogens. (40 FR 21402, May 25, 1976).
U.S. Environmental Protection Agency, 1980. Guidelines and Methodology
for the Preparation of Health Effects Assessment Chapters of the Ambient
Water Quality Criteria Documents. (45 FR 79347, November 28, 1980).
U.S. Environmental Protection Agency, 1986a. Technical Background
Document to Support Rulemaking Pursuant to CERCLA Section 102, Volume 3.
U.S. Environmental Protection Agency, 1986b. Guidelines for Carcinogen
Risk Assessment. (51 FR 33992-34003, September 24, 1986).
37
(A-47)
-------
(A-48)
-------
APPENDIX
HAZARD RANKING OF POTENTIAL CARCINOGENS
A-l
(A-49)
-------
(A-50)
-------
HAZARD RANKING OP POTENTIAL CARCIHOGENS

Substance
CASBN
Degree of
Humans
Evidence
Animals
Weigbt-
of-Evidence
Group
Potency
Factor
Potency
Group
Haza r
Hanki
1
Acatamide, H-fluocen-2-y1
00053963
Inadequate
Sufficient
B2
38.51
2
HED
2
Acrylonitrile
00107131
Limited
Sufficient
B1
2.28f
2
MED
3
Aldnn
00309002
Inadequate
Sufficient
B2
180 .00
1
HIGH
4
An i t r o 1 •
00061825
Inadequate
Sufficient
B2
3.07
2
MED
5
Arsenic
07440382
Sufficient
Inadequate
A
142.31
1
HIGH
6
Arsenic acid
01327522
07778394
d
No Data
d
d
1
HIGH
7
Arsenic disulfide
01303328
d
No Data
d
d
1
HIGH
8
Arsenic pentoxide
01303282
d
No Data
d
d
1
HIGH
9
Arsenic trichloride
07784341
d
No Data
d
d
1
HIGH
10
Arsenic trioxide
01327533
Sufficient
Inadequate
d
d
1
HIGH
11
Arsenic trisulfide
01303339
d
No Data
d
«9
d
1
HIGH
12
Cacodylic acid
00075605
No Data
Inadequate
Hone
None
„ b
None
1 3
Calciua arsenate
07778441
d
No Data
d
d
1
HIGH
14
Calciun arsenite
52740166
d
No Data
d
d
1
HIGH
15
Cupric acetoarsenite
12002038
d
Inadequate
d
d«9
d
1
HIGH
16
Dichlorophenylarsine
00696286
Ho Data
Inadequate
None
None
None^
17
Diethylarsine
00692422
Ho Data
Ho Data
i9
None
Hone
b
Hone
18
Lead arsenate
07784409
d
Inadequate
d
d
1
HIGH
19
Potassium arsenate
07784410
d
No Data
d
d
1
HIGH
20
Potassium arsenite
10124502
Sufficient
Inadequate
d
d
1
HIGH
21
Sodium arsenate
07631892
d
No Data
d
d
1
HIGH
22
Sodium arsenite
07784465
d
No Data
d
d
1
HIGH
23
Asbestos
01332214
Sufficient
Sufficient
A
P
P
HIGH
24
Auramnt
00492808
Inadequate
Sufficient
B2
0.96
3
LOW
25
Asaserine
00115026
Ho Data
Sufficient
B2
a
2
HED
26
Azi ndina
0015156 4
Ho Data
Sufficient
B2
344.89
1
HIGH
27
Benz(c)acridine
00225514
Inadequate
Limited
C
1765.38
1
MED
28
Banz(a)anthracene
00056553
Ho Data
Sufficient
B2
20.34
2
MED
29
Benzene
00071432
Sufficient
Limited
A
0.27f
3
MED
30
Benzidine and its salts
00092875
Sufficient
Sufficient
A
2220.11£
1
HIGH
31
Benzo(bl(luoranthene
00205992
Ho Data
Sufficient
B2
i
1
HIGH
32
Banzo(k}fluoranthene
00207089
Ho Data
Inadequate
D
None
None
b
Hone
33
Benzo(a)pyrene
00050328
Inadequate
Sufficient
B2
159.31
1
HIGH
-------
HAZARD RANKING OF POTENTIAL CARCINOGENS (Continued)

Substance
CASRN
Degree of
Humans
Evidence
Animals
Weight-
of-Bvidence
Group
Potency
Factor
Potency
Group
Uaia
Bank
34
Bensotnchloride
00098077
Linted
Sufficient
B1
112.26
1
HIGH
35
Benzyl chloride
00100447
Inadequate
Sufficient
B2
0.66
3
LOW
36
Beryllium
07440417
Inadequate
Sufficient
B2U
79.70u
2
MED
37
Beryllium chloride
07787475
No Data
No Data
u
19744.00U
1
HIGH
38
Beryllium fluoride
07787497
No Data
Sufficient
u
19744.00U
1
HIGH
39
Beryllium nitrate
13597994
No Data
No Data
u
19744 .00U
1
HIGH
40
alpha - BHC
00319846
No Data
Sufficient
B2
54 .52
2
HED
41
beta - BHC
00319857
No Data
Limited
C
1 .74
2
LOW
42
gamma - BHC (Lindane)
00058899
Inadequate
Sufficient/
Limited
B2/C™
1.83
2
MED
43
Bis(2-chloroethyl) ether
00111444
No Data
Sufficient
B2
13.29
2
MED
44
Bia(chloromethy1) ether
00542881
Sufficient
Sufficient
A
1384.6
1
HIGH
45
Bis(2-ethylhexyl ) phthalate
00117817
No Data
Sufficient
B2
0.015
3
LOW
46
Cadmium
07440439
Limited
Sufficient
B1
57.87k
2
MED
47
Cadmium acetate
00543908
k
No Data
k
k
2
MED
48
Cadmium bromide
07789426
k
No Data
k
k
2
MED
49
Cadmun chloride
10108642
k
Sufficient
k
k
2
MED
SO
Carbon tetrachloride
00056235
Inadequate
Sufficient
B2
59 .93
2
MED
51
Chlorambucil
00305033
Limited
Sufficient
B1
a
2
MED
52
Chlordane
00057749
Inadequate
Sufficient
B2
15.13
2
MED
53
Chlornaphaxine
00494031
Inadequate
Limited
C
a
2
LOW
54
Chloroform
00067663
Inadequate
Sufficient
B2
1.97
2
MED
55
Chloromethyl methyl ether (technical grade)
00107302
Sufficient
Inadequate
A
n
1
HIGH
56
4-Chloro-o-toluidine, hydrochloride
03165933
No Data
Sufficient
B2
0 .29
3
LOW
57
Chromium9
07440473
Sufficient
Sufficient
A*
388 .999
1
HIGH
58
Ammonium bichromate
07789095
9
No Data
9
9
1
HIGH
59
Ammonium chromate
07788989
9
No Data
9
9
1
HIGH
60
Calcium chromate
13765190
9
Sufficient
9
9
1
HIGH
61
Chronic acid
11115745
9
Inadequate
9
9
1
HIGH
£2
Lithium chromate
14307358
9
Ho Data
9
9
1
HIGH
63
Potassium bichromate
07778509
9
Inadequate
9
9
1
HIGH
64
Potassium chromate
07789006
9
Inadequate
9
9
1
HIGH
65
Sodium bichromate
10588019
9
Inadequate
9
9
1
HIGH
-------
HAZARD RANKING OF POTENTIAL CARCINOGENS (Continued)
Weight-
Degree of Evidence of-Bvidence Potency Potancy Hazard
Substanca	CASRN	Hunans	Aniaals	Group	Factor Group	Ranking
66
Sodiua cbroaate
07775113
9
Inadequate
9
9 1
HIGH
67
Strontlun chromate
07789062
9
Inadequate
9
9 1
HIGH
68
Chrysena
00218019
Inadequate
Sufficient
B2
a 2
20.58* 2
MED
69
Coke Oven Eaissions
H.A.
Sufficient
Sufficient
A
HIGH
70
Creosote
08001S89
Limited
Sufficient
Bl"
ab 1
HIGH
71
Cyclophosphamide
00050180
Limited
Sufficient
B1
17.53 2
NED
72
Daunonycin
20830813
Ro Data
Sufficient
B2
a 2
HED
73
DDD
00072548
Inadequate
Sufficient
B2
1.30 2
MED
74
DDE
00072559
Inadequate
Sufficient
B2
3.95 2
MED
75
DDT
00050293
Inadequate
Sufficient
B2
5.58 2
MED
76
Diallate
02303164
No Data
Limited
C
1.68 2
LOW
77
Diaminotoluene (nixed)
00095807
Ho Data
Sufficient
B2
2.94 2
MED
78
Dibenz[a,h| anthracene
00053703
Ho Data
Sufficient
B2
352.56 1
HIGH
79
1,2:7,8-Dibeniopyrene
00189559
Inadequate
Sufficient
B2
a 2
MED
80
1,2-Dibrono-3-chlo ropropane
00096128
No Data
Sufficient
B2
79.37 2
MED
81
3,3'-Dichlorobenzidine
00091941
No Data
Sufficient
B2
8.35 2
MED
82
1,2-Dichloroethane
00107062
Ho Data
Sufficient
B2
0.13 3
LOW
83
1,1-Dichloroethylene (Vinylidena chloride)
00075354
Ho Data
Limited
C
4.15 2
LOW
84
Dieldnn
00060571
Inadequate
Sufficient
B2
235.66 1
HIGH
85
1,2:3, 4-Diepoxybutanp
01464535
Ho Data
sufficient
B2
27.94 2
MED
86
1,2-Diethylhydrazine
01615801
Ho Data
Sufficient
B2
a 2
MED
87
Dlethylstilbestrol
00056531
Sufficient
Sufficient
A
4739.72 1
HIGH
88
Dihydrosafrole
00094586
No Data
Sufficient
B2
1.08 2
MED
89
3,3'-Dmethoxybenzidine
00119904
Ho Data
Sufficient
B2
0.05 3
LOW
90
Dimethyl sulfate
00077781
Inadequate
Sufficient
B2
a 2
MED
91
Diaethylaminoazobenzene
00060117
Ho Data
Sufficient
B2
105.00 1
HIGH
92
7,12-Diaethylbenz(a(anthracene
00057976
Ho Data
Sufficient
B2
191,138.13 1
HIGH
93
3,3'-Diaetby1benzidine
00119937
Ho Data
Limited
C
31.02 2
LOW
94
Diaethylcarbaaoyl chloride
00079447
Inadequate
Sufficient
B2
505.15 1
HIGH
95
1,1-Dimethylhydrazine
00057147
Ro Data
Sufficient
B2
13.44 2
MED
96
1,2-Dimethylhydrazine
00540738
Ho Data
Sufficient
B2
B2"3
5353.70 1
3.82e3 2
HIGH
97
Dimtrotoluene (mixed)
25321146
Ho Data
Sufficient
MED
-------
HAZARD RANKING OF POTENTIAL CARCINOGENS (Continued)
Weight-
Degree of Evidence of-Evidence Potency Potency Hazard
Substance	CASRN	Humans	Animals	Group	Factor Group	Ranking
98
2 , 4-Dinitrotoluene
00121142
No Data
Sufficient
B2
3.82 2
HED
99
2,6-Dinitrotoluene
00606202
No Data
Limited
C
a 2
LOW
100
1,4-Dioxane
00123911
Inadequate
Sufficient
B2
0.034 3
LOW
101
1,2-Diphenylhydrazine
00122667
No Data
Sufficient
B1
4.57 2
HED
102
Epichlorohydrin
00106898
Inadequate
Sufficient
82
0.37 3
LOW
103
Ethyl carbamate (urathana)
OOOS1796
No Data
Sufficient
B2
0.64 3
LOW
104
Ethyl 4 , 4'-dichlorobenxilate
00510156
Inadequate
Sufficient
B2
1.79 2
NED
105
Ethylene dibrom.de
00106934
Inadequate
Sufficient
B2
390.00 1
HIGH
106
Ethylene oxide
00075218
Limited/
Sufficient
B1/B2™
1.46 2
MED
Inadequate
107
Ethylenethiourea
00096457
No
Data
Sufficient
B2
1.30 2
HED
108
Ethyl methanesulfonate
00062500
No
Data
Sufficient
B2
292.80 1
HIGH
109
Formaldehyde
00050000
Inadequate
sufficient
B2
20.66 2
HED
110
Glycidylaldehyde
00765344
No
Data
Sufficient
B2
2.90 2
HED
111
Heptachlor
00076448
Inadequa te
Sufficient
B2
117.00 1
HIGH
112
Heptachlor epoxide
01024573
No
Data
Sufficient
B2
289.93 1
HIGH
113
Hexachlorobensene
00118741
No
Data
Sufficient
B2
11.75 2
HED
114
Hexachlorobutadiene
00087683
No
Da t a
Limited
C
0.59 3
LOW
115
Hexachloroethane
00067721
No
Data
Limited
C
0.08 3
LOW
116
Hydrazine
00302012
Inadequate
Sufficient
B2
107.16 1
HIGH
117
Indeno(l,2,3-cd)pyrene
00193395
No
Data
Limited
C
a 2
LOW
118
Isosafrole
00120581
Ho
Data
Sufficient
B2
0.54 3
LOW
119
Eepone
00143500
No
Data
Sufficient
B2
47.95 2
HED
120
Lasloca rpine
00303344
No
Data
Sufficient
B2
37.66 2
HED
121
Lead acetate
00301042
Ho
Data
Sufficient
B2
7.09 2
HED
122
Lead phosphate
07446277
Ho
Data
Sufficient
B2*
a 2
HED
123
Lead subacetate
01335326
No
Data
Sufficient
B2
0.17 3
LOW
124
Melphalan
00148823
Limited
Sufficient
Bl'2
810.37 1
HIGH
125
Methyl chloride
00074873
No
Data
Limited
C
0.050 2
LOW
126
3-Hethylcholanthrene
00056495
No
Data
Sufficient
B2
21.56 2
HED
127
4,4 '-Methy1eneb13(2-chloroaniline)
00101144
Inadequate
Sufficient
B2
1.22 2
HED
128
Methyl iodide
00074884
Ho
Data
Limited
C
a 2
LOW
-------
HAZARD BANKING OP POTENTIAL CAECINOGENS (Continued)
129
130
131
132
133
134
135
136
137
138
139
140
141
142
> 143
l!n 144
Ul
^ 14S
14 6
147
148
149
150
151
152
153
154
155
156
157
158
159
160
161
Weight—
Degree of Evidence of-Evidence Potency Potency Hazard
Substance	CAS&N	Humans	Aniuls	Group	Factor Group	Hanking
H—Hethy1-N'-nit ro-H-nitrosoquanidine
00070257
Inadequate
Sufficient
B2
55.76 2
NED
Metbylthiouracil
00056042
Inadequate
Sufficient
B2
28.57 2
NED
Nitoaycin c
00050077
No Data
Sufficient
B2
a 2
NED
1-Haphthylaaine
00134327
Inadequate
Inadequate
D
Hone None
„ b
Rone
2-Naphthylaaine
00091596
Sufficient
Sufficient
A
5.OS 2
HIGH
Nickel
07440020
Sufficient
Liaited
A
8.00 2
HIGH
Nickel aaaoniua sulfate
15699180
No Data
No Data
¦ 7
87 *7
LOW
Nickel carbonyl
13463393
Inadequate
Sufficient
B2
a 2
NED
Nickel chloride
07718549
Inadequate
Inadequate
¦ 7
a 7 «7
LOW
Nickel cyanide
00S57197
Ho Data
Ho Data
¦ 7
a 7 s7
LOW
Nickel hydroxide
12054487
No Data
Liaited
C
«7 *7
LOW
Nickel nitrate
14216752
No Data
No Data
*7
«7 «7
LOW
Nickel sulfate
07786814
No Data
Liaited
C
s7 s7
LOW
2-Nitropropano
00079469
Inadequate
Sufficient
B2
a 2
MED
H-Hitrosodi-n-butylaaine
00924163
No Data
Sufficient
B2
43.70 2
MED
N-Nitroaodiethanolaaine
01116547
No Data
sufficient
B2
ab 1
HIGH
N-Nitroaodiethylaaine
00055185
Ho Data
sufficient
B2
968.65 1
HIGH
H-Nitrosodiaethylaaine
00062759
Ho Data
Sufficient
B2
25.55 2
NED
H-Nitrosodi-n-propylaaine
00621647
No Data
Sufficient
B2
a 2
MED
H-Nitroao-N-ethylurea
00759739
Ho Data
sufficient
B2
8 . 74 2
MED
N-Nltroso-H-aethylurea
00684935
Ho Data
Sufficient
B2
10544.00 1
HIGH
N-Hitroso-N-aethylurethane
00615532
Inadequate
Sufficient
B2
ab 1
HIGH
H-Nitrosoaethylvinylanine
04549400
Ho Data
Sufficient
B2 *
a 2
MED
N-Nitrosopiperidine
00100754
Inadequate
Sufficient
B2
25.79 2
MED
H-Nitrosopyrrolidine
00930552
Inadequate
Sufficient
B2
279.13 1
HIGH
5-Nltro-o-toluidine
00099558
Inadequate
Liaited
C
0.17 3
LOW
Pentachloroethane
00076017
Ho Data
Liaited
C
0.66 3
LOW
Pentacbloromtrobenzene
00082688
Ho Data
Liaited
c
1.42Z1° 2
LOW
Pentachlorophenol
00087865
Inadequate
No Data
D
Hone Hone
„ b
None
Phenacetin
00062442
Inadequate
Sufficient
B2
O.OB 3
LOW
Polychlorinated biphenyls (PCBs)
01336363
Inadequate
Sufficient
B2
50.47' 2
MED
Aroclor 1016
12674112
Inadequate
No Data
t
t 2
MED
Aroclor 1221
11104282
Inadequate
No Data
t
t 2
MED
-------
HAZARD RANKING OP POTENTIAL CARCINOGENS (Continued)

Substance
CASRN
Degree of
Huoans
Evidence
Animals
Weight-
of-Bvidence
Group
Potency
Pacto r
Potency
Group
Hazard
Ranking
162
Aroclor 1232
11141165
Inadequate
Ho Data
t
t
2
MED
163
Aroclor 1242
53469219
Inadequate
Ho Data
t
t
2
MED
164
Aroclor 1248
12672296
Inadequate
Ho Data
t
t
2
MED
16 S
Aroclor 1254
11097691
Inadequate
Sufficient
B2
t
2
MED
166
Aroclor 1260
11096825
Inadequate
Sufficient
B2
50.47
2
MED
167
1,3-Propane sultone
01120714
No Data
Suff icient
B2
34 .83
2
MED
168
1, 2-Propylenimine
00075558
No Data
Sufficient
B2
4 .64
2
MED
169
Saccharin
00081072
Inadequate
Lmi ted
C
0 . 0064
3
LOW
170
Saf role
00094597
No Data
Sufficient
B2
0 . 20
3
LOW
171
Seleniua sulfide
07488564
Inadequate
Sufficient
B2
0.93
3
LOW
172
Streptosotocin
18883664
No Data
Sufficient
B2
109.08
1
HIGH
173
2 , 3,7,8-Totrachlo rodibenzo-p-dloxin (TCDD)
01746016
Inadequate
Sufficient
B2
659,000
1
HIGH
174
1,1,1,2-Tetrachloroetbane
00630206
Inadequate
Sufficient
B2
0 .83
3
LOW
175
1,1,2,2-Tet rachloroethano
00079345
Inadequate
Lmi ted
C
1 .66
2
LOW
176
Tot rachlorootbylene
00127184
Inadequate
Sufficient
B2
0.31
3
LOW
177
Thioacetamide
00062555
Inadequate
Suff icient
B2
24 .76
2
MED
178
Thiourea
00062566
No Data
Sufficient
B2
1 .05
2
MED
179
o-Toluidine
00095534
Inadequate
Sufficient
B2
0 .069
3
LOW
180
p-Toluidine
00106490
Ho Data
Sufficient
B2
0.94
3
LOW
181
o-Toluidine hydrochloride
00636215
Inadequate
Sufficient
B2
0 .069
3
LOW
182
Toxaphene
08001352
Inadequate
Sufficient
B2
9.79
2
MED
183
1,1,2-Trichloroethane
00079005
No Data
Lmited
C
0 . 36
3
LOW
184
Tricbloroethylene
00079016
Inadequate
Sufficient
B2
0 . 070
3
LOW
185
Tnchlorophenol (mixed)
25167822
Inadequate
Sufficient
B2»4
O.OB*4
3
LOW
186
2,4, 5-Trichlorophenol
00095954
Inadequate
Inadequate
D
Hone
Hone
Noneb
187
2,4,6-Tnchlorophenol
00088062
Ho Data
Sufficient
B2
0 .08
3
LOW
188
Tris(2,3-dibromopropyl) phosphate
00126727
Ho Data
Sufficient
B2
9.76
2
MED
189
Trypan blue
00072571
Ho Data
Sufficient
B2
5.01
2
MED
190
Uracil Bustard
00066751
Ho Data
Sufficient
B2
a
2
MED
191
Vinyl chloride
00075014
Sufficient
Sufficient
A
0.14
3
MED
-------
FOOTNOTES
GBBBBAL FOOTHOTBS
a Data available act inadequate for calculating a potency factor and no quantitative inferences can be made. Hence, the
substance is assigned to Potency Group 2, the aid-range potency group.
ab The bioassay used to calculate the potency factor suggest that the substance aay be highly carcinogenic (i.e., all
treated aniaals got tumors and therefore there is no basis for calculating a specific EDjg dose). Hence, the
substance is assigned to Potency Group 1.
b Ho RQ can be assigned based on potential carcinogenicity. Other primary criteria nust be used for assigning HQs.
f Potency factor estimate is derived from human epidemiology data.
m When the weight of evidence is expressed as a range, for example, B2/C, the hasard ranking is based on the higher
weight-of-evidence group.
s This particular compound is not classified due to the inadequate nature or nonexistence of data. However, there is a
potential of its being converted into a carcinogenic form when released into the environaent. For reportable quantity
ranking purposes it should be considered as having a weight of evidence siailar to that of the known carcinogenic form.
CHEMICAL-SPECinC FOOTHOTBS
d Arsenic—The weight of evidence for the carcinogenicity of inorganic arsenic coapounds is based on positive hunan
studies in which exposure was by either water or air. The weight of evidence is group A. The exact species of
inorganic arsenic that is directly carcinogenic to humans is not known, but it is assumed that since arsenic is
chemically convertible among the chemical species both in vitro and in vivo, that all inorganic species of arsenic are
.	of equal concern. The potency factor is the same as that given for "arsenic" (potency factor = 142.31). Arsenic
*1*	trionde and potassium orsenite are classified as having sufficient human evidence because human studies that
ui	specifically identify those compounds have been conducted and show sufficient evidence of causal association.
—i
Chromium—Grouping is based on weight of evidence for chroaate production workers and animal data which indicate that
the inhalation of hexavalent chroaiua is carcinogenic. The potency estimate is based on epidemiological data for the
inhalation of hexavalent chromium by chromate workers (potency factor = 388.99).
i Benso(b)fluoranthene—Calculated, using the potency factor estimate for benso ( a ) py rene as a reference.
k Cadmium weight of evidence and potency are based on epidemiology data for cadaiua workers exposed to cadmium oxide
and/or cadmium fume. Although huaan data for cadmium salts are lacking, due to the responsiveness of aniaals to
soluble cadmium compounds, especially cadmium chloride, the weight of evidence for cadaiua acetate, bromide and
chloride are considered to be the same as those cadmium compounds to which workers are exposed.
n Chloromethyl methyl ether (CMHBI—Technical grade chloromethyl methyl ether is contaminated with 1% - 8%
bis(chloromethy1)ether which is a known human carcinogen. Hence the human evidence for this compound and the hasard
ranking is based on the evidence for bis(chloromethyl)ether.
Asbestos—A potency factor estimate for asbestos is inappropriate here because the carcinogenic potential of asbestos
is related to specific fiber shapes, sixes, and atmospheric concentrations. Air concentrations are usually measured
either as a number of fibers or mass. However, no direct relationship exists between air, fib^r/ml (75 microns)
concentrations (by the phase contrast light microscope method) and mass concentrations in mg/m (determined by
electron microscopy). The relationship depends on the type of environment sample, the type of asbestos in the air,
and the size of the fibers. As a delibrate policy choice, asbestos is assigned a "HIGH* hasard ranking, as are most
group "A" substances.
-------
FOOTNOTES
GBSEBAL FOOTBOTBS (Cont.)
t PCBs—The Aroclora ita mixtures of polychlorin>tad biphenyls (PCBs). The manufacturing process for commercial PCB
products, sucta as the Aroclora, yields products composed of a mixture of 20-60 different PCB compounds. Individual
lots of Aroclors of the same average cblorine content may differ greatly in both their components and amount of each
component. Only Aroclors 1254 and 1260 have bean tested for carcinogenic potential and both produce a positive
response. Therefore, for the purpose of HQ hazard ranking, all Aroclors are considered to have carcinogenic potential
similar to Aroclor 1254, and Arocolor 1260.
u Beryllium—Every soluble beryllium compound that has been tested, including beryllium sulfate, fluoride, oxide,
phosphate, as well as beryl ore, sine beryllium silicate, and beryllium metal have been shown to be carcinogenic. It
is therefore considered highly likely that all soluble forms of beryllium are carcinogenic in animals. The potency
factor for all soluble forms of beryllium is based on beryllium sulfate exposure in rats. It is believed that these
forms of beryllium would pose a similar hazard to humans. The potency factor for beryllium metal is based on human
occupational exposure to much less soluble forms of beryllium, mostly beryllium oxides.
v BenzolaIpyrene—This compound is generally found in the environment as part of a complex mixture of polycyclic aromatic
hydrocarbons. Benco(aIpyrene has been found to be carcinogenic in animals and thus its presence in the mixtures
usually indicates the presence of a known animal carcinogen. Many mixtures containing benso(a)pyrene have also been
causally related to human cancer, e.g., soots, tars, coke oven emissions, cigarette smoke. Therefore, benzo(a )pyrene
should be treated as a human carcinogen.
x	creosote—There are no adequate studies of workers exposed to creosote wood preservatives. It has been demonstrated
*—s	that chimney sweeps exposed to tha creosote from the burning of wood or coal have an elevated risk of cancer. In
"j*	addition, creosote, including creosote wood preservative, contains many of the compounds in other polycyclic aromatic
in	hydrocarbon mixtures such as roofing tar pitch and coke oven emissions that have been found to be carcinogenic.
00
y	Lead phosphate—The animal evidence is based in part on consistent findings for other inorganic lead salts.
z N-Nitrosomethy1vinylamine—Bo control data for animal studies exists. However, based on more than one study and
structure-activity relationship with other nitrosamines, the weight of evidence is considered to be sufficient.
z2 Helphalan—The "limited" designation given to the human evidence for carcinogenicity is based only upon three
independent series of cases of multiple myelomas that were treated with melphalan. The case studies represent meager
evidence of the carcinogenicity of melphalan and hence the evidence is less than "limited" but greater than
"inadequate."
z3 Dimtrotoluene—In the absence of analytical data, it should be considered that the mixture contains 2,4-dinitrotoluene
which is a potential human carcinogen. Therefore, for hazard ranking purposes, the mixture should be considered as
hazardous as 2,4-dinitrotoluene.
z4 Trichlorophenol—In the absence of analytical data, it should be considered that the mixture contains
2,4,6-tricblorophenol which is a potential human carcinogen. Therefore, for hazard ranking purposes, the mixture
should be considered as hazardous as 2 ,4 , 6-trichlorophenol.
-------
FOOTNOTES
GEBEBJU. FOOTHOTBS (Cont.)
z7 Nickel—The latest Health Assessment Document on Nickel (CAG Sept., 198S Draft Final) states that the nickel Ion (Ni+2)
could be the ultimate carcinogenic Corn of nickal. Although this is unproven, it is considered prudent to Bake this
assumption for covalent nickal ((oris that generate Bi + 2) and nickel salts. Proven carcinogenic forms of nickel are
nickel refinery dust and nickal subsulfide (both in man) and nickel carbonyl (demonstrated in test animals). The
former two substances are in weight-of-evidence group A, while the latter substance is in weight-of-evidence group B2.
The salts of nickel show soma carcinogenic activity (see HAD, pp. 206-208). The testing of these nickel salts is
inconclusive for assessment of cancer at this time due to limitations of the data base on these nickel salts, but since
there is soma cancer activity it is recommended by the CAG that the hazard ranking under CEBCLA be reported as 'LOW."
This "LOW* hasard ranking reflects the current data base on the nickel salts.
z9 Organic arsenic compounds are considered to be chemically different from the inorganic arsenic compounds such that they
are assessed for carcinogenicity separately from the inorganic arsenic compounds. There are no data (weight-of-
evidence group O) implicating organic arsenic compounds so that the carcinogenicity is indeterminate at this time.
zlO Pentachloronitrobenxene - The potency estimate is for technical grade pentachloronitrobeniene, which contains the
probable human carcinogen hexachlorobensene.
NOTE: The gaps in the letters assigned to the footnotes in this table exist so that consistency with the numbers assigned
to the footnotes in the summary table in OHEA-C-073 (Appendix A in "Technical Background Document to Support
Rulemaking Pursuant to CEBCLA Section 102, Volume 3 (Proposed Rulemaking)," March 1985), is maintained.
-------
Appendix B
EVALUATION OF THE POTENTIAL CARCINOGENICITY OF
CHLOROFORM
IN SUPPORT OF REPORTABLE QUANTITY ADJUSTMENTS
PURSUANT TO CERCLA SECTION 102
B-l
-------
B-2
-------
Evaluation of the Potential Carcinogenicity of
Chloroform
(67-66-3)
In Support of Reportable Quantity Adjustments
Pursuant to CERCLA Section 102
Prepared by:
Carcinogen Assessment Group
Office of Health and Environmental Assessment, ORO
U.S. Environmental Protection Agency
Vashington, O.C. 20460
June 9, 1986
(B-3)
-------
DISCLAIMER
This document is a preliminary draft. It has not been formally released
by the U.S. Environmental Protection Agency and should not, at this
stager be construed to represent Agency policy. It is being circulated
for comments on its technical merit and policy implications.
ii
(B-4)
-------
PREFACE
This report summarizes and evaluates information on the potential
carcinogenicity of chloroform, as part of the methodology used to adjust
the statutory RQ of this CERCLA hazardous substance. Pertinent
epidemiologic and toxicologic data vere obtained through on-line searches
and from hard-copy sources. On-line searches vere extended as far back as
the data bases vould allov. Retrieval of historical data was accomplished
through searches of hard-copy sources and bibliographies of relevant
publications. Every attempt has been made to rely upon primary
publications as opposed to data summaries or-abstracts contained in
secondary sources such as monographs, surveys, review articles, criteria
documents, etc. The on-line data bases that vere searched included
CHEMLINE (National Library of Medicine (NLM)), RTECS (NLM), Toxicology
Data Bank (NLM), TOXLINE (NLM), CANCERLINE (NLM), and Chemical Abstracts
(DIALOG Information Services). Unpublished data vas not used in this
evaluation. This report draws largely on information supplied by the
Syracuse Research Corporation in document number SRC-TR-83-539.
The purpose of ranking hazardous substances based on potential
carcinogenicity is to provide part of the technical background for the
Emergency Response Division in the Office of Emergency and Remedial
Response to adjust Reportable Quantities (RQs) under Section 102 of the
Comprehensive Environmental Response, Compensation, and Liability Act of
1980 (CERCLA).
iii
( B — 5 )
-------
ABSTRACT
Chloroform is a probable human carcinogen, classified as veight-of-
evidence Group B2 under EPA's Proposed Guidelines for Carcinogen Risk
Assessment (U.S. EPA, 1984). Evidence on potential carcinogenicity from
animal studies is "Sufficient," and the evidence from human studies is
"Inadequate."
The potency factor (F) for chloroform is estimated to be 1.97
(ng/kg/day)~* placing it in potency group 2 according to the CAG's
methodology for evaluating potential carcinogens (U.S. EPA, 1986).
Combining the veight-of-evidence group and the potency group, chloroform
is assigned a "MEDIUM" hazard ranking for the purposes of RQ adjustment.
iv
(B — 6)
-------
TABLE OF CONTENTS
Page
1.0	WEIGHT OF EVIDENCE	1-1
1.1	ANIMAL STUDIES	1-1
1.2	HUMAN STUDIES	1-2
1.3	VEIGHT-OF-EVTDENCE ASSIGNMENT 	 		1-3
2.0 POTENCY	2-1
3.0 HAZARD RANKING	3-1
4.0 REFERENCES	4-1
APPENDIX A: SUMMARY OF SIGNIFICANT HUMAN AND/OR ANIMAL STUDIES
APPENDIX B: REPORT ON CARCINOGENESIS BIOASSAY OF CHLOROFORM
TABLES
Table 2-1. DERIVATION OF POTENCY FACTOR (F)	2-2
V
(B-7)
-------
(B-8)
-------
1.0 WEIGHT OF EVIDENCE
1.1 ANIMAL STUDIES
Chloroform produced a statistically significant increase in the incidence
of hepatocellular carcinomas in male and female B6C3F1 mice, and renal
epithelial tumors (combined malignant and benign) in male Osborne-Mendel
rats, when administered at maximally and one-half maximally tolerated
doses by gavage for 78 weeks (NCI, 1976). A carcinogenic response of
similarly treated female Osborne-Mendel rats was not apparent in this
study.
A statistically significant increase in the incidence of renal epithelial
tumors (malignant and benign) was found in another study in which male
ICI mice were treated with chloroform in either toothpaste or arachis oil
by gavage for 80 weeks (Roe et al., 1979). Similar treatment with
chloroform in toothpaste did not, however, produce a carcinogenic
response in female ICI mice, or in male mice of the CBA, C57BL or CF/1
strains. A carcinogenic response was not observed in male or female
Sprague-Dawley rats given chloroform in toothpaste by gavage for 80
weeks, but early mortality was high in both control and treated groups
(Palmer et al., 1979). Gavage doses of chloroform in toothpaste did not
elicit a carcinogenic effect in male or female dogs treated for 7 years
(Heyvood et al., 1979). It should be noted that the results of
preliminary toxicity tests and the carcinogenicity studies indicate that
the doses of chloroform in toothpaste used in the above studies
approached maximally tolerated levels.
Hepatomas were found in NLC mice that were given 0.1 ml doses of 40X
chloroform twice weekly by stomach tube for an unspecified period of time
1-1
(B-9)
-------
(Rudali, 1967), and in female strain A mice that vere given doses of
chloroform by gavage once every 4 days for a total of 30 doses at levels
(0.6 to 2.4 rng/kg) that produced liver necrosis (Eschenbrenner and
Miller, 1945). These studies are deficient, hovever, because small
numbers of animals vere examined, the duration of the studies vas shorter
than the lifetime of the animals, and control data for NLC mice vere not
reported. Chloroform vas ineffective at maximally tolerated and lover
doses in a strain A mouse pulmonary tumor bioassay (i.p. injection)
(Theiss et al., 1977), and did not elicit a carcinogenic response in mice
(CS7 x DBA2 - Fl) that vere given single or 8 daily subcutaneous doses of
200 ug during the first veek of life and observed for their lifetime (Roe
et al., 1968).
1.2 HUMAN STUDIES
Epidemiologic cancer studies dealing vith chloroform per se have not been
conducted, but ecological and case control studies (Alavanja et al.,
1978; Cantor et al., 1978; Brenniman et al., 1978; Hogan et al., 1979;
Struba, 1979; Gottlieb et al., 1981; Young et al., 1981) consistently
support the association of an increased risk of bladder, colon, and
rectal cancer vith exposure to trihalomethanes in chlorinated drinking
vater (U.S. EPA, 1982). This association is statistically significant
but veak, vith risk ratios generally ranging from 1.1-2.0; a risk ratio
as high as 3.6 vas reported for cancer of the colon by Young et al.
(1981). Although the risk ratios derived in these studies could be
explained by the confounding effects of uncontrolled influences such as
smoking, diet, air pollution, occupation, and lifestyle, the consistent
finding of a statistically significant excess of cancer across several
independent and diverse study populations supports the finding of a
definite risk (U.S. EPA, 1982).
Chloroform appears to be the predominant contaminant in chlorinated
drinking vater, and may, therefore, be a contributing factor in the
etiology of the cancers identified above (U.S. EPA, 1982). Many other
1-2
(B-10)
-------
organic contaminants as well as trihalomethanes are present in
chlorinated drinking vater, but they are generally found at much lower
concentrations than chloroform. Although there is a suggestion of an
increased risk of cancer of the bladder, rectum, and large intestine from
exposure to chlorinated drinking vater, it should be emphasized that the
presence of these other substances (some of vhich are carcinogenic) make
it impossible to implicate chloroform directly as the cause. If an
increased risk of cancer at these sites from exposure to chloroform truly
exists, it could also possibly be due to an intermediate in the natural
synthesis of chloroform (U.S. EPA, 1982).
1.3 VEIGHT-OF-EVIDENCE ASSESSMENT
Oral exposure to chloroform has induced hepatocellular carcinomas in male
and female B6C3F1 mice, renal epithelial tumors in male Osborne-Mendel
rats and male ICI mice, and hepatomas in NLC and female strain A mice.
This evidence is sufficient for concluding that chloroform is
carcinogenic in experimental animals. There appears to be an increased
risk of cancer of the bladder, rectum, and large intestine from exposure
to chlorinated drinking vater, and by inference to chloroform, but the
EPA classification of human evidence vould be inadequate at best. Thus,
using the EPA Proposed Guidelines for Carcinogen Risk Assessment (U.S.
EPA, 1984) for evaluating the overall veight of evidence to humans,
chloroform is most appropriately classified as a Group B2 chemical.
Appendix A contains summaries o£ the significant human and/or animal
studies cited in this reviev.
1-3
(B-ll)
-------
2.0 POTENCY
The potency factor (F) for chloroform is estimated to be 1.97
(mg/kg/day)"*, placing it in potency group 2 under CAG's methodology for
evaluating potential carcinogens (U.S. EPA, 1986). Table 2-1 contains
data from the selected study used to derive the potency factor for
chloroform. Appendix B contains the complete primary reference for this
study.
2-1
(B-12)
-------
Table 2-1. Derivation of Potency Factor(F)
Agent: Chlorofora
t— NJ
U>
REFERENCE:
EXPOSURE BOUTE:
SPECIES:
STRAIN:
SEX :
VEHICLE OR PHYSICAL STATE:
BODY WEIGHT:
DURATION OF TREATMENT:
DURATION OF STUDY:
LIFESPAN OF ANIMAL:
TARGET ORGAN:
TUMOR TYPE:
EXPERIMENTAL DOSES/
EXPOSURE.
TRANSFORMED DOSES:*1
(mg/kg/day):
TUMOR INCIDENCE:
ANIMAL POTENCY:
(lag/kg/day)
HUMAN POTENCY:
< mg/kg/day >
NCI, 1976
oral (gavaga)
aics
B6C3F1
F
corn oil
0.03 kg*
516 days
644 - 6S1 days
710 daysb
liver
hepatocellular carcinoma
477 ng/kg/dayC
28a
39/4 1
0	104
1	.97
238 mg/kg/day
143
16/45
0 ng/kg/day
0
0/20
. Repoited
D ,	i
Assumed
c
^ Exposuies wore 5 days/week. Duration of study was assuned to be 647 days.
To derive the transforaed dose fron the experiaentai dose data: experimental dose (ng/kg/day) x 5 (treatment days/week)/ 1
(days/week) * duration of treatment (days)/ duration of study (days).
* See Appendix B for a reproduction of the report on this study.
-------
(B-14)
-------
3.0 HAZARD RANKING
Based on the veight-of-evidence Group B2 for chloroform, and the potency
factor (F) of 1.97 (mg/kg/day)"*, chloroform receives a hazard ranking
of "MEDIUM."
3-1
(B — 15)
-------
(B-16)
-------
4.0 REFERENCES
Alavanja, M., I. Goldstein and M. Susser, 1978. A Case Control Study of
Gastrointestinal and Urinary Tract Cancer Mortality and Drinking Water
Chlorination. pp. 395-409 in Water Chlorination: Environmental Impact
and Health Effects, Vol. 2. R.L. Jolley, 3. Gorchey, D.H. Hamilton, Jr.,
Eds. Ann Arbor Science Publishers, Ann Arbor, MI. (Reviewed in U.S.
EPA, 1982).
Brenniman, G.R., J. Vasilomanolakis-Lagos, J. Amsel, T. Namekata and A.H.
Wolff, 1978. Case-Control Study of Cancer Deaths in Illinois Communities
Served by Chlorinated or Nonchlorinated Water, pp. 1043-1057 in R.J.
Jolley, H. Gorchen, and H. Hamilton, Jr., Eds. Water Chlorination:
Environmental Impact and Health Effects. Ann Arbor Science Publishers,
Ann Arbor, MI. (Reviewed in U.S. EPA, 1982).
Cantor, K.P., R. Hoover, T.J. Mason and L.J. McCabe, 1978. Association
of Cancer Mortality with Halomethanes in Drinking Water. J. Natl. Cancer
Inst. 61(4): 979-985. (Reviewed in U.S.EPA, 1982).
Eschenbrenner, A.B. and E. Miller, 1945. Induction of Hepatomas in Mice
by Repeated Oral Administration of Chloroform with Observations on Sex
Differences. J. Natl. Cancer Inst. 5: 251-255.
Gottlieb, M.S., J.K. Carr and D.T. Morriss, 1981. Cancer and Drinking
Water in Louisiana: Colon and Rectum. Int. Epidemiol. 10(2): 117-125.
(Reviewed in U.S. EPA, 1982).
Heywood, R., R.J. Sortwell, P.R.B. Noel, et al., 1979. Safety Evaluation
of Toothpaste Containing Chloroform. III. Long-Term Study in Beagle
Dogs. J. Environ. Pathol. Toxicol. 2: 835-851.
4-1
(B-17)
-------
Hogan, M.D., P. Chi, D.G. Hoel and T.J. Mitchell, 1979. Association
Between Chloroform Levels in Finished Drinking Water Supplies and Various
Site-Specific Cancer Mortality Rates. J. Environ. Pathol. Toxicol. 2:
873-887. (Reviewed in U.S. EPA, 1982).
NCI (National Cancer Institute), 1976. Report on Carcinogenesis Bioassay
of Chloroform. Natl. Tech. Inf. Serv. PB-264018. Springfield, VA.
Palmer, A.K., A.E. Street, F.J.C. Roe, A.N. Worden and N.J. Van Abbe,
1979. Safety Evaluation of Toothpaste Containing Chloroform. II. Long-
Term Studies in Rats. J. Environ. Pathol. Toxicol. 2: 821-833.
Roe, F.J.C., R.L. Carter and B.C.V. Mitchley, 1968. Test of Chloroform
and 8-Hydroxyquinoline for Carcinogenicity Using Newborn Mice. Br. Emp.
Cancer Campgn. 46: 13. (Reviewed in U.S. EPA, 1982).
Roe, F.J.C., A.K. Palmer, A.N. Worden and N.J. Van Abbe, 1979. Safety
Evaluation of Toothpaste Containing Chloroform. I. Long-Term Studies in
Mice. J. Environ. Pathol. Toxicol. 3: 799-819.
Rudali, G., 1967. Oncogenic Activity of Some Halogenated Hydrocarbons
Used in Therapeutics. UICC Monogt. Ser. 7: 138-143. (Reviewed in U.S.
EPA, 1982).
Struba, R.J., 1979. Cancer and Drinking Water Quality. Ph.D. Thesis.
University of North Carolina, Chapel Hill, NC. 156p. Available from
University Microfilms International, Ann Arbor, MI, Publ. No. 8022514.
(Reviewed in U.S. EPA, 1982).
Theiss, J.C., G.C. Stoner, N.B. Shimkin and E.fC. Weisburger, 1977. Test
for Carcinogenicity of Organic Contaminants of United States Drinking
Waters by Pulmonary Tumor Response in Strain A Mice. Cancer Res. 37:
2717-2720.
4-2
(B-18)
-------
U.S. EPA (Environmental Protection Agency), 1982. Evaluation of the
Carcinogenicity of Chloroform. Chapter Prepared for Health Effects
Assessment Document for Chloroform. Available from NTIS, NTIS No.
PB86-134.
U.S. EPA (Environmental Protection Agency), 1984. Proposed Guidelines
for Carcinogen Assessment, 49 FR 46294-46307, November 23, 1984.
U.S. EPA (Environmental Protection Agency), 1986. Methodology for
Evaluating Reportable Quantity Adjustments Pursuant to CERCLA Section
102, 0HEA-C-073, June, 1986.
7oung, T.B., M.S. Kanarek and A.A. Tslatis, 1981. Epidemiology Study of
Drinking Vater Chlorination and Wisconsin Female Cancer Mortality. J.
Natl. Cancer Inst. 67(6): 1191-1198. (Reviewed in U.S. EPA, 1982).
4-3
(B-19)
-------
(B — 2 0)
-------
APPENDIX A
(B — 2 1)
-------
Tabla I. Aniaal
l(«nLt Chiorofora
Reference: Haywood et •!., 1919
Dom	Duration	Duration	Purity	Vehicle or	Tuaor
Exposure Spec lea/	or	of	of	of	Pltyalaal	Tuaor	Incldenae
Bouto Strain	Sat Exposure	Troalaent	Study	Coa pound	State Target Organ	Type	(P value)
ca
I
to
to
dogs/
beagle
dogs/
beagle
0, 1%, or )0 316 weeks	39S-399 weeks pharmaceutical tooth-
ag/kg/day*	paatg
base In
gelatin
oapsule
0, 15. or 30 376 weeks	395-399 weeks pharoaceutlaal tootli-
ag/kg/day	pasta
base In
gelatin
capsule
Ho treatment related neoplaatlo e(Teats
observed In either oo« when caapared with
vehlole, untreated, or alternative non-
ohlororora toothpaste eontrola*
Mo treatment related neoplaatlo effeota
observed In either sea when oaapared with
vehicle, untreated, or alternative non-
chlorofora toothpaate controls
quatm or ewidehck
Strengths of Study: The coa pound was edalnlatered by • natural route. Histopathologic*! examinations were perforaed on principal
tissues and organs) electron alorosooplo exaalnattons were perfqraed on liver and kidney sect Ions fro a 2 untreated
controls and 3 dogs froa the 30 ag/kg/day group. Hange-rindlng testing suggested that a aailaally tolerated dose
was approaahed.
weakness of Study:
Relatively small nuabera of dogs were treated, and It Is not certain If 7 years was long enough for carcinogenicity
testing with reaped to the Ilfespsn (13-14 years).
Overall Adequacy:
Adequate
a Exposures were 6 days/week
|)
Sane formulation that uas used In the Hoe et al., 1979 study.
(J
6 dogs/sea were Initially tested In treated and control groups, with the eiceptlon of the vehlole controls (16 dogs/sex).
-------
Table ft. Inlaal
Agents Chlorofora
Referenoei NCI, 1976
Eipoeure
Haute
Speolea/
Strain
Sei
Do 30
or
Eiposure
Duration
of
Treataent
Duration
of
Study
Purity
of
Coa pound
Vetilole or
ftiyal6al
State
Target Organ
Tuaor
Type
Tuaor
Inoldenoe
(P value)
8
i-a to/
Oaborne-
Hendal
M
180 ig/kg/day,
5 days/week
70 weeka
III weeka
981
corn oil
kidney
epithelial
tuaora
12/50®
(P.0.01*)°
to 8
1
N>
CO
rata/
Oaborne-
Hendel
H
90 ag/kg/day,
5 days/week
78 week*
III weeks
981
aom oil
kidney
epithelial
tuaora
*/50b
<(•=>0.266)°
N-/
8
rata/
Osborne-
Henilel
H
0 ag/kg/day
(aatohed
oontrola)
N*
III weeka
Nt
aorn oil
kidney
epithelial
tuaora
0/19
CP=0.002)
8
rata/
Oaborne-
Heiuiel
P
200 ng/kg/day0,
5 days/week
78 weeka
III weeka
981
corn oil
thyroid
t
tuaora
I0/H9
(P=0.121)
8
rata/
Oaborne-
Mendel
F
100 ag/kg/day*,
5 days/week
78 Neeka
III weeka
9BS
aorn oil
thyroid
tuaora'
B/*9
(PsO.216) *°
8
rata/
Oaborne-
Hendel
f
0 ag/kg/day
(aatohed
oontrolaI
Uk
III weeka
Mt
corn oil
thyroid
tuaora'
t/i9 A -
(PaO.057)
8
alee/
B6C3FI
M
277 ag/kg/day'1
5 days/week
78 ueeka
92-9) weeka
9B»
corn oil
liver
hepatocellular
earolnoaa
HI/US
(P<0.00l)°
8
nice/
I)6C]F 1
H
1)8 ag/kg/day'1
5 days/week
78 weeka
92-9) weeka
98 %
aorn oil
liver
hepatooellular
earolnoaa
18/50
-------
Table A. Inlul
teferencei MCI, 1976 (cant.)
Eiposure
Bouts
Speoles/
Strain
Sea
Dose
or
Eaposure
Ouratlon Duration
of of
Treataent Study
Purity
of
Caa pound
Vehicle or
physical
State
Target Organ
Tuaor
Type
Tuaor
Incidence
(P value)
s
alee/
B6C3FI
H
0 ag/kg/day
(aatched
controls)
NA
92-91 weeks
Ml
corn oil
liver
hepatocellular
carolnoaa
1/18
(P<0.00l)d
8
alee/
BfcCJFI
9
117 ag/kg/day*
5 days/week
78 weeks
92-9] weeks
981
corn oil
liver
hepatocellular
oarclnoaa
19/'1
(P<0.00l)°
8
alee/
B6CJFI
9
2)8 ag/kg/day8
5 days/week
71 weeks
92-9) weeks
98*
corn oil
liver
hepatocellular
carolnocM
36/»5
(P<0.00»)°
8
alee/
B6CJFI
9
0 ag/kg/day
(aatched
controls)
Mk
92-91 weeks
HI
corn oil
liver
hepatocellular
carolnoaa
0/20
(P<0.00Oa





QUALITY OP EVIDENCE




Strengths of Study:
The coa pound was adalnlstered via t natural route for a significant portion of the lifespan. Two dose levels
were caployed and ooaprehenslve histological eiaalnatlons were perforaed.

Weakness
or Study:
The nuaber of aatched vehicle controls was saall (20 anlaals/sea).




Overal 1
Adequacy:
Adequate







3 10 with tubular call adenocarclnooa and 2 with tubular call adenoaa.
b
2 with tubular cell adenocarolnoaa and 2 with tubular cell adanoaa.
c Fischer Eiact teat, coapared to aatched controls (C*0, I9B2).
J Arattage teat Tor linear trend In proportion (NCI, 1976).
£
Tloe-uelghted average doses reflecting Initial doae levels of 250 and 125 ag/kg/day that were lowered to 1B0 and 90 ag/kg/day after
22 weeks In the high and low doae feaale groups, respectively.
f
Includes folllcular-cell and C-cell thyroid tumors.
a
Incidences of total thyroid tuoors not considered significant since tba two epithelial cell types (footnote f) have distinctly different
embryonic origins and physiologic functions.
11 Tlne-welgted average doae reflecting Initial dose levels of 200 and 120 ag/kg/day (oales) and 400 and 200 ag/kg/day (fesaales)f these
doses were Increased after 18 weeks to ]Q0 and 150 ng//kg/day (aales) and to 500 and 250 ag/kg/day for females.
Incidences of total thyroid timors la statistically olgnlftcant (P<0.05) nhen cor pared with colony controls.
NA = Hoi applicable
-------
Tabic ft. tnlul
l|«ntt Chloroform
Roferenoot Palmer ot al., 1979
Eapoaure
Boule
Speolea/
Strain
Sea
Do so
or
Eapoaure
Duration
of
Treatment
Duration
or
Study
Purity
or
Coo pound
Vehicle or
Phyaloal
State
Tumor
Target Organ Type
Tumor
Incidence
-
paate
mammary gland total tumors
Malignant
21/50
(Pa0.09%)
6/5° .
(Ps0.056)a
8
rata/
SPF
Sprague-
Dauley
r
0 ng/kg/day
(vehicle
control)
Nt
95 weeks
N*
toothg
pasta
mammary gland total tumors
aallgnant
16/50
1/50
-------
Trtlt A. Inlul
IthnnMi falMr et •!., 1979 (coot.)
Dom	puretIon	duration	Purity	Veblole or	Tiaeor
wpmurt Spwln/	or	of	of	of	Miysioal	TUaor	Inoideno*
Route Strain Sea lapoauro	IrulpMi	Study	Coa pound	Stat* Target Organ	Typo	CP value)
qua»n of
Strengths of Studyi
W Uealutesa of Studyi
to
ON
Overall Adequacy!
Consents!
Tbe coapound waa adalnlatared by a natural rpule for • algnlflaant portion of the llfaapan (aeoond study)*
Ulatopathologloal aaaalnatlona were apparently ooaprehenaive.
Intercurrent inspiratory dlaaaaa naoaaaltatad preaature toralnation of the firat audy. Tba aeoood study eaployod
only ona doaa level, and wa characterised by blgb portallty In botb treated.and oeotrol anlaala.
Adequate
Tbe results of this study are not indloatlve of aaaaary gland oarnlnogenloltyi Inoreaaed lnoldenoea of liver
or kidney tuaora were not observed. TreatBent-related non-neoplaatlo toilolty waa observed in botb studies.
It la not elear bow eblorofora absorption in toothpeate would ooapare with that in rats si***) ohlorofora in
a liquid vehlole.
Expoa
6 daya/wcck.
Saae forauletloa that was ueed In tbe Roe et al., 1979 atudy.
cCaes^rlan-derlved specific pethogen—free Spragua-Dauley rata.
d
Significance of Fischer Exact test ss reported by CAfi (I9U).
HA " Not applicable
-------
Tabla I. Inlul
l(«ati Cblarofora
gererenoei |m tt it., 1979
Exposure
tout*
Speoioa/
Strain
3oa
Doh
or
Sipoaura
Duration
of
Trailaani
Duration
of
Study
Purity
of
Coa pound
Vabiola or
Pbyalaal
State
Target Organ
Yuaor
Typa
Tuaor
Inoldanoa
(P value)
EXTERlMm
I









•
aloe/
ICI
H
60 ai/kf/day
60 waaka*
96 waaka
pbaraaoautloal
tootbr
paata
kidney
apltballal
8/52°
«
•lot/
ICI
M
IT .ag/kg/day
00 waaka*
96 weaka
pharaaoeutloal
tootbc,
paata
kidney
epithelial
0/S2
s
aloe/
ICI
M
0 »g/kg/day
(vabiola
control)
MA
96 waaka
R1
tootbr
paata
kidney
apitbalial
0/10H
experiment
2









s
1
alaa/
ICI
M
60 ag/kg/day
60 waaka*
104 waaka
pharaaooutloal
tootbr
paata
kidney
apltballal
9/19°
1
' g
aloe/
ICI
H
0 ag/kg/day
(vabiola
controlI
Nt
10% waaka i
Ml
tootbr
paata
kidney
apltballal
6/217
EXFEBIHEHT
1









a
aloe/
ICI
M
60 ag/kg/day
60 waaka*
97-99 waaka
pharaaooutlaal
tootbr
paata
kidney
apltballal
5/*7°
s
¦too/
ICI
N
0 ag/kg/day
(vabiola
control)
M
97-99 waaka
N*
tOOUlr
paata
kidney
apltballal
l/»9
-------
Table A. Animal
Reference: Roe et al., 1979 (cont.)
Dose	Duration	Duration	Purity	Vehicle or	Tumor
Exposure Species/	or	of	of	or	Physical	Tumor	Incidence
Route Strain	Sex Exposure	Treatment	Study	Compound	State Target Organ	Type	(P value)
g	mice/
1CI
g	aloe/
^ ICI
w
I
t-o
oo
*—'
Strengths of Study:
Weakness or Study:
Overall Adequacy:
Comments:
60 mg/lcg/day 80 weeks*
97-99 weeks pharmaceutical arachls
oil
0 ng/kg/day
(vehicle
control)
NA
97-99 weeks
QUALITY OF EVIDENCE
NA
arachls
oil
kidney
kidney
epithelial
epithelial
The compound was administered For a significant portion of the lifespan by a natural route. Hultiple experiments
with one strain of mouse and single experiments with three other strains of mice were performed (see Comments).
Comprehensive histological examinations were performed in Experiment 1; the brain, lungs, liver, and kidneys were
examined in Experiments 2 and 3* High-purity chloroform (I.e., without haloalkane or phosgene contaminants) was
used.
Female C57BL, CBA, and CF/1 mice (Experiment 3, see Comments) were not tested.
Adequate
Experiment 1
Experiment 2
Experiment 3
Increased Incidences of kidney tumors were not observed in similarly treated female ICI mice.
Female ICI mice were not tested. Treatment with eucalyptol or peppermint oil alone (footnote b) at
several dose levels did not elicit kidney tumor development, indicating that this effect Is due to
chloroform.
Increased Incidences of kidney tumors were not observed in similarly treated male mice of strains
C57B1., CBA, or CF/1. The higher Incidence of kidney tumors in the ICI mice treated with chloroform in
arachls oil than in those treated with chloroform in toothpaste may reflect a difference in
absorption of chloroform.
12/H8C
1/50
6 days/week treatment
b
Toothpaste formulation Included peppermint oil and eucalyptol (essential oils) as flavor components.
Includes malignant (e.g., hypernephroma) and benign (e.g., adenoma) tumors.
HA > Not applicable
-------
APPENDIX B
(B-29)
-------
NOTICE
THIS DOCUMENT HAS BEEN .REPRODUCED
FROM THE BEST COPY FURNISHED US BY
THE SPONSORING AGENCY. ALTHOUGH IT
IS RECOGNIZED THAT CERTAIN PORTIONS ARE
ILLEGIBLE, IT IS BEING RELEASED
IN THE INTEREST OF MAKING AVAILABLE
AS MUCH INFORMATION AS POSSIBLE.
0274B
(B-30)
-------
U.S. DEPARTMENT OF COMMERCE
National Technical Information Service
P&-264 018
Report on Carcinogenesis
Bioassay of Chloroform
National Cancer Inst, Bethesda, Md Carcinogenesis Program
1 Mar 76	•
i
\
(B-31)
-------
( B — 3 2)
-------
REPORT ON CARCINOGENESIS BIOASSAY OF
CHLOROFORM
Carcinogenesis Program. Olvlslcn of Cancer Cause and Prevention
National Career Institute
March 1, 1976
Sumvuft A ca/tdnegzncAiA bica&Aay otf US? gjutdz zhloA.c$c*m i«u cenductcd
uiing QAboAnz-MzndzZ AeutA and 86C3Fj inicz. CiIoao(c-vi> v.-u adniniitfAzd
QJtslZtj (by gavage] in com ail to 50 animal* oj eac/i itx Aid cut ti:e do&z
ZzvzU (ivz timti, pen wzzk &c*. 73 ux.zki. Rata wc ita,*Zzd on 'at at
51 day* orf agz and 4ac.ti(iccd rtrf-tc* 111 wdu. The dae LzvcZi i<*K ma£u
xi'.i 90 and ISO mg/kg body wtight. Feiralz -tats tfzn.it \tan.tzd at 125 and
250 irg/kg, tzduczd to 90 and HO mg/kg a{tzn. 22 tczdis, icith an aveutge
tzvel orf 100 and 200 mg/kg {a*, tiie. itudy. A dzcMa&z -ui iw.vival >ze.Cz
and iczigkt gain tau zvidznt fa*. all tAzatld gxcup4. TV. moAt significant
obi equation (P « .0016] ua& kiebizy zpitkzLuzt tumcAi in rralz tali
incidoxczi 0$: 01 in cantAati, IS in the. lave doAZ and l*% in thz lu'gh
doAZ QACtipA. AIthaugh an inCAZOAZ in tkytoid tim&Li Kai alic cbitAvtd in
txzAtzd icmJLz na£A, HuLa binding y.ua not con&idsAtd biaicgiazVLtj iigni^icmU.
*(tce it'SAC itaAtzd on tui-t at 35 daxjb and iacti(iczd ajtz>t 92-C •' 'recti.
Initial dosz Izvzti wtte 100 and ZOO mg/kg $o* mlej end 'SO and 1C0 mg/L-g
ic" ioKite. mice.. Thziz IzvzJU u.*ete incnta&zd afttz/i IS c.'ec&i *c 15C,'500 and
?50/S00 mg/kg f.upzztbizlij bo that thz average icvtLi ivt'.i t3S rj'.d 77? ra/Kt\
railA and III and 477 mg/kg {andLz nice.. Su.wiva.i' TrtfCJ a»:r cxiai t
flairs i'ZAZ ccnps.xs.bic. {cm • c.i ¦>'••
. ¦ * r" 'aU m) C*	iv wi. ff r ' '.j'> wi * J%? i ^'>u . . . ¦ * * v! *	>	I
r.c '	dsiK. .zi '.?r':z~.cd	c.' rz'^.cd *. c ; ..i..	. --
'l • i.	Cu	i	:d i- •.r-C:,iv
' ¦"	'"a".* ¦c'i: >¦ " .
(B-33)
-------
!~2r~v ^ " i ^ •* ^
f-i <-Z~ Oio
r\ C--CI'!S:':!!S ;i"'-3S-Y "f
CHL0?ry
Carc'';wesis g*:?*ai. rivislor ;f Cancer Cause »*i Preventlcfi
National Cancer Institute
March J, 1976
COKT'13'.'V-S: Th1j resort r-esents a syncrsis of results of a carcinogenesis iioassay
con:„cte: :y tre Carclnoqe' Sloassay and Program Resources Sranch, Carcinogenesis
Prejras, Iiv1s1;n of Cancer Cause and Prevention, National Career Institute ('.CI),
Bet'ssda, ^ary'jid. This research was corcucted at the Hazleton Laboratories iwlca,
Ince-porated, ".'snna, VirgrMa, initially under direct contract to the ?CI are
currently »rCer a suiesntrtst to Tracor Jttco, Incorporated, Prime Contracter for the
NCI Carci'sger.esls Sioassay Progran.
The results of t*1i study *ere reviewed ard this report was prepared by Ors. P. Page'
and U. Sa'fiottl'. *'s. J. w. Chase' functioned as fxecutlve Secretary for the report
review, *-11e *s. P. *. Stefnour' was resrmsible for the consolidation anc technical
presarat':.*: o< the re:srt. The exejrlnental desigr, includlr^ dose levels we»!
deteflrf: ty t*e f:C! project officers, Ors. J. H. Weisburger'.2 and E. K. Weisburgerl;
prlrcipai investigators fcr the ce-.tract were CVs. ft. 8. Powers3, R. «. YcelkerJ,
U. i. 01|:rJ.4 a«d W. «.>»therfcolti3,5; chemical analysis was performed ty Tr. C. t.
Guytcwt-: tecfc*ics' sursrv-sor of i?»1^al treatments and experiments was f's. k,. J.
Petrovics^: the rax*5's?y »as sua^rvisw! ty Pr. 8 V. Yoelker; microscopic diariosn
was conc.ited iy Drs, :. -. senr.e', J. P. rerrell', and R. T. Kabem'anrJ, ard reviewed
by r.-s. C. ". Eirror.i and *. A. Swire'; data collection and data preparation crndon,
\\r~. ' «.
8	-	' ~~~~~'".", '?7» i.	'trev'.. Pcc**	* ."«•»% r	^
\
(B-34)
-------
TABLE Of COHTSMTS
Page
I. Introduction	 1
II.	Materials and Methods	 1
Oesign of Chronic Studies				1
Chemicals		6
Animals	.		6
Animal Maintenance	..		7
Clinical and Pathology Examinations		8
Data Recording and Statistical Analysis			9
III.	Results	 10
A.	Rats	 10
1.	Survival			 10
2.	Body Weights, Pood Conjunction and Clinical Signs		 10
3.	Pathology	 13
B.	K1ce	27
1.	Survival			 27
2.	Bedy Weights, Food Consumption and Clinical Signs	27
3.	Pathology					30
IV. Discussion	38
References	 44
Appendix Summary of Tumors Cbserveo in Rats	 45
Appendix r: Summary sf Tumors Observed in Mice	 55
(B-35)
-------

!
• . f 4f •.f
•izzn Car: moires is Bicassay of C^lorc'tr-
'¦.. "r' i *r • - - -
f arcr. 1, . r/c
4.
i. ^rcincgenesis Program, Division of Cancer Cats* a"d
P«-avor** r^ncpr Tnctlfnfo
8. t'erisrmini O-ji.ii.-c.ob Kryi.
Nasaris; Orgia<'*tii»n Saiam ind .Address
Cardr.crenesis Program
Qlvislor of Cancer Cause and Prevention
13* Type »r Repot k Period
Conrvo
Technical flecort
"ationa. Cancer Institute
Bethesc*, Maryland 20014
14.
1J. i^ipltaasstrr
li. Antticii

USP graie Chloroform was bloassayed using both sexes cf Osbcme-^endel rats ana
B5C3F1 "ice. Two dose levels were administered by oral cavage five times per
week for 78 weeks. A decrease in survival rate and weight gain was evident for
all treated groups. A significant increase in kidney aoithelial tumors was ob-
served in male rats. Highly significant increases ir lesatocellular carcincra
were observed in both sexes of mice, "odular hyperplasia of the liver was observed
in many low dose male mice which had not developed hepatocellular carcincna.
17. \
-------
I. INTRCOUCHQ1.':
Chloroform (CHClj), also known as trichloromethaie, 1s primarily used
(935} 1n the manufacture of fluorocarbons for refrigerants, prcrellarts,
and plastics. The remainder 1s used for many purposes includlrg
extracting and purifying antibiotics, as an Industrial solvent, in
preparation of dyes, drugs and pesticides, as a component of sere
toothpastes, cough medicines, liniments, salves. In photographic
processing and 1n Industrial drycleanlng (1). Chloroform was selected
for carcinogenesis bloassay as one agent in a study of halogenated
alkanes that occur 1n the general and occupational environment
of humans. Chloroform was included 1n this study because of its
chemical structure, use, and prior suspicion of carcinogenicity (2).
II. MATERIALS AHD METHODS:
Design of Chronic Studies - The experiment's bfc:.1c design consisted
of administering chloroform at two dose levels to groups of 5C animals
of each sex and spedes. Thus, 400 treated aniens divided Into S
groups were used. Treatment was by oral gavage 5 times per week for
78 weeks with sacrifice of surviving rats at 111 wee
-------
toxicity study 1n which chloroform was ailrinlstered for 6 weeks at
various ^ose levels fo11o»ed by an addltlcal 2 weeks of observotion.
The parameters evaluated In the toxicity study were mainly survival,
weight differences and clinical/necropsy ctservation.,.
The dose levels for male rats were 160 and 90 mg/kg throughout the
chronic study. For female rats, 1t was necessary to lower the doses
from starting levels of 250 and 125 mg/kg to 160 and 90 irg/kg after
22 weeks. The Initial dose levels for mice were 200 and 100 mg/kg
for males and 400 and 200 mg/kg for females. These were Increased
slightly after 18 weeks to 3C0/150 mg/kg for males and 5C0/250 mg/kg
for females since 1t was considered that the animals could tolerate
a higher dose. Actual doses, days an treatment at each.dose, "time
weighted average dose levels", and estimated average daily doses
for each g/oup are presented 1n Table I. The average doses ranged
from 36-90 milligrams for rats and 4-14 ellllgrams for mice.
Three types of cc.irols were used .n this study, "matched" controls,
"colony" controls and "positive" controls. The "matched" controls
were animals as nearly Identical to the chlorc'orm-treated animals
as possible. They were from the same scvrce, <<1th Identical ani—al
care, housed in sa.-e rcc and received i Hke cuantltv c* the ver-'cls,
^ • *
ccrr oil, as the treat3C jmrjij. lats »?re icsicrs'i :c	-ri
aatc^ed control orcups ? -ardcmzec! -'irer. s'jch t>i" cne w'lr-
CB-38)
-------
TaliIf I. Po'.aqe Schedule - Chlorcf"-:.
DOSE
miATMrnT
HHf uricHiro
td
I
OJ
VO
f r» ens
5|K
POSAGf
CROUP
nosf
LfVfL
(Ni/KG)
PCB100
(DAYS)
AVC. DOSC llVfl
(NRAO<
ftjl
(<«>
N
Low
mum
Final
90
546
90

H
High
Initial
Final
180
546
180

F
Low
Initial
Final
m
90
154
392
100

r
High
Initial
Final
250
180
154
392
200
Mice
(ueciri)
M
Low
Initial
Final
100
1:0
126
420
138

H
High
Initial
Final
200
300
126
420
277

F
Low
Initial
Final
200
250
126
420
238

F
High
Initial
Final
400
soo
126
420
477
fSTlKAUO AVf.
0051 /AN I J'At /PA V
IMP
SO
40
16
70
4
0
7
14
I. iii
1	- l>n-,c iiilmlnlstcrcd In corn oil 5 i/wcck
2	- 1 lac-welijlited average dose » l(dose * treatoent period In days)/ z(no. diys receiving each do*wj.
3	- Oascd upon average weight as presented In Figures 2 end 9.
-------
weight in each group was approximately t"? sare. The matched control
groups of rice were started on the vehic"^ treatment 1 week earlier
than the chloroform-treated mice but were otherwise comparable.
"Colony" control animals were of sane strain and source, and were
started on test within 3 months of the cfrloroform-trefted animals.
They were maintained in the same manner and received com oil as
described for the chloroform "matched" controls. The colony control
Included the chloroform-matched controls plus matched controls to
other chemicals that were tested simultaneously. The "matched"
controls consisted of 20 for each sex of each species, whereas the
colony controls consisted of 99 male and 98 female rats and T> male
and 80 female mice. £11 colony control *1ce were housed 1n the
same room whereas colony control rats were housed in two different
rooms.
"Positive" control animals were of sare strain and source, also
housed in the same way. Thpse, however, received » known carcinogen,
carbon tetrachloride, and were included as a control for the entire
series of halogenated chemicals on test. The purpose of the positive
control was to verify the sensTtiv'ty the test anirab to
carcinogenicity by ^a'o^enated crs-icT- a<*c to serve is a che:- on
procedures and tecnn-cves. "v>e emer--*"*..!'	f:- irs ca'.:n
tetracHirics test ..is essential"..' : vo :s c~'	'-jd\
(8-40)
-------
e.rcspi "at ^3 Josi le-.eU rf.ie- £7 and %}-i "/""Cv.cs. For ::lcny
jmJ CO. controls, only the 2.ita relatinc to total t^-ors, tr:';r
ijeciMc ".ajions of o:"Cfr- ;re prcscrtc; trr ar-\-.is	-:r.
co*-? arise-1 fiourss.
(B-4 1)
-------
C^ricals - The material te-ted was 'JSP z'-.is ;Morofor- purchased
from Aldrlch Chemical Company, Inc., 9^C \est Sdlnt Paul Aver.ua,
Milwaukee, Wisconsin. USP grade chlorofrrm sh:u1d be at least 99.OX
chloroform and 0.5-1.OX ethyl alcohol. Ethyl aicohol 1s added by the
manufacturer as a stabilizer. The purity was checked by Hazleton
Laboratories America, Inc., using gas-Hcu1d chromatography (glc) with
flame Ionization detector and Infrared srectrcretry. Approximately 9£S
of the glc peak area was chloroform with ethyl alcohol accounting for
the remainder. Infrared spectrometry ard glc analysis at Intervals
during the bloassay Indicated no significant change in chemical
composition.
Chloroform was administered by oral gavace using corn oil as a
vehicle. Fresh solutions of chloroform in corn oil were prepared
weekly *n amounts sufficient to treat aV. anirals, sealed, and
refrigerated until use. The concentratlc.n of chloroform 1n corn
oil was 10X for rats and 2-5% for mice. The com oil was purchased
from a distributor, C. F. Sauer Corpany, 3ichr;nd, Virginia. Per
safety purposes, the test solutions were ralntalned cold to minimize
volatilization, and dosing was conducted under a hood.
Animals - Rats and i?1ce of both sexes, c::air5-i thrcugh contracts
of the Division of Cancer Treatrer.t, '.'CI, were used 1n trese tests.
7Ke rats were 0s^orr9-"ende! strain gercr Bitte'1? "arcr-il
Instituze, Colucb'js, C*n, anc t^e * 'te ::r2r-\ hyi.--ds	.
(B-42)
-------
from Crirles 5,.\.er Breeding Labcatcnes, Ire., W''-nnc,:cn, ":ssi:":se
Upon receipt, animal* were quarantined for 7-10 days, Ceterrlned ::
be free fror observable disease or parasites and randomly assigns:
to the experlrental groups.
Animal Maintenance - All animals were housed In te"%erature and f-nidi
controlled rooms. Incoming air was filtered through 2-inch thick
disposable fiberglass filters at a rate providing 12 changes of ":am
air per hour. Lighting was provided on a 12-hour per day cycle. 3ats
were Individually housed in suspended steel, w1re-«nesh cages and -ice
1n polypropylene cages. Ten mice were housed 1n each cage. Clea*
cages with bedding (San1-chips, manufactured by Shjrfire) were provide
twice each week for mice, while the rat cages were changed weekly.
food containers were changed and sterilized once * week for the *frst
10 weeks and once a month thereafter.' Sterile glass water bottles
were provided three times a week fer mice and twice a week for rats.
Food (Wayne Laboratory 81ox Peal) and water were consuned ad 11turn.
Racks were rotated in the room and positlo: .d at random. The rats
were housed in a room 1n which 1,1,2,2-tetrachloroethane, 3-chk-o-
propene, ethylene dlbromide and carbon tetrachloride t»ere also test
Chloroforr-treated mice were housed In the saire room as mice rtrciivir-
1,1,2,2-titrachlorcethane, 3-chloroprorenp, chl:-cpicrin, ', 1-c-:wlo-:
stha-e, t-'ch'oroethylene, sulfo'ene, lodc'om:, etf'y'a-e - *" n t c - * ic,
7
(B-43)
-------
retpylchlcrcfon", !, l,2-*rlchloroi"tnane, tetrach teroethylene,
hexachlorcethane, carton disulfide, trichlcrofluorometha.ie, carbon
tetrachloride, ethylene dihronde and dlbrorachloropropane. Vehicle
matched control groups were housed in the sare roan as their respective
treated groups.
Clinical/Pathelcqy Eaarinations - All animals were Inspected twice
dally. Body weights and food consumption were recorded weekly for
the first 10 weeks ani i*orthly thereafter. Animals apoearlng
moribund w.ien exarlred were sacrificed and irmediately necropsled.
In the chronic study a recropsy was performed on each animal reyardless
of whether it died, -as sacrificed early or survived to term''nation.
Anlrals »-ere ares'het»*ed, exsanguinated and immediately necropsled.
The following tissues were taken fror sacrificed animals and where
possible from these fourd dead: brain, pituitary, adrenal, thyroid,
parathyroid, trachea, escpnagus, thymus, salivary gland, lymph nodes
(mesenteric and cervical!. heart, nasal passages, lung, spleen, liver,
kidney, storach, vail intestine, large, intestine, pancreas, urinary
oladder, prcstate or uterus, testis with epididymis, seminal vesicles,
ovary, skin with r-jmry gland, njscle, nerve, bone, bone marrow, ari
tissue masses.
Tissues were ortrorved " iT". buffered for-alin, srbedded in parjff4-,
;e:t"C6d.	¦„ t*" y<-.it ?> y' ir ar.d °os"", i1"1 ex.""ned
(B-44)
-------
microscopically. Because sane tissues (especial'y sirall organs) were
lost during the gross autopsy, and the histologic preparation process,
the denominator used for a particular organ, tissue or lesion in
Appendixes A and B, does not necessarily ecual the number of animals
placed on experiment 1n each group.
The pathologic T1nd1ngs of the Experimental Pathology Laboratories and
Hazleton Laboratories America, Inc., were reviewed by pathologists
at Tracor Jitco, Inc., and the National Cancer.Institute, with special
attention given to hepatic and renal lesions.
Data Recording and Statistical Analysis - Pertinent data on this
experiment have been recorded 1n an automatic data processing system,
the Carcinogenesis Bloassay Oata System (3). The data eleirents
Include descriptive information on the chenical, animals, experimental
design, clinical observations, survival, animal we
-------
for linear trend in proportions (6a). This analysis determines if
the slope of a dose-recponss plot 1s statistically different fron
zero (P < .05), assuming a linear trend. If the associated statistic
which detects departure from linear trend was significant, then the
Fisher Exact Test (6b) was used to compare controls to each dose
level. A correction for simultaneous comparison of controls was
made using the Bonfarronl Inequality (7). Thus, a corrected
P value < .05 was also deemed significant.
III. RESULTS:
A. Bats
1.	Survival » As illustrated 1n Figure 1, the survival rate
for both male and female rats treated with chloroform was
considerably less than for controls. While decreased survival
appeared dote-related, the difference between high and low
dose females became substantial only after 70 wee
-------
110
riijiiv I. Survival Curves for Rats(Ch)oroforo)



CI (MIM
O iOmum
A MCMDOM
I
\\
-4 V-

A ,A ---
A
A
L
'A..),
1
it
4'
A
I*- ~.
4I4MII Ml»
r	[
«9	t0
IMI 0»iiVST MIMI
-------
I
I
J „
I
"f
° s
2 S
a a
3 a
o	o
a o	a o « o
o 4 A a 4 a
A
-o- o r 0
' O
a o a o
o. a
a
a ¦ a
« •
0 ft a
A I
a
A
°S
AS
39et

0 carom
MAtC RATS
t«M OKttUO* nUfSIS
o a o 0 0 o a
A A
A A
alo °
BO
a 0	. a o o o
a	o o ° 9
n	9 ° '	-
Q	oo
O	A A a
d> a	a a .
a	a a
a
-------
during the first 10 weeks of the study in all treatrent croucs,
1 ov« to moderate numbers of animals develcoed a hunched appearance,
urine stains on the Icwer abdomen, redness of the eyelids and
apparent weight loss. Ourlng the remainder of the first year
of the study, a large percentage of the test animals were hunched
and wheezing, and the urine staining continued. The first
palpable nodule was noted at week 50 in the lew dose male group.
Ourlng the second year of the study, the incidence of che above
described clinical signs gradually increased in-all test groups.
In addition, rough halrccat, stains on halrcoat, localized alopecia
on extremities or trunk, sores on the body, head, and particularly
on the tall were also noted. Both matched and colony control
groups began to exhibit similar signs in the 70th week and
by 110 weeks clinical observations were essentially the same
1n the test and control groups. Several palpable nodules and
tissue masses were noted in all groups during the Tatter part
of the second year. Occasionally, the small nodules palpated
at one observ&ti-n period were not palpable al a later tine or
were replaced by snail sores. These nodules were apparently
small subcutaneous abscesses whicl* dralred and Sealed.
3. 3ethology - Of the 20Q tmatecf ar.d <-atck*d csrtrc' rats
entt-ed into study, fcur ..gre lest (*.«c "¦ss'm intf %o
(B-49)
-------
dutolvidd). Histc?2tholoq1c findings cf tt,-;rs »rs t»t:ul2:=d
In Apcsndix A. Frcs an examination of Appendix A, differer:es
1n turor incidences between chloroform-treated and controls were
apparent only for kidney tumor; In males and females and t.Kyro1
-------
in.UJ. Analysis o f Total Tuwort inJ Specific Liver. Kidney and Thyroid Tumors - Ban (*"t''ro*ln
MALE	FEMALE
.		nnmEon	 —coimwre	 -¦
INCATi'tfNT :
COLONY
MATCHED
LOU
HIGH
COLON*
KATCHEO
low
hich
IttUt runor*8eai . j
„
9/19
24/50
20/50

12/20
24/<9
24/48
Anirul*/Anlmil*2

47*
48X
40X
..
60X
49X
50X
i> Viluc3 4

.2347#
	
—
	
.2733#
..
..
1 In- to Tuccr (weeks)

95
70
42
--
108
73
49
tl.,; jtocellular ^
1/99
0/19
0/50
1/50
0/98
0/20
0/49
0/48
f _r; ir.CT.l/Anlaali
11
0*
OX
2X
OX
OX
74
OX
1 Yoi e1 4
.3)66
.1497
—
—
1.000
1.000
--
—
T i • to luror (weeks)
9/
—
--
. Ill
—
—
--
--
: uno) rpithellal Turcors/
0/99
0/19
4/50
12/50
0/98
0/20
0/49
2/48
r 1 t jli?
0*
01
8*
24X
o* ,
W A
OX
41

.COCO*
.0016*


.0592*
.W626
..

I ;-i- (3 Tuner (weeks)
--
—
102
80
--
--
--
10?
11..r >11J iL'iOrs/
8/99
4/19
• 3/49
4/48
1/38
1/19
ert
10/46

fX
21t •
6X
81
IX
5X
i t
?2X
P Vjli »
.48741
. 1 l?3l


.0000*
.GS74
. -\
• A
Ii . In lu" ..r (t.LC'ks)
101
103
111
III
110
lie
73
49
' at Ttraln.il
261
371
iex
?8«
51X
75X
45X
29*
; :li Ifui1 (III hi ck||
1 - fidl of chlerofurn 1r -irn oil adnlnlsUred by gavage five timet per week.
- b.;»od on antral* whoje tissues were examined front a specific organ.
1 - frt tail ? value froa Arallige test for linear trend In proportions, unless otherwise stated.
I In--, tt li^liclitn of f(r*t tumor (at death).
!> - rjia .V( -rti-re treat linear trend (for departure statistic; P < .05). Fisher Exact Test Is used comparing
cml', to a do*e level. Bcnferronl (7) correction for simultaneous comparison of controls Is Included.
¦> - v 11ui* i..., ..ted using enact test (Co*. Analysis of Blnjry Data) as the number of tutors Is too snail
I0i Arritj.*o method.
* ¦ f t1111 leal ly significant (P < .05).
.¦ - ? vji-c Qivcn in direction of negative trend.
-------
as shOrtfi by the data presented in Table III. Primary eiithc'lal
tfors v-ere observed In the kidneys and renal pelvis of 18 r»ts.
all chlcroform-treated. Of these, 16 were 1n males: 12 in the
high dose group and 4 at the low dose. The other two tumors were
1n the high dose female group. The observation of two Sidney
tirsors In the high dose female group was noc significant when
corpared with colony controls (P » -0592). No primary epithelial
tumor of the kidney was round In any of the *9 low dose females
or 197 controls. Figure 3 Illustrates the percentages o* animals
with these tumors according to experimental group. In addition
to the purely ep1thp*1a1 tumors, four malignant mixed turors.
and three hamartomas were also observed. However, these were fourd
1n both the colony control and treated groups, and not considered
treatment related.
Two male rats had more than ri.e primary renal tumor: a low Cose
male with both a malignant mixed turor ana a tubular cell adenoma
1n the left kidney, and a high dose male with both a tubular cell
carcinoma *.id a tubular cell adenoma 1n the right kidney.
Of the T3 tumors of renal tubular-cell epithelium cbsenad ir.
12 of tfe 50 high dose male rats, ten were carcinoids irl tr^se
adenomas: two of the carcinomas were fourt:.to Mve -et'stasi:;-?.
Tv*c carc'nc^as md two adenomas of r?ral tubular er'tiie' •*?. r-re
i-onc r'C low nosf1 i"le	Cr.s c:irc-"c-: jf
1*
(B-52)
-------
100
90
BO-
IO
60
Ml
40
10
20
10
0-
MALE BATS
FEMALE RATS
(I2/S0I 24*
(4/S0I I*
10/99) 0»
10/lfll 0*
<2/4014X
(0/981 0%
(0/20J OK (0/49) OX
LOlOfJV UATCHEO LOW	HIGH	COLONY HATCHED LOW HIGH
CONTROL CONTROL DOSE	DOSE	CONTROL CONTROL OOSE DOSE
Qure 3. Comparison of Incidences of Epithelial Tumors of Kidney and Renal Pelvis
(Chloroform)
-------
tubula* epithelium and one squamous cell carcinoma arising frcm
renal :e1v1c transitional epithelium we^e observed among the 48
high d;se female rats. The tubular-cell adenocarcinoma widely
metasti«ized.
MtcroscaMcally, the appearance of these epithelial tumors varied
from circumscribed, well-differentiated tubular-cell adenomas to
highly oleomorphic, pcorly differentiated carcinomas which had
invaded and metastasized. The cells in adenomas were relatively
unlforr and polygonal, with abundant eosinophilic cytoplasm.
Nuclei were central or basal 1n location, with minimal atyoia
and little increase 1n mitotic index (Fiaure 4). Most carcinomas
were vary large and replaced a considerable portion of the renal
parenchyma. They were poorly circumscribed and infiltrated
surrounding normal tissues. These were of irregular sheets, nests,
and tutular arrangements of cells with varying degrees of anaplasia
and increaseo nuclear/cytoplasmic ratio (Figures S and 6). The
nests cf cells were often surrounded by a del leal* fibrovascular
stroma, and central necrosis was sometimes present 1n the more
anaplastic neoplasms. Rarely, a papillary glandular pattern was
observe:.
T!"3 ss. 5" rsnal tumors that were not surely c-?
strc^a!, and fatty tlssje cc-ipcrent;. Fc." of " esc
{'.'.j	Sose mile rf* arc two ".n naie	con"-: .'s}
* C
(B-54)
-------
histologically malignant and were classified as malignant mixed
tumors (Figure 7). The other three tumors (one each from low dose
male, high dose male and male colony controls) appeared benign and
were classified as hamartomas. In addition to these seven tumors,
one hemangioma also occurred In the kidney of a high dose female
rat.
Criteria for differentiating malignant from benign primary tumors
of the kidney, both purely epithelial and mixed types, included:
loss of normal cellular architecture; evidence of Invasion of
renal parenchyma, vessels, or adjacent tissues; cellular atypla
Including nuclear/cytoplasmic ratio; prominent nuc'ieoll;
numerous and/or abnormal mitotic figures; and abnormal size and
shape of neoplastic cells. Evidence of metastasis, although
observed 1n several tumors, was not a requirement for classification
of tumors as nalignant.
Malignant mlxet tumors a.id hamartomas have been seen in a low
spontaneous Incidence at several laboratories In aged 0^borne-Mendel
rats used on the Bloassay Program, occurring with equal frequency
1n control and test^ rats. In contrast, purely epithelial t-jmors cf
We renal tubules or renal pelvic transitional epithelium rarely
occur spontaneously in these Osbom«»-"endel rats.
!9
(B-55)
-------

r Irvire
(B-56)
-------
©9 * ;
p?
*
Q
n ¦• j*	
^•J'~	' SwK ir i»
"^r¥i. •*:, &vV •., ' «•*
$2
ricure s, Tuiuljr c®1! carcincra, kidney. 3ot, -*;h dcse -ale.
and «csin, "trC.
". "a'-'rra". -
-------
Follfcular cell and C-cell tumors of the thyroid gland were
observed 1n both control and test groups. Follicular eel!
adercmas appeared microscopically as well circumscribed, usually
single masses composed of enlarged follicles lined by hyperbaso-
philic follicular cells. The cells were Increased 1n number,
either by papillary infolding of simple cuboldal or columnar
epithelium into the follicular lumen, or stratification of follicular
cells surrounding the lumen. Oistinct compression of surrounding
norral thyroid parenchyma, usually with some evidence of fibrous
encaasulation, was present. Follicular architecture and cytology
within the mass differed markedly from that of the adjacent normal
thyroid parenchyma. Follicular cell lesions were classifed as
carcinoma based upon the presence of anaplasia and histologic
arrangement 1n disorderly nests and/or sheets. Areas with
papillary patterns were also often present. Fibrous stroma often
Intermingled with, but did not encapsulate the tumors. Some of
the carcinomas encompassed the entire thyrcld lobe, and the fibrous
Strega present made it impossible to recognize the normal thyroid
capsule.
C-cell lesions were classified as adenomas when the proliferating
C-caMs were present In ncdular rasses v.-hich widely separatee
thyrttd follicles ami distorted r.oml 'ollicuiar architecture.
In larger, rr«re discrc-*.2, nodulor 1iors, trie croii'oratir.c
(B-58)
-------
.-C5"s fc=rc :-;sent as interlacing bur-dies of e'cncitsa, ;:mr'
eel's. r»fan tr:s polyhedral to SDherlcal sf'ice ciar2::sr'.j*.ic
of normal C»cells. In the one rat 1n which the C-cell lessen
w*s classified as a carcinoma, microscopic evidence of capsular
Invasion and multiple pulmonary metastases was present.
The incidences of female rats with thyroid tumors was statistically
higher than controls at both dose levels (P ¦ .05) as was the
departure from linear trend when comparing treated with ttre eoleny
controls. In contrast, the Incidence 1n males was reversed (not
significant at P ¦ .05) with a higher percentage of controls with
thyroid tumors than chloroform-treated animals. The evaluation
of "total" thyroid tumors was not considered valid since two
epithelial cell types of the thyroid (follicular cell and C-ceil)
were observed, having distinctly different embryonic origins ar.i
physiologic functions. Based upon this and the variability of
observed spontaneous Incidence of these tumors in this rat strafn
and laboratory with opposite and Inconsistent effects in rales and
females, the thyroid differences were not considered of biological
significance. The incidences of these different cell types Is
presented In Table IV.
Tjfrle TV. 'fidci".? of T|
-------
Only tuo fepatocel1c1ar carcinomas were observed among all rats
In the study, one In a male colony control dying at 97 weeks,
and the other a high dose male rat that died at 111 weeks. Necslast'c
nodi^es occurred In the liver of 10/197 test rats (5.OS) and 2/197
colony control rat' (1**. Such nodules have recently been defined
morphologically and designated as neoplastic nodules (8). As such,
they have been categorized and coded as neoplasms when observed
In this study.
Table V shows a comparison of the survival of rats receiving
chloroform and the known carcinogen, carbon tetrachloride
with pooled colony controls at 90 and 110 weeks.
Table V. Comparison of Survival of Colony Control*. Cfclorofonn and
	Carbon Tetrachloride-Treated Bats	
AfllKAL ',-OUP
CHlOROFOSf
tcttto	75	rrr
KO. WfcEKS UCFKS

CARPOK TfTPiCHLORIPE
7TTTIE	71	TTC-
f.U. WEEKS WEEKS
Hales Controls 100 67 28
low Dose	SO 39 27
Hlgi. toM SO 27 14
100
so
so
67 26
34 14
34 7
Ftsales Co"trols ICO 75 SI
Lew Ooie	50 ?8 23
HlgK Dose SO	ZS IS
100
SO
50
75 51
38 20
21 14
1A
(B-60)
-------
T-s incierces of loth ~soatccellular carcinomas and neoplastic
ncc-jles in colony controls and in rats receiving ehlorcfom or
carbon tetrachloride are given in Table VI.
Tul« VI. Ineldenws of L'ver Turcrs • Colony Controls, Chloroforn and
	Carton T>tr»eh';"1ie - 'retted Pats		
ani»hi eocp
KfstrccrLtnjw
CARCirOHA
NEOPLASTIC
"OOl'LE

Ch^k^vr LnM
ecu
CNlC.'tFW
LLli
Kfc.*S Controls
1/W
1/99
0/99
0/99
Low Case
0/50
2/50
1/50
2/50
His" Cose
1/50
2/SO
2/50
1/SO
FTJfALES Cortrols
0/98
0/98
2/98
2/98
L5» Jose
0/4?
4/49
4/49
2/49
nose
0/«
1/49
3/48
3/49
Kumerccis other neoplasms, that often occur spontaneously in aged
laboratory rats, were observed in test and control grcuos without
significant differences 1n frequency. These included fibrous
blstlscytcmas of subcutls, hemangiomas and hemanglosarcomas
cf spleen and other crgans, pituitary adenomas, adrenal tumors,
and isTet cell turors of pancreas; hematopoietic tumors,
neserthjnal and ejithellal mammary tumors, endometrial stromal
calyps ard astrscytoras of the brain.
!n a;:fticr to :-nor«, numerous inflamnatory, degenerative,
I'd	Issuer.: ccitonly seen in aged rats recurred
-itr	tr.i1 freejency in treated arc c:-*.rol am.-i's.
(B-61)
-------
These Included pericholangitis and biliary hyperplasia, chronic
nephritis with tuiular dilatation and epithelial hyperplasia
of the renal pelvis, subacute to chronic prostatitis, and
atrophy of seminiferous epithelium of the testes.
Hon-neoplastic, possibly treatment-related lesions were observed
in the lungs, liver, urinary bladder, and spleen as described
1n the following paragraphs.
Although Inflammatory pulmonary lesions occurred in all groups
of control and test rats, there was a distinct difference in the
nature and stverity of the lesions between treated and control
groups. Control rats of both sexes had pulmonary lesions
characteristic of the Mycop 1 asma-associated chronic pneumonia
observed very conmonly 1n aged laboratory rats; I.e., peribronchial
and perivascular lymphoid aggregates and accumulation of alveolar
macrophages in interstitlum and alveoli. While the compound-treated
rats of both sexes and at both dose levels had lesions similar
to the controls, the lesions were more severe and occurred 1n a
higher incidence. In addition, lungs of many animals (approximately
2GX) contained foreign-body giant cells and large marcophages
filled v:1th a fire grar.ular material which in sere sections staired
bro'./n with r5natcxylin and eosm.
(B-62)
-------
Nscr.s*s Z' repatlc nrercnyria occurred In cMoro*orw-T.r?!teted ~'C3 roth se*?s. eood ccn^-cri^ri . . -^c
cc.~r*r*.no 'r2-it—-re 1 effect
(B-63)
-------
t
1
ft
£
>
! A
• /•
-------
>
5
>
I
J
i
A-
MALE MICS
n
m
*4
u
M
«
m
ffVMITWVflHIMl
i
i
s
I
I
I
FEMALE MICS
n
«o
«0
4
Tiut on ITVO* •
FLrur® 9. Grovrh Carves for Ilicd - C.lorriarr.
(B-65)
-------
During the first 10 months of tne study, the appearance and behavior
of the treated and control nice were generally caroarable, Alopecia
(generalized and/or localized), sores on the back and other parts of
the body, small palpable nodules on lower midline and/or Inguinal
areas were noted in Increasing numbers of male mice, beginning at week
9 and persisting during the study. After 42 weeks of treatment,
bloating or abdominal distension was noted 1n the high dose females
and beginning 1n week 78 In the	week 86, nearer
all high dose females and more than 505 of the high dose males had
abdominal distention. This was also apparent 1n eight low dose
females, ''ecroosy of these animals confirmed tiie preserce of Hver
lesions* the majority of which were subsequently diagnosed as
hepatocellular carcinomas.
3. Pathology - Twenty of the 240 treated and control animals were
lost to the study. Of these, IS (6X) ware autolyzed, 4 were missing,
and 1 was accidentally killed. Although most losses were In the
high dose croups, the Influence on the results was negligible.
Histopathologic findings of all tumors observed are tabulated 1n
Appendix 8. From an examination of Appendix B, differences In turor
Incidences between chloroform-treated and controls were apparent
only for tc.al tutors ara hepatocellular carcinoma in both ma'es
and fenales. These data were statistically analyzed and the
results pressntec: in	vTI. In aoa^tcn :c those resul:s
(B-66)
-------
03
I
ON
IjMi'JII. Analytic of Total Tuw»irs tnd Specific Liver. Kidney and Thyroid Tumors - Mice (Chloroform)
HALE	fCHALC
ll.( AIM) l(T
tONTHOLS
CW ON*	HATCHfO LOU	HI fill
CONTROLS
COLONV HAICIirO
l.ital luuor-Ocarlng
An iniu Is/Animals'
I* Valued	|
1 i.ir hi Iiiimir (works)
4/18
22X
.0000*
72
26/50
S2X
6ft
44/4S
90*
54
?/20
10*
.0000*
27
ILfdtcccllular .	®/"
I .ii i i<.imaH 11
i' V i In' <1	.	.0000*
T ixo to Tucior (weeks)* 72
1/18
4X
.0000*
72
in/so
JfiX
60
44/45
98*
54
I/CO
I*
90
o/ro
o*
IliyrolJ Tuirors/	0/77	0/17
Anlirjls?	OX	OX
r 4 l.ooo	l.ooo
J'fLi to Tunor (weeks)
0/48
OX
0/4]
OX
O/PO
OX
1.000
0/20
OX
1.000
Sji . :val At Ternlnal
*jcrlfIce (92 weeks)
40X
50X
65X
65X
61X
75X
LOU
iiir.ii
37/45
82X
66
39/41
95X
67
36/45
F*r
.0Wi0»*
6h
3V41
•IV -
6/
0/45
OX
0/40
OX
K L iny f|i I tlic 11al 1/77	1/18 1/50 ?/45 0/80 0/20
lu. r.rs//nlmals< IX	6X 2X 4X OX OX
( . .1414	.4073 -- - 1.000 1.000
Jjl-10 l"'lr (necks)	92	 92	92	9?		--
0/41
OX
C/36
OX
75X
20 X
1	-	Oral dose of chloroform In corn oil adnlnlstered by gavage five timet per week.
2	-	Bd'.cd on animals whose tissues were examined from a specific organ.
1 -	I'liL'-tall P value from Araltago test for linear trend In proportions, unless otherwise stated.
< -	T iir; lo detection of first tumor (at death).
C -	Ti.Ua ilipirlure from linear trend (for departure statistic; P < .05). Fisher Enact Test Is used comparing
t.iiltuk to a ilusc levo). Sonfrrronl (7) correction for simultaneous comparison of controls is included.
» -	Statistically significant (P * .05).
-------
the incidence of kidney epithelial and thyroid tumors are
presented for cc^parison purposes as statistical differences
of these tumor types were observed in rats.
The Incidence of total tumors was greatly elevated In fcoth rale
and female mice at both dose levels. The Increase Is due to the
occurrence of a specific type of tumor, hepatocellular carcinoma.
A significantly Increased Incidence of hepatocellular carcinomas
was found in all treated groups of mice (P < .001). These "lesions
were observed in treated animals dying as early as 54-60 weeks.
Figure 10 illustrates the incidences of hepatocellular carcinomas.
The hepatocellular carcinomas observed 1n the various test and control
groups comprised the full spectrum of morphology of this entity. The
tumors varied from those composed of we11-differentiated hepatocytes
with a relatively uniform arrangejrent to those which were very
anaplastic and poorly differentiated with numtrous mitotic figures.
Various types of hepatocellular carcinomas described in the
literature were seen, Including those with an orderly cord-like
arrangement of neoplastic cells (Figure 11), those with a pseudo-
glandular pattern resembling adenocardncna, and those exposed of
sheets of highly anaplastic cells with little tendency t; fcr- a
card or gland-liice arrangement. The diagrosis hecatccsllu'-ir
carcinc-a was ori-arily based z- lv. stolcgic cn»ract^r^'.t, :s z* :h<-
(B-68)
-------
neoplasm. Hepatocellular carcinomas were found to have metastasized
to the lung In two low dose males (Figure 12), and two high dose
fenales, and to the kidney In a high dose male.
Few nice receiving carbon tetrachloride survived until the
planned termination of the test, compared with a considerable
number in each of the chloroform-treated groups as shown In
Table VIII.
Table VIII. Comparison of Survival of Colony Control - Vehicle and
	CMorof;~- and C»*6on Tetrachloride-Treated ?1ce
CKCaOfOPH	CAR BOW	L0B.!06

INITIAL
/£
90
INITIAL
/a
TT37
ANIKAL eaoup
W.
XEEVS
WEEKS
no.
WEEKS
VEE«
Males Controls
77
S3
38
77
53
38
Lew Dbse
50
43
37
SO
11
0
High Oose
SO
41
3S
so
2
0
Femalei Control*
80
71
65
80
71
65
Low Oose
SO
43
36
so
10
0
High Cose
SO
36
11
SO
4
1
Hepatocellular carcinomas were found in practically all mice receiving
carbon tetrachloride, including those dying before tennination cf the
(B-69)
-------
100
90
10-
10
60
SO
40
30
10
10
0
MALE MICE	(44/45) 9BW
(IB/50) 3G-1
(5/71) G% (1/18) 6*
FEMALE MICE
139 -a n
136/45) 80";
M/BOI IK
(0/70) 0*
COLONY MATCHED LOW	HIGH
CONTROL CONTROL OOSE OOSE
COLONY MATCHED LOW	HIGH
CONRTOL CONTROL DOSE	OOSE
10. Comparison of Incidences of
Hepatocellular Carcinoma (Clilorofon
-------
> ^
- -5 :iA-	•

••> .-Ai	.irtSS*!
:	; -~at?!,
*a-v r . _
,:i ' y.- ••
^ . ^ * tfv-
a ~
Pierre 'i. '451 •i"fsr',Tfv*?"?	tr*h«cu1*r '¦ec-jtocc^uls- C2*,-,'nc*"';.
;&r. '-'oj* , rs--	• vstoyjlr ?*d :r:ir.
-s 1C. *"ic •	c-rv ?:.«c. "m;. !c.
" T " C ~ 1 • *3 • ' ?i'" !.I'	*¦ P V ! ^ .
(B-71)
-------
test. The incidence of liver tumors was somewhat greater in carbon
tetrac-.lorlde-treated mice (especially at the lower dose levels) than
1n chlcroform-treated mice as shown in Table IX.
Table IX. Csrparfson of Hepatocellular Carcinoma Incidence In Colony
Control - Vehicle Treated and Chloroform- and Carbon
	Tetrachlor1de»Treated Mice	
ttWAl G70VP
CHIOROPORM
carbon treecHicrae
Hales
Controls
5/77
5/77

Lev Oose
18/50
49/49

High Dose
44/45
47/48
Females
Controls
1/80
1/80

low Cose
36/45
40/40

High Cose
39/41
43/45
TJiese liver tumors In carbon tetrachlorlde-tre^ted mice varied
greatly 1n appearance from lesions which contained well differentiated
hepatic cells that had a relatively uniform arrangement of the
cords to very anaplastic liver cells having large hyperchrcnatlc
nuclei, often with Inclusion bodies, and with vacuolated, pale
cytoplasm. Arrangement of the neoplastic liver cells varied from
short stubby cords to nests of hepatic cells and occasionally acinar
arrangements, mitotic figures were cffen present. Sere cf the turcrs
were characterized by discrete areas of Manly anaplastic cells
surrc.^ded by relatively well differentiaie£ tuirc c^lls. "he
r.ec:'j--it ::CLr-*ra m t*>? CC1	nee '..ere s,-,'jr ¦'
c:oe;-i*.ce *o t":•-cte-: in •.'iKircfrr^"-tre5teu ~
(B-72)
-------
The test »ae< at wnlc- the fir:: ani<-»1 c'ed in „.~ich a hepatocellular
carcinoma v»as observe: 1n each croup is given in "able X.
Table X. Cs-jarison of to Liver Tuner Cetect1;n in Colony Control -
	Chloroform, and TarSon yetracbloHrie->efteS *Mce	
ANIKSl (SOUP
CHlOrCrOPf*
ct tetrachloride
Males Controls
n
72
Low Oose
GO
48
High D»e
«4
26
Females Controls
90
90
Low Oose
66
16
High Oose
b7
19
In addition to the higher Incidence, hepatocellular carcinomas were
observed rcuch earlier In carbon tetr2chlor10e-t"eated mice than In the
chloroforn-treated mice. Tumors in control mice were observed much
later than with either other compound.
A very snail number of non-hepat1c spontaneous tumors were observed
1n the various control and test groups, but no significant differences
were observed.
Non-neoplastlc hepatic proliferative changes were found in both the high
and low dose mice ofItath sexes. Of these, lesions of the li%er
classified as nodular hyperplasia occurred i- 1C cf £0 low dc:e rales,
6 of 4S ':w dose fena'ss, and 1 of £1 high ccss 'scales. Hepatic
necrcsis -is observer :n six -ice (a*' treat?;', ' lew cose r.'lo,
4 1c-. czir -stales a-: 1 hi'jr rtse
C B-73)
-------
A variety of Inflarratory, degenerative, and proliferative lesions
occurred in both cc'trol and treated groups of mice. There was
a gen
-------
rats, the pathologists did not attach any biolcgical significance to
those findings (see page 23). The observation of liver cancer was not
totally unexpected, on the basis of earlier studies with chloroform
(9, 10), however, the increased Incidence of kidney tumors had not been
predicted.
The previous chloroform studies were conducted 30 years ago (1945-1946) by
Eschenbrenner and filer (9, 10) and suggested the potential hepato-
carcinogeniclty of chloroform. In those studies chloroform was administered
by stomach tube to Strain A mice. Thirty doses (at five different
concentrations) were given at 4-day intervals for a l?0-day treatment
period with sacrifice 1 month following the last treatment. Hepatomas
were found In 7/15 female nice at the highest dose levels; no hepatic
tumor was observed in any male nor female at the lower dose levels.
The results of the present study clearly support and extend the findings
of Eschenbrenner and Miller, that chloroform administered by gastric
gavage can induce hepatocellular proliferative lesions, Including
hepatocellular carcinomas, in mice. In this study a high incidence
of hepatocellular carcinomas was observed in both males and females, while
a high Incidence was found only in ferales in the eschenbrenner and Miller
study. Tk.is right :e attributed not only tc a sex difference in
jusc?:tib*1ity of ;-e Strain A reuse, but a'tc to the shorter duration
:f t--?atr:*"t ('"O i:ys) and earlier sacrifice (at ":f days aftpr st:rt
2?
(B-75)
-------
The tern "hepatocellular carcinoma" was used for proliferative lesions
of the Mvers 1n mice which, 1n the judgment of the pathologists,
had the potential or the capacity for progressive growth, invasion,
and metastasis and for causing death of the host. This Judgrent
was based upon the cytologic and histologic features of the reoplasms
and the knowledge that lesions with the same morphologic characteristics
have exhibited malignant biologic behavior. The observation of nodular
hyperplasia In many male mice at the low dose without hepatocellular
carcinosis, while virtually all high dose males had hepatocellular
carcinomas, would tend to support the hypothesis that nodular hyperplasia
1s a stage in the development of carcinoma.
The teres "neoplastic nodule" and "hepatocellular carcinoma" used to
diagnose proliferative hepatic lesions in rats were based on the
morphologic criteria and nomenclature recently reported from a workshop
on the classification of specific hepatocellular lesions in rsts (3).
The observation of kidney tumors in rats and liver tumors In rice
Illustrates species differences in organ specificity and sensitivity.
In regard to t*e choice of animal models, the Osborne-fendel r*t was
se^ctec aeca'.se of the experience gained by the Food ard Dr.:
Adr'nlstraticr, where this strain has been used for many year? a >
ge-i-il :-rpc:: test ar'-«»l. In sedition, *. vis '-.rr./n tc. b?
(B-76)
-------
sensitive to the carcinogenic effects of CC14 administered by
subcutaneous Injection (11). The 86C2F^ strain of mouse has been
extensively used by tJCI for carcinogenesis bloassays. Current
experience with this strain 1n our Program Indicates an Incidence
of hepatocellular carcinomas In control nice of approximately 5-10%
in males and 15 1n females. The matched and colony control animals
in this study conformed well to this expected incidence.
From the relatively low response of the rats to CCl^ (< 5% with
hepatocellular carcinomas), 1t would appear that the Osborne-Mendel
rats used 1n these studies were less sensitive to hepatocarcinogenicity
than those used by ?.euber (11). In contrast, nearly 100% of the
CCl^-treated mice developed hepatocellular carcinomas with many
occurring 1n animals dying 1n the first year. While 1t would appear
that the mouse was more sensitive to CCl^ than chloroform, the greater
dose levels of CC14 (5-9 x that of chloroform), should be considered.
A concern in any testing program 1s the possible Influence of extraneous
factors. Because several other compounds were on test in the same rooms
wfth the present test animals, the possibility of;a low level exposure
ta these ccuounds in the air must be considered. The absence cf an
increased incidence cf Urors 1n controls is evidence against any alrect
c-;nourced effect of such respiratory exposure, but the possibility
be e"',rif,ated tfat the effects ctservpd were- accsrtuited :y
(B-77)
-------
concurrent e*:osures to these contaminants. No experimental studies
of cross contamir.it1on or sinultareous administration are available.
We would not expect a protective effect from simultaneous exposure to
other halogenated solvents, and 1t 1s highly unlikely that an
Interaction of possible airborne contaminant amounts of solvents with
the Mg.i doses of chloroform used would bring about false positives.
With mice, stringent precautions against cross contamination were
employed. The mice were kept in cages with filter tops which limited
the amcunt cf expired chemical in the air available for inhalation
by other antnals, the total air in each room was changed 10 to 15 times
per hour, and the mouse racks were transported to another room with
a large hooi for the daily intubations, Furthermore, the hepato-
carcinrmas in mice were pre-ent at a greater than P ¦ 0.01 level of
significance and were produced by doses of chloroform of 90-477 rwi/kg,
wfilch are several thousand-fold greater than any possible contamination
could *iave been. A dose related effect was observed and, any possible
chemical In general room air did not affect controls-. Thus, although
this rtam jrrarts^ent is not 'desirable as is stated in the KCI
Guide'^nes 'or C*rc1ncgen Sioassay in Small Rodents (12), there is
ro eviencs the -esults wou'd have been different wit1: a single
ccmp:.*a a r::r.
(B-78)
-------
The methodology used in these studies differs from that currently
adopted by MCI (12) in that: (a) the testing for subchronic toxicity
was for 42 rather than 90 days; (b) the dosage was changed during the
test; (c) the period of treatment was for 18 rather than 24 months;
(d) the number of matched controls was 20 rather than 50; and (e) several
volatile compounds were tested 1n the sane room. In spite of these
limitations, this bloassay Is considered a valid test for carcinogenic
effect. While the induction of hepatocellular carcinoma in mice, and
epithelial tumors of the kidney In rats were highly significant, even
using the small matched control groups, the use of pooled colony
controls further increased the validity of these differences.
flue to changes in dosage of chloroform during the study and the use
of only two dose levels, a quantitative assessment of a dose-response
relationship is not considered feasible. However, a linear dose trend
was seen for both hepatocellular carcinomas 1n mice and renal epithelial
tumors in the male rat.
(B-79)
-------
REFERENCES
1.	Criteria *er j Pec:--'ended Standard...Occuoatlonal ExoosLire to
Chlc-ofon. U.S. WS. CDC. MIOiH. ohew Putii. fio. iHlQSr) 75-114.
«asr., O.C., U.S. Govt. Print. Off., 1974, 120 pp.
2.	International Agency for Research on Cancer: IARC Monographs on the
Evaluation of Carcinogenic Risk of Chemicals to Man. Geneva 27,
Switzerland, WHO, '972, Volume 1, pp 61-65.
3.	Linhart, M. S., Cocjer, J. A., Martin, R. I., Page, N. P. and
Peters, J. A-.: Carcinogenesis.Bloassay Oata System. J. Comp.
Bior.sd. Res. 7: 230-248, 1974.
4.	Berenblum, I. (Ed.): Carcinogenicity Testing. UICC Technical
Report Series, Volure 2. Geneva, Switzerland' International Union
Against Cancer, 1969, 56 pp.
5.	Kaplan, E. L. and Meier, P.: Nonparametric Estimation from Incomplete
Observations. J. Arer. Statist. Ass. 53: 457-481,
6.	Armitags, P.: Statistical Methods in Wedical Research, J. Wiley
and Sons, New Yoric, 1971. p 363, (a) p i35.
7.	Miller, R. S., Jr.: Simultaneous Statistical Inference. McGraw-Hill,
New York, 1966, p 8.
8.	Squire, R. A. and Levitt, M. H.: Report of a Workshop on Classification
of S;ec1fic Hepatocellular Lesions in Rats. Cancer Res. 35: 3214-3233,
1975.		
9.	Eschenbrenner, A. B.: Induction of hepatomas In mice by repeated
oral administration of chloroform, with observations on sex differences.
J. Mat 1. Cancer Inst. 5: 251-255, 1945.
10.	tschenbrenner, A. 9. and Wilier, E.: Liver necrosis and the induction
of carbon tetrach.uride hepatomas in strain A mice. 0. Rati. Cancer
Inst. 6: 325-341, 1946.
11.	'euber, f*. 0., and Glover, E. I.: Cirrhosis and carcinoma of the
liver In -ale rats riven subcutaneous carbon tetrachloride, J. ':atl.
'ancsr Ipst. 44: 119-423, 1970.
12.	-ontic, J., Pace, and Saffiotti, II.: Guidelines for f'rr.ir-risnesis
•iQeStay •* Sra'l ;::?rits. 'J.S. DHFW, PKS, '"iH, r!CI. l'r\n ?uc.. .".c.
. M-. /o-;-i. rtdS"., j.i.. , U.S. Govt. Pr-nt. Off. (In Press).
dC
(B-80)
-------
APPENDIX A
SUMMARY OF TUMORS OBSERVED IK RATS
(CHLOROFORM)
45
(B-8 1)
-------
•-ijI EATS WITH primary Tl'VOPS BY AHATCVTC SITE (CHIC?:FOR*"
(®e#C£KftceS *" SvSTg* ANO CSGAN *as	PISEC CN Th.g ff F6CTIV C NU"?6R r« 4NI-USI
'	control uaw"ocsI
|MfCrW« Wj«9#» Of ANIM4«.S*	l« (100*1 10 tioctl 50 11*111
ANtMACS «|Th ?«(»*#? TU-OHS	9 <47t> 2* (««t| 2C t *>CX I
iNrecu^iriar s*!^*
suBCur nss^e
nwus fisrjocYTo«A
MLISNANT M8«dUS fclSriGCYTQKA
pmoiA
SKIN
*|«At01ClSTW0«ii
S0UA1CUS CELL CABCtNQPA
2 (tit)
« (1211	t (2*1
2 UIXI
1
I
« (Ml
1
2
I
I 12(1
I
0 (Oti
2 1**1
I
I
0 (CXI
afSPtHATtat stste*
LUNG
ALVE-3LA4-CELL tC£NC»
0 (OS)
0/t9 (0*1
I (2*1
0 10*1
l/n<» ( 2*1 0/«.» (0*1
1
C1«CULAT3#t STST6*
MONS
ofccsrrvs j*sre«
uve«
MONASTIC XOCUUf
HEPATOCELLULAR CAflCINQMA
SXAUL INTSSTIME
'ie>!SA«cc«A
o IO«l
0/19 (0X1
0/19 10*1
t 12*1
1/30 (2S1
1
0/50 (OS)
* <»*i
3/5C (6*1
2
I
1/5* (2*1
I
UMNABY ST J rat
*iwe*
TUMJIAR-CELL *CENOCA0CtNONA
TU8UIAQ—CELL ACENOMt
HAKAiT0*4
xtxti rye" x»tiCN»«T
0 (Oil
0/19 (01)
* (I2tl
13 (26'I
6/50 (121)	13/«1 (2AII
2	ta**(^i
2	3
I	I
2«1 I 1
ENCCC*I«< SYS"X
want:
?OLt I CilL A"-CELL rABftNC»A
PILL :C'JL 4=—''.':U »OEMO*»
C-Cili lOS'tC*
7 (17*1
*/H (21*.
2
I
1
9 ( 10*1
t U2U
' M'z 'f(C; iCC33P!'ir. rr paf.iw sy'TFu.	-
• =	j$ [NOictrei n.g	-•Js'-e
(*.*» Wis (*11
2
1
2	2
* v\ ' * T	i : C .
: * 'u"-*• ^

(B-82)
-------
cgntfcl
ewccaiHft ststp* teoMi
~ituitmt
CMHC*0W<08« iCCWi
UMKll
WWiHGlOSAaCCJU
PM«CCm»0"CCYT0H4
p«c»Eutc inters
ISUT-€SIL C«CImO#»
:SLET-CELL *CENQ»4
0/16 tOt)
*/*+ tltl 1/W IJtl
*	I
Z/19 llltt	IO«l 0/«.« lilt
I
I
1/16 C6I» 2/30 «M» l/t.9 (ZT1
I
I	1	1
MeriTOPotenc syste*
IflH*
KClrtCtO^iflCO.**
t tssi
1/17 I AS)
I
4 taxi
2 (*U
WH (fttj 2/*fl <<•!!
1
J	2
B«paaoucrive systb*
m«»mv CL<*tO
iOWOCMC INQ>«
I (SI1
l/l» (HI
I
a (os) a (ot)
O/SO 101) 0/«« (0*1
MAvnuS SYSTEM
aa«i*r
israocr rci
0 (Of 1
a/is tot)
1 (2*1
I utl
1/10 12*1 1/iO I2«)
1	i
MUSCULOSK&LSTit. SYSTEM
NflNC
SPEC Ml SENSE OflC&MS
nCne
*<.L OT-E» SYSTEMS
winns o«C4ns
*ETicuu-
o 10*1
1 (itl
I li?)
I
* cr.yis iap c"SET accounts!*. ro oacaji s*srE». 'PfCtfitc CG*?. jua	*>oe.
(B-83)
-------
TA-LE AT. fJi.S PA'S Wl'- PKimftV ~.,MOaS BY AHATOMIC SITE (CHLOROFORM) (COHTIfflJ-?
(WC£irtCES - OOS*
ruwe*
TOTlt Uitm its b(TM Bt^tCN TU*OKS	5 (2611	16 (13*1	10 170S I
TOTAL BENIGN Tu*«3*S	9	IS	II
rem mt"«.s -tTw •tucfttxr tu«qbs	* uiti ic <20*1	i« mti
rant mucnmt ru-:*s	*	n	is*
• ent^is 4«s nfPSET L'.caaofNc ™ oac** systfk, spfciptc c»g** »no tu*cp tycc.
(B-84)
-------
TA3LE A2. FB{ALE PATS WITV ' f.yCPS 5Y ANATOMIC SITE fCHLOROFORM)	
(Pt«ci*ricgs system iNn anew u; siseo as the effective h-j^peb cf «m»iisi
CONTPOl	™-LOti™OUSF ;T0^"s«r
EFFECTIVE MtMflE# OF
tNtMIS M|TM PAtHtaY TU*OtH
INTtCUX'Nriflr SYSTFM
suacur tissue
upov
SKIN
Pt»tU0»»
20 11 GOT I
12 160(1
«« (tooti <•« (init)
l< t*«tl J* IJCTl
0 cost*
9 (Oil
0 (Ott
2 (*»»
I (21)
t
: 12*1
t
o ton
o 11*1
o i o<>
MWunftY system
IUNG
MUiiNUif F18B0US MtSTT2C*TC,,»
0 (OfI
0/20 <0*1
I 12*)
l/« (211
I
o co«j
a/o cti
Ct#CULATO*Y SYSTEM
NONE
QIGF5TIVF syste*
ltvt»
MOFUSTtC MCOUie
•UUCJIMT FIB'OUS MSTtCCYTC*
PftNCAb*S
MAltWWtT PltHQUS M(STICCTTC«t
S1LS OUC*
M*MA4TQMt
U«fM4#V SYSTEK
MONEY
>»i(.rw*Nr siaanus wtsnrcYTc*
PgMAMCIOPA
TUBUL.l«-CfLL 4C5NaC4#CX,-C.'«ft
(EMM. '?LVIS
SSWCL'S CELL Ci»CINC»ft
2 (10(1
2/20 (lOtt
2
0/20 (0*1
4/20 IOTI
0 (OSI
0/20 (OS)
9/20 (Oti
5 liOt?
* 19*1
S/*<	I 10*1 J/"" (6*1
* 3
1
l/«."	(21) C/v« (fltJ
1
0/44	(031 l/td lit]
I
I I2«l
3 • 6tl
l/*S (211 2/*« (*« titt
i
• C(XU»M 1®S «e*SFT iCCC'CtUft " rsr>s SY5Tt», S->SCI*ir ncrl4*	TU**CS 1»«?.
•««XI Nu«-i£a IN fiaenrnesss l.';c;:irCS r*E sy?es 3r »E T a £ r a s J i6C T-J«c
-------
TAsLE A2. FS'-'ALS CATS WITH PSl^ARY ^JKORS 8Y ANATOMIC SIT? (CHLOaOFOTM) (CONTINUED)
IPfACENTAGES 8T SYST?» tNO 0«CA* »«€ 8*SE0 ON Tne ELECTIVE NL/*8frt Cf «NI«aiSJ
control LCw"casI""""N7HM"rnii
cioootNS stste*
PfTUtTMV
CMSQMiPMcae »oe*o»»«
rnvROto
mu:cuii«-ceu *ofioiu
•OUICULia-CEU CARCtKOm
c-ciul icsNcxt
c-tEUL
AO*fN«l
CO*TICl'. *OENO»»
PMtocHi>c»cevTQ»k
hncr«»ti; islets
msr-csu. c«cino»«
ISLCT-CEIC »GE*0"»
« (%9St
IT IJ51J
12 I2«l
1/19 U*>
I
6/20 1)0X1 10/*?	(Hi) J/45 t7tl
* 10 J
8/4?	(16') 10/4* (22*1
I *
1 2
6 3
l*"< I)
1/4*	(2*) 0/*? (0*1
I
2/20 I10H
1
I
2/20 II CI)
I
I
0/4* 10*) 0/4P tOTI
NCMtTOPOlSTtC SY5TE*
SPtetN
"C.'iHOICU
0 10*1
0/20 1011
I 12*1
c ten
i/*« i2ti a/»s coo
i
MPHOOUCrtwS SVSTJ-*
mttmtar »»
*OENOCi*CINQ«*
UTE«US
SCU*"CUS CELL CiBCtNaci
6N0C*€T5t4l STPn»at f>CLT®
He»aNc:csA«c»'»
cv »«~
|itiic»fit Ft0«cus ««IST tccrrc-i
G«MJUirSA-C:ll Ui-ga
I uoti
i; urn
14 (2**1
7/20 125*1 13/48	<27*1 11 /*>t (;<•«I
I
T 9	7
3	I
2	2
1/20 15*1
I
a/20 
S6EM*'f C^'iN *'<'J rn—«"»-« <
Ct «c14:tit:¦ 'uMCss
(B-86)
-------
TABLE A2. FgttLg	P"TVARY TVMORS 8Y AHATOMTC SfTE (CKLCa.OPOBM) (CQNHNUgn
(wcenr»c« it vr*Tc» kna cacin »»i sa*eo oh T»e e**ecrivc wee* c
control ioToesi
wscuLCS
0/*« (OSI 1/4T (2*1
I
srecui szNie qrcms
M3H#
HI OThsa STSTM?
xesem1-'*
«UG'*tHT Piaac-s »*isrtcctrQM4
Pieuat
MtusvMT •ib»cjs MtsrtijCTTC"*-
0 (Ot)
0/20 to?)
0/70 (OS)
I I2*J
0 t«ri
l/4< (2*1  0/«7 t0*>
t
TUNRA
TOT»l *M«4iS WITH MMCM ru*0*S	12 <40«l
rarii aeNtSM rufous	i?
TCT*l tMtHS WITK MUGN4»r TUHO«S	3 us»»
total MLlGstMr ry»3*$	5
23 (471) 23 («¦«<)
)6	tT
& IU*I
6
S (H*J
10
• cniu«m A«e c«set icccpoing to c>cut s*ste«, s»fcmc r«r.4« tun tut® typp.
si
(B-87)
-------
(B-88)
-------
APP-HPTX 8
SUMMARY OF TUMC?.S OBSERVED IN MICE
(CHLCROFORM)
(B-89)
-------
t*3le r. »-:e u::s wr-» pp;».v*y ~.m$ sy anatomic site (cuicaorosM}
(»£«C!sT*r,rs jr system *no «t anr.i^ ise etsEo an the E*«crtvE nu»9e» cr iwuisi
I
I
1
i
1
i
•
CCA*POL
IC* CCS6

fMCCTivu su«4(a ;r 4*i»4is *
ANIMALS
18 (lOOit
* (22tl
JO 1
it, <42ti
«s 1 tcoo
4* (•)»*)
stste1*
0 (ott *
I (291
i (?*>
S*f\
MMQSUCQKt
0/1® ton
i/«« tit)
t
0/44 (0*1
sutcor tissue
•isbosmcoj"*
0/18 (0«4
*!TlCLXU*-CiUL 5tiCO"*l
ute t«*»
l
J/10 t 6T1
J
3/*4 (Tt>
2
1
CT«Ca*Ta*t SVSTE"



«rac



otersuv* s*st?»
2 lltS)
20 I«01)
4* |4«{]
uw»
-e«»ncen.'A4i» cwci*:**
•ericucu—cell s4. Z'' »
tv. n;* ,.CC-»
0/18 irn
0/50 IO*f
!/ •' ( -i; t
• •' ''i' CSf4N
»¦ "-'i1 fi -;s;; .
. ' • i i -
' > r - TI .
•' 'i ;¦ f
•tin.;-: !.¦
: > " - '.
¦ > s
(B-90)
-------
TABLE B1. "UE ."ICE WITH PRIMARY TUTORS BY ANATOMIC SITE (CHLOROFORM) (CONTINUED)
(PERCENTAGES 8T SYSTEM tHO BY OPCAN APE ?ASSO ON THE EFPfCTtVe NU"9ER OP iNI»»!.$)
ccntpcl	rTc^'ca^i
HfNtTQPQIBTIC SYSTEM
IYHPN NOOg
•ETtCULU<*-CELL JAftCOM*
LYNPMaSAacON*
SPLEEM
ftgrtcutuf-csLt sapcqua
UrfPHCSAftCCA
SONC NtPAQU
LYMPMOS*acaM4
0 (Of)
0/18 (Oil
o/is tati
o/ia lot)
1 (2*1
3 17(1
1/90 (2*> 3/49 (7*1
1
l/«4 (2*) 2/49 K«1
I	t
I
0/90 (C«) 1/49 (2(1
I
¦eppeoucTtve system
TH5TIS
sertoli-cell ru»oft
0 10*1
0/18 (OX)
1 (2T J
1/90 I 2*1
t
0 (0*1
0/49 ton
NCPVOUS SY*TE»
MA(N
- lYNPMOMaCQNA
0 10*1
e/i9 (o*i
2 (4*1
2/9C (4«J
2
0 (0«)
C/44 10(1
musculo;*elstal system
none
SPFCIAL SENSE ORGANS
HOW
ALU 0™ER STSTBMS
"*JUTtP*.6 0#GANS
UYl«PH0SAaCC'«4
0 (0*>
0 (0*1
1 (2.11
I (>*)
I
0 (0*»
0 (0*1
TU*0» SU"»»PY
TOTAL *Nt»tlS -ITM PsSJCN TUTORS	3 CI7*1 9 (10*1	* Ifltt
TOTAL ru"CQS	3 S 4
TOMt i'iCiLS » I tm »4{.rrj.i.Nr fj"C»S	I (All 22 (4411 4* (Sdti
r5tal "ALic»Asr «	t 2* 10
o	S Aae sft tccc?oi>; t n rr.r.** srSTf, tt:r car.ii x\a ri.*o
-------
TABLE 52. PSUI: .'(TCE WITW ?W-:Y TUMORS 3r ANATOMIC SITE (CHLOROFORM)
(»e«ci*r»cjs *r iTSTf" ino ev c*:i* am amc on t*( e'wcrive KL^et cp 4*i»us>
ccmpol lc» oose -ich ecu
IMSCrtv* snH«ra a*	20 1100*1 *6 1100*1 <.1 uonn
MlMlkS	ryocas	2 (1011	37 l»OM it (9911
tMTI&MWTMY Svr«M
None
»fSPtt*TOft* SYStCM
LUNG
uveon»-cEu aojnch*
w6losa»co"*
0 (Oil*
0/29 (OX)
3 (7TI
3/** (7*>
1
2
0 (0X1
O/tl OXI
CIUCUiATRar srtTI"
NONE
oiecsrive srsir»
uvti
tH9kfCCSl.LUV.iA CMCIN0M4
"*«10SMC0»*
0 (OX)
0/20 (C*l
3i (ecu
34 I9«U
3T/*1 1*2*) 39/H IS!tl
16	3*»«(2I
2
u»t**rr irsre*
NCM
(NCK1t!<.t '.UTt*
40*!riiL
»*«0;MQHOCTfOlM
0 1011
e/20 10x1
e to*>
1 t (!)
a/4.3 (CX) l/M (2*1
I
f«»4-3Pat*TtC S»STE*
smew
»»euosA«cc«*
c tctt
0/19 COT)
t ( 2" J
L/<>6 (2X1
I
0 (Oil

1/20 (5X1 0/<>0 IC-) .l/Jb too
I
•	;*rtr* ; - = 01
is *\a rh.-ti:
mZ :-*ak i»5TF"«. SPfCirn
:irjl rw-	o* >¦ fc:11s;u 1
• > ri r.
'v 9 C .
59
(B-92)
-------
TABLE 8?. FF'ME >'TCE WITH Pi>pWPY Tir^S 3Y AWATCHfC SITE {CHLOROFORM) (CO'iTIM ED)
IMBCfNTACeS 8* SYSTEM tNO >~ OBf.iN A*£ ?*SfO ON THt EFFECT IVF NUXACR Of ANI*USt
cOfiroQc
(.Cw OC« flC* COS?
ure»us
*aehociaciNO»«4
IW)Q««TaiOI. sraaMAL SAACCJU
1/20 (5*1
I
l**Ul
0/42 IO*t 0/31 (Hi
N€«VQIJS VfStfN
WW6
«JSCULQS
4 1411
2
1
1
0 1011
o ca«)
tuwj# s» >¦*»»«¦*
TOSit iSifUS m(T»	TU-OBS
roTAi. oetidt ru*ja$
TOT«l	WtTc WIllCHtMr rti«C8S
TOT41 /tHICKMr rUi«0*S
I IJ*I
t
1 M*l
I
l fit)
1
3? (sati
*2
1 I2*»
I
39
• Cd.U«"• 9ft56*irt«esis i-.ntcsTis Nui-ss* ce »ci4iT4SUE; !u»cs
(B-93)
-------
Appendix C
DATA FOR EVALUATION OF
BIODEGRADATION, HYDROLYSIS AND PHOTOLYSIS (BHP)
C-l
-------
C-2
-------
APPENDIX C
DATA FOR EVALUATION OF BIODEGBADATION, HYDROLYSIS I PHOTOLYSIS (BHP)
Hazardous Substance
CAS Ho.I B
Data / Comments
2-Acotylaminofluoraa*
Acrylonitnle
53963
107131
No data
Acrylonitrile is subject to biodegradation (Kuchinskii, tt al. 1977;
Panova, at al. 1977; Anon, 1977; Schnee, at al. 1977; Kato and
laauuri, 1976; Mlkami, at al. 1974).
Measurement of biochemical oxygen demand has shown 25 to 70%
degradation within 10 days (Hann and Jensen, 1970).
Biodegradation of acrylonitnla is reported to occur readily at
concentrations less than 20 og/1 under anaerobic conditions.
Acclimated sludge can degrade 35% of the pollutant at concentration
levels of 500 ng/1. (Ref.l)
Biodegradation by autant microorganisms: 500 mg/1 8 20°C
% disruption: parent: 84% in 24 hours
mutant: 100% in 4.0 hours (Bef.2)
BOD,_10 = 25% removal 6 20 C with 1-year acclimated sewage seed;
feed cone. = 100-1000 mg/1
BOD^_10 " 67% removed 8 20°C with 27-day acclimated seed; feed
cone, a 50 mg/1
BOD.g = 60% IhOD, 100% removed 9 20°C with 8-day acclimated
seed; feed conc. = 10 mg/1
BOD. a 60% ThOD, 100% removed 0 20°C with 30+ -day acclimated
seed; feed conc. = 40 mg/1
BOD,. = 70+% IhOD, 95+% removed 6 22-25°C with 21-day
acclimated seed; feed conc. 89 mg/1 (Kef.6)
Biological effects: Inhibition of bacteria cell multiplication starts
at 53 mg/1 (Pseudomonas putida) (Bef.2)
Hydrolysis is not environmentally significant. (Kef.l )
Direct photolysis is improbable in aquatic environments. (Baf.l )
Photo-oxidation in the troposphere is a major fate process (half-life
~4 hours). (Bef.l)
Volatilisation is the most likely major transport process. (Bef.l )
-------
DATA FOR EVALUATION OP BIODEGRAQATION, HYDROLYSIS k PHOTOLYSIS (BHP) - Continued
Hazardous substance
I CAS Ho. | B I U
P I Data / Comments
Aldrtn
1 1 1
j 309002| |
1 1 1
1 1 1
1 1 1
1 1 1
1 1 1
1 1 1
1 1 1
1 1 1
1 1 1
1 1 1
1 1 1
1 1 1
1 1 1
1 1 1
I 1 1
1 1 1
1
| There does appear to be biological transforation of aldrin to
j dieldrin. - (Bef.l)
1
| Hydrolysis is not an important process (half-life >4 years). (Haf.l)
1
| Direct photolysis is slow. Indirect photolysis nay be important (one
j expt., half-life » 1 day). (Bef.l)
1
| Volatilisation of aldrin fron aquatic systeas is an important
| process, with half-lives on the order of a few hours to a few days.
| (Ref.l)
1
| Bioccumulation is an important process. Ihe results of terrestrial-
| aquatic microcosm experiments indicate that bioconcentration factors
j for aldrin in aquatic systems will be approximately 10 -10 .
| (Bef.l)
i
Amitrole
1 1 1
| 61825| |
i i i
1 1 1
1
| Amitrole is resistant to hydrolysis and the action of oxidising
| agents. (Bef.4)
1
Ammonium bichromate
| 7789095| |
i i i
1 1 1
1
| Inorganic.
j Can bioconcentrate (chromate) (Ref.3)
i
Ammonium chromate
1 1 1
j 7788989| |
i i i
i i i
1
| Inorganic.
| Can bloconcentrate (chromate) (Rof.3)
i
Aroclor 1016
1 1 1
|12674112| |
i i i
i i i
i i i
i i i
i i i
i i i
i i i
i i i
i i i
i i i
i i I
i
| Available evidence indicates that polychlorinated biphenyls,
j especially those with four or more chlorine atoms per molecule, are
| persistent in the environment. (Bef.l)
1
| PCBs are strongly resistant to both acidic and basic hydrolysis.
| (Bef.l)
1
| There is experimental evidence that the heavier PCBs (five chlorines,
| or more per molecule) can be photolyzed by ultraviolet light, but
| there are no data to indicate that this process is operative in the
| environment. (Bef.l)
|
Axoclor 1221
1 1 1
j11104282| |
i i i
i i i
i i i
i i i
i i i
i i i
i i i
i i i
i i i
i i i
i i i
1
| Available evidence indicates that polychlorinated biphenyls,
| especially those with four or more chlorine atoms per molecule, are
| persistent in the environment. (Bef.l)
1
| PCBs are strongly resistant to both acidic and basic hydrolysis.
| (Bef.l)
1
| There is experimental evidence that the heavier PCBs (five chlorines,
| or more per molecule) can be photolyxed by ultraviolet light, but
| there are no data to indicate that this process is operative in the
| environment. (Ref.l)
1
-------
DATA FOB EVALUATION OF BIODEGRADATION, HYDROLYSIS & PHOTOLYSIS (BHP) - Continued
Hazardous Substance
I CAS No.| B
H I P I Data / Comments
Aroclor
1232
1 1
|111411651
1 1
1 1
1 1
1 1
1 1
1 1
1 1
1 1
1 1
1 1
| I
1 1
| | Available evidence indicates that polychlorinated biphenyls,
| | especially those with four or more chlorine atoms per molecule, are
| | persistent in the environment. (Ref.l)
1 1
| | FCBs are strongly resistant to both acidic and basic hydrolysis.
I | (Ref.l)
1 1
| | there is experimental evidence that the heavier PCBs (five chlorines,
j | or more per molecule) can be photolysed by ultraviolet light, but
j j there are no data to indicate that this process is operative in the
| | environment. (Bef.l)
¦ i
Aroclor
1242
1 1
|53469219|
i i
i i
i i
i i
i i
i i
i i
i i
i i
i i
¦ i
1 1
| | Available evidence indicates that polychlorinated biphenyls,
| | especially those with four or more chlorine atoms per molecule, are
| | persistent in the environment. (Ref.l)
1 1
| | PCBs are strongly resistant to both acidic and basic hydrolysis.
I | (Ref.l)
1 1
| | There is experimental evidence that the heavier PCBs (five chlorines,
j | or more per molecule) can be photolysed by ultraviolet light, but
| | there are no data to indicate that this process is operative in the
| | environment. (Bef.l)
1 I
Aroclor
1248
1 1
|12672296|
i i
i i
i i
i i
i i
i i
i i
i i
i i
i i
i t
1 1
| | Available evidence indicates that polychlorinated biphenyls,
| | especially those with four or more chlorine atoms per molecule, are
j | persistent in the environment. (Ref.l)
1 1
| | PCBs are strongly resistant to both acidic and basic hydrolysis.
I | (Ref.l)
j | There is experimental evidence that the heavier PCBs (five chlorines,
| | or more per molecule) can be photolysed by ultraviolet light, but
j j there are no data to indicate that this process is operative in the
| | environment. (Ref.l)
I i
Aroclor
1254
1 1
111097691|
i i
i i
i i
i i
i i
i i
i i
i i
i i
i i
i i
1 1
| | Available evidence indicates that polychlorinated biphenyls,
| | especially those with four or more chlorine atoms per molecule, are
| | persistent in the environment. (Bef.l)
1 1
| | PCBs are strongly resistant to both acidic and basic hydrolysis.
| | (Ref.l)
1 1
| | There is experimental evidence that the heavier PCBs (five chlorines,
| | or more per molecule) can be photolysed by ultraviolet light, but
| | there are no data to indicate that this process is operative in the
| | environment. (Ref.l)
1 1
-------
DATA FOB EVALUATION OP BIODEGRADAXION, HYEKOLXSIS t PHOTOLYSIS (BUP) - Continued
Hazardous Substance
I CAS Bo.| B | H
P ) Data / Comments
Aroclor 1260
1 1 1
|U096825| |
1 1 1
1 1 1
1 1 1
1 1 1
1 1 1
1 1 1
1 1 1
1 1 1
1 1 1
1 1 1
1 1 1
i
| Available evidence indicates that polychlorinated biphenyls,
| especially those with four or mora chlorine atoms per molecule, are
| persistent in the environment. (Ref.l)
1
| PCBs are strongly resistant to both acidic and basic hydrolysis,
j (Ref.l)
1
| There is experimental evidence that the heavier PCBs (five chlorines,
| or more per molecule) can be photolyxed by ultraviolet light, but
| there are no data to indicate that this process is operative in the
| environment. (Ref.l)
I
Arsenic
1 1 1
j 7440362| |
i i i
i i i
i i i
i t i
i i i
i i i
I I I
1
| Arsenic is metabolized by a number of organisms to organoarsenicals,
| thereby increasing arsenic mobility in the environment. (Ref.l)
1
| Photolysis is not an important process. (Hef.l)
1
| Bioaccumuiation appears to be most significant in lower trophic
| levels. (Bef.l)
1
Arsenic acid
1 1 1
j 1327522| j
| 7778394| |
i i i
1
| Inorganic.
1
i
Arsenic disulfide
1 1 1
| 1303328) |
t i i
1
| Inorganic.
i
Arsenic pentoxide
1 1 1
| 1303282| |
I I I
1
| Inorganic.
i
Arsenic trichloride
1 1 1
| 7784341| |
l 1 l
1
| Inorganic.
I
Arsenic tnoxidc
1 1 1
j 1327533) |
I I I
1
| Inorganic.
i
Arsenic tnsulfide
1 1 1
| 1303339| j
1 1 1
1
| Inorganic.
i
Asbestos
1 1 1
j 1332214| |
1 1 1
1 1 1
1 1 1
1 t 1
1 1 1
1 1 1
1 1 1
1
| "Asbestos is stable	 and is not prone to significant chemical or
| biological degradation in the aquatic environment. After introduction
| into surface waters, asbestos remains in suspension until physical
| degradation or chemical coagulation allows it to settle into the
j sediment layer. (Ref.l)
1
| Asbestos is not affected by photolytic processes. (Ref.l)
l
Aurawne
| 492808| |
i i i
1
| No data
¦
Azaserme
1 1 1
| 115026| |
l i i
1
| Bo data
i
Aziridine
I 1 1
| 151564| |
I i i
1
| Strong poaoiblity of food chain concentration. (Ref.3)
i
Bens(c]acndine
1 1 1
| 225514) |
I i i
1
| No data
Bens(a]anthracene
1 1 1
| 56553j |
1 1 1
1
| No data
i
-------
DATA FOB EVALUATION OP BXODEGBADAXIOH, HYCBOLYSIS k PHOTOLYSIS (BHP) - Continued
Hazardous Substance
CAS Bo.I B
Data / Comments
Benzene
71432
Benzene can be utilised as the sole source of carbon by several
microorganisms and is probably biodegradable at a slow rate. (Bef.l)
Helfgott et al. (1977) report the biorefractory index of benzene to
be 0.23, indicating that benzene is quite resistant to degradation.
(Kef.1).
BOD. a 2% ThOD 9 20°C with 14-day acclimated seed. (Ref.fi)
BOD, _ " 33% ThOD g 20°C with phenol accliaated seed;
feeoconc. = 250 og/1. (Hef.6)
BODj o 0% ThOD with sewage seed
BOD. a 1.9% ThOD with sewage seed
BOD,. • 24% ThOD with sewage seed
BOD. o 58% ThOD with acclimated sewage seed
Food chain contamination potential—negative (Bef.3)
BODj » 10% ThOD;
33% ThOD oxidation of 500 ppm of benzene by phenol activated sludge
after 12 hrs of aeration. (Ref.2)
BOD10 a 1.2 lb/lb.
Hydrolysis is not a significant fate process. (Hef.l)
Photolysis is unlikely since the ozone layer in the upper ataosphere
effectively filters out wavelengths of light less than 290 mi.
Direct excitation of benzene in the aquatic or atmospheric
environment is unlikely unless a substantial wavelength shift is
caused by the media. (Ref.l)
Direct oxidation of benzene in environmental waters is unlikely. Snog
chamber data, however, indicate that benzene is photo—oxidised at a
rapid rate in the atmosphere. (Bef.l)
Volatilization is the primary transport process. (Bef.l)
-------
DATA FOR EVALUATION OP BIODEGRADATION, HYDROLYSIS & PHOTOLYSIS (BHP) - Continued
Hazardous Substance
| CAS Ho. 1 B | H
P | Data / Comments
Benzidine
1 i 1
| 92875| |
1 1 1
1 1 1
1 1 1
1 1 1
1 1 1
1 1 1
1 1 1
1 1 1
1 1 1
1 1 1
1 1 1
1 1 1
1 1 1
1 1 1
1
| Biodegradation may contribute slightly to the degradation of
| benzidine during sewage plant treatment. No specific information was
| found about environmental degradation. (Bef.l)
1
| There are do data to suggest that hydrolysis of benzidine is an
| environmentlly significant process. (Ref.l)
1
| The capabilty of benzidine to absorb electromagnetic energy in the
| near ultraviolet region Bakes photolysis a distinct possibility.
| Nonetheless, no information was found demonstrating that direct
| photolysis was an environmental fate. (Bef.l)
1
| Lake water degradation experiments (precluding photolysis) suggest a
j half-life of 4 hours. (Ref.3)
1
Benzo[bIfluoranthene
1 1 1
| 205992| |
1 1 1
1 1 1
1 1 1
1
| Tho dissolved portion nay undergo rapid photolysis. Ho specific data
| were found however and the reaction products are quinones; no
| hydrolysis; long time required for biodegradation. (Ref.l)
I
Benzo(k)fluoranthene
1 1 1
| 2070891 |
i i i
i i i
1 1 1
1
| The dissolved portion may undergo rapid photolysis. No specific data
j were found however and the reaction products are quinones; no
| hydrolysis; long time required for biodegradation. (Ref.l)
1
Benzo(a]pyran#
1 1 1
| 50328| |
i i i
i i i
i i i
i i i
i i i
i i i
1
| Photodecomposition products are quinones.
1
| Photolysis half-life = 3 hours in stream, 1.5 hours in clear lake
j (unspecified products);
| Photolysis of benzo[aIpyrene yields a mixture of three quinones;
| Hydrolysis/biodegradation not important. (Ref.l)
I
Benzotnchloride
i i i
| 9B077| |
i ii
1
| No fate and effects data available.
Benzyl chloride
1 1 1
| 100447| |
I I t
1
| No data
1
Beryllium
1 1 1
| 7440417| |
1 1 1
1
| Inorganic
i
Beryllium chloride
1 1 1
j 7787475| |
1 1
1
| Inorganic
i
Beryllium fluoride
| 7787497| |
l l l
1
| Inorganic
i
Beryllium nitrate
1 1 1
113597994| j
1 1
1
| Inorganic
I
alpha - BHC
1 1 1
| 319846| |
1 1 1
1 1 1
1 1 1
1 1 1
1 1 1
1 1 1
1 1 1
1 1 1
1
| Photolysis and hydrolysis are not important processes in removing BHC
j from aquatic environment; apparently some biodegradation of BHC.
| (Ref.l)
i
| Quite stable; does bioconcentrate; does not readily hydrolyze or
j photolyze in H^O. (Ref.3)
j Inhibition of bacteria cell multiplication starts at 75 mg/1. (Ref.2)
1
-------
DATA FOB EVALUATION Of BIODEGRADAXIOH, HYDROLYSIS L PHOTOLYSIS (BUP) - Continued
Hazardous Substance
1 CAS Ho. I B I B
P | Data / Comments
beta - BUC
1 1 i
| 319857| |
1 1 1
1 1 1
1 1 1
1 1 1
1 1 1
1 1 1
1 1 1
1 1 1
| Photolysis and hydrolysis art not important processes in removing BBC
| from aquatic environment; apparently some biodegradation of BUC.
| (Ref.l)
i
| Quite stable; does bioconcentrata; does not readily bydrolyse or
j photoloyze in B^O. (Rot.3)
j Inhibition of bacteria cell multiplication starts at 75 ag/1. (Ref.2)
j
gamma - BHC
1 1 1
j 58099| |
i i i
i i i
i i i
i i i
i i i
i i i
i i i
i i i
1
| Photolysis and hydrolysis are not important processes in removing BHC
| from aquatic environment; apparently soae biodegradation of BUC.
I (Ref.l)
1
| feiite stable; does bioconcentrata; does not readily bydrolyse or
j photoloyze in H^O. (Ref.3)
j Inhibition of bacteria cell multiplication starts at 75 mg/1. (Ref.2)
I
2,2'-Bioxirane
i i i
| 14645351 |
i ii
1
| No data
i
Bis (2-chloroetfayl) ether
1 1 1
| 111444| |
1 1 1
1 1 1
1 1 1
1 1 1
1 1 1
1 1 1
1 1 1
1 1 1
1 1 1
1 1 1
1
| Ho information was found fron which any conclusion regarding
| biodegradation can be reached with any degree of confidence.
| Biodegradation may ba important in acclimated settling ponds. (Ref.l)
1
| Hydrolysis of the carbon—chlorine bonds is a slow but perhaps
| significant process. Half-life "0.5-2 years. (Ref.l)
1
| Direct photolysis is probably not important. (Ref.l)
1
| Potential for accumulation. (Ref.3)
i
Bis(chloromethyl) ether
1 1 1
| 5426611 j X
i i i
i i i
i i i
1 1 1
1
| Biodegradation is not likely. (Ref.l)
j Rapid hydrolysis; half-life = 10-40 sec. (Ref.l)
| The expected degradation products are formaldehyde and HC1.
| Photolysis probably does not occur. (Ref.l)
i
Bis (2-ethylhexyl) phthalate
1 1 1
| 117817| |
1 1 1
1
| 5000-pound RQ (maximum level) already assigned.
1
Cacodylic acid
1 1 1
| 75605| |
I I i
1
| Ho data
i

1 1 I
j 7440439) |
1 1 1
1
| Inorganic
I
Cadmium acetate
1 1 1
| 543906| |
I I I
1
| Inorganic
t
Cadmium bromide
1 1 1
j 7789426) j
I I I
i
| Inorganic
i
Cadmium chloride
1 1 1
110108642 j |
i I I
1
| Inorganic
i
Calcium arsenate
1 1 1
| 7776441| |
i i i
1
| No data
Calcium arsenite
1 1 1
|52740166| |
1 1 1
1
| No data
i
-------
QATA FOB EVALUATION OF BIOOEGBAQKTIOH, HYDROLYSIS k PHOTOLYSIS (BHP) - Continued
Hazardous Substance
1 CAS Ho.| B
H I P I Data / Comments
Calcium chrornate
1 1
j13765190|
1 1
i i
| | No data
| 1
Carbon tetrachloride
t 1
| 56235|
i i
i i
i i
i i
i i
i i
i i
i i
i i
i i
i i
i i
i a
1 1
| | Biodegradation probably occurs at an «xtr«Mly slow rate. (Ref.l)
| j Inhibition of bacteria cell multiplication starts at 30 taq/1. (Ref.2)
i i
| | Hydrolysis is too slow to be a significant fate process; the ninimia
| | hydrolysis rate is 7000 years. (Bef.l)
1 1
| | Photolysis is probably not significant in aquatic systems. Photolysis
j j in the stratosphere is the primary fate of this compound. (Hef.l)
1 1
| | Volatilization is the primary transport process from the aquatic
| | environment. (Ref.l)
1 1
| | Some evidence of bioaccumulation. (Hef.3)
1 1
Chloral
1 1
| 75876 j
i i
i i
1 1
| | Inhibition of bacteria cell multiplication starts at 1.6 mg/1.
I | (Ref.2)
i i
Chlorambucil
i i
| 305033|
i i
1 1
| | Ho data
i i
Chlordana
1 1
j 37749 j
1 1
1 1
1 1
1 1
1 1
1 1
1 1
1 1
1 1
1 1
1 1
1 1
1 1
1 I
1 1
| | Although biodegradation of chlordane is very slow, it may be an
j j important process for ultimate degradation. (Hef.l)
1 1
| | Hydrolysis 1b not an important process (half-life >4 years). (Hef.l)
1 1
| | Photolysis probably requires a sensitiser. (Ref.l)
1 1
| | 45* remained after 24 hours exposure to UV radiation (unspecified
j j products). (Bef.S)
1 1
| | High potential for bioaccumulation; will contaminate food chain,
j j (Bef.1(7)
1 1
| | Volatilization is probably an important process. (Ref.l)
1 1
Chlornaphazine
| 494031|
i i
1 1
| | Bo data
i i
-------
DATA FOB EVALUATION OF BXODEGBADAXIOH, HYDROLYSIS i PHOTOLYSIS (HHP) - Continued
Hazardous Substance
I CAS Bo. I B | H
P | Data / Comments
Chloroform
1 1 1
| 67663| |
1 1 1
1 1 1
1 1 1
1 1 1
1 1 1
1 1 1
1 1 1
1 1 1
1 1 1
1 1 1
1 1 1
1 1 1
1 1 1
l l l
1
| No specific information was found on the biodegradation of
j chloroform. (Bef.l)
| Little or no biodegradation in FOTW.
j Subject to limited biodegradation. (Bef.3)
1
| Hydrolysis is probably not a significant fata process. Half-life = 15
| months — 3500 years. (Hef.l)
1
| Photolysis is probably not significant in aquatic systems. (Bef.l)
1
| The primary fate of this compound is attack by hydroxy1 radicals in
| the troposphere. (Bef.l)
1
| Inhibition of bacteria cell multiplication starts at 125 mg/1. (Ref.2)
I
4-Chloro-o-toluidi.no, hydrochloride
1 1 1
| 3165933| |
l I I
1
| No data
I
Chloromethyl methyl ether
1 1 1
| 107302| | X
1 1 1
1 1 1
1
| Cbloromethyl nothy1 ether undergoes decomposition in water to form
| methanol, formaldehyde, and hydrochloric acid.
1
Chromic acid
1 1 1
|11115745| |
l l I
1
| Inorganic
i
Chromium
1 1 1
| 7440473| |
1 1 1
1
| Inorganic
I
Chrysene
1 1 1
| 218019| |
1 1 1
I
| Ho data
1
Creosote
1 1 1
| 80015S9| |
I I I
1
| No data
a
Cupric acetoarsemte
1 1 1
112002038| |
I II
1
| No data
i
Cyclophosphamide
1 1 1
| 50180| |
1 1 1
l
| Bo data
i
Daunomycin
1 II
|20830813| |
l l l
1
| Bo data
i
DDD
1 1 1
1 72548| |
1 1 1
1 1 1
1 1 1
1 1 1
1 1 1
1 1 1
1 1 1
1 1 1
1 1 1
a
| Biodegradation very slow. (Bef.l)
1
| Hydrolysis is not an important process. Half-life - 570 days 8 pH •>
j 9, 190 years 8 pH = 5. (Bef.l)
1
| Photolysis is not an important process. Half-life <= >150 years in
| HjO. (Hef.l)
j Persistent in water and sediments, will bioaccumulate. (Bef.l)
1
-------
DATA FOB EVALUATION 0? BIODEGBADATIOH, HYDEOLYSXS i PHOTOLYSIS (BHP) - Continued
Hazardous Substance
I CAS Ho. | B | H
P ( Data / Comaents
DDE
1 1 1
1 725591 |
1 1 1
1 1 1
1 1 1
1 1 1
1 1 1
1 1 1
1 1 1
1 1 1
1 1 1
1 1 1
i
| Biodegradation very slow. (Bef.l)
1
] Hydrolysis is not an important process. Half-life = >120 years § pH
| ~ 5. (Ref.l)
1
| Photolysis can be an important process for DOE in water. Half-life
| for photolysis in HO o 1 day in strong sunlight, ti days in weak
j sunlight. (Ref.l)
1
| Bioaccunulation is an important process. (Bef.l)
i
DDI
1 1 1
| 50293| |
i i i
i i i
i i i
i i i
i i i
i i i
i i i
i i i
i i i
i i i
i i i
i i i
i i i
i i i
i i i
i i i
1 1 1
1
| DOT is chemically and biologically quite stable and its degradation
| poses a serious challenge. (Bef.4)
| Biodegradation is not an important removal process. (Bef.l)
| 54% DDT remained after 24-hour exposure to UV radiation (products
j unspecified). (Bef.5)
1
| Hydrolysis may be important under certain conditions,
j Half-life for hydrolysis = " 12 years 9 pH <5
j Half-life for hydrolysis « " 81 days ( pi ¦ S
1
| Direct photolysis is slow; indirect photolysis may be important.
| Half-life for direct photolysis in H^O » >150 years (forms DDE),
j Half-life for indirect photolysis in H^O "7 days (forms DDE).
j High potential for bioaccunulation. (Bef.l)
1
| Volatilisation is an important process. (Bef.l)
I
Diallate
| 2303164| |
i i i
i i i
i i i
i i i
i i i
1 1 1
1
| Diallate is an oily amber or brown liquid, almost insoluble in water
j and denser than water. Soil moisture displaces diallate from its poll
j adsorption sites and forces diallate into the vapor phase. In
j alkaline medium, diallate is hydrolyaed.
| Hydrolysis is at the ester linkage and foras a oarcaptan, CO^, and
j an alkylamina. (Ref.3)
1
2,4-Diaminotoluene
1 1 1
| 95607| |
i (i
1
| Bo data
|
Dibenz(a,b1anthracene
1 1 1
1 53703| |
t 1 i
1
| Bo data
1
Dibsni(a,i]pyrene
t \ \
| 189559| |
i i i
I
| No data
¦
1,2-Dibromo-3-chloropropane
1 1 1
| 96128| j
1 1 1
1
| Ho data
i
-------
DMA FOB EVALUATION OP BIODEGHADATION, HYDROLYSIS k PHOTOLYSIS (BHP) — Continued
Hazardous Substance
CAS Ho.I B
Data / Comments
3,3'-Dichlorobenzidine
91941
1,2-Dichloroethane
107062
O
3,3'-Dichlorobenzidine does not appear to be degraded by aquatic
microorganisms. activated sludge, fish or terrestrial mammals. (Ref.l)
Hydrolysis is probably not inportant. (Ref.l)
Photolysis probably nakes a direct contribution to the aquatic fate
of 3,3'- 30l removed 020 C with 365+ day acclimated sewage
seed; reed conc. = 400 mg^l
BOD. a 9% removed 820 C with 365+ day acclimated seed; feed
conc. • 1000 mg/1 (Ref.6)
BOD. " 0% ThOD; BOD.. = 18% ThOD; subject to some biodegradation;
relatively stable to chemical attack in water. (Ref.3)
BOD. » 7% of ThOD;
Inhibition of bacteria cell multiplication starts at 135 mg/1. (Ref.2)
BODs ° 0.002 lb/lb.
Hydrolysis probably occurs too slowly to be a significant fate
process (half-life ~ 50,000 years). (Ref.l)
Photolysis appears to be insignificant in the aquatic environment.
The slow photo-oxidation in the atmosphere probably leaves some
unreacted compound to diffuse upward above the ozone layer to undergo
photodissociation. (Ref.l)
Photo-oxidation in the troposphere appears to be the predominant fate
of this compound. Photo-oxidation in the aquatic environment occurs
at a slow rate. Direct oxidation at ambient conditions does not
occur significantly in the aquatic or atmospheric environment. (Ref.l)
Volatilization is the primary transport process. (Ref.l)
-------
DATA FOB EVALUATION OF BIODEGRADATIOH, HYDaOLJSIS t PHOTOLYSIS (BUP) - Continued
Hazardous Substance
I CAS NO.| B | a
P | Data / Comments
1,1-Dichloroethylena
1 i 1
1 75354| |
1 1 1
l l l
i
| Little biodegradation in POTW; little photolysis or biodegradation;
j half-life for hydrolysis = 1 year. (Bef.l)
¦
Dichlorophenylarsine
1 1 1
| 696286| |
1 1 1
1
| Ho fate and effects data available.
I
Dieldnn
1 1 1
| 60571| |
1 1 1
1 1 1
1 1 1
1 1 1
1 1 1
1 1 1
1 1 1
1 1 1
1 1 1
1 1 1
1 1 1
1
| Biodegradation is not an important removal process,
j Several authors cite dieldrin as being one of the more
| nonbiodegradable chlorinated pesticides. (Bef.l)
1
| Hydrolysis is not an important process. Half-life for hydrolysis =
j >4 years. (Bef.l)
1
| Direct photolysis may be important. Half-life for photolysis in water
| o 2 months (forms photodieldrin which is toxic). (Bef.l)
| Does bioaccuttulate, will contaminate the food chain. (Baf.3)
Diethylarsine
1 1 1
| 692422| |
1 1 1
1
| Spontaneously flaasoable
1
1,4-Diethylene dioxide
1 1 1
| 123911j |
1 1 1
I I I
1
| Inhibition of bacteria cell multiplication starts at 2700 aq/l.
| (Bef.2)
l
H, U'-Diethylhydragine
1 1 1
| 1615801| |
1 1 1
1
| Ho data
I
Diethylstilbestrol
1 1 1
1 56531| |
I I I
1
| Ho data
I
Dihydrosafrole
1 1 1
| 94586| j
1 1 I
1
| Bo data
j
3,3'-Dimethoxybensidine
1 1 1
| 119904| X j
1 1 1
1 1 1
i i i
j Degradation by aerobactor: 500 og/1 G 30 C (Kef.2)
j % ring disruption: parent: 78% in 120 hr
j mutant: 100% in 36 hr
i
Dime thy lanunoazobenzene
1 1 1
j 60117| j
i i i
I
| Ho data
i
7,12-Dioethylbensla]anthracene
1 1 1
1 57976| |
1 1 1
1
| Ho data
a
3,3'-Dimethylbenxidine
1 1 1
| 119937| |
I I I
1
| Ho data
i
Dimethylearbamoyl chloride
1 1 1
| 79447) |
I I I
1
| Ho data
i
1,1-Dimethylhydraiine
1 1 1
1 57147) |
1 1 1
1
| Ho data
1
1,2-Dimethylhydrazine
1 1 1
| 540738| j
i i i
1
| Ho data
i
Dimethyl sulfate
i 1 1
| 77781| | X
1 1 1
1 1 1
1 1 1
1 1 1
1 1 1
1
| Ho BOD data available.
| Hydrolyses rapidly @ 18 C or higher fon&ing sulfuric acid and
| methanol. (Ref.3)
i
| Will not concentrate in food chain. (Bef.3)
1
-------
DATA FOR EVALUATION OP BIODEGBAOAXION, HYDROLYSIS L PHOTOLYSIS (BHP) - Continued
Hazardous Substance
I CAS Bo. I 8 | 11
P | Data / Consents
Diaitrotoluene
3,4-Dinitrotoluene
1 i i
|253211461 |
j 610399| |
1 1 I
i
| Sea data for 2,4- and 2,6- isomers below.
1
I
2,4-Dinitrotoluene
1 1 1
| 121142| J
i i i
i i i
i i i
i i i
i i i
i i i
i i i
i i i
i i i
i i i
t i i
i i i
i i i
i i i
1 1 1
1
| Biodegradation Is slow but could be significant depending upon
J relative rates of other fate processes. (Ref.l)
j 52% degradation of 100 ppa solution by phenol adapted bacteria in 3
j hours.
j Amenable to biological treatment at POTW when diluted. (Bef.3)
j Inhibition of bacteria cell multiplication starts at 57 ag/1
| (Pseudomonas putida). (Bef.2)
1
| Hydrolysis is highly improbable based on the compounds resistance to
j electrophilic attack. (Bef.l)
1
| Phyotolysis is probably responsible for color development in munition
j plant effluents. (Ref.l)
1
| Oxidation may be important in highly aerated watorB. (Ref.l)
i
2,6-Dinitrotoluene
1 1 1
| 606202| |
i i i
i i i
i i i
i i i
i i i
i i i
i i i
1 1 1
1
| Biodegradation is slow but could be significant depending upon
j relative rates of other fate processes. (Bef.l)
1
| Hydrolysis is highly improbable based on the compound's resistance to
1 electrophilic attack. (Ref.l]
1
| Photolysis is probably responsible for color development in aunition
j plant effluents. (Ref.l)
|
1,2-Diphenylhydrazine
1 1 1
| 122661| |
i i i
i i i
i i i
i i i
i i i
i i i
i i i
i i i
i i i
i i i
i i i
i t i
1
| Vertebrates transform this pollutant to aniline and bensidine; no
| specific data are available. (Ref.l)
i
| Hydrolysis is not expected to occur under environmental conditions.
I (Bef.l)
1
| Although photoreduction to aniline is not expected to proceed
| rapidly, it say make a significant contribution to what nay be the
| main pathway to ultimate destruction. (Bef.l)
1
| Bioaccumulatioa is highly probable based on partition coefficients;
j no environmental data available. (Ref.l)
1
Eplchlorohydrin
1 1 1
| 1068981 |
1 1 1
1 1 1
1 1 1
1 1 1
1
| Biodegradation nay occur. (Bef.3)
I
| inhibition of bacteria cell nultiplic&tion starts at 55 mg/1
j (Pseudomonas putida). (Ref.2)
i
Ethanethioaaide
1 1 1
1 62555| |
i I I
1
| BOD^ 3 0% ThOD. (Ref.2)
2-Ethoxyethanol
1 1 1
| 110805| 1
1 1
1
| Bo data
!
Ethyl carbamate (Urethan)
1 1 1
1 *179*1 1
1 1 1
1
| No data
i
-------
DATA FOR EVALUATION OP BIODEGRAQATION, HYDROLYSIS t PHOTOLYSIS (HHP) - Continued
Hazardous Substance
CAS Bo. | B | H
P I Data / Comments
Ethyl 4,4'-dichlorobenxilate
1 1
5101S6| |
j j
1
| So data
1
Ethyl methanesulfonate
62500| |
I I
1
| Ho data
1
Ethylene dibromide
1 1
106934| |
1 i
1
| Bo data
¦
Ethylene oxide
1 1
¦752191 |
1 1
1 1
1 1
1 1
¦ |
i
| Negative potential for accumulation. (Ref.3)
j Ethylene oxide (b.p. 10.7°C) is flammable and explosive in air
j The aqueous solution is fairly stable, but is slowly hydrolysed to
| ethylene glycol. (Ref.4)
1
Ethylenethiourea
96457| |
1
1
| Ho data
i
Formaldehyde
1 1
50000| X |
1 1
1 1
1 1
1 1
1 1
1 1
1 1
1 1
1 1
1 1
I i
1
| BOD^ 5 a nil t ThOD - less than 1 day acclimated seed
j BOD. , • 52% ThOD - sewage treatment seed
j BOD, o 8t ThOD @20°C with MeOH acclimated seed;
j feed conc. n 500 aq/1. (Ref.6)
1
| Subject to biodegradation and photochemical attack at the unsaturated
j bond;
j BOD. = 47% ThOD, activated sludge
j BODg ° 94% ThOD (Ref.3)
| BODj i 60% ThOD (Ref.2)
Glycidylaldehyde
1 1
765344| j
j j
1
| So data
1
Guanidine, N-nitroso-N-methyl-tT-aitro-
70257| |
I i
1
| Ho data
i
Heptachlor
1 1
76448| |
1 1
1 1
1 1
1 1
1 1
1 1
1 1
1 1
1 1
1 1
1 1
1 1
1 1
1 1
1 1
1
| Slow biodegradation. (Ref.l)
1
| Hydrolysis is a rapid process for heptachlor in solution. Half-life ¦
j 1 to 3 days in the environment, with the hydrolysis products
j 1-hydroxychlordene and heptachlor epoxide.
1
| Stable to hydrolysis.
j Heptachlor is said to be stable to at least 160 C and to light
| moisture, air and oxidising agents, acids and alkali. Heptachlor is
j rather easily converted to the epoxide in soil and plants. (Ref.4)
1
| Will undergo photolysis at undetermined rate to form dechlorinated
| heptachlor isomers and heptachlor epoxide.
1
| High food chain contamination potential. (Ref.3)
1
-------
DATA FOB EVALUATION OF BIODEGRADATION, HYEKOLYSIS t PHOTOLYSIS (BHP) - Continued
Hiurdoua Substance
I CAS Ho.| B | H
P t Data / Comments
Heptachlor epoxide
1 1 1
| 1024573| |
1 1 1
1 1 1
1 1 1
1 1 1
1 1 1
1 1 1
1
| Biodegradation is very slow, but could be important. (R»f.l>
1
| Hydrolysis is not an important process. (Ref.l)
1
| Bo quantitative information was available concerning photolysis.
I (Ref.l)
Hexachlorobeneene
1 1 1
| 118741| |
i i i
i i i
i i i
i i i
i i i
i i i
i i i
i i i
i i i
i i i
1 1 1
I
| Biodegradation occurs extremely slowly, if at all. (Ref.l)
' o
| Degradation by Fseudooonas: 200 mg/1 030 C (Kef.2)
| parent: 0% ring disruption in 120 hours
| mutant: 0% ring disruption in 120 hours
1
| Hydrolysis does not occur in ambient waters. (Ref.l)
j Estimated half-life in river water = 0.3-3 days, in soil 4 years.
| (Ref.3)
1
| Photolysis does not occur readily. (Bef.l)
1
Hexachlorobutadiene
1 1 1
| $7683| |
i i i
1 1 1
1
| No information was found in the reviewed literature on the
| biodegradation or hydrolysis of hexachlorobutadiene.
1
O
l-j
1 1 1
i i i
( i i
1 1 1
1
| Hexachlorobutadiene does not strongly absorb light above 290 mm.
1 Photolysis is therefore probably not important. (Ref.l)
I
1 1 1
i i i
I I i
1
| Positive potential for accumulation from water. (Ref.3)
1
Hexachlorocyclopentadiene
1 1 1
1 77474| |
i i i
i i i
i i i
i t i
t i i
i i t
i i i
i i i
i i i
i i i
i i i
i i i
i i i
i i i
1
X | Biodegradation does not appear to be an important fate process.
I (Ref.l)
1
| Hydrolysis appears to be an important fate process. (Ref.l)
j Half-life for hydrolysis ° 14 days (same product as photolysis),
j Forms RCl. (Ref.l)
t
| Photo-oxidation may occur. (Ref.l)
1
| Bear-surface photolysis is an important process. (Ref.l)
j Half-life for photolysis in water - 11 minutes (forms
| tetrachlorocyclopentadienone hydrate).
1
| Volatilisation appears to be important in flowing waters. (Ref.l)
)
-------
DATA FOB EVALUATION OP BIODEGRADATION, HTOROLXSIS t PHOTOLYSIS (HHP) - Continued
Hazardous Substance
| CAS Ho. | B | H
P I Data / Comments
Hexachloroethane
1 1 1
1 <77211 1
1 1 1
1 1 1
1 1 1
1 1 1
1 1 1
t 1 1
1 1 1
1 1 1
1 1 1
1 1 1
1
| Little or no removal in a POTW.
| Ho specific information was found concerning the biodegradation or
| hydrolysis of hexachloroathane. (Ref.l)
1
| Hexachloroethane probably does not undergo photo-dissociation in the
j aquatic or lower atmospheric environments. Photodissociation in the
| stratosphere may be important. (Ref.l)
1
| Evidence is inconclusive as to the relative importance of
j volatilisation. (Bef.l)
I
Hydrazine
1 1 1
| 302012| |
i i i
i i i
i i i
i i i
i i i
1 1 i
1
| Rapidly reacts with dissolved 0. to form HH.OH and
j decompsition accelerated by UV fight; no potential for
| bioaccumlation. (Ref.3)
1
| Impact on biodegradation processes: 75% inhibition of nitrification
j process of non-acclimated activated sludge at 48 mg/1. (Ref.2)
i
Indeno(1,2,3—cdjpyrene
1 1 1
| 193395| j
1 1 1
1
| Little likelihood of significant biodegradation.
i
Isosafrole
1 1 1
j 120581| |
i i i
1
| Ho data
1
Kepone
1 1 1
| 143500| j
i I i
1
| Bioaccumulates; not amenable to FOOT# treatnent. (Ref.3)
i
Lasiocarpine
1 1 1
| 303344| |
I I I
1
| No data
1
Lead
I 1 1
| 7439921| |
i i i
1
| Metallc lead is not sub3ect to BHP.
i
Lead acetate
1 1 1
| 301042| j
1 1 1
I I I
1
| Inhibition of bacteria cell nultiplicatioa starts at 1.8 ng/1
| (Pseudomonaa putida). (Ref.2)
i
Lead arsenate
1 1 1
| 7784409| |
i i i
1
| Ho data
i
Lead phosphate
1 1 1
| 7446277| |
1 I I
1
| No data
i
Lead subacetate
1 1 1
| 1335326| |
i i i
1
| No data
i
Lithium chromate
1 1 1
|14307358| |
i i i
1
| No data
¦
Melphalan
1 1 1
| 148823| j
I I I
i
| Ho data
i
2-Methylaziridine
1 1 1
1 75558| |
1 1 l
1
| Bo data
I
Methyl chloride
1 1 1
| 74873| j
1 1 1
1 1 1
1 1 1
1 1 1
1 1 1
t 1 1
1 1 1
1
| Biodegradation is probably not important. (Ref. 1) Hydrolysis is
j probably not a significant fate. Half-life^417 days. (Ref 1)
| Photolysis is not significant in aquatic systems,
j The predominant environmental process which is thought to determine
j the fate of of this compound isoxidation in the
j troposphere via attack by hydroxyl radicals. (Ref.l)
j Volatilization is the primary transport process. (Ref.l)
1
-------
DATA FOB EVALUATION OF BIODEGHADATIOff, HTOBOLXSIS 4 PHOTOLYSIS (BHP) - Continued
Hazardous Substance
1 CAS Bo. 1 B 1

3-Mothylcholanthrane
1 1 1
1 56495j |
1 1 1
1 | P 1 Data / Comments
| | No data
i i
4,4 '-Matiiylenabis (2-chloroaniline)
1 1 1
j 10U4 79 hours in aerated distilled H.O at
j j initial conc. of 74 ag/1; no hydrolysis or biode^radation. (Kef.l)
I i
K-Hitrosodi-o-propylamine
1 1 1
| 621647| |
1 1 1
1 1 1
1 I
| | Photolysis similar to dimethyliutrosaaina; half-life is 79 hours in
| | aerated, distilled H^O; no hydrolysis, slow biodegradation. (Hef.l)
-------
DATA FOR EVALUATION OF BIODEGRADATION, HYDROLYSIS L PHOTOLYSIS (BHP) - Continued
Hazardous Substance
I CAS So. | B | H
P | Data / Comments


N-Nitroso-H-etbylures
1 i 1
| 7S9739| |
1 1 1
i
| No data
I


N-Nitroso-N-nethylurea
| 684935| |
1 1 1
I
| No data
1


N-Nitroso-N-oetbylurethane
1 1 1
| 615532) |
1 1 1
1
| No data
j


H-Nitrosomethylvinylamine
| 4549400| |
1 1 1
1
| No data
j


H-Nitrosopiperidlne
1 1 1
| 100754| |
1 1 1
1
| No data
1


N-Nltrosopyrrolidlne
1 1 1
| 930552| |
1 1 1
1
| No data
i


Parathion
1 1 1
| 56182| |
I 1 1
i
| High potential for bioconcentration.
i


1 1 1
1 1 1
1 1 1
i
| Photolysis products are
1
quite toxic. (BeC.5)


1 1 1
1 1 1
1
| Parathion is relatively
resistant to hydrolysis. (Ref.4)


1 1 1
j Hydrolysis half-life:



1 1 1
j (a) half-life £ pH »
3.1 = 4182 hours (Corns Paraxon
(toxic))

1 1 1
j (b) half-life $ pH e
7.4 = 2594 hours (Coras Paraxon
(toxic))

1 1 1
j (c) half-life £ pH «»
10.4 o 33.2 hours (forms Paraxon
(toxic))

1 1 1
j Half-life of Paraxon:



1 1 1
j (a) half-life § pH »
3.1 = 4726 (Corns p-Nitrophenol
(toxic))

1 1 1
j 
-------
DATA FOR EVALUATION OP BIODEGRADATIQH, HYDROLYSIS t PHOTOLYSIS (BHP) - Continued
Hazardous Substance
CAS Bo. I B
Data / Comments
Pentachlorophenol
0
1
N3
67865
Phenacetin
1 1
| 62442)
| 1
Folychlorinated biphenyls (PCBs)
1 |
| 113636)(
1 1
1 I
Potassium arsenate
1 1
I 1
| 7764410 j
I |
Potassium arsanite
1 1
|101245021
¦ •
Potassium bichromate
1 1
| 7773509)
• i
Potassium chromate
| 77S9006]
i i
1,3-Propane sultone
1 1
| 1120114|
1 1
In a well-documented study of a fresh-water lake, two accidental
spills were metabolised to pentachloroanisola and a mixture of
chlorinated phenols. (Ref.l)
Bo specific information was found regarding hydrolysis; hydrolysis is
thought NOV to be an important process. (Bef.l)
Photolysis of pentachlorophenol is reported to occur under natural
conditions and It is probably an important process near the water
surface. (Ref.l)
Photolysis of aqueous PCP by sunlight produces a series of
degradation products in which chlorine atoms are replaced by hydroxyl
groups followed by air-oxidation to quinones and other
reactions. Principal products are C CI (OH)
C,C1. (OH)-C-C.C1 0 (OH),and C,Cl,72 days for
coaplste disappearance. (Set.2}
Wastewater treatment: degradation by Fseudoaonas: 200 aj/1 at 30°C
parent:	7% ring disruption in 120 hours
mutant:	26% ring disruption in 120 hours (Bef.2)
Half-life for photolysis 4.75 hours - 1.5 days; products s
chloranilic acid, chlorinated phenols, chlorinated dihydroxylensenea;
Hydrolysis - not important. Biodegradation — does biodagrade;
products = pentachloroanisole k chlorinate phenols. Bef. ?
Persistent/bioaccumulates. (Kef.?)
No data
PCBa are stable to hydrolysis. (Bef.l)
PCBs are stable to oxidation. (Bef.l)
High potential for bioaccumulation.
BOD - very alow.
Ho data
No data
Bo data
Bo data
So data
-------
DATA FOB EVALUATION OF BIODEGBADAXION, HYDROLYSIS & PHOTOLYSIS (BHF) - Continued
Hazardous Substance
I CAS No.| B I H
P | Data / Comments
Saccharin and salts
1 1 1
| 81072| |
1 1 1
i
| Ho data
1
Safrole
1 1 1
| 94597| |
I I I
1
| No data
i
Sodiua arsenate
1 1 1
| 76318921 |
1 1 i
1
| No data
i
Sodium arsenite
1 1 1
| 7784465| j
i 1 i
1
| No data
i
Sodium bichromate
1 1 1
|10588019| j
i I i
1
| No data
i
Sodiua chromata
1 1 1
j 7775113 j |
i I i
1
| No data
a
Sulfur selemde
1 1 1
| 7488564| |
1 1 1
1
| No data
i
streptozotocin
1188836641 |
i i i
1
| No data
1
Strontium chromata
| 7789062| |
i 1 i
1
| No data
1
2,3,7,8-Tetrachlorodibenzo-p—dioxin
(TCDD)
1 II
| 1746016| |
1 1 1
1 1 1
1 1 1
1 1 1
1 1 1
1 1 1
1 1 1
1 1 1
1
| Half-life for biodegradation in H^O - >1 year. (Rof.l)
| Hydrolysis does not occur, (fief.l)
i
| Can photolyze if reactive substrates are available. (Ref.l)
1
| Bioaccumulation likely. Can photolyze in solvent with 777?. No
j hydrolysis likely.
I
1,1,1,2-Tetrachloroethane
| fi30206| |
i i i
1
| No data
|
1,1,2,2-Tetrachloroethane
1 1 1
| 79345j |
1 1 1
1 1 1
1 1 1
1 1 1
1 1 1
1 1 1
1 1 1
1 1 1
1 1 1
1 1 1
1 1 1
1 1 1
1
| Bioaccumulation unlikely.
| Biodegradation probably occurs at a low rate, if at all. (Ref.l)
1
| Hydrolysis appears to occur too slowly to be a significant fate
| process. (Kef.l)
1
| Photolysis is probably not significant in aquatic systems; photo-
| dissociation in the stratosphere is probably a significant fate
| process for this compound. (Bef.l)
1
| Since the vapor pressure of this compound is reasonably high,
| volatilisation probably serves as the primary transport process.
1
-------
DMA FOR EVALUATION OP BIODEGRADATIOH, HYDROLYSIS t PHOTOLYSIS (BHP) - Continued
Hazardous Substance	| CAS Ho.| B | U | P | Data / Comments	
| CAS Ho.|
Tetrachloroethylene
Thiourea
o-Toluidine
p-Toluidine
o-Toluidine hydrochloride
Toxaphene
127184
62566
95534
106490
636215
8001352
Soma evidence of biodegradation in seavater. (BeM)
There ia evidence that metabolic products of tetrachloroethylene from
higher organisms can be biodegraded by aicrogranisms in sea water.
(Ref.l)
Hydrolysis probably occurs too slowly to be a significant fate
process. Half-life for hydrolysis ° 8.8 hours. (Ref.l)
Photolysis - substance is photo-oxidized before photolysis can occur.
Photolysis probably does not occur. Photo-oxidation destroys
tetrachloroethylene, before it can reach the stratosphere, which is
the region above the ozone layer where direct photolysis could occur.
(Ref.l)
Photolysis gives phosgene and trichloroacetyl chloride.
Photo-oxidation in the troposphere appears to be the predominant fate
of this compound. Photo-oxidation in the aquatic environment occurs
at a slow rate. Direct oxidation at ambient conditions does
not occur in the aquatic or atmospheric environment. (Ref.l)
Volatilization is the primary transport process. (Ref.l)
Impact on water pollution treatment processes: 75% reduction of
nitrification process of nonacclimated activated sludge at 0.075
mg/1. (Ref.2)
45% ThOD (Ref. 3)
BODs
Ho data
Ho data
Does not biodegrade in aerobic systems but does in unaeorobic
systems. (Ref.l)
Half-life for hydrolysis = >10 years. (Ref.l)
Half-life for photolysis in H^O o >10 years. (Ref.l)
Positive potential for bioaccumulation; dehydrohalogenator in strong
sunlight. (Ref.l)
-------
DATA FOB EVALUATION OP BIODEGRADATION, HYDROLYSIS I PHOTOLYSIS (BHP) - Continued
Hazardous Substance
CAS Ho.I B
Data / Comments
1,1,2-Tnchloroethane
79005
Trichloroethylene
79016
0
1
to
-P
Trichlorophenol
2,4,5-Trichlorophenol
25167822
95954
Biodegradation probably occurs at a slow rat*. (Bef.l)
Hydrolysis probably occurs too slowly to be a significant fate
process. (Bef.l)
Photolysis is probably not significant in aquatic systems.
Photodissociation in the stratosphere may be a significant fate of
the compound. (Bef.l)
Volatilisation probably serves as the prioary transport process.
(Ref.1)
There is evidence that metabolic products of trichloroethylene from
higher organisms can be biodegraded by microorganisms in sea water.
(Bef.l)
BOD. = 0% ThOD. (Ref.3)
Inhibition of bacteria cell multiplication starts at 65 mg/1
(Pseudomonas putida). (Ref.2)
Hydrolysis probably occurs too slowly to be a significant fate
process. (Ref.l)
Photolysis probably does not occur since photo-oxidation destroys
trichloroethylene before it can reach the stratosphere. (Ref.l)
Trichloroethylene has a short tropospheric lifetime of approximately
4 days. Photolysis yields phosgene and dichloracetyl chloride.
After 20 days no biochemical oxidation occurred; TCE is concentrated
in aquatic species.
See data for specific isomers.
BOD 0.94 - 4.1% with pure bacteria culture. Half-life in surface
water » 1.9 days.
Hydrolyses at DP (~113°C). Ref. ?
Biodegradation: Decomposition in suspended soils >72 days for
complete disappearance. (Bef.2)
-------
DATA FOR EVALUAXIOB OF BIOOEGBADATIOH, HYDROLYSIS k PHOTOLYSIS (BHF) - Continued
Hazardous Substance
CAS Ho.I a
Data / Comments
2,4,6-Trichlorophenol
88062
o
to Tris(2,3-dibromopropy1) phosphate
Cn
Trypan blue
Uracil mustard
Vinyl chloride
126727
72S71
66751
75014
Biodegradation has been demonstrated in soil samples and in
acclimated sewage sludge but it is uncertain as a process in ambient
surface waters. (Ref.l)
Biodegradation:
(a)	7-10 days needed to remove 95% of 300 ppa
2,4,6-trichlorophenol using sludge bacteria
(b)	at 100 ppm, 70% removed in 3 hours
(c)	in soil 5-13 days for complete removal (Ref.l)
Decomposition in soil suspensions: 5 days for complete disappearance.
(Ref.2)
Degradation by Pseudomonas: 200 mg/1 @30°C
parent: 100% ring disruption in 120 hours
mutant: 100% ring disruption in 50 hours. (Ref.2)
Biochemical oxidation of TCP § 100 ng/1 produced 23% degradation
using a phenol adapted seed.
Hydrolysis is not thought to be an environmentally relevant processs.
(Ref.l)
Photolysis has been reported but the environmental relevance is
uncertain. (Ref.l)
Photolysis - In the presence of electron acceptor can photooxidiie to
semiquinones — (2,6—dichlorobenzoquinones and 2,6—dichlorohydro—
quinone).
Ho data
Do data
No data
Resistant to microbial degradation. (Ref.l)
Hydrolysis is probably not a significant fate of this compound.
Hyrdrolysis half-life ¦ <10 years. (Ref.l)
Photolysis is not a significant fate process since photo—oxidation
destroys vinyl chloride before it can reach the stratosphere. (Ref.l)
Volatilization is the most important transport process for vinyl
chloride. (Ref.l)
-------
DA3A FOB EVALUATION OP BIODEGRADATIQN, HYDROLYSIS & PHOTOLYSIS (BHP) - Continued
Hazardous Substance
CAS Ho.
Data / Comments
REFERENCES:
Bef.l - "Hater-Belated Environmental Pat* of 129 Priority
Pollutants", Vol.1(2, EPA 440/4-79-O29 a(b, December 1979.
Ref.2 - "Handbook of environmental Data an Organic Chemicals", Earel
Verschueren, Van Rostrand Beinhold Company, New York, tnr,
copyright 1977 by Litton Educational Publishing Inc.
Bef.3 - The "Oil and Hazardous Materials Technical Assistance Data
Base" (OHKTADS), accessed as a machine-searchable
database via the EPA/NIH Chemical Information System (CIS).
Bef.4 - "Guidelines for the Disposal of Saall Quantities of Unused
Pesticides," EPA 670/2-75-057, June 1975.
Ref.S - "Report on Environmental Assessment of Pesticide Regulatory
Programs" State Component, Volume 2, State of California
Department of Pood and Agriculture, 1978.
Bef.fi - "Chemical Structure Resistant to Aerobic Biochemical
Stabilization," P.J. Ludzack and M.B. Ettinger,
14th Annual Purdue Industrial Waste Conference, Lafayette, Indiana,
May 5-7, 1959.
0
1
K)
CT)
-------
Appendix D
DERIVATION OF THE MULTISTAGE MODEL
D-l
-------
D-2
-------
APPENDIX D
DERIVATION OF THE MULTISTAGE MODEL
THE USE OF A MATHEMATICAL MODEL
To provide a quantitative measure of the carcinogenic potency of a
chemical, a causal relationship between the chemical dose level and the
occurrence of cancer is required. Such relationships cannot be derived
from fundamental theories, since quantitative theories for human
carcinogenicity do not, as yet exist. Instead, a relatively simple and
practical method has been used to establish this causal relationship. A
mathematical model of carcinogenicity with parameters determined by
fitting the model to experimental data for each of the potentially
carcinogenic chemicals was constructed. In order to do this, the
lifetime probability of cancer is expressed as a simple analytical
function of the continuous dose rate "d" to which a human being or animal
is subjected. The most widely used multistage model assumes the
probability to be of the form:
In practice, cancer could occur in the absence of the chemical. The
non-vanishing "background" effect is expressed in terms of the zero-dose
probability, P(o). It is therefore useful to introduce the quantity,
denoted by A(d), that represents the extra risk over background at the
dose-rate "d":
The quantity A(d), defined by Eq.(2), is a measure of the net effects due
to the particular chemical under consideration. The background effects
controlled by the parameter "qo" have completely dropped out of the
expression for A(d) which follows immediately from (1) and (2).
P(d) = 1 - exp [-(qQ+q1d+q2d2+...+qkdk)l
(1)
A(d) = lP(d)-P(o)]/[l-P(o)].
(2)
A(d) - 1 - exp [-q1d+q2d2+ ...
(3)
D-3
-------
The potency factor for a chemical can now be introduced in terms of a
prespecified level of extra risk. The potency factor, 1/ED^q, is simply
the inverse of the estimated dose, in mg/kg/day, associated with a
lifetime cancer risk, of 10%.
In the lov-dose limit, Eq.(3) reduces simply to
A(d) - q:d	(4)
The simple linear relationship in (4) was used originally by Crump (1979)
to introduce the potency factor q..*, which is given by the lower 95%
1	_5
confidence limit for the dose associated with an additional risk of 10 .
The factor q* is therefore a limit on the slope of the dose response
curve in the low dose limit. An important task involved in applying the
model to a given carcinogen is the statistical procedure used to estimate
the model parameters, q's, in the above equations. A detailed
description of this procedure is given below.
THE MAXIMUM LIKELIHOOD METHOD
The maximum likelihood method is a statistical estimating procedure that
selects the most likely model parameters on the basis of the experimental
evidence. In other words, the model parameters are obtained by
maximizing the probability of occurrence of the observed quantities. To
illustrate the procedure, the often encountered normal distribution is
used as an example. Assume that n independent observations, x^,
x-,...,x , are drawn from a normal distribution, or population, with mean
^	n	^
u and variance a . The probability that these values all occur jointly
is P =f(Xj,X2,...i*n)- Since the n sample values are independent, the
joint density function can be written as the product of the individual
probability density functions:
P = f(x1)f(x2)...f(xn),	(5)
where:
D-4
-------
!(,.) . -L_ exp (-^('l-)2)
1 e/IK	
-------
SL n n 1 ^ *2
~zr =0 = - a+ —3 .Vxru)
a i=l
2
yielding the maximum-likelihood estimate of a in the familiar form:
a2 = (JL) £ (xrS)2	(11)
n i-1 1
In parallel vith the above example, one can now write the joint
probability of occurrence of the observed results for a carcinogenicity
experiment vith q treatment groups as:
Po f (P(d.))xj (1 - P(d.))(Nj"Xj),	(12)
j=l 3	J
where represents the number of the total of animals in the ith
treatment group that are observed to be cancer-bearing at death. The
corresponding log-likelihood function is therefore:
g
L = {Xj In P(dj) + (Mj-Xj) In [1 - P(dj)]J.	(13)
If the lifetime probability of cancer, P(d), is estimated by the
multistage model, i.e., Eq.(l), it can be seen that L is maximized with
respect to the model parameters (q's) by setting the partial derivatives
to zero:
—j»—— =0 , j o 1, 2, ... g.	(14)
«ij-l
In the above, k in Eq. (1) has been set to be (g-1) which is given by the
number of treatment groups in the experiment. Here, it can be seen that
the problem has been reduced to that of applied mathematics, i.e., to
D-6
-------
solve g coupled equations, with fairly complicated analytical
expressions, for g unknown parameters. The required mathematical
algorithms are provided by many standard software procedures. The Agency
used computer code GLOBAL 82 in deriving hazard rankings. There is no
need to further explore the computer code realizing that the
maximum-likelihood estimates of the model parameters are in fact
calculated in terms of the observed quantities g, d^'s, x^'s and
Nj's of the experiment.
CALCULATION OF POTENCY FACTORS
tfith each performance of the maximum-likelihood procedure discussed
above, a set of the estimated model parameters, qQ	*s
obtained. One can return to Eq.(3) and obtain an estimated dose for a
specified A(d) value. The 10% A(d) value has been chosen partly because
it lies in the experimental range and because it avoids low-dose
extrapolation. In general, the full expression for A(d) as given in
Eq.(3), rather than the low-dose limit, Eq.(4), should be used as the
linear relationship and may hold only at very low doses for a given
chemical. By solving Eq.(3) for "d" with A(d) at 10% one immediately
obtains the maximum-likelihood estimate (MLE) of the potency factor
1/EDiq.
The	value so obtained is known in statistics as a "point estimate"
which provides no information on the precision of the estimate.
D-7
-------
Appendix E
A COMPARISON OF CHRONIC TOXICITY AND
POTENTIAL CARCINGENICITY AS PRIMARY CRITERIA
E-l
-------
E-2
-------
Appendix E
A COMPARISON OP CHRONIC TOXICITY AND POTENTIAL CARCINOGENICITY AS PRIMARY
CRITERIA
The agency considers potential carcinogenicity and chronic toxicity
(other than potential carcinogenicity) separately as parts of its primary
criteria for adjusting the statutory RQs of the CERCLA hazardous
substances. The Agency treats these tvo criteria separately even though
potential carcinogenicity can be considered a special type or subset of
chronic toxicity. This section provides the Agency's rationale for
considering potential carcinogenicity separately from other chronic
toxicity effects in adjusting the statutory RQs of the CERCLA hazardous
substances. A complete discussion on hov the Agency applies the chronic
toxicity criterion for adjusting RQs may be found in the reports
"Technical Background Document to Support Rulemaking Pursuant to CERCLA
Section 102, Volume 1," March 1985, and "Technical Background Document to
Support Rulemaking Pursuant to CERCLA Section 102, Volume 2," August
1986, which are available in the public docket on RQ rulemaking.
Chronic toxicity rankings for hazardous substances are derived from the
consideration of dose-related adverse effects. Adverse effects are
defined as any effects that result in functional impairment and/or
pathological lesions that may either affect the performance of an
organism or reduce its ability to combat additional insult. An increased
dose of such substances leads to a more pronounced effect, or an
increasing number of effects. Correspondingly, a decreased dose will lead
to a less pronounced effect, or a decreasing number of effects, until a
"no observed effect level" (NOEL) is reached. Chemical substances acting
in this manner may be considered threshold agents, since the organism can
tolerate continuing exposure to the substance, and either eliminate the
substance or marshall its defenses against the substance in such a manner
that it suffers no observable or measurable harm. Conventional
E-3
-------
toxicological methods have long been available to define "safe levels of
exposure" to these agents. Thus, conventional toxicological methods can
be used in ranking chronic toxicants.
Carcinogenic substances, on the other hand, give dose responses which are
consistent with no threshold in general. Therefore, "safe levels of
exposure" cannot be identified. This difference arises because cancer
seems to be different from other health problems. It is multifactor in
its causation and multistage in its development. First, cancer appears
often to be a disease of DNA damage, misrepair, or incomplete repair.
There is evidence that only a few molecules of a carcinogen are needed to
induce DNA damage. Second, cancer is a progressive process with long
latencies (as much as 10 to 20 years in man). Once the final stage of
carcinogenesis has started, the transformed cells appear to
self-replicate out of control of the normal growth processes. Vhen parts
of this cell mass invade neighboring tissue directly or are transferred
to distant sites through the circulatory system (a process known as
metastasis), malignant tumors (cancer) result. The initiating agent need
not be present once the process has begun. Third, many agents seem to
induce the same cancer. Thus carcinogens should not be considered in
isolation because carcinogens can act additively, at least, to produce
the same tumor. For the sake of argument, assume that a threshold dose
exists for each carcinogen. Even though the individual dose for each
substance might be below its respective threshold dose, the summation of
doses for several substances acting simultaneously or independently in
sequence might exceed the threshold for the individual organism.
Moreover, the sensitivity of individual organisms of the same species is
different. Therefore, meaningful (practical) thresholds cannot be
established even if they do exist for these agents.
Mathematical models have been developed to estimate the magnitude of harm
associated with exposure to various "nonthreshold" agents. Thorough
discussions of these models, their biologic basis, and uncertainties and
E-4
-------
limitations associated with their use can be found in the published
literature (Anderson, 1983 and Crump, 1984). This brief discussion is
intended to give the reader an appreciation that nonconventional
toxicological methods are more appropriate in evaluating the magnitude of
harm posed by carcinogens. The CAG methodology for ranking potential
carcinogens is described, and the application of this methodology to
assign RQs is compared to the chronic toxicity RQ assignments.
A step-vise process is employed in ranking potential carcinogens. First,
the biomedical evidence regarding the likelihood of an agent as a
potential human carcinogen is stratified using the CAG criteria. Second,
on the assumption that the agent is a potential human carcinogen, a
quantitative estimate of the strength (a potency factor) of the agent as
a potential human carcinogen is determined using an appropriate
extrapolation model. Coupling the qualitative weight of evidence to the
potency factor allows a systematic ranking of potential carcinogens.
Because of these fundamental differences, it is appropriate that
different ranking procedures be applied for ranking chronic toxicity and
potential carcinogenicity, even though potential carcinogenicity might be
considered as a form of chronic toxicity . While a superficial
similarity exists in that both methods use some measure of effective dose
level as one factor in developing an overall ranking, the relationship
between dose and response is different in the two. Dose as applied to
chronic toxicity rankings is related to the intensity or extent of the
toxic manifestations. Dose as applied to potential carcinogenicity is
related to the probability that cancer will occur.
The chronic toxicity procedure leads to classifying substances into the
usual five RQ levels. Even though the potential carcinogenicity procedure
could be adapted to yield five levels of ranking, only three were
assigned which are expressed as the 1-, 10-, and 100-pound RQ levels,
E-5
-------
leaving the 1000-pound and 5000-pound levels unused. Restricting
potential carcinogen rankings to the three lovest levels provides
increased protection to the public and the environment in terns of
response to releases of potentially carcinogenic agents.
E-6
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APPENDIX F
EVALUATION OF THE lOO-POUND RQ CAP FOR
POTENTIAL CARCINOGENS USING AIR DISPERSION MODELING
F-l
-------
F-2
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Appendix F
EVALUATION OF THE 100-POUND RQ CAP FOR
POTENTIAL CARCINOGENS USING AIR DISPERSION MODELING
To check the reasonableness of the 100-pound maximum RQ, EPA has
evaluated the cancer risk from releases of various quantities of some
moderate to weak potential carcinogens. The evaluation considered a
plausible scenario in vhich a substance is released into the environment
under the following conditions:
1.	The substance is a stable gas, a volatile liquid, or	an aerosol
that remains suspended in the air for long periods.	A volatile
liquid forms a pool with sufficient surface area	to permit
complete volatilization within 24 hours.
2.	The release occurs during stable meteorological conditions. The
wind speed is 1 meter per second (about 2 miles per hour).
3.	The substance is continuously emitted, or the emission time is
greater than the transit time to the point of exposure. This
makes it possible to ignore diffusion in the direction of
transport.
4.	The substance is released at ground level and moves dovnvind.
Any part of the substance reaching the ground is reflected back
into the air.
5.	The point of exposure is at ground level 30 meters (about 100
feet) directly dovnvind from the point of release.
6.	The duration of exposure is 24 hours.
7.	The person exposed veighs 70 kilograms (about ISO pounds) and
breathes 20 cubic meters of air each day.
F-3
-------
To estimate the concentration of a substance in the air at the point of
exposure, a gaussian dispersion model is used. The general form of the
model is:
3
c	concentration of the substance in the air (mg/m )
r	release rate (mg/s)
x	horizontal distance dovnvind from the point of release (m)
y	horizontal distance perpendicular to dovnvind (m)
z	vertical distance above the ground (m)
h	height of the release (m)
sy	horizontal dispersivity (m)
s vertical dispersivity (m)
z
v vind speed (m/s)
For the scenario under consideration,
x = 30 m
y a 0 m
z o 0 m
h » 0 m
Vol m/s
F-4
-------
For stable meteorological conditions, EPA's Office of Air Programs
(Workbook of Atmospheric Dispersion Estimate, 1970) has estimated
Sy = 2.6 m
s b 1•65 m
z
Using these values in the general model gives the scenario-specific model
3
c o 0.074r s/m
For a release of 1 pound (454,000 mg) in 1 day (86,400 s), the release
rate is 5.255 mg/s, and the concentration is
c = 0.390 mg/m"*
3
In 24 hours an exposed person vho weighs 70 kg and breathes 20 m of
air receives a dose of
(0.390 mg/m^) (20 m^) / (70 kg) = 0.111 mg/kg
EPA's guidelines for carcinogen risk assessment (51 FR 33992-34003)
recommend expressing this cumulative dose as an average daily dose
prorated over a lifetime, in the absence of evidence to the contrary.
Although this approach becomes more problematical as exposures become
less frequent, EPA believes that this is a reasonable approach for this
evaluation. Therefore the average daily dose is
(0.111 mg/kg) / (70 yr x 365 d/yr) = 4.360x10"^ mg/kg/d
F-5
-------
The increased cancer risk, is estimated by multiplying this dose by the
cancer potency and the number of pounds released,
Risk a 4.360xl0~^x Potency x Quantity
The EPA has used this model to evaluate the risks from releases of
several moderate to veak potential carcinogens. These are summarized in
Table 2.
Table 2.
SUBSTANCE
CANCER
POTENCY
RISK RESULTING FROM
1 10 100
A RELEASE OF
1000 5000 LBS
BENZENE
2.9E-02
1E-
-07
IE-
-06
1E-
-05
1E-
-04
6E-
-04
CARBON TETRACHLORIDE
1.3E-01
6E-
-07
6E-
-06
6E-
-05
6E-
-04
3E-
-03
1,2-DICHL0R0ETHANE
9.1E-02
4E-
o
4E-
\£>
O
¦
4E-
-05
4E-
-04
2E-
-03
1,1-DICHL0R0ETHYLENE
1.2E+00
5E-
-06
5E-
-05
5E-
-04
5E-
-03
3E-
-02
DICBLOROMETHANE
1.4E-02
6E-
CO
o
1
6E-
-07
6E-
-06
6E-
-05
3E-
-04
TETRACHLOROETHYLENE
5.1E-02
2E-
-07
2E-
-06
2E-
-05
2E-
-04
1E-
-03
TRICHLOROETHYLENE
1.1E-02
5E-
-08
5E-
f^
o
5E-
-06
5E-
-05
2E-
-04
VINYL CHLORIDE
1.8E-02
8E-
-08
8E-
-07
8E-
-06
8E-
-05
4E-
-04
F-6
-------
EPA concludes that substantial risks can result from releases of 1000 or
more pounds of moderate to veak potential carcinogens. Reporting levels
of 1000 or 5000 pounds are, therefore, not adequate to protect the public
health from releases of potential carcinogens. Consequently, the EPA
will assign reporting levels of 1, 10, or 100 pounds to potential
carcinogens.
F-7
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