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[Federal Register: April 6, 2010 (Volume 75, Number 65)]
[Proposed Rules]               
[Page 17333-17349]
From the Federal Register Online via GPO Access [wais.access.gpo.gov]
[DOCID:fr06ap10-20]                         

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ENVIRONMENTAL PROTECTION AGENCY

40 CFR Part 372

[EPA-HQ-TRI-2010-0006; FRL-9134-1]
RIN 2025-AA28

 
Addition of National Toxicology Program Carcinogens; Community 
Right-to-Know Toxic Chemical Release Reporting

AGENCY: Environmental Protection Agency (EPA).

ACTION: Proposed rule.

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SUMMARY: EPA is proposing to add sixteen chemicals to the list of toxic 
chemicals subject to reporting under section 313 of the Emergency 
Planning and Community Right-to-Know Act (EPCRA) of 1986 and section 
6607 of the Pollution Prevention Act of 1990 (PPA). These sixteen 
chemicals have been classified by the National Toxicology Program (NTP) 
in their Report on Carcinogens (RoC) as ``reasonably anticipated to be 
a human carcinogen.'' EPA believes that these sixteen chemicals meet 
the EPCRA section 313(d)(2)(B) criteria because they can reasonably be 
anticipated to cause cancer in humans. As in past chemical reviews, EPA 
adopted a production volume screen for the development of this proposed 
rule to screen out those chemicals for which no reports are expected to 
be submitted. Based on a review of the available production and use 
information, these sixteen chemicals are expected to be manufactured, 
processed, or otherwise used in quantities that would exceed the EPCRA 
section 313 reporting thresholds.

DATES: Comments must be received on or before June 7, 2010.

ADDRESSES: Submit your comments, identified by Docket ID No. EPA-HQ-
TRI-2010-0006, by one of the following methods:
    www.regulations.gov: Follow the on-line instructions for 
submitting comments.
     E-mail: oei.docket@epa.gov.
     Mail: Office of Environmental Information (OEI) Docket, 
Environmental Protection Agency, Mail Code: 28221T, 1200 Pennsylvania 
Ave., NW., Washington, DC 20460
     Hand Delivery: EPA Docket Center (EPA/DC), EPA West, Room 
3334, 1301 Constitution Ave., NW., Washington, DC 20460. Such 
deliveries are only accepted during the Docket's normal hours of 
operation, and special arrangements should be made for deliveries of 
boxed information.
    Instructions: Direct your comments to Docket ID No. EPA-HQ-TRI-
2010-0006. EPA's policy is that all comments received will be included 
in the public docket without change and may be made available online at 
http://www.regulations.gov, including any personal information 
provided, unless the comment includes information claimed to be 
Confidential Business Information (CBI) or other information whose 
disclosure is restricted by statute. Do not submit information that you 
consider to be CBI or otherwise protected through www.regulations.gov 
or e-mail. The www.regulations.gov Web site is an ``anonymous access'' 
system, which means EPA will not know your identity or contact 
information unless you provide it in the body of your comment. If you 
send an e-mail comment directly to EPA without going through 
www.regulations.gov, your e-mail address will be automatically captured 
and included as part of the comment that is placed in the public docket 
and made available on the Internet. If you submit an electronic 
comment, EPA recommends that you include your name and other contact 
information in the body of your comment and with any disk or CD-ROM you 
submit. If EPA cannot read your comment due to technical difficulties 
and cannot contact you for clarification, EPA may not be able to 
consider your comment. Electronic files should avoid the use of special 
characters, avoid any form of encryption, and be free of any defects or 
viruses.
    Docket: All documents in the docket are listed in the 
www.regulations.gov index. Although listed in the index, some 
information is not publicly available, e.g., CBI or other information 
whose disclosure is restricted by statute. Certain other material, such 
as copyrighted material, will be publicly available only in hard copy. 
Publicly available docket materials are available either electronically 
in www.regulations.gov or in hard copy at the OEI Docket, EPA/DC, EPA 
West, Room 3334, 1301 Constitution Ave., NW., Washington, DC. This 
Docket Facility is open from 8:30 a.m. to 4:30 p.m., Monday through 
Friday, excluding legal holidays. The telephone number for the Public 
Reading Room is (202) 566-1744, and the telephone number for the OEI 
Docket is (202) 566-1752.

FOR FURTHER INFORMATION CONTACT: Daniel R. Bushman, Environmental 
Analysis Division, Office of Information Analysis and Access (2842T), 
Environmental Protection Agency, 1200 Pennsylvania Ave., NW., 
Washington, DC 20460; telephone number: 202-566-0743; fax number: 202-
566-0677; e-mail: bushman.daniel@epa.gov, for specific information on 
this notice. For general information on EPCRA section 313, contact the 
Emergency Planning and Community Right-to-Know Hotline, toll free at 
(800) 424-9346 or (703) 412-9810 in Virginia and Alaska or toll free, 
TDD (800) 553-7672, http://www.epa.gov/epaoswer/hotline/.

SUPPLEMENTARY INFORMATION: 

I. General Information

A. Does this Notice Apply to Me?

    You may be potentially affected by this action if you manufacture, 
process, or otherwise use any of the chemicals

[[Page 17334]]

included in this proposed rule. Potentially affected categories and 
entities may include, but are not limited to:


------------------------------------------------------------------------
                                        Examples of potentially affected
               Category                             entities
------------------------------------------------------------------------
Industry.............................  Facilities included in the
                                        following NAICS manufacturing
                                        codes (corresponding to SIC
                                        codes 20 through 39): 311\*\,
                                        31\2*\, 313\*\, 314\*\, 315\*\,
                                        316, 321, 322, 323\*\, 324,
                                        325\*\, 326\*\, 327, 331, 332,
                                        333, 334\*\, 335\*\, 336,
                                        337\*\, 339\*\, 111998\*\,
                                        211112\*\, 212324\*\, 212325\*\,
                                        212393\*\, 212399\*\, 488390\*\,
                                        511110, 511120, 511130,
                                        511140\*\, 511191, 511199,
                                        512220, 512230\*\, 519130\*\,
                                        541712\*\, or 811490\*\.

                                       * Exceptions and/or limitations
                                        exist for these NAICS codes.

                                       Facilities included in the
                                        following NAICS codes
                                        (corresponding to SIC codes
                                        other than SIC codes 20 through
                                        39): 212111, 212112, 212113
                                        (correspond to SIC 12, Coal
                                        Mining (except 1241)); or
                                        212221, 212222, 212231, 212234,
                                        212299 (correspond to SIC 10,
                                        Metal Mining (except 1011, 1081,
                                        and 1094)); or 221111, 221112,
                                        221113, 221119, 221121, 221122,
                                        221330 (Limited to facilities
                                        that combust coal and/or oil for
                                        the purpose of generating power
                                        for distribution in commerce)
                                        (correspond to SIC 4911, 4931,
                                        and 4939, Electric Utilities);
                                        or 424690, 425110, 425120
                                        (Limited to facilities
                                        previously classified in SIC
                                        5169, Chemicals and Allied
                                        Products, Not Elsewhere
                                        Classified); or 424710
                                        (corresponds to SIC 5171,
                                        Petroleum Bulk Terminals and
                                        Plants); or 562112 (Limited to
                                        facilities primarily engaged in
                                        solvent recovery services on a
                                        contract or fee basis
                                        (previously classified under SIC
                                        7389, Business Services, NEC));
                                        or 562211, 562212, 562213,
                                        562219, 562920 (Limited to
                                        facilities regulated under the
                                        Resource Conservation and
                                        Recovery Act, subtitle C, 42
                                        U.S.C. 6921 et seq.) (correspond
                                        to SIC 4953, Refuse Systems).
Federal Government                     Federal facilities.
------------------------------------------------------------------------

    This table is not intended to be exhaustive, but rather provides a 
guide for readers regarding entities likely to be affected by this 
action. Some of the entities listed in the table have exemptions and/or 
limitations regarding coverage, and other types of entities not listed 
in the table could also be affected. To determine whether your facility 
would be affected by this action, you should carefully examine the 
applicability criteria in part 372 subpart B of Title 40 of the Code of 
Federal Regulations. If you have questions regarding the applicability 
of this action to a particular entity, consult the person listed in the 
preceding ``FOR FURTHER INFORMATION CONTACT'' section.

B. How Should I Submit CBI to the Agency?

    Do not submit CBI information to EPA through www.regulations.gov or 
e-mail. Clearly mark the part or all of the information that you claim 
to be CBI. For CBI information in a disk or CD-ROM that you mail to 
EPA, mark the outside of the disk or CD-ROM as CBI and then identify 
electronically within the disk or CD-ROM the specific information that 
is claimed as CBI. In addition to one complete version of the comment 
that includes information claimed as CBI, a copy of the comment that 
does not contain the information claimed as CBI must be submitted for 
inclusion in the public docket. Information so marked will not be 
disclosed except in accordance with procedures set forth in 40 CFR part 
2.

II. Introduction

    Section 313 of EPCRA, 42 U.S.C. 11023, requires certain facilities 
that manufacture, process, or otherwise use listed toxic chemicals in 
amounts above reporting threshold levels to report their environmental 
releases and other waste management quantities of such chemicals 
annually. These facilities must also report pollution prevention and 
recycling data for such chemicals, pursuant to section 6607 of the PPA, 
42 U.S.C. 13106. Congress established an initial list of toxic 
chemicals that comprised more than 300 chemicals and 20 chemical 
categories.
    EPCRA section 313(d) authorizes EPA to add or delete chemicals from 
the list and sets criteria for these actions. EPCRA section 313(d)(2) 
states that EPA may add a chemical to the list if any of the listing 
criteria in Section 313(d)(2) are met. Therefore, to add a chemical, 
EPA must demonstrate that at least one criterion is met, but need not 
determine whether any other criterion is met. Conversely, to remove a 
chemical from the list, EPCRA section 313(d)(3) dictates that EPA must 
demonstrate that none of the listing criteria in Section 313(d)(2) are 
met. The EPCRA section 313(d)(2) criteria are:
    (A) The chemical is known to cause or can reasonably be anticipated 
to cause significant adverse acute human health effects at 
concentration levels that are reasonably likely to exist beyond 
facility site boundaries as a result of continuous, or frequently 
recurring, releases.
    (B) The chemical is known to cause or can reasonably be anticipated 
to cause in humans--

    (i) Cancer or teratogenic effects, or
    (ii) Serious or irreversible--
    (I) Reproductive dysfunctions,
    (II) Neurological disorders,
    (III) Heritable genetic mutations, or
    (IV) Other chronic health effects.

    (C) The chemical is known to cause or can be reasonably anticipated 
to cause, because of
    (i) Its toxicity,
    (ii) Its toxicity and persistence in the environment, or
    (iii) Its toxicity and tendency to bioaccumulate in the 
environment, a significant adverse effect on the environment of 
sufficient seriousness, in the judgment of the Administrator, to 
warrant reporting under this section.

    EPA often refers to the section 313(d)(2)(A) criterion as the 
``acute human health effects criterion;'' the section 313(d)(2)(B) 
criterion as the ``chronic human health effects criterion;'' and the 
section 313(d)(2)(C) criterion as the ``environmental effects 
criterion.''
    EPA has published in the Federal Register of November 30, 1994 (59 
FR 61432) a statement clarifying its interpretation of the section 
313(d)(2) and (d)(3) criteria for modifying the section 313 list of 
toxic chemicals.

III. Background Information

A. What is the NTP and the Report on Carcinogens?

    The National Toxicology Program (NTP) is an interagency program 
within the Department of Health and Human Services (DHHS) headquartered 
at the National Institute of Environmental Health Sciences (NIEHS) of 
the National Institutes of Health (NIH). The mission of the NTP is to 
evaluate chemicals of public health concern by developing and applying 
tools of modern toxicology and molecular biology. The NTP

[[Page 17335]]

program maintains an objective, science-based approach in dealing with 
critical issues in toxicology and is committed to using the best 
science available to prioritize, design, conduct, and interpret its 
studies. The mission of the NTP includes the evaluation of chemicals 
for their potential to cause cancer in humans.
    As part of their cancer evaluation work, the NTP periodically 
publishes a Report on Carcinogens (RoC) document. The RoC was mandated 
by the U.S. Congress, as part of the Public Health Service Act (Section 
301(b)(4), as amended). The NTP describes the RoC as an informational 
scientific and public health document that identifies and discusses 
agents, substances, mixtures, or exposure circumstances that may pose a 
hazard to human health by virtue of their carcinogenicity. The NTP RoC 
serves as a meaningful and useful compilation of data on (1) the 
carcinogenicity (ability to cause cancer), genotoxicity (ability to 
damage genes), and biologic mechanisms (modes of action in the body) of 
the RoC-listed substances in humans and/or in animals, (2) the 
potential for human exposure to these substances, and (3) the 
regulations and guidelines promulgated by Federal agencies to limit 
exposures to RoC-listed substances. The NTP RoC is published 
periodically, with the most recently published 11th RoC having been 
released on January 31, 2005. The 11th RoC contains the NTP cancer 
classifications from the most recent chemical evaluations as well as 
the classifications from previous versions of the RoC.

B. What are the NTP cancer classifications and criteria?

    The NTP RoC classifies chemicals as either ``known to be a human 
carcinogen'' or ``reasonably anticipated to be a human carcinogen.'' 
The criteria that the NTP uses to list an agent, substance, mixture, or 
exposure circumstance under each classification in the RoC (Ref. 1) are 
as follows:

``Known To Be Human Carcinogen:
There is sufficient evidence of carcinogenicity from studies in 
humans*, which indicates a causal relationship between exposure to the 
agent, substance, or mixture, and human cancer.
Reasonably Anticipated To Be Human Carcinogen:
There is limited evidence of carcinogenicity from studies in humans*, 
which indicates that causal interpretation is credible, but that 
alternative explanations, such as chance, bias, or confounding factors, 
could not adequately be excluded,
or
there is sufficient evidence of carcinogenicity from studies in 
experimental animals, which indicates there is an increased incidence 
of malignant and/or a combination of malignant and benign tumors (1) in 
multiple species or at multiple tissue sites, or (2) by multiple routes 
of exposure, or (3) to an unusual degree with regard to incidence, 
site, or type of tumor, or age at onset,
or
there is less than sufficient evidence of carcinogenicity in humans or 
laboratory animals; however, the agent, substance, or mixture belongs 
to a well-defined, structurally related class of substances whose 
members are listed in a previous Report on Carcinogens as either known 
to be a human carcinogen or reasonably anticipated to be a human 
carcinogen, or there is convincing relevant information that the agent 
acts through mechanisms indicating it would likely cause cancer in 
humans. Conclusions regarding carcinogenicity in humans or experimental 
animals are based on scientific judgment, with consideration given to 
all relevant information. Relevant information includes, but is not 
limited to, dose response, route of exposure, chemical structure, 
metabolism, pharmacokinetics, sensitive sub-populations, genetic 
effects, or other data relating to mechanism of action or factors that 
may be unique to a given substance. For example, there may be 
substances for which there is evidence of carcinogenicity in laboratory 
animals, but there are compelling data indicating that the agent acts 
through mechanisms which do not operate in humans and would therefore 
not reasonably be anticipated to cause cancer in humans.
* This evidence can include traditional cancer epidemiology studies, 
data from clinical studies, and/or data derived from the study of 
tissues or cells from humans exposed to the substance in question that 
can be useful for evaluating whether a relevant cancer mechanism is 
operating in people.''

    The NTP classifications for the potential for a chemical to cause 
cancer are very similar to the EPCRA section 313(d)(2)(B) statutory 
criteria for listing a chemical on the list of toxic chemicals subject 
to reporting under EPCRA section 313: ``(B) The chemical is known to 
cause or can reasonably be anticipated to cause in humans-- (i) cancer 
* * * '' The specific data used by the NTP to classify a chemical as 
``Known To Be Human Carcinogen'' or ``Reasonably Anticipated To Be 
Human Carcinogen'' are consistent with data used by EPA to evaluate 
chemicals for their potential to cause cancer and classify chemicals as 
either ``Carcinogenic to Humans'' or ``Likely to Be Carcinogenic to 
Humans'' (Ref. 2).

C. What is the review process for the RoC?

    Specific details of the nomination and review process for the 
development of the 11th RoC are described in the introduction to the 
11th RoC (Ref. 1). In general, the RoC review process includes 
evaluations by scientists from the NTP, other Federal health research 
and regulatory agencies (including EPA), and nongovernmental 
institutions. The RoC review process includes external peer review and 
several opportunities for public comment. For the 11th RoC, two Federal 
scientific review groups, the NIEHS/NTP Review Committee for the Report 
on Carcinogens RG1 and the NTP Executive Committee Interagency Working 
Group for the Report on Carcinogens RG2, evaluated the classification 
recommendations. An EPA representative was a member of the RG2 
committee. These reviews were followed by a third independent external 
scientific peer review by a standing subcommittee of the NTP Board of 
Scientific Counselors (the RoC Subcommittee). During the entire process 
there were three opportunities for public comment. The Director of the 
NTP received for review all of the recommendations of the review 
groups, the opinion of the NTP Executive Committee, and all public 
comments. After evaluating this information and any other relevant 
information the NTP Director developed recommendations to the 
Secretary, DHHS regarding whether and/or how to classify nominations in 
the RoC. The final draft of the RoC was prepared by the NTP based on 
the NTP Director's recommendations and was submitted it to the 
Secretary, DHHS, for review and approval. Once approved, the Secretary 
submitted RoC to the U. S. Congress as a final document. Submittal of 
the RoC to Congress constituted publication of the report, at which 
time it became available to the public.

IV. EPA's Review of the 11th RoC

A. How did EPA select the NTP RoC chemicals being proposed for 
addition?

    The most recent version of the NTP RoC that EPA previously reviewed 
for

[[Page 17336]]

possible additions to the EPCRA section 313 list was the 6th RoC 
(January 12, 1994, 59 FR 1788). Each new version of the RoC adds newly 
classified chemicals to the existing list. EPA's present review of the 
11th RoC identified 81 chemicals that are not on the EPCRA section 
list, 54 of which were previously reviewed for listing when EPA 
reviewed the 6th RoC. Those previous reviews concluded that the 54 
chemicals that were not proposed for addition would not be 
manufactured, processed, or otherwise used at levels that exceed the 
EPCRA section 313 reporting thresholds. For this review EPA only 
considered the 27 chemicals that had been added to the RoC since the 
6th RoC was published and thus had not been previously reviewed for 
listing. Of the 27 chemicals, EPA determined that 12 are manufactured, 
processed, or otherwise used in quantities sufficient to exceed 
reporting thresholds for at least one facility (Ref. 3). In addition, 4 
chemicals are included for addition to the polycyclic aromatic 
compounds category.
    Section 313(d)(2) of EPCRA provides EPA the discretion to add 
chemicals to the TRI list when there is sufficient evidence to 
establish any of the listing criteria. EPA can add a chemical that 
meets one criterion regardless of its production volume. But as in past 
chemical reviews (e.g., January 12, 1994, 59 FR 1788), EPA adopted a 
production volume screen for the development of this proposed rule to 
screen out those chemicals for which no reports are expected to be 
submitted. If chemicals that did not meet the production volume screen 
were listed, there would be an economic burden for firms that would 
have to determine that they did not exceed the reporting threshold. Yet 
as no reports would be filed, there would be no information to the 
public on these chemicals. EPA feels it is appropriate at this time to 
focus on chemicals for which reports are likely to be filed.
    EPA reviewed the NTP 11th RoC chemical profiles and supporting 
materials for each chemical being proposed for listing in this rule 
(Ref. 4). Given the extensive scientific reviews conducted by the NTP 
for their RoC documents, EPA's review focused on ensuring that there 
were no inconsistencies with how the Agency would consider the 
available data. EPA found no inconsistencies and agrees with the hazard 
conclusions of the NTP 11th RoC for each of the chemicals included in 
this proposed rule.

B. What technical data supports the NTP RoC classifications and EPA's 
proposed additions to the EPCRA section 313 list?

    This section presents the data that supported the NTP 11th RoC 
classifications of each chemical now being proposed for inclusion on 
the EPCRA section 313 list and why EPA believes the data support the 
addition of these chemicals to the EPCRA section 313 list. The NTP 
chemical profiles, the NTP chemical background documents, and the 
references cited within each of the portions of the NTP 11th RoC 
chemical profiles quoted here, are all included in the docket for this 
rulemaking. While they are contained in the docket and are part of the 
rulemaking record, the references within the quotations cited from the 
NTP 11th RoC profile documents in this section are not included in the 
list of references in Unit VI. of this Federal Register notice. The 
full citations for the references contained in the quotations can be 
found in the NTP 11th RoC profile documents cited for each chemical.
    1. 1-Amino-2,4-Dibromoanthraquinone (CAS No. 81-49-2) (Refs. NTP 
Profile/Background document (Refs. 5 and 6)). The NTP has classified 1-
amino-2,4-dibromoanthraquinone as ``reasonably anticipated to be a 
human carcinogen.'' The classification is based on sufficient evidence 
of carcinogenicity in experimental animals. The NTP substance profile 
for 1-amino-2,4-dibromoanthraquinone (Ref. 5) included the following 
summary information of the evidence of carcinogenicity:
``Carcinogenicity
    1-Amino-2,4-dibromoanthraquinone (ADBAQ) is reasonably anticipated 
to be a human carcinogen based on sufficient evidence from studies in 
experimental animals. Orally administered ADBAQ significantly increased 
the incidences of benign and/or malignant tumors at multiple tissue 
sites in two species of animals. ADBAQ caused benign and malignant 
liver tumors in rats and mice of both sexes; tumors of the large 
intestine, kidney, and urinary bladder in male and female rats; and 
tumors of the forestomach and lung in male and female mice (NTP 1996).
    Two cohort studies evaluated the risk of cancer among workers in 
plants manufacturing anthraquinone dyes; however, it is not known 
whether workers were exposed specifically to ADBAQ (Gardiner et al. 
1982, Delzell et al. 1989). Some evidence suggests that anthraquinone 
dye workers may have an increased risk of cancer. Significant excesses 
of esophageal and prostate cancer occurred among workers in some areas 
of a Scottish anthraquinone dyestuffs plant, and excesses of lung and 
central nervous system cancer occurred among workers at a New Jersey 
anthraquinone dye and epichlorohydrin plant (Barbone et al. 1992, 1994, 
Sathiakumar and Delzell 2000). Nevertheless, estimates of risk in all 
studies were based on small numbers of cancer deaths, and workers may 
have been exposed to other carcinogens.
Additional Information Relevant to Carcinogenicity
    Evaluation of ADBAQ's genetic effects has been hindered by ADBAQ's 
limited solubility. ADBAQ caused mutations in some strains of bacteria 
but not in rodent cells, which were tested at lower concentrations 
(Haworth et al. 1983, NTP 1996). In mammalian cells, ADBAQ induced 
chromosomal aberrations (changes in chromosome structure or number) and 
sister chromatid exchange; however, the results varied between 
laboratories and between trials at the same laboratory (Loveday et al. 
1990, NTP 1996). Point mutations in the ras proto-oncogene (a gene 
potentially associated with cancer) occurred at a higher frequency in 
forestomach and lung tumors from the two-year carcinogenicity study of 
ADBAQ-exposed mice than in spontaneous tumors from control mice not 
exposed to ADBAQ. The predominant types of mutations were A to T 
transversions and A to G transitions, suggesting that ADBAQ or its 
metabolites target adenine bases in the ras proto-oncogene (Hayashi et 
al. 2001).
    ADBAQ is rapidly absorbed from the gastrointestinal tract and 
distributed to most soft tissues. The majority of ADBAQ is metabolized, 
and both ADBAQ and its metabolites are excreted in the feces and urine. 
However, the metabolites of ADBAQ have not been identified (NTP 1996). 
The mechanism by which ADBAQ causes cancer is not known; however, there 
is no evidence to suggest that mechanisms of tumor induction observed 
in experimental animals would not occur in humans. Four other 
anthraquinones (2-aminoanthraquinone, 1-amino-2- methylanthraquinone, 
danthron [1,8-dihydroxyanthraquinone], and disperse blue 1) are listed 
in the Report on Carcinogens as reasonably anticipated to be human 
carcinogens.''
    EPA has reviewed the NTP assessment for 1-amino-2,4-
dibromoanthraquinone and agrees that

[[Page 17337]]

1-amino-2,4-dibromoanthraquinone can reasonably be anticipated to cause 
cancer in humans. EPA believes that the evidence is sufficient for 
listing 1-amino-2,4-dibromoanthraquinone on EPCRA section 313 pursuant 
to EPCRA section 313(d)(2)(B) based on the available carcinogenicity 
data for this chemical.
    2. 2,2-bis(Bromomethyl)-1,3-propanediol (CAS No. 3296-90-0) (Refs. 
NTP Profile/Background document (Refs. 7 and 8)). The NTP has 
classified 2,2-bis(bromomethyl)-1,3-propanediol as ``reasonably 
anticipated to be a human carcinogen.'' The classification is based on 
sufficient evidence of carcinogenicity in experimental animals. The NTP 
substance profile for 2,2-bis(bromomethyl)-1,3-propanediol (Ref. 7) 
included the following summary information of the evidence of 
carcinogenicity:
Carcinogenicity
    The flame retardant 2,2-bis(bromomethyl)-1,3-propanediol, technical 
grade (BBMP), is reasonably anticipated to be a human carcinogen based 
on sufficient evidence of carcinogenicity from studies in experimental 
animals which indicates there is increased incidence of malignant tumor 
formation at multiple tissue sites in rats and mice. Two year dietary 
studies of BBMP in F344 rats showed significantly increased incidences 
of neoplasms of the skin, subcutaneous tissue, mammary gland, Zymbal 
gland, oral cavity, esophagus, forestomach, small and large intestines, 
mesothelium, urinary bladder, lung, thyroid gland, and seminal vesicle 
and in the incidence of mononuclear cell leukemia in males, and an 
increase in the incidence of neoplasms of the oral cavity, esophagus, 
mammary gland, and thyroid gland in females. Similar studies in B6C3F1 
mice found increased incidences of neoplasms of the harderian gland, 
lung, and kidney in males and neoplasms of the harderian gland, lung, 
and subcutaneous tissue in females (NTP 1996, Dunnick et al. 1997).
    A study in which BBMP was administered in the feed to male F344 
rats for three months, followed by maintenance on a control diet for up 
to two years, found neoplasms at the same sites as in the two-year 
study of male F344 rats described above. However, this study found 
higher incidences of neoplasms of the oral cavity, forestomach, small 
intestine, large intestine, lung, Zymbal gland, thyroid gland, and 
mesothelium than did the two-year study; these neoplasms were 
considered to be related to BBMP exposure (NTP 1996, Dunnick et al. 
1997).
    No published case reports or epidemiological studies of human 
cancer and exposure to BBMP were found (IARC 2000).
Additional Information Relevant to Carcinogenicity
    BBMP has been shown to be mutagenic in bacterial and mammalian test 
systems, under special conditions. BBMP is mutagenic in Salmonella 
typhimurium strains TA100 and TA1535 only when tested in the presence 
of metabolic activation (30% S9 liver homogenate from induced hamsters) 
(Zeiger et al. 1992). In cultured Chinese hamster ovary cells, BBMP 
induces chromosomal aberrations only in the presence of metabolic 
activation, and it does not induce sister chromatid exchange with or 
without activation. Male and female mice exposed to BBMP under various 
conditions showed significant increases in the frequency of 
micronucleated erythrocytes (NTP 1996).
    No available data suggest that mechanisms thought to account for 
BBMP's induction of tumors in experimental animals would not also 
operate in humans.''
    EPA has reviewed the NTP assessment for 2,2-bis(bromomethyl)-1,3-
propanediol and agrees that 2,2-bis(bromomethyl)-1,3-propanediol can 
reasonably be anticipated to cause cancer in humans. EPA believes that 
the evidence is sufficient for listing 2,2-bis(bromomethyl)-1,3-
propanediol on EPCRA section 313 pursuant to EPCRA section 313(d)(2)(B) 
based on the available carcinogenicity data for this chemical.
    3. Furan (CAS No. 110-00-9) (Refs. NTP Profile/Background document 
(Refs. 9 and 10)). The NTP has classified furan as ``reasonably 
anticipated to be a human carcinogen.'' The classification is based on 
sufficient evidence of carcinogenicity in experimental animals. The NTP 
substance profile for furan (Ref. 9) included the following summary 
information of the evidence of carcinogenicity:
``Carcinogenicity
    Furan is reasonably anticipated to be a human carcinogen based on 
sufficient evidence of malignant tumor formation at multiple tissue 
sites in multiple species of experimental animals (IARC 1995).
    When administered by gavage, furan induced an increase in the 
incidence of hepatic cholangiocarcinoma, hepatocellular adenoma, 
hepatocellular carcinoma, and mononuclear cell leukemia in male and 
female F344/N rats treated for up to 2 years (NTP 1993). Gavage 
administration of furan to male F344 rats for 9, 12, or 13 months 
resulted in high incidences of cholangiocarcinoma by 16 months after 
cessation of treatment (Maronpot et al. 1991, Elmore and Sirica 1993). 
When administered by gavage, furan induced a dose-dependent increase in 
the incidence of hepatocellular adenoma and carcinoma and benign 
pheochromocytoma in male and female B6C3F1 mice treated up 
to 2 years (NTP 1993).
    No adequate human studies of the relationship between exposure to 
furan and human cancer have been reported.
Additional Information Relevant to Carcinogenicity
    In bacteria, furan induced gene mutations in Salmonella typhimurium 
strain TA100 (Lee et al. 1994) and in E. coli containing bacteriophage 
T7 (Ronto et al. 1992), but not in S. typhimurium strains TA98 (Lee et 
al. 1994), TA1535, or TA1537 (Mortelmans et al. 1986). In Drosophila 
melanogaster, it did not induce gene mutations (Foureman et al. 1994). 
In mammalian in vitro systems, it induced gene mutations in mouse 
lymphoma cells (McGregor et al. 1988), DNA damage in Chinese hamster 
ovary (CHO) cells (NTP 1993), and chromosomal damage in CHO cells with 
an exogenous metabolic activation system (NTP 1993, IARC 1995), but it 
did not induce DNA damage in mouse or rat hepatocytes (Wilson et al. 
1992, NTP 1993). In mammalian in vivo systems, furan induced 
chromosomal aberrations in bone marrow of B6C3F1 mice (NTP 
1993), but did not induce DNA damage in bone marrow or hepatocytes of 
B6C3F1 mice (Wilson et al. 1992, NTP 1993) or hepatocytes of 
F344/CrIBr rats (Wilson et al. 1992).
    A current hypothesis for the mechanism of furan-induced 
carcinogenesis is metabolic activation of furan by cytochrome P450 to a 
reactive and cytotoxic intermediate that stimulates cell replication, 
increasing the likelihood of tumor induction (Chen et al. 1995, 
Kedderis et al. 1993). The postulated reactive metabolite is cis-2- 
butene-1,4-dial, which was recently characterized as a furan metabolite 
by Chen et al. (1995). This reactive metabolite probably explains 
furan's binding reactivity with proteins both in vitro (uninduced and 
induced F344 male rat liver microsomes) and in vivo (F344 male rat 
liver protein) in biological systems (Burka et al. 1991, Parmar and 
Burka 1993). Furan metabolites may react with DNA, but Burka et al. 
(1991) did not detect any

[[Page 17338]]

radiotracer in DNA from livers of rats treated with [\14\ C]furan.
    No data were available that would suggest that the mechanisms 
thought to account for tumor induction by furan in experimental animals 
would not also operate in humans.''
    EPA has reviewed the NTP cancer assessment for furan and agrees 
that furan can reasonably be anticipated to cause cancer in humans. EPA 
believes that the evidence is sufficient for listing furan on EPCRA 
section 313 pursuant to EPCRA section 313(d)(2)(B) based on the 
available carcinogenicity data for this chemical.
    4. Glycidol (CAS No. 556-52-5) (Ref. NTP Profile/NTP study (Refs. 
11 and 12)). The NTP has classified glycidol as ``reasonably 
anticipated to be a human carcinogen.'' The classification is based on 
sufficient evidence of carcinogenicity in experimental animals. The NTP 
substance profile for glycidol (Ref. 11) included the following summary 
information of the evidence of carcinogenicity:
``Carcinogenicity
    Glycidol is reasonably anticipated to be a human carcinogen based 
on sufficient evidence of carcinogenicity in experimental animals (NTP 
1990, IARC 2000). Two-year studies were conducted with mice and rats 
that were administered glycidol by gavage. Male rats showed increased 
incidences of mesotheliomas of the tunica vaginalis, fibroadenomas of 
the mammary gland, gliomas of the brain, and neoplasms of the 
forestomach, intestine, skin, Zymbal gland, and thyroid gland. Female 
rats had increased incidences of fibroadenomas and adenocarcinomas of 
the mammary gland, gliomas of the brain, neoplasms of the oral mucosa, 
forestomach, clitoral gland, and thyroid gland, and leukemia. Male 
B6C3F1 mice had increased incidences of neoplasms of the 
harderian gland, forestomach, skin, liver, and lung. Female 
B6C3F1 mice had increased incidences of neoplasms of the 
harderian gland, mammary gland, uterus, subcutaneous tissue, and skin. 
Other neoplasms that may be related to the administration of glycidol 
were fibrosarcomas of the glandular stomach in female rats and 
carcinomas of the urinary bladder and sarcomas of the epididymis in 
male mice (NTP 1990).
    No adequate human studies of the relationship between exposure to 
glycidol and human cancer have been reported (IARC 2000).''
    EPA has reviewed the NTP cancer assessment for glycidol and agrees 
that glycidol can reasonably be anticipated to cause cancer in humans. 
EPA believes that the evidence is sufficient for listing glycidol on 
EPCRA section 313 pursuant to EPCRA section 313(d)(2)(B) based on the 
available carcinogenicity data for this chemical.
    5. Isoprene (CAS No. 78-79-5) (Refs. NTP Profile/Background 
document (Refs. 13 and 14)). The NTP has classified isoprene as 
``reasonably anticipated to be a human carcinogen.'' The classification 
is based on sufficient evidence of carcinogenicity in experimental 
animals. The NTP substance profile for isoprene (Ref. 13) included the 
following summary information of the evidence of carcinogenicity:
Carcinogenicity
    Isoprene is reasonably anticipated to be a human carcinogen based 
on sufficient evidence of tumor formation at multiple organ sites in 
multiple species of experimental animals (Melnick et al. 1994, NTP 
1995, 199[9], Placke et al. 1996). Inhalation exposure of mice to 
isoprene vapors induced increased incidences of neoplasms of the lung, 
liver, harderian gland, forestomach, hematopoietic system, and 
circulatory system. Inhalation exposure of rats to isoprene vapors 
induced increased incidences of neoplasms of the mammary gland, kidney, 
and testis (IARC 1999).
    No adequate human studies of the relationship between exposure to 
isoprene and human cancer have been reported.
Additional Information Relevant to Carcinogenicity
    Isoprene is the 2-methyl analog of 1,3-butadiene, an industrial 
chemical that has been identified as an animal and human carcinogen. 
Isoprene and butadiene are metabolized to monoepoxide and diepoxide 
intermediates by liver microsomal cytochrome P450-dependent 
monooxygenases from several species, including humans. Detoxification 
of these intermediates may occur by hydrolysis catalyzed by epoxide 
hydrolase or conjugation with glutathione catalyzed by glutathione-S-
transferase. The diepoxide intermediates of isoprene and butadiene are 
mutagenic in Salmonella typhimurium, whereas the parent compounds are 
inactive (Gervasi et al. 1985). In mice, isoprene and 1,3-butadiene 
induced sister chromatid exchanges in bone marrow cells and increased 
the frequency of micronucleated erythrocytes in peripheral blood (Tice 
et al. 1987, Tice et al. 1988). Common sites of neoplasm induction by 
isoprene and butadiene include the mammary gland and testis in rats, 
and the liver, lung, harderian gland, forestomach, and circulatory 
system in mice (NTP 199[9]). Lung and harderian gland neoplasms induced 
by isoprene in mice had a high frequency of unique K-ras mutations (A 
to T transversions at codon 61) (Hong et al. 1997).
    No data were available that would suggest that mechanisms thought 
to account for tumor induction by isoprene in experimental animals 
would not also operate in humans.
    EPA has reviewed the NTP cancer assessment for isoprene and agrees 
that isoprene can reasonably be anticipated to cause cancer in humans. 
EPA believes that the evidence is sufficient for listing isoprene on 
EPCRA section 313 pursuant to EPCRA section 313(d)(2)(B) based on the 
available carcinogenicity data for this chemical.
    6. Methyleugenol (CAS No. 93-15-2) (Refs. NTP Profile/Background 
document (Refs. 15 and 16)). The NTP has classified methyleugenol as 
``reasonably anticipated to be a human carcinogen.'' The classification 
is based on sufficient evidence of carcinogenicity in experimental 
animals. The NTP substance profile for methyleugenol (Ref. 15) included 
the following summary information of the evidence of carcinogenicity:
Carcinogenicity
    Methyleugenol is reasonably anticipated to be a human carcinogen 
based on sufficient evidence of carcinogenicity from studies in 
experimental animals, which indicates there is an increased incidence 
of malignant and/or combination of malignant and benign tumors at 
multiple tissue sites in multiple species of experimental animals. In 
animal studies, methyleugenol given orally to rats induced liver and 
stomach tumors in both sexes and kidney, mammary gland, and skin tumors 
in males. Methyleugenol given orally to mice induced benign and 
malignant tumors of the liver. Tumors of the stomach in male mice also 
were considered related to exposure to methyleugenol (NTP [2000]). 
Earlier studies found that methyleugenol and two similar compounds, the 
structurally related allylbenzenes, safrole and estragole, induced 
liver tumors in mice after intraperitoneal injection (IARC 1976, Miller 
et al. 1983). Safrole is listed in the Report on Carcinogens as 
reasonably anticipated to be a human carcinogen and by IARC as possibly 
carcinogenic to humans (Group 2B).
    No adequate human studies of the relationship between exposure to

[[Page 17339]]

methyleugenol and human cancer were found.
Additional Information Relevant to Carcinogenicity
    Mechanistic data indicate that liver tumors induced by 
methyleugenol and structurally related allylbenzenes result from 
metabolism of these compounds to DNA-reactive intermediates. 
Methyleugenol may be bioactivated by three different pathways: (1) 
Hydroxylation at the 1' position of the allylic side chain to yield 1'-
hydroxymethyleugenol, followed by sulfation of this intermediate to 
form 1'- hydroxymethyleugenol sulfate, (2) oxidation of the 2',3'-
double bond of the allylic side chain to form methyleugenol-2,3-oxide, 
and (3) O-demethylation followed by spontaneous rearrangement to form 
eugenol quinone methide. Formation of protein adducts and DNA adducts 
in the livers of animals (and in cultured human hepatocytes) exposed to 
allylbenzenes and induction of liver tumors by these compounds in 
animals have been attributed to activation via the hydroxylation 
pathway, because similar effects were produced by the 1'-hydroxy 
metabolites and because these effects were inhibited by pretreatment 
with sulfotransferase inhibitors (Miller et al. 1983, Boberg et al. 
1983, Randerath et al. 1984, Gardner et al. 1996, NTP [2000]).
    Methyleugenol, safrole, and estragole induce unscheduled DNA 
synthesis in rat hepatocytes, and their corresponding 1'-hydroxy 
metabolites are more potent genotoxic agents than are the parent 
compounds (Howes et al. 1990, Chan and Caldwell 1992). Methyleugenol 
induces morphological transformations in Syrian hamster embryo cells 
(Kerckaert et al. 1996), sister chromatid exchange in Chinese hamster 
ovary (CHO) cells (NTP [2000]), intrachromosomal recombination in yeast 
(Schiestl et al. 1989), and DNA repair in Bacillus subtilis (Sekizawa 
and Shibamoto 1982). Methyleugenol does not induce mutations in 
Salmonella typhimurium (NTP [2000]) or Escherichia coli (Sekizawa and 
Shibamoto 1982), chromosomal aberrations in CHO cells (NTP [2000]), or 
micronucleated erythrocytes in peripheral blood of mice (NTP [2000]). A 
higher frequency of [beta]-catenin mutations was observed in liver 
tumors from mice treated with methyleugenol than in spontaneous liver 
tumors from control mice (Devereux et al. 1999). Methyleugenol's lack 
of mutagenicity in bacteria may be due to the need for sulfation in the 
metabolic activation of methyleugenol to its ultimate mutagenic or 
carcinogenic form.
    EPA has reviewed the NTP cancer assessment for methyleugenol and 
agrees that methyleugenol can reasonably be anticipated to cause cancer 
in humans. EPA believes that the evidence is sufficient for listing 
methyleugenol on EPCRA section 313 pursuant to EPCRA section 
313(d)(2)(B) based on the available carcinogenicity data for this 
chemical.
    7. Nitroarenes (selected) (Refs. NTP Profile. (Ref. 17)). The NTP 
has classified five nitroarenes as ``reasonably anticipated to be a 
human carcinogen.'' The five nitroarenes are: 1,6-Dinitropyrene, 1,8-
Dinitropyrene, 6-Nitrochrysene, 1-Nitropyrene, and 4-Nitropyrene. 1-
Nitropyrene is already on the EPCRA section 313 list under the 
polycyclic aromatic compounds (PACs) category (November 30, 1994, 59 FR 
61485). All of the members of the PACs category are listed based on 
concerns for their carcinogenicity and were listed as a category 
because they are structurally similar and induce a similar toxic effect 
(cancer) (November 30, 1994, 59 FR 61463). Since the four other 
nitroarenes are PACs and are being proposed for listing based on a 
concern for carcinogenicity they are being proposed for addition to the 
PACs category, and not for individual listing.
    The PACs category is one of several categories of chemicals of 
special concern for which reporting is triggered at lowered thresholds. 
40 CFR 372.28(a)(2). The special concern for the PACs category members 
is that they are persistent, bioaccumulative, and toxic (PBT) 
chemicals. More specifically, it is the persistence and bioaccumulative 
properties of these chemicals that led EPA to lower reporting 
thresholds (October 29, 1999, 64 FR 58666). The persistence and 
bioaccumulation data for the four nitroarenes addressed in this 
proposal follows the individual summaries of the cancer data for each 
chemical. In addition to the data for the nitroarenes, there is a 
discussion of the PBT criteria and how it was applied to the PACs 
category.
    a. 1,6-Dinitropyrene (CAS No. 42397-64-8) (Refs. NTP Profile/
Background document (Refs. 17 and 18)). The NTP has classified 1,6-
dinitropyrene as ``reasonably anticipated to be a human carcinogen.'' 
The classification is based on sufficient evidence of carcinogenicity 
in experimental animals. The NTP substance profile for 1,6-
dinitropyrene (Ref. 17) included the following summary information of 
the evidence of carcinogenicity:
``Carcinogenicity
    1,6-Dinitropyrene is reasonably anticipated to be a human 
carcinogen based on sufficient evidence of malignant tumor formation in 
multiple species of experimental animals, at multiple sites and by 
multiple routes of exposure (IARC 1989).
    When administered by subcutaneous injections, 1,6-dinitropyrene 
induced injection-site sarcomas in male mice and male and female rats, 
and leukemia in female rats (Tokiwa et al. 1984, Ohgaki et al. 1985, 
Imaida et al. 1995). Intraperitoneal injections of 1,6-dinitropyrene 
caused an increased incidence of liver-cell tumors in male mice 
(Wislocki et al. 1986) and induced sarcomas of the peritoneal cavity in 
female rats (Imaida et al. 1991). In two studies, squamous cell 
carcinomas of the lung were induced in male rats receiving 1,6-
dinitropyrene by intrapulmonary injection (Maeda et al. 1986, Iwagawa 
et al. 1989). The incidences of myeloid leukemia and lung 
adenocarcinomas were significantly increased in male and female 
hamsters receiving 1,6- dinitropyrene by intratracheal instillation 
(Takayama et al. 1985). 1,6- Dinitropyrene induced carcinoma of the 
pituitary gland in an oral study of short-term duration in rats (Imaida 
et al. 1991).
    No adequate data were available to evaluate the carcinogenicity of 
1,6-dinitropyrene in humans.
Additional Information Relevant to Carcinogenicity
    Intratracheal administration of 1,6-dinitropyrene to rats 
previously inoculated to de-epithelialized trachea with an immortalized 
bronchial cell line, caused tumors when the tracheas were then 
implanted subcutaneously into nude mice (Iizasa et al. 1993). 1,6-
Dinitropyrene is genotoxic in a wide variety of assays in bacteria and 
mammalian cells including human cells. 1,6-Dinitropyrene also 
demonstrates evidence of cell transformation activity in vitro in rat 
tracheal epithelial cells. Metabolic pathways leading to mutagenic and 
clastogenic metabolites and DNA adducts of 1,6-dinitropyrene have been 
described (IARC 1989).
    No data were available that would suggest that the mechanisms 
thought to account for tumor induction by 1,6-dinitropyrene in 
experimental animals would not also operate in humans.''
    EPA has reviewed the NTP cancer assessment for 1,6-dinitropyrene 
and agrees that 1,6-dinitropyrene can reasonably be anticipated to 
cause

[[Page 17340]]

cancer in humans. EPA believes that the evidence is sufficient for 
listing 1,6-dinitropyrene in the PACs category on EPCRA section 313 
pursuant to EPCRA section 313(d)(2)(B) based on the available 
carcinogenicity data for this chemical.
    b. 1,8-Dinitropyrene (CAS No. 42397-65-9) (Refs. NTP Profile/
Background document (Refs. 17 and 18)). The National Toxicology Program 
has classified 1,8-dinitropyrene as ``reasonably anticipated to be a 
human carcinogen.'' The classification is based on sufficient evidence 
of carcinogenicity in experimental animals. The NTP substance profile 
for 1,8-dinitropyrene (Ref. 17) included the following summary 
information of the evidence of carcinogenicity:
``Carcinogenicity
    1,8-Dinitropyrene is reasonably anticipated to be a human 
carcinogen based on sufficient evidence of malignant tumor formation in 
multiple species of experimental animals, at multiple sites, and by 
multiple routes of exposure (IARC 1989). When administered by 
subcutaneous injections, 1,8-dinitropyrene induced injection-site 
sarcomas in male mice and male and female rats, and leukemia in female 
rats (Imaida et al. 1995, Ohgaki et al. 1984, 1985, Otofuji et al. 
1987). Intraperitoneal injections of 1,8-dinitropyrene induced sarcomas 
of the peritoneal cavity, leukemia, and mammary adenocarcinoma in 
female rats (Imaida et al. 1991, 1995). The incidences of mammary 
tumors, including adenocarcinomas, were increased in female rats 
receiving 1,8- dinitropyrene by gavage (Imaida et al. 1991, IARC 1989).
    No adequate data were available to evaluate the carcinogenicity of 
1,8-dinitropyrene in humans.
Additional Information Relevant to Carcinogenicity
    1,8-Dinitropyrene is genotoxic in a wide variety of assays in 
bacteria and mammalian cells demonstrating evidence of cell 
transformation activity in vitro, and metabolic pathways leading to 
mutagenic and clastogenic metabolites and DNA adducts have been 
described (IARC 1989).
    No data were available that would suggest that the mechanisms 
thought to account for tumor induction of 1,8-dinitropyrene in 
experimental animals would not also operate in humans.''
    EPA has reviewed the NTP cancer assessment for 1,8-dinitropyrene 
and agrees that 1,8-dinitropyrene can reasonably be anticipated to 
cause cancer in humans. EPA believes that the evidence is sufficient 
for listing 1,8-dinitropyrene in the PACs category on EPCRA section 313 
pursuant to EPCRA section 313(d)(2)(B) based on the available 
carcinogenicity data for this chemical.
    c. 6-Nitrochrysene (CAS No. 7496-02-8) (Refs. NTP Profile/
Background document (Refs. 17 and 19)). The National Toxicology Program 
has classified 6-nitrochrysene as ``reasonably anticipated to be a 
human carcinogen.'' The classification is based on sufficient evidence 
of carcinogenicity in experimental animals. The NTP substance profile 
for 6-nitrochrysene (Ref. 17) included the following summary 
information of the evidence of carcinogenicity:
``Carcinogenicity
    6-Nitrochrysene is reasonably anticipated to be a human carcinogen 
based on sufficient evidence of carcinogenicity at multiple sites in 
multiple species of experimental animals (IARC 1989). In seven studies, 
when administered by intraperitoneal injection, 6-nitrochrysene caused 
lung tumors in male and female mice and also induced liver tumors in 
female and/or male mice in three of these studies and malignant 
lymphoma in one study (Busby et al. 1985, 1989, El-Bayoumy et al. 1992, 
Li et al. 1994, Fu et al. 1994, Imaida et al. 1992, Wislocki et al. 
1986). Dysplastic and/or adenomatous lesions of the colon were 
increased in male and female rats, and colon adenocarcinomas were 
increased in male rats receiving 6-nitrochrysene by intraperitoneal 
injection (Imaida et al. 1992). Mammary fibroadenoma, adenocarcinoma, 
and spindle cell sarcomas were increased in female rats receiving 6-
nitrochrysene by injection into the mammary gland (El-Bayoumy et al. 
1993).
    No data were available to evaluate the carcinogenicity of 6-
nitrochrysene in humans.
Additional Information Relevant to Carcinogenicity
    6-Nitrochrysene induced skin tumors, mainly papillomas, in a dermal 
initiation-promotion study in which 6-nitrochrysene was used as the 
initiator, followed by promotion with a phorbol ester (El-Bayoumy et 
al. 1982). It also caused lung and forestomach tumors when given by 
intraperitoneal injection to transgenic mice carrying a human hybrid c- 
Ha-ras gene (Ogawa et al. 1996). 6-Nitrochrysene is genotoxic in 
several assays in bacteria and mammalian cells and induces cell 
transformation in finite lifespan cells in vitro. Metabolic pathways 
leading to mutagenic and clastogenic metabolites and DNA adducts have 
been described (IARC 1989). The presence of 6-nitrochrysene- DNA 
adducts in tumor target tissue supports the possibility that tumors 
induced by this chemical are at least in part a result of chemical-
induced DNA damage. No data were available that would suggest that the 
mechanisms thought to account for tumor induction by 6-nitrochrysene in 
experimental animals would not also operate in humans.''
    EPA has reviewed the NTP cancer assessment for 6-nitrochrysene and 
agrees that 6-nitrochrysene can reasonably be anticipated to cause 
cancer in humans. EPA believes that the evidence is sufficient for 
listing 6-nitrochrysene in the PACs category on EPCRA section 313 
pursuant to EPCRA section 313(d)(2)(B) based on the available 
carcinogenicity data for this chemical.
    d. 4-Nitropyrene (CAS No. 57835-92-4) (Refs. NTP Profile/Background 
document (Refs. 17 and 20)). The National Toxicology Program has 
classified 4-nitropyrene as ``reasonably anticipated to be a human 
carcinogen.'' The classification is based on sufficient evidence of 
carcinogenicity in experimental animals. The NTP substance profile for 
4-nitropyrene (Ref. 17) included the following summary information of 
the evidence of carcinogenicity:
``Carcinogenicity
    4-Nitropyrene is reasonably anticipated to be a human carcinogen 
based on sufficient evidence of malignant tumor formation at multiple 
tissue sites in multiple species of experimental animals (IARC 1989). 
Intraperitoneal injections of 4-nitropyrene caused an increased 
incidence of liver tumors in male mice, lung tumors in male and female 
mice (Wislocki et al. 1986), and mammary adenocarcinomas in female rats 
(Imaida et al. 1991). When administered by subcutaneous injections, 4-
nitropyrene induced sarcomas at the injection site, and increased 
incidences of mammary adenocarcinomas, leukemia, and tumors of the 
Zymbal gland in female rats (Imaida et al. 1995, IARC 1989). In two 
studies, female rats receiving mammary gland injections of 4-
nitropyrene showed an increased incidence of mammary tumors (Imaida et 
al. 1991, El-Bayoumy et al. 1993).
    No data were available to evaluate the carcinogenicity of 4-
nitropyrene in humans.

[[Page 17341]]

Additional Information Relevant to Carcinogenicity
    Although not as reactive or potent as some of the mononitro- or 
dinitropyrenes, 4-nitropyrene is genotoxic in bacterial cells and 
induces cell transformation in BALB cells in vitro. Metabolic pathways 
for 4-nitropyrene, leading to mutagenic and likely DNA adducts, have 
also been described (IARC 1989).
    No data were available that would suggest that the mechanisms 
thought to account for tumor induction by 4-nitropyrene in experimental 
animals would not also operate in humans.''
    EPA has reviewed the NTP cancer assessment for 4-nitropyrene and 
agrees that 4-nitropyrene can reasonably be anticipated to cause cancer 
in humans. EPA believes that the evidence is sufficient for listing 4-
nitropyrene in the PACs category on EPCRA section 313 pursuant to EPCRA 
section 313(d)(2)(B) based on the available carcinogenicity data for 
this chemical.
    e. Nitroarene persistence and bioaccumulation data. The above four 
nitroarenes are being proposed for addition to the PACs category, the 
members of which have been classified as PBT chemicals with lower 
reporting thresholds (October 29, 1999, 64 FR 58666). For purposes of 
EPCRA section 313 reporting, EPA established persistence half-life 
criteria for PBT chemicals of 2 months in water/sediment and soil and 
2-days in air, and established bioaccumulation criteria for PBT 
chemicals as a bioconcentration factor (BCF) or bioaccumulation factor 
(BAF) of 1,000 or higher. Chemicals meeting the PBT criteria were 
assigned 100 pound reporting thresholds. With regards to setting the 
EPCRA section 313 reporting thresholds, EPA set lower reporting 
thresholds (10 pounds) for those PBT chemicals with persistence half-
lifes of 6 months or more in water/sediment or soil and with BCF or BAF 
values of 5,000 or higher, these chemicals were considered highly PBT 
chemicals. At the time of the lowering of the thresholds for the PACs 
category, the persistence and bioaccumulation data for the current 
members in the category showed variation in these characteristics 
(October 29, 1999, 64 FR 58713). The PACs persistence data included air 
half-lifes of 2 hours to 4 days, surface water half-lifes of 79 days to 
44 years, and soil half-lifes of 20 days to 14.6 years. The PACs 
bioaccumulation data ranged from BCFs of 800 to 31,440. EPA determined 
that while there was variation in the persistence and bioaccumulation 
data for the members of the PACs category, the best way to report these 
chemicals was as one single category (October 29, 1999, 64 FR 58725). 
While much of the persistence and bioaccumulation data for the PACs 
chemicals exceeded what EPA classified as highly persistent and 
bioaccumulative for setting reporting thresholds, EPA decided not to 
assign the PACs category the lower 10 pound reporting threshold because 
of the variability of the persistence and bioaccumulation data across 
members of the category (October 29, 1999, 64 FR 58726).
    Since little data is available on the persistence of the four 
nitroarenes being proposed for listing, the data for 1-nitropyrene, a 
member of the PACs category, was used to estimate the persistence 
properties of the four nitroarenes (Ref. 21). 1-nitropyrene is a 
structural isomer of 4-nitropyrene and very close chemical analog of 
the other nitroarenes. The persistence data for 1-nitropyrene cited in 
the PBT chemical rule included air half lives of 10 hours to 4 days and 
surface water half lives of 16 to 44 years (October 29, 1999, 64 FR 
58713). Based on EPA's assessment (Ref. 21), the four nitroarenes are 
expected to have similar persistence properties due to structural 
similarities and comparability of the available data.
    Most of the bioaccumulation data for the members of the PACs 
category were calculated using a regression-derived equation (Ref. 22). 
The regression equation used to estimate the BCF values for the PACs 
category members for PBT chemical rule was: log BCF = 0.77 log Kow - 
0.70 + correction factor. The estimated BCF value for 1-nitropyrene 
cited in the PBT rule was 908 (Ref. 22). The most recent equations for 
BCF calculations use the equation: log BCF = 0.6598 log Kow - 0.333 + 
correction factor (Ref. 21). The results using results both equations 
to calculate BCF values for the four nitroarenes are as follows: The 
calculated BCF values for 1,6- and 1,8-dinitropyrene ranged from 480-
660, for 6-nitrochrysene they ranged from 1600 to 2600, and for 4-
nitropyrene they ranged from 630-910 (Ref. 21).
    EPA believes that the persistence and bioaccumulation data for the 
four nitroarenes is sufficiently similar to that for the current 
members of the PACs category that they should be included in the PACs 
category with the current 100 pound category reporting threshold.
    8. o-Nitroanisole (CAS No. 91-23-6) (Refs. NTP Profile/Background 
document (Refs. 23 and 24)). The National Toxicology Program has 
classified o-nitroanisole as ``reasonably anticipated to be a human 
carcinogen.'' The classification is based on sufficient evidence of 
carcinogenicity in experimental animals. The NTP substance profile for 
o-nitroanisole (Ref. 23) included the following summary information of 
the evidence of carcinogenicity:
``Carcinogenicity
    o-Nitroanisole is reasonably anticipated to be a human carcinogen 
based on sufficient evidence of malignant tumor formation at multiple 
tissue sites in multiple species of experimental animals (NTP 1993).
    When administered in the diet to male and female rats, o-
nitroanisole induced increased incidences of mononuclear cell leukemia 
and neoplasms of the urinary bladder, kidney, and large intestine. When 
administered in the diet to mice, o-nitroanisole induced increased 
incidences of benign and malignant hepatocellular neoplasms in males 
and increased incidences of hepatocellular adenomas in females.
    No adequate human studies of the relationship between exposure to 
o-nitroanisole and human cancer have been reported (IARC 1996).
Additional Information Relevant to Carcinogenicity
    o-Nitroanisole is genotoxic in a wide variety of bacteria and 
mammalian cellular assays, and mutagenic and carcinogenic metabolites 
have been described (NTP 1993, IARC 1996).
    No data were available that would suggest that the mechanisms 
thought to account for tumor induction by o-nitroanisole in 
experimental animals would not also operate in humans.''
    EPA has reviewed the NTP cancer assessment for o-nitroanisole and 
agrees that o-nitroanisole can reasonably be anticipated to cause 
cancer in humans. EPA believes that the evidence is sufficient for 
listing o-nitroanisole on EPCRA section 313 pursuant to EPCRA section 
313(d)(2)(B) based on the available carcinogenicity data for this 
chemical.
    9. Nitromethane (CAS No. 75-52-5) (Refs. NTP Profile/Background 
document (Refs. 25 and 26)). The National Toxicology Program has 
classified nitromethane as ``reasonably anticipated to be a human 
carcinogen.'' The classification is based on sufficient evidence of 
carcinogenicity in experimental animals. The NTP substance profile for 
nitromethane (Ref. 25) included the following summary information of 
the evidence of carcinogenicity:

[[Page 17342]]

``Carcinogenicity
    Nitromethane is reasonably anticipated to be a human carcinogen 
based on sufficient evidence of carcinogenicity in experimental 
animals. When administered by inhalation, nitromethane significantly 
increased the combined incidences of benign and malignant tumors at 
three tissue sites in mice and at a different tissue site in rats. In 
mice, nitromethane caused harderian gland and lung tumors in both sexes 
and liver tumors in females. In rats, nitromethane caused mammary gland 
tumors in female F344/N rats but did not cause any increased tumors in 
Long-Evans rats (exposed to lower levels) (NTP 1997). The International 
Agency for Research on Cancer (2000) also has concluded that there was 
sufficient evidence for the carcinogenicity of nitromethane in 
experimental animals.
    No studies evaluating the carcinogenicity of nitromethane in humans 
were found in the published literature.
Additional Information Relevant to Carcinogenicity
    The mechanism by which nitromethane causes cancer is not known. 
Nitromethane did not cause mutations in bacteria and does not appear to 
cause genetic damage in mammalian test systems. In cultured mammalian 
cells, nitromethane did not cause chromosomal aberrations (changes in 
chromosome structure or number), sister chromatid exchange, or 
micronucleus formation (a sign of chromosome damage or loss). 
Inhalation exposure of mice to nitromethane did not cause micronucleus 
formation in the erythrocytes (red blood cells), in either bone marrow 
or peripheral (circulating) blood (IARC 2000). In cultured Syrian 
hamster embryo cells, nitromethane induced cell transformation (a step 
in tumor formation) (Kerckaert et al. 1996, NTP 2002).
    Nitromethane appears to be absorbed by inhalation; the available 
data suggest that dermal absorption is negligible. Metabolism of 
nitromethane by experimental animals in vivo has not been 
characterized. Metabolism of nitromethane by liver microsomes from 
Fischer 344 rats resulted in formation of only trace amounts of 
formaldehyde (IARC 2000).''
    EPA has reviewed the NTP cancer assessment for nitromethane and 
agrees that nitromethane can reasonably be anticipated to cause cancer 
in humans. EPA believes that the evidence is sufficient for listing 
nitromethane on EPCRA section 313 pursuant to EPCRA section 
313(d)(2)(B) based on the available carcinogenicity data for this 
chemical.
    10. Phenolphthalein (CAS No. 77-09-8) (Refs. NTP Profile/Background 
document (Refs. 27 and 28)). The National Toxicology Program has 
classified phenolphthalein as ``reasonably anticipated to be a human 
carcinogen.'' The classification is based on sufficient evidence of 
carcinogenicity in experimental animals. The NTP substance profile for 
phenolphthalein (Ref. 27) included the following summary information of 
the evidence of carcinogenicity:
``Carcinogenicity
    Phenolphthalein is reasonably anticipated to be a human carcinogen 
based on sufficient evidence of increased incidence of malignant and/or 
combination of malignant and benign tumors in multiple tissue sites and 
in multiple species (IARC 2000). In a two-year B6C3F1 mouse 
carcinogenicity study, NTP (1996) concluded that phenolphthalein, 
administered in feed, induced significant increases in the incidence of 
histiocytic sarcoma and lymphomas of thymic origin in males and females 
and malignant lymphoma (all types) and benign ovarian sex cord stromal 
tumors in females. In the corresponding Fischer 344 rat dietary 
carcinogenicity study, phenolphthalein induced significant increases in 
the incidence of benign pheochromocytoma of the adrenal medulla in 
males and females and renal tubule adenoma in males (NTP 1996). In a 6-
month dietary study with female heterozygous p53-deficient transgenic 
mice, phenolphthalein induced a significant increase in the incidence 
of malignant lymphoma of thymic origin (Dunnick et al. 1997).
    A few epidemiological studies have investigated the association 
between the use of phenolphthalein-containing laxatives and colon 
cancer or adenomatous colorectal polyps. No consistent association was 
found. Cancers at other sites have not been investigated in humans 
(IARC 2000).
Additional Information Relevant to Carcinogenicity
    The malignant thymic lymphomas induced by phenolphthalein in female 
heterozygous p53-deficient transgenic mice exhibited a loss of the 
normal p53 allele, suggesting the involvement of a mutagenic mechanism 
in tumor induction and/or progression (Dunnick et al. 1997).
    Phenolphthalein causes enhanced oxygen radical production in in 
vitro systems. In vivo, reduction of phenoxyl radicals could allow 
reformation of phenolphthalein, establishing a futile cycle of 
oxidation and reduction, thereby generating more free radical species. 
Thus, phenolphthalein may be a significant source of oxidative stress 
in physiological systems.
    Although negative for mutagenicity and DNA damage in bacteria, 
phenolphthalein exhibits genetic activity in several in vitro and in 
vivo mammalian assays. Phenolphthalein was positive for the induction 
of chromosomal aberrations in cultured Chinese hamster ovary cells in 
the presence of metabolic activation and induced hprt gene mutations, 
chromosomal aberrations, and morphological transformation in Syrian 
hamster embryo cells. Phenolphthalein was also positive for the 
induction of micronucleated erythrocytes in mice following multiple, 
but not single, treatments administered by gavage or dosed feed. 
Phenolphthalein also induced micronuclei in female heterozygous p53-
deficient transgenic mice exposed via dosed feed for 26 weeks. Abnormal 
sperm were induced in male mice, but not male rats, treated with 
phenolphthalein via dosed feed for 13 weeks. Phenolphthalein was 
negative for Na/K ATPase gene mutations and aneuploidy in Syrian 
hamster embryo cells.
    No data were available that would suggest that the mechanisms 
thought to account for tumor induction by phenolphthalein in 
experimental animals would not also operate in humans. Phenolphthalein 
causes oxidative stress and also demonstrates the capability to alter 
tumor suppressor gene pathways, which are both mechanisms believed to 
be involved in human cancer.''
    EPA has reviewed the NTP cancer assessment for phenolphthalein and 
agrees that phenolphthalein can reasonably be anticipated to cause 
cancer in humans. EPA believes that the evidence is sufficient for 
listing phenolphthalein on EPCRA section 313 pursuant to EPCRA section 
313(d)(2)(B) based on the available carcinogenicity data for this 
chemical.
    11. Tetrafluoroethylene (CAS No. 116-14-3) (Refs. NTP Profile/
Background document (Refs. 29 and 30)). The National Toxicology Program 
has classified tetrafluoroethylene as ``reasonably anticipated to be a 
human carcinogen.'' The classification is based on sufficient evidence 
of carcinogenicity in experimental animals. The NTP substance profile 
for tetrafluoroethylene (Ref. 29) included the following summary 
information of the evidence of carcinogenicity:

[[Page 17343]]

``Carcinogenicity
    Tetrafluoroethylene (TFE) is reasonably anticipated to be a human 
carcinogen based on sufficient evidence of malignant tumor formation at 
multiple sites in multiple species of experimental animals (NTP 1997). 
When administered by inhalation to F344 rats, TFE induced renal tubule 
neoplasms, hepatocellular neoplasms, liver hemangiosarcoma, and 
mononuclear cell leukemia. When administered by inhalation to 
B6C3F1 mice, TFE induced liver hemangiomas and 
hemangiosarcomas, hepatocellular neoplasms, and histiocytic sarcomas.
    No adequate human studies of the relationship between exposure to 
TFE and human cancer have been reported (IARC 1999).
Additional Information Relevant to Carcinogenicity
    In prokaryotic systems, TFE was negative for the induction of gene 
mutations in Salmonella typhimurium with and without S9 activation. In 
mammalian systems in vitro, TFE was also negative for the induction of 
gene mutations in Chinese hamster ovary cells (HSDB 2001). No increases 
in the frequency of micronucleated erythrocytes were observed in 
peripheral blood samples obtained from TFE-exposed mice (NTP 1997).
    The frequency of H-ras codon 61 mutations observed in TFE-induced 
hepatocellular neoplasms (15%) was significantly less than the 
corresponding frequency (56 to 59%) in spontaneous liver neoplasms of 
B6C3F1 mice, suggesting that TFE induces liver neoplasms via 
a ras-independent pathway (NTP 1997).
    The kidney-specific toxicity and carcinogenicity of TFE is most 
likely related to the selective uptake and subsequent processing of 
TFE-glutathione conjugates by renal [beta]-lyase (Miller and Surh 1994, 
Anders et al. 1988). In rats, a TFE cysteine conjugate is bioactivated 
in the kidney to a difluorothionacetyl fluoride, the putative reactive 
metabolite for TFE-induced nephrotoxicity (NTP 1997).
    No data were available that would suggest that the mechanisms 
thought to account for tumor induction by TFE in experimental animals 
would not also operate in humans.''
    EPA has reviewed the NTP cancer assessment for tetrafluoroethylene 
and agrees that tetrafluoroethylene can reasonably be anticipated to 
cause cancer in humans. EPA believes that the evidence is sufficient 
for listing tetrafluoroethylene on EPCRA section 313 pursuant to EPCRA 
section 313(d)(2)(B) based on the available carcinogenicity data for 
this chemical.
    12. Tetranitromethane (CAS No. 509-14-8) (Refs. NTP Profile/NTP 
study (Refs. 31 and 32)). The National Toxicology Program has 
classified tetranitromethane as ``reasonably anticipated to be a human 
carcinogen.'' The classification is based on sufficient evidence of 
carcinogenicity in experimental animals. The NTP substance profile for 
tetranitromethane (Ref. 31) included the following summary information 
of the evidence of carcinogenicity:
``Carcinogenicity
    Tetranitromethane is reasonably anticipated to be a human 
carcinogen based on sufficient evidence of carcinogenicity in 
experimental animals. Exposure to tetranitromethane in a two-year 
inhalation bioassay caused a dose-related increase in alveolar/
bronchiolar neoplasms to nearly all mice and rats exposed to 
concentrations of 2 and 5 ppm respectively. The incidences of these 
neoplasms in lower exposure concentration groups (2 ppm for rats and 
0.5 ppm for mice) were 66% and 44% in male and female rats, 
respectively, and 54% and 48% in male and female mice, respectively 
(NTP 1990). The majority of animals with alveolar/bronchiolar neoplasms 
had neoplasms diagnosed as carcinomas, and these neoplasms frequently 
metastasized to a variety of organs. Squamous cell carcinomas of the 
lung were also markedly increased in rats exposed to 5 ppm. This 
particular type of neoplasm has been found in only 3 of approximately 
1,600 untreated control male rats and in none of a similar number of 
untreated female controls (NTP 1990).
    No adequate human studies of the relationship between exposure to 
tetranitromethane and human cancer have been reported (IARC 1996).''
    EPA has reviewed the NTP cancer assessment for tetranitromethane 
and agrees that tetranitromethane can reasonably be anticipated to 
cause cancer in humans. EPA believes that the evidence is sufficient 
for listing tetranitromethane on EPCRA section 313 pursuant to EPCRA 
section 313(d)(2)(B) based on the available carcinogenicity data for 
this chemical.
    13. Vinyl Fluoride (CAS No. 75-02-5) (Refs. NTP Profile/Background 
document (Refs. 33 and 34)). The National Toxicology Program has 
classified vinyl fluoride as ``reasonably anticipated to be a human 
carcinogen.'' The classification is based on sufficient evidence of 
carcinogenicity in experimental animals. The NTP substance profile for 
vinyl fluoride (Ref. 33) included the following summary information of 
the evidence of carcinogenicity:
``Carcinogenicity
    Vinyl fluoride is reasonably anticipated to be a human carcinogen 
based on sufficient evidence of carcinogenicity in experimental 
animals. Both male and female rats exposed to vinyl fluoride by 
inhalation showed increased incidences of hepatic hemangiosarcoma, 
hepatocellular adenoma or carcinoma, and Zymbal gland carcinoma. Both 
male and female mice exposed to vinyl fluoride by inhalation showed 
increased incidences of hepatic hemangiosarcoma, bronchiolar-alveolar 
adenoma or adenocarcinoma, hepatocellular adenoma, and harderian gland 
adenoma. Female mice also showed an increased incidence of mammary 
gland adenocarcinoma (Bogdanffy et al. 1995, IARC 1995).
    The tumor responses of laboratory animals to vinyl fluoride are 
similar to their responses to vinyl chloride, a known human carcinogen 
(IARC 1987), and to vinyl bromide, a probable human carcinogen (IARC 
1986). A unique feature of vinyl chloride carcinogenicity is that vinyl 
chloride induces rare hepatic hemangiosarcomas in experimental animals 
and is causally associated with excess risk of liver hemangiosarcoma in 
epidemiological studies of exposed workers. The fact that vinyl 
fluoride, vinyl chloride, and vinyl bromide all induce rare 
hemangiosarcomas of the liver in experimental animals and induce the 
formation of similar DNA adducts suggests a possible common mechanism 
of carcinogenicity for all three of these chemicals.
    No adequate human studies of the relationship between exposure to 
vinyl fluoride and human cancer were found.
Additional Information Relevant to Carcinogenicity
    Vinyl fluoride is mutagenic in Salmonella typhimurium with the 
addition of a rat liver homogenate metabolic activation system. In 
addition, vinyl fluoride induces gene mutations and chromosomal 
aberrations in Chinese hamster ovary cells (with metabolic activation), 
sex-linked recessive lethal mutations in Drosophila melanogaster, and 
micronuclei in bone marrow cells of female mice (IARC 1995).
    Vinyl fluoride likely is metabolized in a manner similar to vinyl 
chloride: Oxidation via cytochrome P450 to fluoroethylene oxide, 
followed by

[[Page 17344]]

rearrangement to 2-fluoroacetaldehyde, which is oxidized to 
fluoroacetic acid. Human, rat, and mouse liver microsomes metabolize 
vinyl fluoride at similar rates (Cantoreggi and Keller 1997). Vinyl 
fluoride metabolites form covalent DNA adducts. Inhalation exposure of 
rats and mice to vinyl fluoride produced a dose-related increase in the 
formation of the promutagenic adduct N \2\,3- ethenoguanine in their 
liver DNA (Swenberg et al. 1995).
    No available data suggest that mechanisms by which vinyl fluoride 
induces tumors in experimental animals would not also operate in 
humans.''
    EPA has reviewed the NTP cancer assessment for vinyl fluoride and 
agrees that vinyl fluoride can reasonably be anticipated to cause 
cancer in humans. EPA believes that the evidence is sufficient for 
listing vinyl fluoride on EPCRA section 313 pursuant to EPCRA section 
313(d)(2)(B) based on the available carcinogenicity data for this 
chemical.

V. Rationale for Listing

    The NTP RoC document undergoes significant scientific review and 
public comment. The NTP review mirrors the review EPA has historically 
done to assess chemicals for listing under EPCRA section 313 on the 
basis of carcinogenicity. The conclusions regarding the potential for 
chemicals in the NTP RoC to cause cancer in humans are based on 
established sound scientific principles. EPA believes that the NTP RoC 
is an excellent and reliable source of information on the potential for 
chemicals covered in the NTP RoC to cause cancer in humans. Based on 
EPA's review of the data contained in the 11th NTP RoC, EPA has 
determined that the chemicals in this proposed rule can reasonably be 
anticipated to cause cancer. Therefore, EPA believes that the evidence 
is sufficient for listing all of the chemicals in this proposed rule on 
the EPCRA section 313 toxic chemical list pursuant to EPCRA section 
313(d)(2)(B) based on the available carcinogenicity data for these 
chemicals as presented in the 11th RoC.
    EPA considers chemicals that can reasonably be anticipated to cause 
cancer to have moderately high to high chronic toxicity. EPA does not 
believe that it is appropriate to consider exposure for chemicals that 
are moderately high to highly toxic based on a hazard assessment when 
determining if a chemical can be added for chronic effects pursuant to 
EPCRA section 313(d)(2)(B) (see 59 FR 61440-61442). Therefore, in 
accordance with EPA's standard policy on the use of exposure 
assessments (59 FR 61432), EPA does not believe that an exposure 
assessment is necessary or appropriate for determining whether any of 
the chemicals in this proposed rule meet the criteria of EPCRA section 
313(d)(2)(B).

VI. References

    EPA has established an official public docket for this action under 
Docket ID No. EPA-HQ-TRI-2010-0006. The public docket includes 
information considered by EPA in developing this action, including the 
documents listed below, which are electronically or physically located 
in the docket. In addition, interested parties should consult documents 
that are referenced in the documents that EPA has placed in the docket, 
regardless of whether these referenced documents are electronically or 
physically located in the docket. For assistance in locating documents 
that are referenced in documents that EPA has placed in the docket, but 
that are not electronically or physically located in the docket, please 
consult the person listed in the above FOR FURTHER INFORMATION CONTACT 
section.
    1. NTP, 2005. National Toxicology Program. Introduction: Report on 
Carcinogens, Eleventh Edition. Released January 31, 2005. U.S. 
Department of Health and Human Services, Public Health Service, 
National Toxicology Program, Research Triangle Park, NC 27709.
    2. USEPA. Guidelines for Carcinogen Risk Assessment. Risk 
Assessment Forum, U.S. Environmental Protection Agency, Washington, DC, 
March 2005.
    3. USEPA, OEI. Economic Analysis of the Proposed Rule to add 16 
Chemicals to the EPCRA Section 313 List of Toxic Chemicals. February 
16, 2010.
    4. USEPA, OEI. Memorandum from Mark Miller, PhD, Toxicologist, 
Analytical Support Branch to Nicole Paquette, PhD, Chief, Analytical 
Support Branch. January 28, 2010. Subject: Review of National 
Toxicology Program (NTP) Cancer Classification Data for Sixteen 
Chemicals.
    5. NTP, 2005. National Toxicology Program. 11th Report on 
Carcinogens--1-Amino-2,4-dibromoanthraquinone Substance Profile. 
Released January 31, 2005. U.S. Department of Health and Human 
Services, Public Health Service, National Toxicology Program, Research 
Triangle Park, NC 27709.
    6. NTP, 2002. Report on Carcinogens Background Document for 1-
Amino-2,4-dibromoanthraquinone. September 19, 2002. Prepared for, U.S. 
Department of Health and Human Services, Public Health Service, 
National Toxicology Program, Research Triangle Park, NC 27709. Prepared 
by, Technology Planning and Management Corporation Canterbury Hall, 
Suite 310, 4815 Emperor Blvd., Durham, NC 27703. Contract Number N01-
ES-85421.
    7. NTP, 2005. National Toxicology Program. 11th Report on 
Carcinogens--2,2-bis(Bromomethyl)-1,3-propanediol Substance Profile. 
Released January 31, 2005. U.S. Department of Health and Human 
Services, Public Health Service, National Toxicology Program, Research 
Triangle Park, NC 27709.
    8. NTP. Report on Carcinogens Background Document for 2,2-
bis(Bromomethyl)-1,3-propanediol (Technical Grade). Prepared for, U.S. 
Department of Health and Human Services, Public Health Service, 
National Toxicology Program, Research Triangle Park, NC 27709. Prepared 
by, Technology Planning and Management Corporation, Canterbury Hall, 
Suite 310, 4815 Emperor Blvd., Durham, NC 27703. Contract Number N01-
ES-85421.
    9. NTP, 2005. National Toxicology Program. 11th Report on 
Carcinogens--Furan Substance Profile. Released January 31, 2005. U.S. 
Department of Health and Human Services, Public Health Service, 
National Toxicology Program, Research Triangle Park, NC 27709.
    10. NTP, 1999. National Toxicology Program Report on Carcinogens 
Background Document for Furan. March 1999. Prepared for, November 18-
19, 1996, Meeting of the Report on Carcinogens Subcommittee of the 
Board of Scientific Counselors. Prepared by, Integrated Laboratory 
Systems, Research Triangle Park, NC 27709. NIEHS Contract No. N01-ES-
25346.
    11. NTP, 2005. National Toxicology Program. 11th Report on 
Carcinogens--Glycidol Substance Profile. Released January 31, 2005. 
U.S. Department of Health and Human Services, Public Health Service, 
National Toxicology Program, Research Triangle Park, NC 27709.
    12. NTP, 1990. Toxicology and Carcinogenesis Studies of Glycidol 
(CAS No. 556-52-5) In F344/N Rats and B6C3F1 Mice (Gavage Studies). 
Technical Report Series No. 374. NIH Publication No. 90-2829, March 
1990. National Toxicology Program, Research Triangle Park, NC. 229 pp.
    13. NTP, 2005. National Toxicology Program. 11th Report on 
Carcinogens--Isoprene Substance Profile. Released January 31, 2005. 
U.S. Department of Health and Human Services, Public Health Service, 
National Toxicology Program, Research Triangle Park, NC 27709.

[[Page 17345]]

    14. NTP, 1999. National Toxicology Program Report on Carcinogens 
Background Document for Isoprene. March 1999. Prepared for, December 2-
3, 1998, Meeting of the Report on Carcinogens Subcommittee of the NTP 
Board of Scientific Counselors. Prepared by, Integrated Laboratory 
Systems, Research Triangle Park, NC 27709. NIEHS Contract No. N01-ES-
25346.
    15. NTP, 2005. National Toxicology Program. 11th Report on 
Carcinogens--Methyleugenol Substance Profile. Released January 31, 
2005. U.S. Department of Health and Human Services, Public Health 
Service, National Toxicology Program, Research Triangle Park, NC 27709.
    16. NTP, 2000. Report on Carcinogens Background Document for 
Methyleugenol. December 13-14, 2000, Meeting of the NTP Board of 
Scientific Counselors Report on Carcinogens Subcommittee. Prepared for, 
U.S. Department of Health and Human Services, Public Health Service, 
National Toxicology Program, Research Triangle Park, NC 27709. Prepared 
by, Technology Planning and Management Corporation, Canterbury Hall, 
Suite 310, 4815 Emperor Blvd., Durham, NC 27703. Contract Number N01-
ES-85421.
    17. NTP, 2005. National Toxicology Program. 11th Report on 
Carcinogens--Nitroarenes (Selected) Substance Profile. Released January 
31, 2005. U.S. Department of Health and Human Services, Public Health 
Service, National Toxicology Program, Research Triangle Park, NC 27709.
    18. NTP, 1999. National Toxicology Program Report on Carcinogens 
Background Document for 1,6-Dinitropyrene and 1,8-Dinitropyrene. Final 
March 1999. Prepared for, November 18-19, 1996, Meeting of the Report 
on Carcinogens Subcommittee of the NTP Board of Scientific Counselors. 
Prepared by, Integrated Laboratory Systems, Research Triangle Park, NC 
27709. NIEHS Contract No. N01-ES-25346.
    19. NTP, 1999. National Toxicology Program Report on Carcinogens 
Background Document for 6-Nitrochrysene. Final March 1999. Prepared 
for, November 18-19, 1996, Meeting of the Report on Carcinogens 
Subcommittee of the NTP Board of Scientific Counselors. Prepared by, 
Integrated Laboratory Systems, Research Triangle Park, NC 27709. NIEHS 
Contract No. N01-ES-25346.
    20. NTP, 1999. National Toxicology Program Report on Carcinogens 
Background Document for 4-Nitropyrene. Final March 1999. Prepared for, 
November 18-19, 1996, Meeting of the Report on Carcinogens Subcommittee 
of the NTP Board of Scientific Counselors. Prepared by, Integrated 
Laboratory Systems, Research Triangle Park, NC 27709. NIEHS Contract 
No. N01-ES-25346.
    21. USEPA/OEI. Technical Support Document: Bioaccumulation and 
Persistence Data for Selected Nitroarenes. Office of Environmental 
Information, Environmental Analysis Division, Analytical Support 
Branch, November 2009.
    22. USEPA/OPPT. Technical Support Document for Determination of 
Bioaccumulation (BAF) and Bioconcentration (BCF) Values for Persistent 
Bioaccumulative Toxic (PBT) Chemicals and for Identification of PBT 
Chemicals. Jerry Smrchek, PhD, Biologist, Existing Chemicals Assessment 
Branch, Risk Assessment Division. September 1998.
    23. NTP, 2005. National Toxicology Program. 11th Report on 
Carcinogens--o-Nitroanisole Substance Profile. Released January 31, 
2005. U.S. Department of Health and Human Services, Public Health 
Service, National Toxicology Program, Research Triangle Park, NC 27709.
    24. NTP, 1999. National Toxicology Program Report on Carcinogens 
Background Document for o-Nitroanisole. Final March 1999. Prepared for, 
November 18-19, 1996, Meeting of the Report on Carcinogens Subcommittee 
of the NTP Board of Scientific Counselors. Prepared by, Integrated 
Laboratory Systems, Research Triangle Park, NC 27709. NIEHS Contract 
No. N01-ES-25346.
    25. NTP, 2005. National Toxicology Program. 11th Report on 
Carcinogens--Nitromethane Substance Profile. Released January 31, 2005. 
U.S. Department of Health and Human Services, Public Health Service, 
National Toxicology Program, Research Triangle Park, NC 27709.
    26. NTP, 2002. Final Report on Carcinogens Background Document for 
Nitromethane. March 25, 2002. Prepared for, U.S. Department of Health 
and Human Services, Public Health Service, National Toxicology Program, 
Research Triangle Park, NC 27709. Prepared by, Technology Planning and 
Management Corporation, Canterbury Hall, Suite 310, 4815 Emperor Blvd., 
Durham, NC 27703. Contract Number N01-ES-85421.
    27. NTP, 2005. National Toxicology Program. 11th Report on 
Carcinogens--Phenolphthalein Substance Profile. Released January 31, 
2005. U.S. Department of Health and Human Services, Public Health 
Service, National Toxicology Program, Research Triangle Park, NC 27709.
    28. NTP, 1999. National Toxicology Program Report on Carcinogens 
Background Document for Phenolphthalein. Final March 1999. Prepared 
for, October 30-31, 1997, Meeting of the Report on Carcinogens 
Subcommittee of the NTP Board of Scientific Counselors. Prepared by, 
Integrated Laboratory Systems, Research Triangle Park, NC 27709. NIEHS 
Contract No. N01-ES-25346.
    29. NTP, 2005. National Toxicology Program. 11th Report on 
Carcinogens--Tetrafluoroethylene Substance Profile. Released January 
31, 2005. U.S. Department of Health and Human Services, Public Health 
Service, National Toxicology Program, Research Triangle Park, NC 27709.
    30. NTP, 1999. National Toxicology Program Report on Carcinogens 
Background Document for Tetrafluoroethylene. Final March 1999. Prepared 
for, October 30-31, 1997, Meeting of the Report on Carcinogens 
Subcommittee of the NTP Board of Scientific Counselors. Prepared by, 
Integrated Laboratory Systems, Research Triangle Park, NC 27709. NIEHS 
Contract No. N01-ES-25346.
    31. NTP, 2005. National Toxicology Program. 11th Report on 
Carcinogens--Tetranitromethane Substance Profile. Released January 31, 
2005. U.S. Department of Health and Human Services, Public Health 
Service, National Toxicology Program, Research Triangle Park, NC 27709.
    32. NTP, 1990. Toxicology and Carcinogenesis Studies of 
Tetranitromethane (CAS No. 509-14-8) in F344/N Rats and B6C3F1 Mice 
(Inhalation Studies). Technical Report Series No. 386. NIH Publication 
No. 90-2841. Research Triangle Park, NC and Bethesda, NC: National 
Toxicology Program. 207 pp.
    33. NTP, 2005. National Toxicology Program. 11th Report on 
Carcinogens--Vinyl Fluoride Substance Profile. Released January 31, 
2005. U.S. Department of Health and Human Services, Public Health 
Service, National Toxicology Program, Research Triangle Park, NC 27709.
    34. NTP. Final Report on Carcinogens Background Document for Vinyl 
Fluoride. Meeting of the NTP Board of Scientific Counselors Report on 
Carcinogens Subcommittee. Prepared for, U.S. Department of Health and 
Human Services, Public Health Service, National Toxicology Program, 
Research Triangle Park, NC 27709. Prepared by, Technology Planning and 
Management Corporation, Canterbury Hall, Suite 310,

[[Page 17346]]

4815 Emperor Blvd, Durham, NC 27703. Contract Number N01-ES-85421.

VIII. Statutory and Executive Order Reviews Associated With This 
Action?

A. Executive Order 12866, Regulatory Planning and Review

    This action is not a ``significant regulatory action'' under the 
terms of Executive Order (EO) 12866 (58 FR 51735, October 4, 1993) and 
is therefore not subject to review under the EO.

B. Paperwork Reduction Act

    This proposed rule does not contain any new information collection 
requirements that require additional approval by the Office of 
Management and Budget (OMB) under the Paperwork Reduction Act (PRA), 44 
U.S.C. 3501 et seq. Currently, the facilities subject to the reporting 
requirements under EPCRA 313 and PPA 6607 may use either the EPA Toxic 
Chemicals Release Inventory Form R (EPA Form 1B9350-1), or the EPA 
Toxic Chemicals Release Inventory Form A (EPA Form 1B9350-2). The Form 
R must be completed if a facility manufactures, processes, or otherwise 
uses any listed chemical above threshold quantities and meets certain 
other criteria. For the Form A, EPA established an alternative 
threshold for facilities with low annual reportable amounts of a listed 
toxic chemical. A facility that meets the appropriate reporting 
thresholds, but estimates that the total annual reportable amount of 
the chemical does not exceed 500 pounds per year, can take advantage of 
an alternative manufacture, process, or otherwise use threshold of 1 
million pounds per year of the chemical, provided that certain 
conditions are met, and submit the Form A instead of the Form R. In 
addition, respondents may designate the specific chemical identity of a 
substance as a trade secret pursuant to EPCRA section 322 42 U.S.C. 
11042: 40 CFR part 350.
    OMB has approved the reporting and recordkeeping requirements 
related to Form R, supplier notification, and petitions under OMB 
Control number 2070-0093 (EPA Information Collection Request (ICR) No. 
1363.15); those related to Form A under OMB Control number 2070-0143 
(EPA ICR No. 1704.09); and those related to trade secret designations 
under OMB Control number 2070-0078 (EPA ICR No. 1428). As provided in 5 
CFR 1320.5(b) and 1320.6(a), an Agency may not conduct or sponsor, and 
a person is not required to respond to, a collection of information 
unless it displays a currently valid OMB control number. The OMB 
Control numbers relevant to EPA's regulations are listed in 40 CFR part 
9, 48 CFR chapter 15, and displayed on the information collection 
instruments (e.g., forms, instructions).
    For Form R, EPA estimates the industry reporting and recordkeeping 
burden for collecting this information to average, in the first year, 
approximately $4,615 per Form R (for a total first year cost of 
$858,299 based on 16,069 total burden hours). In subsequent years, the 
burden for collecting this information is estimated to average $1,553 
per Form R (for a total cost of $288,902 based on 5,517 total burden 
hours). These estimates include the time needed to become familiar with 
the requirement (first year only); review instructions; search existing 
data sources; gather and maintain the data needed; complete and review 
the collection information; and transmit or otherwise disclose the 
information. The actual burden on any facility may be different from 
this estimate depending on the complexity of the facility's operations 
and the profile of the releases at the facility. Upon promulgation of a 
final rule, the Agency may determine that the existing burden estimates 
in the ICRs need to be amended in order to account for an increase in 
burden associated with the final action. If so, the Agency will submit 
an information collection worksheet (ICW) to OMB requesting that the 
total burden in each ICR be amended, as appropriate.
    The Agency would appreciate any comments or information that could 
be used to: (1) Evaluate whether the proposed collection of information 
is necessary for the proper performance of the functions of the Agency, 
including whether the information will have practical utility; (2) 
evaluate the reasonableness of the Agency's estimate of the burden of 
the proposed collection of information, including the validity of the 
methodology and assumptions used; (3) enhance the quality, utility, and 
clarity of the information to be collected; and (4) minimize the burden 
of the collection of information on those who are to respond, including 
through the use of appropriate automated electronic, mechanical, or 
other technological collection techniques or other forms of information 
technology, e.g., permitting electronic submission of responses. Please 
submit your comments within 90 days as specified at the beginning of 
this proposal. Copies of the existing ICRs may be obtained from Rick 
Westlund, Collection Strategies Division, U.S. Environmental Protection 
Agency (2822T), 1200 Pennsylvania Ave., NW., Washington, DC 20460 or by 
calling (202) 566-1672.

C. Regulatory Flexibility Act (RFA), as Amended by the Small Business 
Regulatory Enforcement Fairness Act of 1996 (SBREFA), 5 U.S.C. 601 et 
seq.

    The RFA generally requires an agency to prepare a regulatory 
flexibility analysis of any rule subject to notice and comment 
rulemaking requirements under the Administrative Procedure Act or any 
other statute unless the agency certifies that the rule will not have a 
significant economic impact on a substantial number of small entities. 
Small entities include small businesses, small organizations, and small 
governmental jurisdictions. For purposes of assessing the impacts of 
today's rule on small entities, small entity is defined as: (1) A 
business that is classified as a ``small business'' by the Small 
Business Administration at 13 CFR 121.201; (2) a small governmental 
jurisdiction that is a government of a city, county, town, school 
district or special district with a population of less than 50,000; and 
(3) a small organization that is any not-for-profit enterprise which is 
independently owned and operated and is not dominant in its field.
    Of the 109 entities estimated to be impacted by this proposed rule, 
41 are small businesses. Of the affected small businesses, all 41 have 
cost impacts of less than 1% in both the first and subsequent years of 
the rulemaking. No small businesses are projected to have a cost impact 
of 1% or greater. In the first year, of the 41 estimated cost impacts, 
there is a maximum impact of 0.616% and a minimum impact of less than 
0.001%. Facilities eligible to use Form A (those meeting the 
appropriate activity threshold which have 500 pounds per year or less 
of reportable amounts of the chemical) will have a lower burden. No 
small governments or small organizations are expected to be affected by 
this action. Thus this rule is not expected to have a significant 
adverse economic impact on a substantial number of small entities. A 
more detailed analysis of the impacts on small entities is located in 
EPA's economic analysis support document (Ref. 3).
    After considering the economic impacts of today's rule on small 
entities, I certify that this action will not have a significant 
economic impact on a substantial number of small entities. We continue 
to be interested in the potential impacts of the proposed rule on small 
entities and welcome comments on issues related to such impacts.

[[Page 17347]]

D. Unfunded Mandates Reform Act

    This rule does not contain a Federal mandate that may result in 
expenditures of $100 million or more for State, local, and tribal 
governments, in the aggregate, or the private sector in any one year. 
EPA's economic analysis indicates that the total cost of this rule is 
estimated to be $859,072 in the first year of reporting. Thus, this 
rule is not subject to the requirements of sections 202 or 205 of UMRA.
    This rule is also not subject to the requirements of section 203 of 
UMRA because it contains no regulatory requirements that might 
significantly or uniquely affect small governments. Small governments 
are not subject to the EPCRA section 313 reporting requirements.

E. Executive Order 13132 (Federalism)

    This action does not have federalism implications. It will not have 
substantial direct effects on the States, on the relationship between 
the national government and the States, or on the distribution of power 
and responsibilities among the various levels of government, as 
specified in Executive Order 13132. This action relates to toxic 
chemical reporting under EPCRA section 313, which primarily affects 
private sector facilities. Thus, Executive Order 13132 does not apply 
to this action.
    In the spirit of Executive Order 13132, and consistent with EPA 
policy to promote communications between EPA and State and local 
governments, EPA specifically solicits comment on this proposed action 
from State and local officials.

F. Executive Order 13175: Consultation and Coordination With Indian 
Tribal Governments

    This action does not have tribal implications, as specified in 
Executive Order 13175 (65 FR 67249, November 9, 2000). This action 
relates to toxic chemical reporting under EPCRA section 313, which 
primarily affects private sector facilities. Thus, Executive Order 
13175 does not apply to this action. In the spirit of Executive Order 
13175, and consistent with EPA policy to promote communications between 
EPA and Indian Tribal Governments, EPA specifically solicits additional 
comment on this proposed action from tribal officials.

G. Executive Order 13045: Protection of Children From Environmental 
Health Risks and Safety Risks

    This action is not subject to EO 13045 (62 FR 19885, April 23, 
1997) because it is not economically significant as defined in EO 
12866, and because the Agency does not believe the environmental health 
or safety risks addressed by this action present a disproportionate 
risk to children. This action relates to toxic chemical reporting under 
EPCRA section 313, which primarily affects private sector facilities.

H. Executive Order 13211: Actions Concerning Regulations That 
Significantly Affect Energy Supply, Distribution, or Use

    This action is not subject to Executive Order 13211 (66 FR 28355 
(May 22, 2001)), because it is not a significant regulatory action 
under Executive Order 12866.

I. National Technology Transfer and Advancement Act

    Section 12(d) of the National Technology Transfer and Advancement 
Act of 1995 (``NTTAA''), Public Law 104-113, 12(d) (15 U.S.C. 272 note) 
directs EPA to use voluntary consensus standards in its regulatory 
activities unless to do so would be inconsistent with applicable law or 
otherwise impractical. Voluntary consensus standards are technical 
standards (e.g., materials specifications, test methods, sampling 
procedures, and business practices) that are developed or adopted by 
voluntary consensus standards bodies. NTTAA directs EPA to provide 
Congress, through OMB, explanations when the Agency decides not to use 
available and applicable voluntary consensus standards.
    This proposed rulemaking does not involve technical standards. 
Therefore, EPA is not considering the use of any voluntary consensus 
standards.

J. Executive Order 12898: Federal Actions To Address Environmental 
Justice in Minority Populations and Low-Income Populations

    Executive Order (EO) 12898 (59 FR 7629 (Feb. 16, 1994)) establishes 
Federal executive policy on environmental justice. Its main provision 
directs Federal agencies, to the greatest extent practicable and 
permitted by law, to make environmental justice part of their mission 
by identifying and addressing, as appropriate, disproportionately high 
and adverse human health or environmental effects of their programs, 
policies, and activities on minority populations and low-income 
populations in the United States.
    EPA has determined that this proposed rule will not have 
disproportionately high and adverse human health or environmental 
effects on minority or low-income populations because it does not 
affect the level of protection provided to human health or the 
environment. This proposed rule adds additional chemicals to the EPCRA 
section 313 reporting requirements. By adding chemicals to the list of 
toxic chemicals subject to reporting under section 313 of EPCRA, EPA 
would be providing communities across the United States (including 
minority populations and low income populations) with access to data 
which they may use to seek lower exposures and consequently reductions 
in chemical risks for themselves and their children. This information 
can also be used by government agencies and others to identify 
potential problems, set priorities, and take appropriate steps to 
reduce any potential risks to human health and the environment. 
Therefore, the informational benefits of the proposed rule will have a 
positive impact on the human health and environmental impacts of 
minority populations, low-income populations, and children.

List of Subjects in 40 CFR Part 372

    Environmental protection, Community right-to-know, Reporting and 
recordkeeping requirements, and Toxic chemicals.

    Dated: March 31, 2010.
Lisa P. Jackson,
Administrator.
    Therefore, it is proposed that 40 CFR part 372 be amended as 
follows:

PART 372--[AMENDED]

    1. The authority citation for part 372 continues to read as 
follows:

    Authority:  42 U.S.C. 11023 and 11048.


Sec.  372.28  [Amended]

    2. In Sec.  372.28, the table in paragraph (a)(2) under the heading 
``Polycyclic aromatic compounds (PACs): (This category includes only 
those chemicals listed below)'' is amended by adding four new entries 
in alphabetical order to read as follows:


Sec.  372.28  Lower thresholds for chemicals of special concern.

    (a) * * *
    (2) * * *

[[Page 17348]]



------------------------------------------------------------------------
                                                             Reporting
                      Category name                          threshold
------------------------------------------------------------------------

                                * * * * *
Polycyclic aromatic compounds (PACs): (This category                 100
 includes only those chemicals listed below)............

                                * * * * *
42397-64-8 1,6-Dinitropyrene............................
42397-65-9 1,8-Dinitropyrene............................

                                * * * * *
07496-02-8 6-Nitrochrysene..............................

                                * * * * *
57835-92-4 4-Nitropyrene................................
------------------------------------------------------------------------

Sec.  372.65  [Amended]

    3. Section 372.65 is amended as follows:
    a. In the table to paragraph (a) by adding new entries in 
alphabetical order.
    b. In the table to paragraph (b) by adding new entries in numerical 
order.
    c. In the table to paragraph (c) under the heading ``Polycyclic 
aromatic compounds (PACs): (This category includes only those chemicals 
listed below)'' by adding four entries in alphabetical order.


Sec.  372.65  Chemicals and chemical categories to which the part 
applies.

* * * * *
    (a) * * *

------------------------------------------------------------------------
                                                              Effective
              Chemical name                    CAS No.           date
------------------------------------------------------------------------

                              * * * * * * *
1-Amino-2,4-dibromoanthraquinone........         00081-49-2         1/11

                              * * * * * * *
2,2-bis(Bromomethyl)-1,3-propanediol....        003296-90-0         1/11

                              * * * * * * *
Furan...................................         00110-00-9         1/11

                              * * * * * * *
Glycidol................................         00556-52-5         1/11

                              * * * * * * *
Isoprene................................         00078-79-5         1/11

                              * * * * * * *
Methyleugenol...........................         00093-15-2         1/11

                              * * * * * * *
o-Nitroanisole..........................         00091-23-6         1/11

                              * * * * * * *
Nitromethane............................         00075-52-5         1/11

                              * * * * * * *
Phenolphthalein.........................         00077-09-8         1/11

                              * * * * * * *
Tetrafluoroethylene.....................         00116-14-3         1/11

                              * * * * * * *
Tetranitromethane.......................         00509-14-8         1/11

                              * * * * * * *
Vinyl Fluoride..........................         00075-02-5         1/11

                              * * * * * * *
------------------------------------------------------------------------

    (b) * * *

------------------------------------------------------------------------
                                                              Effective
             CAS No.                     Chemical name           date
------------------------------------------------------------------------

                               * * * * * *
00075-02-5.......................  Vinyl Fluoride..........         1/11

                               * * * * * *
00075-52-5.......................  Nitromethane............         1/11

                               * * * * * *
00077-09-8.......................  Phenolphthalein.........         1/11

[[Page 17349]]



                               * * * * * *
00078-79-5.......................  Isoprene................         1/11

                               * * * * * *
00081-49-2.......................  1-Amino-2,4-                     1/11
                                    dibromoanthraquinone.

                               * * * * * *
00091-23-6.......................  o-Nitroanisole..........         1/11

                               * * * * * *
00093-15-2.......................  Methyleugenol...........         1/11

                               * * * * * *
00110-00-9.......................  Furan...................         1/11

                               * * * * * *
00116-14-3.......................  Tetrafluoroethylene.....         1/11

                               * * * * * *
00509-14-8.......................  Tetranitromethane.......         1/11

                               * * * * * *
00556-52-5.......................  Glycidol................         1/11

                               * * * * * *
03296-90-0.......................  2,2-bis(Bromomethyl)-1,3-        1/11
                                    propanediol.

                               * * * * * *
------------------------------------------------------------------------

    (c) * * *

------------------------------------------------------------------------
                                                              Effective
                       Category name                             date
------------------------------------------------------------------------

                               * * * * * *
Polycyclic aromatic compounds (PACs): (This category
 includes only those chemicals listed below)...............

                               * * * * * *
42397-64-8 1,6-Dinitropyrene...............................         1/11
42397-65-9 1,8-Dinitropyrene...............................         1/11

                               * * * * * *
07496-02-8 6-Nitrochrysene.................................         1/11

                               * * * * * *
57835-92-4 4-Nitropyrene...................................         1/11
------------------------------------------------------------------------

[FR Doc. 2010-7756 Filed 4-5-10; 8:45 am]
BILLING CODE 6560-50-P
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