Federal Register / Vol. 75, No. 65 / Tuesday, April 6, 2010 / Proposed Rules 17333 

the Rules section of this Federal 

Register. 

FOR FURTHER INFORMATION CONTACT: 

Zach Hedgpeth, U.S. EPA, Region 10, 

1200 Sixth Avenue, Mail stop WCM– 

122, Seattle, Washington 98101, e-mail: 

hedgpeth.zach@epa.gov, phone number 

(206) 553–1217. 

SUPPLEMENTARY INFORMATION: In the 

‘‘Rules and Regulations’’ section of this 

Federal Register, the EPA is codifying 

and incorporating by reference the 

State’s hazardous waste program as an 

direct final rule. The EPA did not make 

a proposal prior to the direct final rule 

because we believe these actions are not 

controversial and do not expect 

comments that oppose them. We have 

explained the reasons for this 

codification and incorporation by 

reference in the preamble to the direct 

final rule. Unless we get written 

comments which oppose this 

incorporation by reference during the 

comment period, the direct final rule 

will become effective on the date it 

establishes, and we will not take further 

action on this proposal. If we get 

comments that oppose these actions, we 

will withdraw the direct final rule and 

it will not take effect. We will then 

respond to public comments in a later 

final rule based on this proposal. You 

may not have another opportunity for 

comment. If you want to comment on 

this action, you must do so at this time. 

For additional information, please see 

the direct final rule published in the 

‘‘Rules and Regulations’’ section of this 

Federal Register. 

Authority: This action is issued under the 

authority of sections 2002(a), 3006 and 

7004(b) of the Solid Waste and Disposal Act, 

as amended, 42 U.S.C. 6912(a), 6926, 6974(b). 

Dated: March 11, 2010. 

Dennis J. McLerran, 

Regional Administrator, EPA Region 10. 

[FR Doc. 2010–7649 Filed 4–5–10; 8:45 am] 

BILLING CODE 6560–50–P 

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. 

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 email 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; email: 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 


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included in this proposed rule. 

Potentially affected categories and 

entities may include, but are not limited 

to: 

Category Examples of potentially affected entities 

Industry ............................... Facilities included in the following NAICS manufacturing codes (corresponding to SIC codes 20 through 39): 311*, 

312*, 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 


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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 subpopulations, 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 


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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 


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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 


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radiotracer in DNA from livers of rats 

treated with [14C]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-Stransferase. 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 


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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) Odemethylation 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 b-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 shortterm 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 


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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, ElBayoumy 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 chemicalinduced 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. 


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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, onitroanisole 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 onitroanisole 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 onitroanisole 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: 


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‘‘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 twoyear 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: 


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‘‘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 TFEglutathione conjugates by renal b-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 TFEinduced 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 


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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. 


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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 oNitroanisole. 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, 


sroberts on DSKD5P82C1PROD with PROPOSALS
17346 Federal Register / Vol. 75, No. 65 / Tuesday, April 6, 2010 / Proposed Rules 

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. 


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Federal Register / Vol. 75, No. 65 / Tuesday, April 6, 2010 / Proposed Rules 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. 

§ 372.28 [Amended] 

2. In § 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: 

§ 372.28 Lower thresholds for chemicals 

of special concern. 

(a) * * * 

(2) * * * 


sroberts on DSKD5P82C1PROD with PROPOSALS
17348 Federal Register / Vol. 75, No. 65 / Tuesday, April 6, 2010 / Proposed Rules 

Category name Reporting 

threshold 

* * * * * 

Polycyclic aromatic compounds (PACs): (This category includes only those 

chemicals listed below) ..... 100 

* * * * * 

42397–64–8 1,6- 

Dinitropyrene.

42397–65–9 1,8- 

Dinitropyrene.

Category name Reporting 

threshold 

* * * * * 

07496–02–8 6- 

Nitrochrysene.

* * * * * 

57835–92–4 4-Nitropyrene.

§ 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. 

§ 372.65 Chemicals and chemical 

categories to which the part applies. 

* * * * * 

(a) * * * 

Chemical name CAS No. Effective 

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) * * * 

CAS No. Chemical name Effective 

date 

* * * * * * 

00075–02–5 ................................................ Vinyl Fluoride .................................................................................................................. 1/11 

* * * * * * 

00075–52–5 ................................................ Nitromethane .................................................................................................................. 1/11 

* * * * * * 

00077–09–8 ................................................ Phenolphthalein .............................................................................................................. 1/11 


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CAS No. Chemical name Effective 

date 

* * * * * * 

00078–79–5 ................................................ Isoprene .......................................................................................................................... 1/11 

* * * * * * 

00081–49–2 ................................................ 1-Amino-2,4-dibromoanthraquinone ............................................................................... 1/11 

* * * * * * 

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-propanediol ........................................................................... 1/11 

* * * * * * 

(c) * * * 

Category name Effective 

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 

FEDERAL COMMUNICATIONS 

COMMISSION 

47 CFR Part 27 

[WTB Docket No. 07–293; FCC 10–46] 

Operations of Wireless 

Communications Services in the 2.3 

GHz Band 

AGENCY: Federal Communications 

Commission. 

ACTION: Proposed rule. 

SUMMARY: The Federal Communications 

Commission (Commission) seeks 

comment on revising the performance 

requirements for the 2.3 GHz Wireless 

Communications Service (WCS) band. 

The Commission is seeking comment on 

possible revision of the performance 

requirements (also known as buildout or 

construction requirements) for the 2.3 

GHz WCS band to ensure that that the 

spectrum is used intensively in the 

public interest. 

DATES: Interested parties may file 

comments on or before April 21, 2010, 

and reply comments on or before May 

3, 2010. Written comments on the 

Paperwork Reduction Act proposed 

information collection requirements 

must be submitted by the public, Office 

of Management and Budget (OMB), and 

other interested parties on or before 

June 7, 2010. 

ADDRESSES: You may submit comments, 

identified by WTB Docket No. 07–293, 

by any of the following methods: 

• Federal eRulemaking Portal: http:// 

www.regulations.gov. Follow the 

instructions for submitting comments. 

• Federal Communications 

Commission Web site: http:// 

www.fcc.gov/cgb/ecfs. Follow the 

instructions for submitting comments. 

• E-mail: ecfs@fcc.gov, and include 

the following words in the body of the 

message, ‘‘get form.’’ A sample form and 

directions will be sent in response. 


sroberts on DSKD5P82C1PROD with PROPOSALS