Document ID: EPA-HQ-TRI-2017-0434-0001
Agency: epa
Document Type: Proposed Rule
Title: Community Right-to-Know Toxic Chemical Release Reporting: Addition of Certain Chemicals
Posted Date: 2021-10-18T04:00Z

[Federal Register Volume 86, Number 198 (Monday, October 18, 2021)]
[Proposed Rules]
[Pages 57614-57629]
From the Federal Register Online via the Government Publishing Office [www.gpo.gov]
[FR Doc No: 2021-22112]

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ENVIRONMENTAL PROTECTION AGENCY

40 CFR Part 372

[EPA-HQ-TRI-2017-0434; FRL-5927-03-OCSPP]
RIN 2070-AK26

Addition of Certain Chemicals; Community Right-to-Know Toxic 
Chemical Release Reporting

AGENCY: Environmental Protection Agency (EPA).

ACTION: Proposed rule.

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SUMMARY: In response to a petition filed under the Emergency Planning 
and Community Right-to-Know Act (EPCRA), EPA is proposing to add 12 
chemicals to the list of toxic chemicals subject to the reporting 
requirements under EPCRA and the Pollution Prevention Act (PPA). EPA 
believes that each of the 12 chemicals meets the EPCRA criteria. In 
addition, based on the available bioaccumulation and persistence data, 
EPA believes that one chemical should be classified as a persistent, 
bioaccumulative, and toxic (PBT) chemical and designated as a chemical 
of special concern with a 100-pound reporting threshold.

DATES: Comments must be received on or before December 17, 2021.

ADDRESSES: Submit your comments, identified by docket identification 
(ID) number EPA-HQ-TRI-2017-0434, using the Federal eRulemaking Portal 
at http://www.regulations.gov. Follow the online instructions for 
submitting comments. Do not submit electronically any information you 
consider to be Confidential Business Information (CBI) or other 
information whose disclosure is restricted by statute.
    Due to the public health concerns related to COVID-19, the EPA 
Docket Center (EPA/DC) and Reading Room is closed to visitors with 
limited exceptions. The staff continues to provide remote customer 
service via email, phone, and webform. For the latest status 
information on EPA/DC services and docket access, visit https://www.epa.gov/dockets.

FOR FURTHER INFORMATION CONTACT: For technical information contact: 
Daniel R. Bushman, Toxics Release Inventory Program Division (7410M), 
Office of Pollution Prevention and Toxics, Environmental Protection 
Agency, 1200 Pennsylvania Ave. NW, Washington, DC 20460-0001; telephone 
number: (202) 566-0743; email: [email protected].
    For general information contact: The Emergency Planning and 
Community Right-to-Know Hotline; telephone numbers: toll free at (800) 
424-9346 (select menu option 3) or (703) 348-5070 in the Washington, DC 
Area and International; or go to https://www.epa.gov/home/epa-hotlines.

SUPPLEMENTARY INFORMATION:

I. General Information

A. Does this action apply to me?

    You may be potentially affected by this action if you own or 
operate a facility that manufactures, processes, or otherwise uses any 
of the 12 chemicals included in this proposed rule. The following list 
of North American Industrial Classification System (NAICS) codes is not 
intended to be exhaustive, but rather provides a guide to help readers 
determine whether this document applies to them. Potentially affected 
facilities may include:
     Facilities included in the following NAICS manufacturing 
codes (corresponding to Standard Industrial Classification (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*, 
113310, 211130*, 212324*, 212325*, 212393*, 212399*, 488390*, 511110, 
511120, 511130, 511140*, 511191, 511199, 512230*, 512250*, 519130*, 
541713*, 541715* 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 (corresponds to SIC code 12, Coal Mining (except 
1241)); or 212221, 212222, 212230, 212299 (corresponds to SIC code 10, 
Metal Mining (except 1011, 1081, and 1094)); or 221111, 221112, 221113, 
221118, 221121, 221122, 221330 (limited to facilities that combust coal 
and/or oil for the purpose of generating power for distribution in 
commerce) (corresponds to SIC codes 4911, 4931, and 4939, Electric 
Utilities); or 424690, 425110, 425120 (limited to facilities previously 
classified in SIC code 5169, Chemicals and Allied Products, Not 
Elsewhere Classified); or 424710 (corresponds to SIC code 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 code 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.) (corresponds to SIC code 4953, Refuse Systems).
     Federal facilities: 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 under FOR FURTHER INFORMATION CONTACT.

B. What action is the Agency taking?

    In response to a petition, EPA is proposing to add 12 chemicals to 
the EPCRA section 313 toxic chemical list. As discussed in more detail 
later in this document, EPA believes that each of the 12 chemicals 
meets the EPCRA section 313(d)(2)(B) and/or (C) criteria for listing. 
EPA is also proposing to classify one chemical as a PBT chemical of 
special concern with a 100-pound reporting threshold.

C. What is the Agency's authority for taking this action?

    This action is issued under EPCRA sections 313(d), 313(e)(1) and 
328, 42 U.S.C. 11023(d), 11023(e)(1) and 11048. EPCRA is also referred 
to as Title III of the Superfund Amendments and Reauthorization Act of 
1986.
    EPCRA section 313, 42 U.S.C. 11023, requires owners/operators of 
certain facilities that manufacture, process, or otherwise use listed 
toxic chemicals in amounts above reporting threshold levels to report 
their facilities' environmental releases and other waste management 
information on such chemicals annually. These facility owners/operators 
must also report pollution prevention and recycling data for such 
chemicals, pursuant to section 6607 of the PPA, 42 U.S.C. 13106.
    Under EPCRA section 313(c), Congress established an initial list of 
toxic chemicals subject to EPCRA toxic chemical reporting requirements 
that

[[Page 57615]]

was comprised of 308 individually listed 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 EPCRA section 313(d)(2) are met. Therefore, to add a 
chemical, EPA must determine 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 determine that none of the criteria in EPCRA section 313(d)(2) 
are met. The listing criteria in EPCRA section 313(d)(2)(A)-(C) are as 
follows:
     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.
     The chemical is known to cause or can reasonably be 
anticipated to cause in humans: Cancer or teratogenic effects, or 
serious or irreversible reproductive dysfunctions, neurological 
disorders, heritable genetic mutations, or other chronic health 
effects.
     The chemical is known to cause or can be reasonably 
anticipated to cause, because of its toxicity, its toxicity and 
persistence in the environment, or 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 EPCRA section 313(d)(2)(A) criterion as the 
``acute human health effects criterion;'' the EPCRA section 
313(d)(2)(B) criterion as the ``chronic human health effects 
criterion;'' and the EPCRA section 313(d)(2)(C) criterion as the 
``environmental effects criterion.''
    Under EPCRA section 313(e)(1), any person may petition EPA to add 
chemicals to or delete chemicals from the list. EPA issued a statement 
of policy in the Federal Register of February 4, 1987 (52 FR 3479) 
(FRL-3101-6) providing guidance regarding the recommended content of 
and format for petitions. On May 23, 1991 (56 FR 23703) (FRL-3802-2), 
EPA issued guidance regarding the recommended content of petitions to 
delete individual members of the metal compounds categories reportable 
under EPCRA section 313. EPA published in the Federal Register of 
November 30, 1994 (59 FR 61432) (FRL-4922-2) a statement clarifying its 
interpretation of the EPCRA section 313(d)(2) and (d)(3) criteria for 
modifying the EPCRA section 313 list of toxic chemicals.

II. What is the description of the petition and EPA's response?

A. Who submitted the petition and what was requested?

    On May 6, 2014, EPA received a petition from the Toxics Use 
Reduction Institute (TURI) requesting the addition of 25 chemicals to 
the EPCRA section 313 toxic chemicals list (Ref. 1). The petitioner 
believes that each of these 25 chemicals meets the EPCRA section 
313(d)(2) listing criteria and that the 25 chemicals should be added to 
the EPCRA section 313 toxic chemical list so that releases can be 
monitored and reported. The 25 chemicals, listed by name and Chemical 
Abstracts Service Registry Number (CASRN), are shown here (note that 
some chemical names are different than those used in the petition 
because they are listed here using the EPA Registry Name):

 Azodicarbonamide; 123-77-3
 1-Bromopropane; 106-94-5
 4-Chlorobenzotrichloride; 5216-25-1
 Cyclododecane; 294-62-2
 Dibutyltin dichloride; 683-18-1
 1,3-Dichloro-2-propanol; 96-23-1
 Dimethylacetamide; 127-19-5
 2,3-Dinitrotoluene; 602-01-7
 2,5-Dinitrotoluene; 619-15-8
 Formamide; 75-12-7
 1,2,5,6,9,10-Hexabromocyclododecane; 3194-55-6
 1,3,4,6,7,8-Hexahydro-4,6,6,7,8,8-hexamethylcyclopenta[g]-2-
benzopyran; 1222-05-5
 Hexahydrophthalic anhydride; 85-42-7
 N-Hydroxyethylethylenediamine; 111-41-1
 N-Methylformamide; 123-39-7
 Methylhexahydrophthalic anhydride; 25550-51-0
 Nitrilotriacetic acid trisodium salt; 5064-31-3
 Nonylphenol; 25154-52-3
 Octabromodiphenyl ether; 32536-52-0
 p-(1,1,3,3-Tetramethylbutyl)phenol; 140-66-9
 1,2,3-Trichlorobenzene; 87-61-6
 Triglycidyl isocyanurate; 2451-62-9
 Tris(2-chloroethyl) phosphate; 115-96-8
 Tris(1,3-dichloro-2-propyl) phosphate; 13674-87-8
 Tris(dimethylphenol) phosphate; 25155-23-1

B. How is EPA responding to the petition?

    As discussed in Unit I.B., EPA is proposing to add 12 of the 25 
chemicals included in the TURI petition to the EPCRA section 313 toxic 
chemicals list. In separate, unrelated actions, three of the 25 
chemicals (1-bromopropane (November 23, 2015 (80 FR 72906) (FRL-9937-
12-OEI)), nonylphenol (September 30, 2014 (79 FR 58686) (FRL-9915-59-
OEI)) and 1,2,5,6,9,10-hexabromocyclododecane (November 28, 2016 (81 FR 
85440) (FRL-9953-28)) have already been added to the EPCRA section 313 
chemical list. Of the remaining 10 chemicals, EPA has determined that 
the available data for nine chemicals are not sufficient for EPA to 
find that the chemicals meet the EPCRA section 313 listing criteria for 
human health or ecological effects (Refs. 2 and 3). Therefore, EPA is 
not proposing to add the nine chemicals listed here:

 Azodicarbonamide; 123-77-3
 4-Chlorobenzotrichloride; 5216-25-1
 Cyclododecane; 294-62-2
 Dimethylacetamide; 127-19-5
 2,3-Dinitrotoluene; 602-01-7
 2,5-Dinitrotoluene; 619-15-8
 Hexahydrophthalic anhydride; 85-42-7
 Methylhexahydrophthalic anhydride; 25550-51-0
 N-Methylformamide; 123-39-7

    In addition, EPA is not proposing to add octabromodiphenyl ether 
(OctaBDE) (32536-52-0) to the EPCRA section 313 toxic chemical list. 
EPA issued a significant new use rule (SNUR) that requires notification 
to EPA 90 days prior to the intended manufacture or import for any use 
of OctaBDE ether after January 1, 2005 (June 13, 2006 (71 FR 34015) 
(FRL-7743-2); 40 CFR 721.10000). The lack of significant new use 
notices (SNUNs) under this SNUR indicates that there has been no non-
exempt manufacture or import for any use of OctaBDE in the United 
States since January 1, 2005. There have also been no submissions for 
OctaBDE under the Chemical Data Reporting (CDR) Rule (https://www.epa.gov/chemical-data-reporting) since 2006. In a 2008 evaluation, 
the United Nations noted that as of 2005, the manufacture and import of 
OctaBDE had been phased out by industry and estimated that most of the 
remaining processing of OctaBDE in the United States was likely 
negligible and only occurring where remaining stockpiles were being 
used up or in waste processing facilities (http://chm.pops.int/portals/0/repository/poprc4/unep-pops-poprc.4-6.english.pdf). Given that the 
phase out occurred more than ten years ago, it is even more likely 
today that there is a negligible amount of OctaBDE remaining that is 
processed or otherwise

[[Page 57616]]

used by facilities in the United States. Therefore, EPA is not 
proposing to add octabromodiphenyl ether to the EPCRA section 313 list 
since EPA expects that no TRI reports would be filed for this chemical. 
EPCRA section 313(d)(2) 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. However, consistent with the 
Agency's previously articulated position on the use of manufacturing 
volume thresholds (e.g., 58 FR 63500, December 1, 1993) (FRL-4904-6) 
and as in past chemical reviews (e.g., 59 FR 61432, November 30, 1994) 
(FRL-4922-2), 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. Since the production volume screen 
indicates that no reports would be filed for such chemicals, there 
would be no information provided to the public. EPA feels it is 
appropriate at this time to focus on chemicals for which reports are 
likely to be filed.
    In addition to proposing to add 1,3,4,6,7,8-hexahydro-4,6,6,7,8,8-
hexamethylcyclopenta[g]-2-benzopyran to the EPCRA section 313 toxic 
chemical list, EPA is proposing to add this chemical to the list of 
chemicals of special concern. There are several chemicals and chemical 
categories on the EPCRA section 313 chemical list that have been 
classified as chemicals of special concern because they are PBT 
chemicals (see 40 CFR 372.28(a)(2)). In a final rule published in the 
Federal Register of October 29, 1999 (64 FR 58666) (FRL-6389-11), EPA 
established the PBT classification criteria for chemicals on the EPCRA 
section 313 chemical list. 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. Most 
chemicals meeting the PBT criteria are assigned 100-pound reporting 
thresholds. EPA set lower reporting thresholds (10 pounds) for those 
PBT chemicals with persistence half-lives of 6 months or more in water, 
sediment, or soil and with BCF or BAF values of 5,000 or higher, since 
these chemicals are considered highly PBT chemicals. The data presented 
in this proposed rule support classifying 1,3,4,6,7,8-hexahydro-
4,6,6,7,8,8-hexamethylcyclopenta[g]-2-benzopyran as a PBT chemical and 
designating it as a chemical of special concern with a 100-pound 
reporting threshold.

III. What are the 12 chemicals that EPA is proposing to add?

    The 12 chemicals that EPA is proposing to add are shown here listed 
by name and CASRN (note that some chemical names are different than 
those used in the petition because they are listed here using the EPA 
Registry Name):

 Dibutyltin dichloride; 683-18-1
 1,3-Dichloro-2-propanol; 96-23-1
 Formamide; 75-12-7
 1,3,4,6,7,8-Hexahydro-4,6,6,7,8,8-hexamethylcyclopenta[g]-2-
benzopyran; 1222-05-5
 N-Hydroxyethylethylenediamine; 111-41-1
 Nitrilotriacetic acid trisodium salt; 5064-31-3
 p-(1,1,3,3-Tetramethylbutyl)phenol; 140-66-9
 1,2,3-Trichlorobenzene; 87-61-6
 Triglycidyl isocyanurate; 2451-62-9
 Tris(2-chloroethyl) phosphate; 115-96-8
 Tris(1,3-dichloro-2-propyl) phosphate; 13674-87-8
 Tris(dimethylphenol) phosphate; 25155-23-1

    EPA has determined that each of these chemicals have production and 
use levels that would result in TRI reports being filed (Ref. 4).

IV. What is the Agency's evaluation of the toxicity of the 12 
chemicals?

    EPA prepared hazard assessment documents that reviewed the 
available data on human health (Ref. 5) and/or ecological effects (Ref. 
6) associated with each of the 12 chemicals being proposed for addition 
to the EPCRA section 313 toxic chemical list. Brief summaries of the 
available human health and ecological effects information that support 
listing these chemicals under EPCRA section 313 are provided in this 
Unit. Readers should consult the support documents (Refs. 5 and 6) for 
more detailed information.
    1. Dibutyltin dichloride (CASRN 683-18-1). Monkey, rat, and mouse 
studies indicate that dibutyltin dichloride (DBTC) exposure during 
early pregnancy may result in embryo/fetal lethality following exposure 
to doses as low as 2.5 milligrams per kilogram per day (mg/kg/day) 
(Refs. 7, 8, 9, 10, 11, and 12). In these studies, decreased pre/post 
implantation loss, increased resorption, and/or decreased number of 
live fetuses/pups were accompanied by maternal body weight effects and/
or clinical signs of toxicity. However, Ema and Harazono (Ref. 7) 
indicated that body weight effects alone did not account for 
reproductive effects, as effects observed at 15.2 mg/kg/day from 
gestation day 0-3 or 4-7 were significantly different than those 
observed in pair-fed controls that had similar body weights.
    Several studies in rats indicate that maternal exposure to DBTC 
during the period of organogenesis causes external, skeletal, and/or 
visceral malformations and decreased body weight in fetuses at oral 
doses >=5 mg/kg/day (Refs. 8, 9, 10, and 13). An increased incidence of 
external and skeletal malformations was observed in fetuses from dams 
exposed to doses as low as 5 mg/kg/day DBTC (lowest dose tested) from 
gestation day 7-15 (Ref. 8). Maternal toxicity was not observed in this 
study until 7.5 mg/kg/day (Ref. 8).
    In summary, the available literature provides evidence that DBTC 
can be reasonably anticipated to cause serious or irreversible 
reproductive and developmental toxicity in humans. Based on the 
observed effects and dose levels, EPA considers DBTC to have moderately 
high to high toxicity. EPA believes that there is sufficient evidence 
for listing DBTC on the EPCRA section 313 toxic chemicals list pursuant 
to EPCRA section 313(d)(2)(B) based on the available reproductive and 
developmental toxicity data.
    DBTC is toxic to aquatic organisms with experimentally determined 
acute and chronic toxicity values lower than 1 milligram per liter (mg/
L). The acute aquatic toxicity values for DBTC are as low as 16.7 
[micro]g DBTC/L (96-hour median effect concentration (EC50) 
for growth) in the green algae (Scenedesmus obliquus) (Ref. 14) and 
chronic aquatic toxicity values are as low as 20 [micro]g/L for 
dibutyltin (DBT) (33-day lowest-observed-effect-concentration (LOEC) 
for reduction in shell length) in larvae of the blue mussel (Mytilus 
edulis), and 38 [micro]g DBTC/L (210-day LOEC for reduced body weight 
and reduced stores of energy substrates) in the duck mussel (Anodonta 
anatina) (Ref. 15).
    Several studies reported effects of short-term exposure to DBTC on 
estuarine and marine invertebrates. Salazar and Salazar (Ref. 16) 
observed a significant effect on mortality in mysids (Metamysidopsis 
elongata) exposed to DBTC at 56 [micro]g/L for 96 hours, while no 
effect on mortality was observed at concentrations of <=11 [micro]g 
DBTC/L; the

[[Page 57617]]

96-hour LC50 was between 11 and 56 [micro]g DBTC/L. Thom et 
al. (Ref. 17) exposed the embryos of Pacific oysters (Crassostrea 
gigas) to DBTC and found a 48-hour EC50 of 142 [micro]g 
DBTC/L (55.5 [micro]g tin (Sn)/L), based on abnormal larval 
development, and a 48-hour LC50 of 171 [micro]g DBTC/L (66.9 
[micro]g Sn/L). In addition to affecting the survival and growth of 
aquatic organisms, DBTC has been shown to have adverse effects on the 
development of aquatic invertebrates at concentrations of 1 mg/L or 
less by causing abnormalities in the embryos of the Pacific oyster (C. 
gigas) (Ref. 18), preventing development of embryos of the tunicate 
(Styela plicata) to the larval stage (Ref. 19), and increasing the 
duration of zoeal development and reducing the dry weight of megalops 
larvae of the mud crab (Rhithropanopeus harrisii) (Ref. 20). 
Additionally, fish have been found to be more sensitive to DBTC in 
early life stages than as adults (Ref. 21). DBTC has been observed to 
cause histological changes in the liver, kidney, thymus, eye, and/or 
skin of Japanese medaka (Oryzias latipes) and guppy (Poecilia 
reticulata) (Refs. 22 and 23), reduced resistance to bacterial 
challenge in the rainbow trout (Oncorhynchus mykiss) (Ref. 21), and 
increased chromosomal aberrations in the land snail (Truncatella 
subcylindrica) (Ref. 24).
    In summary, there is evidence for both acute and chronic toxicity 
to aquatic organisms exposed to DBTC. DBTC has been shown to cause 
lethality and impair growth and development in a wide range of aquatic 
species. The acute and chronic aquatic toxicity values indicate that 
DBTC is toxic at low concentrations and thus is highly toxic to aquatic 
organisms. EPA believes that the evidence is sufficient to list DBTC on 
the EPCRA section 313 toxic chemicals list pursuant to EPCRA section 
313(d)(2)(C) based on the available ecotoxicity information for this 
chemical.
    2. 1,3-Dichloro-2-propanol (CASRN 96-23-1). Evidence from an 
unpublished 2-year bioassay indicates that 1,3-dichloro-2-propanol 
(DC2P) is carcinogenic in male and female rats (Refs. 25 and 26) 
following exposure to 240 mg/L in drinking water in rats of both sexes 
(19.31 mg/kg/day in males; 29.83 mg/kg/day in females). At the 78-week 
interim sacrifice, hepatocellular carcinomas were significantly 
increased in the high-dose male and female groups. At the termination 
of the study, exposure-related increases in neoplastic lesions were 
observed in the liver, kidney, and tongue; neoplasms observed in the 
thyroid may also be exposure-related. Additionally, 25 percent of liver 
carcinomas in high-dose females metastasized to the lung. Survival was 
reduced in both sexes at 240 mg/L over the second year of the study. 
Significant exposure-related changes in clinical chemistry observed 
predominantly in high-dose animals were indicative of liver damage and 
multiple non-neoplastic lesions were observed in both sexes at all 
doses in a dose- and duration-dependent manner.
    It is reasonable to conclude that DC2P is genotoxic because of the 
preponderance of positive in vitro assays, though a limited number of 
in vivo studies reported negative results (Refs. 27, 28, 29, 30, 31, 
32, 33, 34, 35, 36, 37, 38, 39, 40 (as cited in Ref. 41), and 42 (as 
cited in Ref. 39)). The California EPA concluded that DC2P was 
``clearly shown through scientifically valid testing according to 
generally accepted principles to cause cancer.'' (Ref. 43). Under the 
2005 U.S. EPA guidelines (Ref. 44), DC2P is considered likely to be 
carcinogenic to humans based on strong evidence of carcinogenicity in 
male and female rats in a single adequate study and supporting 
mutagenicity data.
    In summary, the available literature provides evidence that DC2P 
can be reasonably anticipated to cause cancer in humans. EPA considers 
chemicals that can reasonably be anticipated to cause cancer to have 
moderately high to high chronic toxicity. EPA believes that there is 
sufficient evidence for listing DC2P on the EPCRA section 313 toxic 
chemicals list pursuant to EPCRA section 313(d)(2)(B) based on the 
available carcinogenicity data.
    3. Formamide (CASRN 75-12-7). Available data from oral studies, 
including a 2-generation study, indicate that formamide is both a 
reproductive and developmental toxicant at doses >=87 mg/kg/day (Refs. 
45, 46, 47, 48, 49, 50, 51, and 52). These effects, including decreased 
pregnancy rates, increased days to litter, decreased live pups/litter, 
increased post implantation loss, and fetal variations, were observed 
in rats, mice, and rabbits, which serves to strengthen the conclusion 
on the potential reproductive and developmental toxicity of formamide. 
In two of the gestational exposure studies, fetal effects occurred at 
doses lower than overt maternal toxicity (decreased fetal body weights 
were observed in Sprague Dawley rats at 100 mg/kg/day and increased 
postimplantation loss and fetal variations were observed in NZ white 
rabbits at 113 mg/kg/day), suggesting that the developing organism is a 
sensitive target for formamide. The available dermal toxicity data 
suggest that formamide can cause developmental effects, including 
decreased fetal body weight and increased fetal variations and 
malformations at >=310 mg/kg/day in rats (Refs. 45, 53, 54, and 55).
    In summary, the available literature provides evidence that 
formamide can be reasonably anticipated to cause serious or 
irreversible reproductive and developmental toxicity in humans. Based 
on the observed effects and dose levels, EPA considers formamide to 
have moderately high to high toxicity. EPA believes that there is 
sufficient evidence for listing formamide on the EPCRA section 313 
toxic chemicals list pursuant to EPCRA section 313(d)(2)(B) based on 
the available reproductive and developmental toxicity data.
    4. 1,3,4,6,7,8-Hexahydro-4,6,6,7,8,8-hexamethylcyclopenta[g]-2-
benzopyran (CASRN 1222-05-5). 1,3,4,6,7,8-Hexahydro-4,6,6,7,8,8-
hexamethylcyclopenta[g]-2-benzopyran (HHCB) is toxic to aquatic 
organisms, with experimentally determined acute and chronic toxicity 
values lower than 1 mg/L. The experimental data for HHCB from aquatic 
toxicity studies includes acute toxicity endpoint values as low as 723 
[micro]g/L in algae (72-hour EC50 for inhibition of biomass 
in the microalgal species (Pseudokirchneriella subcapitata) (Ref. 56 as 
cited in Ref. 57), 153 [micro]g/L in aquatic invertebrates (96-hour 
EC50 in the mussel (Lampsilis cardium) (Ref. 58)), and 950 
[micro]g/L (concentration that is lethal to 50% of the test organisms 
(LC50)) in fish (O. latipes) larvae (Ref. 59). Chronic 
studies also indicate a high concern for environmental hazard with 
maximum acceptable toxicant concentration (MATC) values as low as 98 
[micro]g/L (36-day MATC for effects on larval survival, growth, and 
development in the fathead minnow (Pimephales promelas) (Ref. 60 as 
cited in Ref. 57)) and 4.7 [micro]g/L in fish (14-day MATC for 
oxidative stress in goldfish (Carassius auratus) (Ref. 61)). Chronic 
studies in aquatic invertebrates have found a MATC as low as 53 
[micro]g/L (6-day MATC based on inhibition of larval development rate 
in the copepod (Acartia tonsa) (Ref. 62 as cited in Ref. 63)).
    HHCB bioaccumulates in aquatic organisms. Experimentally-derived 
BCFs as high as 1,584 in fish (Lepomis macrochirus) (Ref. 64) and 2,692 
in benthic worms (Lumbriculus variegatus) (Ref. 65 as cited in Ref. 63) 
have been reported. BCFs for HHCB calculated using the Estimation 
Programs Interface SuiteTM (EPI Suite\TM\) (Ref. 66) were 
3,629 using the regression-based method and 1,231 using the Arnot-Gobas 
model for upper trophic level species, while the bioaccumulation factor 
(BAF)

[[Page 57618]]

calculated by EPI Suite\TM\ was 1,826 (Ref. 67). There are no data 
available to evaluate the potential for HHCB to biomagnify through the 
food chain. Studies have consistently found half-lives longer than two 
months for HHCB in soils and sediments (Ref. 68). Envirogen (Ref. 69 as 
cited in Ref. 63) reported half-lives in river sediment at 79 days, 
forest soil at 95 days, sludge amended soil at 105 days, and 
agricultural soil at 239 days. DiFrancesco et al. (Ref. 70 as cited in 
Ref. 63) reported half-lives between 140-145 days in four types of 
sludge-amended soils.
    In summary, the available data demonstrate that HHCB can cause 
acute and chronic toxicity to aquatic organisms at concentrations at or 
below 1 mg/L. The acute and chronic aquatic toxicity values indicate 
that HHCB is highly toxic to aquatic organisms. In addition, HHCB 
bioaccumulates and is persistent in the environment. EPA believes that 
the evidence is sufficient to list HHCB on the EPCRA section 313 toxic 
chemicals list pursuant to EPCRA section 313(d)(2)(C) based on the 
available ecotoxicity information for this chemical alone and also 
based on its toxicity and persistence in the environment, and toxicity 
and tendency to bioaccumulate.
    EPA believes that the available bioaccumulation and persistence 
data for HHCB support a classification of HHCB as a persistent, 
bioaccumulative, and toxic (PBT) chemical. HHCB has been shown to be 
bioaccumulative in aquatic species with BCF values greater than 1,000 
and to be persistent in soil and sediment for at least 2 months. 
Therefore, consistent with EPA's established policy for PBT chemicals 
(See 64 FR 58666, October 29, 1999) (FRL-6389-11), EPA is proposing to 
designate HHCB as a chemical of special concern with a 100-pound 
reporting threshold.
    5. N-Hydroxyethylethylenediamine (CASRN 111-41-1). Several rat 
studies, including pre-mating though early lactation oral exposure and 
gestational oral exposure, indicate that maternal exposure to N-
hydroxyethylethylenediamine can cause malformations of the great 
vessels in offspring at gavage doses >=10 mg/kg/day, particularly 
aortic aneurysms (Refs. 71, 72, 73, 74, and 75). Other observed 
malformations included aneurysms of the pulmonary trunk, dilations of 
the carotids and descending aorta, and abnormal course of the carotids. 
While some of these studies (Refs. 71, 73, and 74) presented a limited 
consideration of material endpoints and lacked litter-based statistics, 
studies incorporating these elements reported similar developmental 
effects (Refs. 72 and 75). Aortic aneurysms were also observed at 
intraperitoneal injection doses >=10 mg/kg/day (Refs. 71 and 76). 
Available evidence indicates that, at high enough doses, prenatal 
exposure is adequate to induce great vessel malformations; however, the 
critical period appears to extend into the early postnatal period since 
incidence and severity of great vessel malformations was increased when 
exposure extended into the postnatal period (Refs. 77, 78, 79, 80, and 
81). This may, in part, explain why no vessel malformations were 
observed at doses up to 50 mg/kg-day on GD 6-19 and examination of 
fetuses on GD 20 in the EPSDG study (Ref. 75), while aneurysms were 
observed with dosing at >=10 mg/kg-day on GD 14-20 and examination of 
pups on PND 1 in the Xu et al. study (Ref. 71).
    Mechanistic studies indicate that great vessel malformation may be 
due to decreased expression of collagen type 1 and 3 in the walls of 
the great vessels (Ref. 71). A recent study by Chen et al. (Ref. 82) 
concluded that HEED causes significant morphological, biochemical, and 
biomechanical alterations in the extracellular matrix in neonatal 
aortic vascular smooth muscle cells. Additionally, Moore et al. (Ref. 
83) exposed dams to HEED and confirmed exposure of offspring both in 
utero and during lactation. HEED did not, however, appear to 
specifically concentrate in the great vessels of offspring.
    In summary, the available literature provides evidence that N-
hydroxyethyl-ethylenediamine can be reasonably anticipated to cause 
serious or irreversible developmental toxicity in humans. Based on the 
observed effects and dose levels, EPA considers N-hydroxyethyl-
ethylenediamine to have moderately high to high toxicity. EPA believes 
that there is sufficient evidence for listing N-
hydroxyethylethylenediamine on the EPCRA section 313 toxic chemicals 
list pursuant to EPCRA section 313(d)(2)(B) based on the available 
developmental toxicity data.
    6. Nitrilotriacetic acid trisodium salt (CASRN 5064-31-3). Evidence 
from bioassays of 18-24 months indicates that nitrilotriacetic acid 
trisodium salt (NTA) compounds are carcinogenic in rats and mice (Refs. 
84 and 85). Tumors were significantly increased at dietary doses 
>=1,200 mg/kg/day in rats of both sexes, >=590 mg/kg/day in male mice, 
and 2,600 mg/kg/day in female mice, and at drinking water doses of 81 
mg/kg/day in male rats (only dose tested, females not evaluated). 
Exposure-related increases in neoplastic lesions were observed in the 
urinary tract of male and female rats and mice (kidney, ureter, and/or 
bladder), adrenal glands (female rats), liver (female rats), pituitary 
gland (male rats), and hematopoietic system (male mice). Significant 
non-neoplastic and pre-neoplastic lesions were also observed in the 
kidney, lung, bladder, and ureter, especially at the highest doses (at 
dietary doses >=1,200 mg/kg/day in rats and at drinking water doses of 
81 mg/kg/day in male rats). In rats, nitrilotriacetic acid trisodium 
salt monohydrate (Na3NTA[middot]H2O) was a renal 
and bladder tumor promoter, but NTA did not promote bladder tumors 
(Refs. 86, 87, 88, 89, 90, and 91). In both the cancer bioassays and 
promotion studies featuring multiple dose levels, NTA compounds were 
effective at higher doses while showing no activity at lower doses. 
This suggests that high levels may be required for promotion or 
tumorigenicity. Specific doses that induce activity, however, appear to 
differ with route (i.e., carcinogenicity seen at lower doses via 
drinking water than via diet). Genotoxicity data, in general, indicate 
that NTA compounds do not induce direct genetic effects, although there 
is some evidence that they may interfere with normal segregation of 
chromosomes (Refs. 92, 93, and 94).
    Under the U.S. EPA 2005 guidelines (Ref. 44), NTA is considered 
likely to be carcinogenic to humans, based on evidence of 
carcinogenicity in male and female rats and mice in three adequate 
dietary bioassays reported by the National Cancer Institute (Ref. 85), 
along with supporting evidence of carcinogenicity from a drinking water 
study using only one dose level (Ref. 84) and tumor promoting activity 
of Na3NTA[middot]H2O (Refs. 86, 87, 88, 89, 90, and 91). In addition, 
the National Toxicology Program concluded that ``Nitrilotriacetic acid 
is reasonably anticipated to be a human carcinogen based on sufficient 
evidence of carcinogenicity from studies in experimental animals.'' and 
noted that ``exposure to the trisodium salt had the same effects in 
rats and also caused kidney tumors and cancer of the ureter in female 
rats (Refs. 84 and 85).''
    In summary, the available literature provides evidence that 
nitrilotriacetic acid trisodium salt can be reasonably anticipated to 
cause cancer in humans. EPA considers chemicals that can reasonably be 
anticipated to cause cancer to have moderately high to high chronic 
toxicity. EPA believes that there is sufficient evidence for listing 
nitrilotriacetic acid trisodium salt on the

[[Page 57619]]

EPCRA section 313 toxic chemicals list pursuant to EPCRA section 
313(d)(2)(B) based on the available carcinogenicity data.
    7. p-(1,1,3,3-Tetramethylbutyl)phenol (CASRN 140-66-9). p-(1,1,3,3-
Tetramethylbutyl)phenol (TMBP) is toxic to aquatic organisms with 
experimentally determined acute and chronic toxicity values lower than 
1 mg/L. The experimental data for TMBP include acute toxicity endpoint 
values as low as 47.9 [micro]g/L in aquatic invertebrates (96-hour 
LC50 in mysid shrimp (Mysidopsis bahia) (Ref. 95)), 120 
[micro]g/L in fish (14-day LC50 in rainbow trout (O. mykiss) 
(Ref. 96)), and 0.2 [micro]g/L in amphibians (24-hour LOEC for early 
sexual differentiation in bullfrog tadpoles (Rana catesbeiana) (Ref. 
97)). Chronic toxicity endpoint values are as low as 0.03 [micro]g/L in 
aquatic invertebrates (21-day MATC for delayed nauplii development in 
the copepod (Tigriopus japonicas) (Ref. 98)), 1 [micro]g/L in fish (35-
day LOECs for reduced growth in rainbow trout larvae (O. mykiss) (Ref. 
99)), and 0.002 [micro]g/L in amphibians (48-week LOEC for 
malformations and abnormalities and developmental delay in Northern 
leopard frog tadpoles (Rana pipiens) (Refs. 100 and 101)). The majority 
of chronic toxic effects on aquatic organisms were due to endocrine 
disruption. For example, TMBP mimics the effects of 17[beta]-estradiol 
by binding to the estrogen receptor and acting as an estrogen agonist 
(Refs. 99, 102, 103, 104, and 105). Examples of estrogenic effects 
caused by TMBP in male fish include induction of synthesis of 
vitellogenin (an egg yolk protein precursor that is not usually 
synthesized in male fish, but can be induced by estrogen), inhibition 
of testicular growth and spermatogenesis, and reduction of the 
gonadosomatic index (gonad mass as a percentage of total body mass) 
(Refs. 106, 107, and 108).
    TMBP bioaccumulates in aquatic organisms. Whole fish wet weight 
based BCFs determined under controlled experimental conditions at 
steady state were 471 in rainbow trout (O. mykiss) and 261 in Japanese 
medaka (O. latipes) (Refs. 109 and 110). Wet weight based field BAFs in 
fish were similar, ranging from 46 to 297 (Ref. 111). Maximum BAF 
values for the blue mussel (M. edulis) were 1,280 when converted to a 
wet weight basis (Refs. 112 and 113). A maximum value for phytoplankton 
was 2,510 when converted to a wet weight basis (Refs. 112 and 113). 
BCFs for TMBP calculated using the Estimation Programs Interface 
Suite\TM\ (EPI Suite\TM\) (Ref. 66) were also similar: 243 using the 
regression-based method and 302 using the Arnot-Gobas model for upper 
trophic level species. There was some evidence of biomagnification in 
fish species preying on mussels and in herring gulls feeding on fish 
(Ref. 112).
    In summary, the available data demonstrate that TMBP can cause 
acute and chronic toxicity to aquatic organisms at low concentrations 
indicating that TMBP is highly toxic to aquatic organisms. TMBP can 
cause lethality and impair growth and reproduction and is also an 
endocrine disruptor that may lead to estrogenic effects. TMBP has the 
potential to bioaccumulate in aquatic organisms and there is limited 
evidence for biomagnification of TMBP. EPA believes that the evidence 
is sufficient to list TMBP on the EPCRA section 313 toxic chemicals 
list pursuant to EPCRA section 313(d)(2)(C) based on the available 
ecotoxicity information for this chemical alone and also based on its 
toxicity and tendency to bioaccumulate.
    8. 1,2,3-Trichlorobenzene (CASRN 87-61-6). 1,2,3-Trichlorobenzene 
(1,2,3-TCB) is toxic to aquatic organisms with experimentally 
determined acute and chronic toxicity values lower than 1 mg/L. The 
experimental data for 1,2,3-TCB include acute toxicity endpoint values 
as low as 330 [micro]g/L in aquatic invertebrates (96-hour 
LC50 in the mysid shrimp (M. bahia) (Ref. 114)) and 350 
[micro]g/L in fish (96-hour LC50 in the guppy (P. 
reticulata) (Ref. 115)). Chronic toxicity endpoint values are as low as 
22 [micro]g/L in aquatic invertebrates (28-day MATC for inhibition of 
reproduction and growth in M. bahia (Ref. 116)) and 44 [micro]g/L in 
fish (42-day MATC for reduced growth in the mosquitofish (Gambusia 
affinis) (Ref. 117)).
    1,2,3-TCB bioaccumulates in aquatic organisms. There are 
experimentally-derived BCF values in fish over 1,000 and as high as 
5,600 for the fathead minnow (P. promelas) (Ref. 118). A 
biomagnification factor (BMF) of 2.3 was estimated by Hendriks et al. 
(Ref. 119) for an aquatic food chain.
    In summary, based on experimental data from both acute and chronic 
studies of aquatic organisms, 1,2,3-TCB is toxic to aquatic organism at 
low concentrations. The acute and chronic aquatic toxicity values 
indicate that 1,2,3-TCB is highly toxic to aquatic organisms. In 
addition, 1,2,3-TCB has been shown to be highly bioaccumulative in 
fish. EPA believes that the evidence is sufficient to list 1,2,3-TCB on 
the EPCRA section 313 toxic chemicals list pursuant to EPCRA section 
313(d)(2)(C) based on the available ecotoxicity information for this 
chemical alone and also based on its toxicity and tendency to 
bioaccumulate.
    9. Triglycidyl isocyanurate (CASRN 2451-62-9). Available animal 
toxicology studies on triglycidyl isocyanurate (TGIC) provide evidence 
of male reproductive toxicity. For example, a subchronic (13 week) oral 
exposure study in rats exposed to 0, 0.72, 2.08, and 7.32 mg/kg/day 
TGIC reported a dose-dependent decrease in the mean number of 
spermatozoa (0.0%, 5.1%, 13.5%, and 23.1%, respectively) with 
statistical significance at the high dose (Ref. 120). No mortalities, 
clinical signs of toxicity, or effects on any fertility parameters were 
observed during the study. However, although no significant effects on 
male rat fertility were observed, a decrease in sperm count could have 
biological significance in humans since it is well-known that the human 
male is of relatively low fertility and thus may be at greater risk 
from effects on sperm parameters than are males of the common 
laboratory animal model species (Ref. 121).
    Supplemental data from shorter-term exposure studies in mice also 
provide some additional supporting evidence for male reproductive 
effects following exposure to TGIC. For example, in spermatogonial 
cytogenics assays, decreased spermatogonial cell survival was reported 
in NS mice exposed orally to a single dose of 115 mg/kg/day (Ref. 122), 
but not in CD-1 mice exposed by inhalation (Ref. 122). In a dose-range 
finding study, ICR mice demonstrated decreased spermatogonial cell 
survival at 667 mg/kg/day administered via oral gavage (Ref. 123). The 
differences in responses among these studies may be due to differences 
in sensitivity between mice strain and route of exposure. In dominant 
lethal assays, although impairment of reproductive performance 
(decreased mating index) in CD-1 mice exposed via inhalation was 
reported, it occurred at the same level (49.6 mg/m\3\) exhibiting 10% 
mortality, decreased body weight, as well as clinical signs of 
toxicity, and may not be indicative of reproductive effects (Ref. 124). 
Likewise, ICR mice exposed orally failed to show an impairment of male 
mice impregnating unexposed females at 550 mg/kg/day (Ref. 125). Of the 
few genotoxicity studies of TGIC identified in the literature, TGIC did 
not induce chromosomal aberrations in spermatogonial cells in mice 
(Ref. 126) but did induce both sister chromatid exchange and 
chromosomal aberrations in Chinese hamster ovary cells in vitro (Ref. 
127 and Ref. 128).
    In summary, the available data indicate that the male reproductive

[[Page 57620]]

system, particularly spermatogonia and spermatozoa, may be a target of 
TGIC toxicity. Effects on sperm measurements were seen across two 
species (rats and mice) and routes of exposure (oral and inhalation) 
following subchronic and shorter-term exposures and collectively 
provide sufficient evidence of male reproductive toxicity. Based on the 
observed effects and dose levels, EPA considers TGIC to have moderately 
high to high toxicity. Therefore, EPA believes there is sufficient 
evidence for listing TGIC on the EPCRA section 313 toxic chemicals list 
pursuant to EPCRA section 313(d)(2)(B) based on the available 
reproductive toxicity data.
    10. Tris(2-chloroethyl) phosphate (CASRN 115-96-8). The National 
Toxicology Program (NTP) (Ref. 129) performed 2-year oral bioassays of 
tris(2-chloroethyl) phosphate (TCEP) in male and female rats and mice. 
The NTP concluded there is clear evidence of carcinogenicity in both 
male and female rats based on renal tubule adenomas observed at 88 mg/
kg/day and noted that mononuclear cell leukemia and thyroid follicular 
cell neoplasms in both sexes may also be exposure related. A 
significant increase in the incidence of renal tubule adenomas in male 
and female rats was observed at 88 mg/kg/day. From the mouse bioassay, 
the NTP concluded that there was equivocal evidence for carcinogenicity 
in male mice based on a marginal increase in renal tubule cell 
neoplasms and in female mice based on a marginal increase in harderian 
gland neoplasms in the main study group (14% incidence at 350 mg/kg/day 
versus 6% incidence in controls). The incidence of harderian gland 
tumors in females (main study and interim sacrifice groups combined) 
was statistically increased at the high dose of 350 mg/kg/day (p 
<=0.05) with a significant dose-related trend (p <=0.05). Significant 
non-neoplastic and pre-neoplastic lesions occurred in both male and 
female rats at 88 mg/kg/day (in the brain stem, cerebrum, and kidney) 
and in both male and female mice at >=175 mg/kg/day (in the kidney). 
Genotoxicity data indicate that TCEP is not mutagenic, and evidence for 
clastogenicity and cell transformation is limited and inconsistent 
(Refs. 130, 131, 132, 133, 134, 135, 136 as cite in Ref. 129, 137, and 
138).
    Under the U.S. EPA 2005 guidelines (Ref. 44), TCEP is considered 
likely to be carcinogenic to humans, based on clear evidence of 
carcinogenicity in male and female rats and equivocal evidence in male 
and female mice in adequate studies performed by NTP (Ref. 129). In 
2009, EPA's Office of Research and Development reached the same 
conclusion when it derived the provisional peer-reviewed toxicity 
values for TCEP (Ref. 139).
    Available data indicate that TCEP causes reproductive toxicity in 
mice, including sperm alterations and decreases in fertility in treated 
males and altered sex ratios in pups. A two-generation study with 
continuous breeding protocol showed that oral exposure to TCEP caused a 
decrease in the number of live male pups/litter and an altered sex 
ratio at 175 mg/kg/day and decreases in the numbers of litters/pair and 
live pups/litter at 350 mg/kg/day; a crossover breeding trial indicated 
that these effects were predominantly due to effects in male mice, 
including decreased fertility and sperm alterations (Ref. 140). Dose-
related sperm alterations in mice have also been reported following 
oral exposure to 700 mg/kg/day TCEP for 16 weeks (Ref. 141). Sperm 
effects were also noted in an inhalation study in male rats 
continuously exposed to >=0.5 mg/m\3\ for 4 months, with decreased 
litter size and increased pre- and post-implantation loss observed when 
males exposed to 1.5 mg/m\3\ were mated to na[iuml]ve females (Ref. 142 
as cited in Ref. 140). There was no evidence of adverse effects in the 
female reproductive system in either the two-generation study with 
crossover trial or the subchronic reproductive screen (Refs. 129 and 
141). A gestational exposure study found no evidence for developmental 
toxicity resulting from TCEP exposure (Refs. 143 and 144).
    In summary, the available literature provides evidence that TCEP 
can be reasonably anticipated to cause cancer and serious or 
irreversible reproductive toxicity in humans. EPA considers chemicals 
that can reasonably be anticipated to cause cancer to have moderately 
high to high chronic toxicity. In addition, based on the observed 
reproductive effects and dose levels causing those effects, EPA 
considers TCEP to have moderately high to high toxicity. EPA believes 
that there is sufficient evidence for listing TCEP on the EPCRA section 
313 toxic chemicals list pursuant to EPCRA section 313(d)(2)(B) based 
on the available cancer and reproductive toxicity data.
    11. Tris(1,3-dichloro-2-propyl) phosphate (CASRN 13674-87-8). 
Evidence from a 2-year bioassay indicates that tris(1,3-dichloro-2-
propyl) phosphate (TDCPP) is carcinogenic in male and female rats (Ref. 
145). Tumors were significantly increased at >=20 mg/kg/day in rats of 
both sexes. Exposure-related increases in neoplastic lesions were 
observed in the kidney (both sexes at high dose), liver (both sexes), 
testes (males), and adrenal glands (females). Significant non-
neoplastic lesions were also observed in the kidney and liver of male 
and female rats and in the epididymides and seminal vesicles of male 
rats. Genotoxicity data indicate that TDCPP is mutagenic in bacteria 
with metabolic activation, although assays for mutagenicity in 
mammalian cells and fruit flies were negative (Refs. 146, 147, 148, 
149, 150 and 151). Assays for clastogenicity in mammalian cells in 
vitro were positive with activation, but in vivo studies were negative 
(Refs. 146, 148, and 152). Results for cell transformation were mixed 
(Refs. 146 and 151).
    The California EPA concluded that TDCPP was ``clearly shown through 
scientifically valid testing according to generally accepted principles 
to cause cancer.'' (Ref. 153). Under the U.S. EPA 2005 guidelines (Ref. 
44), TDCPP is considered likely to be carcinogenic to humans, based on 
strong evidence of carcinogenicity in male and female rats with 
multiple tumors in a single yet largely adequate chronic cancer 
bioassay study and supporting mutagenicity data of both the primary 
compound and metabolites, in bacteria.''
    In summary, the available literature provides evidence that TDCPP 
can cause cancer at multiple sites in rats and can be reasonably 
anticipated to cause cancer in humans based on the animal data and the 
overall weight of mutagenicity and genotoxicity in bacteria and 
mammalian cells. EPA considers chemicals that can reasonably be 
anticipated to cause cancer to have moderately high to high chronic 
toxicity. EPA believes that there is sufficient evidence for listing 
TDCPP on the EPCRA section 313 toxic chemicals list pursuant to EPCRA 
section 313(d)(2)(B) based on the available carcinogenicity data.
    TDCPP is toxic to aquatic organisms both from acute and chronic 
exposures with acute toxicity below 10 mg/L and chronic toxicity below 
0.1 mg/L. Observed acute aquatic toxicity values are as low as 1,400 
[micro]g/L (96-hour LC50) in rainbow trout (O. mykiss) (Ref. 
154). Chronic aquatic toxicity values are below 0.1 mg/L and are as low 
as 22 [micro]g/L (142-hour MATC for decreases in body weight and whole-
body thyroxin (T4) content) in zebrafish (Danio rerio) (Ref. 155) and 
20 [micro]g/L (116-hour LOEC for effects on mRNA expression of genes 
for estrogen and progesterone receptors and vitellogenin) in D. rerio 
(Ref. 156). EPA has previously determined that TDCPP is persistent in 
the environment with a half-life >60 days (Ref. 157).

[[Page 57621]]

    In summary, the acute toxicity data for TDCPP for fish range from 1 
to 10 mg/L and chronic aquatic toxicity values range from 20 to 1,000 
[micro]g/L. TDCPP has also been shown to be persistent in the 
environment. Based on experimental data from both acute and chronic 
studies of aquatic organisms, TDCPP is toxic to aquatic organism at low 
concentrations. The acute and chronic aquatic toxicity values along 
with the persistence data indicate that TDCPP is highly toxic to 
aquatic organisms. EPA believes that the evidence is sufficient to list 
TDCPP on the EPCRA section 313 toxic chemicals list pursuant to EPCRA 
section 313(d)(2)(C) based on the available ecotoxicity data and its 
persistence in the environment.
    12. Tris(dimethylphenol) phosphate (CASRN 25155-23-1). In a one-
generation reproductive/developmental toxicity screening study in rats, 
the pregnancy index was significantly decreased by tris(dimethylphenol) 
phosphate (TDMPP) at gavage doses as low as 200 mg/kg/day as 
demonstrated by the reduced number of implantations and the decreased 
number of gravid dams and successful parturitions (Ref. 158 as cited in 
Ref. 159). While these effects were shown to be reversible in the 
recovery group (i.e., animals maintained for 4 weeks without exposure, 
after which rats were mated), they were accompanied by significant 
effects on organ weight and histological changes at doses as low as 25 
mg/kg/day. These treatment-related organ weight and histological 
changes were also partly reversible in the recovery group.
    In summary, the available data provides evidence that TDMPP can be 
reasonably anticipated to cause serious or irreversible reproductive 
toxicity in humans. Based on the observed effects and dose levels, EPA 
considers TDMPP to have moderately high to high toxicity. EPA believes 
that there is sufficient evidence for listing TDMPP on the EPCRA 
section 313 toxic chemicals list pursuant to EPCRA section 313(d)(2)(B) 
based on the available reproductive toxicity data.

V. Why is EPA proposing to list the 12 chemicals and lower the 
reporting threshold for HHCB?

A. What is EPA's rationale for listing the 12 chemicals?

    Based on EPA's review of the available toxicity data, EPA believes 
that the 12 chemicals EPA is proposing to add to the EPCRA section 313 
toxic chemical list can reasonably be anticipated to cause either 
adverse chronic human health effects at moderately low to low doses 
and/or environmental effects at low concentrations. EPA believes that 
the data show that these 12 chemicals have moderately high to high 
human health toxicity and/or are highly toxic to aquatic organisms. 
Therefore, EPA believes that the evidence is sufficient for listing all 
12 of the chemicals in this proposed rule on the EPCRA section 313 
toxic chemicals list pursuant to EPCRA section 313(d)(2)(B) and/or (C).
    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 human health effects pursuant to EPCRA section 313(d)(2)(B) 
(see 59 FR 61440-61442). EPA also does not believe that it is 
appropriate to consider exposure for chemicals that are highly toxic 
based on a hazard assessment when determining if a chemical can be 
added for environmental effects pursuant to EPCRA section 313(d)(2)(C) 
(see 59 FR 61440-61442). Therefore, in accordance with EPA's standard 
policy on the use of exposure assessments (see November 30, 1994 (59 FR 
61432, FRL-4922-2), 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) 
or (C).

B. What is EPA's rationale for lowering the reporting threshold for 
HHCB?

    EPA believes that the available bioaccumulation and persistence 
data for HHCB support a classification of HHCB as a PBT chemical. HHCB 
has been shown to be bioaccumulative in aquatic species with BCF values 
greater than 1,000 and to persist in soils and sediments with half-
lives greater than 2 months. Therefore, consistent with EPA's 
established policy for PBT chemicals (see 64 FR 58666, October 29, 
1999) (FRL-6389-11), EPA is proposing to establish a 100-pound 
reporting threshold for HHCB.

VI. References

    The following is a listing of the documents that are specifically 
referenced in this document. The docket includes these documents and 
other information considered by EPA, including documents that are 
referenced within the documents that are included in the docket, even 
if the referenced document is not itself physically located in the 
docket. For assistance in locating these other documents, please 
consult the person listed under FOR FURTHER INFORMATION CONTACT.

1. Petition from the Massachusetts Toxics Use Reduction Institute 
(TURI), University of Massachusetts Lowell, 600 Suffolk St., Suite 
501, Lowell, MA 01854, May 6, 2014.
2. USEPA, OPPT. Memorandum from Jocelyn Hospital, Toxicologist, 
Regulatory Development Branch to David Turk, Chief, Regulatory 
Development Branch. December 8, 2016. Subject: Review of Toxics Use 
Reduction Institute (TURI) Petition Chemicals.
3. USEPA, OPPT. Memorandum from Kara Koehrn and Thomas Forbes, 
Regulatory Development Branch, to David Turk, Chief, Regulatory 
Development Branch. February 16, 2017. Subject: Review of Toxics Use 
Reduction Institute (TURI) Petition Chemicals.
4. USEPA, OPPT. 2018. Economic Analysis of the Proposed Rule to Add 
Twelve Chemicals Identified in a Petition from the Toxics Use 
Reduction Institute to the EPCRA Section 313 List of Toxic 
Chemicals. November 7, 2018.
5. USEPA, OPPT. 2016. Human Health Review of Chemicals from the 
Toxics Use Reduction Institute (TURI) Petition. Office of Pollution 
Prevention and Toxics, Toxics Release Inventory Program Division, 
Regulatory Developmental Branch. March 29, 2016.
6. USEPA, OPPT. 2017. Ecological Toxicity Review of Chemicals from 
the Toxics Use Reduction Institute (TURI) Petition. Office of 
Pollution Prevention and Toxics, Toxics Release Inventory Program 
Division, Regulatory Developmental Branch. July 18, 2017.
7. Ema, M. and A. Harazono. 2000. Adverse effects of dibutyltin 
dichloride on initiation and maintenance of rat pregnancy. Reprod. 
Toxicol. 14(5): 451-456.
8. Ema, M., T. Itami, and H. Kawasaki. 1991. Teratogenicity of di-n-
butyltin dichloride in rats. Toxicol. Lett. 58(3): 347-356.
9. Ema, M., T. Itami, and H. Kawasaki. 1992. Susceptible period for 
the teratogenicity of di-n-butyltin dichloride in rats. Toxicol. 
73(1): 81-92.
10. Ema, M., R. Kurosaka, H. Amano, and Y. Ogawa. 1995. Comparative 
developmental toxicity of butyltin trichloride, dibutyltin 
dichloride and tributyltin chloride in rats. J. Appl. Toxicol. 
15(4): 297-302.
11. Ema, M., K. Fukunishi, M. Matsumoto, A. Hirose, E. Kamata, and 
T. Ihara. 2007. Developmental toxicity of dibutyltin dichloride in 
cynomolgus monkeys. Reprod. Toxicol. 23(1): 12-19.
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cover letter dated 05/09/88. Submitted under TSCA Section 4; EPA 
Document No. FYI-OTS-0588-0615; OTS0000615-0.
115. van Hoogen, G and A. Opperhuizen. 1988. Toxicokinetics of 
chlorobenzenes in fish. Environ. Toxicol. Chem. 7:213-219.
116. Chemical Manufacturers Association. 1988b. Chronic toxicity of 
1,2,3-trichlorobenzene to mysid shrimp (Mysidopsis bahia) with cover 
letter dated 11/14/88. Springborn Life Science, Inc. Submitted under 
TSCA Section 4; EPA Document No. 40-88201001; OTS0523010.
117. Chaisuksant, Y., Y. Qiming, and D.W. Connell. 1998. Effects of 
halobenzenes on growth rate of fish (Gambusia affinis). Ecotox. 
Environ. Safe. 39:120-130.
118. Sijm, D.T H M. and A. van der Linde. 1995. Size-dependent 
bioconcentration kinetics of hydrophobic organic chemicals in fish 
based on diffusive mass transfer and allometric relationships. 
Environ. Sci. Technol. 29:2769-2777.
119. Hendriks, A.J., Pieters, H., and de Boer, J. 1998. Accumulation 
of metals, polycyclic (halogenated) aromatic hydrocarbons, and 
biocides in zebra mussel and eel from the Rhine and Meuse Rivers. 
Environ. Toxicol. Chem. 17:1885-1898.
120. Ciba-Geigy. 1995. Support: 13-Week toxicity study and fertility 
study of Araldite PT-810 by oral route (dietary admixture) in male 
rats, with cover letter dated 4-26-96. Ciba-Geigy Corporation. 
Submitted under TSCA Section 8(e). OTS0503914-17.
121. USEPA. 1996. Guidelines for Reproductive Toxicity Risk 
Assessment. Federal Register 61(212):56274-56322. U.S. Environmental 
Protection Agency. Washington, DC Available online at https://www.epa.gov/sites/default/files/2014-11/documents/guidelines_repro_toxicity.pdf.
122. Nissan. 1992. Supplement: Triglycidyl isocyanurate: chromosome 
analysis in mouse spermatogonial cells, comparative

[[Page 57625]]

inhalation study with cover letter dated 091892. Nissan Chemical 
American Corporation. Submitted under TSCA Section 8E. OTS0503914-
14. 89-920000133.
123. Ciba-Geigy. 1988. Initial submission: Subchronic dose selection 
study on 1,3,5-tris(oxiranylmethyl-1,3,5-triazine-2,4,6(1h,3h,5h)-
trione with cover letter dated 08/07/92. Ciba-Geigy Corporation. 
Submitted under TSCA Section 8ECP. OTS0555023. 88-920008205.
124. BRRC. 1992. Dominant lethal assay of inhaled PL-90-910 dust in 
CD-1 mice. In: Support: 1,3,5-triglycidylisocyanurate: Dominant 
lethal assay in CD-1 mice with cover letter dated 11-09-92. Busy Run 
Research Center Submitted under TSCA to the U.S. Environmental 
Protection Agency Section 8(e). OTS0503914-15.
125. Ciba-Geigy. 1989. Mutagenicity test on Araldite PT-810 in the 
mouse spermatogonial cell cytogenetic assay and dominant lethal 
assay in mice with cover letter dated 061989 (final reports). Ciba-
Geigy Corporation. Submitted under TSCA Section 8E. OTS0503914-4. 
89-890000197.
126. Nissan. 1992. Supplemental information from Nissan chemical 
America Corp to USEPA concerning triglycidyl isocyanurate: 5-Day 
repeat exposure inhalation toxicity study in the male mouse w-
attach. Nissan Chemical American Corporation. Submitted under TSCA 
Section 8E. OTS0503914-13. 89-920000049.
127. Loveday, KS; Anderson, BE; Resnick, MA; Zeiger, E. 1990. 
Chromosome aberration and sister chromatid exchange tests in Chinese 
hamster ovary cells in vitro: V. Results with 46 chemicals. Environ 
Mol Mutagen 16: 272-303.
128. Sofuni, T; Matsuoka, A; Sawada, M; Ishidate, MJ; Zeiger, E; 
Shelby, MD. 1990. A comparison of chromosome aberration induction by 
25 compounds tested by two Chinese hamster cell (CHL and CHO) 
systems in culture. Mutat Res 241: 175-214.
129. NTP. 1991. NTP toxicology and carcinogenesis studies of tris(2-
chloroethyl) phosphate (CAS No. 115-96-8) in F344/N rats and B6C3F1 
mice (gavage studies). National Toxicology Program Technical Report 
Series 391: 1-233.
130. Aceto Chemical Company Inc. 1977. Nine studies on tris (2-
chloroethyl) phosphate and tris (chloropropyl) phosphate with cover 
letter dated 02-09-89. Submitted to the U.S. Environmental 
Protection Agency under TSCA Section 8(d).
131. F[ouml]llmann, W., and J. Wober. 2006. Investigation of 
cytotoxic, genotoxic, mutagenic, and estrogenic effects of the flame 
retardants tris-(2-chloroethyl)-phosphate (TCEP) and tris-(2 
chloropropyl)-phosphate (TCPP) in vitro. Toxicol. Lett. 161(2): 124-
134.
132. Haworth, S., T. Lawlor, K. Mortelmans, W. Speck, and E. Zeiger. 
1983. Salmonella mutagenicity test results for 250 chemicals. 
Environ. Mutagen. 5(Suppl 1): 3-142.
133. Galloway, S.M., M.J. Armstrong, C. Reuben, S. Colman, B. Brown, 
C. Cannon, A.D. Bloom, F. Nakamura, M. Ahmed, S. Duk, J. Rimpo, B.H. 
Margolin, M.A. Resnick, B. Anderson, and E. Zeiger. 1987. Chromosome 
aberrations and sister chromatid exchanges in Chinese hamster ovary 
cells: Evaluations of 108 chemicals. Environ. Mol. Mutagen. 10 
(Suppl. 10): 1-175.
134. Nakamura, A., N. Tateno, S. Kojima, M.A. Kaniwa, and T. 
Kawamura. 1979. The mutagenicity of halogenated alkanols and their 
phosphoric acid esters for Salmonella typhimurium. Mutat. Res. 
66(4): 373-380.
135. Sala, M., Z.G. Gu, G. Moens, and I. Chouroulinkov. 1982. In 
vivo and in vitro biological effects of the flame retardants 
tris(2,3-dibromopropyl) phosphate and tris(2-
chlorethyl)orthophosphate. Eur. J. Cancer Clin. Oncol. 18(12): 1337-
1344.
136. Simmon, V.F. and K. Kauhanen. 1978. In vitro microbiological 
mutagenicity assays of tris(2-chloroethyl)phosphate. Report 11 (as 
cited in Ref. 125).
137. Simmon, V.F., K. Kauhanen, and R.G. Tardiff. 1977. Mutagenic 
activity of chemicals identified in drinking water. Dev. Toxicol. 
Environ. Sci. 2: 249-258.
138. Vogel, E.W. and M.J. Nivard. 1993. Performance of 181 chemicals 
in a Drosophila assay predominantly monitoring interchromosomal 
mitotic recombination. Mutagenesis 8(1): 57-81.
139. USEPA. 2009. Provisional peer-reviewed Toxicity values for 
tris(2-chloroethyl) phosphate (CAS No. 115-96-8). U.S. Environmental 
Protection Agency. Washington, DC Available at: http://hhpprtv.ornl.gov/issue_papers/Tris2chloroethylphosphate.pdf.
140. NTP. 1991. Final report on the reproductive toxicity of tris(2-
chloroethyl)phosphate reproduction and fertility assessment in Swiss 
CD-1 mice when administered via gavage. NTIS Technical Report 
129170(253).
141. Morrissey, R. E., B.A. Schwetz, J.C. Lamb, M.D. Ross, J.L. 
Teague, and R.W. Morris. 1988. Evaluation of rodent sperm vaginal 
cytology and reproductive organ weight data from National Toxicology 
Program 13-week studies. Fundam. Appl. Toxicol. 11(2): 343-358.
142. Shepel'skaia, N R. and NE Dyshginevich. 1981. Experimental 
study of the gonadotoxic effect of tri- (chloroethyl)-phosphate. 
Gig. Sanit. (6): 20-21 (as cited in Ref. 136).
143. NIOSH. 1983. Screening of priority chemicals for potential 
reproductive hazard (Final Report) with attachments and cover sheet. 
Atlanta, GA: Centers for Disease Control, U.S. Department of Health 
and Human Services.
144. Hardin, B.D., R.L. Schuler, J.R. Burg, G.M. Booth, K.P. 
Hazelden, K.M. Mackenzie, V.J. Piccirillo, and K.N. Smith. 1987. 
Evaluation of 60 chemicals in a preliminary developmental toxicity 
test. Teratogen. Carcinogen. Mutagen. 7: 29-48.
145. Stauffer Chemical Company. 1981. A two-year oral toxicity/
carcinogenicity study of FYROL FR-2 in rats. (Volume I-IV). (Final 
Reports) with attachments, cover sheets and letter dated 09-30-81. 
Submitted to the U.S. Environmental Protection Agency under TSCA 
Section 8(e), pages 580-2180.
146. Brusick, D., D. Matheson, D.R. Jagannath, S. Goode, H. 
Lebowitz, M. Reed, G. Roy, and S. Benson. 1979. A comparison of the 
genotoxic properties of tris(2,3-dibromopropyl)phosphate and 
tris(1,3-dichloro-2-propyl)phosphate in a battery of short-term 
bioassays. J. Environ. Pathol. Toxicol. 3(1-2): 207-226.
147. Gold, M.D., A. Blum, and B.N. Ames. 1978. Another flame 
retardant, tris-(1,3-dichloro-2-propyl)-phosphate, and its expected 
metabolites are mutagens. Science 200(4343): 785-787.
148. Ishidate, M.J. 1981. Application of chromosomal aberration 
tests in vitro to the primary screening for chemicals with 
carcinogenic and/or genetic hazards. Tests Courts Cancerog Quo 
Vadis: 57-79.
149. Lynn, R.K., K. Wong, C. Garvie-Gould, and J.M. Kennish. 1981. 
Disposition of the flame retardant, tris(1,3-dichloro-2-propyl) 
phosphate, in the rat. Drug Metab. Disp. 9(5): 434-441.
150. Mortelmans, K., S. Haworth, T. Lawlor, W. Speck, B. Tainer, and 
E. Zeiger. 1986. Salmonella mutagenicity tests. 2. Results from the 
testing of 270 chemicals. Environ. Mutagen. 8(Suppl 7): 1-119.
151. Soderlund, E.J., E. Dybing, J.A. Holme, J.K. Hongslo, E. 
Rivedal, T. Sanner, and S.D. Nelson. 1985. Comparative genotoxicity 
and nephrotoxicity studies of the two halogenated flame retardants 
tris(1,3-dichloro-2-propyl)phosphate and tris(2,3-
dibromopropyl)phosphate. Acta Pharmacol. Toxicol. 56(1): 20-29.
152. Bloom, SE 1984. Sister chromatid exchange studies in the chick 
embryo and neonate: Actions of mutagens in a developing system. 
Basic Life Sci. 29B: 509-533.
153. OEHHA 2011. Evidence on the Carcinogenicity of Tris(1,3-
dichloro-2-propyl)phosphate.
154. Jenkins, C.A. 1990. FYROL FR-2: Acute toxicity to rainbow 
trout. Life Science Research Limited, Suffolk, U.K. Report No. 90/
AKL027/0234, 20 pp. TSCA 8D; OTS0528355, DCN: 86-910000061.
155. Wang, Q., K. Liang, J. Liu, L. Yang, Y. Guo, C. Liu, and B. 
Zhou. 2013. Exposure of zebrafish embryos/larvae to TDCPP alters 
concentrations of thyroid hormones and transcriptions of genes 
involved in the hypothalamic-pituitary-thyroid axis. Aquatic 
Toxicol. 126: 207-213.
156. Liu, C., Q. Wang, K. Liang, J. Liu, B. Zhou, X. Zhang, H. Liu, 
J.P. Giesy, and H. Yu. 2013. Effects of tris(1,3-dichloro-2-propyl) 
phosphate and triphenyl phosphate on receptor-associated mRNA 
expression in zebrafish embryos/larvae. Aquatic Toxicol. 128-129: 
147-157.
157. USEPA. 2015. Flame Retardants Used in Flexible Polyurethane 
Foam: An Alternatives Assessment Update. Design for the Environment, 
August 2015, EPA 744-R-15-002.
158. Akzo Nobel Functional Chemicals LLC. 2004. Combined repeated 
dose with

[[Page 57626]]

reproductive and developmental toxicity study in rats by oral 
gavage. Submitted to the U.S. Environmental Protection Agency under 
TSCA Section 8(e).
159. ECHA. 2010. Background Document to the Committee for Risk 
Assessment on a Proposal for Harmonised Classification and Labelling 
of Trixylyl Phosphate. EC number: 246-677-8. CAS number: 25155-23-1. 
European Chemicals Agency. Final 27 January 2010.

VII. What are the statutory and Executive Orders reviews associated 
with this action?

    Additional information about these statutes and Executive Orders 
can be found at http://www2.epa.gov/laws-regulations/laws-and-executive-orders.

A. Executive Order 12866: Regulatory Planning and Review and Executive 
Order 13563: Improving Regulation and Regulatory Review

    This action is not a significant regulatory action and was 
therefore not submitted to the Office of Management and Budget (OMB) 
for review under Executive Orders 12866 (58 FR 51735, October 4, 1993) 
and 13563 (76 FR 3821, January 21, 2011).

B. Paperwork Reduction Act (PRA)

    This action does not contain any new information collection 
activities that require additional approval by OMB under the PRA, 44 
U.S.C. 3501 et seq. OMB has previously approved the information 
collection activities contained in the existing regulations and has 
assigned OMB control numbers 2070-0212 (EPA ICR No. 2613.02, entitled 
``Toxic Chemical Release Reporting'') and 2050-0078 (EPA ICR No. 
1428.11, entitled ``Trade Secret Claims for Community Right-to-Know and 
Emergency Planning''). Currently, the facilities subject to the 
reporting requirements under EPCRA section 313 and PPA section 6607 may 
use either the EPA Toxic Chemicals Release Inventory Form R (EPA Form 
9350-1), or the EPA Toxic Chemicals Release Inventory Form A (EPA Form 
9350-2). 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 Forms A and R, supplier notification, and petitions under 
OMB Control number 2070-0212 and those related to trade secret 
designations under OMB Control 2050-0078. 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 and displayed on the information collection instruments (e.g., forms, 
instructions).

C. Regulatory Flexibility Act (RFA)

    I certify that this action will not have a significant economic 
impact on a substantial number of small entities under the RFA, 5 
U.S.C. 601 et seq. The small entities subject to the requirements of 
this action are small manufacturing facilities. The Agency has 
determined that of the 488 entities estimated to be impacted by this 
action, 449 are small businesses; no small governments or small 
organizations are expected to be affected by this action. All 449 small 
businesses affected by this action are estimated to incur annualized 
cost impacts of less than 1% of annual revenue or sales. Thus, this 
action 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 provided in EPA's economic analysis (Ref. 
4).

D. Unfunded Mandates Reform Act (UMRA)

    This action does not contain an unfunded mandate of $100 million or 
more as described in UMRA, 2 U.S.C. 1531-1538, and does not 
significantly or uniquely affect small governments. This action is not 
subject to the requirements of UMRA because it contains no regulatory 
requirements that might significantly or uniquely affect small 
governments. EPA did not identify any small governments that would be 
impacted by this action. EPA's economic analysis indicates that the 
total cost of this action is estimated to be $2,057,000 in the first 
year of reporting (Ref. 4).

E. Executive Order 13132: Federalism

    This action does not have federalism implications as specified in 
Executive Order 13132 (64 FR 43255, August 10, 1999). 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.

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.

G. Executive Order 13045: Protection of Children From Environmental 
Health Risks and Safety Risks

    EPA interprets Executive Order 13045 (62 FR 19885, April 23, 1997) 
as applying only to those regulatory actions that concern environmental 
health or safety risks that EPA has reason to believe may 
disproportionately affect children, per the definition of ``covered 
regulatory action'' in section 2-202 of the Executive Order. This 
action is not subject to Executive Order 13045 because it does not 
concern an environmental health risk or safety risk.

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 (NTTAA)

    This rulemaking does not involve any technical standards subject to 
NTTAA section 12(d) (15 U.S.C. 272 note).

J. Executive Order 12898: Federal Actions To Address Environmental 
Justice in Minority Populations and Low-Income Populations

    The EPA believes that this action is not subject to Executive Order 
12898 (59 FR 7629, February 16, 1994) because it does not establish an 
environmental health or safety standard. This regulatory action adds 
additional chemicals to the EPCRA section 313 reporting requirements; 
it does not have

[[Page 57627]]

any impact on human health or the environment. This action does not 
address any human health or environmental risks and does not affect the 
level of protection provided to human health or the environment. The 
addition of these chemicals to the EPCRA section 313 reporting 
requirements will provide information that government agencies and 
others can use to identify potential problems, set priorities, and help 
inform activities.

List of Subjects in 40 CFR Part 372

    Environmental protection, Community right-to-know, Reporting and 
recordkeeping requirements, and Toxic chemicals.

    Dated: October 6, 2021.
Michal Freedhoff,
Assistant Administrator, Office of Chemical Safety and Pollution 
Prevention.

    Therefore, for the reasons stated in the preamble, it is proposed 
that 40 CFR chapter I be amended as follows:

PART 372--TOXIC CHEMICAL RELEASE REPORTING: COMMUNITY RIGHT-TO-KNOW

0
1. The authority citation for part 372 continues to read as follows:

    Authority: 42 U.S.C. 11023 and 11048.

0
2. In Sec.  372.28, amend the table in paragraph (a)(1) by:
0
a. Revising the third column header to read ``Reporting threshold (in 
pounds),'' and
0
b. Adding the chemical ``1,3,4,6,7,8-Hexahydro-4,6,6,7,8,8-
hexamethylcyclopenta[g]-2- benzopyran'' in alphabetical order.
    The revision and addition read as follows:

Sec.  372.28  Lower thresholds for chemicals of special concern.

    (a) * * *
    (1) * * *

                       Table to Paragraph (a) (1)
------------------------------------------------------------------------
                                                             Reporting
              Chemical name                   CAS No.      threshold (in
                                                              pounds)
------------------------------------------------------------------------
 
                              * * * * * * *
1,3,4,6,7,8-Hexahydro-4,6,6,7,8,8-             1222-05-5             100
 hexamethylcyclopenta[g]-2- benzopyran..
 
                              * * * * * * *
------------------------------------------------------------------------

* * * * *
0
3. Amend Sec.  372.65 by:
0
a. Adding new entries in alphabetical order in table 1 to paragraph (a) 
for ``Dibutyltin dichloride,'' ``1,3-Dichloro-2-propanol,'' 
``Formamide,'' ``1,3,4,6,7,8-Hexahydro-4,6,6,7,8,8-
hexamethylcyclopenta[g]-2- benzopyran,'' ``N-
Hydroxyethylethylenediamine,'' ``Nitrilotriacetic acid trisodium 
salt,'' ``p-(1,1,3,3-Tetramethylbutyl)phenol,'' ``1,2,3-
Trichlorobenzene,'' ``Triglycidyl isocyanurate,'' ``Tris(2-chloroethyl) 
phosphate,'' ``Tris(1,3-dichloro-2-propyl) phosphate,'' and 
``Tris(dimethylphenol) phosphate''; and
0
b. Adding new entries in alphabetical order in the table 2 to paragraph 
(b) for ``Formamide,'' ``1,2,3-Trichlorobenzene,'' ``1,3-Dichloro-2-
propanol,'' ``N-Hydroxyethylethylenediamine,'' ``Tris(2-chloroethyl) 
phosphate,'' ``p-(1,1,3,3-Tetramethylbutyl)phenol,'' ``Dibutyltin 
dichloride,'' ``1,3,4,6,7,8-Hexahydro-4,6,6,7,8,8-
hexamethylcyclopenta[g]-2- benzopyran,'' ``Triglycidyl isocyanurate,'' 
``Nitrilotriacetic acid trisodium salt,'' ``Tris(1,3-dichloro-2-propyl) 
phosphate,'' and ``Tris(dimethylphenol) phosphate''.
    The additions read as follows:

Sec.  372.65  Chemicals and chemical categories to which this part 
applies.

* * * * *
    (a) * * *

                        Table 1 to Paragraph (a)
------------------------------------------------------------------------
              Chemical name                   CAS No.     Effective date
------------------------------------------------------------------------
 
                              * * * * * * *
Dibutyltin dichloride...................        683-18-1          1/1/23
 
                              * * * * * * *
1,3-Dichloro-2-propanol.................         96-23-1          1/1/23
 
                              * * * * * * *
Formamide...............................         75-12-7          1/1/23
 
                              * * * * * * *
1,3,4,6,7,8-Hexahydro-4,6,6,7,8,8-             1222-05-5          1/1/23
 hexamethylcyclopenta[g]-2- benzopyran..
 
                              * * * * * * *
N-Hydroxyethylethylenediamine...........        111-41-1          1/1/23
 
                              * * * * * * *
Nitrilotriacetic acid trisodium salt....       5064-31-3          1/1/23
 
                              * * * * * * *
p-(1,1,3,3-Tetramethylbutyl)phenol......        140-66-9          1/1/23
 

[[Page 57628]]

 
                              * * * * * * *
1,2,3-Trichlorobenzene..................         87-61-6          1/1/23
 
                              * * * * * * *
Triglycidyl isocyanurate................       2451-62-9          1/1/23
 
                              * * * * * * *
Tris(2-chloroethyl) phosphate...........        115-96-8          1/1/23
 
                              * * * * * * *
Tris(1,3-dichloro-2-propyl) phosphate...      13674-87-8          1/1/23
 
                              * * * * * * *
Tris(dimethylphenol) phosphate..........      25155-23-1          1/1/23
 
                              * * * * * * *
------------------------------------------------------------------------

* * * * *
    (b) * * *

                        Table 2 to Paragraph (b)
------------------------------------------------------------------------
          CAS No.                   Chemical name         Effective date
------------------------------------------------------------------------
 
                              * * * * * * *
75-12-7....................  Formamide..................          1/1/23
 
                              * * * * * * *
87-61-6....................  1,2,3-Trichlorobenzene.....          1/1/23
 
                              * * * * * * *
96-23-1....................  1,3-Dichloro-2-propanol....          1/1/23
 
                              * * * * * * *
111-41-1...................  N-                                   1/1/23
                              Hydroxyethylethylenediamin
                              e.
 
                              * * * * * * *
115-96-8...................  Tris(2-chloroethyl)                  1/1/23
                              phosphate.
 
                              * * * * * * *
140-66-9...................  p-(1,1,3,3-                          1/1/23
                              Tetramethylbutyl)phenol.
 
                              * * * * * * *
683-18-1...................  Dibutyltin dichloride......          1/1/23
 
                              * * * * * * *
1222-05-5..................  1,3,4,6,7,8-Hexahydro-               1/1/23
                              4,6,6,7,8,8-
                              hexamethylcyclopenta[g]-2-
                              benzopyran.
 
                              * * * * * * *
2451-62-9..................  Triglycidyl isocyanurate...          1/1/23
 
                              * * * * * * *
5064-31-3..................  Nitrilotriacetic acid                1/1/23
                              trisodium salt.
 
                              * * * * * * *
13674-87-8.................  Tris(1,3-dichloro-2-propyl)          1/1/23
                              phosphate.
 
                              * * * * * * *
25155-23-1.................  Tris(dimethylphenol)                 1/1/23
                              phosphate.
 
                              * * * * * * *
------------------------------------------------------------------------

[[Page 57629]]

[FR Doc. 2021-22112 Filed 10-15-21; 8:45 am]
BILLING CODE 6560-50-P