57614 Federal Register / Vol. 86, No. 198 / Monday, October 18, 2021 / Proposed Rules 
eligible to apply time credits under 18 
U.S.C. 3632(d)(4)—including the extent to which any of the statutory provisions listed in this notice might affect the ability of some or all D.C. Code offenders to apply time credits—and not on the other contents of the November 25, 2020, proposed rule. 
Issued under rulemaking authority 
vested in the Attorney General in 5 U.S.C. 301; 28 U.S.C. 509, 510 and delegated to the Director, Bureau of Prisons in 28 CFR 0.96. 
Michael D. Carvajal, 
Director, Federal Bureau of Prisons. 
[FR Doc. 2021–22613 Filed 10–15–21; 8:45 am] 
BILLING CODE P 
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. 
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: bushman.daniel@epa.gov. 
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 
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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 
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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 mg DBTC/L (96-hour median effect concentration (EC
50) for growth) 
in the green algae (Scenedesmus obliquus) (Ref. 14) and chronic aquatic toxicity values are as low as 20 mg/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 mg 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 mg/L for 96 hours, while no effect on mortality was observed at concentrations of ≤11 mg DBTC/L; the 
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96-hour LC 50was between 11 and 56 mg 
DBTC/L. Thom et al. (Ref. 17) exposed 
the embryos of Pacific oysters (Crassostrea gigas) to DBTC and found a 48-hour EC
50of 142 mg DBTC/L (55.5 
mg tin (Sn)/L), based on abnormal larval development, and a 48-hour LC
50of 171 
mg DBTC/L (66.9 mg 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 mg/L in algae (72-hour EC
50for inhibition of biomass in the 
microalgal species (Pseudokirchneriella subcapitata) (Ref. 56 as cited in Ref. 57), 153 mg/L in aquatic invertebrates (96- 
hour EC
50in the mussel (Lampsilis 
cardium) (Ref. 58)), and 950 mg/L (concentration that is lethal to 50% of the test organisms (LC
50)) 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 mg/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 mg/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 mg/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 Suite
TM(EPI SuiteTM) (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) 
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calculated by EPI SuiteTMwas 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 (Na
3NTA·H 2O) 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·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 
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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 mg/L in aquatic invertebrates (96-hour LC
50in mysid 
shrimp (Mysidopsis bahia) (Ref. 95)), 120 mg/L in fish (14-day LC
50in rainbow 
trout (O. mykiss) (Ref. 96)), and 0.2 mg/ 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 mg/L in aquatic invertebrates (21-day MATC for delayed nauplii development in the copepod (Tigriopus japonicas) (Ref. 98)), 1 mg/L in fish (35- day LOECs for reduced growth in rainbow trout larvae (O. mykiss) (Ref. 99)), and 0.002 mg/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 17b- 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 
SuiteTM) (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 mg/L in aquatic invertebrates (96-hour LC
50in the mysid 
shrimp (M. bahia) (Ref. 114)) and 350 mg/L in fish (96-hour LC
50in the guppy 
(P. reticulata) (Ref. 115)). Chronic toxicity endpoint values are as low as 22 mg/L in aquatic invertebrates (28-day MATC for inhibition of reproduction and growth in M. bahia (Ref. 116)) and 44 mg/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 
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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
3for 
4 months, with decreased litter size and increased pre- and post-implantation loss observed when males exposed to 1.5 mg/m
3were mated to naı ¨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 mg/L (96-hour LC
50) 
in rainbow trout (O. mykiss) (Ref. 154). 
Chronic aquatic toxicity values are below 0.1 mg/L and are as low as 22 mg/ L (142-hour MATC for decreases in body weight and whole-body thyroxin (T4) content) in zebrafish (Danio rerio) 
(Ref. 155) and 20 mg/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). 
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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 mg/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. 
12. Ema, M., S. Fujii, T. Ikka, M. Matsumoto, 
A. Hirose, and E. Kamata. 2007. Early pregnancy failure induced by dibutyltin dichloride in mice. Environ. Toxicol. 22(1): 44–52. 
13. Noda, T., S. Morita, and S. Baba. 1993. 
Teratogenic effects of various di-n- butyltins with different anions and butyl(3-hydroxybutyl)tin dilaurate in rats. Toxicol. 85(2–3): 149–160. 
14. Huang, G., Z. Bai, S. Dai, and Q. Xie. 
1993. Accumulation and toxic effect of 
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organometallic compounds on algae. 
Appl. Organomet. Chem. 7: 373–380. 
15. Holwerda, D.A. and H.J. Herwig. 1986. 
Accumulation and metabolic effects of di-n-butyltin dichloride in the freshwater clam, Anodonta anatina. Bull. Environ. 
Contam. Toxicol. 36: 756–762. 
16. Salazar, M.H. and S.M. Salazar. 1989. 
Acute effects of (bis)tributyltin oxide on marine organisms. Naval Ocean Systems Center, San Diego, California. Technical Report 1299. 
17. Thom, R.M., L.M. Karle, and J.Q. Word. 
1991. Static acute 48-hour toxicity test of dibutyltin dichloride (DBT) to oyster larvae. Battelle Pacific Northwest Laboratories, Sequim, WA, USA, BNW No. 12716, pp 1–72. TSCA 8E; OTS0540381, DCN: 88–920004033. 
18. Thom, R.M., L.M. Karle, and J.Q. Word. 
1991. Static acute 48-hour toxicity test of 
dibutyltin dichloride (DBT) to oyster larvae. Battelle Pacific Northwest Laboratories, Sequim, WA, USA, BNW No. 12716, pp 1–72. TSCA 8E; OTS0540381, DCN: 88–920004033. 
19. Cima, F., L. Ballarin, G. Bressa, G. 
Martinucci, and P. Burighel. 1996. Toxicity of organotin compounds on embyros of a marine invertebrate (Styela plicata; Tunicata). Ecotoxicol. Environ. 
Saf. 35: 174–182. 
20. Laughlin, R.B., Jr. and W. French. 1989. 
Population-related toxicity responses to two butyltin compounds by zoeae of the mud crab Rhithropanopeus harrisii. Marine Biol. 102: 397–401. 
21. de Vries, H., A.H. Penninks, N.J. Snoeij, 
and W. Seinen. 1991. Comparative toxicity of organotin compounds to rainbow trout (Oncorhynchus mykiss) yolk sac fry. Sci. Total Environ. 103: 229–243. 
22. Wester, P.W. and J.H. Canton. 1987. 
Histopathological study of Poecilia reticulata (Guppy) after long-term 
exposure to bis(tri-n-butyltin)oxide (TBTO) and di-n-butyltindichloride (DBTC). Aquat. Toxicol. 10: 143–165. 
23. Wester, P.W., J.H. Canton, A.A.J. Van 
Iersel, E.I. Krajnc, and H.A.M.G. Vaessen. 1990. The toxicity of bis(tri-n- butyltin)oxide (TBTO) and di-n- butyltindichloride (DBTC) in the small fish species Oryzias latipes (medaka) and Poecilia reticulata (guppy). Aquat. Toxicol. 16: 53–72. 
24. Vitturi, R., C. Mansueto, E. Catalano, L. 
Pellerito, and M.A. Girasolo. 1992. Spermatocyte chromosome alterations in Truncatella subcylindrica (L., 1767) (Mollusca, Mesogastropoda) following exposure to dibutyltin(IV) and tributyltin(IV) chlorides. Appl. Organomet. Chem. 6: 525–532. 
25. Hercules, Inc. 1986. 104 Week chronic 
toxicity and oncogenicity study with 1,3 dichloropropan-2-ol in the rat (Part 1) with cover letter dated 080389. Submitted to the U.S. Environmental Protection Agency under TSCA section 8E. 
26. Hercules, Inc. 1986. 104-Week chronic 
toxicity and oncogenicity study 1,3- dichloropropanol-2-ol in the rat report (Part 1) with cover letter dated 110889 (appendices). Submitted to the U.S. 
Environmental Protection Agency under TSCA section 8E. 
27. Frei, H. and F.E. Wurgler. 1997. The 
vicinal chloroalcohols 1,3-dichloro-2- propanol (DC2P), 3-chloro-1,2- propanediol (3CPD) and 2-chloro-1,3- propanediol (2CPD) are not genotoxic in vivo in the wing spot test of Drosophila 
melanogaster. Mutat. Res. 394(1–3): 59– 68. 
28. 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: 785–787. 
29. Hahn, H., E. Eder, and C. Deininger. 1991. 
Genotoxicity of 1,3-dichloro-2-propanol in the SOS chromotest and in the Ames test. Elucidation of the genotoxic mechanism. Chem. Biol. Interact. 80(1): 
73–88. 
30. Hercules, Inc. 1990. Letter from Hercules 
Inc to U.S. EPA regarding submission of final reports on 3 mutagenicity studies with attachments. Submitted to the U.S. Environmental Protection Agency under TSCA section 8(e). 
31. Lynn, R.K., K. Wong, C. Garvie-Gould, 
and M. Kennish. 1981. Disposition of the flame retardant, tris(1,3-dichloro-2- propyl) phosphate, in the rat. Drug Metab. Dispos. 9(5): 434–441. 
32. Nakamura, A., N. Tateno, S. Kojima, M. 
Kaniwa, and T. Kawamura. 1979. The mutagenicity of halogenated alkanols and their phosphoric acid esters for Salmonella typhimurium. Mutat. Res. 66(4): 373–380. 
33. Ohkubo T., T. Hayashi, E.Watanabe, H. 
Endo, S. Goto, O. Endo, T. Mizoguchi, and Y. Mori. 1995. Mutagenicity of chlorohydrins. Nippon Suisan Gakkaishi 61(4): 596–601. 
34. Painter, R.B. and R. Howard. 1982. The 
HeLa DNA-synthesis inhibition test as a rapid screen for mutagenic carcinogens. Mutat. Res. 92(1–2): 427–438. 
35. Silhankova, L., F. Smid, M. Cerna, J. 
Davidek, and J. Velisek. 1982. Mutagenicity of glycerol chlorohydrines and of their esters with higher fatty acids present in protein hydrolysates. Mutat. Res. 103(1): 77–81. 
36. Stolzenberg, S.J. and C.H. Hine. 1980. 
Mutagenicity of 2- and 3-carbon halogenated compounds in the salmonella/mammalian-microsome test. Environ. Mutagen. 2: 59–66. 
37. von der Hude, W., M. Scheutwinkel, U. 
Gramilich, B. Fibler, and A. Basler. 1987. Genotoxicity of three-carbon compounds evaluated in the SCE test in vitro. Environ. Mutagen. 9(4): 401–410. 
38. von Der Hude, W., C. Behm, R. Gurtler, 
and A. Basler. 1988. Evaluation of the SOS chromotest. Mutat. Res. 203: 81–94. 
39. Zeiger, E., B. Anderson, S. Haworth, T. 
Lawlor, and K. Mortelmans. 1988. Salmonella mutagenicity tests. IV. Results from the testing of 300 chemicals. Environ. Mol. Mutagen. 11(Suppl 12): 1–158. 
40. Howe, J. 2002. 1,3-Dichloropropan-2-ol 
(1,3–DCP): Induction of micronuclei in the bone marrow of treated rats. Report No. 2150/1–D6172 from Covance 
Laboratories Ltd., Harrogate, North Yorkshire, England. Available from the Food Standards Agency (as cited in Ref. 41). 
41. NTP. 2005. 1,3-Dichloro-2-propanol [CAS 
No. 96–23–1]. Review of toxicological literature. Prepared by Integrated Laboratory Systems, Inc., Research Triangle Park, North Carolina, for the National Toxicology Program, National Institute of Environmental Health Sciences. 
42. Beevers, C. 2003. 1,3-Dichloroproan-2-ol 
(1,3–DCP): Induction of unscheduled DNA synthesis in rat liver using an in vivo/in vitro procedure. Report No. 2150/ 3–D6173 from Covance Laboratories Ltd., Harrogate, North Yorkshire, England. Available from the Food Standards Agency (as cited in Ref. 41). 
43. OEHHA. 2010. Evidence on the 
Carcinogenicity of 1,3-Dichloro-2- 
propanol. https://oehha.ca.gov/media/ 
downloads/proposition-65/13- dcphida.pdf. 
44. U.S. EPA. 2005. Guidelines for 
carcinogen risk assessment. U.S. Environmental Protection Agency, Office of Pollution Prevention Toxics. Washington, DC EPA/630/P=03/001F. Available at http://www2.epa.gov/sites/ production/files/2013-09/documents/ cancer_ guidelines_ final_ 3-25-05.pdf. 
45. BASF Corp. 1982. Reports on teratogenic 
effects of commercially available ink and the influence and teratogenic effects of formamide (five enclosures) with cover letter dated 08–09–82. Submitted to the U.S. Environmental Protection Agency under TSCA Section 4. 
46. Fail, P.A., J.D. George, T.B. Grizzle, and 
J.J. Heindel. 1998. Formamide and dimethylformamide: Reproductive assessment by continuous breeding in mice. Reprod. Toxicol. 12(3): 317–332. 
47. George, J.D., C.J. Price, M.C. Marr, C.B. 
Myers, and G.D. Jahnke. 2000. Evaluation of the developmental toxicity of formamide in Sprague-Dawley (CD) rats. Toxicol. Sci. 57(2): 284–291. 
48. George, J.D., C.J. Price, M.C. Marr, C.B. 
Myers, and G.D. Jahnke. 2002. Evaluation of the developmental toxicity of formamide in New Zealand white rabbits. Toxicol. Sci. 69(1): 165–174. 
49. NTP. 1992. Final report on the 
reproductive toxicity of formamide (FORM) (CAS no. 75–12–7) in CD–1 Swiss mice: Volume 1 NTIS Technical Report 109213(327). 
50. NTP. 1992. Final report on the 
reproductive toxicity of formamide (FORM) (CAS no. 75–12–7) CD–1 (trade name) Swiss mice: Volume 2. Laboratory supplement. NTIS Technical Report 109221(249). 
51. NTP. 1998. Final report on the 
developmental toxicity of formamide (CAS No. 75–12–7) administered by gavage to Sprague-Dawley CD¥ rats on 
gestational days 6–19. NTIS Technical Report 139701(106). 
52. NTP. 2001. Developmental toxicity 
evaluation of formamide (CAS No. 75– 12–7) administered by gavage to New 
VerDate Sep<11>2014 18:10 Oct 15, 2021 Jkt 256001 PO 00000 Frm 00012 Fmt 4702 Sfmt 4702 E:\FR\FM\18OCP1.SGM 18OCP1jspears on DSK121TN23PROD with PROPOSALS157623 Federal Register / Vol. 86, No. 198 / Monday, October 18, 2021 / Proposed Rules 
Zealand white rabbits on gestational 
days 6 through 29. NTIS Technical Report 104060(460). 
53. Stula, E.F. and W.C. Krauss. 1977. 
Embryotoxicity in rats and rabbits from cutaneous application of amide-type solvents and substituted ureas. Toxicol. Appl. Pharmacol. 41: 35–55. 
54. Dupont Chemical Company. 1967. Initial 
submission: The effects of DMF, MMF, & formamide on embryonic development in rats with cover letter dated 10–15–92. Submitted to the U.S. Environmental Protection Agency under TSCA Section 8ECP. 
55. Dupont Chemical Company. 1992. Initial 
submission: Embryotoxicity in rats and rabbits from application of formamide & other chemicals to skin during organogenesis with cover letter dated 10–15–92. Submitted to the U.S. 
Environmental Protection Agency under TSCA Section 8ECP. 
56. Van Dijk, A. 1997. Acute toxicity of 
HHCB to Pseudokirchneriella subcapitata. Report to the RIFM, RCC 
Umweltchemie AG Project 380632 (as cited Ref. 57). 
57. Balk, F. and R.A. Ford. 1999. 
Environmental risk assessment for the polycyclic musks, AHTN and HHCB: II. Effect assessment and risk characterization. Toxicol Lett 111:81–94. 
58. Gooding, M.; T.J. Newton; M.R. Bartsch; 
K.C. Hornbuckle. 2006. Toxicity of synthetic musks to early life stages of the freshwater mussel Lampsilis cardium. Arch. Environ. Contam. Toxicol. 51:549– 558. 
59. Yamauchi, R, H. Ishibashi, M. Hirano, 
and T. Mori. 2008. Effects of synthetic polycyclic musks on estrogen receptor, vitellogenin, pregnane X receptor, and Cytochrome P450 3A gene expression in the livers of male medaka (Oryzias latipes). Aquatic Toxicology 90: 261– 268. 
60. Croudace, CP, J.E. Caunter, P.A. Johnson. 
1997. HHCB: Chronic toxicity to fathead minnow (Pimephales promelas) embryos and larvae. Report to RIFM, Zeneca Project Report BL 5934/B (as cited in Ref. 57). 
61. Chen, F., J. Gao, Q. Zhou. 2012. Toxicity 
assessment of simulated urban runoff containing polycyclic musks and cadmium in Carassius auratus using oxidative stress biomarkers. Environmental Pollution 162: 91–97. 
62. Bj<rnestad, E. 2007. Acartia tonsa larval 
development test with ‘‘HHCB’’. Project No. 54464, GLP Study No 91328/700, DHI Denmark. Report to International Flavors & Fragrances Hilversum, NL (as cited in Ref. 63). 
63. European Commission. 2008. European 
Union Risk Assessment Report for 1,3,4,6,7,8-hexahydro-4,6,6,7,8,8- hexamethylcyclopenta-g-2-benzopyran (1,3,4,6,7,8-hexahydro-4,6,6,7,8,8- hexamethylin-deno[5,6–C]pyran-HHCB), CAS No. 1222–05–5, EINECS No. 214– 916–9, Risk Assessment, Final Approved Version. Office for Official Publications of the European Communities, Luxembourg, The Netherlands. 64. Balk, F., and R.A. Ford. 1999. 
Environmental risk assessment for the 
polycyclic musks AHTN and HHCB in the EU: I. Fate and exposure assessment. Toxicol. Lett. 111:57–79. 
65. Artola-Garciana, E. 2002. Distribution 
behaviour of polycyclic musks in sewage treatment plants and in biota. Interpretation of data using free and total concentration measurements. Thesis at Institute for Risk Assessment Sciences IRA, Utrecht, The Netherlands (as cited in Ref. 63). 
66. USEPA. 2012. EPI Suite results for CAS 
1222–05–5, HHCB. EPI Suite
TMv4.11. 
U.S. Environmental Protection Agency. Available online at http://www.epa.gov/ opptintr/exposure/pubs/episuitedl.htm (accessed November 12, 2015). 
67. Arnot, J.A. and F.A.P.C. Gobas. 2003. A 
generic QSAR for assessing the 
bioaccumulation potential of organic chemicals in aquatic food webs. QSAR Comb. Sci. 22:337–345. 
68. USEPA. 2014. TSCA Work Plan Chemical 
Risk Assessment, HHCB, 1,3,4,6,7,8- Hexahydro-4,6,6,7,8,8- hexamethylcyclopenta-g-2-Benzopyran, CASRN: 1222–05–5. U.S. Environmental Protection Agency. 
69. Envirogen. 1998. Fate of HHCB in Soil 
Microcosms. Envirogen, Inc. Princeton Research Centre, report submitted to International Flavors and Fragrances, Lawrenceville, NJ (as cited in Ref. 63). 
70. DiFrancesco, A. M., P. C. Chiu, L. J. 
Standley, H. E. Allen, and D. T. Salvito. 2004. Dissipation of Fragrance Materials in Sludge-Amended Soils. Environmental Science and Technology, 38(1), 194–201. 
71. Xu, Y., S. Treumann, S; R. Rossbacher, S. 
Schneider, and P.J. Boor. 2014. Dissecting aortic aneurysm induced by N-(2-aminoethyl) ethanolamine in rat: Role of defective collagen during development. Birth Defects Res A Clin Mol Teratol 100: 924–933. 
72. Schneider, S., S. Treumann, and N.P. 
Moore. 2012. Malformations of the great vessels in the neonatal rat induced by N- (2-aminoethyl)ethanolamine. Birth Defects Res B Dev. Reprod. Toxicol. 95: 95–106. 
73. EPSDG. 2009. Additional interim results 
of a preliminary experiment to explore the p.o. (gavage) administration of ABEA (CAS No. 111–41–1) to pregnant female rats of various strains and in separate laboratories. Ethyleneamines Product Stewardship Discussion Group. Submitted under TSCA Section 8E. 89090000355. 8EHQ–0809–17477B. 
74. EPSDG. 2009. Interim results of a 
preliminary experiment to explore the p.o. (gavage) administration of AEEA (CAS No. 111–41–1) to pregnant female rats of various strains and in separate laboratories. Ethyleneamines Product Stewardship Discussion Group. Submitted under TSCA Section 8E. 8EHQ–0409–17477A. 88090000201. 
75. EPSDG. 2003. Oral prenatal 
developmental toxicity study in rats. Ethyleneamines Product Stewardship Discussion Group. Submitted under TSCA Section 8(e). 8EHQ–1203–15167 
D. 89040000064. 
76. EPSDG. 2008. Interim results of a 
preliminary experiment to explore the intrapertioneal (i.p.) route of administration of AEEA (CAS No. 111– 41–1). Ethyleneamines Product Stewardship Discussion Group. Submitted under TSCA Section 8(e). 8EHQ–1008–17311A. 88090000035. 
77. Moore, N.P.; Tornesi, B.; Yano, B.L.; et al. 
2012a. Developmental sensitivity to the induction of great vessel malformations by N-(2-aminoethyl)ethanolamine. Birth Defects Res B Dev Reprod Toxicol 95: 116–122. 
78. EPSDG. 2006a. [Interim results of a probe 
developmental toxicity study with AEEA (CAS No. 111–41–1)]. Ethyleneamines Product Stewardship Discussion Group. Submitted under TSCA Section 8E. 
8EHQ–1106–16670A. 88070000088. 
79. EPSDG. 2005b. Revised results of a 
reproductive and developmental toxicity follow-up probe study in rats by oral gavage. Ethyleneamines Product Stewardship Discussion Group. Submitted under TSCA Section 8E. 89050000409. 8EHQ–0505–15167 F. 
80. EPSDG. 2004. A reproductive and 
developmental toxicity follow-up probe study in rats by oral gavage. Ethyleneamines Product Stewardship Discussion Group. Submitted under TSCA Section 8E. 8EHQ–0404–15167 E. 89040000140. 
81. EPSDG. 2003a. Interim results of a 
histopathology processing and examination study in rats (a follow-up study to an OECD 421 study). Ethyleneamines Product Stewardship Discussion Group. Submitted under TSCA Section 8E. 8EHQ–1103–15167 C. 89040000033. 
82. Chen, Z; Xu, Y; Bujalowski, P; 
Oberhauser, AF; Boor, PJ. 2015. N-(2- Aminoethyl) Ethanolamine-Induced Morphological, Biochemical, and Biophysical Alterations in Vascular Matrix Associated With Dissecting Aortic Aneurysm. Toxicol Sci 148:421– 32. 
83. Moore, NP; Saghir, SA; Clark, AJ; Hansen, 
SC; Carney, EW; Marshall, VA; Rasoulpour, RJ: Bartels, MJ. 2012b. Toxicokinetic profile of N-(2- aminoethyl)ethanolamine in the female Wistar rat and distribution into the late gestation fetus and milk. Birth Defects Res B Dev Reprod Toxicol 95:107–15. 
84. Goyer, R.A., H.L. Falk, M. Hogan, D.D. 
Feldman, and W. Richter. 1981. Renal tumors in rats given trisodium nitrilotriacetic acid in drinking water for 2 years. J. Natl. Cancer Inst. 66(5): 869– 880. 
85. National Cancer Institute (NCI). 1977. 
Bioassays of nitrilotriacetic acid (NTA) and nitrilotriacetic acid, trisodium salt, monohydrate (Na3–NTA–H2O) for possible carcinogenicity. Carcinogenesis Technical Report Series 6: 1–203. 
86. Fukushima, S., Y. Kurata, S. Tamano, K. 
Inoue, and N. Ito. 1985. Promoting effect of trisodium nitrilotriacetate monohydrate on urinary bladder 
VerDate Sep<11>2014 18:10 Oct 15, 2021 Jkt 256001 PO 00000 Frm 00013 Fmt 4702 Sfmt 4702 E:\FR\FM\18OCP1.SGM 18OCP1jspears on DSK121TN23PROD with PROPOSALS157624 Federal Register / Vol. 86, No. 198 / Monday, October 18, 2021 / Proposed Rules 
carcinogenesis in rats. Jpn. J. Cancer Res. 
(Gann) 76(9): 823–827. 
87. Hiasa, Y., Y. Kitahori, N. Konishi, N. 
Enoki, T. Shimoyama, and A. Miyashiro. 1984. Trisodium nitrilotriacetate monohydrate: promoting effects on the development of renal tubular cell tumors in rats treated with N-ethyl-N- hydroxyethylnitrosamine. J. Natl. Cancer Inst. 72(2): 483–489. 
88. Hiasa, Y., Y. Kitahori, N. Konishi, and T. 
Shimoyama. 1985. Dose-related effect of trisodium nitrilotriacetate monohydrate on renal tumorigenesis initiated with N- ethyl-N-hydroxyethylnitrosamine in rats. Carcinogenesis 6(6): 907–910. 
89. Hiasa, Y., Y. Kitahori, N. Konishi, T. 
Shimoyama, and A. Miyashiro. 1985. Trisodium nitriloacetate monohydrate: Promoting effect in urinary bladder carcinogenesis in rats treated with N- 
butyl-N-(4-hydroxybutyl)nitrosamine. J. Natl. Cancer Inst. 74(1): 235–239. 
90. Kitahori, Y., N. Konishi, T. Shimoyama, 
and Y. Hiasa. 1985. Dose-dependent promoting effect of trisodium nitrilotriacetate monohydrate on urinary bladder carcinogenesis in Wistar rats pretreated with N-butyl-N-(4- hydroxybutyl)nitrosamine. Jpn. J. Cancer Res. (Gann) 76(9): 818–822. 
91. Kitahori, Y., T. Shimoyama, M. Ohshima, 
H. Matsuki, H. Hashimoto, S. Minami, N. Kinishi, K and Y. Hiasa. 1988. Effects of trisodium nitrilotriacetate monohydrate, nitrilotriacetic acid and ammonium chloride on urinary bladder carcinogenesis in rats pretreated with N- bis(2-hydroxypropyl) nitrosamine. Cancer Lett. 43(1–2): 105–110. 
92. Costa, R., A. Russo, M. Zoardan, F. 
Pacchierotti, A. Tavella, and A.G. Lewis. 1988. Nitrilotriacetic acid (nta) induces aneuploidy in drosophila and mouse germ-line cells. Environ. Mol. Mutagen. 12: 397–407. 
93. Ramel, C., and J. Magnusson. 1979. 
Chemical induction of non-disjunction in Drosophila. Environ. Health Perspect. 31: 29–66. 
94. Zordan, M., U. Graf, D. Singer, C. 
Belrame, L. Dalla Valle, M. Osti, R. Costa, and A.G. Lewis. 1991. The genotoxicity of nitrilotriacetic acid (NTA) in a somatic mutation and recombination test in Drosophila melanogaster. Mutat. Res. 262(4): 253– 262. 
95. Cripe, G.M., A. Ingley-Guezou, L.R. 
Goodman, and J. Forester. 1989. Effect of food availability on the acute toxicity of four chemicals to Mysidopsis bahia (Mysidacea) in static exposures. Environ. Toxicol. Chem. 8:333–338. 
96. CMA (Chemical Manufacturing 
Association). 1984. Dynamic 14-day acute toxicity of octylphenol to rainbow trout (Final). Submitted under TSCA Section 4; EPA Document No. 40– 8418133; OTS0527135. 
97. Mayer, L.P., C.A. Dyer, C.R. Propper. 
2003. Exposure to 4-tert-octylphenol accelerates sexual differentiation and disrupts expression of steroidogenic Factor 1 in developing bullfrogs. Environ. Health Persp. 111:557–561. 98. Marcial, H.S., A. Hagiwara, T.W. Snell. 
2003. Estrogenic compounds affect 
development of harpacticoid copepod Tigriopus japonicus. Environ. Toxicol. Chem. 22:3025–3030. 
99. Ashfield, L.A., T.G. Pottinger, J.P. 
Sumpter. 1998. Exposure of female juvenile rainbow trout to alkylphenolic compounds results in modifications to growth and ovosomatic index. Environ. Toxicol. Chem. 17:679–686. 
100. Croteau, M.C., C.J. Martyniuk, V.L. 
Trudeau and D.R.S. Lean. 2008. Chronic exposure of Rana pipiens tadpoles to UVB radiation and the estrogenic chemical 4-tert-octylphenol. J. Toxicol. Environ. Health A 71:134–144. 
101. Croteau, M.C., M. Davidson, P. Duarte- 
Guterman, M. Wade, J.T. Popesku, S. Wiens D.R.S.Lean and Trudeau, VL. 2009. Assessment of thyroid system 
disruption in Rana pipiens tadpoles chronically exposed to UVB radiation and 4-tert-octylphenol. Aquat Toxicol 95:81–92. 
102. White, R; Jobling, S; Hoare, SA; et al. 
(1994) Environmentally persistent alkylphenolic compounds are estrogenic. Endocrinology 135:175–182. 
103. Andersen, HR; Wollenberger, L; Halling- 
S<rensen, B; et al. (2001) Development of copepod nauplii to copepodites—a parameter for chronic toxicity including endocrine disruption. Environ Toxicol Chem 20:2821–2829. 
104. Jobling, S; Sumpter, JP. (1993) Detergent 
components in sewage effluent are weakly oestrogenic to fish: An in vitro study using rainbow trout (Oncorhynchus mykiss) hepatocytes. Aquat Toxicol 27:361–372. 
105. Cruz-Li, EI. (2004) Effects of ammonium 
perchlorate, 4(tert-octyl)phenol and their mixture on zebrafish (Danio rerio) Lubbock, Texas: Ph.D. Thesis, Texas Tech University. 
106. Holland Toomey, B; Monteverdi, GH; Di 
Giulio, RT. (1999) Octylphenol induces vitellogenin production and cell death in fish hepatocytes. Environ Toxicol Chem 18:734–739. 
107. Jobling, S; Sheahan, D; Osborne, JA; et 
al. (1996) Inhibition of testicular growth 
in rainbow trout (Oncorhynchus mykiss) exposed to estrogenic alkylphenolic chemicals. Environ Toxicol Chem 15:194–202. 
108. Gronen, S; Denslow, N; Manning, S; et 
al. (1999) Serum vitellogenin levels and 
reproductive impairment of male Japanese medaka (Oryzias latipes) exposed to 4-tert-octylphenol. Environ Health Perspect 107:385–390. 
109. Ferreira-Leach, A.M. and E.M. Hill. 
2001. Bioconcentration and distribution of 4-tert-octylphenol residues in tissues of the rainbow trout (Oncorhynchus mykiss). Mar. Environ. Res. 51:75–89. 
110. Tsuda, T., A. Takino, K. Muraki, H. 
Harada, and M. Kojima. 2001. Evaluation of 4-nonylphenols and 4-tert-octylphenol contamination of fish in rivers by laboratory accumulation and excretion experiments. Water Res. 35:1786–1792. 
111. Tsuda, T., A. Takino, M. Kojima, H. 
Harada, K. Muraki, and M. Tsuji. 2000. 4-Nonylphenols and 4-tert-octylphenol 
in water and fish from rivers flowing into Lake Biwa. Chemosphere 41:757–762. 
112. Staniszewska, M., L. Falkowska, P. 
Grabowski, Kwasniak, S. Mudrak- Cegiolka, A.R. Reindl, A. Sokolowski, E. Szumilo, and A. Zgrundo. 2014. Bisphenol A, 4-tert-octylphenol, and 4- nonylphenol in the Gulf of Gdan ´sk 
(Southern Baltic). Arch. Environ. Contam. Toxicol. 67:335–347. 
113. Stephen, C.E., D.I. Mount, D.J. Hansen, 
J.H. Gentile, G.A. Chapman, and W.A. Brungs. 1985. Guidelines for Deriving Numerical National Water Quality Criteria for the Protection of Aquatic Organisms and Their Uses. U.S. EPA, Office of Research and Development, Environmental Research Laboratories, Duluth, MN; Narragansett, RI; and Corvallis, OR., 98 pp. 
114. Chemical Manufacturers Association. 
1988. Status report on aquatic toxicity 
tests on 1,2,3- and 1,2,4-trichlorobenzene with 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 
VerDate Sep<11>2014 18:10 Oct 15, 2021 Jkt 256001 PO 00000 Frm 00014 Fmt 4702 Sfmt 4702 E:\FR\FM\18OCP1.SGM 18OCP1jspears on DSK121TN23PROD with PROPOSALS157625 Federal Register / Vol. 86, No. 198 / Monday, October 18, 2021 / Proposed Rules 
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. Fo ¨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 
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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 
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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 
■1. The authority citation for part 372 
continues to read as follows: Authority: 42 U.S.C. 11023 and 11048. 
■2. In § 372.28, amend the table in 
paragraph (a)(1) by: 
■a. Revising the third column header to 
read ‘‘Reporting threshold (in pounds),’’ and 
■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: 
§ 372.28 Lower thresholds for chemicals 
of special concern. 
(a) * * * 
(1) * * * 
TABLE TO PARAGRAPH (a) (1) 
Chemical name CAS No. Reporting 
threshold 
(in pounds) 
*******  
1,3,4,6,7,8-Hexahydro-4,6,6,7,8,8-hexamethylcyclopenta[g]-2- benzopyran ........................................................ .. 1222–05–5 100 
*******  
* * * * * 
■3. Amend § 372.65 by: 
■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 
■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: 
§ 372.65 Chemicals and chemical 
categories to which this part applies. 
* * * * * 
(a) * * * 
TABLE 1 TOPARAGRAPH (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-hexamethylcyclopenta[g]-2- benzopyran ........................................................ .. 1222–05–5 1/1/23 
*******  
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 
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TABLE 1 TOPARAGRAPH (a)—Continued 
Chemical name CAS No. Effective 
date 
*******  
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 TOPARAGRAPH (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-Hydroxyethylethylenediamine ........................................................................................................................... 1/1/23 
*******  
115–96–8 .......... Tris(2-chloroethyl) phosphate ................................................................................ ............................................... 1/1/23 
*******  
140–66–9 .......... p-(1,1,3,3-Tetramethylbutyl)phenol ....................................................................................................................... 1/1/23 
*******  
683–18–1 .......... Dibutyltin dichloride ........................................................................................ ...................................................... 1/1/23 
*******  
1222–05–5 ........ 1,3,4,6,7,8-Hexahydro-4,6,6,7,8,8-hexamethylcyclopenta[g]-2- benzopyran ....................................... ................ 1/1/23 
*******  
2451–62–9 ........ Triglycidyl isocyanurate ...................................................................................... .................................................. 1/1/23 
*******  
5064–31–3 ........ Nitrilotriacetic acid trisodium salt .......................................................................... ................................................ 1/1/23 
*******  
13674–87–8 ...... Tris(1,3-dichloro-2-propyl) phosphate .......................................................................... ........................................ 1/1/23 
*******  
25155–23–1 ...... Tris(dimethylphenol) phosphate ................................................................................. .......................................... 1/1/23 
*******  
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[FR Doc. 2021–22112 Filed 10–15–21; 8:45 am] 
BILLING CODE 6560–50–P 
DEPARTMENT OF COMMERCE 
National Oceanic and Atmospheric 
Administration 
50 CFR Part 622 
[Docket No. 211006–0204] 
RIN 0648–BK36 
Fisheries of the Caribbean, Gulf of 
Mexico, and South Atlantic; Reef Fish Fishery of the Gulf of Mexico; Lane Snapper Management Measures and Proposed Rule 
AGENCY : National Marine Fisheries 
Service (NMFS), National Oceanic and Atmospheric Administration (NOAA), Commerce. 
ACTION : Proposed rule; request for 
comments. 
SUMMARY : NMFS proposes to implement 
management measures described in a framework action to the Fishery Management Plan for the Reef Fish Resources of the Gulf of Mexico (FMP) as prepared by the Gulf of Mexico Fishery Management Council (Council). For Gulf of Mexico (Gulf) lane snapper, this proposed rule would modify the annual catch limit (ACL) and revise an accountability measure (AM). The purposes of this proposed rule are to prevent overfishing of lane snapper and achieve optimum yield (OY). This proposed rule would also make minor administrative changes to replace outdated NMFS website addresses and language about required software for the Individual Fishing Quota (IFQ) programs. 
DATES : Written comments must be 
received by November 2, 2021. 
ADDRESSES : You may submit comments 
on the proposed rule identified by ‘‘NOAA–NMFS–2021–0073’’ by any of the following methods: 
•Electronic Submission: Submit all 
electronic public comments via the Federal e-Rulemaking Portal. Go to www.regulations.gov and enter [NOAA– 
NMFS–2021–0073] in the Search box. Click on the ‘‘Comment’’ icon, complete the required fields, and enter or attach your comments. 
•Mail: Submit all written comments 
to Dan Luers, NMFS Southeast Regional Office, 263 13th Avenue South, St. Petersburg, FL 33701. 
Instructions: Comments sent by any 
other method, to any other address or individual, or received after the end of the comment period, may not be considered by NMFS. All comments received are a part of the public record and will generally be posted for public viewing on www.regulations.gov without change. All personal identifying information (e.g., name, address), 
confidential business information, or otherwise sensitive information submitted voluntarily by the sender will be publicly accessible. NMFS will accept anonymous comments (enter ‘‘N/A’’ in the required fields if you wish to remain anonymous). 
Electronic copies of the framework 
action, which includes an environmental assessment, a fishery impact statement, a Regulatory Flexibility Act analysis, and a regulatory impact review, may be obtained from the Southeast Regional Office website at https://www.fisheries.noaa.gov/action/. 
FOR FURTHER INFORMATION CONTACT : Dan 
Luers, NMFS Southeast Regional Office, telephone: 727–824–5305, email: daniel.luers@noaa.gov. 
SUPPLEMENTARY INFORMATION : NMFS and 
the Council manage the Gulf reef fish fishery, which includes lane snapper, under the FMP. The Council prepared the FMP and NMFS implements the FMP through regulations at 50 CFR part 622 under the authority of the Magnuson-Stevens Fishery Conservation and Management Act (Magnuson-Stevens Act). 
Background 
The Magnuson-Stevens Act requires 
NMFS and regional fishery management 
councils to prevent overfishing and achieve, on a continuing basis, the OY from federally managed fish stocks. These mandates are intended to ensure fishery resources are managed for the greatest overall benefit to the nation, particularly with respect to providing food production and recreational opportunities, and protecting marine ecosystems. 
Unless otherwise noted, all weights in 
this proposed rule are in round weight. 
Lane snapper occur in estuaries and 
shelf waters of the Gulf, and are particularly abundant off south and southwest Florida. Lane snapper in the Gulf exclusive economic zone (EEZ) are managed as a single stock with a stock ACL of 301,000 lb (136,531 kg) that was implemented in 2012 (76 FR 82044; December 29, 2011). This stock ACL is based on average landings from 1999 through 2008. The Council has also established a stock annual catch target (ACT) that is set 14 percent below the ACL, at 259,000 lb (117,480 kg), but the ACT is not codified in the regulations and is not linked to any specific management action, such as a closure. 
The fishing season is open year-round, January 1 through December 31. However, the current AM for lane snapper specifies that if combined commercial and recreational landings exceed the stock ACL in a fishing year, then during the following fishing year, if the stock ACL is reached or is projected to be reached, the commercial and recreational sectors will be closed for the remainder of the fishing year. 
In 2016, a Southeast Data, 
Assessment, and Review (SEDAR) stock assessment (SEDAR 49 2016, ‘‘SEDAR 49’’) was completed for lane snapper and determined that the size of the lane snapper stock was similar to previous estimates. The Council’s Scientific and Statistical Committee (SSC) reviewed SEDAR 49, accepted the assessment as the best scientific information available, and made recommendations to the Council to revise the catch limits. However, because the catch limits based on SEDAR 49 were similar to the established catch limits, the Council decided not to act on the SSC’s recommendation. 
As described in this framework 
action, Gulf lane snapper landings exceeded the stock ACL each year from 2016 through 2019. In 2017, NMFS notified the Council that landings in 2017 exceeded the overfishing limit (OFL), resulting in overfishing. Subsequently, NMFS estimated that 2018 landings did not exceed the 2018 OFL, but did exceed the ACL, and that a closure would be needed in 2019 should the ACL be projected to be met. On December 13, 2019, NMFS closed fishing for lane snapper for the remainder of the year based on a projection that the ACL would be caught. Despite this closure, the ACL was exceeded in 2019. Review of recent landings data indicate this ACL was also exceeded in 2020. 
In 2019, in response to landings data 
that indicated lane snapper experienced overfishing in 2017 and exceeded its ACL in 2018, the Council requested that the NMFS Southeast Fisheries Science Center provide an updated, interim analysis to include landings data from 2015–2018 (SEDAR 49 Update 2019). However, the updated analysis used recreational catch estimate values that were calculated using landings from the 
previous Marine Recreational Information Program (MRIP) Coastal Household Telephone Survey rather than the newer MRIP Fishing Effort Survey (FES). Thus, the Council’s SSC requested that the recreational data used to calculate the estimated catch limits for lane snapper be converted to values directly comparable to those collected 
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