Proposed Rule2021-22112
Addition of Certain Chemicals; Community Right-to-Know Toxic Chemical Release Reporting
Primary source
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Published
October 18, 2021
Issuing agencies
Environmental Protection Agency
Abstract
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.
Full Text
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<title>Federal Register, Volume 86 Issue 198 (Monday, October 18, 2021)</title>
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[Federal Register Volume 86, Number 198 (Monday, October 18, 2021)]
[Proposed Rules]
[Pages 57614-57629]
From the Federal Register Online via the Government Publishing Office [<a href="http://www.gpo.gov">www.gpo.gov</a>]
[FR Doc No: 2021-22112]
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ENVIRONMENTAL PROTECTION AGENCY
40 CFR Part 372
[EPA-HQ-TRI-2017-0434; FRL-5927-03-OCSPP]
RIN 2070-AK26
Addition of Certain Chemicals; Community Right-to-Know Toxic
Chemical Release Reporting
AGENCY: Environmental Protection Agency (EPA).
ACTION: Proposed rule.
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SUMMARY: In response to a petition filed under the Emergency Planning
and Community Right-to-Know Act (EPCRA), EPA is proposing to add 12
chemicals to the list of toxic chemicals subject to the reporting
requirements under EPCRA and the Pollution Prevention Act (PPA). EPA
believes that each of the 12 chemicals meets the EPCRA criteria. In
addition, based on the available bioaccumulation and persistence data,
EPA believes that one chemical should be classified as a persistent,
bioaccumulative, and toxic (PBT) chemical and designated as a chemical
of special concern with a 100-pound reporting threshold.
DATES: Comments must be received on or before December 17, 2021.
ADDRESSES: Submit your comments, identified by docket identification
(ID) number EPA-HQ-TRI-2017-0434, using the Federal eRulemaking Portal
at <a href="http://www.regulations.gov">http://www.regulations.gov</a>. 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 <a href="https://www.epa.gov/dockets">https://www.epa.gov/dockets</a>.
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: <a href="/cdn-cgi/l/email-protection#84e6f1f7ece9e5eaaae0e5eaede1e8c4e1f4e5aae3ebf2"><span class="__cf_email__" data-cfemail="462433352e2b2728682227282f232a0623362768212930">[email protected]</span></a>.
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 <a href="https://www.epa.gov/home/epa-hotlines">https://www.epa.gov/home/epa-hotlines</a>.
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:
<bullet> 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.)
<bullet> 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).
<bullet> Federal facilities: To determine whether your facility
would be affected by this action, you should carefully examine the
applicability criteria in part 372, subpart B of Title 40 of the Code
of Federal Regulations. If you have questions regarding the
applicability of this action to a particular entity, consult the person
listed under FOR FURTHER INFORMATION CONTACT.
B. What action is the Agency taking?
In response to a petition, EPA is proposing to add 12 chemicals to
the EPCRA section 313 toxic chemical list. As discussed in more detail
later in this document, EPA believes that each of the 12 chemicals
meets the EPCRA section 313(d)(2)(B) and/or (C) criteria for listing.
EPA is also proposing to classify one chemical as a PBT chemical of
special concern with a 100-pound reporting threshold.
C. What is the Agency's authority for taking this action?
This action is issued under EPCRA sections 313(d), 313(e)(1) and
328, 42 U.S.C. 11023(d), 11023(e)(1) and 11048. EPCRA is also referred
to as Title III of the Superfund Amendments and Reauthorization Act of
1986.
EPCRA section 313, 42 U.S.C. 11023, requires owners/operators of
certain facilities that manufacture, process, or otherwise use listed
toxic chemicals in amounts above reporting threshold levels to report
their facilities' environmental releases and other waste management
information on such chemicals annually. These facility owners/operators
must also report pollution prevention and recycling data for such
chemicals, pursuant to section 6607 of the PPA, 42 U.S.C. 13106.
Under EPCRA section 313(c), Congress established an initial list of
toxic chemicals subject to EPCRA toxic chemical reporting requirements
that
[[Page 57615]]
was comprised of 308 individually listed chemicals and 20 chemical
categories.
EPCRA section 313(d) authorizes EPA to add or delete chemicals from
the list and sets criteria for these actions. EPCRA section 313(d)(2)
states that EPA may add a chemical to the list if any of the listing
criteria in EPCRA section 313(d)(2) are met. Therefore, to add a
chemical, EPA must determine that at least one criterion is met, but
need not determine whether any other criterion is met. Conversely, to
remove a chemical from the list, EPCRA section 313(d)(3) dictates that
EPA must determine that none of the criteria in EPCRA section 313(d)(2)
are met. The listing criteria in EPCRA section 313(d)(2)(A)-(C) are as
follows:
<bullet> 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.
<bullet> 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.
<bullet> 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):
<bullet> Azodicarbonamide; 123-77-3
<bullet> 1-Bromopropane; 106-94-5
<bullet> 4-Chlorobenzotrichloride; 5216-25-1
<bullet> Cyclododecane; 294-62-2
<bullet> Dibutyltin dichloride; 683-18-1
<bullet> 1,3-Dichloro-2-propanol; 96-23-1
<bullet> Dimethylacetamide; 127-19-5
<bullet> 2,3-Dinitrotoluene; 602-01-7
<bullet> 2,5-Dinitrotoluene; 619-15-8
<bullet> Formamide; 75-12-7
<bullet> 1,2,5,6,9,10-Hexabromocyclododecane; 3194-55-6
<bullet> 1,3,4,6,7,8-Hexahydro-4,6,6,7,8,8-hexamethylcyclopenta[g]-2-
benzopyran; 1222-05-5
<bullet> Hexahydrophthalic anhydride; 85-42-7
<bullet> N-Hydroxyethylethylenediamine; 111-41-1
<bullet> N-Methylformamide; 123-39-7
<bullet> Methylhexahydrophthalic anhydride; 25550-51-0
<bullet> Nitrilotriacetic acid trisodium salt; 5064-31-3
<bullet> Nonylphenol; 25154-52-3
<bullet> Octabromodiphenyl ether; 32536-52-0
<bullet> p-(1,1,3,3-Tetramethylbutyl)phenol; 140-66-9
<bullet> 1,2,3-Trichlorobenzene; 87-61-6
<bullet> Triglycidyl isocyanurate; 2451-62-9
<bullet> Tris(2-chloroethyl) phosphate; 115-96-8
<bullet> Tris(1,3-dichloro-2-propyl) phosphate; 13674-87-8
<bullet> 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:
<bullet> Azodicarbonamide; 123-77-3
<bullet> 4-Chlorobenzotrichloride; 5216-25-1
<bullet> Cyclododecane; 294-62-2
<bullet> Dimethylacetamide; 127-19-5
<bullet> 2,3-Dinitrotoluene; 602-01-7
<bullet> 2,5-Dinitrotoluene; 619-15-8
<bullet> Hexahydrophthalic anhydride; 85-42-7
<bullet> Methylhexahydrophthalic anhydride; 25550-51-0
<bullet> 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 (<a href="https://www.epa.gov/chemical-data-reporting">https://www.epa.gov/chemical-data-reporting</a>) 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 (<a href="http://chm.pops.int/portals/0/repository/poprc4/unep-pops-poprc.4-6.english.pdf">http://chm.pops.int/portals/0/repository/poprc4/unep-pops-poprc.4-6.english.pdf</a>). Given that the
phase out occurred more than ten years ago, it is even more likely
today that there is a negligible amount of OctaBDE remaining that is
processed or otherwise
[[Page 57616]]
used by facilities in the United States. Therefore, EPA is not
proposing to add octabromodiphenyl ether to the EPCRA section 313 list
since EPA expects that no TRI reports would be filed for this chemical.
EPCRA section 313(d)(2) provides EPA the discretion to add chemicals to
the TRI list when there is sufficient evidence to establish any of the
listing criteria. EPA can add a chemical that meets one criterion
regardless of its production volume. However, consistent with the
Agency's previously articulated position on the use of manufacturing
volume thresholds (e.g., 58 FR 63500, December 1, 1993) (FRL-4904-6)
and as in past chemical reviews (e.g., 59 FR 61432, November 30, 1994)
(FRL-4922-2), EPA adopted a production volume screen for the
development of this proposed rule to screen out those chemicals for
which no reports are expected to be submitted. If chemicals that did
not meet the production volume screen were listed, there would be an
economic burden for firms that would have to determine that they did
not exceed the reporting threshold. Since the production volume screen
indicates that no reports would be filed for such chemicals, there
would be no information provided to the public. EPA feels it is
appropriate at this time to focus on chemicals for which reports are
likely to be filed.
In addition to proposing to add 1,3,4,6,7,8-hexahydro-4,6,6,7,8,8-
hexamethylcyclopenta[g]-2-benzopyran to the EPCRA section 313 toxic
chemical list, EPA is proposing to add this chemical to the list of
chemicals of special concern. There are several chemicals and chemical
categories on the EPCRA section 313 chemical list that have been
classified as chemicals of special concern because they are PBT
chemicals (see 40 CFR 372.28(a)(2)). In a final rule published in the
Federal Register of October 29, 1999 (64 FR 58666) (FRL-6389-11), EPA
established the PBT classification criteria for chemicals on the EPCRA
section 313 chemical list. For purposes of EPCRA section 313 reporting,
EPA established persistence half-life criteria for PBT chemicals of 2
months in water, sediment and soil and 2 days in air, and established
bioaccumulation criteria for PBT chemicals as a bioconcentration factor
(BCF) or bioaccumulation factor (BAF) of 1,000 or higher. Most
chemicals meeting the PBT criteria are assigned 100-pound reporting
thresholds. EPA set lower reporting thresholds (10 pounds) for those
PBT chemicals with persistence half-lives of 6 months or more in water,
sediment, or soil and with BCF or BAF values of 5,000 or higher, since
these chemicals are considered highly PBT chemicals. The data presented
in this proposed rule support classifying 1,3,4,6,7,8-hexahydro-
4,6,6,7,8,8-hexamethylcyclopenta[g]-2-benzopyran as a PBT chemical and
designating it as a chemical of special concern with a 100-pound
reporting threshold.
III. What are the 12 chemicals that EPA is proposing to add?
The 12 chemicals that EPA is proposing to add are shown here listed
by name and CASRN (note that some chemical names are different than
those used in the petition because they are listed here using the EPA
Registry Name):
<bullet> Dibutyltin dichloride; 683-18-1
<bullet> 1,3-Dichloro-2-propanol; 96-23-1
<bullet> Formamide; 75-12-7
<bullet> 1,3,4,6,7,8-Hexahydro-4,6,6,7,8,8-hexamethylcyclopenta[g]-2-
benzopyran; 1222-05-5
<bullet> N-Hydroxyethylethylenediamine; 111-41-1
<bullet> Nitrilotriacetic acid trisodium salt; 5064-31-3
<bullet> p-(1,1,3,3-Tetramethylbutyl)phenol; 140-66-9
<bullet> 1,2,3-Trichlorobenzene; 87-61-6
<bullet> Triglycidyl isocyanurate; 2451-62-9
<bullet> Tris(2-chloroethyl) phosphate; 115-96-8
<bullet> Tris(1,3-dichloro-2-propyl) phosphate; 13674-87-8
<bullet> Tris(dimethylphenol) phosphate; 25155-23-1
EPA has determined that each of these chemicals have production and
use levels that would result in TRI reports being filed (Ref. 4).
IV. What is the Agency's evaluation of the toxicity of the 12
chemicals?
EPA prepared hazard assessment documents that reviewed the
available data on human health (Ref. 5) and/or ecological effects (Ref.
6) associated with each of the 12 chemicals being proposed for addition
to the EPCRA section 313 toxic chemical list. Brief summaries of the
available human health and ecological effects information that support
listing these chemicals under EPCRA section 313 are provided in this
Unit. Readers should consult the support documents (Refs. 5 and 6) for
more detailed information.
1. Dibutyltin dichloride (CASRN 683-18-1). Monkey, rat, and mouse
studies indicate that dibutyltin dichloride (DBTC) exposure during
early pregnancy may result in embryo/fetal lethality following exposure
to doses as low as 2.5 milligrams per kilogram per day (mg/kg/day)
(Refs. 7, 8, 9, 10, 11, and 12). In these studies, decreased pre/post
implantation loss, increased resorption, and/or decreased number of
live fetuses/pups were accompanied by maternal body weight effects and/
or clinical signs of toxicity. However, Ema and Harazono (Ref. 7)
indicated that body weight effects alone did not account for
reproductive effects, as effects observed at 15.2 mg/kg/day from
gestation day 0-3 or 4-7 were significantly different than those
observed in pair-fed controls that had similar body weights.
Several studies in rats indicate that maternal exposure to DBTC
during the period of organogenesis causes external, skeletal, and/or
visceral malformations and decreased body weight in fetuses at oral
doses >=5 mg/kg/day (Refs. 8, 9, 10, and 13). An increased incidence of
external and skeletal malformations was observed in fetuses from dams
exposed to doses as low as 5 mg/kg/day DBTC (lowest dose tested) from
gestation day 7-15 (Ref. 8). Maternal toxicity was not observed in this
study until 7.5 mg/kg/day (Ref. 8).
In summary, the available literature provides evidence that DBTC
can be reasonably anticipated to cause serious or irreversible
reproductive and developmental toxicity in humans. Based on the
observed effects and dose levels, EPA considers DBTC to have moderately
high to high toxicity. EPA believes that there is sufficient evidence
for listing DBTC on the EPCRA section 313 toxic chemicals list pursuant
to EPCRA section 313(d)(2)(B) based on the available reproductive and
developmental toxicity data.
DBTC is toxic to aquatic organisms with experimentally determined
acute and chronic toxicity values lower than 1 milligram per liter (mg/
L). The acute aquatic toxicity values for DBTC are as low as 16.7
[micro]g DBTC/L (96-hour median effect concentration (EC<INF>50</INF>)
for growth) in the green algae (Scenedesmus obliquus) (Ref. 14) and
chronic aquatic toxicity values are as low as 20 [micro]g/L for
dibutyltin (DBT) (33-day lowest-observed-effect-concentration (LOEC)
for reduction in shell length) in larvae of the blue mussel (Mytilus
edulis), and 38 [micro]g DBTC/L (210-day LOEC for reduced body weight
and reduced stores of energy substrates) in the duck mussel (Anodonta
anatina) (Ref. 15).
Several studies reported effects of short-term exposure to DBTC on
estuarine and marine invertebrates. Salazar and Salazar (Ref. 16)
observed a significant effect on mortality in mysids (Metamysidopsis
elongata) exposed to DBTC at 56 [micro]g/L for 96 hours, while no
effect on mortality was observed at concentrations of <=11 [micro]g
DBTC/L; the
[[Page 57617]]
96-hour LC<INF>50</INF> was between 11 and 56 [micro]g DBTC/L. Thom et
al. (Ref. 17) exposed the embryos of Pacific oysters (Crassostrea
gigas) to DBTC and found a 48-hour EC<INF>50</INF> of 142 [micro]g
DBTC/L (55.5 [micro]g tin (Sn)/L), based on abnormal larval
development, and a 48-hour LC<INF>50</INF> of 171 [micro]g DBTC/L (66.9
[micro]g Sn/L). In addition to affecting the survival and growth of
aquatic organisms, DBTC has been shown to have adverse effects on the
development of aquatic invertebrates at concentrations of 1 mg/L or
less by causing abnormalities in the embryos of the Pacific oyster (C.
gigas) (Ref. 18), preventing development of embryos of the tunicate
(Styela plicata) to the larval stage (Ref. 19), and increasing the
duration of zoeal development and reducing the dry weight of megalops
larvae of the mud crab (Rhithropanopeus harrisii) (Ref. 20).
Additionally, fish have been found to be more sensitive to DBTC in
early life stages than as adults (Ref. 21). DBTC has been observed to
cause histological changes in the liver, kidney, thymus, eye, and/or
skin of Japanese medaka (Oryzias latipes) and guppy (Poecilia
reticulata) (Refs. 22 and 23), reduced resistance to bacterial
challenge in the rainbow trout (Oncorhynchus mykiss) (Ref. 21), and
increased chromosomal aberrations in the land snail (Truncatella
subcylindrica) (Ref. 24).
In summary, there is evidence for both acute and chronic toxicity
to aquatic organisms exposed to DBTC. DBTC has been shown to cause
lethality and impair growth and development in a wide range of aquatic
species. The acute and chronic aquatic toxicity values indicate that
DBTC is toxic at low concentrations and thus is highly toxic to aquatic
organisms. EPA believes that the evidence is sufficient to list DBTC on
the EPCRA section 313 toxic chemicals list pursuant to EPCRA section
313(d)(2)(C) based on the available ecotoxicity information for this
chemical.
2. 1,3-Dichloro-2-propanol (CASRN 96-23-1). Evidence from an
unpublished 2-year bioassay indicates that 1,3-dichloro-2-propanol
(DC2P) is carcinogenic in male and female rats (Refs. 25 and 26)
following exposure to 240 mg/L in drinking water in rats of both sexes
(19.31 mg/kg/day in males; 29.83 mg/kg/day in females). At the 78-week
interim sacrifice, hepatocellular carcinomas were significantly
increased in the high-dose male and female groups. At the termination
of the study, exposure-related increases in neoplastic lesions were
observed in the liver, kidney, and tongue; neoplasms observed in the
thyroid may also be exposure-related. Additionally, 25 percent of liver
carcinomas in high-dose females metastasized to the lung. Survival was
reduced in both sexes at 240 mg/L over the second year of the study.
Significant exposure-related changes in clinical chemistry observed
predominantly in high-dose animals were indicative of liver damage and
multiple non-neoplastic lesions were observed in both sexes at all
doses in a dose- and duration-dependent manner.
It is reasonable to conclude that DC2P is genotoxic because of the
preponderance of positive in vitro assays, though a limited number of
in vivo studies reported negative results (Refs. 27, 28, 29, 30, 31,
32, 33, 34, 35, 36, 37, 38, 39, 40 (as cited in Ref. 41), and 42 (as
cited in Ref. 39)). The California EPA concluded that DC2P was
``clearly shown through scientifically valid testing according to
generally accepted principles to cause cancer.'' (Ref. 43). Under the
2005 U.S. EPA guidelines (Ref. 44), DC2P is considered likely to be
carcinogenic to humans based on strong evidence of carcinogenicity in
male and female rats in a single adequate study and supporting
mutagenicity data.
In summary, the available literature provides evidence that DC2P
can be reasonably anticipated to cause cancer in humans. EPA considers
chemicals that can reasonably be anticipated to cause cancer to have
moderately high to high chronic toxicity. EPA believes that there is
sufficient evidence for listing DC2P on the EPCRA section 313 toxic
chemicals list pursuant to EPCRA section 313(d)(2)(B) based on the
available carcinogenicity data.
3. Formamide (CASRN 75-12-7). Available data from oral studies,
including a 2-generation study, indicate that formamide is both a
reproductive and developmental toxicant at doses >=87 mg/kg/day (Refs.
45, 46, 47, 48, 49, 50, 51, and 52). These effects, including decreased
pregnancy rates, increased days to litter, decreased live pups/litter,
increased post implantation loss, and fetal variations, were observed
in rats, mice, and rabbits, which serves to strengthen the conclusion
on the potential reproductive and developmental toxicity of formamide.
In two of the gestational exposure studies, fetal effects occurred at
doses lower than overt maternal toxicity (decreased fetal body weights
were observed in Sprague Dawley rats at 100 mg/kg/day and increased
postimplantation loss and fetal variations were observed in NZ white
rabbits at 113 mg/kg/day), suggesting that the developing organism is a
sensitive target for formamide. The available dermal toxicity data
suggest that formamide can cause developmental effects, including
decreased fetal body weight and increased fetal variations and
malformations at >=310 mg/kg/day in rats (Refs. 45, 53, 54, and 55).
In summary, the available literature provides evidence that
formamide can be reasonably anticipated to cause serious or
irreversible reproductive and developmental toxicity in humans. Based
on the observed effects and dose levels, EPA considers formamide to
have moderately high to high toxicity. EPA believes that there is
sufficient evidence for listing formamide on the EPCRA section 313
toxic chemicals list pursuant to EPCRA section 313(d)(2)(B) based on
the available reproductive and developmental toxicity data.
4. 1,3,4,6,7,8-Hexahydro-4,6,6,7,8,8-hexamethylcyclopenta[g]-2-
benzopyran (CASRN 1222-05-5). 1,3,4,6,7,8-Hexahydro-4,6,6,7,8,8-
hexamethylcyclopenta[g]-2-benzopyran (HHCB) is toxic to aquatic
organisms, with experimentally determined acute and chronic toxicity
values lower than 1 mg/L. The experimental data for HHCB from aquatic
toxicity studies includes acute toxicity endpoint values as low as 723
[micro]g/L in algae (72-hour EC<INF>50</INF> for inhibition of biomass
in the microalgal species (Pseudokirchneriella subcapitata) (Ref. 56 as
cited in Ref. 57), 153 [micro]g/L in aquatic invertebrates (96-hour
EC<INF>50</INF> in the mussel (Lampsilis cardium) (Ref. 58)), and 950
[micro]g/L (concentration that is lethal to 50% of the test organisms
(LC<INF>50</INF>)) in fish (O. latipes) larvae (Ref. 59). Chronic
studies also indicate a high concern for environmental hazard with
maximum acceptable toxicant concentration (MATC) values as low as 98
[micro]g/L (36-day MATC for effects on larval survival, growth, and
development in the fathead minnow (Pimephales promelas) (Ref. 60 as
cited in Ref. 57)) and 4.7 [micro]g/L in fish (14-day MATC for
oxidative stress in goldfish (Carassius auratus) (Ref. 61)). Chronic
studies in aquatic invertebrates have found a MATC as low as 53
[micro]g/L (6-day MATC based on inhibition of larval development rate
in the copepod (Acartia tonsa) (Ref. 62 as cited in Ref. 63)).
HHCB bioaccumulates in aquatic organisms. Experimentally-derived
BCFs as high as 1,584 in fish (Lepomis macrochirus) (Ref. 64) and 2,692
in benthic worms (Lumbriculus variegatus) (Ref. 65 as cited in Ref. 63)
have been reported. BCFs for HHCB calculated using the Estimation
Programs Interface Suite<SUP>TM</SUP> (EPI Suite\TM\) (Ref. 66) were
3,629 using the regression-based method and 1,231 using the Arnot-Gobas
model for upper trophic level species, while the bioaccumulation factor
(BAF)
[[Page 57618]]
calculated by EPI Suite\TM\ was 1,826 (Ref. 67). There are no data
available to evaluate the potential for HHCB to biomagnify through the
food chain. Studies have consistently found half-lives longer than two
months for HHCB in soils and sediments (Ref. 68). Envirogen (Ref. 69 as
cited in Ref. 63) reported half-lives in river sediment at 79 days,
forest soil at 95 days, sludge amended soil at 105 days, and
agricultural soil at 239 days. DiFrancesco et al. (Ref. 70 as cited in
Ref. 63) reported half-lives between 140-145 days in four types of
sludge-amended soils.
In summary, the available data demonstrate that HHCB can cause
acute and chronic toxicity to aquatic organisms at concentrations at or
below 1 mg/L. The acute and chronic aquatic toxicity values indicate
that HHCB is highly toxic to aquatic organisms. In addition, HHCB
bioaccumulates and is persistent in the environment. EPA believes that
the evidence is sufficient to list HHCB on the EPCRA section 313 toxic
chemicals list pursuant to EPCRA section 313(d)(2)(C) based on the
available ecotoxicity information for this chemical alone and also
based on its toxicity and persistence in the environment, and toxicity
and tendency to bioaccumulate.
EPA believes that the available bioaccumulation and persistence
data for HHCB support a classification of HHCB as a persistent,
bioaccumulative, and toxic (PBT) chemical. HHCB has been shown to be
bioaccumulative in aquatic species with BCF values greater than 1,000
and to be persistent in soil and sediment for at least 2 months.
Therefore, consistent with EPA's established policy for PBT chemicals
(See 64 FR 58666, October 29, 1999) (FRL-6389-11), EPA is proposing to
designate HHCB as a chemical of special concern with a 100-pound
reporting threshold.
5. N-Hydroxyethylethylenediamine (CASRN 111-41-1). Several rat
studies, including pre-mating though early lactation oral exposure and
gestational oral exposure, indicate that maternal exposure to N-
hydroxyethylethylenediamine can cause malformations of the great
vessels in offspring at gavage doses >=10 mg/kg/day, particularly
aortic aneurysms (Refs. 71, 72, 73, 74, and 75). Other observed
malformations included aneurysms of the pulmonary trunk, dilations of
the carotids and descending aorta, and abnormal course of the carotids.
While some of these studies (Refs. 71, 73, and 74) presented a limited
consideration of material endpoints and lacked litter-based statistics,
studies incorporating these elements reported similar developmental
effects (Refs. 72 and 75). Aortic aneurysms were also observed at
intraperitoneal injection doses >=10 mg/kg/day (Refs. 71 and 76).
Available evidence indicates that, at high enough doses, prenatal
exposure is adequate to induce great vessel malformations; however, the
critical period appears to extend into the early postnatal period since
incidence and severity of great vessel malformations was increased when
exposure extended into the postnatal period (Refs. 77, 78, 79, 80, and
81). This may, in part, explain why no vessel malformations were
observed at doses up to 50 mg/kg-day on GD 6-19 and examination of
fetuses on GD 20 in the EPSDG study (Ref. 75), while aneurysms were
observed with dosing at >=10 mg/kg-day on GD 14-20 and examination of
pups on PND 1 in the Xu et al. study (Ref. 71).
Mechanistic studies indicate that great vessel malformation may be
due to decreased expression of collagen type 1 and 3 in the walls of
the great vessels (Ref. 71). A recent study by Chen et al. (Ref. 82)
concluded that HEED causes significant morphological, biochemical, and
biomechanical alterations in the extracellular matrix in neonatal
aortic vascular smooth muscle cells. Additionally, Moore et al. (Ref.
83) exposed dams to HEED and confirmed exposure of offspring both in
utero and during lactation. HEED did not, however, appear to
specifically concentrate in the great vessels of offspring.
In summary, the available literature provides evidence that N-
hydroxyethyl-ethylenediamine can be reasonably anticipated to cause
serious or irreversible developmental toxicity in humans. Based on the
observed effects and dose levels, EPA considers N-hydroxyethyl-
ethylenediamine to have moderately high to high toxicity. EPA believes
that there is sufficient evidence for listing N-
hydroxyethylethylenediamine on the EPCRA section 313 toxic chemicals
list pursuant to EPCRA section 313(d)(2)(B) based on the available
developmental toxicity data.
6. Nitrilotriacetic acid trisodium salt (CASRN 5064-31-3). Evidence
from bioassays of 18-24 months indicates that nitrilotriacetic acid
trisodium salt (NTA) compounds are carcinogenic in rats and mice (Refs.
84 and 85). Tumors were significantly increased at dietary doses
>=1,200 mg/kg/day in rats of both sexes, >=590 mg/kg/day in male mice,
and 2,600 mg/kg/day in female mice, and at drinking water doses of 81
mg/kg/day in male rats (only dose tested, females not evaluated).
Exposure-related increases in neoplastic lesions were observed in the
urinary tract of male and female rats and mice (kidney, ureter, and/or
bladder), adrenal glands (female rats), liver (female rats), pituitary
gland (male rats), and hematopoietic system (male mice). Significant
non-neoplastic and pre-neoplastic lesions were also observed in the
kidney, lung, bladder, and ureter, especially at the highest doses (at
dietary doses >=1,200 mg/kg/day in rats and at drinking water doses of
81 mg/kg/day in male rats). In rats, nitrilotriacetic acid trisodium
salt monohydrate (Na<INF>3</INF>NTA[middot]H<INF>2</INF>O) was a renal
and bladder tumor promoter, but NTA did not promote bladder tumors
(Refs. 86, 87, 88, 89, 90, and 91). In both the cancer bioassays and
promotion studies featuring multiple dose levels, NTA compounds were
effective at higher doses while showing no activity at lower doses.
This suggests that high levels may be required for promotion or
tumorigenicity. Specific doses that induce activity, however, appear to
differ with route (i.e., carcinogenicity seen at lower doses via
drinking water than via diet). Genotoxicity data, in general, indicate
that NTA compounds do not induce direct genetic effects, although there
is some evidence that they may interfere with normal segregation of
chromosomes (Refs. 92, 93, and 94).
Under the U.S. EPA 2005 guidelines (Ref. 44), NTA is considered
likely to be carcinogenic to humans, based on evidence of
carcinogenicity in male and female rats and mice in three adequate
dietary bioassays reported by the National Cancer Institute (Ref. 85),
along with supporting evidence of carcinogenicity from a drinking water
study using only one dose level (Ref. 84) and tumor promoting activity
of Na3NTA[middot]H2O (Refs. 86, 87, 88, 89, 90, and 91). In addition,
the National Toxicology Program concluded that ``Nitrilotriacetic acid
is reasonably anticipated to be a human carcinogen based on sufficient
evidence of carcinogenicity from studies in experimental animals.'' and
noted that ``exposure to the trisodium salt had the same effects in
rats and also caused kidney tumors and cancer of the ureter in female
rats (Refs. 84 and 85).''
In summary, the available literature provides evidence that
nitrilotriacetic acid trisodium salt can be reasonably anticipated to
cause cancer in humans. EPA considers chemicals that can reasonably be
anticipated to cause cancer to have moderately high to high chronic
toxicity. EPA believes that there is sufficient evidence for listing
nitrilotriacetic acid trisodium salt on the
[[Page 57619]]
EPCRA section 313 toxic chemicals list pursuant to EPCRA section
313(d)(2)(B) based on the available carcinogenicity data.
7. p-(1,1,3,3-Tetramethylbutyl)phenol (CASRN 140-66-9). p-(1,1,3,3-
Tetramethylbutyl)phenol (TMBP) is toxic to aquatic organisms with
experimentally determined acute and chronic toxicity values lower than
1 mg/L. The experimental data for TMBP include acute toxicity endpoint
values as low as 47.9 [micro]g/L in aquatic invertebrates (96-hour
LC<INF>50</INF> in mysid shrimp (Mysidopsis bahia) (Ref. 95)), 120
[micro]g/L in fish (14-day LC<INF>50</INF> in rainbow trout (O. mykiss)
(Ref. 96)), and 0.2 [micro]g/L in amphibians (24-hour LOEC for early
sexual differentiation in bullfrog tadpoles (Rana catesbeiana) (Ref.
97)). Chronic toxicity endpoint values are as low as 0.03 [micro]g/L in
aquatic invertebrates (21-day MATC for delayed nauplii development in
the copepod (Tigriopus japonicas) (Ref. 98)), 1 [micro]g/L in fish (35-
day LOECs for reduced growth in rainbow trout larvae (O. mykiss) (Ref.
99)), and 0.002 [micro]g/L in amphibians (48-week LOEC for
malformations and abnormalities and developmental delay in Northern
leopard frog tadpoles (Rana pipiens) (Refs. 100 and 101)). The majority
of chronic toxic effects on aquatic organisms were due to endocrine
disruption. For example, TMBP mimics the effects of 17[beta]-estradiol
by binding to the estrogen receptor and acting as an estrogen agonist
(Refs. 99, 102, 103, 104, and 105). Examples of estrogenic effects
caused by TMBP in male fish include induction of synthesis of
vitellogenin (an egg yolk protein precursor that is not usually
synthesized in male fish, but can be induced by estrogen), inhibition
of testicular growth and spermatogenesis, and reduction of the
gonadosomatic index (gonad mass as a percentage of total body mass)
(Refs. 106, 107, and 108).
TMBP bioaccumulates in aquatic organisms. Whole fish wet weight
based BCFs determined under controlled experimental conditions at
steady state were 471 in rainbow trout (O. mykiss) and 261 in Japanese
medaka (O. latipes) (Refs. 109 and 110). Wet weight based field BAFs in
fish were similar, ranging from 46 to 297 (Ref. 111). Maximum BAF
values for the blue mussel (M. edulis) were 1,280 when converted to a
wet weight basis (Refs. 112 and 113). A maximum value for phytoplankton
was 2,510 when converted to a wet weight basis (Refs. 112 and 113).
BCFs for TMBP calculated using the Estimation Programs Interface
Suite\TM\ (EPI Suite\TM\) (Ref. 66) were also similar: 243 using the
regression-based method and 302 using the Arnot-Gobas model for upper
trophic level species. There was some evidence of biomagnification in
fish species preying on mussels and in herring gulls feeding on fish
(Ref. 112).
In summary, the available data demonstrate that TMBP can cause
acute and chronic toxicity to aquatic organisms at low concentrations
indicating that TMBP is highly toxic to aquatic organisms. TMBP can
cause lethality and impair growth and reproduction and is also an
endocrine disruptor that may lead to estrogenic effects. TMBP has the
potential to bioaccumulate in aquatic organisms and there is limited
evidence for biomagnification of TMBP. EPA believes that the evidence
is sufficient to list TMBP on the EPCRA section 313 toxic chemicals
list pursuant to EPCRA section 313(d)(2)(C) based on the available
ecotoxicity information for this chemical alone and also based on its
toxicity and tendency to bioaccumulate.
8. 1,2,3-Trichlorobenzene (CASRN 87-61-6). 1,2,3-Trichlorobenzene
(1,2,3-TCB) is toxic to aquatic organisms with experimentally
determined acute and chronic toxicity values lower than 1 mg/L. The
experimental data for 1,2,3-TCB include acute toxicity endpoint values
as low as 330 [micro]g/L in aquatic invertebrates (96-hour
LC<INF>50</INF> in the mysid shrimp (M. bahia) (Ref. 114)) and 350
[micro]g/L in fish (96-hour LC<INF>50</INF> in the guppy (P.
reticulata) (Ref. 115)). Chronic toxicity endpoint values are as low as
22 [micro]g/L in aquatic invertebrates (28-day MATC for inhibition of
reproduction and growth in M. bahia (Ref. 116)) and 44 [micro]g/L in
fish (42-day MATC for reduced growth in the mosquitofish (Gambusia
affinis) (Ref. 117)).
1,2,3-TCB bioaccumulates in aquatic organisms. There are
experimentally-derived BCF values in fish over 1,000 and as high as
5,600 for the fathead minnow (P. promelas) (Ref. 118). A
biomagnification factor (BMF) of 2.3 was estimated by Hendriks et al.
(Ref. 119) for an aquatic food chain.
In summary, based on experimental data from both acute and chronic
studies of aquatic organisms, 1,2,3-TCB is toxic to aquatic organism at
low concentrations. The acute and chronic aquatic toxicity values
indicate that 1,2,3-TCB is highly toxic to aquatic organisms. In
addition, 1,2,3-TCB has been shown to be highly bioaccumulative in
fish. EPA believes that the evidence is sufficient to list 1,2,3-TCB on
the EPCRA section 313 toxic chemicals list pursuant to EPCRA section
313(d)(2)(C) based on the available ecotoxicity information for this
chemical alone and also based on its toxicity and tendency to
bioaccumulate.
9. Triglycidyl isocyanurate (CASRN 2451-62-9). Available animal
toxicology studies on triglycidyl isocyanurate (TGIC) provide evidence
of male reproductive toxicity. For example, a subchronic (13 week) oral
exposure study in rats exposed to 0, 0.72, 2.08, and 7.32 mg/kg/day
TGIC reported a dose-dependent decrease in the mean number of
spermatozoa (0.0%, 5.1%, 13.5%, and 23.1%, respectively) with
statistical significance at the high dose (Ref. 120). No mortalities,
clinical signs of toxicity, or effects on any fertility parameters were
observed during the study. However, although no significant effects on
male rat fertility were observed, a decrease in sperm count could have
biological significance in humans since it is well-known that the human
male is of relatively low fertility and thus may be at greater risk
from effects on sperm parameters than are males of the common
laboratory animal model species (Ref. 121).
Supplemental data from shorter-term exposure studies in mice also
provide some additional supporting evidence for male reproductive
effects following exposure to TGIC. For example, in spermatogonial
cytogenics assays, decreased spermatogonial cell survival was reported
in NS mice exposed orally to a single dose of 115 mg/kg/day (Ref. 122),
but not in CD-1 mice exposed by inhalation (Ref. 122). In a dose-range
finding study, ICR mice demonstrated decreased spermatogonial cell
survival at 667 mg/kg/day administered via oral gavage (Ref. 123). The
differences in responses among these studies may be due to differences
in sensitivity between mice strain and route of exposure. In dominant
lethal assays, although impairment of reproductive performance
(decreased mating index) in CD-1 mice exposed via inhalation was
reported, it occurred at the same level (49.6 mg/m\3\) exhibiting 10%
mortality, decreased body weight, as well as clinical signs of
toxicity, and may not be indicative of reproductive effects (Ref. 124).
Likewise, ICR mice exposed orally failed to show an impairment of male
mice impregnating unexposed females at 550 mg/kg/day (Ref. 125). Of the
few genotoxicity studies of TGIC identified in the literature, TGIC did
not induce chromosomal aberrations in spermatogonial cells in mice
(Ref. 126) but did induce both sister chromatid exchange and
chromosomal aberrations in Chinese hamster ovary cells in vitro (Ref.
127 and Ref. 128).
In summary, the available data indicate that the male reproductive
[[Page 57620]]
system, particularly spermatogonia and spermatozoa, may be a target of
TGIC toxicity. Effects on sperm measurements were seen across two
species (rats and mice) and routes of exposure (oral and inhalation)
following subchronic and shorter-term exposures and collectively
provide sufficient evidence of male reproductive toxicity. Based on the
observed effects and dose levels, EPA considers TGIC to have moderately
high to high toxicity. Therefore, EPA believes there is sufficient
evidence for listing TGIC on the EPCRA section 313 toxic chemicals list
pursuant to EPCRA section 313(d)(2)(B) based on the available
reproductive toxicity data.
10. Tris(2-chloroethyl) phosphate (CASRN 115-96-8). The National
Toxicology Program (NTP) (Ref. 129) performed 2-year oral bioassays of
tris(2-chloroethyl) phosphate (TCEP) in male and female rats and mice.
The NTP concluded there is clear evidence of carcinogenicity in both
male and female rats based on renal tubule adenomas observed at 88 mg/
kg/day and noted that mononuclear cell leukemia and thyroid follicular
cell neoplasms in both sexes may also be exposure related. A
significant increase in the incidence of renal tubule adenomas in male
and female rats was observed at 88 mg/kg/day. From the mouse bioassay,
the NTP concluded that there was equivocal evidence for carcinogenicity
in male mice based on a marginal increase in renal tubule cell
neoplasms and in female mice based on a marginal increase in harderian
gland neoplasms in the main study group (14% incidence at 350 mg/kg/day
versus 6% incidence in controls). The incidence of harderian gland
tumors in females (main study and interim sacrifice groups combined)
was statistically increased at the high dose of 350 mg/kg/day (p
<=0.05) with a significant dose-related trend (p <=0.05). Significant
non-neoplastic and pre-neoplastic lesions occurred in both male and
female rats at 88 mg/kg/day (in the brain stem, cerebrum, and kidney)
and in both male and female mice at >=175 mg/kg/day (in the kidney).
Genotoxicity data indicate that TCEP is not mutagenic, and evidence for
clastogenicity and cell transformation is limited and inconsistent
(Refs. 130, 131, 132, 133, 134, 135, 136 as cite in Ref. 129, 137, and
138).
Under the U.S. EPA 2005 guidelines (Ref. 44), TCEP is considered
likely to be carcinogenic to humans, based on clear evidence of
carcinogenicity in male and female rats and equivocal evidence in male
and female mice in adequate studies performed by NTP (Ref. 129). In
2009, EPA's Office of Research and Development reached the same
conclusion when it derived the provisional peer-reviewed toxicity
values for TCEP (Ref. 139).
Available data indicate that TCEP causes reproductive toxicity in
mice, including sperm alterations and decreases in fertility in treated
males and altered sex ratios in pups. A two-generation study with
continuous breeding protocol showed that oral exposure to TCEP caused a
decrease in the number of live male pups/litter and an altered sex
ratio at 175 mg/kg/day and decreases in the numbers of litters/pair and
live pups/litter at 350 mg/kg/day; a crossover breeding trial indicated
that these effects were predominantly due to effects in male mice,
including decreased fertility and sperm alterations (Ref. 140). Dose-
related sperm alterations in mice have also been reported following
oral exposure to 700 mg/kg/day TCEP for 16 weeks (Ref. 141). Sperm
effects were also noted in an inhalation study in male rats
continuously exposed to >=0.5 mg/m\3\ for 4 months, with decreased
litter size and increased pre- and post-implantation loss observed when
males exposed to 1.5 mg/m\3\ were mated to na[iuml]ve females (Ref. 142
as cited in Ref. 140). There was no evidence of adverse effects in the
female reproductive system in either the two-generation study with
crossover trial or the subchronic reproductive screen (Refs. 129 and
141). A gestational exposure study found no evidence for developmental
toxicity resulting from TCEP exposure (Refs. 143 and 144).
In summary, the available literature provides evidence that TCEP
can be reasonably anticipated to cause cancer and serious or
irreversible reproductive toxicity in humans. EPA considers chemicals
that can reasonably be anticipated to cause cancer to have moderately
high to high chronic toxicity. In addition, based on the observed
reproductive effects and dose levels causing those effects, EPA
considers TCEP to have moderately high to high toxicity. EPA believes
that there is sufficient evidence for listing TCEP on the EPCRA section
313 toxic chemicals list pursuant to EPCRA section 313(d)(2)(B) based
on the available cancer and reproductive toxicity data.
11. Tris(1,3-dichloro-2-propyl) phosphate (CASRN 13674-87-8).
Evidence from a 2-year bioassay indicates that tris(1,3-dichloro-2-
propyl) phosphate (TDCPP) is carcinogenic in male and female rats (Ref.
145). Tumors were significantly increased at >=20 mg/kg/day in rats of
both sexes. Exposure-related increases in neoplastic lesions were
observed in the kidney (both sexes at high dose), liver (both sexes),
testes (males), and adrenal glands (females). Significant non-
neoplastic lesions were also observed in the kidney and liver of male
and female rats and in the epididymides and seminal vesicles of male
rats. Genotoxicity data indicate that TDCPP is mutagenic in bacteria
with metabolic activation, although assays for mutagenicity in
mammalian cells and fruit flies were negative (Refs. 146, 147, 148,
149, 150 and 151). Assays for clastogenicity in mammalian cells in
vitro were positive with activation, but in vivo studies were negative
(Refs. 146, 148, and 152). Results for cell transformation were mixed
(Refs. 146 and 151).
The California EPA concluded that TDCPP was ``clearly shown through
scientifically valid testing according to generally accepted principles
to cause cancer.'' (Ref. 153). Under the U.S. EPA 2005 guidelines (Ref.
44), TDCPP is considered likely to be carcinogenic to humans, based on
strong evidence of carcinogenicity in male and female rats with
multiple tumors in a single yet largely adequate chronic cancer
bioassay study and supporting mutagenicity data of both the primary
compound and metabolites, in bacteria.''
In summary, the available literature provides evidence that TDCPP
can cause cancer at multiple sites in rats and can be reasonably
anticipated to cause cancer in humans based on the animal data and the
overall weight of mutagenicity and genotoxicity in bacteria and
mammalian cells. EPA considers chemicals that can reasonably be
anticipated to cause cancer to have moderately high to high chronic
toxicity. EPA believes that there is sufficient evidence for listing
TDCPP on the EPCRA section 313 toxic chemicals list pursuant to EPCRA
section 313(d)(2)(B) based on the available carcinogenicity data.
TDCPP is toxic to aquatic organisms both from acute and chronic
exposures with acute toxicity below 10 mg/L and chronic toxicity below
0.1 mg/L. Observed acute aquatic toxicity values are as low as 1,400
[micro]g/L (96-hour LC<INF>50</INF>) in rainbow trout (O. mykiss) (Ref.
154). Chronic aquatic toxicity values are below 0.1 mg/L and are as low
as 22 [micro]g/L (142-hour MATC for decreases in body weight and whole-
body thyroxin (T4) content) in zebrafish (Danio rerio) (Ref. 155) and
20 [micro]g/L (116-hour LOEC for effects on mRNA expression of genes
for estrogen and progesterone receptors and vitellogenin) in D. rerio
(Ref. 156). EPA has previously determined that TDCPP is persistent in
the environment with a half-life >60 days (Ref. 157).
[[Page 57621]]
In summary, the acute toxicity data for TDCPP for fish range from 1
to 10 mg/L and chronic aquatic toxicity values range from 20 to 1,000
[micro]g/L. TDCPP has also been shown to be persistent in the
environment. Based on experimental data from both acute and chronic
studies of aquatic organisms, TDCPP is toxic to aquatic organism at low
concentrations. The acute and chronic aquatic toxicity values along
with the persistence data indicate that TDCPP is highly toxic to
aquatic organisms. EPA believes that the evidence is sufficient to list
TDCPP on the EPCRA section 313 toxic chemicals list pursuant to EPCRA
section 313(d)(2)(C) based on the available ecotoxicity data and its
persistence in the environment.
12. Tris(dimethylphenol) phosphate (CASRN 25155-23-1). In a one-
generation reproductive/developmental toxicity screening study in rats,
the pregnancy index was significantly decreased by tris(dimethylphenol)
phosphate (TDMPP) at gavage doses as low as 200 mg/kg/day as
demonstrated by the reduced number of implantations and the decreased
number of gravid dams and successful parturitions (Ref. 158 as cited in
Ref. 159). While these effects were shown to be reversible in the
recovery group (i.e., animals maintained for 4 weeks without exposure,
after which rats were mated), they were accompanied by significant
effects on organ weight and histological changes at doses as low as 25
mg/kg/day. These treatment-related organ weight and histological
changes were also partly reversible in the recovery group.
In summary, the available data provides evidence that TDMPP can be
reasonably anticipated to cause serious or irreversible reproductive
toxicity in humans. Based on the observed effects and dose levels, EPA
considers TDMPP to have moderately high to high toxicity. EPA believes
that there is sufficient evidence for listing TDMPP on the EPCRA
section 313 toxic chemicals list pursuant to EPCRA section 313(d)(2)(B)
based on the available reproductive toxicity data.
V. Why is EPA proposing to list the 12 chemicals and lower the
reporting threshold for HHCB?
A. What is EPA's rationale for listing the 12 chemicals?
Based on EPA's review of the available toxicity data, EPA believes
that the 12 chemicals EPA is proposing to add to the EPCRA section 313
toxic chemical list can reasonably be anticipated to cause either
adverse chronic human health effects at moderately low to low doses
and/or environmental effects at low concentrations. EPA believes that
the data show that these 12 chemicals have moderately high to high
human health toxicity and/or are highly toxic to aquatic organisms.
Therefore, EPA believes that the evidence is sufficient for listing all
12 of the chemicals in this proposed rule on the EPCRA section 313
toxic chemicals list pursuant to EPCRA section 313(d)(2)(B) and/or (C).
EPA does not believe that it is appropriate to consider exposure
for chemicals that are moderately high to highly toxic based on a
hazard assessment when determining if a chemical can be added for
chronic human health effects pursuant to EPCRA section 313(d)(2)(B)
(see 59 FR 61440-61442). EPA also does not believe that it is
appropriate to consider exposure for chemicals that are highly toxic
based on a hazard assessment when determining if a chemical can be
added for environmental effects pursuant to EPCRA section 313(d)(2)(C)
(see 59 FR 61440-61442). Therefore, in accordance with EPA's standard
policy on the use of exposure assessments (see November 30, 1994 (59 FR
61432, FRL-4922-2), EPA does not believe that an exposure assessment is
necessary or appropriate for determining whether any of the chemicals
in this proposed rule meet the criteria of EPCRA section 313(d)(2)(B)
or (C).
B. What is EPA's rationale for lowering the reporting threshold for
HHCB?
EPA believes that the available bioaccumulation and persistence
data for HHCB support a classification of HHCB as a PBT chemical. HHCB
has been shown to be bioaccumulative in aquatic species with BCF values
greater than 1,000 and to persist in soils and sediments with half-
lives greater than 2 months. Therefore, consistent with EPA's
established policy for PBT chemicals (see 64 FR 58666, October 29,
1999) (FRL-6389-11), EPA is proposing to establish a 100-pound
reporting threshold for HHCB.
VI. References
The following is a listing of the documents that are specifically
referenced in this document. The docket includes these documents and
other information considered by EPA, including documents that are
referenced within the documents that are included in the docket, even
if the referenced document is not itself physically located in the
docket. For assistance in locating these other documents, please
consult the person listed under FOR FURTHER INFORMATION CONTACT.
1. Petition from the Massachusetts Toxics Use Reduction Institute
(TURI), University of Massachusetts Lowell, 600 Suffolk St., Suite
501, Lowell, MA 01854, May 6, 2014.
2. USEPA, OPPT. Memorandum from Jocelyn Hospital, Toxicologist,
Regulatory Development Branch to David Turk, Chief, Regulatory
Development Branch. December 8, 2016. Subject: Review of Toxics Use
Reduction Institute (TURI) Petition Chemicals.
3. USEPA, OPPT. Memorandum from Kara Koehrn and Thomas Forbes,
Regulatory Development Branch, to David Turk, Chief, Regulatory
Development Branch. February 16, 2017. Subject: Review of Toxics Use
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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 Gda[nacute]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 <a href="https://www.epa.gov/sites/default/files/2014-11/documents/guidelines_repro_toxicity.pdf">https://www.epa.gov/sites/default/files/2014-11/documents/guidelines_repro_toxicity.pdf</a>.
122. Nissan. 1992. Supplement: Triglycidyl isocyanurate: chromosome
analysis in mouse spermatogonial cells, comparative
[[Page 57625]]
inhalation study with cover letter dated 091892. Nissan Chemical
American Corporation. Submitted under TSCA Section 8E. OTS0503914-
14. 89-920000133.
123. Ciba-Geigy. 1988. Initial submission: Subchronic dose selection
study on 1,3,5-tris(oxiranylmethyl-1,3,5-triazine-2,4,6(1h,3h,5h)-
trione with cover letter dated 08/07/92. Ciba-Geigy Corporation.
Submitted under TSCA Section 8ECP. OTS0555023. 88-920008205.
124. BRRC. 1992. Dominant lethal assay of inhaled PL-90-910 dust in
CD-1 mice. In: Support: 1,3,5-triglycidylisocyanurate: Dominant
lethal assay in CD-1 mice with cover letter dated 11-09-92. Busy Run
Research Center Submitted under TSCA to the U.S. Environmental
Protection Agency Section 8(e). OTS0503914-15.
125. Ciba-Geigy. 1989. Mutagenicity test on Araldite PT-810 in the
mouse spermatogonial cell cytogenetic assay and dominant lethal
assay in mice with cover letter dated 061989 (final reports). Ciba-
Geigy Corporation. Submitted under TSCA Section 8E. OTS0503914-4.
89-890000197.
126. Nissan. 1992. Supplemental information from Nissan chemical
America Corp to USEPA concerning triglycidyl isocyanurate: 5-Day
repeat exposure inhalation toxicity study in the male mouse w-
attach. Nissan Chemical American Corporation. Submitted under TSCA
Section 8E. OTS0503914-13. 89-920000049.
127. Loveday, KS; Anderson, BE; Resnick, MA; Zeiger, E. 1990.
Chromosome aberration and sister chromatid exchange tests in Chinese
hamster ovary cells in vitro: V. Results with 46 chemicals. Environ
Mol Mutagen 16: 272-303.
128. Sofuni, T; Matsuoka, A; Sawada, M; Ishidate, MJ; Zeiger, E;
Shelby, MD. 1990. A comparison of chromosome aberration induction by
25 compounds tested by two Chinese hamster cell (CHL and CHO)
systems in culture. Mutat Res 241: 175-214.
129. NTP. 1991. NTP toxicology and carcinogenesis studies of tris(2-
chloroethyl) phosphate (CAS No. 115-96-8) in F344/N rats and B6C3F1
mice (gavage studies). National Toxicology Program Technical Report
Series 391: 1-233.
130. Aceto Chemical Company Inc. 1977. Nine studies on tris (2-
chloroethyl) phosphate and tris (chloropropyl) phosphate with cover
letter dated 02-09-89. Submitted to the U.S. Environmental
Protection Agency under TSCA Section 8(d).
131. F[ouml]llmann, W., and J. Wober. 2006. Investigation of
cytotoxic, genotoxic, mutagenic, and estrogenic effects of the flame
retardants tris-(2-chloroethyl)-phosphate (TCEP) and tris-(2
chloropropyl)-phosphate (TCPP) in vitro. Toxicol. Lett. 161(2): 124-
134.
132. Haworth, S., T. Lawlor, K. Mortelmans, W. Speck, and E. Zeiger.
1983. Salmonella mutagenicity test results for 250 chemicals.
Environ. Mutagen. 5(Suppl 1): 3-142.
133. Galloway, S.M., M.J. Armstrong, C. Reuben, S. Colman, B. Brown,
C. Cannon, A.D. Bloom, F. Nakamura, M. Ahmed, S. Duk, J. Rimpo, B.H.
Margolin, M.A. Resnick, B. Anderson, and E. Zeiger. 1987. Chromosome
aberrations and sister chromatid exchanges in Chinese hamster ovary
cells: Evaluations of 108 chemicals. Environ. Mol. Mutagen. 10
(Suppl. 10): 1-175.
134. Nakamura, A., N. Tateno, S. Kojima, M.A. Kaniwa, and T.
Kawamura. 1979. The mutagenicity of halogenated alkanols and their
phosphoric acid esters for Salmonella typhimurium. Mutat. Res.
66(4): 373-380.
135. Sala, M., Z.G. Gu, G. Moens, and I. Chouroulinkov. 1982. In
vivo and in vitro biological effects of the flame retardants
tris(2,3-dibromopropyl) phosphate and tris(2-
chlorethyl)orthophosphate. Eur. J. Cancer Clin. Oncol. 18(12): 1337-
1344.
136. Simmon, V.F. and K. Kauhanen. 1978. In vitro microbiological
mutagenicity assays of tris(2-chloroethyl)phosphate. Report 11 (as
cited in Ref. 125).
137. Simmon, V.F., K. Kauhanen, and R.G. Tardiff. 1977. Mutagenic
activity of chemicals identified in drinking water. Dev. Toxicol.
Environ. Sci. 2: 249-258.
138. Vogel, E.W. and M.J. Nivard. 1993. Performance of 181 chemicals
in a Drosophila assay predominantly monitoring interchromosomal
mitotic recombination. Mutagenesis 8(1): 57-81.
139. USEPA. 2009. Provisional peer-reviewed Toxicity values for
tris(2-chloroethyl) phosphate (CAS No. 115-96-8). U.S. Environmental
Protection Agency. Washington, DC Available at: <a href="http://hhpprtv.ornl.gov/issue_papers/Tris2chloroethylphosphate.pdf">http://hhpprtv.ornl.gov/issue_papers/Tris2chloroethylphosphate.pdf</a>.
140. NTP. 1991. Final report on the reproductive toxicity of tris(2-
chloroethyl)phosphate reproduction and fertility assessment in Swiss
CD-1 mice when administered via gavage. NTIS Technical Report
129170(253).
141. Morrissey, R. E., B.A. Schwetz, J.C. Lamb, M.D. Ross, J.L.
Teague, and R.W. Morris. 1988. Evaluation of rodent sperm vaginal
cytology and reproductive organ weight data from National Toxicology
Program 13-week studies. Fundam. Appl. Toxicol. 11(2): 343-358.
142. Shepel'skaia, N R. and NE Dyshginevich. 1981. Experimental
study of the gonadotoxic effect of tri- (chloroethyl)-phosphate.
Gig. Sanit. (6): 20-21 (as cited in Ref. 136).
143. NIOSH. 1983. Screening of priority chemicals for potential
reproductive hazard (Final Report) with attachments and cover sheet.
Atlanta, GA: Centers for Disease Control, U.S. Department of Health
and Human Services.
144. Hardin, B.D., R.L. Schuler, J.R. Burg, G.M. Booth, K.P.
Hazelden, K.M. Mackenzie, V.J. Piccirillo, and K.N. Smith. 1987.
Evaluation of 60 chemicals in a preliminary developmental toxicity
test. Teratogen. Carcinogen. Mutagen. 7: 29-48.
145. Stauffer Chemical Company. 1981. A two-year oral toxicity/
carcinogenicity study of FYROL FR-2 in rats. (Volume I-IV). (Final
Reports) with attachments, cover sheets and letter dated 09-30-81.
Submitted to the U.S. Environmental Protection Agency under TSCA
Section 8(e), pages 580-2180.
146. Brusick, D., D. Matheson, D.R. Jagannath, S. Goode, H.
Lebowitz, M. Reed, G. Roy, and S. Benson. 1979. A comparison of the
genotoxic properties of tris(2,3-dibromopropyl)phosphate and
tris(1,3-dichloro-2-propyl)phosphate in a battery of short-term
bioassays. J. Environ. Pathol. Toxicol. 3(1-2): 207-226.
147. Gold, M.D., A. Blum, and B.N. Ames. 1978. Another flame
retardant, tris-(1,3-dichloro-2-propyl)-phosphate, and its expected
metabolites are mutagens. Science 200(4343): 785-787.
148. Ishidate, M.J. 1981. Application of chromosomal aberration
tests in vitro to the primary screening for chemicals with
carcinogenic and/or genetic hazards. Tests Courts Cancerog Quo
Vadis: 57-79.
149. Lynn, R.K., K. Wong, C. Garvie-Gould, and J.M. Kennish. 1981.
Disposition of the flame retardant, tris(1,3-dichloro-2-propyl)
phosphate, in the rat. Drug Metab. Disp. 9(5): 434-441.
150. Mortelmans, K., S. Haworth, T. Lawlor, W. Speck, B. Tainer, and
E. Zeiger. 1986. Salmonella mutagenicity tests. 2. Results from the
testing of 270 chemicals. Environ. Mutagen. 8(Suppl 7): 1-119.
151. Soderlund, E.J., E. Dybing, J.A. Holme, J.K. Hongslo, E.
Rivedal, T. Sanner, and S.D. Nelson. 1985. Comparative genotoxicity
and nephrotoxicity studies of the two halogenated flame retardants
tris(1,3-dichloro-2-propyl)phosphate and tris(2,3-
dibromopropyl)phosphate. Acta Pharmacol. Toxicol. 56(1): 20-29.
152. Bloom, SE 1984. Sister chromatid exchange studies in the chick
embryo and neonate: Actions of mutagens in a developing system.
Basic Life Sci. 29B: 509-533.
153. OEHHA 2011. Evidence on the Carcinogenicity of Tris(1,3-
dichloro-2-propyl)phosphate.
154. Jenkins, C.A. 1990. FYROL FR-2: Acute toxicity to rainbow
trout. Life Science Research Limited, Suffolk, U.K. Report No. 90/
AKL027/0234, 20 pp. TSCA 8D; OTS0528355, DCN: 86-910000061.
155. Wang, Q., K. Liang, J. Liu, L. Yang, Y. Guo, C. Liu, and B.
Zhou. 2013. Exposure of zebrafish embryos/larvae to TDCPP alters
concentrations of thyroid hormones and transcriptions of genes
involved in the hypothalamic-pituitary-thyroid axis. Aquatic
Toxicol. 126: 207-213.
156. Liu, C., Q. Wang, K. Liang, J. Liu, B. Zhou, X. Zhang, H. Liu,
J.P. Giesy, and H. Yu. 2013. Effects of tris(1,3-dichloro-2-propyl)
phosphate and triphenyl phosphate on receptor-associated mRNA
expression in zebrafish embryos/larvae. Aquatic Toxicol. 128-129:
147-157.
157. USEPA. 2015. Flame Retardants Used in Flexible Polyurethane
Foam: An Alternatives Assessment Update. Design for the Environment,
August 2015, EPA 744-R-15-002.
158. Akzo Nobel Functional Chemicals LLC. 2004. Combined repeated
dose with
[[Page 57626]]
reproductive and developmental toxicity study in rats by oral
gavage. Submitted to the U.S. Environmental Protection Agency under
TSCA Section 8(e).
159. ECHA. 2010. Background Document to the Committee for Risk
Assessment on a Proposal for Harmonised Classification and Labelling
of Trixylyl Phosphate. EC number: 246-677-8. CAS number: 25155-23-1.
European Chemicals Agency. Final 27 January 2010.
VII. What are the statutory and Executive Orders reviews associated
with this action?
Additional information about these statutes and Executive Orders
can be found at <a href="http://www2.epa.gov/laws-regulations/laws-and-executive-orders">http://www2.epa.gov/laws-regulations/laws-and-executive-orders</a>.
A. Executive Order 12866: Regulatory Planning and Review and Executive
Order 13563: Improving Regulation and Regulatory Review
This action is not a significant regulatory action and was
therefore not submitted to the Office of Management and Budget (OMB)
for review under Executive Orders 12866 (58 FR 51735, October 4, 1993)
and 13563 (76 FR 3821, January 21, 2011).
B. Paperwork Reduction Act (PRA)
This action does not contain any new information collection
activities that require additional approval by OMB under the PRA, 44
U.S.C. 3501 et seq. OMB has previously approved the information
collection activities contained in the existing regulations and has
assigned OMB control numbers 2070-0212 (EPA ICR No. 2613.02, entitled
``Toxic Chemical Release Reporting'') and 2050-0078 (EPA ICR No.
1428.11, entitled ``Trade Secret Claims for Community Right-to-Know and
Emergency Planning''). Currently, the facilities subject to the
reporting requirements under EPCRA section 313 and PPA section 6607 may
use either the EPA Toxic Chemicals Release Inventory Form R (EPA Form
9350-1), or the EPA Toxic Chemicals Release Inventory Form A (EPA Form
9350-2). The Form R must be completed if a facility manufactures,
processes, or otherwise uses any listed chemical above threshold
quantities and meets certain other criteria. For the Form A, EPA
established an alternative threshold for facilities with low annual
reportable amounts of a listed toxic chemical. A facility that meets
the appropriate reporting thresholds, but estimates that the total
annual reportable amount of the chemical does not exceed 500 pounds per
year, can take advantage of an alternative manufacture, process, or
otherwise use threshold of 1 million pounds per year of the chemical,
provided that certain conditions are met, and submit the Form A instead
of the Form R. In addition, respondents may designate the specific
chemical identity of a substance as a trade secret pursuant to EPCRA
section 322, 42 U.S.C. 11042, 40 CFR part 350.
OMB has approved the reporting and recordkeeping requirements
related to Forms A and R, supplier notification, and petitions under
OMB Control number 2070-0212 and those related to trade secret
designations under OMB Control 2050-0078. As provided in 5 CFR
1320.5(b) and 1320.6(a), an Agency may not conduct or sponsor, and a
person is not required to respond to, a collection of information
unless it displays a currently valid OMB control number. The OMB
control numbers relevant to EPA's regulations are listed in 40 CFR part
9 and displayed on the information collection instruments (e.g., forms,
instructions).
C. Regulatory Flexibility Act (RFA)
I certify that this action will not have a significant economic
impact on a substantial number of small entities under the RFA, 5
U.S.C. 601 et seq. The small entities subject to the requirements of
this action are small manufacturing facilities. The Agency has
determined that of the 488 entities estimated to be impacted by this
action, 449 are small businesses; no small governments or small
organizations are expected to be affected by this action. All 449 small
businesses affected by this action are estimated to incur annualized
cost impacts of less than 1% of annual revenue or sales. Thus, this
action is not expected to have a significant adverse economic impact on
a substantial number of small entities. A more detailed analysis of the
impacts on small entities is provided in EPA's economic analysis (Ref.
4).
D. Unfunded Mandates Reform Act (UMRA)
This action does not contain an unfunded mandate of $100 million or
more as described in UMRA, 2 U.S.C. 1531-1538, and does not
significantly or uniquely affect small governments. This action is not
subject to the requirements of UMRA because it contains no regulatory
requirements that might significantly or uniquely affect small
governments. EPA did not identify any small governments that would be
impacted by this action. EPA's economic analysis indicates that the
total cost of this action is estimated to be $2,057,000 in the first
year of reporting (Ref. 4).
E. Executive Order 13132: Federalism
This action does not have federalism implications as specified in
Executive Order 13132 (64 FR 43255, August 10, 1999). It will not have
substantial direct effects on the States, on the relationship between
the national government and the States, or on the distribution of power
and responsibilities among the various levels of government.
F. Executive Order 13175: Consultation and Coordination With Indian
Tribal Governments
This action does not have tribal implications as specified in
Executive Order 13175 (65 FR 67249, November 9, 2000). This action
relates to toxic chemical reporting under EPCRA section 313, which
primarily affects private sector facilities. Thus, Executive Order
13175 does not apply to this action.
G. Executive Order 13045: Protection of Children From Environmental
Health Risks and Safety Risks
EPA interprets Executive Order 13045 (62 FR 19885, April 23, 1997)
as applying only to those regulatory actions that concern environmental
health or safety risks that EPA has reason to believe may
disproportionately affect children, per the definition of ``covered
regulatory action'' in section 2-202 of the Executive Order. This
action is not subject to Executive Order 13045 because it does not
concern an environmental health risk or safety risk.
H. Executive Order 13211: Actions Concerning Regulations that
Significantly Affect Energy Supply, Distribution, or Use
This action is not subject to Executive Order 13211 (66 FR 28355,
May 22, 2001), because it is not a significant regulatory action under
Executive Order 12866.
I. National Technology Transfer and Advancement Act (NTTAA)
This rulemaking does not involve any technical standards subject to
NTTAA section 12(d) (15 U.S.C. 272 note).
J. Executive Order 12898: Federal Actions To Address Environmental
Justice in Minority Populations and Low-Income Populations
The EPA believes that this action is not subject to Executive Order
12898 (59 FR 7629, February 16, 1994) because it does not establish an
environmental health or safety standard. This regulatory action adds
additional chemicals to the EPCRA section 313 reporting requirements;
it does not have
[[Page 57627]]
any impact on human health or the environment. This action does not
address any human health or environmental risks and does not affect the
level of protection provided to human health or the environment. The
addition of these chemicals to the EPCRA section 313 reporting
requirements will provide information that government agencies and
others can use to identify potential problems, set priorities, and help
inform activities.
List of Subjects in 40 CFR Part 372
Environmental protection, Community right-to-know, Reporting and
recordkeeping requirements, and Toxic chemicals.
Dated: October 6, 2021.
Michal Freedhoff,
Assistant Administrator, Office of Chemical Safety and Pollution
Prevention.
Therefore, for the reasons stated in the preamble, it is proposed
that 40 CFR chapter I be amended as follows:
PART 372--TOXIC CHEMICAL RELEASE REPORTING: COMMUNITY RIGHT-TO-KNOW
0
1. The authority citation for part 372 continues to read as follows:
Authority: 42 U.S.C. 11023 and 11048.
0
2. In Sec. 372.28, amend the table in paragraph (a)(1) by:
0
a. Revising the third column header to read ``Reporting threshold (in
pounds),'' and
0
b. Adding the chemical ``1,3,4,6,7,8-Hexahydro-4,6,6,7,8,8-
hexamethylcyclopenta[g]-2- benzopyran'' in alphabetical order.
The revision and addition read as follows:
Sec. 372.28 Lower thresholds for chemicals of special concern.
(a) * * *
(1) * * *
Table to Paragraph (a) (1)
------------------------------------------------------------------------
Reporting
Chemical name CAS No. threshold (in
pounds)
------------------------------------------------------------------------
* * * * * * *
1,3,4,6,7,8-Hexahydro-4,6,6,7,8,8- 1222-05-5 100
hexamethylcyclopenta[g]-2- benzopyran..
* * * * * * *
------------------------------------------------------------------------
* * * * *
0
3. Amend Sec. 372.65 by:
0
a. Adding new entries in alphabetical order in table 1 to paragraph (a)
for ``Dibutyltin dichloride,'' ``1,3-Dichloro-2-propanol,''
``Formamide,'' ``1,3,4,6,7,8-Hexahydro-4,6,6,7,8,8-
hexamethylcyclopenta[g]-2- benzopyran,'' ``N-
Hydroxyethylethylenediamine,'' ``Nitrilotriacetic acid trisodium
salt,'' ``p-(1,1,3,3-Tetramethylbutyl)phenol,'' ``1,2,3-
Trichlorobenzene,'' ``Triglycidyl isocyanurate,'' ``Tris(2-chloroethyl)
phosphate,'' ``Tris(1,3-dichloro-2-propyl) phosphate,'' and
``Tris(dimethylphenol) phosphate''; and
0
b. Adding new entries in alphabetical order in the table 2 to paragraph
(b) for ``Formamide,'' ``1,2,3-Trichlorobenzene,'' ``1,3-Dichloro-2-
propanol,'' ``N-Hydroxyethylethylenediamine,'' ``Tris(2-chloroethyl)
phosphate,'' ``p-(1,1,3,3-Tetramethylbutyl)phenol,'' ``Dibutyltin
dichloride,'' ``1,3,4,6,7,8-Hexahydro-4,6,6,7,8,8-
hexamethylcyclopenta[g]-2- benzopyran,'' ``Triglycidyl isocyanurate,''
``Nitrilotriacetic acid trisodium salt,'' ``Tris(1,3-dichloro-2-propyl)
phosphate,'' and ``Tris(dimethylphenol) phosphate''.
The additions read as follows:
Sec. 372.65 Chemicals and chemical categories to which this part
applies.
* * * * *
(a) * * *
Table 1 to Paragraph (a)
------------------------------------------------------------------------
Chemical name CAS No. Effective date
------------------------------------------------------------------------
* * * * * * *
Dibutyltin dichloride................... 683-18-1 1/1/23
* * * * * * *
1,3-Dichloro-2-propanol................. 96-23-1 1/1/23
* * * * * * *
Formamide............................... 75-12-7 1/1/23
* * * * * * *
1,3,4,6,7,8-Hexahydro-4,6,6,7,8,8- 1222-05-5 1/1/23
hexamethylcyclopenta[g]-2- benzopyran..
* * * * * * *
N-Hydroxyethylethylenediamine........... 111-41-1 1/1/23
* * * * * * *
Nitrilotriacetic acid trisodium salt.... 5064-31-3 1/1/23
* * * * * * *
p-(1,1,3,3-Tetramethylbutyl)phenol...... 140-66-9 1/1/23
[[Page 57628]]
* * * * * * *
1,2,3-Trichlorobenzene.................. 87-61-6 1/1/23
* * * * * * *
Triglycidyl isocyanurate................ 2451-62-9 1/1/23
* * * * * * *
Tris(2-chloroethyl) phosphate........... 115-96-8 1/1/23
* * * * * * *
Tris(1,3-dichloro-2-propyl) phosphate... 13674-87-8 1/1/23
* * * * * * *
Tris(dimethylphenol) phosphate.......... 25155-23-1 1/1/23
* * * * * * *
------------------------------------------------------------------------
* * * * *
(b) * * *
Table 2 to Paragraph (b)
------------------------------------------------------------------------
CAS No. Chemical name Effective date
------------------------------------------------------------------------
* * * * * * *
75-12-7.................... Formamide.................. 1/1/23
* * * * * * *
87-61-6.................... 1,2,3-Trichlorobenzene..... 1/1/23
* * * * * * *
96-23-1.................... 1,3-Dichloro-2-propanol.... 1/1/23
* * * * * * *
111-41-1................... N- 1/1/23
Hydroxyethylethylenediamin
e.
* * * * * * *
115-96-8................... Tris(2-chloroethyl) 1/1/23
phosphate.
* * * * * * *
140-66-9................... p-(1,1,3,3- 1/1/23
Tetramethylbutyl)phenol.
* * * * * * *
683-18-1................... Dibutyltin dichloride...... 1/1/23
* * * * * * *
1222-05-5.................. 1,3,4,6,7,8-Hexahydro- 1/1/23
4,6,6,7,8,8-
hexamethylcyclopenta[g]-2-
benzopyran.
* * * * * * *
2451-62-9.................. Triglycidyl isocyanurate... 1/1/23
* * * * * * *
5064-31-3.................. Nitrilotriacetic acid 1/1/23
trisodium salt.
* * * * * * *
13674-87-8................. Tris(1,3-dichloro-2-propyl) 1/1/23
phosphate.
* * * * * * *
25155-23-1................. Tris(dimethylphenol) 1/1/23
phosphate.
* * * * * * *
------------------------------------------------------------------------
[[Page 57629]]
[FR Doc. 2021-22112 Filed 10-15-21; 8:45 am]
BILLING CODE 6560-50-P
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</html>Indexed from Federal Register on October 18, 2021.
This is legal information, not legal advice. Laws vary by jurisdiction and change frequently. Always verify current law with official sources and consult a licensed attorney in your jurisdiction for advice on your specific situation.