Document ID: EPA-HQ-TRI-2022-0262-0263
Agency: epa
Document Type: Rule
Title: Addition of Diisononyl Phthalate Category; Community Right-to-Know Toxic Chemical Release Reporting
Posted Date: 2023-07-14T04:00Z

[Federal Register Volume 88, Number 134 (Friday, July 14, 2023)]
[Rules and Regulations]
[Pages 45089-45098]
From the Federal Register Online via the Government Publishing Office [www.gpo.gov]
[FR Doc No: 2023-14642]

[[Page 45089]]

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ENVIRONMENTAL PROTECTION AGENCY

40 CFR Part 372

[EPA-HQ-TRI-2022-0262; FRL-2425.1-03-OCSPP]
RIN 2025-AA17

Addition of Diisononyl Phthalate Category; Community Right-to-
Know Toxic Chemical Release Reporting

AGENCY: Environmental Protection Agency (EPA).

ACTION: Final rule.

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SUMMARY: The Environmental Protection Agency (EPA) is adding a 
diisononyl phthalate (DINP) category to the list of toxic chemicals 
subject to the reporting requirements under the Emergency Planning and 
Community Right-to-Know Act (EPCRA) and the Pollution Prevention Act 
(PPA). In this action, EPA is adding the DINP category to the toxic 
chemical list as a category defined to include branched alkyl di-esters 
of 1,2 benzenedicarboxylic acid in which alkyl ester moieties contain a 
total of nine carbons. The DINP category meets the EPCRA chronic human 
health effects toxicity criterion because the members of the category 
can reasonably be anticipated to cause serious or irreversible 
reproductive dysfunctions as well as other serious or irreversible 
chronic health effects in humans, specifically, developmental, kidney, 
and liver toxicity.

DATES: The final rule is effective on September 12, 2023.

ADDRESSES: The docket for this action, identified by docket 
identification (ID) number EPA-HQ-TRI-2022-0262, is available at 
https://www.regulations.gov. Additional instructions on visiting the 
docket, along with more information about dockets generally, is 
available at https://www.epa.gov/dockets.

FOR FURTHER INFORMATION CONTACT:
    For technical information contact: Rachel Dean, Data Gathering and 
Analysis Division (7406M), Office of Pollution Prevention and Toxics, 
Environmental Protection Agency, 1200 Pennsylvania Ave. NW, Washington, 
DC 20460-0001; telephone number: (202) 566-1303; email: 
[email protected].
    For general information contact: The Emergency Planning and 
Community Right-to-Know Hotline; telephone numbers: toll free at (800) 
424-9346 (select menu option 3) or (703) 348-5070 in the Washington, DC 
Area and International; or go to https://www.epa.gov/home/epa-hotlines.

SUPPLEMENTARY INFORMATION: 

I. Executive Summary

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 
chemicals in the diisononyl phthalate (DINP) category. 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. Facilities 
subject to reporting under EPCRA section 313 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*, 212323*, 212390*, 488390*, 512230*, 512250*, 5131*, 
516210*, 519290*, 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): 
211130* (corresponds to SIC code 1321, Natural Gas Liquids, and SIC 
2819, Industrial Inorganic Chemicals, Not Elsewhere Classified); or 
212114, 212115, 212220, 212230, 212290*; or 2211*, 221210*, 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, 424710 
(corresponds to SIC code 5171, Petroleum Bulk Terminals and Plants); 
425120 (limited to facilities previously classified in SIC code 5169, 
Chemicals and Allied Products, Not Elsewhere Classified); 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). *Exceptions and/or limitations exist for 
these NAICS codes.
     Federal facilities.
     Facilities that the EPA Administrator has specifically 
required to report to TRI pursuant to a determination under EPCRA 
section 313(b)(2).
    A more detailed description of the types of facilities covered by 
the NAICS codes subject to reporting under EPCRA section 313 can be 
found at: https://www.epa.gov/toxics-release-inventory-tri-program/tri-covered-industry-sectors. To determine whether your facility would be 
affected by this action, you should carefully examine the applicability 
criteria in 40 CFR part 372, subpart B. 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 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 PPA section 6607, 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 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 the Administrator 
determines, in his judgment, that there is sufficient evidence to 
establish that 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 delete a chemical from the list, EPCRA 
section 313(d)(3) dictates that EPA must determine that there is not 
sufficient evidence to establish any of the criteria described in EPCRA 
section 313(d)(2). 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

[[Page 45090]]

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) 
providing guidance regarding the recommended content of and format for 
petitions. On May 23, 1991 (56 FR 23703), 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.

C. What action is the Agency taking?

    In response to a petition, EPA is adding DINP as a category to the 
list of toxic chemicals subject to the reporting requirements under 
section 313 of EPCRA. As discussed in more detail later in this 
document, EPA is concluding that the members of the DINP category meet 
the EPCRA section 313(d)(2)(B) criterion for listing.
    Additionally, as indicated in the supplemental proposal and as is 
now being finalized via this rulemaking, EPA is listing DINP as a 
chemical category that includes all branched alkyl di-esters of 1,2 
benzenedicarboxylic acid in which alkyl ester moieties contain a total 
of nine carbons. This category includes but is not limited to the 
chemicals covered by the CAS numbers and names identified by EPA at the 
time of this rulemaking. In the supplemental proposal, EPA identified 
the following chemicals: Diisononyl phthalate (CAS Number 28553-12-0), 
Branched dinonyl phthalate (CAS Number 71549-78-5), Branched dinonyl 
phthalate (CAS Number 14103-61-8), and Di(C8-10, C9 rich) branched 
alkyl phthalate (CAS Number 68515-48-0). EPA has since identified that 
Bis(7-methyloctyl) phthalate (CAS Number 20548-62-3) and Bis(3-
ethylheptan-2-yl) benzene-1,2-dicarboxylate (CAS Number 111983-10-9) 
also meet the definition of DINP being used for this listing and thus 
are also being included in the listing at 40 CFR 372.65(c) to assist 
facilities in identifying members of the DINP chemical category.
    Further, in response to public comments and further review of 
available information, EPA has updated the 2022 Technical Review of 
DINP (Ref. 1) provided with the supplemental notice of proposed 
rulemaking (87 FR 48128, August 8, 2022). The updated 2023 Technical 
Review of DINP (Ref. 2) is in the docket for this rule. For the reasons 
more fully explained in the updated 2023 Technical Review of DINP (Ref. 
2), EPA is now listing the DINP category based on our conclusion that 
it is reasonably anticipated to cause serious or irreversible 
reproductive dysfunctions and other serious or irreversible chronic 
health effects in humans, including developmental, kidney, and liver 
toxicity. EPA has determined that the DINP can reasonably be 
anticipated to cause serious or irreversible chronic human health 
effects at moderately low to low doses and thus data show that DINP has 
moderately high to high human health toxicity.
    As indicated previously, EPCRA section 313(d)(2) states that EPA 
may add a chemical to the list if the Administrator determines, in his 
judgment, that there is sufficient evidence to establish that 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. Accordingly, 
EPA is basing this addition on its conclusion that DINP is reasonably 
anticipated to cause serious or irreversible reproductive dysfunctions 
and other serious or irreversible chronic health effects in humans, 
including developmental, kidney, and liver toxicity.
    Given multiple endpoint findings of serious or irreversible chronic 
noncancer health effects, it was not necessary for the Agency to rely 
on hazards related to cancer concerns as a basis for a TRI listing of a 
DINP chemical category. The Agency is not, with this action, taking a 
position as to whether or not DINP presents cancer concerns that would 
support a TRI listing of the chemical category. In response to comments 
received on the supplemental proposal, EPA has updated it hazard 
analysis to include additional literature on cancer-related research on 
DINP. However, EPA is forgoing further analysis of this particular 
topic as it relates to the EPCRA 313 listing criteria. Given 
forthcoming additional hazard analyses being conducted by the EPA 
(e.g., pursuant to section 6 of the Toxic Substances Control Act) and 
ensuring that the Agency has adequate resources to conduct its other 
TRI activities, EPA has determined it appropriate to reduce the scope 
of analysis for purposes of this listing.

D. Why is the Agency taking this action?

    EPA is taking this action in response to a petition submitted under 
EPCRA section 313(e)(1) (Ref.3). In this case, EPA is granting the 
petition to list DINP. Additional details about the petition are 
included in the 2000 proposed rule and the 2022 supplemental proposed 
rule (87 FR 48128, August 8, 2022).

E. What are the estimated incremental impacts of this action?

    EPA prepared an economic analysis for this action entitled, 
``Economic Analysis for the Addition of Diisononyl Phthalate Category; 
Community Right-to-Know Toxic Chemical Release Reporting'' (Ref. 4), 
which presents an analysis of the costs of the addition of the DINP 
category. EPA estimates that this action would result in an additional 
198 to 396 reports being filed annually. EPA estimates that the costs 
of this action will be approximately $968,546 to $1,935,041 in the 
first year of reporting and approximately $461,212 to $921,448 in the 
subsequent years. In addition, EPA has determined that of the 181 to 
365 small businesses affected by this action, none are estimated to 
incur annualized cost impacts of more than 1%. Thus, this action is not 
expected to have a significant adverse economic impact on a substantial 
number of small entities.

II. Summary of Proposed Rule

    On September 5, 2000 (65 FR 53681; FRL-6722-3), in response to a 
petition filed under the EPCRA, EPA issued a proposed rule to add a 
DINP category to the list of toxic chemicals subject to the reporting 
requirements under EPCRA section 313 and PPA section 6607. EPA proposed 
to add this chemical category

[[Page 45091]]

to the EPCRA section 313 toxic chemical list based on the Agency's 
preliminary conclusion that this category met the EPCRA chronic human 
health effects toxicity criterion. In response to comments on the 
proposal, EPA revised its hazard assessment for DINP and issued a 
notice of data availability (NODA) requesting comments on the revised 
hazard assessment (70 FR 34437, June 14, 2005 (FRL-7532-4)). In the 
NODA, EPA proposed to list DINP based on serious or irreversible 
chronic health effects including liver, kidney, and developmental 
toxicity but reserved judgment on whether cancer was an endpoint of 
concern for DINP. On August 8, 2022 (87 FR 48128; FRL-2425.1-04-OCSPP), 
EPA published a supplemental proposal, providing updated supporting 
materials for the proposal (e.g., hazard assessment for DINP (i.e., 
2022 Technical Review of DINP) (Ref. 1)).

III. Summary of Comments Received and EPA Responses

    EPA received 15 comments on the supplemental proposed rule. Two 
comments came from trade associations: the American Chemistry Council 
(ACC) and the National Association of Chemical Distributors (NACD). Two 
comments came from environmental/public interest groups: Earthjustice 
(including Alaska Community Action on Toxics, Breast Cancer Prevention 
Partners, Center for Environmental Health, Center for Food Safety, 
Defend Our Health, Learning Disabilities Association of America, Sierra 
Club) and Environmental Defense Fund (EDF). One comment also came from 
an individual company: UPC Technology Corporation (UPC). Nine of the 
on-topic comments came from both private citizens and an anonymous 
commenter. There was also one off-topic anonymous comment. This unit 
provides summaries of the most significant comments and EPA's 
responses. A complete set of comments and EPA's detailed responses can 
be found in the Response to Comments (RTC) document that is available 
in the docket for this rulemaking (Ref. 5).

A. Comments Supporting EPA's Proposed Listing of DINP

    Earthjustice, EDF, and all private citizens and the anonymous 
commenter expressed support for EPA's proposed addition of DINP to the 
TRI list. Additionally, Earthjustice urged EPA to work quickly to 
publish the rule as EPCRA does not require multiple toxicity endpoints 
for listing.

B. Comments on the Listing Standard

    Comment: UPC disagreed with EPA's proposed listing. UPC claimed 
that adding DINP to the TRI chemicals list will cause companies to 
shift away from DINP, instead dealing with chemicals which have not 
been as well reviewed as DINP, and might be more toxic than DINP, and 
that listing DINP would create a barrier to international trade. They 
cited European Chemicals Agency 's (ECHA's) 2018 decision not to label 
DINP as a hazardous chemical as justification for why DINP would not 
satisfy EPCRA's requirements for listing.
    EPA response: EPA respectfully disagrees with the commenter that 
DINP does not meet the TRI chemical listing criteria specified in EPCRA 
section 313(d)(2). Additionally, the fact that a chemical is not on a 
given organization's ``hazardous chemical'' list does not mean that the 
chemical fails to meet the EPCRA section 313(d)(2) listing criteria. 
The Agency's full rationale for listing the DINP category is detailed 
in the 2023 Technical Review of DINP (Ref. 2) and Response to Comments 
(Ref. 5).
    Comment: ACC also disagreed with EPA's proposed listing of DINP. 
They asserted that EPA did not apply the correct legal standard because 
the Agency did not list DINP based on ``cancer, birth defects, or 
serious or irreversible reproductive dysfunctions, neurological 
disorders, or heritable genetic mutations.'' ACC also asserts that EPA 
improperly put the onus on the commenters to prove that DINP is not 
adverse to humans, rather than EPA showing that it is adverse to 
humans; and that EPA is assuming or ``suspects'' that DINP is a hazard, 
rather than having sufficient information that it does, in fact, meet 
the listing criteria.
    EPA response: Section 313(d)(2) of EPCRA sets out the legal 
standard for adding new chemicals to the TRI list, and EPA applied this 
standard when deciding to add DINP. Commenters incorrectly describe 
this standard, which allows for listing based on sufficient evidence to 
establish any one of several criteria, including that 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 Agency reasonably 
relied on hazards identified from animal studies which could plausibly 
be extrapolated to humans based on a weight of evidence (WoE) 
evaluation of health hazards posed by DINP in determining that DINP can 
reasonably be anticipated to cause one or more serious or irreversible 
chronic health effects in humans.
    As documented in the 2023 Technical Review of DINP (Ref. 2), the 
evidence available to EPA is sufficient to establish that DINP can 
reasonably be anticipated to cause in humans serious or irreversible 
reproductive dysfunctions as well as other serious or irreversible 
chronic health effects in humans, specifically, developmental, kidney, 
and liver toxicity. This evidence includes evidence of developmental 
toxicity, such as: reduced pup weights, skeletal variations, and 
dilated renal pelvises; and also evidence of reproductive dysfunctions 
such that ``gestational exposure to DINP has been shown to induce 
effects consistent with the spectrum of effects such as reduced fetal 
testicular testosterone, decreased AGD, increased male pup nipple 
retention, altered reproductive organ weight, testicular pathology, and 
a low incidence of reproductive tract malformation in some studies 
(such effects are sometimes generally referred to as `phthalate 
syndrome').'' (Ref. 2). This evidence also includes evidence of other 
serious or irreversible chronic health effects; specifically, non-
cancer liver and kidney toxicity.
    Comment: ACC points to studies in non-human primates to argue that 
primates are much less sensitive to DINP than are rodents. ACC argues 
that the timeline of the primate studies was similar to that of rodent 
studies, so they should be considered.
    EPA response: The commenter's argument does not consider the 
explanation that the short study duration (especially relative to the 
lifespan of the test species) accounts for the lack of treatment-
related effects, and instead attributes the differential toxicity to 
differences in species sensitivity. ACC was referring to a 14-day study 
in macaques (Ref. 6) and a 90-day study in marmosets (Ref. 7). The 
marmoset study did show decreases in body weights and body weight gains 
in both sexes. However, the non-human primate studies were not further 
evaluated due to being considered insufficient in study design and 
duration to evaluate DINP for carcinogenicity as well as for potential 
reproductive and developmental effects.

C. Comments Related to Hazard: Cancer

    Comment: ACC commented on EPA's proposal to list DINP based on 
cancer as an endpoint, and stated that the EPA could not list DINP on 
the TRI simply because it was on the California Prop 65 list. ACC 
further commented that certain animal tumors discussed in the

[[Page 45092]]

2022 Technical Review of DINP (Ref. 1) as evidence for listing DINP due 
to carcinogenicity (including alpha-2u-globulin-mediated kidney cancers 
in male rats, mononuclear cell leukemia (MNCL), and PPAR[alpha]-
mediated liver tumors) are not indicative of human hazard. The comment 
claimed that there is significant evidence to show that all three DINP-
induced rodent tumors are specific to rodents and not relevant to human 
cancer.
    EPA response: EPA's decision to list DINP on the TRI is based on 
EPA's analysis of the available data, and not, as the commenter appears 
to suggest, on a decision made by another regulatory body. Moreover, as 
explained in greater detail in the Response to Comments (Ref. 5), EPA 
has decided not to rely on a cancer endpoint for this action to add a 
DINP chemical category to the TRI chemical list.
    As explained in greater detail in the 2023 Technical Review of DINP 
(Ref. 2), in this action EPA is adding DINP to the TRI chemical list 
based on toxicity data demonstrating that these chemicals can be 
reasonably anticipated to cause serious or irreversible reproductive 
dysfunctions and other serious or irreversible chronic human health 
effects, including developmental, liver, and kidney effects. EPA 
revised the 2022 Technical Review of DINP (Ref. 1) regarding the 
evaluation of MNCL and tumors in the liver and kidney, in addition to 
including a new section on ``Tumors Observed in Other Organs'' under 
the Conclusions on Carcinogenicity Section of the 2023 Technical Review 
of DINP (Ref. 2). This section provides a brief discussion of the data 
for pancreatic islet cell carcinomas, testicular interstitial (Leydig) 
cell carcinomas and uterine adenocarcinomas. EPA did not, however, base 
its decision to list DINP on these data.

D. Comments Related to Hazard: Reproductive Dysfunctions and 
Developmental Toxicity

    Comment: ACC asserted that, ``in addition to animal evidence, human 
evidence, where available, would be crucial to the EPA's evaluation, 
including the developmental endpoint for DINP. However, neither the 
EPA's Supplemental Notice nor the Revised Technical Review for DINP 
includes any of the growing epidemiological evidence''.
    EPA response: The Agency acknowledges that the evidence of 
developmental hazard presented to support the listing of DINP on the 
TRI focused on the evidence in developmental toxicity and reproduction 
studies in laboratory animals. The Agency determined that this evidence 
is extensive and unambiguous in interpretation. EPA notes that the 
epidemiology data on developmental hazard, although pertinent, do not 
negate the importance of the animal data, especially given the extent 
of evidence provided by animal data. Further, inconsistent results make 
it difficult to draw a definitive conclusion on hazard concerns from 
epidemiological data on DINP. Therefore, EPA determined that the 
epidemiological studies are not required to inform the Agency's 
decision to list DINP on the TRI. EPA's discussion of the 
epidemiological data referenced by ACC in its comment is addressed 
further in the Response to Comment document (Ref. 5). Furthermore, the 
Agency does not consider the lack of presentation of epidemiological 
evidence to detract from the strength of evidence of both developmental 
and reproductive hazard posed by DINP represented in the animal 
studies.
    Comment: Reduced pup weights were reversible or transient, 
inconsistently observed, not statistically significant, and did not 
cause any adverse effects in older rats, so they should not be 
considered ``serious or irreversible'' effects.
    EPA response: EPA disagrees with the characterization of the body 
weight decreases as transient, which is typically interpreted in 
evaluation of toxicology studies as the effect being temporary in the 
presence of continued exposure. In the two major studies cited (both 
discussed in Waterman et al., 2000 (Ref. 8)), statistical significance 
was achieved at multiple timepoints. Particularly in the two-generation 
study (Ref. 8), the decreased F1 offspring body weights became more 
pronounced in statistical significance and in magnitude difference from 
controls, and occurred at lower doses as the post-natal period 
proceeded. The effects of DINP on body weight occurred in both sexes 
and across generations and generally increased in significance and 
magnitude with time; and importantly, occurred at lower doses in 
offspring compared to parents.
    Regarding ACC's comment that reduced pup weight results are 
inconsistent, EPA acknowledges that in some studies with shorter 
exposure durations, longer term effects on growth may not be apparent. 
In the study by Clewell et al. (Ref. 9), pregnant rats were 
administered DINP in the diet from gestational day (GD) 12 through 
postnatal day (PND) 14. However, even with this shorter exposure 
duration, dams exhibited reduced body weight, body weight gain, and 
food consumption during gestation and lactation at 750 mg/kg/day. 
Offspring body weights of males were decreased at PND 14 at the high 
dose on PND 2 ([darr]12%) and dose-dependently at both the mid- and 
high-dose on PND 14 ([darr]10-27%) at termination of dosing. The fact 
that the male offspring body weights were not significantly decreased 
by PND 49-50 ([darr]4%; NS) with no exposure to DINP since PND 14 (~35 
days) does not equate to transient decreases (those that occur with 
continued exposure).
    Furthermore, an additional study showed that decreased body weights 
persisted after the treated period ended. Masutomi et al. (Ref. 10) 
evaluated developmental effects in the offspring of female Sprague-
Dawley rats exposed to DINP in the diet at concentrations of 0, 400, 
4,000, or 20,000 ppm from GD 15 to PND 10. Even though treatment ceased 
on PND 10, prepubertal body weights of offspring were still 
significantly decreased on PND 27. Importantly, the decreased body 
weight in male offspring occurred at a lower dose than affected 
maternal body weights, indicating heightened relative sensitivity of 
male offspring exposed in utero compared to parents. Finally, it is 
important to note that these decreases were substantial, with decreases 
of 18% in mid-dose males and 39-47% in high dose males and females, and 
were highly significant (p<0.01). This supporting evidence shows that 
adverse effects are seen in prepubertal rats born to exposed pregnant 
females; it can be reasonably expected that results would persist into 
adulthood.
    In short, the decreases in body weight and weight gain in the 
animals in the reproduction and developmental toxicity studies on DINP 
are ``serious,'' in part, because they increase in magnitude and 
significance with time exposed and across generations and occur at 
lower doses in offspring than in parents.
    Comment: ACC questioned EPA's use of skeletal effects and dilated 
renal pelvises as evidence of DINP toxicity to developmental health. 
ACC stated that the conclusions of the ECHA and Australia's National 
Industrial Chemicals Notification and Assessment Scheme (NICNAS) are 
that supernumerary ribs are common anomalies in rodents which can only 
be ``indicative of slight developmental effects.'' ACC asserted that 
animals in multi-generation studies thrived and there was no evidence 
of adverse effects related to these variations. ACC also asserted that 
the agency itself is unsure of the biological relevance of increased

[[Page 45093]]

rib variations in rats. For the renal pelvises effects, ACC stated that 
the dilated renal pelvises reported in Waterman et al. (2000) (Ref. 8) 
and Hellwig et al. (1997) (Ref. 11) are transient, of doubtful 
biological and statistical significance, and occur only at maternally 
toxic doses.
    EPA response: Supernumerary ribs are larger (longer) structures 
with distal cartilage present and are likely to be permanent, 
ultimately remaining as distinct ribs; whereas ossification sites are 
smaller (shorter) structures without distal cartilage and are likely to 
be transient.
    The developmental variations seen in Waterman et al. (1999) (Ref. 
12) include significantly increased incidences of rudimentary lumbar 
ribs at 500 and 1,000 mg/kg-day, compared to controls. Additionally, 
incidences of supernumerary cervical ribs were significantly increased 
at 1000 mg/kg-day, compared to controls. The authors noted that 
supernumerary lumbar ribs ``have been associated with nonspecific 
maternal toxicity''; however, this does not preclude its relevance, and 
it is important to note that significantly increased incidences of 
rudimentary lumbar ribs were noted at a dose lower than that at which 
maternal toxicity was observed. Furthermore, no corroborating findings 
of delayed fetal ossification, which would suggest that fetal effects 
were secondary to maternal effects, were reported at the high dose in 
this study. ACC has taken the Agency's statement from the 2022 
Technical Review of DINP (Ref. 1) out of context. The full statement 
was: ``Therefore, although the biological significance of a 
statistically significant increase in rib variations is uncertain, the 
Agency believes that the dose-related response observed in the Waterman 
et al. (1999) (Ref. 12) study may represent growth alterations that are 
indicative of DINP's potential to disrupt normal developmental patterns 
and produce a developmental hazard.'' The Agency reiterates its 
conclusion that DINP can reasonably be anticipated to be 
developmentally toxic to humans.
    EPA acknowledges that the dilated renal pelvises observed in 
Hellwig et al. (1997) (Ref. 11) were consistently increased over 
controls only at the high dose of 1000 mg/kg-day. However, the fact 
that this fetal finding in this study was noted at a dose that was 
toxic to the maternal animals does not preclude its toxicological 
relevance to offspring. And it is important to note that, for DINP-3, 
increased dilated renal pelvises observed at 1000 mg/kg-day were 
accompanied in some instances by renal malformations (e.g., 
hydroureter, agenesis or absence of kidney). Furthermore, in the 
developmental toxicity study in rats conducted by Waterman et al. 
(1999) (Ref. 12), fetal and litter incidences of dilated renal pelvis 
were statistically significant and dose-dependently increased in all 
treated groups, whereas maternal toxicity, as evidenced by decreased 
body weights and weight gains during treatment, was affected only at 
the high dose of 1000 mg/kg-day. EPA disagrees with the 
characterization that dilated renal pelvis is a ``normal developmental 
phenomenon'' (as stated by NICNAS), but acknowledges that the 
toxicological relevance is dependent upon the incidence and severity. 
Nevertheless, the commenters mischaracterized NICNAS's conclusion on 
these variations. The full statement from NICNAS reads: ``These 
variations are relatively common in rodents; however, the induced 
frequencies (78% vs 25% control for rudimentary lumbar ribs, and 26% vs 
0% control for dilated renal pelvises) were outside historical control 
ranges and thus interpreted as indicative of slight developmental 
effects.'' (Ref. 13, emphases added). Therefore, NICNAS also 
interpreted the renal pelvis and additional lumbar ribs to be 
indicative of adverse effects of DINP.
    To summarize, dilated renal pelvises incidences in these studies 
are treatment-related, and it remains to be seen whether the findings 
are reversible/transient because that depends on the severity of the 
effects. However, it is the Agency's determination that dilated renal 
pelvises, in addition to renal malformations, even at doses with 
observed maternal toxicity, are biologically significant, and 
contribute to the WoE for DINP as a developmental toxicant.
    Comment: ACC asserted that DINP does not cause a serious or 
irreversible effect on anogenital distance (AGD) or nipple retention in 
animals, citing a lack of statistical significance in Clewell et al. 
(2013) (Ref. 14) for AGD and Gray et al. (2000) (Ref. 15) for nipple 
retention. ACC stated that these effects, if they occur, are only 
transient and do not persist into adulthood. Finally, ACC asserts that 
DINP is not associated with male reproductive malformations in humans.
    EPA response: EPA acknowledges that there is some inconsistency in 
reporting of significant effects on AGD across available studies of 
DINP and that permanent, statistically significant reductions in AGD 
have not been reported in adult offspring following gestational 
exposure to DINP. However, reduced AGD in males is only one of many 
effects that make up phthalate syndrome (or androgen insufficiency 
syndrome). As described in EPA's 2023 Technical Review of DINP (Ref. 
2), gestational exposure to DINP has been shown to induce effects 
consistent with the spectrum of effects that comprise phthalate 
syndrome (e.g., reduced fetal testicular testosterone, decreased AGD, 
increased male pup nipple retention, altered reproductive organ weight, 
testicular pathology, and a low incidence of reproductive tract 
malformation in some studies). Therefore, EPA still considers a 
decrease in AGD to be a potential adverse and serious outcome of DINP 
exposure and a reflection of the suite of effects that comprise 
phthalate syndrome.
    EPA also acknowledges that there is some inconsistency in reporting 
of nipple retention across available studies of DINP. In Gray et al. 
(2000) (Ref. 15), the finding of permanent nipples in DINP-treated rats 
was accompanied by several abnormalities in the testes, including 
testicular atrophy, epididymal agenesis with hypospermatogenesis, and 
scrotal fluid-filled testis devoid of spermatids. This syndrome may 
result from inhibition of fetal testis hormone production during sexual 
differentiation, a process that is critical in all mammals including 
humans. Furthermore, the finding of nipple retention was not 
exclusively noted in Gray et al. (2000) (Ref. 15). For example, Boberg 
et al. (2011) (Ref. 16) demonstrated a dose-dependent and statistically 
significant increase in the number of retained nipples in DINP-exposed 
(GD 7 to PND 19) male pups on PND 13 at 750 mg/kg-day (3.14) and 900 
mg/kg-day (3.17) compared to controls (1.98), which ACC failed to 
mention when citing the findings in the study at PND 90.
    In addition to the male reproductive malformations noted in the two 
studies by Gray et al. (2000 (Ref. 15), 2023 (Ref. 17)), EPA discussed 
the findings of ten additional studies in its 2023 Technical Review of 
DINP (Ref. 2) which support the WoE for serious adverse impacts on the 
male reproductive tract. Such effects include: decreased body weight at 
the onset of puberty; decreased weights of the testes, levator ani plus 
bulbocavernosus muscles (LABC), and seminal vesicles; decreased 
testosterone, percent motile sperm, and AGD; increased incidences of 
multinucleated gonocytes (MNGs) in testes, large Leydig cell 
aggregates, degeneration of stage XIV meiotic spermatocytes, vacuolar 
degeneration of Sertoli cells, and scattered cell debris in the 
epididymal ducts; and effects on male copulatory

[[Page 45094]]

behavior (reduced number of mounts, intromissions, and ejaculations).
    Phthalate syndrome may result from inhibition of fetal testis 
hormone production during sexual differentiation, a process that is 
critical in all mammals including humans. EPA concludes that humans can 
reasonably be anticipated to be affected if exposed to sufficient 
concentrations of DINP or its metabolites at critical stages of 
reproductive development.

E. Comments Related to Hazard: Liver Toxicity

    Comment: ACC commented on EPA's identification of spongiosis 
hepatis as a treatment-related lesion in rats exposed to DINP, and the 
Agency's position that the occurrence is relevant to human health; more 
specifically, ACC asserted that the mere fact that a lesion is 
treatment-related in a rat does not mean it will occur in humans. ACC 
further stated that the effect did not occur in mice exposed to similar 
levels of DINP, and that it is not a serious or irreversible effect, 
even in rats, because EPA did not state whether spongiosis hepatis is 
linked to any other adverse pathological or toxicological process 
detrimental to the health of affected rats. ACC added that liver enzyme 
changes in studies appeared to be sporadic and not indicative of 
serious liver damage. ACC concluded that spongiosis hepatis is not 
relevant to human health.
    Response: EPA disagrees with ACC's conclusion and maintains that 
the finding of spongiosis hepatis in rats has human relevance as one of 
multiple indicators of adverse outcomes to the liver post-DINP 
exposure. While the human relevance of spongiosis hepatis, in 
particular, is unclear, that does not preclude its relevance in a WoE 
evaluation of evidence of hepatotoxicity in the rat, and the Agency 
does not consider the lack of evidence of a direct human correlate of 
spongiosis hepatis to detract from the extrapolation of that evidence 
in animals to relevance to human health. The Agency references Lington 
et al. (1997) (Ref. 18) for the co-occurring findings of other 
histopathology effects in the liver due to DINP treatment including 
focal necrosis, hepatopathy associated with leukemia, and 
hepatocellular enlargement in both sexes, in addition to sinusoid 
ectasia in males. The Agency also references Moore et al. (1998a) (Ref. 
19) and Bio/dynamics (1987) (Ref. 20) for co-occurring findings in the 
liver, including cytoplasmic eosinophilia, diffuse hepatocellular 
enlargement, and increased pigment in both sexes, and additionally 
individual cell degeneration/necrosis in the males. Moore et al. 
(1998b) (Ref. 21) also conducted a 2-year study in mice and found 
similar adverse treatment-related effects on the liver. In all these 
studies, increases in key indicator enzymes were also observed.
    The Agency acknowledges that treatment-related effects on the liver 
are often along a continuum, with effects early on and at lower doses 
reflecting an adaptive response (often indicated by increased liver 
weights and/or hepatocellular hypertrophy) but progressing to an 
adverse response at prolonged or higher doses, characterized by adverse 
findings in clinical chemistry and histopathology. While induction of 
CYP450s as a metabolic activation response of the liver may be an 
adaptive response, increases in ALT are indicative of liver damage and 
inherently adverse, and the clinical interpretation of this finding is 
conserved across species, including humans. For certain enzymes (e.g., 
ALT), increases, as well as various enzymatic activities when 
considered with other effects such as histopathology lesions, are 
adverse effects and support the conclusion that DINP induces serious 
chronic effects in the liver beyond liver enlargement. Thus, the Agency 
disagrees with ACC's assertion that the increases in liver weights and 
enzymes seen in these studies are an adaptive response or are non-
serious in the total weight of evidence.

F. Comments Related to Hazard: Kidney Toxicity

    Comment: ACC commented that: (a) DINP does not cause and cannot 
reasonably be anticipated to cause rodent chronic progressive 
nephropathy (CPN) in human kidneys, as no human analog exists; (b) 
while EPA may ``speculate,'' per ACC's characterization, that chemicals 
that cause CPN in rodents may cause other kidney effects in humans, 
such ``speculation'' is not appropriate for a TRI listing; and (c) even 
the EPA's ``speculation'' is unlikely to be supported, as there is 
minimal evidence that DINP is associated with any kidney disease in 
humans. ACC further points to the lack of adverse effects seen in 
primate studies as evidence that DINP is not relevant to human health.
    EPA response: Although the mechanism of DINP-induced kidney 
toxicity may not be clear, the kidneys are clearly a target of DINP-
induced toxicity which can reasonably be anticipated to cause serious 
or irreversible chronic health effects in humans, as evidenced by 
increases in absolute and relative kidney weights, clinical chemistry 
(e.g., increased blood urea nitrogen), urinalysis changes, and findings 
in gross pathology (e.g., granular pitted/rough kidneys), and 
histopathology (e.g., reduction in the tubular space and oedema of 
epithelial cells in the glomeruli, a loss of loop points in the 
glomerular capillaries, increased granular casts and regenerative/
basophilic tubules) in rats and mice. EPA disagrees with ACC's 
conclusion that the changes in kidney weights in rats are not relevant 
to human kidney toxicity, and asserts that the lack of an effect in the 
primate studies ACC mentioned is plausibly related to the shorter 
duration of dosing relative to the life span of the animal instead of 
indicating a lack of relevance to humans. (See the ``Generally: EPA has 
Failed to Apply the Correct Legal Standard in this Case'' section.) 
Given that increased kidney weight appears as a consistent effect among 
other kidney injuries following DINP exposure, EPA believes it to be 
relevant in the WoE supporting DINP kidney toxicity. EPA acknowledges 
that, in a letter to the U.S. EPA IRIS Program (NIEHS 2019) (Ref. 22), 
U.S. NTP concluded that the ``morphological spectrum of CPN have no 
analog in the human kidney and that CPN is distinct entity in the rat 
(Hard et al., 2009) (Ref. 23).'' However, NTP also acknowledged that 
``The etiology of CPN is unknown and represents a complex disease 
process in rats. Given the fact that there is no definitive 
pathogenesis for this multifactorial disease process, it cannot be 
fully ruled out that chemicals which exacerbate CPN in rats may have 
the potential to exacerbate disease processes in the human kidney.'' 
Subsequently, the EPA IRIS Program in its toxicological reviews of 
tert-Butanol (EPA 2021a) (Ref. 24) and ethyl tertiary butyl ether (EPA 
2021b) (Ref. 25) (chemicals which cause CPN in male and female rats) 
concluded that ``a chemical that exacerbates CPN in rats could also 
exacerbate disease processes in the human kidney'' and that other 
effects in the kidney were observed that were not confounded by alpha 
2u-globulin related processes, and kidney toxicity was selected as the 
basis of the oral noncancer reference doses that were derived. 
Similarly, for DINP, available studies demonstrate a spectrum of 
effects on the kidney. Given the WoE when considering the other effects 
involving the kidney, and EPA's position, based on the Agency's 
technical expertise, that chemicals which exacerbate CPN in rodents 
could also exacerbate disease processes in the human kidney, DINP can 
reasonably be anticipated to cause serious and/or

[[Page 45095]]

irreversible harm to the kidney based on the literature reviewed.
    Furthermore, the EPA disagrees with ACC's assertion that the kidney 
toxicity seen in female mice is irrelevant to human health. Although 
[alpha]-2u-globulin MOA is male rat-specific and has been shown not to 
be relevant to humans, the MOA for kidney toxicity for female rats and 
male and female mice remains unclear and so in order to be protective 
of human health, EPA maintains that CPN is relevant to human health and 
contributes to the WoE for kidney toxicity for this non-cancer 
endpoint. A study by Ma et al. (Ref. 26) found that oxidative stress 
may be involved in the hepatic and renal toxicities associated with 
DINP exposure. In order to be protective of human health, the EPA 
maintains that oxidative stress-related mechanism are relevant to human 
health. EPA would like to direct ACC's attention to the ``Conclusions 
on Chronic Non-cancer Toxicity'' section 2.5.6.2 on ``Kidney Effects'' 
in the 2023 Technical Review of DINP (Ref. 2) for further details.

G. Comments Related to Exposure

    Comment: ACC argued that due to its physico/chemical properties, 
community exposure to DINP via environmental release is negligible.
    EPA response: As EPA has previously stated, including in the 
supplemental proposal for this rulemaking (87 FR 48128), it is not 
appropriate to consider exposure for chemicals that are moderately high 
to highly toxic based on a hazard assessment when determining if a 
chemical should be added for chronic human health effects pursuant to 
EPCRA section 313(d)(2)(B) (see 59 FR 61440-61442). EPA concludes that 
DINP can reasonably be anticipated to cause serious or irreversible 
chronic human health effects at moderately low to low doses including 
serious or irreversible reproductive dysfunctions as well as other 
serious or irreversible chronic health effects in humans, specifically, 
developmental, kidney, and liver toxicity. The data for DINP 
demonstrates that DINP has moderately high to high human health 
toxicity. For listings pursuant to EPCRA section 313(d)(2)(A), EPA must 
consider whether ``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.'' However, even pursuant to such listings, the 
Agency need not confirm that communities are actually exposed to the 
given chemical, but rather that concentration levels of concern are 
reasonably likely to exist beyond a facility's boundaries as a result 
of releases. Further, listings based on EPCRA section 313(d)(2)(B) (as 
well as EPCRA section 313(d)(2)(C)) do not require an exposure 
assessment, but rather are based on hazard alone.
    Therefore, in accordance with EPA's standard policy on the use of 
exposure assessments (see November 30, 1994 (59 FR 61432, FRL-4922-2), 
an exposure assessment is neither necessary nor appropriate for 
determining whether DINP meets the criteria of EPCRA section 
313(d)(2)(B).
    Additionally, EPA notes that EPCRA indicates that TRI reporting 
forms are intended to provide information to governments and the public 
to inform persons about releases of toxic chemicals to the environment, 
assist in the conduct of research and data gathering, and to aid in the 
development of regulations and other similar purposes (see EPCRA 
section 313(h)). Accordingly, even if releases are very small, the data 
reported is still useful. For example, such reporting might indicate 
that a toxic chemical being used in the community is not being released 
at levels of concern, which would be reassuring to residents. Further, 
how the public or any particular entity may make use of TRI data on a 
particular chemical need not factor into whether or not that chemical 
is on the TRI list of chemicals.

IV. Summary of the Final Rule

    EPA is finalizing the addition of a DINP category to the EPCRA 
section 313 list of toxic chemicals. Based on EPA's review of the 
available toxicity data, EPA has determined that these chemicals can be 
reasonably anticipated to cause serious or irreversible reproductive 
dysfunctions as well as serious or irreversible chronic human health 
effects in humans, including developmental, kidney, and liver toxicity. 
Therefore, EPA has determined that the evidence is sufficient for 
listing the DINP category on the EPCRA section 313 toxic chemicals list 
pursuant to EPCRA section 313(d)(2)(B).

V. 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. USEPA. Technical Review of Diisononyl Phthalate. Office Pollution 
Prevention and Toxics, Data Gathering and Analysis Division and 
Existing Chemicals Risk Assessment Division. April 11, 2022.
2. USEPA. Technical Review of Diisononyl Phthalate [updated]. Office 
Pollution Prevention and Toxics, Data Gathering and Analysis 
Division and Existing Chemicals Risk Assessment Division. June 2023.
3. Letter to EPA Administrator Carol M. Browner, Re: Petition to Add 
Diisononyl Phthalate (DINP) to the Emergency Planning and Community 
Right-to-Know Act Section 313 List of Toxic Chemicals. From Laurie 
Valeriano, Policy Director, Wastington Toxics Coalition. February 
24, 2000.
4. USEPA. Economic Analysis for the Addition of Diisononyl Phthalate 
Category; Community Right-to-Know Toxic Chemical Release Reporting. 
Prepared by Abt Associates. April 20, 2023.
5. USEPA. Response to Comments Received on the August 8, 2022, 
Proposed Rule (87 FR 48128): Addition of Diisononyl Phthalate 
Category; Community Right-to-Know Toxic Chemical Release Reporting. 
June 2023.
6. Pugh, G.; Isenberg, J.S.; Kamendulis, L.M.; Ackley, D.C.; Clare, 
L.J.; Brown, R.; Lington, A.W.; Smith, J.H.; and Klaunig, J.E. 2000. 
Effects of di-isononyl phthalate, di-2-ethylhexyl phthalate, and 
clofibrate in cynamolgus monkeys. Toxicol. Sci. 56:181-188.
7. Hall, M.; Matthews, A.; Webley, L.; and Harling R. 1999. Effects 
of di-isononyl phthalate (DINP) on peroxisomal markers in the 
marmoset--DINP is not a peroxisome proliferator. J. Toxicol. Sci. 
24: 237-244.
8. Waterman, S.J.; Keller, L.H.; Trimmer, G.W.; Freeman, J.J.; 
Nikiforov, A.I.; Harris, S.B., Nicolich, M.J.; and McKee, R.H. 2000. 
Two generation reproduction study in rats given di-isononyl 
phthalate in the diet. Reprod. Toxicol. 14(1):21-36.
9. Clewell, R. 2011. A Dose Response Study of the Effects on Male 
Rat Sexual Development After Administration of Diisononyl Phthalate 
to the Pregnant and Lactating Dam. Performing laboratory: The Hamner 
Institutes for Health Sciences, Research Triangle Park, NC. 
Laboratory Study Number: 10003. Sponsor: ExxonMobil Biochemical 
Sciences Inc., location not reported.
10. Masutomi, N.; Shibutani, M.; Takagi, H.; Uneyama, C.; Takahashi, 
N.; Hirose, M. 2003. Impact of dietary exposure to methoxychlor, 
genistein, or diisononyl phthalate during the perinatal period on 
the development of the rat endocrine/reproductive systems in later 
life. Toxicology 192:149-170.
11. Hellwig, J.; Freudenberger, H.; and Jackh, R. 1997. Differential 
prenatal toxicity of branched phthalate esters in rats. Food and 
Chem. Toxicol. 35:501-512.

[[Page 45096]]

12. Waterman, S.J.; Ambroso, J.L.; Keller, L.H.; Trimmer, G.W.; 
Nikiforov, A.I.; Harris, S.B. 1999. Developmental toxicity of di-
isodecyl and di-isononyl phthalates in rats. Reprod. Toxicol. 
13(2):131-136.
13. Australia NICNAS, Priority existing chemical assessment report 
no. 35. Diisononyl phthalate. September 2012, Australian Government 
Department of Health and Ageing: Sydney, Australia. https://www.industrialchemicals.gov.au/sites/default/files/PEC35-Diisononyl-phthalate-DINP.pdf.
14. Clewell, R.A., et al., 2013. A dose response study to assess 
effects after dietary administration of diisononyl phthalate (DINP) 
in gestation and lactation on male rat sexual development. Reprod 
Toxicol. 35:70-80.
15. Gray, L.E.; Jr, Ostby, J.; Furr, J.; Price, M.; Rao 
Veeramachaneni, D.N.; and Parks, L. 2000. Perinatal exposure to the 
phthalates DEHP, BBP, and DINP, but not DEP, DMP, or DOTP, alters 
sexual differentiation of the male rat. Toxicol. Sci. 58:350-365.
16. Boberg, J., et al., 2011. Reproductive and behavioral effects of 
diisononyl phthalate (DINP) in perinatally exposed rats. Reprod 
Toxicol. 31(2):200-9.
17. Gray, L.E. 2023. Biologically relevant reductions in fetal 
testosterone and Insl3 induced by in utero exposure to high levels 
of di-isononyl phthalate (DINP) in male rats. Toxicol. and Appl. 
Pharmacol. 465:116454. https://doi.org/10.1016/j.taap.2023.116454.
18. Lington, A.W.; Bird M.G.; Plutnick, R.T.; Stubblefield, W.A.; 
and Scala, R.A. 1997. Chronic toxicity and carcinogenic evaluation 
of diisononyl phthalate in rats. Fundam. Appl. Toxicol 36: 79-89.
19. Moore, M.R. 1998a. Oncogenicity study in rats with 
di(isononyl)phthalate including ancillary hepatocellular 
proliferation and biochemical analyses. TSCATS Doc# 89980000308. Old 
Doc 8EHQ099813083. Fiche # OTS05562832. Submitted by Aristech 
Chemical Corporation. Produced by Covance Laboratories 2598-104.
20. Bio/dynamics. (1987). A chronic toxicity carcinogenicity feeding 
study in rats with Santicizer 900 with cover letter dated 06/05/87 
[TSCA Submission]. (EPA/OTS Doc #86870000362). St. Louis, MO: 
Monsanto Company.
21. Moore M.R. 1998b. Oncogenicity study in mice with 
di(isononyl)phthalate including ancillary hepatocellular 
proliferation and biochemical analyses. TSCATS Doc# 89990000046. Old 
Doc 8EHQ119813083. Fiche # OTS05562833. Submitted by Aristech 
Chemical Corp. Produced by Covance 2598-105.
22. National Institute of Environmental Health Sciences (NIEHS). 
2019. Letter to U.S. EPA IRIS Program. https://heronet.epa.gov/heronet/index.cfm/reference/details/reference_id/5098230.
23. Hard GC, Johnson KJ, Cohen SM. 2009. A comparison of rat chronic 
progressive nephropathy with human renal disease-implications for 
human risk assessment. Crit Rev Toxicol. 39(4):332-346.
24. USEPA. 2021a. Toxicological Review of tert-Butyl Alcohol (tert- 
Butanol) [CASRN 75-65-0]. EPA/635/R-20/370Fa. Integrated Risk 
Information System, Center for Public Health and the Environmental 
Assessment, Office of Research and Development. Washington, DC. 
https://iris.epa.gov/static/pdfs/1036tr.pdf.
25. USEPA. 2021b. Toxicological Review of Ethyl Tertiary Butyl Ether 
[CASRN 637-92-3]. EPA/635/R-20/400Fa. Integrated Risk Information 
System, Center for Public Health and the Environmental Assessment, 
Office of Research and Development. Washington, DC. https://iris.epa.gov/static/pdfs/1034tr.pdf.
26. Ma P. et al., 2014. Oral exposure of Kunming mice to diisononyl 
phthalate induces hepatic and renal tissue injury through the 
accumulation of ROS. Protective effect of melatonin. Food Chem 
Toxicol, 68: 247-56.

VI. Statutory and Executive Order Reviews

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

A. Executive Order 12866: Regulatory Planning and Review and 14094: 
Modernizing Regulatory Review

    This action is not a significant regulatory action as defined in 
Executive Order 12866 (58 FR 51735, October 4, 1993), as amended by 
Executive Order 14094 (88 FR 21879, April 11, 2023), and was therefore 
not subject to a requirement for Executive Order 12866 review.

B. Paperwork Reduction Act (PRA)

    This action does not impose any new information collection burden 
under the PRA, 44 U.S.C. 3501 et seq. Burden is defined in 5 CFR 
1320.3(b). OMB has previously approved the information collection 
activities contained in the existing regulations and has assigned OMB 
control numbers 2070-0212 and 2050-0078.
    Currently, the facilities subject to the reporting requirements 
under EPCRA section 313 and PPA section 6607 may use either EPA Toxic 
Chemicals Release Inventory Form R (EPA Form 9350-1), or 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 (EPA Information Collection Request (ICR) 
No. 2613.02) and those related to trade secret designations under OMB 
Control 2050-0078 (EPA ICR No. 1428). As provided in 5 CFR 1320.5(b) 
and 1320.6(a), an Agency may not conduct or sponsor, and a person is 
not required to respond to, a collection of information unless it 
displays a currently valid OMB control number. The OMB control numbers 
relevant to EPA's regulations are listed in 40 CFR part 9 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 no small governments or small organizations are 
expected to be affected by this action; and that of the 198 to 396 
entities estimated to be impacted by this action, 181 to 365 are small 
businesses. All small businesses affected by this action are estimated 
to incur annualized cost impacts of less than 1%. 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 located 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. The action imposes 
no enforceable duty on any state, local or tribal governments and EPA 
did not identify any small governments that would be impacted by this 
action. EPA's economic analysis indicates that the total industry cost 
of this action is estimated to be $968,546 to $1,935,041 in the first 
year of

[[Page 45097]]

reporting and $461,212 to $921,448 in subsequent years (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), because 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), because it will 
not have substantial direct effects on tribal governments, on the 
relationship between the Federal government and the Indian tribes, or 
on the distribution of power and responsibilities between the Federal 
government and Indian tribes. 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 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 Executive Order 13045. This 
action is not subject to Executive Order 13045, because it does not 
concern an environmental health or safety risk. Since this action does 
not concern human health, EPA's Policy on Children's Health also does 
not apply.
    Although this action does not concern an environmental health or 
safety risk, the data collected as a result of this action will provide 
information about releases to the environment that could be used to 
inform the public on potential exposures to toxic chemical releases, 
pursuant to the right-to-know principles. EPA also believes that the 
information obtained as a result of this action could be used by 
government agencies, researchers, and others to identify potential 
problems, set priorities, and take appropriate steps to reduce any 
potential exposures and related human health or environmental risks 
identified as a result of increased knowledge of exposures to DINP.

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 technical standards under the 
NTTAA section 12(d), 15 U.S.C. 272.

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

    Executive Order 12898 (59 FR 7629, February 16, 1994) directs 
federal agencies, to the greatest extent practicable and permitted by 
law, to make environmental justice part of their mission by identifying 
and addressing, as appropriate, disproportionately high and adverse 
human health or environmental effects of their programs, policies, and 
activities on minority populations (people of color and/or indigenous 
peoples) and low-income populations.
    EPA believes that it is not practicable to assess whether the human 
health or environmental conditions that exist prior to this action 
result in disproportionate and adverse effects on people of color, low-
income populations and/or indigenous peoples. This action adds a 
chemical category to the EPCRA section 313 reporting requirements; it 
does not directly address any human health or environmental risks and 
does not affect the level of protection provided to human health or the 
environment. However, EPA believes that the information obtained as a 
result of this action could be used by the public (including people of 
color, low-income populations and/or Indigenous peoples) to inform 
their behavior as it relates to sources of DINP exposure, or by 
government agencies and others to identify potential problems, set 
priorities, and take appropriate steps to reduce those exposures, as 
well as assess any potential human health or environmental risks.

K. Congressional Review Act (CRA)

    This action is subject to the CRA, 5 U.S.C. 801 et seq., and EPA 
will submit a rule report to each House of the Congress and to the 
Comptroller General of the United States. This action is not a ``major 
rule'' as defined by 5 U.S.C. 804(2).

List of Subjects in 40 CFR Part 372

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

    Dated: July 6, 2023.
Michal Freedhoff,
Assistant Administrator, Office of Chemical Safety and Pollution 
Prevention.

    Therefore, for the reasons set forth in the preamble, EPA is 
amending 40 CFR part 372 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.  372.65, adding in alphabetical order an entry to Table 3 in 
paragraph (c) for ``Diisononyl Phthalates (DINP)'' to read as follows:

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

* * * * *
    (c) * * *

                        Table 3 to Paragraph (c)
------------------------------------------------------------------------
                     Category name                        Effective date
------------------------------------------------------------------------
 
                              * * * * * * *
Diisononyl Phthalates (DINP): Includes branched alkyl          1/1/2024
 di-esters of 1,2 benzenedicarboxylic acid in which
 alkyl ester moieties contain a total of nine carbons.
 (This category includes but is not limited to the
 chemicals covered by the CAS numbers and names listed
 here).................................................
    28553-12-0 Diisononyl phthalate....................
    71549-78-5 Branched dinonyl phthalate..............

[[Page 45098]]

 
    14103-61-8 Bis(3,5,5-trimethylhexyl) phthalate.....
    68515-48-0 Di(C8-10, C9 rich) branched alkyl
     phthalates........................................
    20548-62-3 Bis(7-methyloctyl) phthalate............
    111983-10-9 Bis(3-ethylheptan-2-yl) benzene-1,2-
     dicarboxylate.....................................
 
                              * * * * * * *
------------------------------------------------------------------------

[FR Doc. 2023-14642 Filed 7-13-23; 8:45 am]
BILLING CODE 6560-50-P