[Federal Register Volume 70, Number 113 (Tuesday, June 14, 2005)]
[Proposed Rules]
[Pages 34437-34440]
From the Federal Register Online via the Government Publishing Office [www.gpo.gov]
[FR Doc No: 05-11664]
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ENVIRONMENTAL PROTECTION AGENCY
40 CFR Part 372
[TRI-2005-0004; FRL-7532-4]
RIN 2025-AA17
Addition of Diisononyl Phthalate Category; Community Right-to-
Know Toxic Chemical Release Reporting; Notice of Data Availability
AGENCY: Environmental Protection Agency (EPA).
ACTION: Proposed rule, notice of data availability.
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SUMMARY: On September 5, 2000, EPA issued a proposed rule, in response
to a petition filed under section 313(e)(1) of the Emergency Planning
and Community Right-to-Know Act (EPCRA), to add a diisononyl phthalate
(DINP) category to the list of toxic chemicals subject to the reporting
requirements under EPCRA section 313 and section 6607 of the Pollution
Prevention Act (PPA). EPA proposed to add this chemical category to the
EPCRA section 313 toxic chemical list pursuant to its authority to add
chemicals and chemical categories because EPA believes this category
meets the EPCRA section 313(d)(2)(B) toxicity criterion. The purpose of
today's action is to inform interested parties that, in an effort to
ensure adequate opportunities for input from all affected parties, EPA
is making available for public comment a revised hazard assessment for
DINP.
DATES: Comments must be received on or before September 12, 2005.
ADDRESSES: Submit your comments, identified by Docket ID No. TRI-2005-
0004, by one of the following methods:
Federal eRulemaking Portal: http://www.regulations.gov.
Follow the on-line instructions for submitting comments.
Agency Web site: http://www.epa.gov/edocket. EDOCKET,
EPA's electronic public docket and comment system, is EPA's preferred
method for receiving comments. Follow the on-line instructions for
submitting comments.
E-mail: [email protected].
Mail: Office of Environmental Information (OEI) Docket,
Environmental Protection Agency, Mail Code: 28221T, 1200 Pennsylvania
Ave., NW., Washington, DC, 20460, Attention Docket ID No. TRI-2005-
0004.
Hand Delivery: EPA Docket Center, (EPA/DC) EPA West, Room
B102, 1301 Constitution Ave., NW., Washington, DC, 20004, telephone:
202-566-1744, Attention Docket ID No. TRI-2005-0004. Such deliveries
are only accepted during the Docket's normal hours of operation, and
special arrangements should be made for deliveries of boxed
information.
Instructions: Direct your comments to Docket ID No. TRI-2005-0004.
EPA's policy is that all comments received will be included in the
public docket without change and may be made available online at http://www.epa.gov/edocket, including any personal information provided,
unless the comment includes information claimed to be Confidential
Business Information (CBI) or other information whose disclosure is
restricted by statute. Do not submit information that you consider to
be CBI or otherwise protected through EDOCKET, regulations.gov, or e-
mail. The EPA EDOCKET and the Federal regulations.gov Web sites are
``anonymous access'' systems, which means EPA will not know your
identity or contact information unless you provide it in the body of
your comment. If you send an e-mail comment directly to EPA without
going through EDOCKET or regulations.gov, your e-mail address will be
automatically captured and included as part of the comment that is
placed in the public docket and made available on the Internet. If you
submit an electronic comment, EPA recommends that you include your name
and other contact information in the body of your comment and with any
disk or CD-ROM you submit. If EPA cannot read your comment due to
technical difficulties and cannot contact you for clarification, EPA
may not be able to consider your comment. Electronic files should avoid
the use of special characters, any form of encryption, and be free of
any defects or viruses.
Docket: All documents in the docket are listed in the EDOCKET index
at: http://www.epa.gov/edocket. Although listed in the index, some
information is not publicly available, i.e., CBI or other information
whose disclosure is restricted by statute. Certain other material, such
as copyrighted material, is not placed on the Internet and will be
publicly available only in hard copy form. Publicly available docket
materials are available either electronically in EDOCKET or in hard
copy at the OEI Docket, EPA/DC, EPA West, Room B102, 1301 Constitution
Ave., NW., Washington, DC. The Public Reading Room is open from 8:30
a.m. to 4:30 p.m., Monday through Friday, excluding legal holidays. The
telephone number for the Public Reading Room is 202-566-1744, and the
telephone number for the OEI Docket is 202-566-1752.
FOR FURTHER INFORMATION CONTACT: Daniel R. Bushman, Toxics Release
Inventory Program Division, Office of Information Analysis and Access
(2844T), Environmental Protection Agency, 1200 Pennsylvania Ave., NW.,
Washington, DC 20460; telephone number: 202-566-0743; fax number: 202-
566-0741; e-mail: [email protected], for specific
information on this proposed rule, or for more information on EPCRA
section 313, the Emergency Planning and Community Right-to-Know
Hotline, Environmental Protection Agency, Mail Code 5101, 1200
Pennsylvania Ave., NW., Washington, DC 20460, Toll free: 1-800-424-
9346, in Virginia and Alaska: 703-412-9810 or Toll free TDD: 1-800-553-
7672.
SUPPLEMENTARY INFORMATION:
I. General Information
A. Does This Notice Apply To Me?
You may be potentially affected by this notice if you manufacture,
process, or otherwise use DINP. Potentially affected categories and
entities may include, but are not limited to:
[[Page 34438]]
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Category Examples of potentially affected entities
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Industry............................................ SIC major group codes 10 (except 1011, 1081, and 1094); 12
(except 1241); or 20 through 39; or industry codes 4911
(limited to facilities that combust coal and/or oil for
the purpose of generating power for distribution in
commerce); or 4931 (limited to facilities that combust
coal and/or oil for the purpose of generating power for
distribution in commerce); or 4939 (limited to facilities
that combust coal and/or oil for the purpose of
generating power for distribution in commerce); or 4953
(limited to facilities regulated under the Resource
Conservation and Recovery Act, subtitle C, 42 U.S.C.
section 6921 et seq.); or 5169; or 5171; or 7389 (limited
to facilities primarily engaged in solvent recovery
services on a contract or fee basis).
Federal Government.................................. Federal facilities.
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This table is not intended to be exhaustive, but rather provides a
guide for readers regarding entities likely to be affected by this
action. Other types of entities not listed in the table could also be
affected. To determine whether your facility would be affected by this
action, you should carefully examine the applicability criteria in part
372 subpart B of Title 40 of the Code of Federal Regulations. If you
have questions regarding the applicability of this action to a
particular entity, consult the person listed in the preceding FOR
FURTHER INFORMATION CONTACT section.
B. How Should I Submit CBI To the Agency?
Do not submit information that you consider to be CBI
electronically through EPA's electronic public docket or by e-mail.
Commenters wishing to submit proprietary information for consideration
must clearly distinguish such information from other comments and
clearly label it as CBI. Send submissions containing such proprietary
information directly to the following address only, and not to the
public docket, to ensure that proprietary information is not
inadvertently placed in the docket: Attention: OEI Document Control
Officer, Mail Code: 2822T, U.S. EPA, 1200 Pennsylvania Ave., NW.,
Washington, DC, 20460. You may claim information that you submit to EPA
as CBI by marking any part or all of that information as CBI (if you
submit CBI on disk or CD ROM, mark the outside of the disk or CD ROM as
CBI and then identify electronically within the disk or CD ROM the
specific information that is CBI). The EPA will disclose information
claimed as CBI only to the extent allowed by the procedures set forth
in 40 CFR part 2.
In addition to one complete version of the comment that includes
any information claimed as CBI, a copy of the comment that does not
contain the information claimed as CBI must be submitted for inclusion
in the public docket and EPA's electronic public docket. If you submit
the copy that does not contain CBI on disk or CD ROM, mark the outside
of the disk or CD ROM clearly that it does not contain CBI. Information
not marked as CBI will be included in the public docket and EPA's
electronic public docket without prior notice. If you have any
questions about CBI or the procedures for claiming CBI, please consult
the person identified in the FOR FURTHER INFORMATION CONTACT section.
II. What Did EPA Propose and What Is the Purpose of This Notice?
In response to a petition to add diisononyl phthalate (DINP) to the
EPCRA section 313 list of toxic chemicals, EPA published a proposed
rule to add a DINP category to the EPCRA section 313 list (65 FR 53681,
September 5, 2000). The proposed rule was based on information
contained in the hazard assessment for DINP that was developed in
response to the petition (Ref. 1). In response to comments on the
proposal, EPA revised its hazard assessment for DINP. The purpose of
this notice is to allow the public an opportunity to comment on a
revised hazard assessment that EPA has developed for DINP (Ref. 2).
A. What Preliminary Determinations Did EPA Reach in the Proposed Rule?
After a review of the data available at the time, the Agency
preliminarily determined that there was sufficient evidence to support
the conclusion that DINP can reasonably be anticipated to cause
carcinogenicity and liver, kidney, and developmental toxicity. The
preliminary findings were summarized as follows.
DINP has been shown to cause developmental toxicity in prenatal
rats. This developmental toxicity included significant decreases in
the mean body weight of pups from two generations which may result
in serious developmental delays in growth throughout the lifetime.
In addition, skeletal variations were observed which may interfere
with normal nerve function and blood flow. Kidney effects in fetuses
were observed which might lead to progressive kidney damage and
impaired kidney function.
DINP has been shown to cause chronic liver and kidney toxicity
in rats and mice. The liver effects are indicators of the serious
liver damage produced by DINP and are early indicators of the tissue
damage which leads to DINP-induced tumors. In addition to chronic
liver toxicity, biochemical indicators of chronic kidney toxicity
were evident in male and female rats. Also, chronic progressive
irreversible kidney damage (nephropathy) occurred in female mice
which lead to early mortality.
DINP has been shown to be a liver carcinogen in rats and mice,
to induce kidney tumors in male rats, and to increase the incidence
of mononuclear cell leukemia. (65 FR 53686, September 5, 2000).
EPA EAPA also stated that:
EPA currently believes that it is reasonable to anticipate that
all members of the DINP category as described will exhibit
carcinogenicity and liver, kidney, and developmental toxicity in
humans and that creating a category of DINP is the most appropriate
way to list this class of chemicals. (65 FR 53686, September 5,
2000).
B. Why Has EPA Issued This Notice?
EPA received significant comments on its original hazard assessment
for DINP both during the comment period for the proposed rule and in
later submissions to the Agency. Based on the comments EPA received,
the Agency decided to revise the DINP hazard assessment and subject the
document to a peer review process. The revised DINP hazard assessment
was reviewed by experts within EPA and then by a group of external peer
reviewers. Based on these reviews EPA made additional revisions to the
DINP hazard assessment. The comments received from the external peer
reviewers and EPA's responses to those comments have been placed in the
docket for this notice (Ref. 3). The revisions to the hazard assessment
have an impact on the preliminary conclusions that EPA reached in the
proposed rule. Therefore, EPA is making the revised DINP hazard
assessment available for public comment through the publication of this
notice.
III. How Has the Hazard Assessment Changed?
The original DINP hazard assessment has been updated to include the
most recent data available on the toxicity of DINP and has been revised
based on public comments and on feedback from internal and external
peer reviewers. Based on public comment, the revised hazard assessment
has been expanded
[[Page 34439]]
to include a more extensive discussion of each human health endpoint of
concern. The significant substantive changes to the hazard assessment
are discussed in the following sections.
A. What Changes Have Been Made to the Discussion of Carcinogenicity?
1. Liver Cancer. In the original DINP hazard assessment (Ref. 1),
EPA stated that DINP was a liver carcinogen in rats and mice and could
reasonably be anticipated to cause cancer in humans. Liver tumors were
demonstrated in three independent chronic studies in rats and mice
(Refs. 4, 5, and 6). At that time, EPA acknowledged that there was an
ongoing scientific discussion regarding the role of peroxisome
proliferation and peroxisome proliferation activating receptor-/ (PPAR/
) activation in rodent liver tumors and its relevance to human cancer.
In accordance with EPA's cancer guidelines (Ref. 7), however, the
data were considered insufficient to demonstrate that a response in
animals was not relevant to any human situation. Therefore, the default
assumption that positive effects in animal studies indicate that DINP
could have carcinogenic potential in humans was warranted. Based on
this default assumption, EPA's position in the original hazard
assessment was that DINP could reasonably be anticipated to cause
cancer in humans.
Recently, the Office of Prevention, Pesticides and Toxics
Substances (OPPTS) presented a draft of a proposed OPPTS science policy
on PPAR[alpha]mediated hepatocarcinogenicity to the Federal
Insecticide, Fungicide, and Rodenticide Act (FIFRA) Science Advisory
Panel (SAP), a Federal advisory committee. The SAP serves as the
primary scientific peer review mechanism of OPPTS under Section 25(d)
of FIFRA. The guidance document described an approach OPPTS proposed to
use to evaluate the scientific information regarding the mode of action
of PPAR/ activating chemicals, such as DINP, in rodent liver tumors and
the relevance of this mode of action for human liver cancer. EPA is
currently reviewing the responses from the FIFRA SAP and will notify
the public on a science policy decision. EPA therefore reserves
judgment on whether DINP can reasonably be anticipated to cause liver
cancer in humans, pending the results of this EPA review. The revised
DINP hazard assessment has been updated to include a discussion of
EPA's ongoing review.
2. Mononuclear Cell Leukemia. In the original DINP hazard
assessment (Ref. 1), EPA stated that there were clear, statistically
significant increases in the incidences of mononuclear cell leukemia
(MNCL) in two independent chronic oral studies using Fischer rats.
Fischer rats (F-344) had an increased mortality due to MNCL in DINP-
treated rats suggesting that DINP is associated with the elevated
incidence, progression and severity of MNCL. The tumor findings may be
biologically significant because the time to onset of tumor was shorter
and the disease was more severe in treated animals compared to the
timing of onset and severity in control animals. EPA believes that it
is therefore highly unlikely that these findings were unrelated to
treatment. EPA notes, however, that there are several sources of
uncertainty in the interpretation of the MNCL data. These include a
high and variable background rate of MNCL and a lack of information on
the mode of action for induction of MNCL. Furthermore, some scientists
believe that MNCL may be a rodent-specific cancer of unclear relevance
to human cancer. EPA is reviewing the scientific question of the
biological relevance of MNCL and human cancer. As a result of these
scientific uncertainties, EPA reserves judgment on the human
significance of MNCL and whether DINP can reasonably be anticipated to
cause cancer in humans.
Because the data currently available do not permit a clear
conclusion on the relevance of DINP-induced liver tumors and MNCL at
this time, EPA reserves judgment on whether DINP can reasonably be
anticipated to cause cancer in humans.
B. What Changes Have Been Made to the Discussion of Chronic Liver
Toxicity?
In the original DINP hazard assessment (Ref. 1), EPA stated that
DINP could reasonably be anticipated to cause chronic liver toxicity
based on increased liver weight, increased liver enzyme activities, and
chronic liver lesions based on two chronic studies in rats (Refs. 4 and
5). In the revised hazard assessment, the chronic liver lesion is
described in more detail and identified as spongiosis hepatis. The
incidence of spongiosis hepatis was dose-related and significantly
elevated in male rats chronically treated with DINP in two independent
studies conducted by different laboratories. The incidence of
spongiosis hepatis was not elevated in female rats or in male or female
mice. Based on the available data, the Agency has identified a No
Observed Adverse Effect Level (NOAEL) of 15 milligrams per kilogram per
day (mg/kg/day) and a Lowest Observed Adverse Effect Level (LOAEL) of
152 mg/kg/day for the Lington et al. study (Ref. 4) and a NOAEL of 88
mg/kg/day and a LOAEL of 359 mg/kg/day for the Moore study (Ref. 5),
based on indications of serious liver damage (i.e., a statistically
significant increased incidence of spongiosis hepatis and increased
liver weight and liver enzyme activities) in male rats chronically
exposed to DINP for two years.
The Agency believes that the existing data support the conclusion
that the increased incidence of spongiosis hepatis in dosed rats is
clearly related to DINP treatment. In further evaluating the data for
hepatic spongiosis, the Agency considered (1) The possibility that the
occurrence of spongiosis hepatis and induction of peroxisome
proliferation were related; (2) the possibility that the occurrence of
spongiosis hepatis was a consequence of MNCL; (3) the relationship of
spongiosis hepatis to hepatocellular cancer; and (4) the human
relevance of hepatis spongiosis.
EPA believes that the occurrence of spongiosis hepatis is not
likely to be related to the occurrence of peroxisome proliferation,
hepatocellular cancer, or MNCL. Spongiosis hepatis is a lesion of the
perisinusoidal cells of the liver (the Ito cells) whereas the
carcinogenic and other toxic effects of DINP on the liver involved
hepatocytes, which are the predominant cell type in the liver. This
lesion has been found in livers of rodents and fish following exposure
to substances (e.g., nitrosamines) that induce cancer in these species
(Ref. 8). Both chronic studies of DINP (Refs. 4 and 5) reported
increased incidences of treated male rats with spongiosis hepatis. EPA
has determined that spongiosis hepatis is relevant to human health and
that determination is discussed in detail in the revised hazard
assessment (Ref. 2, section II.E.1).
Spongiosis hepatis was also considered to be a significant finding
by the authoritative scientific panel, the U.S. Consumer Product Safety
Commission's (CPSC) Chronic Hazard Advisory Panel (CHAP) on DINP in
their final report (Ref. 9). In addition to the CPSC panel report, a
Histopathology Peer Review and Pathology Working Group convened by
Experimental Pathology Laboratories (ELP) (Ref. 10) independently
evaluated the liver slides from rats chronically treated with DINP and
confirmed that the spongiosis hepatitis was increased in male rats of
both chronic rodent studies. These findings support EPA's position that
chronic liver toxicity is an endpoint of concern for DINP. At the time
of the development of the original DINP hazard assessment, EPA had not
[[Page 34440]]
reviewed the ELP report (Ref. 10), or seen the CHAP report (Ref. 9)
that discusses the ELP report conclusions because the final CHAP report
was not available.
IV. How Does the Revised Hazard Assessment Impact EPA's Previous
Conclusions About the Toxicity of DINP?
In the previous DINP hazard assessment (Ref. 1), carcinogenicity
was determined to be a significant concern for DINP. However, based on
the revised hazard assessment (Ref. 2), at this time EPA reserves
judgment on whether cancer is an endpoint of concern for DINP. This
conclusion may change in the future depending on how EPA resolves the
issues concerning the human relevance of the types of tumors that DINP
has been shown to cause. The revised hazard assessment also provides a
more detailed and specific discussion about the ability of DINP to
cause chronic liver toxicity than that contained in the previous hazard
assessment. The revised discussion on chronic liver toxicity provides
additional support to the previous conclusion that DINP causes chronic
liver toxicity.
The revised DINP hazard assessment does not affect the previous
conclusions from the original DINP hazard assessment that developmental
and chronic kidney toxicity are endpoints of concern for DINP. In
addition, nothing in the revised DINP hazard assessment affects EPA's
previous conclusion that the addition of DINP as a category of
chemicals, rather than individual chemical listings, would be
appropriate.
V. What Type of Comments Is EPA Interested In Receiving?
EPA is requesting comments on all parts of the revised hazard
assessment. However, EPA is specifically interested in comments on the
sections of the revised hazard assessment that deal with
carcinogenicity and chronic liver toxicity. EPA also requests
commenters to provide any additional data or information on the human
relevance of any of the adverse effects discussed in the revised hazard
assessment.
VI. References
EPA has established an official public docket for this action under
Docket ID No. TRI-2005-0004. The previous docket number for the
proposed rule was OEI-100004 and was assigned prior to the development
of EPA's electronic public docket and comment system. Therefore, EPA is
creating a new electronic docket number for this action. All the
materials submitted to docket number OEI-100004 have been transferred
to docket number TRI-2005-0004. The public docket includes information
considered by EPA in developing this proposed rule, including the
documents listed below, which are electronically or physically located
in the docket. In addition, interested parties should consult documents
that are referenced in the documents that EPA has placed in the docket,
regardless of whether these referenced documents are electronically or
physically located in the docket. For assistance in locating documents
that are referenced in documents that EPA has placed in the docket, but
that are not electronically or physically located in the docket, please
consult the person listed in the above FOR FURTHER INFORMATION CONTACT
section.
1. USEPA, OEI. 2000. Technical Review of Diisononyl Phthalate.
Office of Environmental Information, Becki Madison, Christine
Augustyniak, Ron Bloom, Candace Brassard, Ossi Meyn, Nicole Paquette,
Pam Russell, and John Scalera.
2. USEPA, OEI. 2005. Revised Technical Review of Diisononyl
Phthalate, March 4, 2005. Office of Environmental Information,
Environmental Analysis Division, Analytical Support Branch. Amy Newman,
Candace Brassard, Kathryn Montague, Nicole Paquette, Ph.D., and John
Scalera.
3. USEPA, OEI. 2005. Response to External Peer Review Comments on
the Revised Technical Review for Diisononyl Phthalate, April 2005.
4. Lington, A.W.; Bird M.G.; Plutnick, R.T.; Stubblefield, W.A.;
and Scala, RA. 1997. Chronic toxicity and carcinogenic evaluation of
diisononyl phthalate in rats. Fundam. Appl. Toxicol 36: 79-89.
5. Moore, M.R., 1998. 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.
6. Moore M.R., 1998. 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.
7. USEPA. 1999. Draft Revised Guidelines for Carcinogen Risk
Assessment. NCEA-F-0644, July 1999.
8. Stoebel, P.; Mayer, F.; Zerban, H., Bannasch, P. 1995.
Spongiotic pericytoma: a benign neoplasm deriving from the
perisinusoidal cells in rat liver. Am. J. Pathol. 146:903-913.
9. Chronic Hazard Advisory Panel on Diisononyl Phthalate. Report to
the U.S. Consumer Product Safety Commission. June 2001. U.S. Consumer
Product Safety Commission, Bethesda, MD.
10. Experimental Pathology Laboratories, 1999. Histology peer
review and pathology working group review of selected lesions of the
liver and spleen in male and female F344 rats exposed to DINP. EPL
Project number 303-013, Pathology Report.
List of Subjects in 40 CFR Part 372
Environmental protection, Chemicals, Community right-to-know,
Hazardous substances, Intergovernmental relations, Reporting and
recordkeeping requirements, Superfund.
Dated: June 7, 2005.
Kimberly T. Nelson,
Assistant Administrator for Office of Environmental Information and
Chief Information Officer.
[FR Doc. 05-11664 Filed 6-13-05; 8:45 am]
BILLING CODE 6560-50-P