[Federal Register: March 7, 2006 (Volume 71, Number 44)]
[Proposed Rules]
[Page 11483-11504]
[DOCID:fr07mr06-32]

-----------------------------------------------------------------------

Part IV

Environmental Protection Agency

-----------------------------------------------------------------------

40 CFR Part 723

Premanufacture Notification Exemption for Polymers; Amendment of
Polymer Exemption Rule to Exclude Certain Perfluorinated Polymers;
Proposed Rule

-----------------------------------------------------------------------

ENVIRONMENTAL PROTECTION AGENCY

40 CFR Part 723

[EPA-HQ-OPPT-2002-0051; FRL-7735-5]
RIN 2070-AD58

Premanufacture Notification Exemption for Polymers; Amendment of
Polymer Exemption Rule to Exclude Certain Perfluorinated Polymers

AGENCY: Environmental Protection Agency (EPA).

ACTION: Proposed rule.

-----------------------------------------------------------------------

SUMMARY: EPA is proposing to amend the polymer exemption rule, which
provides an exemption from the premanufacture notification (PMN)
requirements of the Toxic Substances Control Act (TSCA), to exclude
from eligibility polymers containing as an integral part of their
composition, except as impurities, certain perfluoroalkyl moieties
consisting of a CF3- or longer chain length. This proposed exclusion
includes polymers that contain any one or more of the following:
Perfluoroalkyl sulfonates (PFAS); perfluoroalkyl carboxylates (PFAC);
fluorotelomers; or perfluoroalkyl moieties that are covalently bound to
either a carbon or sulfur atom where the carbon or sulfur atom is an
integral part of the polymer molecule. If finalized as proposed, any
person who intends to manufacture (or import) any of these polymers not
already on the TSCA Inventory would have to complete the TSCA
premanufacture review process prior to commencing the manufacture or
import of such polymers. EPA believes this proposed change to the
current regulation is necessary because, based on recent information,
EPA can no longer conclude that these polymers ``will not present an
unreasonable risk to human health or the environment,'' which is the
determination necessary to support an exemption under TSCA, such as the
polymer exemption rule.

DATES: Comments must be received on or before May 8, 2006.

ADDRESSES: Submit your comments, identified by docket identification
(ID) number EPA-HQ-OPPT-2002-0051, by one of the following methods:
     http://www.regulations.gov. Follow the on-line

instructions for submitting comments.
     E-mail<EMAIL_ADDRESS>     Mail: Document Control Office (7407M), Office of Pollution
Prevention and Toxics (OPPT), Environmental Protection Agency, 1200
Pennsylvania Ave., NW., Washington, DC 20460-0001.
     Hand Delivery: OPPT Document Control Office (DCO), EPA
East Bldg., Rm. 6428, 1201 Constitution Ave., NW., Washington, DC.
Attention: Docket ID number EPA-HQ-OPPT-2002-0051. The DCO is open from
8 a.m. to 4 p.m., Monday through Friday, excluding legal holidays. The
telephone number for the DCO is<PHONE_NUMBER>. 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 number EPA-HQ-OPPT-
2002-0051. EPA's policy is that all comments received will be included
in the public docket without change and may be made available on-line
at http://www.regulations.gov, 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 regulations.gov or e-
mail. The regulations.gov website is an ``anonymous access'' system,
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 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
regulations.gov index. Although listed in the index, some information
is not publicly available, e.g., 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 electronically through regulations.gov or in
hard copy at the OPPT Docket, EPA Docket Center (EPA/DC), EPA West, Rm.
B102, 1301 Constitution Ave., NW., Washington, DC. The EPA Docket
Center 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<PHONE_NUMBER>, and the telephone number for the
OPPT Docket is<PHONE_NUMBER>.

FOR FURTHER INFORMATION CONTACT: For general information contact: Colby
Lintner, Regulatory Coordinator, Environmental Assistance Division
(7408M), Office of Pollution Prevention and Toxics, Environmental
Protection Agency, 1200 Pennsylvania Ave., NW., Washington, DC 20460-
0001; telephone number:<PHONE_NUMBER>; e-mail address:
<EMAIL_ADDRESS>
    For technical information contact: Geraldine Hilton, Chemical
Control Division (7405M), Office of Pollution Prevention and Toxics,
Environmental Protection Agency, 1200 Pennsylvania Ave., NW.,
Washington, DC 20460-0001; telephone number:<PHONE_NUMBER>; e-mail
address<EMAIL_ADDRESS>
SUPPLEMENTARY INFORMATION:

I. General Information

A. Does this Action Apply to Me?

    You may be potentially affected by this action if you manufacture
or import polymers that contain as an integral part of their
composition, except as impurities, certain perfluoroalkyl moieties
consisting of a CF3- or longer chain length (``affected polymers''). As
specified in the proposed regulatory text (Sec.  723.250(d)(6)), this
includes polymers that contain any one or more of the following: PFAS;
PFAC; fluorotelomers; or perfluoroalkyl moieties that are covalently
bound to either a carbon or sulfur atom where the carbon or sulfur atom
is an integral part of the polymer molecule. Persons who import or
intend to import polymers that are covered by the final rule would be
subject to TSCA section 13 (15 U.S.C. 2612) import certification
requirements, and to the regulations codified at 19 CFR 12.118 through
12.127 and 127.28. Those persons must certify that they are in
compliance with the PMN requirements. The EPA policy in support of
import certification appears at 40 CFR part 707, subpart B. Importers
of formulated products that contain a polymer that is a subject of this
proposed rule as a component (for example, for use as a water-proof
coating for textiles or as a top anti-reflective coating (TARC) used to
manufacture integrated circuits) may also be potentially affected. A
list of potential monomers and reactants that could be used to
manufacture polymers

that would be affected by this rulemaking may be found in the public
docket (Ref. 1). Potentially affected entities may include, but are not
limited to:
     Chemical manufacturers or importers (NAICS 325), e.g.,
persons who manufacture (defined by statute to include import) one or
more of the subject chemical substances.
     Chemical exporters (NAICS 325), e.g., persons who export,
or intend to export, one or more of the subject chemical substances.
    This listing 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 this unit could also be
affected. The North American Industrial Classification System (NAICS)
codes have been provided to assist you and others in determining
whether this action might apply to certain entities. To determine
whether you or your business may be affected by this action, you should
carefully examine the applicability provisions in 40 CFR 723.250. If
you have any questions regarding the applicability of this action to a
particular entity, consult the technical person listed under FOR
FURTHER INFORMATION CONTACT.

B. What Should I Consider as I Prepare My Comments for EPA?

    1. Submitting CBI. Do not submit this information to EPA through
regulations.gov or e-mail. Clearly mark the part or all of the
information that you claim to be CBI. For CBI information in a disk or
CD ROM that you mail to EPA, 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 claimed as CBI. In addition to one
complete version of the comment that includes 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.
Information so marked will not be disclosed except in accordance with
procedures set forth in 40 CFR part 2.
    2. Tips for preparing your comments. When submitting comments,
remember to:
    i. Identify the document by docket number and other identifying
information (subject heading, Federal Register date, and page number).
    ii. Follow directions. The Agency may ask you to respond to
specific questions or organize comments by referencing a Code of
Federal Regulations (CFR) part or section number.
    iii. Explain why you agree or disagree; suggest alternatives and
substitute language for your requested changes.
    iv. Describe any assumptions and provide any technical information
and/or data that you used.
    v. If you estimate potential costs or burdens, explain how you
arrived at the estimate.
    vi. Provide specific examples to illustrate your concerns and
suggested alternatives.
    vii. Explain your views as clearly as possible, avoiding the use of
profanity or personal threats.
    viii. Make sure to submit your comments by the comment period
deadline identified.

II. Background

A. What Action is the Agency Taking?

    The Agency is proposing to exclude from the polymer exemption rule
(40 CFR 723.250), which exempts certain chemical substances from TSCA
section 5 PMN requirements, polymers containing as an integral part of
their composition, except as impurities, certain perfluoroalkyl
moieties consisting of a CF3- or longer chain length. This exclusion
includes polymers that contain any one or more of the following: PFAS;
PFAC; fluorotelomers; or perfluoroalkyl moieties that are covalently
bound to either a carbon or sulfur atom where the carbon or sulfur atom
is an integral part of the polymer molecule. The effective date of the
final rule would be one year from the date of publication of the final
rule. Manufacture or import of any of these polymers not already on the
TSCA Inventory, including polymers currently being produced under the
polymer exemption rule, would no longer be eligible for the polymer
exemption and, in the case of continued manufacture or import after the
effective date of the final rule, would require completion of the
premanufacture review requirements under TSCA section 5(a)(1)(A) and 40
CFR part 720 prior to the effective date of the final rule. After
expiration of the one year period between the publication date of the
final rule and the effective date, the PMN requirement would apply in
full to manufacturers and importers of all polymers that are subject to
the final rule.
    EPA is actively working with industry to develop more complete data
on affected polymers. In light of these efforts, certain publicly
available and confidential business information regarding the specific
chemicals manufactured, current production volumes, uses/applications,
environmental fate and effects, and toxicity of the polymeric materials
that would be subject to this proposed rule has been made and continues
to be made available to EPA on an ongoing basis. Accordingly, EPA may
supplement the public docket for this proposed rule with relevant non-
confidential business information as it is received by the Agency. Non-
confidential information related to this proposed rule may also be
found in administrative record number (AR) AR-226, which is the public
administrative record that the Agency has established for
perfluorinated chemicals generally. Interested parties should consult
AR-226 for additional information on PFAS, PFAC, fluorotelomers, or
other perfluoroalkyl moieties. To receive an index of AR-226, contact
the EPA Docket Center by telephone:<PHONE_NUMBER> or e-mail:
<EMAIL_ADDRESS>
    Additional information may be found in EPA Docket ID No. OPPT-2003-
0012, which covers the Agency's enforceable consent agreement (ECA)
process for certain of these chemicals. Instructions on accessing an
EPA public docket are provided at the beginning of this document under
ADDRESSES.

B. What is the Agency's Authority for Taking This Action?

    Section 5(a)(1)(A) of TSCA requires persons to notify EPA at least
90 days before they manufacture or import a new chemical substance for
commercial purposes. Section 3(9) of TSCA defines a ``new chemical
substance'' as any substance that is not on the Inventory of Chemical
Substances compiled by EPA under section 8(b) of TSCA. Section 5(h)(4)
of TSCA authorizes EPA, upon application and by rule, to exempt the
manufacturer or importer of any new chemical substance from part or all
of the provisions of section 5 if the Agency determines that the
manufacture, processing, distribution in commerce, use, or disposal of
such chemical substance, or any combination of such activities will not
present an unreasonable risk of injury to human health or the
environment. Section 5(h)(4) also authorizes EPA to amend or repeal
such rules. EPA is acting under these authorities to amend the polymer
exemption rule at 40 CFR 723.250.

C. Why is the Agency Taking This Action?

    1. Polymers containing PFAS or PFAC. EPA is proposing to amend the
polymer exemption rule, last amended in 1995, because the Agency has
received information which suggests that polymers containing PFAS or
PFAC may degrade and release fluorochemical

residual compounds into the environment. Once released, PFAS or PFAC
are expected to persist in the environment, are expected to
bioaccumulate, and are expected to be highly toxic. Accordingly, EPA
believes that it can no longer make the determination that the
manufacturing, processing, distribution in commerce, use, or disposal
of polymers containing PFAS or PFAC ``will not present an unreasonable
risk to human health or the environment'' as required under TSCA
section 5(h)(4).
    PFAS or PFAC are used in a variety of polymeric substances to
impart oil and water resistance, stain and soil protection, and reduced
flammability. The same features that make the polymeric coatings
containing PFAS or PFAC useful, allow the polymeric compound to be
stable to the natural environmental conditions that produce
degradation. It has been demonstrated that PFAS or PFAC-containing
compounds can undergo degradation (chemical, microbial, or photolytic)
of the non-fluorinated portion of the molecule leaving the remaining
perfluorinated acid untouched (Ref. 2). Further degradation of the
perfluoroalkyl residual compounds is extremely difficult. Even under
routine conditions of municipal waste incinerators (MWIs), the Agency
believes that the PFAS and PFAC produced by oxidative thermal
decomposition of the polymers will remain intact (the typical
conditions of a MWI are not stringent enough to cleave the carbon-
fluorine bonds) to be released into the environment. EPA has evidence
that polymers containing PFAS or PFAC may degrade, possibly by
incomplete incineration, and release these perfluorinated chemicals
into the environment (Ref. 3).
    EPA has received data on the PFAS and PFAC chemicals
perfluorooctane sulfonate (PFOS) and perfluorooctanoic acid (PFOA),
respectively. Biological sampling recently revealed the presence of
PFOS and PFOA in fish, birds, and mammals, including humans across the
United States and in other countries. The widespread distribution of
the chemicals suggests that PFOS and PFOA may bioaccumulate. PFOS and
PFOA have a high level of toxicity and have shown liver, developmental,
and reproductive toxicity at very low dose levels in exposed laboratory
animals (Ref. 4).
    Although the Agency has far more data on PFOS and PFOA than on
other PFAS and PFAC chemicals, EPA believes that other PFAS and PFAC
chemicals of CF3- or longer chain length may share similar toxicity,
persistence and bioaccumulation characteristics. Based on currently
available information, EPA believes that, while all PFAS and PFAC
chemicals are expected to persist, the length of the perfluorinated
chain may have an effect on the other areas of concern for these
chemicals: Bioaccumulation and toxicity. PFAS and PFAC chemicals with
longer carbon chain lengths may be of greater concern (Refs. 5, 6, and
7). EPA has insufficient evidence at this time, however, to
definitively establish a lower carbon chain length limit to meet the
``will not present an unreasonable risk'' finding, which is the
determination necessary to support an exemption under section 5(h)(4)
of TSCA.
    The Agency, working in cooperation with the fluorochemical
industry, has been investigating the physicochemical properties, the
environmental fate and distribution, and the toxicity of PFAS and PFAC
chemicals, including polymers already in production. These data help
the Agency to evaluate these polymers to ascertain any potential risks
on a case-by-case basis.
    2. Polymers containing fluorotelomers or other perfluoroalkyl
moieties. EPA is also proposing to exclude from the exemption polymers
that contain fluorotelomers, or that contain perfluoroalkyl moieties of
a CF3- or longer chain length that are covalently bound to either a
carbon or sulfur atom where the carbon or sulfur atom is an integral
part of the polymer molecule. EPA has received data on various
perfluorinated chemical substances that indicate potential concerns and
that the Agency should evaluate polymers that contain these
perfluoroalkyl moieties through the PMN process. For example, the
fluorotelomer alcohol 2-(perfluorooctyl)ethanol [678-39-7], also known
as 8-2 alcohol, has been shown to degrade to form PFOA when exposed to
activated sludge during accelerated biodegradation studies (Ref. 8).
    Initial test data from a study in rats dosed with fluorotelomer
alcohol and other preliminary animal studies on various telomeric
products containing fluorocarbons structurally similar to PFAC or PFAS
have demonstrated a variety of adverse effects including liver, kidney
and thyroid effects (Ref. 9).
    Preliminary investigations have demonstrated the presence of
fluorotelomer alcohols in the air in 6 different cities (Ref. 10). This
finding is significant because it is indicative of widespread
fluorotelomer alcohol distribution and it further indicates that air
may be a route of exposure to these chemicals, which can ultimately
become PFOA. Fluorotelomer alcohols are generally incorporated into the
polymers via covalent ester linkages, and it is possible that
degradation of the polymers may result in release of the fluorotelomer
alcohols to the environment.
    Based on the presence of fluorotelomer alcohols in the air, the
growing data demonstrating that fluorotelomer alcohols metabolize or
degrade to generate PFOA (Ref. 11), the preliminary toxicity data on
certain compounds containing fluorotelomers (such as the 8-2 alcohol),
and the possibility that polymers containing fluorotelomers as an
integral part of the polymer composition may degrade in the environment
thereby releasing fluorotelomer alcohols or other perfluoroalkyl-
containing substances, EPA believes that it can no longer conclude that
polymers containing fluorotelomers as an integral part of the polymer
composition ``will not present an unreasonable risk of injury to health
or the environment'' as required for an exemption under section 5(h)(4)
of TSCA. Therefore, EPA is proposing to exclude polymers that contain
such fluorotelomers from the polymer exemption at 40 CFR 723.250.
    Although EPA does not have specific data demonstrating that
polymers containing perfluoroalkyl moieties other than PFAS, PFAC, or
fluorotelomers present the same concerns as those containing PFAS,
PFAC, or fluorotelomers, EPA is nevertheless proposing to exclude
polymers containing perfluoroalkyl groups, consisting of a CF3- or
longer chain length, that are covalently bound to either a carbon or
sulfur atom where the carbon or sulfur atom is an integral part of the
polymer molecule from the polymer exemption. Based on available data
which indicates that compounds containing PFAS or PFAC may degrade in
the environment thereby releasing the PFAS or PFAC moiety, and that
fluorotelomers may degrade in the environment to form PFAC, EPA
believes that it is possible for polymers containing these other types
of perfluoroalkyl moieties to also degrade over time in the environment
thereby releasing the perfluoroalkyl moiety. EPA also believes that
once released, such moieties may potentially degrade to form PFAS or
PFAC. EPA does not believe, therefore, that it can continue to make the
``will not present an unreasonable risk of injury to health or the
environment'' finding for such polymers and is proposing to exclude
them from the polymer exemption. EPA is specifically requesting comment
on this aspect of the proposed rule. Please see Unit VII. of this
document for

specific information that EPA is interested in obtaining to evaluate
whether continued exemption for polymers containing fluorotelomers or
perfluoroalkyl moieties that are covalently bound to either a carbon or
sulfur atom where the carbon or sulfur atom is an integral part of the
polymer molecule is appropriate.

D. Would Manufacturers or Importers of Affected Polymers That Were
Previously Manufactured Under the Terms of the Polymer Exemption Rule
Need to Complete the PMN Review Process or to Cease Production?

    This proposed rule would allow manufacturers or importers of
affected polymers, who are in full compliance with the terms of the
polymer exemption rule, to continue manufacture or import for a period
of one year after the date of publication of the final rule. However,
after the one-year period, polymers that are subject to the final rule
(including affected polymers made under the polymer exemption rule
since promulgation of the 1995 amendment to the rule) would no longer
be eligible for exemption under the polymer exemption rule. Therefore,
a person who intends to continue manufacturing or importing polymers
subject to the final rule without interruption would have to complete
the PMN review process before the effective date in order to comply
with the final rule. Manufacturers or importers of polymers that are
already on the Inventory of Chemical Substances compiled and published
under section 8(b) of TSCA (15 U.S.C. 2607(b)) would not be affected by
this proposed amendment. The PMN requirements in section 5(a) of TSCA
apply only to new chemical substances which are those that are not
included on the Inventory of Chemical Substances. However, several of
the polymers that are already included on the Inventory of Chemical
Substances are subject to control actions under TSCA section 5,
including section 5(e) consent orders and section 5(a)(2) Significant
New Use Rules (SNURS).

III. Summary of This Proposed Rule

A. Polymers Containing PFAS or PFAC

    EPA is proposing to amend the polymer exemption rule (40 CFR
723.250) to exclude polymers containing PFAS or PFAC consisting of a
CF3- or longer chain length from eligibility under the polymer
exemption. This exclusion would be codified at 40 CFR 723.250(d)(6).
EPA has received data on PFOS (a PFAS chemical containing a
perfluoroalkyl moiety with eight carbon atoms) and PFOA (a PFAC
chemical containing a perfluoroalkyl moiety with seven perfluorinated
carbon atoms), that indicate that these chemicals are expected to
persist and have the potential to bioaccumulate and be hazardous to
human health and the environment. PFOS and PFOA have been found in the
blood of workers exposed to the chemicals and in the general
populations of the United States and other countries. They have also
been found in many terrestrial and aquatic animal species worldwide.
PFAS and PFAC chemicals used in the production of polymers may be
released into the environment by degradation. It is possible,
therefore, that the widespread presence of PFOS and PFOA in the
environment may be due, in part, to the degradation of such polymers
and the subsequent release of the PFAS and PFAC components into the
environment. However, the method of degradation and environmental
distribution is uncertain.
    Animal test data for PFOS and PFOA have shown liver, developmental,
and reproductive toxicity at very low exposure levels. Animal test data
indicate that PFOA may cause cancer, and an epidemiologic study
reported an increased incidence of bladder cancer mortality in a small
number of workers at a plant that manufactures perfluorinated
chemicals. The number of carbon atoms on the PFAS/PFAC component may
influence the bioaccumulation potential and the toxicity. In
particular, there is some evidence that PFAS/PFAC moieties with longer
carbon chains may present greater concerns for bioaccumulation
potential and toxicity than PFAS/PFAC moieties with shorter carbon
chains (Refs. 5, 6, and 7). Although there is insufficient
understanding available at present to determine the carbon number below
which PFAS and PFAC chemicals ``will not present an unreasonable
risk,'' efforts are underway to develop a better understanding of the
environmental fate, bioaccumulation potential, and human and
environmental toxicity of PFAS and PFAC chemicals with shorter carbon
chains. At this time, however, EPA can no longer conclude that polymers
containing PFAS or PFAC will not present an unreasonable risk to human
health or the environment. Therefore, this proposed amendment would
exclude polymers containing PFAS or PFAC from eligibility for exemption
from TSCA section 5(a)(1)(A) reporting requirements for new chemical
substances.

B. Polymers Containing Fluorotelomers or Other Perfluoroalkyl Moieties

    EPA is also proposing to exclude from the polymer exemption rule
polymers that contain fluorotelomers, or that contain perfluoroalkyl
moieties of a CF3- or longer chain length that are covalently bound to
either a carbon or sulfur atom where the carbon or sulfur atom is an
integral part of the polymers molecule. EPA has concerns with respect
to the potential health and environmental effects of these substances
and the Agency believes that polymers containing such moieties should
be subject to the premanufacture review process so that EPA can better
evaluate and address these concerns.
    As discussed in Unit IV.E., there is a growing body of data
demonstrating that fluorotelomer alcohols metabolize or degrade to
generate PFOA. Initial studies have also demonstrated toxic effects of
certain compounds containing fluorotelomers (derived from the 8-2
alcohol). Preliminary investigations have found that fluorotelomer
alcohols were present in the air above several cities, indicating that
these substances may be widely distributed and that air may be a route
of exposure. EPA believes that polymers containing fluorotelomers or
perfluoroalkyl moieties that are covalently bound to either a carbon or
sulfur atom where the carbon or sulfur atom is an integral part of the
polymers molecule may degrade in the environment thereby releasing
fluorotelomer alcohols or other perfluoroalkyl-containing substances.
Accordingly, EPA can no longer conclude that polymers containing
fluorotelomers and these other perfluoroalkyl moieties ``will not
present an unreasonable risk of injury to health or the environment''
as required for an exemption under section 5(h)(4) of TSCA. Therefore,
EPA is proposing to exclude such polymers from the polymer exemption at
40 CFR 723.250.

C. Proposed Implementation

    EPA is proposing to delay the implementation of the final rule in
order to provide current manufacturers or importers of the affected
polymers who are in full compliance with the terms of the existing
polymer exemption rule, additional time to come into compliance with
the amendment proposed without disrupting their ability to manufacture
or import those polymers.
    To do this, EPA is proposing to establish an effective date for the
final rule that is one year after the date of publication of the final
rule. After expiration of the one year implementation period, polymers
that

are subject to the final rule (including affected polymers made under
the polymer exemption rule) would no longer be eligible for exemption.
Therefore, a person who intends to manufacture or import polymers
subject to the final rule must complete the TSCA premanufacture review
process before the effective date. EPA believes that the one year
period between the publication date of the final rule and the effective
date of the final rule would provide adequate time for current
manufacturers and importers of the polymers subject to the final rule
to prepare and submit PMNs for those polymers and for EPA to review the
PMNs.
    As an alternative to the one year effective date, EPA could
establish an effective date of the final rule as 30 days after its
publication in the Federal Register, the minimum required by section
553(c) of the Administrative Procedure Act, but provide an extended
compliance date for those who, prior to the effective date of the final
rule, had already initiated the manufacture or import of polymers that
are subject to the final rule. Under this approach, the TSCA section
5(a)(1)(A) requirement to submit a PMN for a new chemical substance
would be re-established with respect to polymers that are subject to
the final rule, beginning 30 days after publication of the final rule
in the Federal Register. However, those who are manufacturing or
importing polymers under the existing exemption would have one year
from the effective date to complete the PMN process. EPA is
specifically requesting comment on this or other alternatives for
implementing the final rule that would achieve the purposes of TSCA
section 5 without disrupting ongoing manufacture or import of
currently-exempt polymers.

IV. Proposed Rule

A. History Subsequent to the 1995 Amendment to the Polymer Exemption
Rule

    The 1995 amendments to the polymer exemption rule expanded the
polymer exemption to include polymers made from reactants that contain
certain halogen atoms, including fluorine. The best available
information in 1995 indicated that most halogen containing compounds,
including unreactive polymers containing PFAS and PFAC chemicals, were
chemically and environmentally stable and would not present an
unreasonable risk to human health and the environment. In 1999,
however, the 3M Company (3M) provided the Agency with preliminary
reports that indicated widespread distribution of PFOS in humans and
animals (Refs. 12, 13, and 14). In addition, on May 16, 2000, 3M
announced that it would phase out perfluorooctanyl chemistry in light
of the persistence of certain fluorochemicals and their detection at
extremely low levels in the blood of the general population and
animals. 3M indicated that production of these chemicals would be
substantially discontinued by the end of 2000 (Ref. 15). Based on this
information from 3M, EPA began to investigate potential risks from PFOS
and other perfluorinated chemicals, as well as polymers containing
these chemicals. EPA believes that polymers containing PFAS or PFAC
chemicals may degrade, releasing these chemicals into the environment
where they are expected to persist. The number of carbon atoms on the
PFAS or PFAC molecule, whether as a single compound, or as a component
of a polymer, may influence bioaccumulation potential and toxicity. EPA
also believes that polymers containing fluorotelomers or perfluoroalkyl
moieties that are covalently bound to either a carbon or sulfur atom
where the carbon or sulfur atom is an integral part of the polymer
molecule may degrade, releasing these substances into the environment
where they may further degrade into PFAS or PFAC.

B. Defining Polymers That Are Subject to This Proposed Rule

    1. Polymers containing PFAS or PFAC. This proposed rule applies to
a large group of polymers containing one or more fully fluorinated
alkyl sulfonate or carboxylate groups. None of these polymers occur
naturally. Such polymers are considered ``new chemical substances''
under TSCA if they have not been included in the Inventory of Chemical
Substances compiled and published under section 8(b) of TSCA (15 U.S.C.
2607(b)). For a list of examples of the Ninth Collective Index of
chemical names and CAS Registry Numbers (CASRN) of chemical substances
used to make polymers that are subject to this proposed rule amendment,
see Ref.1. EPA has concerns for the perfluorinated carbon atoms in the
Rf substituent, below, when that Rf unit is associated with the polymer
through the carbonyl (PFAC) or sulfonyl (PFAS) group. How these
materials are incorporated into the polymer is immaterial (they may be
counter ions, terminal/end capping agents, or part of the polymer
backbone).
     O
     [par]
    PFAC Rf--C--Hetero atom (typically N or O)-Polymer

     Rf = Perfluoroalkyl CF3- or greater

     O
     [par]
    PFAS Rf--S--Hetero atom (typically N or O)-Polymer
     [par]
     O
    This proposed rule would specifically exclude from the polymer
exemption at 40 CFR 723.250 polymers that contain any PFAS or PFAC
group consisting of a CF3- or longer chain length. EPA has increasing
concerns as the number of carbon atoms that are perfluorinated in any
individual Rf substituent increases. PFOA (perfluorooctanoate) is a
PFAC (see top structure) which has 7 carbon atoms in the Rf moiety (CAS
nomenclature rules count the carbonyl carbon atom as the eighth carbon
for naming purposes, hence the octanoate terminology). PFOS
(perfluorooctane sulfonate) is a PFAS (see bottom structure) which has
8 carbon atoms in the Rf moiety. Generally, the longer the chain of
perfluorinated C atoms, the greater the persistence and retention time
in the body; furthermore, the C8 chain length has been associated with
adverse health effects.
    Most of the toxicity data currently available on PFAS and PFAC
chemicals pertain to the PFOS potassium salt (PFOSK) and the PFOA
ammonium salt

(APFO). There is some evidence that PFAS/PFAC moieties with longer
carbon chains may present greater concerns than PFAS/PFAC moieties with
shorter carbon chains (Refs. 5, 6, and 7). However, EPA has
insufficient information at this time to determine a limit for which
shorter chain lengths ``will not present an unreasonable risk to human
health or the environment.''
    2. Polymers containing fluorotelomers or other perfluoroalkyl
moieties. EPA is also proposing to exclude polymers that contain
fluorotelomers, or that contain perfluoroalkyl moieties of a CF3- or
longer chain length that are covalently bound to either a carbon or
sulfur atom where the carbon or sulfur atom is an integral part of the
polymer molecule.
    Fluorotelomers: One method that is commonly used to incorporate
perfluorinated compounds into polymers is to use fluorotelomers, such
as perfluoroalkyl ethanol. Telomerization is the reaction of a telogen
with a polymerizable ethylenic compound to form low molecular weight
polymeric compounds, commonly referred to as ``telomers.'' For example,
the reaction of pentafluoroethyl iodide (a telogen) with
tetrafluoroethylene forms a fluorotelomer iodide intermediate which is
then reacted with ethylene and converted into perfluoroalkyl ethanol.
This chemical can be further reacted to form a variety of useful
materials which may subsequently be incorporated into the polymer (Ref.
16). The fluorochemical group formed by the telomerization process is
predominantly straight chain, and depending on the telogen used
produces a product having an even number of carbon atoms. However, the
chain length of the fluorotelomer varies widely. A representative
structure for these compounds is:
    F-(CF2-CF2)x-Anything (often CH2-CH2-O-Polymer) x >= 1
    Other perfluoroalkyl moieties: Perfluoroalkyl moieties that are
covalently bound to either a carbon or sulfur atom where the carbon or
sulfur atom is an integral part of the polymer molecule can be attached
to the polymers using conventional chemical reactions. A representative
structure for these compounds is:
    F-(CF2)x-(C,S)-Polymer x >= 1

C. Concerns With Respect to Polymers Containing PFAS, PFAC,
Fluorotelomers, or Other Perfluoroalkyl Moieties

    EPA is proposing to amend the polymer exemption rule because the
Agency has received information which suggests that polymers containing
certain perfluoroalkyl moieties consisting of a CF3- or longer chain
length (i.e., PFAS, PFAC, fluorotelomers, or perfluoroalkyl moieties
that are covalently bound to either a carbon or sulfur atom where the
carbon or sulfur atom is an integral part of the polymer molecule) may
degrade and release fluorochemical residual compounds into the
environment. Once released, these substances are expected to persist in
the environment, may bioaccumulate, and may be highly toxic. The
evidence suggests that fluorotelomers and perfluoroalkyl moieties that
are covalently bound to either a carbon or sulfur atom where the carbon
or sulfur atom is an integral part of the polymer molecule do persist
in the environment, and that they can be metabolically transformed into
PFAC, which bioaccumulates and is toxic. The following sections will
summarize the concerns the Agency has for PFAS, PFAC, fluorotelomers,
or perfluoroalkyl moieties that are covalently bound to either a carbon
or sulfur atom where the carbon or sulfur atom is an integral part of
the polymer molecule.

D. Summary of Data on PFAS and PFAC

    1. Use and production volume data for PFOS. PFAS chemicals have
been in commercial use since the 1950's. There were three main
categories of use: Surface treatments, paper protectors (including food
contact papers), and performance chemicals (Ref. 3). The various
surface treatment and paper protection uses constituted the largest
volume of PFOS production and therefore, were believed to present the
greatest source of widespread human and environmental exposure to PFOS.
    Until the year 2000, 3M was the largest manufacturer of PFAS
chemicals in the United States. On May 16, 2000, following discussions
with the Agency, 3M issued a press release announcing that it would
discontinue the production of perfluorooctanyl chemicals used in the
manufacture of some of its repellent and surfactant products. In its
statement, 3M committed to ``substantially phase out production'' by
the end of calendar year 2000 (Ref. 17). In subsequent correspondence
with the Agency, 3M provided a schedule documenting its complete plan
for discontinuing all manufacture of specific PFOS and related
chemicals for most surface treatment and paper protection uses
(including food contact uses regulated by the Food and Drug
Administration (FDA)) by the end of 2000, and for discontinuing all
manufacture for any uses by the end of 2002 (Ref. 15).
    The 3M phase-out plan eliminated many of these chemicals from
further distribution in commerce. The largest production volume (both
initially produced and removed from commerce) was for polymers. Other
PFAS chemicals, however, continue to be manufactured or imported by
other companies and may be of concern. EPA followed the voluntary 3M
phase-out with the promulgation of a SNUR under TSCA section 5. The
SNUR limits any future manufacture or importation of PFOS before EPA
has had an opportunity to review activities and risks associated with
the proposed manufacture or importation (Ref. 17a).
    PFAS chemicals produced for surface treatment applications provide
soil, oil, and water resistance to personal apparel and home
furnishings. Specific applications in this use category include
protection of apparel and leather, fabric/upholstery, and carpeting.
Applications are undertaken in industrial settings such as textile
mills, leather tanneries, finishers, fiber producers, and carpet
manufacturers. PFAS chemicals are also used in aftermarket treatment of
apparel and leather, upholstery, carpet, and automobile interiors, with
the application performed by both the general public and professional
applicators (Ref. 3). In 2000, the domestic production volume of PFAS
chemicals for this use category was estimated to be 2.4 million pounds
(Ref. 15).
    PFAS chemicals produced for paper protection applications provide
grease, oil, and water resistance to paper and paperboard as part of a
sizing agent formulation. Specific applications in this use category
include food contact applications (plates, food containers, bags, and
wraps) regulated by the FDA under 21 CFR 176.170, as well as non-food
contact applications (folding cartons, containers, carbonless forms,
and masking papers). The application of sizing agents is undertaken
mainly by paper mills and, to some extent, converters, who manufacture
bags, wraps, and other products from paper and paperboard (Ref. 3). In
2000, the domestic production volume of PFOS chemicals for this use
category was estimated to be 2.7 million pounds (Ref. 15).
    PFAS chemicals in the performance chemicals category are used in a
wide variety of specialized industrial, commercial, and consumer
applications. Specific applications include fire fighting foams, mining
and oil well surfactants, acid mist suppressants for metal plating and
electronic etching baths, alkaline cleaners, floor polishes,
photographic film, denture cleaners,

shampoos, chemical intermediates, coating additives, carpet spot
cleaners, and as an insecticide in bait stations for ants (Ref. 3). In
2000, the domestic production volume of PFAS chemicals for this use
category was estimated to be 1.5 million pounds (Ref. 15).
    2. Use and production volume data for PFOA. The largest use for
PFOA is as a chemical intermediate. Its salts are used in emulsifier
and surfactant applications, including as a fluoropolymer
polymerization aid in the production of fluoropolymers and
fluoroelastomers. This proposed rule does not require PMN notification
for polymers where APFO is used exclusively as a polymerization aid and
is not incorporated into the polymer structure.
    Until the year 2000, 3M was also the largest manufacturer and
importer of PFOA and its salts in the United States. Subsequent to its
May 16, 2000 announcement (see Unit IV.D.1.), 3M provided clarification
that this announcement included PFOA as well as PFOS, indicating that
it was phasing out certain FLUORAD Brand specialty materials that
contained PFOA and its salts (Ref. 4). Following the phase-out by 3M,
DuPont began to manufacture PFOA in the United States, and is currently
the sole U.S. producer (Ref. 18). The Fluoropolymer Manufacturers Group
has stated that DuPont will not sell APFO outside the fluoropolymer
industry (Ref. 18a).
    The four principal use categories for salts of PFOA include uses
as:
     A fluoropolymer polymerization aid in the industrial
synthesis of fluoropolymers and fluoroelastomers such as
polytetrafluoroethylene (PTFE) and polyvinylidene fluoride (PVDF), with
a variety of industrial and consumer uses (Refs. 19, 20, and 21).
     A post-polymerization processing aid to stabilize
suspensions of fluoropolymers and fluoroelastomers prior to further
industrial processing (Ref. 19).
     A processing aid for factory-applied fluoropolymer
coatings on architectural fabrics, metal surfaces, and fabricated or
molded parts (Ref. 20).
     An extraction agent in ion-pair reversed-phased liquid
chromatography (Ref. 22).
    PTFE and PVDF account for the largest volumes of fluoropolymer
production (Ref. 23). PFOA is also used in other fluoropolymer and
fluoroelastomer manufacturing and processing. In addition, 3M used PFOA
in the industrial synthesis of a fluoroacrylic ester, which is used in
an industrial coating application (Ref. 19).
    The fluoropolymers manufactured with PFOA as a polymerization aid
are used to produce a wide variety of industrial and consumer products.
These products include: High performance lubricants; personal care
products; architectural fabrics; films; cookware, breathable membranes
for apparel; protective industrial coatings; wire and cable insulation;
semiconductor chip manufacturing equipment; pump seals, liners and
packing; medical tubing; aerospace devices; automotive hoses and
tubing; and, a wide variety of electronic products (Ref. 24). The
fluoropolymer industry has informed EPA that it does not intend to
incorporate PFOA into the polymer structure for these uses (Ref. 24).
However, if PFOA were to be incorporated into the structure of a
polymer, this proposed rule amendment would require PMN notification.
    3. Exposure data for PFOS and PFOA. PFOS and PFOA have been
detected at low levels in the blood of humans and wildlife throughout
the United States, providing clear evidence of widespread exposure to
these chemicals (Refs. 4 and 25). Studies are underway to determine the
sources of exposure for PFOS and PFOA. Several potential pathways may
account for the widespread exposure to these chemicals.
    For PFOS, these pathways may have included:
     Dietary intake from the consumption of food wrapped in
paper containing PFOS derivatives.
     Inhalation from aerosol applications of PFOS-containing
consumer products.
     Inhalation, dietary, or dermal exposures resulting from
manufacturing, as well as industrial, commercial, and consumer use and
disposal of PFOS-containing chemicals and products.
    Because PFOA is not used directly in consumer products, its
exposure pathways may result from manufacturing and industrial uses and
disposal of PFOA-derived chemicals and products, typically used as
processing aids for fluoropolymer manufacturing. EPA has data
indicating that PFOA is released into the environment from industrial
discharges to air, water, and land (Refs. 19, 20, 26). Canadian
research has found that thermolysis of fluoropolymers, e.g., PTFE, can
liberate small quantities of perfluorocarboxylic acids, which include
PFOA (Ref. 27). However, the extreme conditions needed to produce these
PFAC products make this source of PFAC an improbable contributor to the
environmental availability of PFAC.
    Data indicate that PFOA may also be produced by the degradation or
metabolism of fluorotelomer alcohols (Refs. 8 and 48), suggesting
exposures to PFOA may result from releases from fluorotelomer
manufacturing and processing, and from the use and disposal of
fluorotelomer-containing products.
    4. Environmental fate of PFAS and PFAC. Little information is
available on the fate of high molecular weight PFAS and PFAC polymers
in the environment. Based on their chemical structures they are
expected to be stable, with many derivatives being non-volatile, but
few studies are available to allow confirmation.
    EPA cannot currently conduct a definitive assessment of the
environmental fate and transport of PFOS- and PFOA-derived chemicals.
Conventional modeling programs are based on ``traditional'' organic
compounds which contain carbon and hydrogen. These models are not
designed to account for the physical-chemical properties and
environmental behavior of perfluorinated compounds. Therefore, these
models provide results that are not representative of perfluorinated
chemicals.
    PFOS and PFOA may be expected to be similar in their resistance to
hydrolysis, biodegradation and photolysis, however, they may have
differences in adsorption/desorption, transport, distribution and
bioaccumulation. Based on available data, PFOS and PFOA are expected to
persist in the environment.
    PFOS and PFOA are stable to hydrolysis. The 3M Environmental
Laboratory (Refs. 28 and 29) performed studies of the hydrolysis of
PFOS and PFOA. The study procedures were based on EPA's OPPTS
Harmonized Test Guideline 835.2110. Results were based on the observed
concentrations of PFOS and PFOA in buffered aqueous solutions as a
function of time. Based on these studies, it was estimated that the
hydrolytic half-lives of PFOS and PFOA at 25[deg]C are greater than 41
and 92 years, respectively.
    PFOS and PFOA do not measurably biodegrade in the environment. The
biodegradation of PFOA was investigated using acclimated sludge
microorganisms and a shake culture study modeled after the Soap and
Detergent Association's presumptive test for degradation (Ref. 30).
Neither thin-layer nor liquid chromatography detected the presence of
any metabolic products over the course of 2
1/89/21/13/23/85/83/8 months, indicating that PFOA does not
readily undergo biodegradation. In a related study PFOA was not
measurably degraded in activated sludge inoculum (Ref. 31). Several
other studies conducted between 1977 to 1987 did

not show PFOA biodegradation either; however, the results are
questionable due to methodological problems (Refs. 32, 33, 34, and 35).
Similar results have been reported for PFOS. No measurable
biodegradation of PFOS in activated sludge, sediment, aerobic soil,
anaerobic sludge, or pure culture studies were found (Ref. 36).
    PFOS and PFOA appear to be stable to photolysis. Direct photolysis
of PFOA was examined by Todd (Ref. 37) and photodegradation was not
observed. Hatfield (Ref. 38) studied both direct and indirect
photolysis utilizing techniques based on EPA and the Organization for
Economic Cooperation and Development (OECD) guidance documents. There
was no conclusive evidence of direct or indirect photolysis. A PFOA
half-life in the environment was estimated to be greater than 349 days.
    PFOA appears to be mobile in soils, and there is conflicting data
on the mobility of PFOS in soils. The adsorption-desorption of PFOA and
PFOS were studied by 3M using 14C-labeled test chemicals in distilled
water with a Brill sandy loam soil. The study reported a soil
adsorption coefficient (Koc) of 14 for PFOA, and a
Koc of 45 for PFOS, indicating that both PFOS and PFOA have
high mobility in Brill sandy loam soil. The Koc value for
PFOA, and possibly PFOS, however, is questionable due to the lack of
accurate information on the purity of the 14C-labeled test substance
(Refs. 39 and 40). In another 3M study using OECD method 106 to measure
the sorption of PFOS (Ref. 41), it was reported that the chemical
strongly adsorbed to all of the soil/sediment/sludge matrices tested.
The test substance, once adsorbed, did not desorb readily, even when
extracted with an organic solvent. Koc values more than 3
orders of magnitude higher than those reported by Welsh were observed.
DuPont evaluated PFOA in a soil absorption/desorption study and found
that the average absorption of PFOA in various soils tested at 1:1
soil:solution ratio ranged from 40.8% to 81.8%, and the highest average
desorption coefficient (Kd) value, 22.5 mL/g, was found in
sludge (Ref. 42). The data from the 3M and DuPont studies, while of
high quality, are of limited utility in understanding the movement of
PFOA released to soil. Batch sorption studies, because of their limited
nature, do not provide all the information needed to understand the
behavior of PFOA in the environment. The data raised additional
questions, and are not sufficient to understand the behavior of PFOA in
soil to allow EPA to determine whether soil is an important pathway for
human and environmental exposure to PFOA.
    Both substances have low vapor pressures and Henry's Law constants
(HLCs ), which suggest low potential for volatilization from water. The
estimated HLCs for PFOS are 1.4 E-7, 2.4 E-8, 4.7 E-9 , 3 E-9 atm-m\3\/
mole (atmospheres per meter cubed per mole), utilizing the vapor
pressure of 3.3 E-9 atm at 20[deg]C and water solubility values of 12,
25, 370, and 570 (mg/L) in unfiltered seawater, filtered seawater,
fresh water and pure water, respectively. For PFOA, the estimated HLCs
is <  3.8 x 10E-10 atm-m\3\/mole based on a vapor pressure of 9.1 E-8
atm and > 100 g/L solubility in water.
    Even though PFOS and PFOA have relatively low vapor pressures, it
is possible that they can be adsorbed on suspended particles. This is
because PFOS and PFOA are considered semi-volatile organic compounds,
i.e., substances with vapor pressures between about 10 E-4 to 10 E-11
atm at ambient temperatures (Ref. 43). The potential adsorption of PFOS
and PFOA onto particulate matter might also create an exposure pathway.
    EPA believes that PFAS and PFAC chemicals may bioaccumulate, but is
uncertain as to the mechanism. Three studies have been conducted that
attempted to determine the bioaccumulation potential of PFOS and PFOA.
In the first study using the fathead minnow, the calculated
bioconcentration factor (BCF) was 1.8 for APFO (Ref. 46). However,
questions were raised about the analytical techniques, high test
chemical concentration and short test duration of the study. In a
Japanese study using carp, the bioaccumulation potential of PFOA was
low, with apparent bioaccumulation factors ranging from 3.1-9.1 (Ref.
45). In the final study using bluegill sunfish from the 3M Decatur
plant, no fluorochemicals were detected in the river water-exposed fish
(Ref. 44). However, interpretation of the study was problematic. For
instance, effluent concentrations of subject fluorochemicals were not
characterized; the protocol for fish exposure was not found; there was
no information on the Tennessee river water or effluent used, whether
there was an opportunity for depuration of the fish prior to sacrifice,
or the cause of death for the 12 dead fish; and the study did not
differentiate between bioaccumulation of the test compound and sorption
onto the fish surface. These studies in fish on the bioaccumulation of
these chemicals suggest relatively low bioaccumulation potential.
However, the detection of PFOS and to a lesser extent PFOA in wild
animals indicates the possibility of accumulation of the chemicals in
biota. PFOS and PFOA appear to have higher bioaccumulation factors than
other PFAS and PFAC chemicals. Thus, the widespread presence of these
chemicals in living organisms also suggests that PFOS and PFOA may
bioaccumulate.
    5. Health effects of PFAS and PFAC. Most of the Agency's concerns
for the health effects of polymers subject to this proposed rule focus
on the perfluoroalkyl moiety, which may be released into the
environment. The Agency's non-confidential data for health effects of
PFAS and PFAC chemicals are on PFOS (as PFOSK) and PFOA (as APFO). EPA
has insufficient evidence to determine that polymers containing PFAS or
PFAC with any number of carbons on the perfluoroalkyl moiety ``will not
present an unreasonable risk to human health or the environment'' and
is proposing to exclude polymers that contain these chemicals from
eligibility for the exemption. Below is a summary of the results of
toxicological and epidemiological studies on PFOS and PFOA.
    i. Health effects of PFOS. All of the data summarized in Unit
IV.D.5.i., as well as the primary references, are detailed in the OECD
``Hazard Assessment of Perfluorooctane sulfonate (PFOS) and its Salts''
(Ref. 25).
    Toxicology studies show that PFOS is well absorbed orally and
distributes primarily in the serum and liver. PFOS can also be formed
as a metabolite of other perfluorinated sulfonates. It does not appear
to be further metabolized. Elimination from the body is slow and occurs
via both urine and feces. The elimination half-life for an oral dose is
7.5 days in adult rats and approximately 200 days in Cynomolgus
monkeys. In humans, the mean elimination half-life of PFOS reported in
9 retired workers appears to be considerably longer, on the order of
years (mean = 8.67 years; range = 2.29-21.3 years; standard deviation =
6.12).
    PFOS has shown moderate acute toxicity by the oral route with a
combined (male and female) rat LD50 of 251 mg/kg. The
LD50 was 233 mg/kg in males and 271 mg/kg in females. A 1-
hour LC50 of 5.2 mg/L in rats has been reported. PFOS was
found to be mildly irritating to the eyes and non-irritating to the
skin of rabbits. PFOS does not induce gene mutation in selected strains
of Salmonella typhimurium or Escherichia coli nor does it induce
chromosomal aberrations in human lymphocytes in culture when tested in
vitro either with or without metabolic activation. PFOS does not induce

 unscheduled DNA synthesis in primary cultures of rat hepatocytes and
is negative when tested in vivo in a mouse bone marrow micronucleus
assay.
    Three 90-day subchronic studies of PFOS have been conducted. One
was a dietary study in rats and two were gavage studies in rhesus
monkeys. In addition, a four week and a 26 week capsule study in
Cynomolgus monkeys and a two-year cancer bioassay in rats, have been
conducted . The primary health effects of concern, based on available
data, are liver effects, developmental effects, and mortality.
Mortality was associated with a steep dose-response across all ages and
species.
    In the rat subchronic study, CD rats, 5/sex/group, were
administered dietary levels of PFOS at 0, 30, 100, 300, 1,000 or 3,000
parts per million (ppm) for 90 days. All of the rats in the 300, 1,000
and 3,000 ppm groups died. Before death, the rats in all groups showed
signs of toxicity including emaciation, convulsions following handling,
hunched back, red material around the eyes, yellow material around the
anogenital region, increased sensitivity to external stimuli, reduced
activity, and moist red material around the mouth or nose. Mean body
weight and average food consumption were reduced in all groups. Animals
in the 100 ppm and 30 ppm dose groups also showed signs of
gastrointestinal effects and hematological abnormalities. At necropsy,
treatment related gross lesions were present in all treated groups and
included varying degrees of discoloration and/or enlargement of the
liver and discoloration of the glandular mucosa of the stomach.
Histologic examination also showed lesions in all treated groups.
    Two 90-day rhesus monkey studies were performed. In the first
study, PFOS was administered to male and female rhesus monkeys at doses
of 0, 10, 30, 100, or 300 mg/kg/day in distilled water by gavage for 90
days. In the second study, PFOS was administered at doses of 0, 0.5,
1.5, or 4.5 mg/kg/day also in distilled water by gavage for 90 days.
None of the monkeys in the first study survived treatment. In the
second study, all monkeys in the 4.5 mg/kg/day group died or were
sacrificed in extremis. Before death all monkeys suffered from similar
signs of toxicity including decreased activity, emesis with some
diarrhea, body stiffening, general body trembling, twitching, weakness,
convulsions, and prostration. At necropsy, several of the monkeys in
the 100 and 300 mg/kg/day groups had a yellowish-brown discoloration of
the liver; histologic examination showed no microscopic lesions.
Congestion, hemorrhage, and lipid depletion of the adrenal cortex was
noted in all treated groups in the first study.
    In the second study, animals in the 30 mg/kg/day dose group had
reduced mean body weight, significant reduction in serum cholesterol
and a 50% reduction in serum alkaline phosphatase activity. At
necropsy, all males and females had marked diffuse lipid depletion in
the adrenals. One male and two females had moderate diffuse atrophy of
the pancreatic exocrine cells with decreased cell size and loss of
zymogen granules. Two males and one female had moderate diffuse atrophy
of the serous alveolar cells characterized by decreased cell size and
loss of cytoplasmic granules. Animals in the 1.5 and 0.5 mg/kg/day dose
group survived to the end of the study and showed signs of decreased
activity and gastrointestinal distress.
    Two additional studies were conducted in Cynomolgus monkeys. In the
first study, male and female Cynomologus monkeys received doses of 0,
0.02, or 2.0 mg/kg/day PFOS in capsules placed directly into the
stomach for 30 days. All animals survived treatment. There were no
test-related effects on clinical observations, body weight, food
consumption, body temperatures, hematology, enzyme levels, cell
proliferation in the liver, testes or pancreas or macroscopic or
microscopic pathology findings.
    In the second study, PFOS was administered to Cynomolgus monkeys by
oral capsule at doses of 0, 0.03, 0.15, or 0.75 mg/kg/day for 26 weeks.
Animals from the 0.15 and 0.75 mg/kg/day groups were assigned to a
recovery group and were held for observation for an additional 26 weeks
after treatment. Two males in the 0.75 mg/kg/day dose group did not
survive the 26 weeks of treatment. The first animal died on day 155. In
addition to being cold to the touch, clinical signs in the first animal
included: Constricted pupils, pale gums, gastrointestinal distress, low
food consumption, hypoactivity, labored respiration, dehydration, and
recumbent position. An enlarged liver was detected by palpation. Cause
of death was determined to be pulmonary necrosis with severe acute
inflammation. The second male was sacrificed in a moribund condition on
day 179. Clinical signs noted included low food consumption, excessive
salivation, labored respiration, hypoactivity and ataxia. The cause of
death was not determined. Males and females in the 0.75 mg/kg/day dose-
group had lower total cholesterol and males and females in the 0.15 and
0.75 mg/kg/day groups had lower high density lipoprotein cholesterol
during treatment. The effect on total cholesterol worsened with time.
By day 182, mean total cholesterol for males and females in the high
dose group were 68% and 49% lower, respectively, than levels in the
control animals. Males in the high dose group also had lower total
bilirubin concentrations and higher serum bile acid concentrations than
males in either the control or other treatment groups. The effect on
total cholesterol was reversed within 5 weeks of recovery and the
effect on high density lipoprotein cholesterol was reversed within 9
weeks of recovery.
    At terminal sacrifice, females in the 0.75 mg/kg/day dose-group had
increased absolute liver weight, liver-to-body weight percentages, and
liver-to-brain weight ratios. In males, liver-to body weight
percentages were increased in the high-dose group compared to the
controls. ``Mottled'' livers and centrilobular or diffuse
hepatocellular hypertrophy and centrilobular or diffuse hepatocellular
vacuolation were also observed in high dose males and females. No PFOS
related lesions were observed either macroscopically or microscopically
at recovery sacrifice indicating that the effects seen at terminal
sacrifice may be reversible.
    The chronic toxicity and carcinogenicity of PFOS have been studied
in rats. The results of the study show that PFOS is hepatotoxic and
carcinogenic, inducing tumors of the liver, and thyroid and mammary
glands. In this study, groups of 40 to 70 male and female Crl:CD
(SD)IGS BR rats were given PFOS in the diets at concentrations of 0,
0.5, 2, 5, or 20 ppm for 104 weeks. A recovery group was given the test
material at 20 ppm for 52 weeks and was observed until death. Five
animals per sex in the treatment groups were sacrificed during weeks 4,
14, and 53.
    At the terminal sacrifice, the livers of animals given 5 or 20 ppm
were enlarged, mottled, diffuse darkened, or focally lightened.
Hepatotoxicity, characterized by significant increases in centrilobular
hypertrophy, centrilobular eosinophilic hepatocytic granules,
centrilobular hepatocytic pigment, or centrilobular hepatocytic
vacuolation was noted in male and/or female rats given 5 or 20 ppm. A
significant increase in hepatocellular centrilobular hypertrophy was
also observed in mid-dose (2 ppm) male rats. For neoplastic effects, a
significant positive trend was noted in the incidences of
hepatocellular adenoma in male rats. A significantly increased
incidence was observed for thyroid follicular cell

adenoma in the high-dose recovery group when compared to the control
group.
    In females, significant positive trends were observed in the
incidences of hepatocellular adenoma and combined hepatocellular
adenoma and carcinoma. A significant increase for combined thyroid
follicular cell adenoma and carcinoma was observed in the mid-high (5.0
ppm) group as compared to the control group. Except for the high-dose
group, increases in mammary tumors were observed in all treatment
groups when compared to the controls.
    Developmental toxicity studies on PFOS have been conducted in rats,
mice and rabbits. The first study administered four groups of 22 time-
mated Sprague-Dawley rats 0, 1, 5, and 10 mg/kg/day PFOS in corn oil by
gavage on gestation days (GD) 6-15. Signs of maternal toxicity
consisted of significant reductions in mean body weights during GD 12-
20 at the high-dose group of 10 mg/kg/day. No other signs of maternal
toxicity were reported. Under the conditions of the study, a no
observed adverse effect level (NOAEL) of 5 mg/kg/day and a lowest
observed adverse effect level (LOAEL) of 10 mg/kg/day for maternal
toxicity were indicated. Developmental toxicity evident at 10 mg/kg/day
consisted of reductions in the mean number of implantation sites,
corpora lutea, resorption sites, and the mean numbers of viable male,
female, and total fetuses, but the differences were not statistically
significant. In addition, unusually high incidences of unossified,
asymmetrical, bipartite, and missing sternebrae were observed in all
dose groups; however, these skeletal variations were also observed in
control fetuses at the same rate and therefore these effects were not
considered to be treatment-related. A fetal lens finding initially
described as a variety of abnormal morphological changes localized to
the area of the embryonal nucleus, was later determined to be an
artifact of the free-hand sectioning technique and therefore not
considered to be treatment-related.
    Groups of 25 pregnant Sprague-Dawley rats were administered 1, 5,
and 10 mg/kg/day PFOS in corn oil by gavage on gestation days (GD) 6-
15. Evidence of maternal toxicity occurred at the 5 and 10 mg/kg/day
dose groups both consisted of hunched posture, anorexia, bloody vaginal
discharge, uterine stains, alopecia, rough haircoat, and bloody crust.
Significant decreases in mean body weight gains during GD 6-8, 6-16,
and 0-20 were also observed in the 5 and 10 mg/kg/day dose groups.
These reductions were considered to be treatment-related since mean
body weight gains were greater than controls during the post-exposure
period (GD 16-20). Significant decreases in mean total food consumption
were observed on GD 17-20 in the10 mg/kg/day dose group, and on GD 7-16
and 0-20 in both the 5 and 10 mg/kg/day dose groups. The mean gravid
uterine weight in the 10 mg/kg/day dose group was significantly lower
when compared with controls. The mean terminal body weights minus the
gravid uterine weights were lower in all treated groups, with
significant decreases at 5 and 10 mg/kg/day. High-dose animals also
exhibited an increased incidence in gastrointestinal lesions. No
significant differences were observed in pregnancy rates, number of
corpora lutea, and number and placement of implantation sites among
treated and control groups. Two dams in the 10 mg/kg/day dose group
were found dead on GD 17. Under the conditions of the study, a NOAEL of
1 mg/kg/day and a LOAEL of 5 mg/kg/day for maternal toxicity were
indicated.
    Significant decreases in mean fetal weights for both males and
females were observed in the 5 and 10 mg/kg/day dose groups.
Statistically significant increases in incomplete closure of the skull
were observed in the low- and high-dose groups but not in the mid-dose
group. Statistically significant increases in the incidences in the
number of litters containing fetuses with visceral anomalies, delayed
ossification, and skeletal variations were observed in the high dose
group of 10 mg/kg/day. These included external and visceral anomalies
of the cleft palate, subcutaneous edema, and cryptorchism as well as
delays in skeletal ossification of the skull, pectoral girdle, rib
cage, vertebral column, pelvic girdle, and limbs. Skeletal variations
in the ribs and sternebrae were also observed. Under the conditions of
the study, a NOAEL of 1 mg/kg/day and a LOAEL of 5 mg/kg/day for
developmental toxicity were indicated.
    In another study, Sprague-Dawley rats and CD-1 mice were
administered doses of 0, 1, 5, or 10 mg/kg/day PFOS in 0.5% Tween-20 by
gavage beginning on gestation day 2 and continuing until term. Half of
the dams were sacrificed on gestation day 21 (rats) or gestation day 17
(mice) and the remaining dams were allowed to deliver. Preliminary
results are available. In rats, there was a significant reduction in
maternal body weight gain at 5 and 10 mg/kg/day. Maternal serum
cholesterol and triglycerides were reduced at 10 mg/kg/day, but liver
weights were comparable to control. At 10 mg/kg/day, there was a
reduction in fetal body weight and an increase in cleft palate and
anasarca. All pups were born alive, but within 4 to 6 hours after birth
all the pups in the 10 mg/kg/day group died, and 95% of the pups in the
5 mg/kg/day group died within 24 hours. In mice, maternal body weight
was unaffected and liver weights were significantly increased at 5 and
10 mg/kg/day; serum triglycerides were reduced at 5 and 10 mg/kg/day.
The incidence of fetal mortality was slightly increased at 10 mg/kg/day
and mean fetal body weights were comparable to control. However,
neonatal body weights were reduced during the first 3 days of life.
Additional studies are underway to further elucidate the dose-response
relationships and to examine the mechanism for the neonatal death.
    Pregnant New Zealand White rabbits, 22 per group, were administered
doses of 0, 0.1, 1.0, 2.5, or 3.75 mg/kg/day PFOS in 0.5% Tween-80 by
gavage on gestation days 7-20 in another study. Maternal toxicity was
evident at doses of 1.0 mg/kg/day and above. One doe in the 2.5 mg/kg/
day group and nine does in the 3.75 mg/kg/day aborted. There was a
significant increase in the incidence of scant feces in the 3.75 mg/kg/
day group. Scant feces were also noted in one and three does in the 1.0
and 2.5 mg/kg/day groups, respectively. Mean maternal body weight gains
were significantly reduced in the 3.75 and 2.5 mg/kg/day group. Mean
food consumption (g/kg/day) was significantly reduced in the 2.5 and
3.75 mg/kg/day dose group. The LOAEL for maternal toxicity was 1.0 mg/
kg/day and the NOAEL was 0.1 mg/kg/day.
    Developmental toxicity was evident at doses of 2.5 mg/kg/day and
above. Mean fetal body weight (male, female, and sexes combined) was
significantly reduced in the 2.5 and 3.75 mg/kg/day groups. There was
also a significant reduction in the ossification of the sternum (litter
averages) in the 2.5 and 3.75 mg/kg/day groups, and a significant
reduction in the ossification of the hyoid (litter averages),
metacarpals (litter averages), and pubis (litter and fetal averages) in
the 3.75 mg/kg/day group. The LOAEL for developmental toxicity was 2.5
mg/kg/day and the NOAEL was 1.0 mg/kg/day.
    In epidemiological studies, cross-sectional, occupational, and a
longitudinal study did not indicate consistent associations between
workers' PFOS serum levels and certain hematology and other clinical
chemistry parameters. In the cross-sectional analysis, workers with the
highest PFOS exposures had significantly higher serum triiodothyronine
levels and significantly lower thyroid hormone binding ratio; however,
hormonal

parameters were not measured longitudinally. In addition, these studies
were conducted on volunteers only, female employees could not be
analyzed due to the small number of women employed at these plants,
different labs and analytical techniques were used to measure PFOS, and
only a small number of employees were common to all of the sampling
periods. In a mortality study of workers exposed to PFOS, most of the
cancer types and non-malignant causes were not elevated. However, a
statistically significant mortality risk of bladder cancer (SMR =
12.77, 95% CI = 2.63-37.35) was reported in 3 male employees. All of
the workers had been employed at the plant for more than 20 years and
all of them had worked in ``high exposure jobs'' for at least 5 years.
Although it is unlikely that this effect would be due to chance or
tobacco smoking, it cannot be ascertained whether fluorochemicals are
responsible for the excess of bladder cancer deaths, or whether other
carcinogens may be present in the workplace.
    In human blood samples, PFOS has been detected in the serum of
occupational and general populations in the parts per billion (ppb) to
ppm range. In the United States, recent blood serum levels of PFOS in
manufacturing employees have been as high as 12.83 ppm, while in the
general population, pooled serum collected from the United States blood
banks and commercial sources have indicated mean PFOS levels ranging
from 29 to 44 ppb. Mean serum PFOS levels from individual samples in
adults and children were approximately 43 ppb.
    Sampling of several wildlife species from a variety of sites across
the United States has shown widespread distribution of PFOS. In recent
analyses, PFOS was detected in the ppb range in the plasma of several
species of eagles, wild birds, and fish. PFOS has also been detected in
the ppb range in the livers of unexposed rats used in toxicity studies,
presumably through a dietary source (fishmeal).
    Although the PFOS levels detected in the blood of the general
population are low, this widespread presence, combined with the
persistence, the bioaccumulative potential, and the reproductive and
subchronic toxicity of the chemical, raises concerns for potential
adverse effects on people and wildlife (wild mammals and birds) over
time should the chemical substances continue to be produced, released,
and accumulate in the environment.
    ii. Health effects of PFOA. All of the data presented in Unit
IV.D.5.ii. are detailed in an EPA hazard assessment of PFOA (Ref. 4).
Primary references can be obtained from that document.
    The primary health effects of concern for PFOA, based on available
data, are liver toxicity and developmental toxicity. Most of the health
effects data for PFOA are on the ammonium salt, APFO. Occupational data
indicate that mean serum levels of PFOA in workers range from 0.84 to
6.4 ppm, with the highest reported level of 81.3 ppm. In non-
occupational populations, mean pooled blood bank and commercial PFOA
samples ranged from 3 to 17 ppb. The mean PFOA level in individual
blood samples (in children and adults) was 5.6 ppb.
    Animal studies have shown that APFO is well absorbed following oral
and inhalation exposure, and to a lesser extent following dermal
exposure. Rats show gender differences in the elimination of APFO. APFO
distributes primarily to the liver, plasma, and kidney, and to a lesser
extent, other tissues of the body including the testis and ovary. It
does not partition to the lipid fraction or adipose tissue. APFO is not
metabolized and there is evidence of enterohepatic circulation of the
compound. Female rats appear to have a secretory mechanism that rapidly
eliminates APFO; this secretory mechanism is either lacking or
relatively inactive in male rats and is not found in monkeys or humans.
    Epidemiological studies on the effects of PFOA in humans have been
conducted on workers. Two mortality studies, as well as studies
examining effects on the liver, pancreas, endocrine system, and lipid
metabolism, have been conducted to date. A longitudinal study of worker
surveillance data has also been conducted. A weak association with PFOA
exposure and prostate cancer was reported in one study; however, this
result was not observed in an update to the study in which the exposure
categories were modified. A non-statistically significant increase in
estradiol levels in workers with high serum PFOA levels (> 30 ppm) was
also reported, but none of the other hormone levels analyzed indicated
any adverse effects.
    The acute oral toxicity of APFO was tested in male and female rats
in three studies. Death occurred at concentrations >= 464 mg/kg.
Abnormal findings upon necropsy (kidney, stomach, uterus) were observed
at 500 mg/kg (higher concentrations were not tested). Clinical signs of
toxicity observed in these three studies included: Red-stained face,
stained urogenital area, wet urogenital area, hypoactivity, hunched
posture, staggered gait, excessive salivation, ptosis, piloerection,
decreased limb tone, ataxia, corneal opacity, and hypothermic to touch.
    The acute inhalation toxicity of APFO was tested in male and female
Sprague-Dawley rats, at a dose level of 18.6 mg/L (nominal
concentration), and exposure duration of one hour. Signs of toxicity
during and up to 14 days after the exposure period included: excessive
salivation, excessive lacrimation, decreased activity, labored
breathing, gasping, closed eyes, mucoid nasal discharge, irregular
breathing, red nasal discharge, yellow staining of the anogenital fur,
dry and moist rales, red material around the eyes, and body tremors.
Upon necropsy, lung discoloration was observed in a higher than normal
incidence of rats (8/10). Based on the study results, the test
substance was not fatal to rats at a nominal exposure concentration of
18.6 mg/L and exposure duration of one hour.
    The acute dermal toxicity of APFO was tested in male and female
rabbits, at a dose level of 2,000 mg/kg, and a 24-hour exposure period.
Dermal irritation consisted of slight to moderate erythema, edema, and
atonia; slight desquamation; coriaceousness; and fissuring. No visible
lesions were observed upon necropsy. The dermal LD50 in
rabbits was determined to be greater than 2,000 mg/kg.
    APFO did not induce mutation in either S. typhimurium or E. coli
when tested either with or without mammalian activation and did not
induce chromosomal aberrations in human lymphocytes also when tested
with and without metabolic activation up to cytotoxic concentrations.
It was recently reported that APFO did not induce gene mutation when
tested with or without metabolic activation in the K-1 line of Chinese
hamster ovary (CHO) cells in culture.
    APFO was tested twice for its ability to induce chromosomal
aberrations in CHO cells. In the first assay, APFO induced both
chromosomal aberrations and polyploidy in both the presence and absence
of metabolic activation. In the second assay, no significant increases
in chromosomal aberrations were observed without activation. However,
when tested with metabolic activation, APFO induced significant
increases in chromosomal aberrations and in polyploidy.
    APFO was tested in a cell transformation and cytotoxicity assay
conducted in C3H 10T1/2 mouse embryo fibroblasts.
The cell transformation was determined as both colony transformation
and foci transformation potential. There was no evidence of

transformation at any of the dose levels tested in either the colony or
foci assay methods.
    Subchronic toxicity studies have been conducted in rats, mice, and
Rhesus and Cynomolgus monkeys. A range-finding and a 6-month toxicity
study in Cynomolgus monkeys was recently conducted. In all species, the
liver is the main target organ. In rats, males had more pronounced
hepatotoxicity and histopathologic effects than females, presumably
because of the gender difference in elimination of APFO. Subchronic
studies in rats and mice with 28 and 90 days of exposure have
demonstrated that the liver is the primary target organ and that males
are far more sensitive than females due to the gender differences in
elimination. In a 90-day study with rhesus monkeys, exposure to doses
of 30 mg/kg/day or higher resulted in death, lipid depletion in the
adrenals, hypocellularity of the bone marrow, and moderate atrophy of
the lymphoid follicles in the spleen and lymph nodes. Chronic dietary
exposure of rats to 300 ppm APFO (14.2 and 16.1 mg/kg/day for males and
females, respectively) for 2 years resulted in increased liver and
kidney weights, hematological effects, and liver lesions in males and
females. In addition, testicular masses were observed in males at 300
ppm and ovarian tubular hyperplasia was observed in females after
exposure to 30 ppm (1.6 mg/kg/day), the lowest dose tested.
    PFOA is immunotoxic in mice. Feeding the mice a diet of 0.02% PFOA
resulted in adverse effects to both the thymus and spleen. Other
effects included suppression of the specific humoral immune response to
horse red blood cells, and suppression of the splenic lymphocyte
proliferation in response to lipopolysacccharide (LPS) and concanavalin
A (ConA). Studies using transgenic mice indicated that the peroxisome
proliferator-activated receptor was involved in causing the adverse
effects to the immune system.
    Several prenatal developmental toxicity studies of APFO, including
two oral studies in rats, one oral study in rabbits, and one inhalation
study in rats, have been conducted. In one study, time-mated Sprague-
Dawley rats (22 per group) were administered doses of 0, 0.05, 1.5, 5,
and 150 mg/kg/day APFO in distilled water by gavage on gestation days
(GD) 6-15. Signs of maternal toxicity consisted of statistically
significant reductions in mean maternal body weights at the high-dose
group of 150 mg/kg/day. Other signs of toxicity that occurred only at
the high dose group included ataxia and death in three rat dams. No
other effects were reported. Administration of APFO during gestation
did not appear to affect the ovaries or reproductive tract of the dams.
Under the conditions of the study, a NOAEL of 5 mg/kg/day and a LOAEL
of 150 mg/kg/day for maternal toxicity were indicated. No significant
differences between treated and control groups were noted for
developmental parameters. A fetal lens finding initially described as a
variety of abnormal morphological changes localized to the area of the
embryonal nucleus, was later determined to be an artifact of the free-
hand sectioning technique and therefore not considered to be treatment-
related. Under the conditions of the study, a NOAEL for developmental
toxicity of 150 mg/kg/day was indicated.
    Another developmental study was also conducted on APFO. The study
design consisted of an inhalation and an oral portion, each with two
trials or experiments. In the first trial the dams were sacrificed on
GD 21; while in the second trial, the dams were allowed to litter and
the pups were sacrificed on day 35-post partum. For the inhalation
portion of the study, the two trials consisted of 12 pregnant Sprague-
Dawley rats per group exposed to 0, 0.1, 1, 10, and 25 mg/m\3\ APFO for
6 hours/day, on GD 6-15. In the oral portion of the study, 25 and 12
Sprague-Dawley rats for the first and second trials, respectively, were
administered 0 and 100 mg/kg/day APFO in corn oil by gavage on GD 6-15.
    In trial one of the inhalation study, treatment-related clinical
signs of maternal toxicity occurred at 10 and 25 mg/m\3\ and consisted
of wet abdomens, chromodacryorrhea, chromorhinorrhea, a general unkempt
appearance, and lethargy in four dams at the end of the exposure period
(high-concentration group only). Three out of 12 dams died during
treatment at 25 mg/m\3\ (on GD 12, 13, and 17). Food consumption was
significantly reduced at both 10 and 25 mg/m\3\. Significant reductions
in body weight were also observed at these concentrations, with
statistical significance at the high-concentration only. Likewise,
statistically significant increases in mean liver weights were seen at
the high-concentration group. The NOAEL and LOAEL for maternal toxicity
were 1 and 10 mg/m\3\, respectively. Similar effects were seen in trial
two and the NOAEL and LOAEL for maternal toxicity were the same in both
trials.
    No effects were observed on the maintenance of pregnancy or the
incidence of resorptions. Mean fetal body weights were significantly
decreased in the 25 mg/m\3\ groups and in the control group pair-fed 25
mg/m\3\. However, interpretation of the decreased fetal body weight is
difficult given the high incidence of mortality in the dams. Under EPA
guidance, data at doses exceeding 10% mortality are generally
discounted. Under the conditions of the study, a NOAEL and LOAEL for
developmental toxicity of 10 and 25 mg/m\3\, respectively, were
indicated. Similar effects were seen in trial two and the same NOAEL
and LOAEL were noted.
    In trial one of the oral study, three out of 25 dams died during
treatment of 100 mg/kg APFO during gestation (one death on GD 11; two
on GD 12). Clinical signs of maternal toxicity in the dams that died
were similar to those seen with inhalation exposure. Food consumption
and body weights were reduced in treated animals compared to controls.
No adverse signs of toxicity were noted for any of the reproductive
parameters such as maintenance of pregnancy or incidence of
resorptions. Likewise, no significant differences between treated and
control groups were noted for fetal weights, or in the incidences of
malformations and variations; nor were there any effects noted
following microscopic examination of the eyes. In trial two of the oral
study, similar observations for clinical signs were noted for the dams
as in trial one. Likewise, no adverse effects on reproductive
performance or in any of the fetal observations were noted.
    An oral two-generation reproductive toxicity study was conducted on
APFO. Five groups of 30 Sprague-Dawley rats per sex per dose group were
administered APFO by gavage at doses of 0, 1, 3, 10, and 30 mg/kg/day
six weeks prior to and during mating. Treatment of the F0 male rats
continued until mating was confirmed, and treatment of the F0 female
rats continued throughout gestation, parturition, and lactation.
    At necropsy, none of the sperm parameters evaluated (sperm number,
motility, or morphology) were affected by treatment at any dose level.
One F0 male rat in the 30 mg/kg/day dose group was sacrificed on day 45
of the study due to adverse clinical signs (emaciation, cold-to-touch,
and decreased motor activity). Necroscopic examination in that animal
revealed a pale and tan liver, and red testes. All other F0 generation
male rats survived to scheduled sacrifice. Statistically significant
increases in clinical signs were also observed in male rats in the
high-dose group that included dehydration, urine-stained abdominal fur,
and ungroomed coat. No treatment-related effects were reported at any
dose

level for any of the mating and fertility parameters assessed. At
necropsy, none of the sperm parameters evaluated (sperm number,
motility, or morphology) were affected by treatment at any dose level.
    At necropsy, statistically significant reductions in terminal body
weights were seen at 3, 10, and 30 mg/kg/day. Absolute weights of the
left and right epididymides, left cauda epididymis, seminal vesicles
(with and without fluid), prostate, pituitary, left and right adrenals,
spleen, and thymus were also significantly reduced at 30 mg/kg/day. The
absolute weight of the seminal vesicles without fluid was significantly
reduced in the 10 mg/kg/day dose group. The absolute weight of the
liver was significantly increased in all dose-groups. Kidney weights
were significantly increased in the 1, 3, and 10 mg/kg/day dose groups,
but significantly decreased in the 30 mg/kg/day group. All organ
weight-to-terminal body weight and ratios were significantly increased
in all treated groups. Organ weight-to-brain weight ratios were
significantly reduced for some organs at the high dose group, and
significantly increased for other organs among all treated groups.
    No treatment-related effects were seen at necropsy or upon
microscopic examination of the reproductive organs, with the exception
of increased thickness and prominence of the zona glomerulosa and
vacuolation of the cells of the adrenal cortex in the 10 and 30 mg/kg/
day dose groups. No treatment-related deaths or adverse clinical signs
were reported in parental females at any dose level. No treatment-
related effects were reported for body weights, body weight gains, and
absolute and relative food consumption values.
    There were no treatment-related effects on estrous cyclicity,
mating or fertility parameters. None of the natural delivery and litter
observations were affected by treatment. Necropsy and histopathological
evaluation were also unremarkable. Terminal body weights, organ
weights, and organ-to-terminal body weight ratios were comparable to
control values for all treated groups, except for kidney and liver
weights. The weights of the left and right kidney, and the ratios of
these organ weights-to-terminal body weight and of the left kidney
weight-to-brain weight were significantly reduced at the highest dose
of 30 mg/kg/day. The ratio of liver weights-to-terminal body weight was
also significantly reduced at 3 and 10 mg/kg/day.
    No effects were reported at any dose level for the viability and
lactation indices of F1 pups. No differences between treated and
control groups were noted for the numbers of pups surviving per litter,
the percentage of male pups, litter size and average pup body weight
per litter at birth. Pup body weight on a per litter basis (sexes
combined) was reduced in the 30 mg/kg/day group throughout lactation,
and statistical significance was achieved on days 1, 5, and 8.
    At 30 mg/kg/day, one pup from one dam died prior to weaning on
lactation day 1 (LD1). Additionally, on lactation days 6 and 8,
statistically significant increases in the numbers of pups found dead
were observed at 3 and 30 mg/kg/day. According to the study authors,
this was not considered to be treatment related because they did not
occur in a dose-related manner and did not appear to affect any other
measures of pup viability including numbers of surviving pups per
litter and live litter size at weighing. An independent statistical
analysis was conducted by EPA. No significant differences were observed
between dose groups and the response did not have any trend in dose.
    Of the pups necropsied at weaning, no statistically significant,
treatment-related differences were observed for the weights of the
brain, spleen, and thymus and the ratios of these organ weights to the
terminal body weight and brain weight.
    No treatment-related adverse clinical signs were observed at any
dose level in F2 generation offspring. No treatment-related adverse
clinical signs were observed at any dose level. Likewise, no treatment-
related effects were reported following necroscopic examination, with
the exception of no milk in the stomach of the pups that were found
dead. The numbers of pups found either dead or stillborn did not show a
dose-response (3/28, 6/28, 10/28, 10/28, and 6/28 in 0, 1, 3, 10, and
30 mg/kg/day dose groups, respectively) and therefore were unlikely
related to treatment.
    No effects were reported at any dose level for the viability and
lactation indices. No differences between treated and control groups
were noted for the numbers of pups surviving per litter, the percentage
of male pups, litter size, and average pup body weight per litter when
measured on LDs 1, 5, 8, 15, or 22. Anogenital distances measured for
F2 male and female pups on LDs 1 and 22 were also comparable among the
five dosage groups and did not differ significantly. Likewise, no
treatment-related effects were reported following necroscopic
examination, with the exception of no milk in the stomach of the pups
that were found dead. The numbers of pups found either dead or
stillborn did not show a dose-response (3/28, 6/28, 10/28, 10/28, and
6/28 in 0, 1, 3, 10, and 30 mg/kg/day dose groups, respectively) and
therefore were unlikely related to treatment.
    No effects were reported at any dose level for the viability and
lactation indices. No differences between treated and control groups
were noted for the numbers of pups surviving per litter, the percentage
of male pups, litter size, and average pup body weight per litter when
measured. Statistically significant increases (p < = 0.01) in the number
of pups found dead were observed on lactation day 1 in the 3 and 10 mg/
kg/day groups. According to the study authors, this was not considered
to be treatment related because they did not occur in a dose-related
manner and did not appear to affect any other measures of pup viability
including numbers of surviving pups per litter and live litter size at
weighing. An independent statistical analysis was conducted by EPA. No
significant differences were observed between dose groups and the
response did not have any trend in dose. Terminal body weights in F2
pups were not significantly different from controls. Absolute weights
of the brain, spleen, and thymus and the ratios of these organ weights-
to-terminal body weight and to brain weight were also comparable among
treated and control groups.
    In summary, under the conditions of the study, the LOAEL for F0
parental males is considered to be 1 mg/kg/day, the lowest dose tested,
based on significant increases in the liver and kidney weights-to-
terminal body weight and to brain weight ratios. A NOAEL for the F0
parental males could not be determined since treatment-related effects
were seen at all doses tested. The NOAEL and LOAEL for F0 parental
females are considered to be 10 and 30 mg/kg/day, respectively, based
on significant reductions in kidney weight and kidney weight-to-
terminal body weight and to brain weight ratios observed at the highest
dose.
    The LOAEL for F1 generation males is considered to be 1 mg/kg/day,
based on significant decreases in body weights and body weight gains,
and in terminal body weights; and significant changes in absolute liver
and spleen weights and in the ratios of liver, kidney, and spleen
weights-to-brain weights; and based on significant, dose-related
reductions in body weights and body weight gains observed prior to and
during cohabitation and during the entire dosing period. A NOAEL for
the F1 males could not be determined since treatment-related effects
were seen at all doses tested.
    The NOAEL and LOAEL for F1 generation females are considered to be

10 and 30 mg/kg/day, respectively, based on statistically significant
increases in postweaning mortality, delays in sexual maturation (time
to vaginal patency), decreases in body weight and body weight gains,
and decreases in absolute food consumption, all observed at the highest
dose tested. The NOAEL for the F2 generation offspring was considered
to be 30 mg/kg/day. No treatment-related effects were observed at any
doses tested in the study. However, it should be noted that the F2 pups
were sacrificed at weaning, and thus it was not possible to ascertain
the potential post-weaning effects that were noted in the F1
generation.
    Carcinogenicity studies in CD rats show that APFO is weakly
carcinogenic, inducing Leydig cell tumors in the male rats and mammary
tumors in the females. The compound has also been reported to be
carcinogenic to the liver and pancreas of male CD rats. The
mechanism(s) of APFO tumorigenesis is not clearly understood. APFO is
not mutagenic. Available data indicate that the induction of tumors by
APFO is due to a non-genotoxic mechanism, involving activation of
receptors and perturbations of the endocrine system. There is
sufficient evidence to suggest that APFO is a PPAR[alpha]-agonist and
that the liver carcinogenicity/toxicity of APFO is mediated by binding
to PPAR[alpha] in the liver. The Agency is currently examining the
scientific knowledge associated with PPAR[alpha]-agonist-induced liver
tumors in rodents and the relevance to humans. Available data suggest
that the induction of Leydig cell tumors (LCT) and mammary gland
neoplasms by APFO may be due to hormonal imbalance resulting from
activation of the PPAR[alpha] and induction of the cytochrome P450
enzyme, aromatase. Preliminary data suggest that the pancreatic acinar
cell tumors are related to an increase in serum level of the growth
factor, cholecystokinin.
    There are limited data on PFOA serum levels in workers and the
general population. Occupational data from plants in the United States
and Belgium that manufacture or use PFOA indicate that mean serum
levels in workers range from 0.84 to 6.4 ppm. In non-occupational
populations, serum PFOA levels were much lower; in both pooled blood
bank samples and in individual samples, mean serum PFOA levels ranged
from 3 to 17 ppb. The highest serum PFOA levels were reported in a
sample of children from different geographic regions in the United
States (range, 1.9 to 56.1 ppb).
    Several wildlife species have been sampled to determine levels of
PFOA. PFOA has rarely been found in fish or in fish-eating bird samples
collected from around the world. PFOA was found in a few mink livers
from Massachusetts, but not found in mink from Louisiana, South
Carolina, and Illinois. PFOA concentrations in river otter livers from
Washington and Oregon were less than the quantification limit of 36 ng/
g, wet wt. PFOA was not detected at quantifiable concentrations in
oysters collected in the Chesapeake Bay and Gulf of Mexico.

E. Summary of Data on Fluorotelomers and Other Perfluoroalkyl Moieties

    EPA has concerns about the potential health and environmental
effects of polymers containing fluorotelomers or perfluoroalkyl
moieties that are covalently bound to either a carbon or sulfur atom
where the carbon or sulfur atom is an integral part of the polymer
molecule. The Agency believes that polymers containing such substances
should be subject to the premanufacture review process so that EPA can
better evaluate and address these concerns. In 1981, the first reports
of fluorotelomer alcohol metabolism were reported and clearly showed
that PFOA was formed from the 8-2 alcohol (Ref. 8). In more recent
research published by 3M and in similar tests reported by the Telomer
Research Program (TRP), 8-2 alcohol has been shown to degrade to form
PFOA when exposed to activated sludge during accelerated biodegradation
studies. A single mechanism had been proposed for the conversion of the
8-2 alcohol to form PFOA, whether through metabolic reaction or
environmental degradation. Each intermediate in the stepwise sequence
of chemical reactions has been identified confirming the proposed
mechanism (Ref. 47 and 48).
    In addition, initial test data from a study in rats dosed with
fluorotelomer alcohol and other preliminary animal studies on various
telomeric products containing fluorocarbons structurally similar to
PFAC or PFAS have demonstrated a variety of adverse effects including
liver, kidney, and thyroid effects (Ref. 9).
    Canadian researchers have developed an analytical methodology to
measure airborne organo-fluorine compounds (Ref. 49). Using this
technique, the researchers monitored air samples in Toronto and were
successful in detecting fluoroorganics, including PFOS derivatives and
fluorotelomer alcohols. DuPont commissioned a preliminary study in
North America by these same researchers and found similar results in
six different U.S. and Canadian cities (Ref. 10). While these studies
are only preliminary and certainly not conclusive, the fact that the
Canadian researchers found fluorotelomer alcohols in the air in six
different cities is significant. This finding is indicative of
widespread fluorotelomer alcohol distribution, and it further indicates
that air may be a route of exposure to these chemicals, which can
ultimately become PFOA. The TRP, in developing radiolabeled 8-2
alcohol, noted the volatile nature of this material and the rampant
loss of non-radio labeled material attributed to a high vapor pressure
(Ref. 50).
    Although the source of the fluorotelomer alcohols cannot be
determined from the study, most (85% of the production volume)
fluorotelomer alcohols produced are used in the manufacture of high
molecular weight polymers. These fluorotelomer alcohols are generally
incorporated into the polymers via covalent ester linkages, and it is
possible that degradation of the polymers may result in release of the
fluorotelomer alcohols to the environment. This hypothesis has been
posed to TRP, which has begun to investigate whether fluorotelomer-
based polymers may be a source of PFOA in the environment (Ref. 51).
    Based on the presence of fluorotelomer alcohols in the air, the
growing data demonstrating that fluorotelomer alcohols metabolize or
degrade to generate PFOA (Ref. 11), the demonstrated toxicity of 8-2
alcohol and certain compounds containing fluorotelomers, and the
possibility that polymers containing fluorotelomers could degrade in
the environment thereby releasing fluorotelomer alcohols or other
perfluoroalkyl-containing substances, EPA can no longer conclude that
such polymers ``will not present an unreasonable risk of injury to
health or the environment'' as required for an exemption under section
5(h)(4) of TSCA. Therefore, EPA is proposing to exclude polymers that
contain fluorotelomers as an integral part of their composition, except
as impurities, from the polymer exemption at 40 CFR 723.250.
    Similarly, EPA does not have specific data demonstrating that
polymers containing perfluoroalkyl moieties other than PFAS, PFAC, or
fluorotelomers present the same concerns as those containing PFAS,
PFAC, or fluorotelomers. Nevertheless, EPA is also proposing to exclude
polymers containing perfluoroalkyl moieties, consisting of a CF3- or
longer chain length, that are covalently bound to either a carbon or
sulfur atom where the carbon or sulfur atom is an integral part of the
polymer molecule from the polymer exemption. Available data indicate
that compounds containing

PFAS or PFAC may degrade in the environment thereby releasing the PFAS
or PFAC moiety, and that fluorotelomers may degrade in the environment
to form PFAC. Based on these data, EPA believes that it is possible
that polymers containing these other types of perfluoroalkyl moieties
could also degrade over time in the environment, thereby releasing the
perfluoroalkyl moiety. EPA also believes that once released, such
moieties may potentially degrade to form PFAS or PFAC. EPA does not
believe, therefore, that it can continue to make the ``will not present
an unreasonable risk of injury to health or the environment'' finding
for such polymers and is proposing to exclude them from the polymer
exemption. EPA is specifically requesting comment on this aspect of the
proposed rule. Please see Unit VII. of this document for specific
information that EPA is interested in obtaining to evaluate whether
continued exemption for polymers containing fluorotelomers or
perfluoroalkyl moieties that are covalently bound to either a carbon or
sulfur atom where the carbon or sulfur atom is an integral part of the
polymer molecule is appropriate.

V. Objectives and Rationale for This Proposed Rule

    The objective of this proposed rule is to amend the polymer
exemption rule to exclude polymers containing as an integral part of
the polymer composition, except as impurities, any one or more of
certain perfluroalkyl moieties consisting of a CF3- or longer chain
length from eligibility for the exemption from TSCA section 5 reporting
requirements allowed under the 1995 amendments to the polymer exemption
rule. In section 5(a)(1)(A) of TSCA, Congress prohibited persons from
manufacturing (including importing) new chemical substances unless such
persons submitted a PMN to EPA at least 90 days before such
manufacture. Pursuant to section 5(h)(4) of TSCA, EPA is authorized to
exempt the manufacturer of any new chemical substance from all or part
of the requirements of section 5 if the Agency determines that the
manufacture, processing, distribution in commerce, use, or disposal of
the substance, or any combination of such activities, will not present
an unreasonable risk of injury to health or the environment. Section
5(h)(4) also authorizes EPA to amend or repeal such rules.
    While TSCA does not contain a definition of unreasonable risk, the
legislative history indicates that the determination of unreasonable
risk requires a balancing of the considerations of both the severity
and probability that harm will occur against the effect of the final
regulatory action on the availability to society of the benefits of the
chemical substance. [House Report 1341, 94\th\ Cong. 2\nd\ Session, 14
(1976)]. This analysis can include an estimate of factors such as
market potential, the effect of the regulation on promoting or
hindering the economic appeal of a substance, environmental effects,
and many other factors that are difficult to define and quantify with
precision. In making a determination of unreasonable risk, EPA must
rely not only on available data, but also on its professional judgment.
Congress recognized that the implementation of the unreasonable risk
standard ``will vary on the specific regulatory authority which the
Administrator seeks to exercise.''
    The polymer exemption rule is intended to exempt from certain
section 5 requirements polymers that EPA believes pose a low risk of
injury to health or the environment. The exemption criteria are
therefore designed to exempt polymers that are of low concern because
of their stability, molecular size, and lack of reactivity, among other
properties. In contrast, EPA has excluded certain polymers from the
exemption where:
     The Agency has insufficient data and review experience to
support a finding that they will not present an unreasonable risk. Or
     The Agency has found that under certain conditions, the
polymers may present risks which require a closer examination of the
conditions of manufacturing, processing, distribution, use, and
disposal during a full 90-day PMN review (i.e., the Agency has
information suggesting that the conditions for an exemption under
section 5(h)(4) are not met).
    This approach allows the Agency to maintain full regulatory
oversight on potentially higher risk polymers while promoting the
manufacture of low-risk polymers.
    Based on the data currently available, EPA believes, for the
reasons that follow it no longer can make a generally-applicable
finding, without additional information, that the manufacture,
processing, distribution in commerce, use, and/or disposal of polymers
containing certain perfluoroalkyl moieties consisting of a CF3- or
longer chain length will not present an unreasonable risk of injury to
health or the environment. This exclusion includes polymers that
contain any one or more of the following: PFAS; PFAC; fluorotelomers;
or perfluoroalkyl moieties that are covalently bound to either a carbon
or sulfur atom where the carbon or sulfur atom is an integral part of
the polymer molecule. To the contrary, EPA believes that the risks
presented by such polymers should be evaluated during the 90-day PMN
review period that Congress contemplated for new chemicals under
section 5(a)(1)(A) of TSCA.
    First, PFOS and PFOA, which are members of the PFAS and PFAC
category of chemicals as defined in Unit IV.B., have a high level of
toxicity and have shown liver, developmental, and reproductive toxicity
at very low dose levels in exposed laboratory animals. The primary
health effects of concern for PFOS, based on available data, are liver
effects, developmental effects, and mortality. The mortality is
associated with a steep dose/response across all ages and species. The
primary health effects of concern for PFOA are liver toxicity and
developmental toxicity. The health effects of PFOS and PFOA are
discussed more fully in Unit IV.D.5. With regard to fluorotelomers, it
has been demonstrated that the fluorotelomer 8-2 alcohol can be
converted to PFOA through metabolic reaction and environmental
degradation. Moreover, initial test data from a study in rats dosed
with fluorotelomer alcohol and other preliminary animal studies on
various telomeric products containing fluorocarbons structurally
similar to PFAC or PFAS have demonstrated a variety of toxic effects.
With regard to polymers containing perfluoroalkyl moieties other than
PFAS, PFAC, or fluorotelomers that would be subject to the rule, EPA
does not have specific data demonstrating that such polymers present
the same concerns as those containing PFAS, PFAC, or fluorotelomers.
Nonetheless, based on available data which indicates that compounds
containing PFAS or PFAC may degrade in the environment thereby
releasing the PFAS or PFAC moiety, and that fluorotelomers may degrade
in the environment to form PFAC, EPA believes that it is possible for
polymers containing perfluoroalkyl moieties that are covalently bound
to either a carbon or sulfur atom where the carbon or sulfur atom is an
integral part of the polymer molecule to also degrade over time in the
environment thereby releasing the perfluoroalkyl moiety. EPA also
believes that once released, such moieties may potentially degrade to
form PFAS or PFAC.
    Second, PFOS and PFOA are expected to persist in the environment
and they may bioaccumulate. These chemicals are stable to hydrolysis,
appear to be stable to photolysis, and do not

measurably biodegrade in the environment. PFOS and PFOA have been found
in the blood of workers exposed to the chemicals and in the general
population of the United States and other countries. They have also
been found in many terrestrial and animal species worldwide. The
widespread distribution of the chemicals suggests that PFOS and PFOA
may bioaccumulate. Exposure and environmental fate data are discussed
more fully in Unit IV.D.3. and Unit IV.D.4. respectively. EPA has also
received preliminary data that indicates that certain perfluoroalkyl
compounds including fluorotelomer alcohols are present in the air in
some large cities. These preliminary data suggest that there may be
widespread distribution of fluorotelomer alcohols and that air may be a
possible route of exposure to such chemicals.
    Third, although the Agency has far more data on PFOS and PFOA than
on other PFAS and PFAC chemicals, EPA believes that other PFAS and PFAC
chemicals may share similar toxicity, persistence and bioaccumulation
characteristics. Based on currently available information, EPA believes
that, while all PFAS and PFAC chemicals are expected to persist, the
length of the perfluorinated chain may have an effect on the other
areas of concern for these chemicals. In particular, there is some
evidence that PFAS/PFAC moieties with longer carbon chains may present
greater concerns for bioaccumulation potential and toxicity than PFAS/
PFAC moieties with shorter carbon chains. (Refs. 5, 6, and 7).
    Fourth, EPA has evidence that polymers containing PFAS or PFAC may
degrade, possibly by incomplete incineration, and release these
perfluorinated chemicals into the environment (Ref. 3). Even under
routine conditions of municipal waste incinerators, the Agency believes
that the PFAS and PFAC produced by oxidative thermal decomposition of
the polymers will remain intact (the typical conditions of a MWI are
not stringent enough to cleave the carbon-fluorine bonds) to be
released into the environment. It has also been demonstrated that PFAS
or PFAC-containing compounds may undergo degradation (chemical,
microbial, or photolytic) of the non-fluorinated portion of the
molecule leaving the remaining perfluorinated acid untouched (Ref. 2).
The Agency further anticipates that a carpet treated with a stain
resistant polymer coating containing fluorochemicals would be exposed
to conditions over time that could lead to the release of chemical
substances which may biodegrade to form PFAC. Further degradation of
the PFAC degradation product is extremely difficult. This possibility
is consistent with the previously cited degradation studies.
    As discussed in Unit II.C.2, EPA does not have specific data
demonstrating that perfluoroalkyl moieties other than PFAS, PFAC, or
fluorotelomers that would be subject to the rule present the same
concerns as PFAS, PFAC, or fluorotelomers. EPA is nevertheless
proposing to exclude polymers containing perfluoroalkyl moieties
consisting of a CF3- or longer chain length that are covalently bound
to either a carbon or sulfur atom where the carbon or sulfur atom is an
integral part of the polymer molecule from the polymer exemption. Based
on the data summarized in Unit V., EPA believes that it is possible for
polymers containing these perfluoroalkyl moieties to degrade in the
environment thereby releasing the perfluoroalkyl moiety. EPA also
believes that once released, such moieties may potentially degrade to
form PFAS or PFAC. EPA believes therefore, that polymers containing
these perfluoroalkyl moieties should be evaluated for potential health
or environmental concerns through the PMN process.
    Efforts are currently underway to develop a better understanding of
the environmental fate, bioaccumulation potential, and human and
environmental toxicity of PFAS and PFAC chemicals as well as
fluorotelomers and other perfluoroalkyl moieties. EPA has insufficient
evidence at this time, however, to definitively establish a carbon
chain length at which PFAS, PFAC, fluorotelomers, or other
perfluoroalkyl moieties that would be subject to the rule will not
present an unreasonable risk of injury to health or the environment,
which is the determination necessary to support an exemption under
section 5(h)(4) of TSCA. Therefore, EPA believes it is reasonable to
exclude from the polymer exemption rule polymers containing as an
integral part of their composition, except as impurities, certain
perfluoroalkyl moieties consisting of a CF3- or longer chain length.
This exclusion includes polymers that contain any one or more of the
following: PFAS; PFAC; fluorotelomers; or perfluoroalkyl moieties that
are covalently bound to either a carbon or sulfur atom where the carbon
or sulfur atom is an integral part of the polymer molecule.

VI. Other Options Considered

A. Exclude Polymers Containing PFAS, PFAC, Fluorotelomers, or
Perfluoroalkyl Moieties That Are Covalently Bound to Either a Carbon or
Sulfur Atom Where the Carbon or Sulfur Atom is an Integral Part of the
Polymer Molecule, But Only if These Perfluoroalkyl Moieties Contain
Greater Than Four Carbon Atoms

    This option would allow an exemption for polymers containing PFAS,
PFAC, fluorotelomers, or perfluoroalkyl moieties that are covalently
bound to either a carbon or sulfur atom where the carbon or sulfur atom
is an integral part of the polymer molecule, where the perfluoroalkyl
moiety contains fewer than five carbon atoms. This option was rejected
because, based on available information, EPA cannot continue to find
that such polymers ``will not present an unreasonable risk to human
health and the environment.'' EPA will continue to evaluate whether
exemptions for polymers containing PFAS, PFAC, fluorotelomers, or
perfluoroalkyl moieties that are covalently bound to either a carbon or
sulfur atom where the carbon or sulfur atom is an integral part of the
polymer molecule with smaller chain lengths in the perfluoroalkyl
moiety are appropriate for future exemption under the polymer exemption
rule.

B. Make the Scope of This Proposed Rule Consistent With the SNURs on
Perfluorooctyl Sulfonates (67 FR 11007; March 11, 2002 and 67 FR 72854;
December 9, 2002)

    These two SNURs cover perfluorooctanesulfonic acid (PFOSH) and
certain of its salts (PFOSS), perfluorooctanesulfonyl fluoride (POSF),
certain higher and lower homologues of PFOSH and POSF, and certain
other chemical substances, including polymers, that are derived from
PFOSH and its homologues. These chemicals are collectively referred to
as perfluoroalkyl sulfonates, or PFAS. Today's proposed rule would
exclude from eligibility polymers containing as an integral part of
their composition, except as impurities, certain perfluoroalkyl
moieties consisting of a CF3- or longer chain length. This exclusion
includes polymers that contain any one or more of the following: PFAS;
PFAC; fluorotelomers; or perfluoroalkyl moieties that are covalently
bound to either a carbon or sulfur atom where the carbon or sulfur atom
is an integral part of the polymer molecule. Therefore, if the proposed
rule were to be made consistent with the SNURs, only PFAS-containing
polymers

would be excluded from the polymer exemption rule. This option would
have continued to allow exemption under the polymer exemption rule for
polymers containing:
     PFAS that are not specifically derived from PFOSH
(specifically, the C4 to C10 carbon chain lengths addressed in the
SNUR).
     PFAC; fluorotelomers; or other perfluoroalkyl moieties,
for which EPA cannot make a ``will not present an unreasonable risk to
human health or the environment'' finding.

C. Exclude From Exemption PFAS (and Not PFAC) Containing Any Number of
Carbon Atoms Deemed Appropriate

    This option was rejected because although it would remove polymers
containing PFAS from exemption under the polymer exemption rule, it
would have continued to allow exemption for polymers containing PFAC,
for which EPA cannot make a ``will not present an unreasonable risk to
human health or the environment'' finding. This option could also
encourage companies to use these chemicals as substitutes for PFOS.

D. Exclude From Exemption All Fluorine-containing Polymers

    This option would have excluded from exemption under the polymer
exemption rule all fluorine-containing polymers. This option was
rejected because EPA does not believe, based on the best available
data, that all polymers containing fluorine present concerns that would
justify excluding them from the exemption. EPA will continue to
evaluate whether exemption for fluorine-containing polymers is
appropriate under the polymer exemption rule.

VII. Request for Comment on Specific Issues

    EPA is requesting specific responses to the following:
     Is exemption for polymers containing perfluoroalkyl
moieties that are covalently bound to either a carbon or sulfur atom
where the carbon or sulfur atom is an integral part of the polymer
molecule and where the perfluoroalkyl moiety consists of a CF3- or
longer chain length appropriate under the polymer exemption rule?
    The Agency is looking for information showing whether or not
polymers containing such substances degrade and release fluorochemical
residual compounds into the environment, and information concerning the
toxicity and bioaccumulation potential of such known or possible
fluorochemical breakdown products.
    In particular, the Agency is also looking for information showing
whether such polymers containing perfluoroalkyl moieties with smaller
chain lengths (i.e., less than 8 carbons) can degrade and release
fluorochemical residual compounds into the environment. If degradation
is shown to occur, the Agency would then want information indicating
whether once released, these compounds exhibit characteristics similar
to PFOS or PFOA in terms of persistence, bioaccumulation, or toxicity,
or otherwise exhibit characteristics of potential concern.
     Those who are manufacturing or importing polymers under
the existing exemption would have one year from the effective date to
complete the PMN process. EPA is specifically requesting comment on
this or other alternatives for implementing the final rule that would
achieve the purposes of TSCA section 5 without disrupting ongoing
manufacture or import of currently-exempt polymers.

VIII. Economic Considerations

    EPA has evaluated the potential costs of eliminating the polymer
exemption for the chemicals described in this proposal. The results of
this evaluation are contained in a document entitled ``Economic
Analysis of the Amendment of the Polymer Exemption Rule To Exclude
Certain Perfluorinated Polymers'' (Ref. 54). A copy of this economic
analysis is available in the public docket for this action, and is
briefly summarized here.
    As a result of the elimination of the polymer exemption for the
chemicals described in this proposal, any person who intends to
manufacture (defined by statute to include import) any of these
polymers, which are not already on the TSCA Inventory, would have to
first complete the TSCA premanufacture review process prior to
commencing the manufacture or import of such polymers. Any person who
relied on the exemption in the past and currently manufactures an
affected polymer would have to complete the TSCA premanufacture review
process to continue the manufacture of such polymers after the
effective date of the final rule. In order to provide an opportunity
for these existing manufacturers to complete the PMN process without
disrupting their manufacture of the affected polymers, the Agency is
seeking comment on approaches for structuring a delayed effective date
or phase in period for the amendment. For purposes of this analysis,
the Agency assumes that existing manufacturers will complete the PMN
process within the first year after the effective date of the final
rule.
    The industry costs for completing and submitting a PMN reporting
form are estimated to be $7,267 per chemical. Because the proposed rule
would eliminate the cost of complying with the recordkeeping and
reporting requirements of the Polymer Exemption Rule, the cost for
completing and submitting a PMN as a result of this proposed amendment
can be reduced by $308, for a net cost of $6,959 per chemical.
    Companies that currently manufacture an affected polymer are
estimated to incur a total cost of $6,959 per chemical. Companies that
do not currently manufacture an affected polymer, but begin to
manufacture such polymers in the future, may also incur potential costs
of $19,416 associated with potential delays in commercialization of the
new chemical. These companies are estimated to incur a total cost of
$26,375 per chemical as a result of this rulemaking (Ref. 52).
    The potential number of PMNs that may be submitted each year if the
proposed rule is finalized was estimated using the 200 polymer reports
received annually under the polymer exemption rule. EPA estimates that
this proposal might affect a maximum of six percent of the 200 polymers
reported annually, and therefore estimates that a maximum of 12 PMNs
may be submitted each year if the proposed rule is finalized. Using the
same estimated number of 12 chemicals per year for the 10 years that
affected polymers were exempt from PMN requirements under the polymer
exemption rule, EPA estimates that a maximum of 120 previously exempt
chemicals (12 chemicals x 10 years) could be expected to complete and
submit a PMN under the final rule. Thus, the Agency estimates that a
maximum of 132 PMNs might be submitted during the first year after the
effective date of the final rule, and that a maximum of 12 PMNs might
be submitted each subsequent year (Ref. 53).
    Using the estimated per chemical costs and the estimated number of
PMNs anticipated, EPA estimates the potential impact of this proposal
on industry to be a total annual costs for existing manufacturers of
$835,080 ($6,959 per chemical costs x 120 chemicals), and a total
annual cost for new manufacturers of $316,500 ($26,375 per chemical
costs x 12). The total annual potential industry compliance costs of
the proposed rule in the first year is estimated to be $1,151,580,
which will decrease to an estimated

annual cost of $316,500 in subsequent years.
    In addition, as was the case prior to the promulgation of the
polymer exemption rule in 1995, the Agency recognizes that the
submission of a PMN may lead to other regulatory actions under TSCA,
for example consent orders issued under TSCA section 5(e). Any such
actions are highly dependent on the circumstances surrounding the
individual PMN (e.g., available information and scientific
understanding about the chemical and its risks at the time the PMN is
being reviewed). Such potential actions and any costs associated with
them would not be a direct result of the proposed amendments to the
polymer exemption rule. Nevertheless, EPA believes it is informative to
provide a brief discussion of the Agency's previous and ongoing
regulatory activities with respect to potentially affected polymers.

IX. References

    These references have been placed in the public docket that was
established under docket ID number EPA-HQ-OPPTS-2002-0051 for this
rulemaking as indicated under ADDRESSES. The public docket includes
information considered by EPA in developing this proposed rule,
including the documents listed below, which are 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 other documents are 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