[Federal Register Volume 71, Number 44 (Tuesday, March 7, 2006)]
[Proposed Rules]
[Pages 11484-11504]
From the Federal Register Online via the Government Publishing Office [www.gpo.gov]
[FR Doc No: 06-2152]



[[Page 11483]]

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Part IV





Environmental Protection Agency





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40 CFR Part 723



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

  Federal Register / Vol. 71, No. 44 / Tuesday, March 7, 2006 / 
Proposed Rules  

[[Page 11484]]


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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.

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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 protected].
     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 (202) 564-8930. 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 (202) 566-1744, and the telephone number for the 
OPPT Docket is (202) 566-0280.

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: (202) 554-1404; e-mail address: [email protected].
    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: (202) 564-8986; e-mail 
address: [email protected].

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

[[Page 11485]]

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: (202) 566-0280 or e-mail: 
[email protected].
    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

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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

[[Page 11487]]

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

[[Page 11488]]

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

[[Page 11489]]

(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,

[[Page 11490]]

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

[[Page 11491]]

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

[[Page 11492]]

 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

[[Page 11493]]

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

[[Page 11494]]

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

[[Page 11495]]

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

[[Page 11496]]

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

[[Page 11497]]

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

[[Page 11498]]

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

[[Page 11499]]

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

[[Page 11500]]

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

[[Page 11501]]

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 
physically located in the docket, please consult the technical person 
listed in FOR FURTHER INFORMATION CONTACT. Reference documents 
identified with an AR are cross-indexed to non-regulatory, publicly 
accessible information files maintained in the TSCA Nonconfidential 
Information Center. Copies of these documents can be obtained as 
described in ADDRESSES.
    1. Memo from Dr. Gregory Fritz (USEPA/OPPT/EETD) to Mary Begley 
(USEPA/OPPT/CCD) re: Polymer Feedstocks Resulting in Excluded Polymers, 
April 18, 2002.
    2. A. Remde and R. Debus, Biodegradability of Fluorinated 
Surfactants Under Aerobic and Anaerobic Conditions, Chemosphere, 32(8), 
1563-1574 (1996).
    3. (AR 226-0550) Fluorochemical Use, Distribution and Release 
Overview. 3M. St. Paul, MN. May 26, 1999.
    4. (AR 226-1093) Seed, Jennifer. Hazard Assessment of 
Perfluorooctanoic Acid and Its Salts-USEPA/EPA/RAD. Washington, DC. 
November 4, 2002.
    5. Kudo, Naomi, et al. Comparison of the Elimination Between 
Perfluorinated Fatty Acids with Different Carbon Chain Lengths in Rats. 
Chemico-Biological Interactions. Vol. 134(2), pp. 203-216, 2001.
    6. Goeke-Flora, Carol M. and Nicholas V. Reo. Influence of Carbon 
Chain Length on the Hepatic Effects of Perfluorinated Fatty Acids, A 
\19\F- and \31\P-NMR Investigation. Chemical Research in Toxicology 
9(4) pp. 689-695, 1996.
    7. (AR 226-1030a109) 3M, Fluorochemical Decompostion Processes - 
April 4, 2001.
    8. (AR 226-1440) Hagen DF, Belisle J, Johnson JD, Venkateswarlu P., 
``Characterization of fluorinated metabolites by a gas chromatographic-
helium microwave plasma detector--the biotransformation of 1H, 1H, 2H, 
2H-perfluorodecanol perfluorooctanoate.'' Analytical Biochemistry 
118(2):336-343, 1981.
    9. (AR 226-1147) DuPont presentation to the Agency at the meeting 
held on November 25, 2002.
    10. (AR 226-1281) Scott Mabury, PI; Interim Annual Report of 
Activities for TRP Grant to University of Toronto; Project years: 1 
September, 2001 to 1 September, 2002.
    11. (AR 226-1141) Presentation materials used by the Telomer 
Research Group in a meeting with EPA on November 25, 2002.
    12. (AR 226-0620) Sulfonated Perfluorochemicals in the Environment: 
Sources, Dispersion, Fate, and Effects. 3M. St. Paul, MN. March 1, 
2000.
    13. (AR 226-0547) The Science of Organic Fluorochemistry. 3M. St. 
Paul, MN. February 5, 1999.
    14. (AR 226-0548) Perfluorooctane Sulfonate: Current Summary of 
Human Sera, Health and Toxicology Data. 3M. St. Paul, MN. January 21, 
1999.
    15. (AR 226-0600) Weppner, William A. Phase-out Plan for PFOS-Based 
Products. 3M. St. Paul, MN. July 7, 2000.
    16. The Use of Fluorochemical Surfactants in Floor Polish. David 
Bultman and Myron Pike. 3M Company. http://home.hanmir.com/~hahnw/news/
3m.html.
    17. 3M Phasing Out Some of its Specialty Materials. 3M News. 3M. 
St. Paul, MN. May 16, 2000.
    17a. Federal Register. (65 FR 62319, October 18, 2000) (FRL-6745-
5); (67 FR 11008; March 11, 2002) (FRL-6823-6); (67 FR 11014, March 11, 
2002) (FRL-6823-7); (67 FR 72854, December 9, 2002) (FRL-7279-1).
    18. (OPPT-2003-0012-0012) Voluntary Actions to Evaluate and Control 
Emissions of Ammonium Perfluorooctanoate (APFO). Letter to Stephen L. 
Johnson from Society of Plastics Industry. March 14, 2003.
    18a. (AR 226-1094) The Society of the Plastics Industry, Inc., 
presentation to the EPA, Sanitized Copy. April 26, 2002.
    19. (AR 226-0043) Voluntary Use and Exposure Information Profile 
for Perfluorooctanesulfonic Acid and Various Salt Forms. 3M Company 
submission to USEPA, dated April 27, 2000.
    20. (AR 226-0595) Voluntary Use and Exposure Information Profile 
for Perfluorooctanoic Acid and Salts. 3M Company submission to USEPA, 
dated June 8, 2000.
    21. Nobuhiko Tsuda, Daikin Industries Ltd., ``Fluoropolymer 
Emulsion for High-Performance Coatings'' in Paint and Coating Industry 
Magazine, June 2001, p. 56-66.
    22. K. Petritis, et al. ``Ion-pair reversed-phase liquid 
chromatography for determination of polar underivatized amino acids 
using perfluorinated carboxylic acids as ion pairing agent'' in Journal 
of Chromatography A, Vol. 833, 1999, pp. 147-155.
    23. Feiring, Andrew E. ``Fluoroplastics,'' in Organofluorine 
Chemistry, Principles and Commercial Applications, edited by R.E. Banks 
et al. Plenum Press, New York. 1994. pp. 339, 356.
    24. (AR 226-0938) EPA/Fluoropolymer Industry Meeting, Sept. 14, 
2000; Teflon Today Online, http://www.Dupont.com/teflon, http://www.gore.com.
    25. (AR 226-1140) Organization for Economic Co-operation and 
Development (OECD), Hazard Assessment of Perfluorooctane sulfonate 
(PFOS) and its Salts, ENV/JM/RD(2002)17/FINAL, Nov. 21, 2002.
    26. (AR 226-0599) Voluntary Use and Exposure Information Profile 
Ammonium Perfluorooctanoate (APFO) CAS Number: 3825-26-1. DuPont 
submission to USEPA, dated June 23, 2000.
    27. Ellis D. A., S. A. Mabury, J. W. Martin and D. C. G. Muir 2001. 
Thermolysis of fluoropolymers as a potential source of halogenated 
organic acids in the environment. Nature: 412, pp. 321-324.
    28. (AR 226-1030a090) 3M Environmental Laboratory. 2001. Hydrolysis 
Reactions of Perfluorooctanoic Acid (PFOA). Lab Request Number E00-
1851. March 30.

[[Page 11502]]

    29. (AR 226-1030a039) 3M Environmental Laboratory. 2001. Hydrolysis 
Reactions of Perfluorooctane Sulfonate (PFOS). Report Number W1878.
    30. Reiner, E.A. 1978. Fate of Fluorochemicals in the Environment. 
Project Number 9970612613. 3M Company, Environmental Laboratory. July 
19.
    31. (AR 226-1030a038) D. Pace Analytical. 2001. The 18-Day Aerobic 
Biodegradation Study of Perfluorooctanesulfonyl-Based Chemistries. 3M 
Company Request, Contract Analytical Project ID: CA097, Minneapolis, 
MN. February 23.
    32. (AR 226-0487) 3M Company. 1977. Ready Biodegradation of FC-143 
(BOD/COD/TOC). Environmental Laboratory. St. Paul, MN.
    33. (AR 226-0492) 3M Company. 1980. Ready Biodegradation of FC-143 
(BOD/COD) Lab Request No. 5625S. Environmental Laboratory. St. Paul, 
MN.
    34. (AR 226-0494) 3M Company. 1985. Ready Biodegradation of FX-1001 
(BOD/COD). Lab Request No. C1006. Environmental Laboratory. St. Paul, 
MN.
    35. (AR 226-0495) Pace Analytical. 1997. Ready Biodegradation of 
FC-126(BOD/COD). 3M Company Lab Request No. E1282. Minneapolis, MN. May 
29.
    36. Springborn Laboratories. 2000. Biodegradation of 
Perfluorooctane Sulfonate (PFOS) I. Study  290.6120, II.Study 
 290.6120, III. Study  290.6120, IV. Pure Culture 
Study. Study  290.6120. Submitted to the 3M Environmental 
Laboratory.
    37. (AR 226-0490) Todd, J.W. 1979. FC-143 Photolysis Study Using 
Simulated Sunlight. Project 9776750202, 3M. Company Technical Report 
No. 002. February 2.
    38. (AR 226-1030a091) Hatfield, T. 2001. Screening Studies on the 
Aqueous Photolytic Degradation of Perfluorooctanoic Acid (PFOA). 3M 
Environmental Laboratory. Lab request number E00-2192. St. Paul, MN.
    39. (AR 226-0488) Boyd, S. 1993. Review of Technical Report 
Summary: Adsorption of FC 95 and FC 143 in Soil. Michigan State 
University. May 19.
    40. Boyd, S.A. 1993. Review of Technical Notebook. Soil Thin Layer 
Chromatography. Number 48277, p 30. Michigan State University.
    41. (AR 226-1030a030) 3M Environmental Laboratory. 2000. Soil 
Adsorption/Desorption Study of Potassium Perfluorooctanesulfonate 
(PFOS). Lab Report Number E00-1311.
    42. (OPPT-2003-0012-0401) Adsorption/desorption of Ammonium 
Perfluorooctanoate to soil (OECD 106). April 17, 2003. Association of 
Plastics Manufacturers in Europe/DuPont.
    43. Bidleman, T.F. 1988. Atmospheric Processes: Wet and Dry 
Deposition of Organic Compounds are Controlled by their Vapor-Particle 
Partitioning. Environmental Science and Technology 22(4), pp. 361-367.
    44. Vraspir, G.A., Mendel, Arthur. 1979. Analysis for 
fluorochemicals in Bluegill Fish. Project 99706 12600: Fate of 
Fluorochemicals. 3M Technical Report Number 14. May 1.
    45. (AR 226-1053) EPA/Society of the Plastics Industry (SPI) 
Fluoropolymers Manufacturers Group (FMG) meeting, January 30, 2002.
    46. (AR 226-0496) 3M Environmental Laboratory. Howell, R.D., 
Johnson, J.D., Drake, J.B, Youngbloom, R.D. 1995. Assessment of the 
Bioaccumulative Properties of Ammonium Perfluorooctanoate: Static. 3M 
Technical Report. May 31.
    47. (AR 226-1149) 3M, Biodegradation screen studies for telomer 
type alcohols Nov. 6, 2002
    48. (AR 226-1262) DuPont Executive Summary--Biodegradation 
Screening Studies of 8-2 Telomer B Alcohol 03/20/03.
    49. (AR 226-1062) Martin, Jonathan W., Muir, Derek C., Moody, 
Cheryl A., Ellis, David A., Kwan, Wai Chi, Solomon, Keith R., Mabury, 
Scott A., ``Collection of Airborne Fluorinated Organics and Analysis by 
Gas Chromatography/Chemical Ionization Mass Spectrometry.'' Analytical 
Chemistry, 74: 584-590, 2002.
    50. (AR 226-1033) DuPont Telomer Research Program Update and Status 
Report--February 21, 2001.
    51. (AR 226-1258) TRP (DuPont), Letter of Intent (LOI) for the 
Telomer Research Program - Appendix 1 Submission March 14, 2003.
    52. U.S. EPA. ``Health and Safety Data Reporting; Submission of 
Lists and Copies of Health and Safety Studies,'' EPA ICR  
0574.12, OMB No. 2070-0012, August 2003.
    53. U.S. EPA. Memo from Dr. Gregory Fritz (USEPA/OPPT/EETD) to Mary 
Begley (USEPA/OPPT/CCD) re: Polymer Exemption Rule Amendment, November 
21, 2001.
    54. U.S. EPA. ``Economic Analysis of the Amendment of the Polymer 
Exemption Rule To Exclude Certain Perfluorinated Polymers,'' Wendy 
Hoffman (USEPA/OPPT/EETD), August 12, 2005.

X. Statutory and Executive Order Reviews

A. Regulatory Planning and Review

    Pursuant to Executive Order 12866, entitled Regulatory Planning and 
Review (58 FR 51735, October 4, 1993), the Office of Management and 
Budget (OMB) has designated this proposed rule as a ``significant 
regulatory action'' under section 3(f) of the Executive Order because 
it may raise novel legal or policy issues arising out of legal 
mandates, the President's priorities, or the principles set forth in 
the Executive Order. This action was therefore submitted to OMB for 
review under this Executive Order, and any changes to this document 
made at the suggestion of OMB have been documented in the public docket 
for this rulemaking.
    EPA has prepared an economic analysis of the potential impacts of 
this proposed revision to the polymer exemption rule. This economic 
analysis (Ref. 54) is available in the public docket for this action 
and is briefly summarized in Unit VIII.

B. Paperwork Reduction Act

    The information collection requirements related to the submission 
of PMNs are already approved by the Office of Management and Budget 
(OMB) under the Paperwork Reduction Act, 44 U.S.C. 3501 et seq. That 
Information Collection Request (ICR) document has been assigned EPA ICR 
number 0574.12 and OMB control number 2070-0012. This proposed rule 
does not impose any new requirements that require additional OMB 
approval.
    Under the PRA, ``burden'' means the total time, effort, or 
financial resources expended by persons to generate, maintain, retain, 
or disclose or provide information to or for a Federal agency. This 
burden estimate includes the time needed to review instructions, search 
existing data sources, gather and maintain the data needed, and 
complete, review, and submit the required PMN, and maintain the 
required records.
    Based on the estimated burden in the existing ICR, if an entity 
were to submit a PMN to the Agency, the annual reporting burden is 
estimated to average between 95 and 114 hours per response, with an 
midpoint respondent burden of 107 hours. This estimate was adjusted to 
account for the elimination of the existing burden related to the 
recordkeeping and reporting requirements in the polymer exemption rule, 
which is estimated to impose a burden on industry of six hours per 
chemical, i.e., two hours for reporting, and four hours for 
recordkeeping. The

[[Page 11503]]

net paperwork burden for submitting a PMN as a result of this proposed 
amendment is therefore estimated to be 101 hours per PMN submission. 
The burden hour cost for this proposed rule is estimated to be $4,459. 
In addition, PMN submissions must be accompanied by a user fee of 
$2,500 (set at $100 for small businesses with annuals sales of less 
than $40 million).
    Based on the high-end assumption of 12 PMN submissions annually, 
the annual burden is estimated to be 1,212 hours (12 x 101 hours). The 
one-time burden for the companies that submit PMNs for chemicals 
already in production is estimated to be a maximum of 12,120 hours (120 
chemicals x 101 hours per submission).
    An agency may not conduct or sponsor, and a person is not required 
to respond to an information collection request subject to the PRA 
unless it displays a currently valid OMB control number. The OMB 
control numbers for EPA's regulations in 40 CFR, after appearing in the 
preamble of the final rule, are listed in 40 CFR part 9 and included on 
any related collection instrument (e.g., on the form or survey).
    Submit any comments on the Agency's need for this information, the 
accuracy of the provided burden estimates, and any suggested methods 
for minimizing respondent burden, including the use of automated 
collection techniques, along with your comments on the proposed rule as 
instructed under ADDRESSES. The Agency will consider any comments 
related to the information collection requirements contained in this 
proposal as it develops a final rule.

C. Regulatory Flexibility Act

    Pursuant to section 605(b) of the Regulatory Flexibility Act (RFA) 
(5 U.S.C. 601 et seq.), the Agency hereby certifies that this proposed 
rule will not have a significant adverse economic impact on a 
substantial number of small entities.
    For purposes of assessing the impacts of today's proposed rule on 
small entities, small entity is defined as:
     A small business as defined by the Small Business 
Administration's (SBA) regulations at 13 CFR 121.201 based on the 
applicable NAICS code for the business sector impacted.
     A small governmental jurisdiction that is a government of 
a city, county, town, school district or special district with a 
population of less than 50,000.
     A small organization that is any not-for-profit enterprise 
which is independently owned and operated and is not dominant in its 
field.
    The regulated community does not include any small governmental 
jurisdictions or small not-for-profit organizations. For small 
businesses, the Agency assessed the impacts on small chemical 
manufacturers in NAICS codes 325 and 324110. The SBA size standards for 
sectors under NAICS 325 range from 500 to 1,000 employees or fewer in 
order to be classified as small. The size standard for NAICS code 
324110, petroleum refineries, is 1,500 employees.
    Based on estimates of the number of PMNs expected to be submitted 
as a result of this action, it appears that 12 or fewer businesses 
would be affected per year. The five companies that manufacture the 
majority of the volume of chemicals that will be affected by the 
polymer exemption rule belong to either or both of the Fluoropolymer 
Manufacturers Group, and the Telomer Research Program. These two 
groups, which have no other members beyond the five companies, are 
negotiating enforceable consent agreements and other voluntary testing 
arrangements with the Agency for testing specific chemicals that would 
be affected by the polymer exemption rule. The two groups have told the 
Agency that their member companies manufacture the majority of the 
volume of chemicals that would be affected by the rule. None of these 
five companies meet the definition of small under the Small Business 
Administration employee size criteria. The remaining volume of 
chemicals that could be affected by the rule is low enough so that even 
if a small company were to be affected, a significant number of 
businesses would not be affected, nor would any individual small 
business experience significant impacts. In addition to the estimated 
impact of having to submit a PMN (see estimates in Unit VIII.), small 
businesses with less than $40 million in annual sales are entitled to a 
reduced user fee of $100 for submitting a PMN, rather than the $2,500 
user fee, which would further reduce any impacts of the rule on small 
businesses.

D. Unfunded Mandates Reform Act

    Based on EPA's experience with past PMNs, State, local, and tribal 
governments have not been affected by this reporting requirement, and 
EPA does not have any reason to believe that any State, local, or 
tribal government will be affected by this rulemaking. As such, EPA has 
determined that this regulatory action does not impose any enforceable 
duty, contain any unfunded mandate, or otherwise have any affect on 
small governments subject to the requirements of sections 202, 203, 
204, or 205 of the Unfunded Mandates Reform Act of 1995 (UMRA) (Public 
Law 104-4).

E. Federalism

    Pursuant to Executive Order 13132, entitled Federalism (64 FR 
43255, August 10, 1999), EPA has determined that this proposed rule 
does not have ``federalism implications,'' because it will not have 
substantial direct effects on the states, on the relationship between 
the national government and the states, or on the distribution of power 
and responsibilities among the various levels of government, as 
specified in the Order. Thus, Executive Order 13132 does not apply to 
this proposed rule.

F. Consultation and Coordination With Indian Tribal Governments

    As required by Executive Order 13175, entitled Consultation and 
Coordination with Indian Tribal Governments (65 FR 67249, November 6, 
2000), EPA has determined that this proposed rule does not have tribal 
implications because it will not have any affect on tribal governments, 
on the relationship between the Federal government and the Indian 
tribes, or on the distribution of power and responsibilities between 
the Federal government and Indian tribes, as specified in the Order. 
Thus, Executive Order 13175 does not apply to this proposed rule.

G. Protection of Children From Environmental Health and Safety Risks

    Executive Order 13045, entitled Protection of Children from 
Environmental Health Risks and Safety Risks (62 FR 19885, April 23, 
1997) does not apply to this proposed rule because this action is not 
designated as an ``economically significant'' regulatory action as 
defined by Executive Order 12866, nor does it establish an 
environmental standard, or otherwise have a disproportionate effect on 
children.

H. Actions That Significantly Affect Energy Supply, Distribution, or 
Use

    This proposed rule is not subject to Executive Order 13211, 
entitled Actions concerning Regulations that Significantly Affect 
Energy Supply, Distribution, or Use (66 FR 28355, May 22, 2001) because 
it is not designated as an ``economically significant'' regulatory 
action as defined by Executive Order 12866, nor is it likely to have 
any significant adverse effect on the supply, distribution, or use of 
energy.

[[Page 11504]]

I. National Technology Transfer Advancement Act

    Section 12(d) of the National Technology Transfer and Advancement 
Act of 1995 (NTTAA), 15 U.S.C. 272 note) directs EPA to use voluntary 
consensus standards in its regulatory activities unless to do so would 
be inconsistent with applicable law or impractical. Voluntary consensus 
standards are technical standards (e.g., materials specifications, test 
methods, sampling procedures, etc.) that are developed or adopted by 
voluntary consensus standards bodies. This proposed rule does not 
impose any technical standards that would require EPA to consider any 
voluntary consensus standards.

J. Environmental Justice

    This proposed rule does not have an adverse impact on the 
environmental and health conditions in low-income and minority 
communities. Therefore, under Executive Order 12898, entitled Federal 
Actions to Address Environmental Justice in Minority Populations and 
Low-Income Populations (59 FR 7629, February 16, 1994), the Agency does 
not need to consider environmental justice-related issues.

List of Subjects in 40 CFR Part 723

    Environmental protection, Chemicals, Hazardous substances, 
Reporting and recordkeeping requirements.


    Dated: February 8, 2006.
Susan B. Hazen,
Acting Assistant Administrator for Prevention, Pesticides and Toxics 
Substances.
    Therefore, it is proposed that 40 CFR part 723 be amended as 
follows:

PART 723--[AMENDED]

    1. The authority citation for part 723 would continue to read as 
follows:

    Authority: 15 U.S.C. 2604.

    2. Section 723.250 is amended as follows:
    a. By adding several definitions in alphabetical order to paragraph 
(b).
    b. By adding a paragraph (d)(6).


Sec.  723.250  Polymers.

* * * * *
    (b) * * *
    Fluorotelomers means the products of telomerization, the reaction 
of a telogen (such as pentafluoroethyl iodide) with an ethylenic 
compound (such as tetrafluoroethylene) to form low molecular weight 
polymeric compounds, which contain an array of saturated carbon atoms 
covalently bonded to each other (C-C bonds) and to fluorine atoms (C-F 
bonds). This array is predominantly a straight chain, and depending on 
the telogen used produces a compound having an even number of carbon 
atoms. However, the carbon chain length of the fluorotelomer varies 
widely. The perfluoroalkyl groups formed by this process are usually, 
but do not have to be, connected to the polymer through a 
functionalized ethylene group as indicated by the following structural 
diagram: (Rf-CH2-CH2-Anything).
    Perfluororalkyl carboxylate (PFAC) means a group of saturated 
carbon atoms covalently bonded to each other in a linear, branched, or 
cyclic array and covalently bonded to a carbonyl moiety and where all 
carbon-hydrogen (C-H) bonds have been replaced with carbon-fluorine (C-
F) bonds. The carbonyl moiety is also covalently bonded to a hetero 
atom, typically, but not necessarily oxygen (O) or nitrogen (N).
    Perfluoroalkyl sulfonate (PFAS) means a group of saturated carbon 
atoms covalently bonded to each other in a linear, branched, or cyclic 
array and covalently bonded to a sulfonyl moiety and where all carbon - 
hydrogen (C-H) bonds have been replaced with carbon - fluorine (C-F) 
bonds. The sulfonyl moiety is also covalently bonded to a hetero atom, 
typically, but not necessarily oxygen (O) or nitrogen (N).
* * * * *
    (d) * * *
    (6) Polymers which contain certain perfluoroalkyl moieties 
consisting of a CF3- or longer chain length. After [insert date 1 year 
after date of publication of the final rule in the Federal Register] a 
polymer cannot be manufactured under this section if the polymer 
contains as an integral part of its composition, except as impurities, 
one or more of the following perfluoroalkyl moieties consisting of a 
CF3- or longer chain length: 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.
    (i) Except as provided in paragraph (d)(6)(ii) of this section, any 
polymer that is subject to paragraph (d)(6) of this section and that 
has been manufactured prior to [insert date 1 year after date of 
publication of the final rule in the Federal Register] may no longer be 
manufactured after [insert date 1 year after date of publication of the 
final rule in the Federal Register] unless that polymer has undergone a 
premanufacture review in accordance with section 5(a)(1)(A) of TSCA and 
40 CFR part 720.
    (ii) Paragraph (d)(6) of this section does not apply to polymers 
which are already on the list of chemical substances manufactured or 
processed in the United States that EPA compiles and keeps current 
under section 8(b) of TSCA.
* * * * *

[FR Doc. 06-2152 Filed 3-6-06; 8:45 am]
BILLING CODE 6560-50-S