```

[Federal Register Volume 76, Number 143 (Tuesday, July 26, 2011)]
[Proposed Rules]
[Pages 44535-44547]
From the Federal Register Online via the Government Printing Office [www.gpo.gov]
[FR Doc No: 2011-18842]

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ENVIRONMENTAL PROTECTION AGENCY

40 CFR Part 799

[EPA-HQ-OPPT-2010-0812; FRL-8880-3]
RIN 2070-AJ83

Testing of Bisphenol A

AGENCY: Environmental Protection Agency (EPA).

ACTION: Advance notice of proposed rulemaking (ANPRM).

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SUMMARY: Bisphenol A (BPA) (Chemical Abstracts Service Registry Number 
(CASRN) 80-05-7), a high production volume (HPV) chemical, is a 
reproductive, developmental, and systemic toxicant in animal studies 
and is weakly estrogenic. EPA is providing this ANPRM to request 
comment on requiring toxicity testing to determine the potential for 
BPA to cause adverse effects, including endocrine-related effects, in 
environmental organisms at low concentrations. EPA is also seeking 
comment on requiring environmental testing consisting of sampling and 
monitoring for BPA in surface water, ground water, drinking water, 
soil, sediment, sludge, and landfill leachate

[[Page 44536]]

in the vicinity of expected BPA releases to determine whether 
environmental organisms may currently be exposed to concentrations of 
BPA in the environment that are at or above levels of concern for 
adverse effects, including endocrine-related effects. This ANPRM is 
directed only toward the environmental presence and environmental 
effects of BPA. EPA is working with the Department of Health and Human 
Services (HHS) on potential human health issues, but is not considering 
any additional testing specifically in regard to human health issues at 
this time.

DATES: Comments must be received on or before September 26, 2011.

ADDRESSES: Submit your comments, identified by docket identification 
(ID) number EPA-HQ-OPPT-2010-0812, by one of the following methods:
     Federal eRulemaking Portal: http://www.regulations.gov. 
Follow the on-line instructions for submitting comments.
     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-2010-0812. 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 DCO'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-
2010-0812. EPA's policy is that all comments received will be included 
in the 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 Web site 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 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 docket index 
available at http://www.regulations.gov. 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, will be publicly available only 
in hard copy. Publicly available docket materials are available 
electronically at http://www.regulations.gov, or, if only available in 
hard copy, at the OPPT Docket. The OPPT Docket is located in the EPA 
Docket Center (EPA/DC) at Rm. 3334, EPA West Bldg., 1301 Constitution 
Ave., NW., Washington, DC. The EPA/DC Public Reading Room hours of 
operation are 8:30 a.m. to 4:30 p.m., Monday through Friday, excluding 
legal holidays. The telephone number of the EPA/DC Public Reading Room 
is (202) 566-1744, and the telephone number for the OPPT Docket is 
(202) 566-0280. Docket visitors are required to show photographic 
identification, pass through a metal detector, and sign the EPA visitor 
log. All visitor bags are processed through an X-ray machine and 
subject to search. Visitors will be provided an EPA/DC badge that must 
be visible at all times in the building and returned upon departure.

FOR FURTHER INFORMATION CONTACT: For technical information contact: 
Mary Dominiak, Chemical Control Division (7405M), Office of Pollution 
Prevention and Toxics, Environmental Protection Agency, 1200 
Pennsylvania Ave., NW., Washington, DC 20460-0001; telephone number: 
(202) 564-8104; e-mail address: dominiak.mary@epa.gov.
    For general information contact: The TSCA-Hotline, ABVI-Goodwill, 
422 South Clinton Ave., Rochester, NY 14620; telephone number: (202) 
554-1404; e-mail address: TSCA-Hotline@epa.gov.

SUPPLEMENTARY INFORMATION:

I. General Information

A. Does this action apply to me?

    You may be potentially affected by this action if you manufacture 
(defined by statute to include import) or process BPA (CASRN 80-05-7). 
BPA is listed on the Toxic Substances Control Act (TSCA) Chemical 
Substance Inventory (TSCA Inventory) under the name phenol, 4,4'-(1-
methylethylidene)bis-. Potentially affected entities may include, but 
are not limited to:
     Chemical manufacturers (including importers) (NAICS codes 
325, 32411), e.g., chemical manufacturing and petroleum refineries of 
BPA.
     Plastics material and resin manufacturers (NAICS code 
325211), e.g., manufacturers and processors of BPA-based polycarbonate 
plastics and epoxy resins.
     Foundries (NAICS codes 331512, 331524, 331528), e.g., 
steel investment foundries, aluminum foundries, and other non-ferrous 
foundries, except die-casting, using BPA in casting sands.
     Paint and coating manufacturers (NAICS code 325510), e.g., 
manufacturers of epoxy-based paints and other coating products that may 
contain BPA.
     Paper recyclers (NAICS codes 322110, 322121, 3222), e.g., 
pulp mills, paper (except newsprint) mills, and converted paper product 
manufacturers that may process waste thermal paper containing BPA.
     Materials recovery facilities (NAICS code 562920), e.g., 
facilities separating and sorting recyclable materials that may handle 
thermal paper, polycarbonates, or food and beverage cans lined with 
BPA-based epoxy coatings.
     Custom compounders of purchased resins (NAICS code 
325991), e.g., facilities where resins are made from recycled 
polycarbonate plastics that may contain BPA.
    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. 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.

[[Page 44537]]

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 ID 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 your estimate in sufficient detail to allow for it to be 
reproduced.
    vi. Provide specific examples to illustrate your concerns and 
suggest 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?

    As a follow-up to the BPA Action Plan released on March 29, 2010 
(Ref. 1), EPA is issuing this ANPRM under TSCA section 4(a) (15 U.S.C. 
2603(a)) to solicit public input on the necessity for and best approach 
to obtain environmental effects, exposure, and pathway information 
relevant to a determination that BPA either does or does not present an 
unreasonable risk of injury to the environment. In particular, EPA 
requests comment on:
    1. Whether EPA should propose requiring specific toxicity testing 
to more fully characterize the effects of BPA on environmental 
organisms at low concentrations.
    2. Whether EPA should propose requiring environmental testing 
consisting of sampling and monitoring, particularly in the vicinity of 
reported releases of BPA into the environment, and what design and 
protocol it should use for such sampling and monitoring, in order to 
identify potential sources and pathways of exposure and determine the 
extent to which environmental organisms may be exposed to BPA 
concentrations of concern as determined by existing data and by 
additional studies that are either already underway or would be 
conducted under a test rule.
    3. EPA additionally requests comment and supporting information 
regarding which TSCA section 4(a)(1) finding authority would be most 
appropriate for the purpose of a BPA test rule proposal, as discussed 
in Unit II.C. Any proposal would ultimately be based on EPA's 
assessment of the relevant information available at the time of 
proposal.

B. What testing is EPA considering in this ANPRM?

    In this ANPRM, EPA is considering requiring both toxicity testing 
for environmental organisms exposed to BPA and environmental testing 
consisting of sampling and monitoring in the vicinity of reported BPA 
releases to measure its environmental presence. The toxicity testing is 
being considered to resolve existing uncertainties concerning the 
potential for BPA to elicit adverse effects in ecologically relevant 
species, including endocrine-related impacts that could occur at low 
doses. The environmental testing is being considered to resolve 
existing uncertainties concerning potential sources of and pathways 
leading to environmental exposures and to determine whether or not the 
concentrations to which organisms currently may be exposed in the 
environment are at or above levels of concern for adverse effects, 
including endocrine-related effects.
    On May 17, 1985, EPA published in the Federal Register a proposed 
rule (50 FR 20691) to require human health and environmental testing in 
response to the TSCA Interagency Testing Committee's (ITC) 14th report 
published in the Federal Register issue of May 29, 1984 (49 FR 22389), 
which designated BPA for priority consideration for health and 
environmental effects. EPA proposed standard freshwater and marine 
acute fish and aquatic invertebrate toxicity tests, and freshwater 
aquatic plant toxicity tests. Test results were submitted in response 
to the proposal for freshwater and marine acute fish, acute aquatic 
invertebrate, and algal toxicity. EPA's final rule published in the 
Federal Register issue of September 18, 1986 (51 FR 33047) (1986 Final 
Rule), terminated the test rule process for environmental effects 
testing for BPA. At the time, EPA determined that the test data were 
adequate and that chronic freshwater organism testing was not needed 
because the LC50 values for the standard acute aquatic 
organism toxicity tests were greater than 1.0 parts per million (ppm) 
(1 milligram/Liter (mg/L)), and the ratios of 48-hour to 96-hour 
LC50 values were not greater than 2. Since the 1986 Final 
Rule, however, several studies on BPA have raised concerns about its 
environmental effects at concentrations less than 1.0 ppm (1 mg/L).
    As stated in the BPA Action Plan (Ref. 1), EPA does not intend to 
initiate regulatory action under TSCA at this time on the basis of 
human health. EPA remains committed to protecting human health, but 
notes that most human exposure, including exposure to children, comes 
through food packaging materials under the jurisdiction of the Food and 
Drug Administration (FDA) in HHS. FDA, together with the Centers for 
Disease Control and Prevention (CDC) and the National Institute of 
Environmental Health Sciences (NIEHS), is investing in important new 
health studies in both animals and humans to better determine and 
evaluate the potential health consequences of BPA exposures. EPA will 
continue to coordinate closely with FDA, CDC, and NIEHS on this 
activity. To the extent that FDA may identify health concerns from BPA 
in food contact materials, EPA will work with FDA to identify and 
assess potential substitutes. Levels of exposure that may be identified 
by the ongoing review as being of concern to human health, including 
children's health, will affect the extent to which EPA would take 
additional action to address potential risks to human health resulting 
from uses within TSCA jurisdiction.
    1. What is currently known about the environmental hazard of BPA? 
The toxicity of BPA has been studied extensively, as indicated in the 
multiple studies cited in the BPA Action Plan (Ref. 1).\1\ There is 
general agreement

[[Page 44538]]

among multiple reviewers, including government regulatory agencies in 
the United States, Japan, the European Union (EU), and Canada, that BPA 
is a reproductive and developmental toxicant at doses in animal studies 
of [gteqt] 50 mg/kilogram-body weight (kg-bw)/day (delayed puberty in 
male and female rats and male mice; discussed in Refs. 2-9); [gteqt] 
235 mg/kg-bw/day (reduced fetal or birth weight or growth early in 
life, effects on testis of male rats; Ref. 9); and [gteqt] 500 mg/kg-
bw/day (possible decreased fertility in mice, altered estrous cycling 
in female rats, and reduced survival of fetuses; Ref. 9). Systemic 
effects (reduction in body weight, changes in relative organ weights, 
and increases in liver toxicity; Refs. 2-8) were observed at doses 
above 5 mg/kg-bw/day (identified as a no observed adverse effect level 
(NOAEL); lowest observed adverse effect level (LOAEL) of 50 mg/kg-bw/
day). There are reports of endocrine-related low-dose effects on 
puberty and neurological development (brain, behavior; Ref. 9) at doses 
in animal studies as low as 2 microgram ([mu]g)/kg-bw/day. There is 
disagreement in the scientific community at large about whether effects 
seen at doses in animals less than 1 mg/kg/day are meaningful and 
relevant to humans. FDA, together with NIEHS and CDC, are engaging in 
additional research to better determine and evaluate the potential 
human health consequences of exposures to BPA, including exposures at 
low doses (Ref. 10). EPA is working with FDA, NIEHS, and CDC on this 
ongoing research, and is not considering any additional testing 
specifically in regard to human health issues at this time.
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    \1\ EPA's response to the request for correction of the 
information provided in the Action Plan that was filed under the 
``Agency's Information Quality Guidelines'' by the American 
Chemistry Council is available at http://www.epa.gov/quality/informationguidelines/iqg-list.html.
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    Many studies have been conducted to determine potential effects of 
BPA exposure on invertebrates, fish, amphibians, reptiles, birds, and 
wild mammals, and a review is provided by Crain et al. (Ref. 11). In 
general, studies have shown that BPA can affect growth, reproduction, 
and development in aquatic organisms. Evidence of sub-lethal effects 
mediated through either endocrine or non-endocrine related mechanisms 
in fish, amphibians, reptiles, and invertebrate aquatic organisms has 
been reported at potentially environmentally relevant exposure levels 
lower than those required for acute toxicity. There is a widespread 
variation in reported values for these sub-lethal effects, but many 
fall in the range of 1 [micro]g/L to 1 mg/L (Ref. 6; also, see 
individual studies noted in Table 2 of Unit II.B.2.).
    The ecological hazard for BPA has been evaluated in three different 
risk assessments performed by the EU, Canada, and Japan (Refs. 7, 6, 
and 8), as summarized in Table 1 of this unit. The different 
methodologies, endpoints, and study results used by each country to 
derive their ecological values highlight the significant uncertainty in 
the estimated hazard values. Japan concluded that ``the current 
exposure levels of BPA will not pose unacceptable risks to the local 
populations of aquatic life, particularly fish'' (Ref. 8). In contrast, 
the EU concluded that although the predicted exposure concentrations 
were significantly below its hazard values, there was a need for 
further information and/or testing on such organisms as freshwater 
snails (Ref. 7).
    Canada used a study (Ref. 12) that reported reduced sperm quality 
and delayed ovulation in brown trout at a very low concentration in 
water (1.75 [micro]g/L). Other effects such as the induction of 
intersex (or testes-ova in males and females), decreased 
spermatogenesis, induction of vitellogenin, delayed or ceased 
ovulation, or histological liver changes were also reported in other 
studies referenced in the EU and Japanese hazard evaluations. However, 
because there were no standardized test guidelines or risk assessment 
guidance for evaluating some of these endocrine-related effects at the 
time of these assessments, the EU and Japan set ecotoxicological hazard 
values based on conventional effects (mortality and reproductive 
effects) from standardized studies. In contrast, Canada concluded in 
its hazard characterization that:

    [c]onsidered together, the data provide strong evidence that 
bisphenol A is capable of eliciting adverse effects: (1) following 
prolonged exposure at levels below those usually seen to elicit 
effects in standard toxicity tests (i.e., tests based on recognized 
methods which evaluate endpoints such as survival, reproduction and 
growth); (2) following brief low-dose exposure, particularly at 
sensitive developmental stages, with effects apparent later in the 
life cycle; (3) on filial generations following parental exposure; 
and (4) using more than one mode of action.
    (Ref. 6)

    Canada concluded that BPA concentrations in water have the 
potential to cause adverse effects on populations of pelagic organisms 
in Canada and concentrations in biota have the potential to cause 
adverse effects in populations of wildlife in Canada, but that there is 
a low risk of direct adverse effects to sediment organisms and to avian 
wildlife species in Canada. In the conclusion of its risk assessment, 
Canada stated that it is considered appropriate to apply a 
precautionary approach when characterizing risk, observing ``it is 
concluded that bisphenol A is entering the environment in a quantity or 
concentration or under conditions that have or may have an immediate or 
long-term harmful effect on the environment or its biological 
diversity'' (Ref. 6).

                                Table 1--Summary of Bisphenol A Ecological Values
----------------------------------------------------------------------------------------------------------------
                                              Predicted no effect
                                                 concentrations
                   Country                      (microgram/Liter                     Endpoints
                                                 ([mu]g/L)) \1\
----------------------------------------------------------------------------------------------------------------
European Union..............................                1.5    The predicted no effect concentration (PNEC)
                                                                    for aquatic organisms (derived by using a
                                                                    statistical analysis of data from available
                                                                    data on freshwater and marine aquatic
                                                                    organisms (in this case, 16 different
                                                                    studies, unpublished and published, from 10
                                                                    different taxonomic groups)) to arrive at a
                                                                    value of 7.5 [mu]g/L, which is divided by an
                                                                    uncertainty factor of 5, resulting in a PNEC
                                                                    of 1.5 [mu]g/L (Ref. 7).
Canada......................................                0.175  This PNEC was derived by using a lowest
                                                                    observed effect concentration (LOEC) of 1.75
                                                                    [mu]g/L for reduced semen quality and
                                                                    delayed ovulation in a brown trout study
                                                                    (Lahnsteiner et al. 2005) and applying an
                                                                    uncertainty factor of 10 (Ref. 6).

[[Page 44539]]

 
Japan.......................................                1.6    The PNEC was derived by using the 16 [mu]g/L
                                                                    no effect concentration (NOEC) for egg
                                                                    hatchability in fathead minnows from the
                                                                    unpublished 3-generation study by Sumpter,
                                                                    et al. (2001) multi-generation fish study
                                                                    and dividing by an uncertainty factor of 10
                                                                    (Ref. 8).
----------------------------------------------------------------------------------------------------------------
\1\ In the European Union, Canada, and Japan, a predicted no effect concentration (PNEC) is compared directly
  with an exposure value to evaluate risk. If the ratio of environmental concentration to PNEC is less than one,
  the risk is generally considered acceptable. As noted in the table, countries use different approaches for
  generating PNECs, and the precise values may differ even when based on the same studies.

    EPA considers that the uncertainty demonstrated by these divergent 
opinions concerning interpretation of the results of existing 
environmental toxicity studies, particularly studies addressing 
potential effects at low levels of exposure, may indicate further 
testing is necessary to resolve the question of whether or not BPA 
presents an unreasonable risk of injury to the environment on the basis 
of those effects. This is due to the combination of the existence of 
measured values, as discussed in Unit II.B.4. and as shown in that 
unit's Table 3, for BPA in U.S. surface waters at a mean-concentration 
range of up to 1.78 [mu]g/L (parts per billion (ppb)) and a single-
maximum concentration of 12 [mu]g/L (ppb); in ground water at a mean-
concentration range of up to 1.9 [mu]g/L (ppb) and a maximum 
concentration of 2.55 [mu]g/L (ppb); and in freshwater sediments at a 
median concentration of 0.6 [mu]g/kg (ppb) dry weight and a maximum 
concentration of 140 [mu]g/kg (ppb) (see Table 3 in Unit II.B.4.), and 
the existence of many hazard studies describing a variety of effects in 
aquatic organisms at some of these concentrations (see Table 2 in Unit 
II.B.2.), leaving little or no room for a reasonable or acceptable 
margin of exposure.
    In order to assess the potential for BPA to harm the environment in 
the United States, EPA considers it important to address two basic 
areas of inquiry relevant to identifying the hazard and exposure 
components of a risk analysis:
    a. What additional hazard information is needed to fully 
characterize the effects of BPA in environmental organisms at low doses 
and potentially environmentally relevant concentrations?
    b. What levels of BPA are present in the environment, particularly 
in areas where environmental exposures are likely to be highest (e.g., 
near BPA manufacturing facilities, polycarbonate and epoxy resin 
manufacturing and processing facilities, foundries, landfills, 
wastewater treatment plants (WWTPs), and other locations associated 
with uses and/or releases of BPA)?
    2. What additional hazard information is needed on the effects of 
BPA on environmental organisms? EPA performed a literature search to 
identify relevant scientific information to assess the acute and 
chronic toxicity of BPA to environmental organisms from 2007 \2\ to the 
present. A total of 468 articles were found (Ref. 13), of which 30 were 
found to be of some relevance (Ref. 14). Since thorough analyses of 
acute and chronic toxicity for ``conventional endpoints'' (which 
generally address immediate effects on survival or reproduction) had 
already been conducted for BPA by Canada, the EU, and Japan (Refs. 6-
8), EPA performed a more detailed evaluation of the scientific 
literature for sub-lethal effects at lower concentrations (
L). These sub-lethal effects in both vertebrates and invertebrates 
could be mediated either through endocrine or non-endocrine-related 
mechanisms. There are many studies indicating such sub-lethal effects 
from BPA exposures at levels that, based on the information discussed 
in Unit II.B.4., appear to be potentially environmentally relevant 
concentrations because they may occur in the environment. Some of these 
studies are included in Table 2 of this unit.
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    \2\ The starting date of 2007 was used to allow for some overlap 
between the thorough searches done by Canada, the EU, and Japan.

       Table 2--Summary of Reported Hazard Effects of Bisphenol A at Potentially Environmentally Relevant
                                                 Concentrations
----------------------------------------------------------------------------------------------------------------
                                                                  Effect  concentrations
           Test organism                       Endpoint              (microgram/Liter     References  (Listed in
                                                                        ([mu]g/L))               Ref. 14)
----------------------------------------------------------------------------------------------------------------
Amphibians:
    Xenopus laevis (African clawed   Inhibited metamorphosis via  22.8..................  Heimeier et al., 2009.
     frog).                           T3 pathways.
    Xenopus laevis.................  High ratio of females to     23....................  Levy et al., 2004.
                                      males--1st study.
    Xenopus laevis.................  High ratio of females to     only at 23............  Levy et al., 2004.
                                      males--2nd study.
Avian:
    Gallus domesticus (chicken)....  Delayed development of       2.....................  Furuya et al., 2006.
                                      wattle, comb, and testes.
    Gallus domesticus..............  Inhibited development of     20....................  Furuya et al., 2006.
                                      seminiferous tubuli and
                                      spermatogenesis.
Fish:
    Dicentrarchus labrax (seabass).  Increased vitellogenin       10....................  Correia et al., 2007.
                                      production.

[[Page 44540]]

 
    Misgurnus anguillicaudatus       Increased vitellogenin       10....................  Lv et al., 2007.
     (Chinese loach).                 production.
    Orizias latipes (medaka).......  Egg hatchability delayed...  13 only...............  Yokota et al., 2000.
    Orizias latipes................  Loss of testicular           50....................  Metcalfe et al., 2001.
                                      structure, increased
                                      fibrotic tissue; decreased
                                      sperm cells.
    Orizias latipes................  Vitellogenin production....  10....................  Kashiwada et al.,
                                                                                           2002.
    Orizias latipes................  Increased female proteins    10....................  Tabata et al., 2001.
                                      (i.e., vitellogenin).
    Orizias latipes................  Decreased egg hatching in    2 only................  Japanese Ministry of
                                      2nd generation.                                      the Environment,
                                                                                           2006.
    Orizias latipes................  Increased male               49.7..................  Japanese Ministry of
                                      hepatosomatic index.                                 the Environment,
                                                                                           2006.
    Pimephales promelas (fathead     Increased vitellogenin       52.8..................  Rhodes et al., 2007
     minnow).                         production.                                          (unpublished).
    Xiphophorus helleri (swordtail   Reduced sword tail length..  20....................  Kwak et al., 2001.
     fish).
    Cyprinus carpio (carp).........  Oviduct formation in males.  32....................  Bowmer & Gimeno, 2001
                                                                                           (unpublished).
    Cyprinus carpio................  Altered sex steroid levels;  1.....................  Mandich et al., 2007.
                                      alterations in testes
                                      structure; oocyte atresia.
Invertebrates:
    Bellamya purificata (snail)....  Enzyme activities in gills   1.....................  Li et al., 2008.
                                      and digestive glands.
    Marisa cornuarietis (ramshorn    Superfeminization..........  1.....................  Oehlmann et al., 2000.
     snail).
    Marisa cornuarietis............  Increased egg and clutch     0.25 at 20 [deg]C.....  Oehlmann et al., 2006.
                                      production per female.
    Marisa cornuarietis............  Increased egg production...  0.25 at 27 [deg]C.....  Oehlmann et al., 2006.
    Marisa cornuarietis............  Increased clutch production  5 at 27 [deg]C........  Oehlmann et al., 2006.
    Potamopyrgus antipodarum         Increased growth/embryo      5 only................  Jobling et al., 2004.
     (snail).                         production.
    Potamopyrgus antipodarum.......  Unshelled embryos..........  30....................  Duft et al., 2003.
    Potamopyrgus antipodarum.......  Increased embryo production  1.....................  Duft et al., 2003.
    Nucella lapillus (marine snail)  Superfeminization; reduced   1.....................  Oehlmann et al., 2000.
                                      sperm/penis length/
                                      prostrate gland in males.
    Acartia tonsa (copepod)........  Increased egg production...  20 (day 10 only)......  Andersen et al., 1999.
    Tigriopus japonicus (intertidal  Delayed development          0.1...................  Marcial et al., 2003.
     copepod).                        (Parent).
    Tigriopus japonicus............  Delayed development (F1)...  0.01..................  Marcial et al., 2003.
    Chironomus riparius............  Delayed emergence (2nd       0.078.................  Watts et al., 2001.
                                      generation).
    Chironomus riparius............  Mouthpart deformities......  0.01..................  Watts et al., 2003.
----------------------------------------------------------------------------------------------------------------

    There is debate in the scientific literature on how best to 
interpret these low-dose, sub-lethal effects of BPA and other chemicals 
on environmental organisms. EPA is concerned that these sub-lethal 
effects may be having a detrimental effect on populations of aquatic 
organisms over time based on the reported increased susceptibility of 
subsequent generations exposed to BPA in multi-generation invertebrate 
and fish studies. For example, in the intertidal copepod (Tigriopus 
japonicus), delayed development was reported in the first generation at 
0.1 [micro]g/L, but at a 10-fold lower concentration of 0.01 [micro]g/L 
in the next generation (Ref. 15). In the freshwater midge (Chironomus 
riparius), the first generation did not have a significant delay in 
emergence time from the egg, but in the second generation emergence was 
delayed at 0.08 [micro]g/L (Ref. 16). Egg hatchability decreased in 
fathead minnows (Pimephales promelas) at 640 [micro]g/L in the first 
(F1) generation, then at 160 [micro]g/L in the second (F2) generation 
(Ref. 17). Although the mechanisms of action leading to effects may be 
different for vertebrate and invertebrate organisms, this suggests the 
potential for increasing developmental and reproductive effects in 
populations of aquatic organisms that have repeated exposures to BPA 
for generations, even at very low concentrations.
    Testing with BPA has been extensive at sub-lethal concentrations, 
but the studies with effects across multiple species generally have 
flaws associated with them, including lack of analytical monitoring, 
small sample size, inadequate replication, or use of inappropriate 
statistical analyses leading to incorrect conclusions of study results. 
Studies in ramshorn snails, for example, resulted in superfeminization 
(e.g., the formation of additional female organs, enlarged accessory 
sex glands, gross malformations of the pallial oviduct, and a 
stimulation of egg and clutch production) at very low concentrations in 
one lab (Ref. 18), but those results were not found in studies by other 
researchers (Refs. 19-21).
    In addition, in some studies, BPA demonstrated effects at very low 
concentrations, but no effects were observed at the higher test 
concentrations. For example, tadpoles exposed to 2.3, 23, and 230 
[micro]g/L of BPA (Ref. 22) before metamorphosis had an increased 
female to male ratio at 23 [micro]g/L only. These types of anomalous 
responses have been reported across multiple species of fish and 
invertebrates for BPA and are characteristic of endocrine-active

[[Page 44541]]

chemicals. They suggest inhibition of reproduction and development at 
low concentrations and overcompensation by the organism at higher 
concentrations in response to a toxicant (Ref. 23).
    It is difficult to interpret this information in a regulatory 
context, because the scientific methods employed in individual academic 
settings to test a hypothesis are not necessarily geared toward meeting 
or establishing generally applicable guidelines for evaluating 
ecotoxicity and setting corresponding regulatory limits or controls. In 
terms of environmental toxicity, EPA considers the currently available 
research as evidence that BPA has the potential to interact with the 
estrogen hormone system. There is some evidence that BPA is also active 
via the thyroid hormone pathway in amphibians and fish (Refs. 24 and 
25). More recent evidence indicates that BPA also acts as an androgen 
receptor antagonist in both mammals and fish (Ref. 26). There are 
currently efforts underway by EPA's Office of Science Coordination and 
Policy (OSCP) through the Endocrine Disruptor Screening Program (EDSP) 
and the Organization for Economic Cooperation and Development (OECD) 
Endocrine Disrupter Testing and Assessment Work Group (EDTAWG), among 
others, to determine the best approach to evaluate and assess such 
effects (Refs. 27-29).
    EPA is inviting comment on the need to further determine the hazard 
of BPA to various ecological species. The purpose of further testing 
would be to produce high quality data that could be used for risk 
assessment purposes for any adverse reproductive or developmental 
effects in different species that might result from the interactions 
identified through the available research.
    3. What are the issues for comment concerning toxicity testing? EPA 
invites comment on whether and what testing should be required to 
further describe the hazard of BPA to various ecological species to 
resolve the low dose effects issue. EPA particularly invites comment on 
the following, for which little or no clarifying hazard information 
appears to be currently available or for which much of the available 
data have been derived from studies of questionable quality or 
uncertain interpretation:
    a. Effects of BPA on fish in long-term tests, including those that 
encompass multiple generations.
    b. Effects of BPA on amphibians at sensitive life stages, 
specifically metamorphosis (thyroid effects) and sexual development/
differentiation (hypothalamic-pituitary-gonadal axis effects).
    c. Effects of BPA on birds over multiple generations.
    d. Effects of BPA on aquatic invertebrate species.
    EPA further invites comment on the availability of current test 
guidelines that could help address these issues. This may include, for 
example, considering the draft recommendations concerning aquatic life 
criteria for contaminants of emerging concern (Ref. 30). Additionally, 
EPA is inviting the public to describe and define where they believe 
there are data gaps concerning the environmental toxicity of BPA, 
especially at low concentrations, or whether and on what basis they 
believe the current data are sufficient to determine whether BPA does 
or does not present an unreasonable risk of injury to the environment.
    4. What levels of BPA are present in the U.S. environment? BPA is 
present in the environment as a result of direct releases from 
manufacturing or processing facilities (Ref. 31). BPA also may be 
present in the environment as a result of fugitive emissions during 
processing and handling, release of unreacted monomer from products 
(Ref. 9), or possibly from degradation of products under certain 
conditions. In addition, although no environmental studies on thermal 
paper have been done in the United States, based on information from 
EPA's review of European and Japanese studies, the use of unconjugated 
BPA in thermal paper also may contribute to environmental releases of 
BPA from paper manufacturing and recycling plants and to the presence 
of BPA in the stream of recycled paper used in toilet paper, paper 
tableware, and other products, and may contribute to the presence of 
BPA in landfills because paper products are a major contributor to the 
U.S. solid waste stream (Refs. 7, 32-36).\3\
---------------------------------------------------------------------------

    \3\ Recent studies also indicate thermal paper may contribute 
directly to human exposure to BPA through dermal contact. In one 
U.S. study, for example, pregnant women who worked as cashiers, who 
presumably had frequent contact with thermal paper used in cash 
register receipts, had the highest urinary BPA concentrations 
compared with pregnant women in other occupations (Ref. 37).
---------------------------------------------------------------------------

    Significant research has been done to document widespread human 
population exposures to BPA in the United States using biomonitoring 
(Refs. 37-41). Although these studies and reports indicate that most 
people in the United States have measurable levels of BPA in their 
bodies, these data do not identify the relative source contributions to 
BPA exposure. Researchers generally accept that food contact uses of 
materials containing BPA, such as polycarbonate bottles or epoxy 
linings in food and beverage cans, are a likely major source of human 
exposure, but the relative contributions of food contact uses, 
potential TSCA uses, or other environmental sources cannot be 
extrapolated reliably from these existing data. For information about 
the multi-agency effort to evaluate the potential human health 
consequences of BPA exposures, see the discussion in Unit II.B.
    According to the Toxics Release Inventory (TRI) Database, total 
release of BPA in the United States in 2007 was 1,132,062 pounds (lbs), 
with releases of 122,965 lbs to air, 6,246 lbs to water, 14,972 lbs 
released on-site to land, and 684,638 lbs transferred off-site to land. 
An additional 32,928 lbs were reported as off-site water transfer to 
Publicly Owned Treatment Works (POTWs), with another 2,759,705 lbs 
transferred to incineration (Ref. 31).
    Some information is available for BPA concentrations in U.S. water 
and other environmental media (see Table 3 in Unit II.B.4., providing 
values from the U.S. studies cited in this discussion). Most 
environmental monitoring results show that the concentrations of BPA in 
surface water bodies are lower than 1 [mu]g/L (ppb), mainly due to its 
partitioning and biodegradability properties (Ref. 42). BPA was 
detected at a median concentration of 0.14 [mu]g/L (ppb) and a maximum 
concentration of 12 [mu]g/L (ppb) in 41.2% of 85 samples collected from 
U.S. streams in 1999 and 2000 (Ref. 43). The maximum concentration of 
12 [mu]g/L (ppb) was much higher than any of the other samples reported 
in the study; the next highest concentration reported was 5.2 [mu]g/L 
(ppb), and as indicated by the median concentration of 0.14 [mu]g/L 
(ppb), BPA concentration in other U.S. waters was much lower. A recent 
review of reports of BPA in surface water found that BPA was reported 
in 26 studies in North America (2 in Canada and 24 in the United 
States) with detection in 80% (852 of 1,068) of surface water samples. 
The median concentration reported was 0.081 [micro]g/L (ppb) and the 
95th percentile concentration was 0.47 [micro]g/L (ppb) (Ref. 44).
    Two studies have addressed individual WWTPs in two different parts 
of the United States. In 2001 and 2002, BPA was not detected above the 
detection limit of 0.0001 [mu]g/L (ppb) in Louisiana in effluent from a 
WWTP, in samples collected from surface waters in Louisiana, or in 
drinking water at various stages of treatment at plants in Louisiana 
(Ref. 45). A 2008 study

[[Page 44542]]

sampled BPA in treated wastewater from the East Bay Municipal Utilities 
WWTP in Oakland, California, and in a variety of locations that 
discharge to this WWTP (Ref. 46). This study reported detecting (limit 
of detection = 0.25 [micro]g/L (ppb)) BPA in two of three treated 
wastewater samples at 0.38 and 0.31 [micro]g/L (ppb). It also reported 
detecting BPA in wastewater generated by a pharmaceutical manufacturer 
(0.295 [micro]g/L (ppb)), an industrial laundry (21.5 [micro]g/L 
(ppb)), and a paper products manufacturer (0.753 [micro]g/L (ppb)).
    While U.S. studies on wastewater are limited to only two State 
locations, a Canadian study published in 2000 reported BPA 
concentrations ranging from 49.9 to 0.031 [micro]g/L (ppb) in sewage 
influent and effluent (generally L (ppb) in the influent 
and L (ppb) in the effluent) and from 36.7 to 0.104 
[micro]g/g (ppm) in raw and digested sewage sludge from multiple WWTPs 
in Canada (Ref. 47). The same authors reported that BPA contamination 
was detected in 100% of sewage samples from 31 WWTPs across Canada with 
concentrations ranging from 0.080 to 4.98 [micro]g/L (ppb) (median 
0.329 [micro]g/L (ppb)) for the influent and from 0.010 to 1.08 
[micro]g/L (ppb)(median 0.136 [micro]g/L (ppb)) for the effluent (Ref. 
48). Based on comparison of influent and effluent levels, they 
estimated that BPA in the influent was removed by the sewage treatment 
process with a median reduction rate of 68%. BPA was detected in sludge 
samples at concentrations ranging from 0.033 to 36.7 [micro]g/g (ppm), 
on a dry weight basis. The authors also reported a wide range of BPA in 
wastewater discharges from industrial facilities in the Toronto, 
Canada, area, with concentrations ranging from 0.23 to 149.2 [micro]g/L 
(ppb). Higher BPA levels in wastewater were associated with facilities 
producing chemicals and chemical products and packaging and paper 
products, and with commercial dry cleaning establishments. BPA 
concentrations in pulp and paper mill sludge ranged from g (ppm), with a median value of 0.076 
[micro]g/g (ppm), on a dry weight basis (Ref. 48). EPA notes that U.S. 
wastewater treatment conditions and industrial and commercial 
discharges may differ from what was found in Canada, but considers this 
Canadian study to be informative.
    Municipal wastewater treatment produces solid byproducts, commonly 
referred to as sewage sludge. After additional treatment to meet 
regulatory standards for pathogen, nutrient, and metal content, this 
treated sewage sludge, now classified as biosolids, may be disposed of 
by land application; biosolids may also be incinerated or disposed of 
in landfills. A U.S. study published in 2006 measured BPA in 9 treated 
biosolids products from WWTPs in 7 States and found that all contained 
between 1,090 and 14,400 [mu]g/kg (ppb) (median 4,690 [mu]g/kg (ppb)) 
(Ref. 49). A 2008 study reported BPA in treated biosolids from a 
municipal U.S. WWTP at 4,600 [mu]g/kg (ppb) and reported 81 [mu]g/kg 
(ppb) in soil that received the land-applied biosolids (Ref. 50). That 
study detected BPA at 81 [mu]g/kg (ppb) in earthworms living in treated 
soil. The authors also reported detecting 147 [mu]g/kg (ppb) in a 
nearby ``control'' soil that did not receive treatment with biosolids. 
That anomalous result was not explained.
    In 2000, the U.S. Geological Survey (USGS) collected samples from 
47 ambient ground water sites (not drinking water wells) in 18 States 
and analyzed them for 65 organic wastewater contaminants. BPA was 
detected in 29.8% of the sampled ground water sites, with a mean 
detected concentration of 1.78 [mu]g/L (ppb) and a range of 1.06 to 
2.55 [mu]g/L (ppb). BPA was among the top 5 most frequently detected 
organic compounds in this study (Refs. 51 and 52).
    In the summer of 2001, the USGS collected samples from 74 sources 
of raw, untreated, drinking water in 25 States and Puerto Rico, in 
areas that were known or suspected to have at least some human and/or 
animal wastewater sources in upstream or upgradient areas. These 
sources comprise 25 ground water and 49 surface water sources of 
drinking water serving populations ranging from one family to more than 
8 million people. BPA was detected in 9.5% of these samples at a 
reporting level of 1 [mu]g/L (ppb). The maximum concentration measured 
in these samples was 1.9 [mu]g/L (ppb) (Refs. 51 and 53).
    Landfill leachate from one U.S. study reported maximum BPA 
concentrations of 1.7 [mu]g/L (ppb) in landfill leachate and 1.4 [mu]g/
L (ppb) in the receiving ground water plume at a landfill on Cape Cod, 
Massachusetts, that was known to be leaking (Ref. 54). Data for other 
landfill sites in the United States were not available, and this single 
point is not representative of the country. Landfill leachate from 
other countries contained more than 500 [mu]g/L (ppb) of BPA (Ref. 42). 
Studies conducted at Japanese landfills resulted in maximum untreated 
leachate concentrations of 17,200 [mu]g/L (ppb) and treated leachate 
concentrations of 5.1 [mu]g/L (ppb) (Ref. 11).
    Wilson et al. (Ref. 55) reported that BPA concentrations in soil 
samples taken from outdoor play areas of homes and daycare centers 
ranged from 4-14 ppb dry weight, with means of 6-7 ppb dry weight. 
Klecka et al. (Ref. 44) reported a median concentration of 0.6 ppb BPA 
in North American freshwater sediments, including non-detected samples; 
BPA concentrations in samples from the United States ranged from 1.4 to 
140 ppb dry weight. Levels in U.S. marine sediments were reported to 
have a median of 3.5 ppb of BPA and to range from 1.5 to 5 ppb dry 
weight (Ref. 56).

                       Table 3--U.S. Reported Environmental Concentrations of Bisphenol A
----------------------------------------------------------------------------------------------------------------
                                     Mean or range of means
              Location                 (parts per  billion         Range (ppb)                References
                                             (ppb))
----------------------------------------------------------------------------------------------------------------
Surface Water......................  L, Table 1 of Unit II.B.1.) with measured concentrations in some 
U.S. waters and sediments, which included values as high as 12 [mu]g/L 
(ppb) (surface water), 2.55 [mu]g/L (ppb) (ground water), and 140 ppb 
sediment (freshwater sediment) (Table 2 of Unit II.B.2.), indicate 
possible risk of injury to aquatic organisms. The single available 
measurement of BPA in leachate from one U.S. landfill site is not 
sufficient to represent or characterize the United States as a whole, 
and landfill leachate data from other countries suggest that BPA 
concentrations in leachate may be significantly higher than 
concentrations in surface water bodies. The direct exposure pathway 
from wastewater to environmental organisms, along with the widespread 
detection of BPA in WWTP sludges, further suggest that land application 
of WWTP sludges may be a significant environmental exposure pathway 
that needs to be better understood.\4\
---------------------------------------------------------------------------

    \4\ EPA's response to the request for correction of the 
information provided in the Action Plan that was filed under the 
``Agency's Information Quality Guidelines'' by the American 
Chemistry Council is available at http://www.epa.gov/quality/informationguidelines/iqg-list.html.
---------------------------------------------------------------------------

    Although most currently available environmental monitoring results 
show that the concentrations of BPA in U.S. water bodies are lower than 
1 [mu]g/L (ppb) (median concentration of 0.14 [mu]g/L (ppb)), these 
environmental measurements represent isolated snapshots in time. 
Because these results come from a variety of studies designed for very 
different purposes and conditions (for example, laboratory analytical 
development contrasted with field monitoring), the data are not readily 
comparable and cannot be assembled into a nationally or regionally 
representative picture. Particularly in light of the corresponding 
uncertainties described in Unit II.B.1. and 2., concerning potential 
BPA hazards at low doses, the existing data do not allow EPA to 
determine how many areas may exceed potential concentrations of 
concern, how often or how long such concentrations may be exceeded, or 
the sources or pathways leading to BPA presence in the environment from 
manufacturing, processing, distribution in commerce, use, or disposal 
that may result in human and environmental exposures. EPA considers 
that these existing data would not be sufficient to determine whether 
or not an unreasonable risk to the environment exists. To help resolve 
these uncertainties, EPA is considering requiring that manufacturers 
and processors of BPA conduct environmental testing consisting of 
targeted sampling and monitoring of surface water, ground water, 
sediment, soil, landfill leachate, and drinking water on and adjacent 
to their properties, specifically in the vicinity of manufacturing 
facilities and such processing facilities as foundries, WWTPs, paper 
and plastics recycling facilities, and other sources of BPA releases as 
identified through TRI reporting and other information. These test data 
could also help guide development of effective risk management actions 
if it should be determined that activities involving BPA present an 
unreasonable risk of injury to aquatic or other environmental systems.
    Fully understanding exposure pathways and in particular the 
magnitude, frequency, and duration of exposure could require a 
nationwide survey of the occurrence of the chemical in environmental 
media associated with production, processing, use, disposal, and 
recycling facilities. However, at this time, EPA is proposing that 
selected monitoring of a more limited scope be conducted to help 
identify the most likely locations of high exposure and the sources and 
pathways of exposure, to determine whether BPA may be present in those 
locations at concentrations that pose a risk of concern to aquatic or 
other systems. Monitoring of aquatic sites and sediments near releases 
(effluents and sludge) from manufacturing and processing sites 
(including on-site WWTPs) reporting high releases under TRI or 
associated with high releases identified from other information, as 
well as monitoring of sites that receive runoff from landfills, would 
be included.
    EPA believes these targeted monitoring data may provide information 
relevant both to the characterization of environmental risk and to the 
potential focus of future risk management activities such as those 
under TSCA section 6, if the data indicate such activities are 
warranted. EPA also considers these data would further inform the issue 
of potential human exposure levels attributable to sources other than 
the direct food

[[Page 44544]]

contact uses believed to be the principal source of human exposure, 
which are regulated by the FDA. As noted earlier in Unit II.B., EPA is 
working with FDA, NIEHS, and CDC on additional research to better 
determine and evaluate the potential human health consequences of 
exposures to BPA, including exposures at low doses. Levels of exposure 
that may be identified by FDA as being of concern to human health, 
including children's health, would affect the extent to which EPA would 
take additional action to address potential risks to human health 
resulting from uses within TSCA jurisdiction, but EPA is not 
considering any additional testing specifically in regard to human 
health issues at this time.\5\
---------------------------------------------------------------------------

    \5\ EPA notes, however, that information obtained on the 
environmental presence of BPA would be relevant to understanding the 
environmental component of human exposures.
---------------------------------------------------------------------------

    In order to be useful to an investigation of potential 
environmental risks posed by BPA, environmental testing must be 
representative and of known quality. To accomplish this, data should be 
collected using approved or recognized sampling, preparation, and 
analytical techniques. Appropriate quality assurance and quality 
controls also should be incorporated in the protocols for collection 
and analyses.
    A further complicating factor in the assessment of potential 
environmental risks posed by BPA is that organisms in the environment, 
rather than being exposed to a single chemical at a time, are likely to 
be exposed simultaneously to multiple chemicals. The presence of other 
endocrine-active chemicals, including other estrogenic chemicals, for 
example, could affect the potential for effects on environmental 
organisms. It may be useful, when monitoring for BPA, to identify the 
total estrogenicity of a sample along with the amount of BPA present.
    Potential methodologies and protocols for use in monitoring 
programs may include ASTM D7574-09 Standard Test Method for 
Determination of Bisphenol A in Environmental Waters by Liquid 
Chromatography/Tandem Mass Spectrometry (Ref. 62); ASTM D5730-04 
Standard Guide for Site Characterization for Environmental Purposes 
With Emphasis on Soil, Rock, the Vadose Zone and Ground Water (Ref. 
63); EPA Method 8270D (SW-846), Semivolatile Organic Compounds by Gas 
Chromatography/Mass Spectrometry (GC/MS), Revision 4 (Ref. 64); and 
other methods cited and described in such publications as Barnes et al. 
(2008) (Ref. 51) and Focazio et al. (2008) (Ref. 53).
    5. What are the issues for comment concerning environmental testing 
consisting of sampling and monitoring? EPA particularly invites comment 
on:
    a. The extent and type of environmental testing that may be 
sufficient to characterize the environmental presence of BPA.
    b. The extent and type of environmental testing that may be 
sufficient to understand sources of and exposure from the high 
concentrations of BPA found in treated biosolids from WWTPs.
    c. Whether environmental testing should be conducted now, or should 
be tiered to occur after the uncertainties associated with the hazards 
of BPA at low concentrations in the environment have been resolved.
    d. The locations where such environmental testing should be 
undertaken, such as manufacturing, processing, recycling, foundry, and 
other use, treatment, and disposal sites identified with BPA releases 
reported under TRI or other information.
    e. The media (e.g., soil, sediment, sludge, WWTP influent and 
effluent, landfill leachate, drinking water, surface water, ground 
water) to be sampled at each such site.
    f. Which parties should be required to conduct the testing and/or 
be potentially responsible for providing reimbursement to those who 
conduct specific tests.
    g. The appropriate methods and protocols to use in such a 
environmental testing program.
    h. Whether such an environmental testing program should include 
measurements for the total estrogenicity of samples collected as well 
as for the concentration of BPA, and what methods and protocols may be 
suitable for generating and interpreting such data.
    i. Whether and what additional environmental testing activities may 
be necessary to understand and characterize non-food-contact uses, 
sources, and environmental pathways that may contribute to exposure to 
BPA. Though, as indicated in Unit II.B., the current focus of this 
ANPRM is on environmental effects, this information would inform the 
multi-agency effort to evaluate the potential human health consequences 
of BPA exposures.
    j. Other information that may provide insight into sources and 
pathways of environmental and human exposure to BPA released into the 
environment. Though, as indicated in Unit II.B., the current focus of 
this ANPRM is on environmental effects, this information would inform 
the multi-agency effort to evaluate the potential human health 
consequences of BPA exposures.
    k. The cost and economic feasibility of such environmental testing, 
for the different types of sites.

C. What is the agency's authority for taking this action?

    EPA is issuing this ANPRM on certain toxicity testing and on 
certain environmental testing consisting of sampling and monitoring for 
the chemical substance BPA under TSCA section 4(a) (15 U.S.C. 2603(a)).
    Section 2(b)(1) of TSCA (15 U.S.C. 2601(b)) states that it is the 
policy of the United States that ``adequate data should be developed 
with respect to the effect of chemical substances and mixtures on 
health and the environment and that the development of such data should 
be the responsibility of those who manufacture [which is defined by 
statue to include import] and those who process such chemical 
substances and mixtures[.]'' To implement this policy, TSCA section 
4(a)(1) provides that EPA shall require by rule that manufacturers or 
processors or both of chemical substances and mixtures conduct testing, 
if the Administrator finds in a final rule that:

    (A)(i) the manufacture, distribution in commerce, processing, 
use, or disposal of a chemical substance or mixture, or that any 
combination of such activities, may present an unreasonable risk of 
injury to health or the environment,
    (ii) there are insufficient data and experience upon which the 
effects of such manufacture, distribution in commerce, processing, 
use, or disposal of such substance or mixture or any combination of 
such activities on health or the environment can reasonably be 
determined or predicted, and
    (iii) testing of such substances or mixture with respect to such 
effects is necessary to develop such data; or
    (B)(i) a chemical substance or mixture is or will be produced in 
substantial quantities, and (I) it enters or may reasonably be 
anticipated to enter the environment in substantial quantities or 
(II) there is or may be significant or substantial human exposure to 
such substance or mixture,
    (ii) there are insufficient data and experience upon which the 
effects of the manufacture, distribution in commerce, processing, 
use, or disposal of such substance or mixture or of any combination 
of such activities on health or the environment can reasonably be 
determined or predicted, and
    (iii) testing of such substance or mixture with respect to such 
effects is necessary to develop such data and
    (C) in the case of a mixture, the effects which the mixture's 
manufacture, distribution in commerce, processing, use or disposal 
or any combination of such activities may have on health or the 
environment may not be reasonably and more efficiently determined or 
predicted by

[[Page 44545]]

testing the chemical substances which comprise the mixture[.]

(15 U.S.C. 2603(a))

    If EPA in a final rule makes an appropriate finding under TSCA 
section 4(a)(1)(A) or (B) for a chemical substance or mixture, the 
Administrator shall require that testing be conducted on that chemical 
substance or mixture. The purpose of the testing would be to develop 
data with respect to the health and environmental effects for which 
there is an insufficiency of data and experience, and which are 
relevant to a determination that the manufacture, distribution in 
commerce, processing, use, or disposal of the substance or mixture, or 
any combination of such activities, does or does not present an 
unreasonable risk of injury to health or the environment. As indicated 
in Unit II.A.3., EPA requests comment and supporting information 
regarding which TSCA section 4(a)(1) finding authority would be most 
appropriate for the purpose of a BPA test rule proposal. Any proposal 
would ultimately be based on EPA's assessment of the relevant 
information available at the time of proposal.
    Once the Administrator has made the relevant findings under TSCA 
section 4(a), EPA may require any health or environmental effects 
testing for which data are insufficient and which are necessary to 
develop the data. EPA need not limit the scope of testing required to 
the factual basis for the TSCA section 4(a)(1)(A)(i) or (B)(i) findings 
as long as EPA also finds that there are insufficient data and 
experience upon which the effects of the manufacture, distribution in 
commerce, processing, use, or disposal of such substance or mixture or 
of any combination of such activities on health or the environment can 
reasonably be determined or predicted, and that testing is necessary to 
develop such data. This approach is explained in more detail in EPA's 
TSCA section 4(a)(1)(B) Final Statement of Policy (B Policy) published 
in the Federal Register issue of May 14, 1993 (58 FR 28736, 28738-
28739).
    Authority for requiring sampling and monitoring for a chemical 
substance or mixture can be found within TSCA section 4. Section 4(a) 
of TSCA authorizes EPA to require the development of data ``which are 
relevant to a determination that the manufacture, distribution in 
commerce, processing, use, or disposal of such substance or mixture, or 
that any combination of such activities, does or does not present an 
unreasonable risk of injury to health and the environment.'' The extent 
to which such activities may affect health or the environment is 
dependent in part upon the human and environmental exposures to the 
chemical substance occasioned by those activities. As an example, TSCA 
section 4(a)(2)(A) specifically addresses testing for persistence of a 
substance. Testing to identify where and in what concentrations a 
chemical substance or mixture may become present in the environment 
contributes to an understanding of human and environmental exposures 
resulting from those activities. As stated in Unit II.B., EPA does not 
intend to initiate regulatory action under TSCA at this time on the 
basis of human health.

III. References

1. EPA. 2010. Bisphenol A Action Plan. Available on-line at http://www.regulations.gov/#!documentDetail;D=EPA-HQ-OPPT-2010-0348-0002.
2. EPA. 1993. Bisphenol A (CASRN 80-05-7) Reference Dose for Chronic 
Oral Exposure (RfD). July 1, 1993. Integrated Risk Information 
System (IRIS). Available on-line at http://www.epa.gov/ncea/iris/subst/0356.htm.
3. FDA. 2008. Draft Assessment of Bisphenol A for Use in Food 
Contact Applications. Available on-line at http://www.fda.gov/ohrms/dockets/AC/08/briefing/2008-0038b1_01_02_FDA%20BPA%20Draft%20Assessment.pdf. Peer review report and 
additional information available on-line at http://www.fda.gov/Food/FoodIngredientsPackaging/ucm166145.htm.
4. European Food and Safety Authority (EFSA). 2006. Opinion of the 
Scientific Panel on Food Additives, Flavourings, Processing Aids and 
Materials in Contact with Food on a Request from the Commission 
Related to 2,2-BIS(4-HYDROXYPHENYL) PROPANE. Question number EFSA-Q-
2005-100. The EFSA Journal. Vol. 428:1-75.
5. EFSA. 2008. Scientific Opinion of the Panel on Food additives, 
Flavourings, Processing aids and Materials in Contact with Food 
(AFC) on a request from the Commission on the toxicokinetics of 
Bisphenol A. The EFSA Journal. Vol. 759:1-10.
6. Canada. 2008. Environment Canada, Health Canada. Screening 
Assessment for the Challenge Phenol, 4,4' (1-methylethylidene)bis- 
(Bisphenol A) Chemical Abstracts Service Registry Number 80-05-7. 
October 2008. Available on-line at http://www.ec.gc.ca/substances/ese/eng/challenge/batch2/batch2_80-05-7_en.pdf.
7. EU. 2010. European Union Risk Assessment Report. CAS: 80-05-7. 
EINECS No.: 201-245-8. Environment Addendum of April 2008 and Human 
Health Addendum of April 2008 (to be read in conjunction with 
published EU RAR of BPA, 2003). 4,4'-ISOPROPYLIDENEDIPHENOL 
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8. Japan's National Institute of Advanced Industrial Science and 
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to Human Reproduction (NTP/CERHR), HHS. 2008. NTP-CERHR Monograph on 
the Potential Human Reproductive and Developmental Effects of 
Bisphenol A. Available on-line at http://cerhr.niehs.nih.gov/evals/bisphenol/bisphenol.pdf.
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11. Crain, D.A.; Eriksen, M.; Iguchi, T.; Jobling, S.; Laufer, H.; 
LeBlanc, G.A.; and Guillette, Jr., L.J. 2007. An ecological 
assessment of Bisphenol A: evidence from comparative biology. 
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12. Lahnsteiner, F.; Berger, B.; Kletzl, M.; and Weismann, T. 2005. 
Effect of Bisphenol A on Maturation and Quality of Semen and Eggs in 
the Brown Trout, Salmo trutta f. fario. Aquatic Toxicology. Vol. 
75:213-224.
13. EPA. 2010. List of References to BPA-Related Environmental 
Studies Published from 2007 through 2010.
14. EPA. 2010. List of References Published from 2007 through 2010 
of Some Relevance to the Environmental Toxicity of BPA, and Older 
Studies of Sub-Lethal Effects Also Cited in Table 2.
15. Marcial, H.S.; Hagiwara, A.; and Snell, T.W. 2003. Estrogenic 
compounds affect development of harpacticoid copepod Tigriopus 
Japonicus. Environmental Toxicology and Chemistry. Vol. 22:3025-
3030.
16. Watts, M.M.; Pascoe, D.; and Carroll, K. 2001. Chronic exposure 
to 17[alpha]-ethinylestradiol and bisphenol A-effects on development 
and reproduction in the freshwater invertebrate Chironomus riparius 
(Diptera: Chironomidae). Aquatic Toxicology. Vol. 55:113-124.
17. Sumpter, J.P.; Tyler, C.R.; Sherazi, A. 2001. Bisphenol-A: 
Multigeneration study with the fathead minnow (Pimephales promelas). 
Brunel University (unpublished; part of study published as Sohoni et 
al., 2001).
18. Oehlmann, J.; Schulte-Oehlmann, U.; Werner, K.; Jagnytsch, O.; 
Lutz, I.; Kresten, K.; Wollenberger, L.; Santos, E.M.; Paull, G.C.; 
Van Look, K.J.W.; and Tyler, C.R. 2008. A Critical Analysis of the 
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19. Forbes, V.E.; Selck, H.; Palmqvist, A.; Aufderheide, J.; 
Warbritton, R.; Pounds, N.; Thompson, R.; van der Hoeven, N.; and 
Caspers, N. 2007. Does bisphenol A induce superfeminization in 
Marisa

[[Page 44546]]

cornuarietis? Part I: Intra- and inter-laboratory variability in 
test endpoints. Ecotoxicology and Environmental Safety. Vol. 66:309-
318.
20. Forbes, V.E.; Aufderheide, J.; Warbritton, R.; Thompson, R.; van 
der Hoeven, N.; and Caspers, N. 2007. Does bisphenol A induce 
superfeminization in Marisa cornuarietis? Part II: Toxicity test 
results and requirements for statistical power analyses. 
Ecotoxicology and Environmental Safety. Vol. 66:319-325.
21. Forbes, V.E; Aufderheide, J.; Warbritton, R.; Thompson, R.; van 
der Hoeven, N.; and Caspers, N. 2008. Effects of bisphenol A on 
fecundity, egg hatchability, and juvenile growth of Maris 
Cornuarietis. Environmental Toxicology and Chemistry. Vol. 27:2332-
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22. Levy, G.; Lutz, I.; Kr[uuml]ger, A.; and Kloas, W. 2004. 
Bisphenol A induces feminization in Xenopus laevis tadpoles. 
Environmental Research. Vol. 94:102-111.
23. Calabrese, E.J. and Baldwin, L.A. 2003. Hormesis at the National 
Toxicology Program (NTP): evidence of hormetic dose responses in NTP 
dose-range studies. Nonlinearity in Biology, Toxicology, and 
Medicine. Vol. 1:455-467.
24. Heimeier, R.A.; Das, B.; Buchholz, D.R.; and Shi, Y. 2009. The 
Xenoestrogen Bisphenol A inhibits postembryonic vertebrate 
development by antagonizing gene regulation by thyroid hormone. 
Endocrinology. Vol. 150:2964-2973.
25. Ramakrishnan, S. and Wayne, N.L. 2008. Impact of bisphenol-A on 
early embryonic development and reproductive maturation. 
Reproductive Toxicology. Vol. 25:177-183.
26. Ankley, G.T.; Jensen, K.M.; Kahl, M.D.; Durhan, E.J.; Makynen, 
E.A.; Cavallin, J.E.; Martinovic, D.; Wehmas, L.C.; Mueller, N.D.; 
and Villeneuve, D.L. 2010. Use of chemical mixtures to differentiate 
mechanisms of endocrine action in a small fish model. Aquatic 
Toxicology. Vol. 99:389-396.
27. EPA. Endocrine Disruptor Screening Program; Policies and 
Procedures for Initial Screening; Notice. Federal Register (74 FR 
17560, April 15, 2009) (FRL-8399-9).
28. EPA. Endocrine Disruptor Screening Program Web site. Available 
on-line at http://www.epa.gov/scipoly/oscpendo.
29. Organization for Economic Co-operation and Development 
Environment Directorate. Endocrine Disruptor Testing and Assessment. 
Available on-line at http://www.oecd.org/document/62/0,3343,en_2649_34377_2348606_1_1_1_1,00.html.
30. EPA. 2008. White Paper. Aquatic Life Criteria for Contaminants 
of Emerging Concern. Draft Document. EPA, Office of Water. 
Washington, DC.
31. EPA. 2009a. Toxics Release Inventory. 2007 Public Data Release, 
Released March 14, 2009. Available on-line at http://www.epa.gov/tri/tridata/index.html.
32. Vinggaard, A.M.: K[ouml]rner, W.; Lund, K.H.; Bolz, U.; and 
Petersen, J.H. 2000. Identification and quantification of estrogenic 
compounds in recycled and virgin paper for household use as 
determined by an in vitro yeast estrogen screen and chemical 
analysis. Chemical Research in Toxicology. Vol. 13:1214-1222.
33. Gehring, M.; Tennhardt, L.; Vogel, D.; Weltin, D.; and 
Bilitewski, B. 2004. Bisphenol A contamination of wastepaper, 
cellulose and recycled paper products. In: Brebbia, C.A.; Kungulos, 
S.; Popov, V.; and Itoh, H. (eds.): Waste Management and the 
Environment II. WIT Transactions on Ecology and the Environment. 
Vol. 78:294-300. Southampton, Boston: WIT Press. Available on-line 
at http://rcswww.urz.tu-dresden.de/~gehring/deutsch/dt/vortr/
040929ge.pdf.
34. Ozaki, A.; Yamaguchi, Y.; Fujita, T.; Kuroda, K.; and Endo, G. 
2004. Chemical analysis and genotoxicological safety assessment of 
paper and paperboard used for food packaging. Food and Chemical 
Toxicology. Vol. 42:1323-1337.
35. Fukazawa, H.; Hoshino, K.; Shiozawa, T.; Matsushita, H.; and 
Terao, Y. 2001. Identification and quantification of chlorinated 
bisphenol A in wastewater from wastepaper recycling plants. 
Chemosphere. Vol. 44:973-979.
36. Terasaki, M.; Shiraishi, F.; Fukazawa, H.; and Makino, M. 2007. 
Occurrence and estrogenicity of phenolics in paper-recycling process 
water: pollutants originating from thermal paper in waste paper. 
Environmental Toxicology and Chemistry. Vol. 26:2356-2366.
37. Braun, J.M.; Kalkbrenner, A.E.; Calafat, A.M.; Bernert, J.T.; 
and Ye, X., et al. 2011 Variability and Predictors of Urinary 
Bisphenol A Concentrations during Pregnancy. Environmental Health 
Perspectives. Vol. 119:131-137.
38. Calafat, A.M.; Kuklenyik, Z.; and Reidy, J.A., et al 2005. 
Urinary concentrations of bisphenol A and 4-nonylphenol in a human 
reference population. Environmental Health Perspectives. Vol. 
113:391-395.
39. Calafat, A.M.; Ye, S; and Wong, L.Y., et al 2008. Exposure of 
the US population to bisphenol A and 4-tertiarty-octylphenol: 2003-
2004. Environmental Health Perspectives. Vol. 116:39-44.
40. Calafat, A.M.; Weuve, J.; Ye, X., et al 2009. Exposure to 
bisphenol A and other phenols in neonatal intensive care unit 
premature infants. Environmental Health Perspectives. Vol. 117:639-
644.
41. CDC, HHS. Fourth National Report on Human Exposure to 
Environmental Chemicals, Update Tables. July 2010. Available on-line 
at http://www.cdc.gov/exposurereport/pdf/Update_Tables.pdf.
42. Tsai, W. 2006. Human Health Risk on Environmental Exposure to 
Bisphenol-A: A Review. Journal of Environmental Science and Health. 
Part C, Vol. 24:225-255.
43. Kolpin, D.W.; Furlong, E.T.; Meyer, M.T.; Thurman, E.M.; Zaugg, 
S.D.; Barber, L.B.; and Buxton, H.T. 2002. Pharmaceuticals, 
hormones, and other organic wastewater contaminants in U.S. streams, 
1999-2000: a national survey. Environmental Science & Technology. 
Vol. 36:1202-1211.
44. Klecka, G.M.; Staples, C.A.; Clark, K.E.; van der Hoeven, N.; 
Thomas, D.E.; and Hentges, S.G. 2009. Exposure Analysis of Bisphenol 
A in Surface Water Systems in North America and Europe. 
Environmental Science & Technology. Vol. 43:6145-6150.
45. Boyd, G.R.; Reemtsma, H.; Grimm, D.A.; and Mitra, S. (2003). 
Pharmaceuticals and personal care products (PPCPs) in surface and 
treated waters of Louisiana, U.S.A. and Ontario, Canada. The Science 
of the Total Environment. Vol. 311:135-149.
46. Jackson, J. and Sutton, R. 2008. Sources of endocrine-disrupting 
chemicals in an urban wastewater, Oakland, CA. The Science of the 
Total Environment. Vol. 405:153-160.
47. Lee, H-B. and Peart, T.E. 2000a. Determination of bisphenol A in 
sewage effluent and sludge by solid-phase and supercritical fluid 
extraction and gas chromatography/mass spectrometry. Journal of the 
Association of Analytical Communities (AOAC) International. Vol. 
83:290-297.
48. Lee, H-B. and Peart, T.E. 2000b. Bisphenol A contamination in 
Canadian municipal and industrial wastewater and sludge samples. 
Water Quality Research Journal of Canada. Vol. 35:283-298.
49. Kinney, C.A.; Furlong, E.T.; Zaugg, S.D.; Burkhardt, M.R.; 
Werner, S.L.; Cahill, J.D.; and Jorgensen, G.R. 2006. Survey of 
Organic Wastewater Contaminants in Biosolids Destined for Land 
Application. Environmental Science & Technology. Vol.--40:7207-7215.
50. Kinney, C.A; Furlong, E.T.; Kolpin, D.W.; Burkhardt, M.R.; 
Zaugg, S.D.; Werner, S.L.; Bossio, J.P.; and Benotti, M.J. 2008. 
Bioaccumulation of pharmaceuticals and other anthropogenic waste 
indicators in earthworms from agricultural soil amended with 
biosolid or swine manure. Environmental Science & Technology. Vol. 
42:1863-1870.
51. Barnes, K.K.; Kolpin, D.W.; Focazio, M.J.; Furlong, E.T.; Meyer, 
M.T.; Zaugg, S.D.; Haack, S.K.; Barber, L.B.; and Thurman, E.M. 
2008a. U. S. Geological Survey. Water-Quality Data for 
Pharmaceuticals and Other Organic Wastewater Contaminants in Ground 
Water and in Untreated Drinking Water Sources in the United States, 
2000-01. Available on-line at http://pubs.usgs.gov/of/2008/1293.
52. Barnes, K.K.; Kolpin, D.W.; Furlong, E.T.; Zaugg, S.D.; Meyer, 
M.T.; and Barber, L.B. 2008b. A National Reconnaissance of 
Pharmaceuticals and Other Organic Wastewater Contaminants in the 
United States: (I) Groundwater. The Science of the Total 
Environment. Vol. 402:192-200.
53. Focazio, M.J.; Kolpin, D.W.; Barnes, K.K.; Furlong, E.T.; Meyer, 
M.T.; Zaugg, S.D.; Barber, L.B.; and Thurman, E.M. 2008. A National 
Reconnaissance for Pharmaceuticals and Other Organic

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Wastewater Contaminants in the United States--(II) Untreated 
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1998. Identification of Alkylphenols and Other Estrogenic Phenolic 
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M.K. 2003. Aggregate exposures of nine preschool children to 
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57. Boyd, G.R.; Palmerib, J.M.; and Grimm, D.A. 2004. 
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in New Orleans, Louisiana, USA. The Science of the Total 
Environment. Vol. 333:137-48.
58. Staples, C.A.; Dorn, P.B.; Klecka, G.M.; O'Block, S.T.; Branson, 
D.R.; and Harris, L.R. 2000. Bisphenol A Concentrations in Receiving 
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Simultaneous Quantification of Polycyclic Aromatic Hydrocarbons 
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Henderson, A.K.; and Reissman, D.B. 2004. Persistence of 
Pharmaceutical Compounds and Other Organic Wastewater Contaminants 
in a Conventional Drinking-Water-Treatment Plant. The Science of the 
Total Environment. Vol. 329:99-113.
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Sonzogni, W. 2005. An Assessment of Endocrine Disrupting Activity 
Changes during Wastewater Treatment through the Use of Bioassays and 
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62. ASTM International (ASTM). 2009. ASTM D7574-09 Standard Test 
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http://www.astm.org/Standards/D7574.htm.
63. ASTM. 2004. ASTM D5730-04 Standard Guide for Site 
Characterization for Environmental Purposes With Emphasis on Soil, 
Rock, the Vadose Zone and Ground Water. Available on-line at http://www.astm.org/Standards/D5730.htm.
64. EPA. 1998. Method 8270D (SW-846), Semivolatile Organic Compounds 
by Gas Chromatography/Mass Spectrometry (GC/MS), Revision 4. 
Available on-line at http://www.epa.gov/sam/pdfs/EPA-8270d.pdf.

IV. Statutory and Executive Order Reviews

    Under Executive Order 12866, entitled ``Regulatory Planning and 
Review'' (58 FR 51735, October 4, 1993), this action was submitted to 
the Office of Management and Budget (OMB) for review. Any changes made 
to this document in response to OMB comments received by EPA during 
that review have been documented in the docket as required by the 
Executive Order.
    Since this document does not impose or propose any requirements, 
and instead seeks comments and suggestions for the Agency to consider 
in possibly developing a subsequent proposed rule, the various other 
review requirements that apply when an agency imposes requirements do 
not apply to this action. Nevertheless, as part of your comments on 
this ANPRM, you may include any comments or information that you have 
regarding this action.
    In particular, any comments or information that would help the 
Agency to assess the potential impact of a rule on small entities 
pursuant to the Regulatory Flexibility Act (RFA) (5 U.S.C. 601 et 
seq.); to consider voluntary consensus standards pursuant to section 
12(d) of the National Technology Transfer and Advancement Act of 1995 
(NTTAA) (15 U.S.C. 272 note); to consider environmental health or 
safety effects on children pursuant to Executive Order 13045, entitled 
``Protection of Children from Environmental Health Risks and Safety 
Risks'' (62 FR 19885, April 23, 1997); or to consider human health or 
environmental effects on minority or low-income populations pursuant to 
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 will consider such comments during the development of 
any subsequent proposed rule as it takes appropriate steps to address 
any applicable requirements.

List of Subjects in 40 CFR Part 799

    Environmental protection, Bisphenol A, BPA, Chemicals, Hazardous 
substances, Reporting and recordkeeping requirements.

    Dated: July 20, 2011.
Stephen. A. Owens,
Assistant Administrator, Office of Chemical Safety and Pollution 
Prevention.
[FR Doc. 2011-18842 Filed 7-25-11; 8:45 am]
BILLING CODE 6560-50-P
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