[Federal Register Volume 76, Number 143 (Tuesday, July 26, 2011)]
From the Federal Register Online via the Government Publishing Office [www.gpo.gov]
[FR Doc No: 2011-18842]
ENVIRONMENTAL PROTECTION AGENCY
40 CFR Part 799
Testing of Bisphenol A
AGENCY: Environmental Protection Agency (EPA).
ACTION: Advance notice of proposed rulemaking (ANPRM).
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
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
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: [email protected].
For general information contact: The TSCA-Hotline, ABVI-Goodwill,
422 South Clinton Ave., Rochester, NY 14620; telephone number: (202)
554-1404; e-mail address: [email protected].
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
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
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
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,
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
vi. Provide specific examples to illustrate your concerns and
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
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
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
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.
\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.
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.
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
Country (microgram/Liter Endpoints
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).
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
\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 (< 100 [mu]g/
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.
\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
Test organism Endpoint (microgram/Liter References (Listed in
([mu]g/L)) Ref. 14)
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.
Xenopus laevis................. High ratio of females to only at 23............ Levy et al., 2004.
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
Dicentrarchus labrax (seabass). Increased vitellogenin 10.................... Correia et al., 2007.
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.
fibrotic tissue; decreased
Orizias latipes................ Vitellogenin production.... 10.................... Kashiwada et al.,
Orizias latipes................ Increased female proteins 10.................... Tabata et al., 2001.
Orizias latipes................ Decreased egg hatching in 2 only................ Japanese Ministry of
2nd generation. the Environment,
Orizias latipes................ Increased male 49.7.................. Japanese Ministry of
hepatosomatic index. the Environment,
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.
Cyprinus carpio (carp)......... Oviduct formation in males. 32.................... Bowmer & Gimeno, 2001
Cyprinus carpio................ Altered sex steroid levels; 1..................... Mandich et al., 2007.
alterations in testes
structure; oocyte atresia.
Bellamya purificata (snail).... Enzyme activities in gills 1..................... Li et al., 2008.
and digestive glands.
Marisa cornuarietis (ramshorn Superfeminization.......... 1..................... Oehlmann et al., 2000.
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.
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.
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.
Tigriopus japonicus............ Delayed development (F1)... 0.01.................. Marcial et al., 2003.
Chironomus riparius............ Delayed emergence (2nd 0.078................. Watts et al., 2001.
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
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
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
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 < 1 [micro]g/L (ppb) in the influent
and < 0.3 [micro]g/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 < 0.02 (below
detection limit) to 3.33 [micro]g/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
Surface Water...................... <0.0001 to 0.14*...... <0.0001 to 12......... Barnes et al., 2008a (Ref.
Boyd et al., 2003 (Ref.
Boyd et al., 2004 (Ref.
Focazio et al., 2008 (Ref.
Klecka et al., 2009 (Ref.
Kolpin et al., 2002 (Ref.
Staples et al., 2000 (Ref.
Zhang et al., 2007 (Ref.
Ground Water....................... NR** to 1.78 [dagger]. <0.003 to 2.55........ Barnes et al., 2008a (Ref.
Barnes et al., 2008b (Ref.
Focazio et al., 2008 (Ref.
Rudel et al., 1998 (Ref.
Drinking Water..................... <0.0001............... <0.0001 to 0.42....... Boyd et al., 2003 (Ref.
Stackelberg et al., 2004
Wastewater......................... <0.0001............... <0.0001 to 25......... Boyd et al., 2003 (Ref.
Drewes et al., 2005 (Ref.
Jackson and Sutton, 2008
Rudel et al., 1998 (Ref.
Tsai, 2006 (Ref. 42).
Soils.............................. 6 to 7................ 4 to 147.............. Kinney et al., 2008 (Ref.
Wilson et al., 2003 (Ref.
Sediment, Fresh.................... 0.6* [dagger][dagger]. 1.4 to 140 Klecka et al., 2009 (Ref.
Sediment, Marine................... 3.5*.................. 1.5 to 5.0............ Stuart et al., 2005 (Ref.
Biosolids.......................... 4,600 to 4,690*....... 1,090-14,400.......... Kinney et al., 2006 (Ref.
Kinney et al., 2008 (Ref.
* Value is median.
** Not reported (NR).
[dagger] Mean of values above reporting limit (1 ppb).
[dagger][dagger] Median value includes non-detected values below the minimum detection limit, while the reported
range includes only detected values.
Although there is disagreement in interpreting some of the effects
observed in studies performed to date with BPA, as described in Unit
II.B.1. and 2., a comparison of the range of the effect levels observed
in many studies and the predicted no effect concentration (PNEC) values
used in three international regulatory risk assessments (0.175 to 1.6
[mu]g/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
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
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
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
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
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-
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.
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
(Bisphenol A). Institute for Health and Consumer Protection, Joint
Research Centre, European Commission. Luxembourg: Publications
Office of the European Union.
8. Japan's National Institute of Advanced Industrial Science and
Technology (AIST). 2007. AIST Risk Assessment Document Series 4.
Bisphenol A. AIST07-A00001-4.
9. National Toxicology Program, Center for the Evaluation of Risks
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.
10. FDA. 2010. U.S. Food and Drug Administration. Update on
Bisphenol A for Use in Food Contact Applications: January 2010.
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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.
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-
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
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17. Sumpter, J.P.; Tyler, C.R.; Sherazi, A. 2001. Bisphenol-A:
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18. Oehlmann, J.; Schulte-Oehlmann, U.; Werner, K.; Jagnytsch, O.;
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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
cornuarietis? Part I: Intra- and inter-laboratory variability in
test endpoints. Ecotoxicology and Environmental Safety. Vol. 66:309-
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.
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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
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22. Levy, G.; Lutz, I.; Kr[uuml]ger, A.; and Kloas, W. 2004.
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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
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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.
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25. Ramakrishnan, S. and Wayne, N.L. 2008. Impact of bisphenol-A on
early embryonic development and reproductive maturation.
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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
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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.
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,
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S.; Popov, V.; and Itoh, H. (eds.): Waste Management and the
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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.
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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.
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37. Braun, J.M.; Kalkbrenner, A.E.; Calafat, A.M.; Bernert, J.T.;
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38. Calafat, A.M.; Kuklenyik, Z.; and Reidy, J.A., et al 2005.
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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
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41. CDC, HHS. Fourth National Report on Human Exposure to
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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.
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.
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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
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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
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48. Lee, H-B. and Peart, T.E. 2000b. Bisphenol A contamination in
Canadian municipal and industrial wastewater and sludge samples.
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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
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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.
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52. Barnes, K.K.; Kolpin, D.W.; Furlong, E.T.; Zaugg, S.D.; Meyer,
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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
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1998. Identification of Alkylphenols and Other Estrogenic Phenolic
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55. Wilson, N.K.; Chuang, J.C.; Lyu, C.; Menton, R.; and Morgan,
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57. Boyd, G.R.; Palmerib, J.M.; and Grimm, D.A. 2004.
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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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in a Conventional Drinking-Water-Treatment Plant. The Science of the
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61. Drewes, J.E.; Hemming, J.; Ladenburger, S.J.; Schauer, J.; and
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
Method for Determination of Bisphenol A in Environmental Waters by
Liquid Chromatography/Tandem Mass Spectrometry. Available on-line at
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
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
[FR Doc. 2011-18842 Filed 7-25-11; 8:45 am]
BILLING CODE 6560-50-P