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EO12866_BPA-Testing_ANPRM_2010-12-10.doc 

EO 12866 Review Draft as submitted.

BILLING CODE 6560–50–P 

ENVIRONMENTAL PROTECTION AGENCY 

 40 CFR Part 799 

 [EPA–HQ–OPPT–2010–0812; FRL–XXXX–X] 

RIN 2070-AJ83 

Testing of Bisphenol A 

AGENCY: Environmental Protection Agency (EPA). 

ACTION: Advance notice of proposed rulemaking. 

SUMMARY: Bisphenol A (BPA, CASRN 80-05-7), a high production volume 

chemical, is a reproductive, developmental, and systemic toxicant in animal studies and is 

weakly estrogenic. EPA is providing this advance notice of proposed rulemaking to 

request comment on requiring toxicity testing to determine the potential for BPA to cause 

endocrine-related and other adverse 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. 
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DATES: Comments must be received on or before [insert date [60] days after date of 

publication in the Federal Register]. 

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 website is 

an “anonymous access” system, which means EPA will not know your identity or contact 
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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 
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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 (identified by 

statute to include import) or process BPA (CASRN 80-05-7). BPA is listed on the 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). 
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 • 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. 

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 
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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. 
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 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 advance notice of proposed rulemaking 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; and 

 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 proposed test rule. 

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 proposed to resolve existing 
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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 proposed 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 endocrinerelated effects. 

 On May 17, 1985, EPA published a Proposed Rule (50 FR 20691) to require 

human health and environmental testing in response to the Interagency Testing 

Committee's (ITC's) designation of 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 (51 FR 33047), published 

September 18, 1986, terminated the test rule process for environmental effects testing for 

bisphenol A. 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 ppm (1 mg/L), and 

the ratio of 48-hour to 96-hour LC50 values were not greater than two. 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). 

1. What Is Currently Known About the Environmental Hazard of BPA? 
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 The toxicity of BPA has been studied extensively, as indicated in the multiple 

studies cited in the Action Plan (Ref. 1). There is general agreement among multiple 

reviewers that BPA is a reproductive and developmental toxicant at doses in animal 

studies of > 50 mg/kg-bw/day (delayed puberty in male and female rats and male mice; 

discussed in Ref. 2-9); > 235 mg/kg-bw/day (reduced fetal or birth weight or growth 

early in life, effects on testis of male rats; Ref. 9); and > 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; Ref. 2-8) were observed at doses above 5 mg/kgbw/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 endocrinerelated low-dose effects on puberty and neurological development (brain, behavior; Ref. 

9) at doses in animal studies as low as 2 μg/kg-bw/day. There is disagreement about 

whether effects seen at doses in animals less than 1 mg/kg/day are meaningful and 

relevant to humans. The Food and Drug Administration (FDA), together with the 

National Institute of Environmental Health Sciences (NIEHS) and the Centers for 

Disease Control and Prevention (CDC), is 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 proposing any additional testing specifically in regard 

to human health issues at this time. 

 Many studies have been conducted to determine potential effects of BPA 

exposure on invertebrates, fish, amphibians, reptiles, birds, and wild mammals, and a 
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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 sublethal 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 μg/L to 1 mg/L. (Ref. 6; also, see individual studies noted 

in Table 2). 

 The ecological hazard for BPA has been evaluated in three different risk 

assessments performed by the European Union (EU), Canada, and Japan (Refs. 7, 6, and 

8), as summarized in Table 1 below. 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 μg/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 
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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 

Country 

Predicted No 

Effect 

Concentrations

1 (μg/L) 

Endpoints 

European 1.5 The predicted no effect concentration (PNEC) for aquatic 
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Table 1: Summary of Bisphenol A Ecological Values 

Country 

Predicted No 

Effect 

Concentrations

1 (μg/L) 

Endpoints 

Union 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 

μg/L, which is divided by an uncertainty factor of 5, resulting 

in a PNEC of 1.5 μg/L (Ref. 7). 

Canada 0.175 This PNEC was derived by using a lowest observed effect 

concentration (LOEC) of 1.75 μg/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 μg/L no effect 

concentration (NOEC) for egg hatchability in fathead minnows 

from the unpublished 3 generation study by Sumpter, et al. 

(2001) multigeneration fish study and dividing by an 

uncertainty factor of 10 (Ref. 8). 

1 In Europe, 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 

shown in Table 3, for BPA in U.S. surface waters at a mean concentration range of up to 

1.78 μg/L (ppb) and a single maximum concentration of 12 μg/L (ppb); in ground water 

at a mean concentration range of up to 1.9 μg/L (ppb) and a maximum concentration of 

2.55 μg/L (ppb); and in freshwater sediments at a median concentration of 0.6 μg/kg 
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(ppb) dry weight and a maximum concentration of 140 μg/kg (ppb) (See Table 3), and 

the existence of many hazard studies describing a variety of effects in aquatic organisms 

at some of these concentrations (See Table 2), leaving little or no room for a reasonable 

or acceptable margin of exposure. 

 There are two principal, initial questions that need to be answered in order to 

assess the potential for BPA to harm the environment in the U.S.: 

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; and 

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 20071

 to 

the present. A total of 645 articles were found (Ref. 13), of which 31 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 European Union, and 

 

1

 The starting date of 2007 was used to allow for some overlap between the thorough searches done by 

Canada, the EU and Japan 
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Japan (Ref. 6-8), EPA performed a more detailed evaluation of the scientific literature for 

sub-lethal effects at lower concentrations (< 100 μg/L). These sub-lethal effects in both 

vertebrates and invertebrates could be mediated either through endocrine or nonendocrine-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. 

Table 2. Summary of Reported Hazard Effects of BPA at 

Potentially Environmentally Relevant Concentrations

Test Organism Endpoint 

Effect 

Conc. 

(μg/L) 

References (Listed 

in Ref. 14) 

Amphibians 

Xenopus laevis (African 

clawed frog)

Inhibited metamorphosis 

via T3 pathways 22.8 Heimeier et al., 2009 

Xenopus laevis 

High ratio of females to 

males-1st study 23 Levy et al., 2004 

Xenopus laevis 

High ratio of females to 

males-2nd study only at 23 Levy et al., 2004 

 

Avian 

Gallus domesticus

(chicken) 

Delayed development of 

wattle, comb and testes 2 Furuya et al., 2006 

Gallus domesticus 

Inhibited development of 

seminiferous tubuli and 

spermatogenesis 20 Furuya et al., 2006 

 

Fish 

Dicentrarchus labrax

(seabass)

Increased vitellogenin 

production 10 Correia et al., 2007 

Misgurnus 

anguillicaudatus (Chinese 

loach)

Increased vitellogenin 

production 10 Lv et al., 2007 

Orizias latipes (medaka) Egg hatchability delayed 13 only Yokota et al., 2000 

Orizias latipes 

Loss of testicular 

structure, increased 

fibrotic tissue; decreased 50 Metcalfe et al., 2001 
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Table 2. Summary of Reported Hazard Effects of BPA at 

Potentially Environmentally Relevant Concentrations

Test Organism Endpoint 

Effect 

Conc. 

(μg/L) 

References (Listed 

in Ref. 14) 

sperm cells. 

Orizias latipes Vitellogenin production 10 

Kashiwada et al., 

2002 

Orizias latipes 

Increased female proteins 

(i.e. vitellogenin) 10 Tabata et al., 2001 

Orizias latipes 

Decreased egg hatching 

in 2nd generation 2 only Japanese MOE, 2006

Orizias latipes 

Increased male 

hepatosomatic index 49.7 Japanese MOE, 2006

Pimephales promelas 

(fathead minnow)

Increased vitellogenin 

production 52.8 

Rhodes et al., 2007-

unpublished 

Xiphophorus helleri 

(swordtail fish) Reduced sword tail length 20 Kwak et al., 2001 

Cyprinus carpio (carp)

Oviduct formation in 

males 32 

Bowmer & Gimeno, 

2001., unpublished 

Cyprinus carpio 

Altered sex steroid levels; 

alterations in testes 

structure; oocyte atresia 1 Mandich et al., 2007 

 

Invertebrates 

Bellamya purificata (snail)

Enzyme activities in gills 

and digestive glands 1 Li et al., 2008 

Marisa cornuarietis 

(ramshorn snail) Superfeminization 1 

Oehlmann et al., 

2000 

Marisa cornuarietis 

Increased egg and clutch 

production per female 

0.25 at 20 

degrees C 

Oehlmann et al., 

2006 

Marisa cornuarietis Increased egg production 

0.25 at 27 

degrees C 

Oehlmann et al., 

2006 

Marisa cornuarietis 

Increased clutch 

production 

5 at 27 

degrees C 

Oehlmann et al., 

2006 

Potamopyrgus 

antipodarum (snail)

Increased growth/embryo 

production 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 
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Table 2. Summary of Reported Hazard Effects of BPA at 

Potentially Environmentally Relevant Concentrations

Test Organism Endpoint 

Effect 

Conc. 

(μg/L) 

References (Listed 

in Ref. 14) 

Nucella lapillus (marine 

snail)

Superfeminization; 

reduced sperm/penis 

length/prostrate gland in 

males 1 

Oehlmann et al., 

2000 

Acartia tonsa (copepod) Increased egg production 

20 (day 10 

only) Andersen et al., 1999

Tigriopus japonicus 

(intertidal copepod)

Delayed development 

(Parent) 0.1 Marcial et al., 2003 

Tigriopus japonicus 

Delayed development 

(F1) 0.01 Marcial et al., 2003 

Chironomus riparius 

Delayed emergence (2nd 

generation) 0.078 Watts et al., 2001 

Chironomus riparius Mouthpart deformities 0.01 Watts et al., 2002 

 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 multigeneration invertebrate and fish studies. 

For example, in the intertidal copepod (Tigriopus japonicus), delayed development was 

reported in the first generation at 0.1 μg/L, but at a 10-fold lower concentration of 0.01 

μg/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 μg/L (Ref. 16). Egg hatchability 

decreased in fathead minnows (Pimephales promelas) at 640 μg/L in the first (F1) 

generation, then at 160 μg/L in the second (F2) generation (Ref. 17). Although the 

mechanisms of action leading to effects may be different for vertebrate and invertebrate 
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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 at very low concentrations 

in one lab (Ref. 18), but those results were not found in studies by other researchers (Ref. 

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 μg/L of BPA (Ref. 22) before 

metamorphosis had an increased female to male ratio at 23 μg/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 
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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 

(Ref. 24, 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 

the EPA 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. (Ref. 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 to identify and establish a dose-response 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. 
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b. Effects of BPA on amphibians at sensitive life stages, specifically metamorphosis 

(thyroid effects) and sexual development/differentiation (hypothalamic-pituitarygonadal 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 

recommendations for 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 U.S., 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, 
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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 (Ref. 32-37). 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. 38). 

 According to the Toxics Release Inventory (TRI) Database, total release of BPA 

in the U.S. in 2007 was 1,132,062 pounds, with releases of 122,965 pounds to air, 6,246 

pounds to water, 14,972 pounds released on-site to land, and 684,638 pounds transferred 

off-site to land. An additional 32,928 pounds were reported as off-site water transfer to 

Publicly Owned Treatment Works (POTWs), with another 2,759,705 pounds transferred 

to incineration (Ref. 31). 

 Some information is available for BPA concentrations in U.S. water and other 

environmental media (see Table 3, 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 μg/L (ppb), mainly due to its partitioning and 

biodegradability properties (Ref. 39). BPA was detected at a median concentration of 

0.14 μg/L (ppb) and a maximum concentration of 12 μg/L (ppb) in 41.2% of 85 samples 

collected from U.S. streams in 1999 and 2000 (Ref. 40). The maximum concentration of 

12 μg/L (ppb) was much higher than any of the other samples reported in the study; the 

next highest concentration reported was 5.2 μg/L (ppb), and as indicated by the median 

concentration of 0.14 μg/L (ppb), BPA concentration in other U.S. waters was much 
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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 percent (852 of 1068) of surface water samples. The median concentration reported 

was 0.081 μg/L (ppb) and the 95th percentile concentration was 0.47 μg/L (ppb) (Ref. 

41). 

 Two studies have addressed individual wastewater treatment plants (WWTPs) in 

two different parts of the U.S. In 2001 and 2002, BPA was not detected above the 

detection limit of 0.0001 μg/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. 42). 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. 43). This study reported 

detecting (limit of detection = 0.25 μg/L (ppb)) BPA in two of three treated wastewater 

samples at 0.38 and 0.31 μg/L (ppb). It also reported detecting BPA in wastewater 

generated by a pharmaceutical manufacturer (0.295 μg/L (ppb)), an industrial laundry 

(21.5 μg/L (ppb)), and a paper products manufacturer (0.753 μg/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 μg/L (ppb) in sewage influent and effluent (generally < 1 μg/L (ppb) in the influent 

and < 0.3 μg/L (ppb) in the effluent) and from 36.7 to 0.104 μg/g (ppm) in raw and 

digested sewage sludge from multiple WWTPs in Canada (Ref. 44). The same authors 

reported that BPA contamination was detected in 100 percent of sewage samples from 31 

WWTPs across Canada with concentrations ranging from 0.080 to 4.98 μg/L (ppb) 
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(median 0.329 μg/L (ppb)) for the influent and from 0.010 to 1.08 μg/L (ppb)(median 

0.136 μg/L (ppb)) for the effluent (Ref. 45). 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 percent. BPA was detected in sludge samples 

at concentrations ranging from 0.033 to 36.7 μg/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 area, with concentrations ranging from 0.23 to 149.2 μg/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 μg/g (ppm), with a median value of 0.076 μg/g (ppm), on 

a dry weight basis (Ref. 45). 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 nine treated biosolids 

products from WWTPs in seven states and found that all contained between 1,090 and 

14,400 μg/kg (ppb) (median 4,690 μg/kg (ppb)) (Ref. 46). A 2008 study reported BPA in 

treated biosolids from a municipal U.S. WWTP at 4,600 μg/kg (ppb) and reported 81 

μg/kg (ppb) in soil that received the land-applied biosolids (Ref. 47). That study detected 
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BPA at 81 μg/kg (ppb) in earthworms living in treated soil. The authors also reported 

detecting 147 μg/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 

groundwater 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 

groundwater sites, with a mean detected concentration of 1.78 μg/L (ppb) and a range of 

1.06 to 2.55 μg/L (ppb). BPA was among the top five most frequently detected organic 

compounds in this study (Ref. 48, 49). 

 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 groundwater 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 μg/L (ppb). 

The maximum concentration measured in these samples was 1.9 μg/L (ppb) (Ref. 48, 50). 

 Landfill leachate from one U.S. study reported maximum BPA concentrations of 

1.7 μg/L (ppb) in landfill leachate and 1.4 μg/L (ppb) in the receiving groundwater plume 

at a landfill on Cape Cod that was known to be leaking (Ref. 51). 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 μg/L (ppb) 

of BPA (Ref. 39). Studies conducted at Japanese landfills resulted in maximum untreated 
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leachate concentrations of 17,200 μg/L (ppb) and treated leachate concentrations of 5.1 

μg/L (ppb) (Ref. 11). 

 Wilson et al. (Ref. 52) 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. 41) reported a median 

concentration of 0.6 ppb BPA in North American freshwater sediments, including 

nondetected 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. 53). 

Table 3: U.S. Reported Environmental Concentrations of BPA 

Location Mean or Range 

of Means (ppb) 

Range (ppb) References 

Surface Water <0.0001 to 0.14* <0.0001 to 12 

Barnes et al. (2008a) (Ref. 48) 

Boyd et al. (2003) (Ref. 42) 

Boyd et al. (2004) (Ref. 54) 

Focazio et al. (2008) (Ref. 50) 

Klecka et al. (2009) (Ref. 41) 

Kolpin et al. (2002) (Ref. 40) 

Staples et al. (2000) (Ref. 55) 

Zhang et al. (2007) (Ref. 56) 

Groundwater NR** to 1.78† <0.003 to 2.55 

Barnes et al. (2008a) (Ref. 48) 

Barnes et al. (2008b) (Ref. 49) 

Focazio et al. (2008) (Ref. 50) 

Rudel et al. (1998) (Ref. 51) 

Drinking Water <0.0001 <0.0001 to 0.42 Boyd et al. (2003) (Ref. 42) 

Stackelberg et al. (2004) (Ref. 57) 

Wastewater <0.0001 <0.0001 to 25 

Boyd et al. (2003) (Ref. 42) 

Drewes et al. (2005) (Ref. 58) 

Jackson and Sutton (2008) (Ref. 43) 

Rudel et al. (1998) (Ref. 51) 

Tsai (2006) (Ref. 39) 

Soils 6 to 7 4 to 147 Kinney et al. (2008) (Ref. 47) 

Wilson et al. (2003) (Ref. 52) 

Sediment, Fresh 0.6*†† 1.4 to 140†† Klecka et al. (2009) (Ref. 41) 

Sediment, 

Marine 3.5* 1.5 to 5.0 Stuart et al. (2005) (Ref. 53) 
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Table 3: U.S. Reported Environmental Concentrations of BPA 

Location Mean or Range 

of Means (ppb) 

Range (ppb) References 

Biosolids 4600 to 4690* 1090-14,400 Kinney et al. (2006) (Ref. 46) 

Kinney et al. (2008) (Ref. 47) 

* Value is median 

** Not Reported 

†

 Mean of values above Reporting Limit (1 ppb) 

†† Median value includes nondetected values below the MDL, 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 μg/L, Table 1) with measured concentrations in some U.S. waters and 

sediments, which included values as high as 12 μg/L (ppb) (surface water), 2.55 μg/L 

(ppb) (ground water), and 140 ppb sediment (freshwater sediment) (Table 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. 

 Although most currently available environmental monitoring results show that the 

concentrations of BPA in U.S. water bodies are lower than 1 μg/L (ppb) (median 
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concentration of 0.14 μg/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 

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, groundwater, 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. 
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 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 section 6 of TSCA, 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. 

 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 
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analytical techniques. Appropriate quality assurance and quality controls also should be 

incorporated in the protocols for collection and analyses. 

 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. 59); 

ASTM D5730-04 Standard Guide for Site Characterization for Environmental Purposes 

With Emphasis on Soil, Rock, the Vadose Zone and Ground Water (Ref. 60); EPA 

Method 8270D (SW-846), Semivolatile Organic Compounds by Gas 

Chromatography/Mass Spectrometry (GC/MS), Revision 4 (Ref. 61); and other methods 

cited and described in such publications as Barnes et al. (2008) (Ref. 48) and Focazio et 

al. (2008) (Ref. 50). 

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. 
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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 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 human exposure to BPA. 

i. Other information that may provide insight into sources and pathways of 

environmental and human exposure to BPA released into the environment. 

j. The cost and economic feasibility of such environmental testing, for the different 

types of sites. 

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

 EPA is issuing this advance notice of proposed rulemaking 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)). 
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 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 subsection 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 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 
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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 testing the chemical substances which comprise 

the mixture[.] (15 U.S.C. § 2603(a)). 

 If EPA makes these findings 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. Id. 

 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 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 
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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 published in the Federal Register at 58 FR 28736, 28738-28739, May 

14, 1993 (B Policy). 

 Authority for requiring sampling and monitoring for a chemical substance or 

mixture can be found within TSCA section 4. Section 4(a) 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, 

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.

III. References 

1. EPA. 2010. Bisphenol A Action Plan. Available online at 

http://www.regulations.gov/search/Regs/home.html#documentDetail?R=0900006480ad7

e0c 

 2. EPA. 1993. Integrated Risk Information System (IRIS) (1993). Accessed at 

http://www.epa.gov/ncea/iris/subst/0356.htm. 
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33 of 43 

 3. FDA. 2008. U. S. Food and Drug Administration. Draft Assessment of 

Bisphenol A for Use in Food Contact Applications. 

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 at 

http://www.fda.gov/Food/FoodIngredientsPackaging/ucm166145.htm. 

 4. European Food and Safety Authority (EFSA). 2006. Scientific Panel on Food 

Additives, Flavourings, Processing Aids and Materials in Contact with Food . Summary 

Opinion of the Scientific Panel on food additives, flavourings, processing aids and 

materials in contact with food (AFC) related to 2,2-BIS(4-HYDROXYPHENYL) 

PROPANE. Question number EFSA-Q-2005-100 November. 

 5. European Food and Safety Authority (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 (2008) 759, 1-10. 

 6. Canada. 2008. Environment Canada, Health Canada. Screening Assessment for 

the Challenge Phenol, 4,4' (1-methylethylidene)bis- (Bisphenol A) CAS 80-05-7. October 

2008. http://www.ec.gc.ca/substances/ese/eng/challenge/batch2/batch2_80-05-7_en.pdf

 7. EU. 2008. European Union Updated Risk Assessment Report. Bisphenol A, 

CAS No: 80-05-7. Institute for Health and Consumer Protection, European Chemicals 

Bureau, European Commission Joint Research Centre, 3rd Priority List, Luxembourg: 

Office for Official Publications of the European Communities. 
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 8. AIST (Japan’s National Institute of Advanced Industrial Science and 

Technology). 2007. AIST Risk Assessment Document Series 4. Bisphenol A. 

 9. NTP/CERHR. 2008. NTP-CERHR Monograph on the Potential Human 

Reproductive and Developmental Effects of Bisphenol A. US Department of Health and 

Human Services. National Toxicology Program. Center for the Evaluation of Risks to 

Human Reproduction. 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. Accessed at 

http://www.fda.gov/NewsEvents/PublicHealthFocus/ucm197739.htm. 

 11. Crain, D.A.; Eriksen, M.; Iguchi, T.; Jobling, S.; Laufer, H.; LeBlanc, G.A.; 

Guillette, Jr., L.J. 2007. An ecological assessment of Bisphenol A: evidence from 

comparative biology. Reprod. Toxicology (24): 225-239. 

 12. Lahnsteiner, F.; Berger, B.; Kletzl, M.: Weismann, T. 2005. Effect of 

Bisphenol A on Maturation and Quality of Semen and Eggs in the Brown Trout, Salmo 

trutta f. fario. Aquatic Tox. 75: 213-224. 

13. Reference to RAD bibliographical list of 645 articles found; list will 

appear in docket. 

 14. Reference to RAD bibliographical list of 31 articles deemed relevant; list 

will appear in docket.

 15. Marcial, H.S.; Hagiwara, A.; Snell, T.W. 2003. Estrogenic compounds 

affect development of harpacticoid copepod Tigriopus Japonicus. Env. Tox. and Chem. 

22(12), 3025–3030. 
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 16. Watts, M.M.; Pascoe, D.; Carroll, K. 2001. Chronic exposure to 17αethinylestradiol and bisphenol A-effects on development and reproduction in the 

freshwater invertebrate Chironomus riparius (Diptera: Chironomidae). Aquat. Tox. 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.; Tyler, 

C.R. 2008. A Critical Analysis of the Biological Impacts of Plasticizers on Wildlife. 

Philos. Trans. R. Soc., B: Biol. Sci. 364(1526): 2047–2062. 

 19. Forbes, V.E.; Selck, H.; Palmqvist, A.; Aufderheide, J.; Warbritton, R.; 

Pounds, N.; Thompson, R.; van der Hoeven, N.; Caspers, N. 2007. Does bisphenol A 

induce superfeminization in Marisa cornuarietis? Part I: Intra- and inter-laboratory 

variability in test endpoints. Ecotox. and Env. Safe. 66, 309–318. 

 20. Forbes, V.E.; Aufderheide, J.; Warbritton, R.; Thompson, R.; van der 

Hoeven, N.; Caspers, N. 2007. Does bisphenol A induce superfeminization in Marisa 

cornuarietis? Part I: Intra- and inter-laboratory variability in test endpoints. Ecotox. and 

Env. Safe. 66, 319–325. 

 21. Forbes, V.E; Aufderheide, J.; Warbritton, R.; Thompson, R.; van der Hoeven, 

N.; Caspers, N. 2008. Effects of bisphenol A on fecundity, egg hatchability, and 

juvenile growth of Maris Cornuarietis. Env. Tox. and Chem. 27 (11), 2332–2340. 
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 22. Levy, G.; Lutz, I.; Krüger, A.; Kloas, W. 2004. Bisphenol A induces 

feminization in Xenopus laevis tadpoles. Environ. Res. 94, 102-111. 

 23. Calabrese, E.J.; Baldwin, L.A. 2003. Hormesis at the National Toxicology 

Program (NTP): evidence of hormetic dose responses in NTP dose-range studies. 

Nonlinearity Biol. Toxicol. Med. 1, 455–467. 

 24. Heimeier, R.A.; Das, B.; Buchholz, D.R.; Shi, Y. 2009. The Xenoestrogen 

Bisphenol A inhibits postembryonic vertebrate development by antagonizing gene 

regulation by thyroid hormone. Endocrinology, 150, 2964-2973. 

 25. Ramakrishnan, S.; Wayne, N.L. 2008. Impact of bisphenol-A on early 

embryonic development and reproductive maturation. Reproductive Toxicology 25, 177–

183. 

 26. Ankley, G.T., K.M. Jensen, M.D. Kahl, E.J. Durhan, E.A. Makynen, J.E. 

Cavallin, D. Martinovic, L.C. Wehmas, N.D. Mueller and D.L. Villeneuve. 2010. Use of 

chemical mixtures to differentiate mechanisms of endocrine action in a small fish model. 

Aquat. Toxicol. 99, 389-396. 

27. EPA. Endocrine Disruptor Screening Program; Policies and Procedures for 

Initial Screening. 74 Fed.Reg. 17560. April 15, 2009. 

 28. EPA. Endocrine Disruptor Screening Program website. Accessed at 

http://www.epa.gov/scipoly/oscpendo/. 

 29. Organization for Economic Co-operation and Development Environment 

Directorate. Endocrine Disruptor Testing and Assessment. Accessed at 

http://www.oecd.org/document/62/0,3343,en_2649_34377_2348606_1_1_1_1,00.html
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 30. EPA. 2008. Aquatic Life Criteria for Contaminants of Emerging Concern 

(Part 1) & Illustration of Recommendations using Data for 17α-Ethinylestradiol (EE2). 

USEPA Office of Water, Washington, DC.

 31. EPA. 2009a. Toxic Release Inventory. 2007 Public Data Release, Released 

March 14, 2009. http://www.epa.gov/tri/tridata/index.htm#pdr

 32. European Union. 2010. Risk Assessment Report, 4,4'-Isopropylidenediphenol 

(Bisphenol-A), CAS No: 80-05-7, (February 2010). 

 33. Vinggaard, A.M.: Körner, W.; Lund, K.H.; Bolz, U.; 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. Chem Res Toxicol. 13(12):1214-22. 

 34. Gehring, M.; Vogel, D.; Tennhardt, L.; Weltin, D.; Bilitewski, B. Undated. 

Bisphenol A contamination of wastepaper, ellulose and recycled paper products. 

http://rcswww.urz.tu-dresden.de/~gehring/deutsch/dt/vortr/040929ge.pdf 

 35. Ozaki, A.; Yamaguchi, Y.; Fujita, T.; Kuroda, K.; Endo, G. 2004. Chemical 

analysis and genotoxicological safety assessment of paper and paperboard used for food 

packaging. Food Chem Toxicol. 42(8):1323-37. 

 36. Fukazawa, H.; Hoshino, K.; Shiozawa, T.; Matsushita, H.; Terao, Y. 2001. 

Identification and quantification of chlorinated bisphenol A in wastewater from 

wastepaper recycling plants. Chemosphere. 44(5):973-9. 

 37. Terasaki, M.; Shiraishi, F.; Fukazawa, H.; Makino, M. 2007. Occurrence and 

estrogenicity of phenolics in paper-recycling process water: pollutants originating from 

thermal paper in waste paper. Environ Toxicol Chem. 26(11):2356-66. 
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 38. Braun J.M., Kalkbrenner A.E., Calafat A.M., Bernert J.T., Ye X., et al. 2010 

Variability and Predictors of Urinary Bisphenol A Concentrations during Pregnancy. 

Environ Health Perspect doi:10.1289/ehp.1002366. 

39. Tsai, W. 2006. Human Health Risk on Environmental Exposure to BisphenolA: A Review. Journal of Environmental Science and Health Part C, 24:225-255. 

 40. Kolpin, D.W.; Furlong, E.T.; Meyer, M.T.; Thurman, E.M.; Zaugg, S.D.; 

Barber, L.B.; Buxton, H.T. 2002. Pharmaceuticals, hormones, and other organic 

wastewater contaminants in U.S. streams, 1999–2000: a national survey. Environ Sci 

Technol 36:1202–1211. 

 41. Klecka, G.M.; Staples, C.A.; Clark, K.E.; van der Hoeven, N.; Thomas, D.E.; 

Hentges, S.G. 2009. Exposure Analysis of Bisphenol A in Surface Water Systems in 

North America and Europe. Environ. Sci. Technol. 2009, 43(16):6145–6150. 

 42. Boyd G.R.; Reemtsma, H.; Grimm, D.A.; Mitra, S. 2003. Pharmaceuticals 

and personal care products (PPCPs) in surface and treated waters of Louisiana, U.S.A. 

and Ontario, Canada. Sci Total Environ 311: 135-149. 

 43. Jackson, J.; Sutton, R. 2008. Sources of endocrine-disrupting chemicals in an 

urban wastewater, Oakland, CA. Sci. Total Env., vol. 405:153-160. 

 44. Lee, H-B; Peart, T.E. 2000. Determination of bisphenol A in sewage effluent 

and sludge by solid-phase and supercritical fluid extraction and gas chromatography/mass 

spectrometry. J AOAC Int. vol. 83:290-7. 

 45. Lee, H-B; Peart, T.F. 2000. Bisphenol A contamination in Canadian 

municipal and industrial wastewater and sludge samples. Water Quality Res. J Canada. 

vol. 35: 283-298. 
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 46. Kinney, C.A.; Furlong, E.T.; Zaugg, S.D.; Burkhardt, M.R.; Werner, S.L.; 

Cahill, J.D.; Jorgensen, G.R. 2006. Survey of Organic Wastewater Contaminants in 

Biosolids Destined for Land Application. Environ. Sci. Technol. Vol. 40:7207–7215. 

 47. Kinney, C.A; Furlong, E.T.; Kolpin, D.W.; Burkhardt, M.R.; Zaugg, S.D.; 

Werner, S.L.; Bossio, J.P.; Benotti, M.J. 2008. Bioaccumulation of pharmaceuticals and 

other anthropogenic waste indicators in earthworms from agricultural soil amended with 

biosolid or swine manure. Environ. Sci. Technol. 2008, vol.42: 1863–1870. 

 48. Barnes, K.K.; Kolpin, D.W.; Focazio, M.J.; Furlong, E.T.; Meyer, M.T.; 

Zaugg, S.D.; Haack, S.K.; Barber, L.B.; 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 at: http://pubs.usgs.gov/of/2008/1293/. 

 49. Barnes, K.K.; Kolpin, D.W.; Furlong, E.T.; Zaugg, S.D.; Meyer, M.T.; 

Barber, L.B. 2008b. A National Reconnaissance of Pharmaceuticals and Other Organic 

Wastewater Contaminants in the United States: (I) Groundwater. Sci.Total Enviro. 402 

(2–3), 192–200. 

 50. Focazio, M.J.; Kolpin, D.W.; Barnes, K.K.; Furlong, E.T.; Meyer, M.T.; 

Zaugg, S.D.; Barber, L.B.; Thurman, E.M. 2008. A National Reconnaissance for 

Pharmaceuticals and Other Organic Wastewater Contaminants in the United States—(II) 

Untreated Drinking Water Sources. Sci. Total Environ. 402(2–3), 201–216. 

 51. Rudel, R.A.; Melly, S.J.; Geno, P.W.; Sun, G.; Brody, J.G. 1998. 

Identification of Alkylphenols and Other Estrogenic Phenolic Compounds in Wastewater, 

Septage, and Groundwater on Cape Cod, MA. Environ. Sci. Technol 32:861-9. 
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 52. Wilson, N.K.; Chuang, J.C.; Lyu, C.; Menton, R.; Morgan, M.K. 2003. 

Aggregate exposures of nine preschool children to persistent organic pollutants at day 

care and home. J. Expo. Anal. Environ. Epidemiol. 13:187-202. 

 53. Stuart, J.D.; Capulong, C.P.; Launer, K.D.; Pan, X. 2005. Analyses of 

phenolic endocrine disrupting chemicals in marine samples by both gas and liquid 

chromatography-mass spectrometry. J. Chromatogr. A. 1079:136-145. 

 54. Boyd, G.R.; Palmerib, J.M.; Grimm, D.A. 2004. Pharmaceuticals and 

Personal Care Products (PPCPs) and Endocrine Disrupting Chemicals (EDCs) in 

Stormwater Canals and Bayou St. John in New Orleans, Louisiana, USA. Sci. Total 

Environ. 333:137-48. 

 55. Staples, C.A.; Dorn, P.B.; Klecka, G.M.; O’Block, S.T.; Branson, D.R.; 

Harris, L.R. 2000. Bisphenol A Concentrations in Receiving Waters Near U.S. 

Manufacturing and Processing Facilities. Chemosphere 40:521-525. 

 56. Zhang, S.; Zhang, Q.; Darisaw, S.; Ehie, O.; Wang, G. 2007. Simultaneous 

Quantification of Polycyclic Aromatic Hydrocarbons (PAHs), Polychlorinated Biphenyls 

(PCBs), and Pharmaceuticals and Personal Care Products (PPCPs) in Mississippi River 

Water, in New Orleans, Louisiana, USA. Chemosphere 66:1057-69. 

 57. Stackelberg, P.E.; Furlong, E.T.; Meyer, M.T.; Zaugg, S.D.; Henderson, A.K.; 

Reissman, D.B. 2004. Persistence of Pharmaceutical Compounds and Other Organic 

Wastewater Contaminants in a Conventional Drinking-Water-Treatment Plant. Sci. Total 

Environ. 329:99-113. 

 58. Drewes, J.E.; Hemming, J.; Ladenburger, S.J.; Schauer, J.; Sonzogni, W. 

2005. An Assessment of Endocrine Disrupting Activity Changes during Wastewater 
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Treatment through the Use of Bioassays and Chemical Measurements. Water Environ. 

Res. 77:12–23. 

 59. ASTM. 2009. ASTM International. ASTM D7574-09 Standard Test Method 

for Determination of Bisphenol A in Environmental Waters by Liquid 

Chromatography/Tandem Mass Spectrometry. 

http://www.astm.org/Standards/D7574.htm. 

 60. ASTM. 2004. ASTM International. ASTM D5730-04 Standard Guide for Site 

Characterization for Environmental Purposes With Emphasis on Soil, Rock, the Vadose 

Zone and Ground Water. http://www.astm.org/Standards/D5730.htm. 

 61. USEPA. 1998. U.S. Environmental Protection Agency. EPA Method 8270D 

(SW-846), Semivolatile Organic Compounds by Gas Chromatography/Mass 

Spectrometry (GC/MS), Revision 4. 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 
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comments on this notice, 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, Chemical testing, Chemicals, 

Hazardous substances, Reports and recordkeeping requirements. 

Dated: ____________________ 
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__________________________________________ 

Assistant Administrator, Office of Chemical Safety and Pollution Prevention.