Federal Register / Vol. 76, No. 143 / Tuesday, July 26, 2011 / Proposed Rules 44535 

rulemaking. EPA has considered these 

requests and has decided to reopen the 

comment period for an additional 15 

days from the date of publication of 

today’s rulemaking. 

This reopening is for the limited 

purpose of public review and comment 

on the potential impacts of the final 

CSAPR on EPA’s proposed rulemaking 

to approve Tennessee’s Regional Haze 

SIP. EPA does not anticipate any 

impacts from the CSAPR on the 

proposed rulemaking on the Tennessee 

Regional Haze SIP. As noted in the 

CSAPR, EPA has not conducted any 

technical analysis to determine whether 

compliance with the CSAPR would 

satisfy Regional Haze Best Available 

Retrofit Technology (BART)-related 

requirements for electric generating 

units (EGUs). For that reason, EPA has 

neither made any determinations nor 

established any presumptions that 

compliance with the CSAPR satisfies 

BART-related requirements for EGUs. 

EPA intends to undertake a separate 

analysis to determine if compliance 

with the CSAPR would provide 

sufficient reductions to satisfy BART 

requirements for EGUs in accordance 

with Regional Haze Rule requirements 

for alternative BART compliance 

options as soon as practicable following 

official promulgation of the CSAPR. 

Dated: July 15, 2011. 

Gwendolyn Keyes Fleming, 

Regional Administrator, Region 4. 

[FR Doc. 2011–18833 Filed 7–25–11; 8:45 am] 

BILLING CODE 6560–50–P 

ENVIRONMENTAL PROTECTION 

AGENCY 

40 CFR Part 52 

[EPA–R09–OAR–2011–0042; FRL–9279–4] 

Revisions to the California State 

Implementation Plan, Northern Sierra 

Air Quality Management District, 

Sacramento Metropolitan Air Quality 

Management District, and South Coast 

Air Quality Management District 

AGENCY: Environmental Protection 

Agency (EPA). 

ACTION: Proposed rule. 

SUMMARY: EPA is proposing to approve 

revisions to the Northern Sierra Air 

Quality Management District 

(NSAQMD), Sacramento Metropolitan 

Air Quality Management District 

(SMAQMD), and South Coast Air 

Quality Management District 

(SCAQMD) portions of the California 

State Implementation Plan (SIP). These 

revisions concern volatile organic 

compound (VOC) emissions from 

gasoline dispensing facilities, polyester 

resin operations, and spray booth 

facilities. We are proposing to approve 

local rules to regulate these emission 

sources under the Clean Air Act as 

amended in 1990 (CAA or the Act). 

DATES: Any comments on this proposal 

must arrive by August 25, 2011. 

ADDRESSES: Submit comments, 

identified by docket number EPA–R09– 

OAR–2011–0042, by one of the 

following methods: 

1. Federal eRulemaking Portal: http://

www.regulations.gov. Follow the on-line 

instructions. 

2. E-mail: steckel.andrew@epa.gov. 

3. Mail or deliver: Andrew Steckel 

(Air-4), U.S. Environmental Protection 

Agency Region IX, 75 Hawthorne Street, 

San Francisco, CA 94105–3901. 

Instructions: All comments will be 

included in the public docket without 

change and may be made available 

online at http://www.regulations.gov, 

including any personal information 

provided, unless the comment includes 

Confidential Business Information (CBI) 

or other information whose disclosure is 

restricted by statute. Information that 

you consider CBI or otherwise protected 

should be clearly identified as such and 

should not be submitted through http://

www.regulations.gov or e-mail. http://

www.regulations.gov is an ‘‘anonymous 

access’’ system, and EPA will not know 

your identity or contact information 

unless you provide it in the body of 

your comment. If you send e-mail 

directly to EPA, your e-mail address 

will be automatically captured and 

included as part of the public comment. 

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: The index to the docket for 

this action is available electronically at 

http://www.regulations.gov and in hard 

copy at EPA Region IX, 75 Hawthorne 

Street, San Francisco, California. While 

all documents in the docket are listed in 

the index, some information may be 

publicly available only at the hard copy 

location (e.g., copyrighted material), and 

some may not be publicly available in 

either location (e.g., CBI). To inspect the 

hard copy materials, please schedule an 

appointment during normal business 

hours with the contact listed in the FOR

FURTHER INFORMATION CONTACT section. 

FOR FURTHER INFORMATION CONTACT: 

David Grounds, EPA Region IX, (415) 

972–3019, grounds.david@epa.gov. 

SUPPLEMENTARY INFORMATION: This 

proposal addresses the following local 

rules: NSAQMD Rule 215, SMAQMD 

Rule 465, and SCAQMD Rules 1132 and 

1162. In the Rules and Regulations 

section of this Federal Register, we are 

approving these local rules in a direct 

final action without prior proposal 

because we believe these SIP revisions 

are not controversial. If we receive 

adverse comments, however, we will 

publish a timely withdrawal of the 

direct final rule and address the 

comments in subsequent action based 

on this proposed rule. Please note that 

if we receive adverse comment on an 

amendment, paragraph, or section of 

this rule and if that provision may be 

severed from the remainder of the rule, 

we may adopt as final those provisions 

of the rule that are not the subject of an 

adverse comment. 

We do not plan to open a second 

comment period, so anyone interested 

in commenting should do so at this 

time. If we do not receive adverse 

comments, no further activity is 

planned. For further information, please 

see the direct final action. 

Dated: February 15, 2011. 

Jared Blumenfeld, 

Regional Administrator, Region IX. 

[FR Doc. 2011–18871 Filed 7–25–11; 8:45 am] 

BILLING CODE 6560–50–P 

ENVIRONMENTAL PROTECTION 

AGENCY 

40 CFR Part 799 

[EPA–HQ–OPPT–2010–0812; FRL–8880–3] 

RIN 2070–AJ83 

Testing of Bisphenol A 

AGENCY: Environmental Protection 

Agency (EPA). 

ACTION: Advance notice of proposed 

rulemaking (ANPRM). 

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 


wreier-aviles on DSKDVH8Z91PROD with PROPOSALS
44536 Federal Register / Vol. 76, No. 143 / Tuesday, July 26, 2011 / Proposed Rules 

in the vicinity of expected BPA releases 

to determine whether environmental 

organisms may currently be exposed to 

concentrations of BPA in the 

environment that are at or above levels 

of concern for adverse effects, including 

endocrine-related effects. This ANPRM 

is directed only toward the 

environmental presence and 

environmental effects of BPA. EPA is 

working with the Department of Health 

and Human Services (HHS) on potential 

human health issues, but is not 

considering any additional testing 

specifically in regard to human health 

issues at this time. 

DATES: Comments must be received on 

or before September 26, 2011. 

ADDRESSES: Submit your comments, 

identified by docket identification (ID) 

number EPA–HQ–OPPT–2010–0812, by 

one of the following methods: 

• Federal eRulemaking Portal: http:// 

www.regulations.gov. Follow the on-line 

instructions for submitting comments. 

• Mail: Document Control Office 

(7407M), Office of Pollution Prevention 

and Toxics (OPPT), Environmental 

Protection Agency, 1200 Pennsylvania 

Ave., NW., Washington, DC 20460– 

0001. 

• Hand Delivery: OPPT Document 

Control Office (DCO), EPA East Bldg., 

Rm. 6428, 1201 Constitution Ave., NW., 

Washington, DC. Attention: Docket ID 

Number EPA–HQ–OPPT–2010–0812. 

The DCO is open from 8 a.m. to 4 p.m., 

Monday through Friday, excluding legal 

holidays. The telephone number for the 

DCO is (202) 564–8930. Such deliveries 

are only accepted during the DCO’s 

normal hours of operation, and special 

arrangements should be made for 

deliveries of boxed information. 

Instructions: Direct your comments to 

docket ID number EPA–HQ–OPPT– 

2010–0812. EPA’s policy is that all 

comments received will be included in 

the docket without change and may be 

made available on-line at http:// 

www.regulations.gov, including any 

personal information provided, unless 

the comment includes information 

claimed to be Confidential Business 

Information (CBI) or other information 

whose disclosure is restricted by statute. 

Do not submit information that you 

consider to be CBI or otherwise 

protected through regulations.gov or email. The regulations.gov Web site is an 

‘‘anonymous access’’ system, which 

means EPA will not know your identity 

or contact information unless you 

provide it in the body of your comment. 

If you send an e-mail comment directly 

to EPA without going through 

regulations.gov, your e-mail address 

will be automatically captured and 

included as part of the comment that is 

placed in the docket and made available 

on the Internet. If you submit an 

electronic comment, EPA recommends 

that you include your name and other 

contact information in the body of your 

comment and with any disk or CD-ROM 

you submit. If EPA cannot read your 

comment due to technical difficulties 

and cannot contact you for clarification, 

EPA may not be able to consider your 

comment. Electronic files should avoid 

the use of special characters, any form 

of encryption, and be free of any defects 

or viruses. 

Docket: All documents in the docket 

are listed in the docket index available 

at http://www.regulations.gov. Although 

listed in the index, some information is 

not publicly available, e.g., CBI or other 

information whose disclosure is 

restricted by statute. Certain other 

material, such as copyrighted material, 

will be publicly available only in hard 

copy. Publicly available docket 

materials are available electronically at 

http://www.regulations.gov, or, if only 

available in hard copy, at the OPPT 

Docket. The OPPT Docket is located in 

the EPA Docket Center (EPA/DC) at Rm. 

3334, EPA West Bldg., 1301 

Constitution Ave., NW., Washington, 

DC. The EPA/DC Public Reading Room 

hours of operation are 8:30 a.m. to 4:30 

p.m., Monday through Friday, excluding 

legal holidays. The telephone number of 

the EPA/DC Public Reading Room is 

(202) 566–1744, and the telephone 

number for the OPPT Docket is (202) 

566–0280. Docket visitors are required 

to show photographic identification, 

pass through a metal detector, and sign 

the EPA visitor log. All visitor bags are 

processed through an X-ray machine 

and subject to search. Visitors will be 

provided an EPA/DC badge that must be 

visible at all times in the building and 

returned upon departure. 

FOR FURTHER INFORMATION CONTACT: For 

technical information contact: Mary 

Dominiak, Chemical Control Division 

(7405M), Office of Pollution Prevention 

and Toxics, Environmental Protection 

Agency, 1200 Pennsylvania Ave., NW., 

Washington, DC 20460–0001; telephone 

number: (202) 564–8104; e-mail address: 

dominiak.mary@epa.gov. 

For general information contact: The 

TSCA-Hotline, ABVI-Goodwill, 422 

South Clinton Ave., Rochester, NY 

14620; telephone number: (202) 554– 

1404; e-mail address: TSCAHotline@epa.gov. 

SUPPLEMENTARY INFORMATION: 

I. General Information 

A. Does this action apply to me? 

You may be potentially affected by 

this action if you manufacture (defined 

by statute to include import) or process 

BPA (CASRN 80–05–7). BPA is listed on 

the Toxic Substances Control Act 

(TSCA) Chemical Substance Inventory 

(TSCA Inventory) under the name 

phenol, 4,4’-(1-methylethylidene)bis-. 

Potentially affected entities may 

include, but are not limited to: 

• Chemical manufacturers (including 

importers) (NAICS codes 325, 32411), 

e.g., chemical manufacturing and 

petroleum refineries of BPA. 

• Plastics material and resin 

manufacturers (NAICS code 325211), 

e.g., manufacturers and processors of 

BPA-based polycarbonate plastics and 

epoxy resins. 

• Foundries (NAICS codes 331512, 

331524, 331528), e.g., steel investment 

foundries, aluminum foundries, and 

other non-ferrous foundries, except diecasting, 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. 


wreier-aviles on DSKDVH8Z91PROD with PROPOSALS
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1EPA’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 

Continued 

B. What should I consider as I prepare 

my comments for EPA? 

1. Submitting CBI. Do not submit this 

information to EPA through 

regulations.gov or e-mail. Clearly mark 

the part or all of the information that 

you claim to be CBI. For CBI 

information in a disk or CD-ROM that 

you mail to EPA, mark the outside of the 

disk or CD-ROM as CBI and then 

identify electronically within the disk or 

CD-ROM the specific information that is 

claimed as CBI. In addition to one 

complete version of the comment that 

includes information claimed as CBI, a 

copy of the comment that does not 

contain the information claimed as CBI 

must be submitted for inclusion in the 

public docket. Information so marked 

will not be disclosed except in 

accordance with procedures set forth in 

40 CFR part 2. 

2. Tips for preparing your comments. 

When submitting comments, remember 

to: 

i. Identify the document by docket ID 

number and other identifying 

information (subject heading, Federal 

Register date and page number). 

ii. Follow directions. The Agency may 

ask you to respond to specific questions 

or organize comments by referencing a 

Code of Federal Regulations (CFR) part 

or section number. 

iii. Explain why you agree or disagree; 

suggest alternatives and substitute 

language for your requested changes. 

iv. Describe any assumptions and 

provide any technical information and/ 

or data that you used. 

v. If you estimate potential costs or 

burdens, explain how you arrived at 

your estimate in sufficient detail to 

allow for it to be reproduced. 

vi. Provide specific examples to 

illustrate your concerns and suggest 

alternatives. 

vii. Explain your views as clearly as 

possible, avoiding the use of profanity 

or personal threats. 

viii. Make sure to submit your 

comments by the comment period 

deadline identified. 

II. Background 

A. What action is the agency taking? 

As a follow-up to the BPA Action 

Plan released on March 29, 2010 (Ref. 

1), EPA is issuing this ANPRM under 

TSCA section 4(a) (15 U.S.C. 2603(a)) to 

solicit public input on the necessity for 

and best approach to obtain 

environmental effects, exposure, and 

pathway information relevant to a 

determination that BPA either does or 

does not present an unreasonable risk of 

injury to the environment. In particular, 

EPA requests comment on: 

1. Whether EPA should propose 

requiring specific toxicity testing to 

more fully characterize the effects of 

BPA on environmental organisms at low 

concentrations. 

2. Whether EPA should propose 

requiring environmental testing 

consisting of sampling and monitoring, 

particularly in the vicinity of reported 

releases of BPA into the environment, 

and what design and protocol it should 

use for such sampling and monitoring, 

in order to identify potential sources 

and pathways of exposure and 

determine the extent to which 

environmental organisms may be 

exposed to BPA concentrations of 

concern as determined by existing data 

and by additional studies that are either 

already underway or would be 

conducted under a test rule. 

3. EPA additionally requests comment 

and supporting information regarding 

which TSCA section 4(a)(1) finding 

authority would be most appropriate for 

the purpose of a BPA test rule proposal, 

as discussed in Unit II.C. Any proposal 

would ultimately be based on EPA’s 

assessment of the relevant information 

available at the time of proposal. 

B. What testing is EPA considering in 

this ANPRM? 

In this ANPRM, EPA is considering 

requiring both toxicity testing for 

environmental organisms exposed to 

BPA and environmental testing 

consisting of sampling and monitoring 

in the vicinity of reported BPA releases 

to measure its environmental presence. 

The toxicity testing is being considered 

to resolve existing uncertainties 

concerning the potential for BPA to 

elicit adverse effects in ecologically 

relevant species, including endocrinerelated impacts that could occur at low 

doses. The environmental testing is 

being considered to resolve existing 

uncertainties concerning potential 

sources of and pathways leading to 

environmental exposures and to 

determine whether or not the 

concentrations to which organisms 

currently may be exposed in the 

environment are at or above levels of 

concern for adverse effects, including 

endocrine-related effects. 

On May 17, 1985, EPA published in 

the Federal Register a proposed rule (50 

FR 20691) to require human health and 

environmental testing in response to the 

TSCA Interagency Testing Committee’s 

(ITC) 14th report published in the 

Federal Register issue of May 29, 1984 

(49 FR 22389), which designated BPA 

for priority consideration for health and 

environmental effects. EPA proposed 

standard freshwater and marine acute 

fish and aquatic invertebrate toxicity 

tests, and freshwater aquatic plant 

toxicity tests. Test results were 

submitted in response to the proposal 

for freshwater and marine acute fish, 

acute aquatic invertebrate, and algal 

toxicity. EPA’s final rule published in 

the Federal Register issue of September 

18, 1986 (51 FR 33047) (1986 Final 

Rule), terminated the test rule process 

for environmental effects testing for 

BPA. At the time, EPA determined that 

the test data were adequate and that 

chronic freshwater organism testing was 

not needed because the LC50 values for 

the standard acute aquatic organism 

toxicity tests were greater than 1.0 parts 

per million (ppm) (1 milligram/Liter 

(mg/L)), and the ratios of 48-hour to 96- 

hour LC50 values were not greater than 

2. Since the 1986 Final Rule, however, 

several studies on BPA have raised 

concerns about its environmental effects 

at concentrations less than 1.0 ppm (1 

mg/L). 

As stated in the BPA Action Plan (Ref. 

1), EPA does not intend to initiate 

regulatory action under TSCA at this 

time on the basis of human health. EPA 

remains committed to protecting human 

health, but notes that most human 

exposure, including exposure to 

children, comes through food packaging 

materials under the jurisdiction of the 

Food and Drug Administration (FDA) in 

HHS. FDA, together with the Centers for 

Disease Control and Prevention (CDC) 

and the National Institute of 

Environmental Health Sciences 

(NIEHS), is investing in important new 

health studies in both animals and 

humans to better determine and 

evaluate the potential health 

consequences of BPA exposures. EPA 

will continue to coordinate closely with 

FDA, CDC, and NIEHS on this activity. 

To the extent that FDA may identify 

health concerns from BPA in food 

contact materials, EPA will work with 

FDA to identify and assess potential 

substitutes. Levels of exposure that may 

be identified by the ongoing review as 

being of concern to human health, 

including children’s health, will affect 

the extent to which EPA would take 

additional action to address potential 

risks to human health resulting from 

uses within TSCA jurisdiction. 

1. What is currently known about the 

environmental hazard of BPA? The 

toxicity of BPA has been studied 

extensively, as indicated in the multiple 

studies cited in the BPA Action Plan 

(Ref. 1).1 There is general agreement 


wreier-aviles on DSKDVH8Z91PROD with PROPOSALS
44538 Federal Register / Vol. 76, No. 143 / Tuesday, July 26, 2011 / Proposed Rules 

available at http://www.epa.gov/quality/ 

informationguidelines/iqg-list.html. 

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 ≥ 

50 mg/kilogram-body weight (kg-bw)/ 

day (delayed puberty in male and 

female rats and male mice; discussed in 

Refs. 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; 

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 lowdose effects on puberty and neurological 

development (brain, behavior; Ref. 9) at 

doses in animal studies as low as 2 

microgram (μg)/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. 

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 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 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 

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 assessment guidance 

for evaluating some of these endocrinerelated 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 

(microgram/Liter 

(μg/L)) 1

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 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). 


wreier-aviles on DSKDVH8Z91PROD with PROPOSALS
Federal Register / Vol. 76, No. 143 / Tuesday, July 26, 2011 / Proposed Rules 44539 

2The starting date of 2007 was used to allow for 

some overlap between the thorough searches done 

by Canada, the EU, and Japan. 

TABLE 1—SUMMARY OF BISPHENOL A ECOLOGICAL VALUES—Continued 

Country 

Predicted no effect 

concentrations 

(microgram/Liter 

(μg/L)) 1

Endpoints 

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) multi-generation fish study and dividing by an uncertainty factor of 10 

(Ref. 8). 

1 In the European Union, Canada, and Japan, a predicted no effect concentration (PNEC) is compared directly with an exposure value to 

evaluate risk. If the ratio of environmental concentration to PNEC is less than one, the risk is generally considered acceptable. As noted in the 

table, countries use different approaches for generating PNECs, and the precise values may differ even when based on the same studies. 

EPA considers that the uncertainty 

demonstrated by these divergent 

opinions concerning interpretation of 

the results of existing environmental 

toxicity studies, particularly studies 

addressing potential effects at low levels 

of exposure, may indicate further testing 

is necessary to resolve the question of 

whether or not BPA presents an 

unreasonable risk of injury to the 

environment on the basis of those 

effects. This is due to the combination 

of the existence of measured values, as 

discussed in Unit II.B.4. and as shown 

in that unit’s Table 3, for BPA in U.S. 

surface waters at a mean-concentration 

range of up to 1.78 μg/L (parts per 

billion (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 (ppb) 

dry weight and a maximum 

concentration of 140 μg/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 μg/L). These sublethal effects in both vertebrates and 

invertebrates could be mediated either 

through endocrine or non-endocrinerelated 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. 

TABLE 2—SUMMARY OF REPORTED HAZARD EFFECTS OF BISPHENOL A AT POTENTIALLY ENVIRONMENTALLY RELEVANT

CONCENTRATIONS

Test organism Endpoint 

Effect 

concentrations 

(microgram/Liter (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. 


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TABLE 2—SUMMARY OF REPORTED HAZARD EFFECTS OF BISPHENOL A AT POTENTIALLY ENVIRONMENTALLY RELEVANT

CONCENTRATIONS—Continued 

Test organism Endpoint 

Effect 

concentrations 

(microgram/Liter (μg/L)) 

References 

(Listed in Ref. 14) 

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 sperm cells.50 ..................................... Metcalfe et al., 2001. 

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 Ministry of the Environment, 2006. 

Orizias latipes ........................ Increased male hepatosomatic index .......... 49.7 .................................. Japanese Ministry of the Environment, 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 °C .................... Oehlmann et al., 2006. 

Marisa cornuarietis ................ Increased egg production ............................. 0.25 at 27 °C .................... Oehlmann et al., 2006. 

Marisa cornuarietis ................ Increased clutch production ......................... 5 at 27 °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. 

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., 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 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 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 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 


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3Recent 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). 

chemicals. They suggest inhibition of 

reproduction and development at low 

concentrations and overcompensation 

by the organism at higher 

concentrations in response to a toxicant 

(Ref. 23). 

It is difficult to interpret this 

information in a regulatory context, 

because the scientific methods 

employed in individual academic 

settings to test a hypothesis are not 

necessarily geared toward meeting or 

establishing generally applicable 

guidelines for evaluating ecotoxicity 

and setting corresponding regulatory 

limits or controls. In terms of 

environmental toxicity, EPA considers 

the currently available research as 

evidence that BPA has the potential to 

interact with the estrogen hormone 

system. There is some evidence that 

BPA is also active via the thyroid 

hormone pathway in amphibians and 

fish (Refs. 24 and 25). More recent 

evidence indicates that BPA also acts as 

an androgen receptor antagonist in both 

mammals and fish (Ref. 26). There are 

currently efforts underway by EPA’s 

Office of Science Coordination and 

Policy (OSCP) through the Endocrine 

Disruptor Screening Program (EDSP) 

and the Organization for Economic 

Cooperation and Development (OECD) 

Endocrine Disrupter Testing and 

Assessment Work Group (EDTAWG), 

among others, to determine the best 

approach to evaluate and assess such 

effects (Refs. 27–29). 

EPA is inviting comment on the need 

to further determine the hazard of BPA 

to various ecological species. The 

purpose of further testing would be to 

produce high quality data that could be 

used for risk assessment purposes for 

any adverse reproductive or 

developmental effects in different 

species that might result from the 

interactions identified through the 

available research. 

3. What are the issues for comment 

concerning toxicity testing? EPA invites 

comment on whether and what testing 

should be required to further describe 

the hazard of BPA to various ecological 

species to resolve the low dose effects 

issue. EPA particularly invites comment 

on the following, for which little or no 

clarifying hazard information appears to 

be currently available or for which 

much of the available data have been 

derived from studies of questionable 

quality or uncertain interpretation: 

a. Effects of BPA on fish in long-term 

tests, including those that encompass 

multiple generations. 

b. Effects of BPA on amphibians at 

sensitive life stages, specifically 

metamorphosis (thyroid effects) and 

sexual development/differentiation 

(hypothalamic-pituitary-gonadal axis 

effects). 

c. Effects of BPA on birds over 

multiple generations. 

d. Effects of BPA on aquatic 

invertebrate species. 

EPA further invites comment on the 

availability of current test guidelines 

that could help address these issues. 

This may include, for example, 

considering the draft recommendations 

concerning aquatic life criteria for 

contaminants of emerging concern (Ref. 

30). Additionally, EPA is inviting the 

public to describe and define where 

they believe there are data gaps 

concerning the environmental toxicity 

of BPA, especially at low 

concentrations, or whether and on what 

basis they believe the current data are 

sufficient to determine whether BPA 

does or does not present an 

unreasonable risk of injury to the 

environment. 

4. What levels of BPA are present in 

the U.S. environment? BPA is present in 

the environment as a result of direct 

releases from manufacturing or 

processing facilities (Ref. 31). BPA also 

may be present in the environment as a 

result of fugitive emissions during 

processing and handling, release of 

unreacted monomer from products (Ref. 

9), or possibly from degradation of 

products under certain conditions. In 

addition, although no environmental 

studies on thermal paper have been 

done in the United States, based on 

information from EPA’s review of 

European and Japanese studies, the use 

of unconjugated BPA in thermal paper 

also may contribute to environmental 

releases of BPA from paper 

manufacturing and recycling plants and 

to the presence of BPA in the stream of 

recycled paper used in toilet paper, 

paper tableware, and other products, 

and may contribute to the presence of 

BPA in landfills because paper products 

are a major contributor to the U.S. solid 

waste stream (Refs. 7, 32–36).3

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 

μg/L (ppb), mainly due to its 

partitioning and biodegradability 

properties (Ref. 42). 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. 43). 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 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 μg/L (ppb) and the 

95th percentile concentration was 0.47 

μg/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 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. 45). A 2008 study 


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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 

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. 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 μg/L (ppb) (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. 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 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, 

Canada, 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. 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 μg/kg (ppb) 

(median 4,690 μg/kg (ppb)) (Ref. 49). 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 landapplied biosolids (Ref. 50). That study 

detected 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 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 μg/L 

(ppb) and a range of 1.06 to 2.55 μg/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 μg/L 

(ppb). The maximum concentration 

measured in these samples was 1.9 μg/ 

L (ppb) (Refs. 51 and 53). 

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 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 μg/L (ppb) of BPA (Ref. 

42). Studies conducted at Japanese 

landfills resulted in maximum untreated 

leachate concentrations of 17,200 μg/L 

(ppb) and treated leachate 

concentrations of 5.1 μg/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 

Location 

Mean or range of means 

(parts per 

billion (ppb)) 

Range (ppb) References 

Surface Water ...................... <0.0001 to 0.14* ................ <0.0001 to 12 .................... Barnes et al., 2008a (Ref. 51). 

Boyd et al., 2003 (Ref. 45). 

Boyd et al., 2004 (Ref. 57). 

Focazio et al., 2008 (Ref. 53). 

Klecka et al., 2009 (Ref. 44). 

Kolpin et al., 2002 (Ref. 43). 

Staples et al., 2000 (Ref. 58). 

Zhang et al., 2007 (Ref. 59). 

Ground Water ...................... NR** to 1.78 † .................... <0.003 to 2.55 ................... Barnes et al., 2008a (Ref. 51). 

Barnes et al., 2008b (Ref. 52). 

Focazio et al., 2008 (Ref. 53). 

Rudel et al., 1998 (Ref. 54). 


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4EPA’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. 

TABLE 3—U.S. REPORTED ENVIRONMENTAL CONCENTRATIONS OF BISPHENOL A—Continued 

Location 

Mean or range of means 

(parts per 

billion (ppb)) 

Range (ppb) References 

Drinking Water ..................... <0.0001 ............................. <0.0001 to 0.42 ................. Boyd et al., 2003 (Ref. 45). 

Stackelberg et al., 2004 (Ref. 60). 

Wastewater .......................... <0.0001 ............................. <0.0001 to 25 .................... Boyd et al., 2003 (Ref. 45). 

Drewes et al., 2005 (Ref. 61). 

Jackson and Sutton, 2008 (Ref. 46). 

Rudel et al., 1998 (Ref. 54) 

Tsai, 2006 (Ref. 42). 

Soils ..................................... 6 to 7 ................................. 4 to 147 ............................. Kinney et al., 2008 (Ref. 50). 

Wilson et al., 2003 (Ref. 55). 

Sediment, Fresh .................. 0.6* †† ................................ 1.4 to 140 †† ...................... Klecka et al., 2009 (Ref. 44). 

Sediment, Marine ................ 3.5* .................................... 1.5 to 5.0 ........................... Stuart et al., 2005 (Ref. 56). 

Biosolids .............................. 4,600 to 4,690* .................. 1,090–14,400 ..................... Kinney et al., 2006 (Ref. 49). 

Kinney et al., 2008 (Ref. 50) 

* Value is median. 

** Not reported (NR). 

† Mean of values above reporting limit (1 ppb). 

†† 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 μg/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 μg/L (ppb) (surface water), 

2.55 μg/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

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 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 to the environment 

exists. To help resolve these 

uncertainties, EPA is considering 

requiring that manufacturers and 

processors of BPA conduct 

environmental testing consisting of 

targeted sampling and monitoring of 

surface water, ground water, sediment, 

soil, landfill leachate, and drinking 

water on and adjacent to their 

properties, specifically in the vicinity of 

manufacturing facilities and such 

processing facilities as foundries, 

WWTPs, paper and plastics recycling 

facilities, and other sources of BPA 

releases as identified through TRI 

reporting and other information. These 

test data could also help guide 

development of effective risk 

management actions if it should be 

determined that activities involving 

BPA present an unreasonable risk of 

injury to aquatic or other environmental 

systems. 

Fully understanding exposure 

pathways and in particular the 

magnitude, frequency, and duration of 

exposure could require a nationwide 

survey of the occurrence of the chemical 

in environmental media associated with 

production, processing, use, disposal, 

and recycling facilities. However, at this 

time, EPA is proposing that selected 

monitoring of a more limited scope be 

conducted to help identify the most 

likely locations of high exposure and 

the sources and pathways of exposure, 

to determine whether BPA may be 

present in those locations at 

concentrations that pose a risk of 

concern to aquatic or other systems. 

Monitoring of aquatic sites and 

sediments near releases (effluents and 

sludge) from manufacturing and 

processing sites (including on-site 

WWTPs) reporting high releases under 

TRI or associated with high releases 

identified from other information, as 

well as monitoring of sites that receive 

runoff from landfills, would be 

included. 

EPA believes these targeted 

monitoring data may provide 

information relevant both to the 

characterization of environmental risk 

and to the potential focus of future risk 

management activities such as those 

under TSCA section 6, if the data 

indicate such activities are warranted. 

EPA also considers these data would 

further inform the issue of potential 

human exposure levels attributable to 

sources other than the direct food 


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5EPA notes, however, that information obtained 

on the environmental presence of BPA would be 

relevant to understanding the environmental 

component of human exposures. 

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

In order to be useful to an 

investigation of potential environmental 

risks posed by BPA, environmental 

testing must be representative and of 

known quality. To accomplish this, data 

should be collected using approved or 

recognized sampling, preparation, and 

analytical techniques. Appropriate 

quality assurance and quality controls 

also should be incorporated in the 

protocols for collection and analyses. 

A further complicating factor in the 

assessment of potential environmental 

risks posed by BPA is that organisms in 

the environment, rather than being 

exposed to a single chemical at a time, 

are likely to be exposed simultaneously 

to multiple chemicals. The presence of 

other endocrine-active chemicals, 

including other estrogenic chemicals, 

for example, could affect the potential 

for effects on environmental organisms. 

It may be useful, when monitoring for 

BPA, to identify the total estrogenicity 

of a sample along with the amount of 

BPA present. 

Potential methodologies and protocols 

for use in monitoring programs may 

include ASTM D7574–09 Standard Test 

Method for Determination of Bisphenol 

A in Environmental Waters by Liquid 

Chromatography/Tandem Mass 

Spectrometry (Ref. 62); ASTM D5730– 

04 Standard Guide for Site 

Characterization for Environmental 

Purposes With Emphasis on Soil, Rock, 

the Vadose Zone and Ground Water 

(Ref. 63); EPA Method 8270D (SW–846), 

Semivolatile Organic Compounds by 

Gas Chromatography/Mass 

Spectrometry (GC/MS), Revision 4 (Ref. 

64); and other methods cited and 

described in such publications as 

Barnes et al. (2008) (Ref. 51) and 

Focazio et al. (2008) (Ref. 53). 

5. What are the issues for comment 

concerning environmental testing 

consisting of sampling and monitoring? 

EPA particularly invites comment on: 

a. The extent and type of 

environmental testing that may be 

sufficient to characterize the 

environmental presence of BPA. 

b. The extent and type of 

environmental testing that may be 

sufficient to understand sources of and 

exposure from the high concentrations 

of BPA found in treated biosolids from 

WWTPs. 

c. Whether environmental testing 

should be conducted now, or should be 

tiered to occur after the uncertainties 

associated with the hazards of BPA at 

low concentrations in the environment 

have been resolved. 

d. The locations where such 

environmental testing should be 

undertaken, such as manufacturing, 

processing, recycling, foundry, and 

other use, treatment, and disposal sites 

identified with BPA releases reported 

under TRI or other information. 

e. The media (e.g., soil, sediment, 

sludge, WWTP influent and effluent, 

landfill leachate, drinking water, surface 

water, ground water) to be sampled at 

each such site. 

f. Which parties should be required to 

conduct the testing and/or be 

potentially responsible for providing 

reimbursement to those who conduct 

specific tests. 

g. The appropriate methods and 

protocols to use in such a 

environmental testing program. 

h. Whether such an environmental 

testing program should include 

measurements for the total estrogenicity 

of samples collected as well as for the 

concentration of BPA, and what 

methods and protocols may be suitable 

for generating and interpreting such 

data. 

i. Whether and what additional 

environmental testing activities may be 

necessary to understand and 

characterize non-food-contact uses, 

sources, and environmental pathways 

that may contribute to exposure to BPA. 

Though, as indicated in Unit II.B., the 

current focus of this ANPRM is on 

environmental effects, this information 

would inform the multi-agency effort to 

evaluate the potential human health 

consequences of BPA exposures. 

j. Other information that may provide 

insight into sources and pathways of 

environmental and human exposure to 

BPA released into the environment. 

Though, as indicated in Unit II.B., the 

current focus of this ANPRM is on 

environmental effects, this information 

would inform the multi-agency effort to 

evaluate the potential human health 

consequences of BPA exposures. 

k. The cost and economic feasibility 

of such environmental testing, for the 

different types of sites. 

C. What is the agency’s authority for 

taking this action? 

EPA is issuing this ANPRM on certain 

toxicity testing and on certain 

environmental testing consisting of 

sampling and monitoring for the 

chemical substance BPA under TSCA 

section 4(a) (15 U.S.C. 2603(a)). 

Section 2(b)(1) of TSCA (15 U.S.C. 

2601(b)) states that it is the policy of the 

United States that ‘‘adequate data 

should be developed with respect to the 

effect of chemical substances and 

mixtures on health and the environment 

and that the development of such data 

should be the responsibility of those 

who manufacture [which is defined by 

statue to include import] and those who 

process such chemical substances and 

mixtures[.]’’ To implement this policy, 

TSCA section 4(a)(1) provides that EPA 

shall require by rule that manufacturers 

or processors or both of chemical 

substances and mixtures conduct 

testing, if the Administrator finds in a 

final rule that: 

(A)(i) the manufacture, distribution in 

commerce, processing, use, or disposal of a 

chemical substance or mixture, or that any 

combination of such activities, may present 

an unreasonable risk of injury to health or the 

environment, 

(ii) there are insufficient data and 

experience upon which the effects of such 

manufacture, distribution in commerce, 

processing, use, or disposal of such substance 

or mixture or any combination of such 

activities on health or the environment can 

reasonably be determined or predicted, and 

(iii) testing of such substances or mixture 

with respect to such effects is necessary to 

develop such data; or 

(B)(i) a chemical substance or mixture is or 

will be produced in substantial quantities, 

and (I) it enters or may reasonably be 

anticipated to enter the environment in 

substantial quantities or (II) there is or may 

be significant or substantial human exposure 

to such substance or mixture, 

(ii) there are insufficient data and 

experience upon which the effects of the 

manufacture, distribution in commerce, 

processing, use, or disposal of such substance 

or mixture or of any combination of such 

activities on health or the environment can 

reasonably be determined or predicted, and 

(iii) testing of such substance or mixture 

with respect to such effects is necessary to 

develop such data and 

(C) in the case of a mixture, the effects 

which the mixture’s manufacture, 

distribution in commerce, processing, use or 

disposal or any combination of such 

activities may have on health or the 

environment may not be reasonably and 

more efficiently determined or predicted by 


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testing the chemical substances which 

comprise the mixture[.] 

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

If EPA in a final rule makes an 

appropriate finding under TSCA section 

4(a)(1)(A) or (B) for a chemical 

substance or mixture, the Administrator 

shall require that testing be conducted 

on that chemical substance or mixture. 

The purpose of the testing would be to 

develop data with respect to the health 

and environmental effects for which 

there is an insufficiency of data and 

experience, and which are relevant to a 

determination that the manufacture, 

distribution in commerce, processing, 

use, or disposal of the substance or 

mixture, or any combination of such 

activities, does or does not present an 

unreasonable risk of injury to health or 

the environment. As indicated in Unit 

II.A.3., EPA requests comment and 

supporting information regarding which 

TSCA section 4(a)(1) finding authority 

would be most appropriate for the 

purpose of a BPA test rule proposal. 

Any proposal would ultimately be based 

on EPA’s assessment of the relevant 

information available at the time of 

proposal. 

Once the Administrator has made the 

relevant findings under TSCA section 

4(a), EPA may require any health or 

environmental effects testing for which 

data are insufficient and which are 

necessary to develop the data. EPA need 

not limit the scope of testing required to 

the factual basis for the TSCA section 

4(a)(1)(A)(i) or (B)(i) findings as long as 

EPA also finds that there are insufficient 

data and experience upon which the 

effects of the manufacture, distribution 

in commerce, processing, use, or 

disposal of such substance or mixture or 

of any combination of such activities on 

health or the environment can 

reasonably be determined or predicted, 

and that testing is necessary to develop 

such data. This approach is explained in 

more detail in EPA’s TSCA section 

4(a)(1)(B) Final Statement of Policy (B 

Policy) published in the Federal 

Register issue of May 14, 1993 (58 FR 

28736, 28738–28739). 

Authority for requiring sampling and 

monitoring for a chemical substance or 

mixture can be found within TSCA 

section 4. Section 4(a) of TSCA 

authorizes EPA to require the 

development of data ‘‘which are 

relevant to a determination that the 

manufacture, distribution in commerce, 

processing, use, or disposal of such 

substance or mixture, or that any 

combination of such activities, does or 

does not present an unreasonable risk of 

injury to health and the environment.’’ 

The extent to which such activities may 

affect health or the environment is 

dependent in part upon the human and 

environmental exposures to the 

chemical substance occasioned by those 

activities. As an example, TSCA section 

4(a)(2)(A) specifically addresses testing 

for persistence of a substance. Testing to 

identify where and in what 

concentrations a chemical substance or 

mixture may become present in the 

environment contributes to an 

understanding of human and 

environmental exposures resulting from 

those activities. As stated in Unit II.B., 

EPA does not intend to initiate 

regulatory action under TSCA at this 

time on the basis of human health. 

III. References 

1. EPA. 2010. Bisphenol A Action Plan. 

Available on-line at http:// 

www.regulations.gov/#!document

Detail;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%20

Assessment.pdf. Peer review report and 

additional information available on-line 

at http://www.fda.gov/Food/Food

IngredientsPackaging/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 

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Centre, European Commission. 

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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. Available on-line at http:// 

www.fda.gov/NewsEvents/

PublicHealthFocus/ucm197739.htm. 

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. Reproductive 

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12. Lahnsteiner, F.; Berger, B.; Kletzl, M.; and 

Weismann, T. 2005. Effect of Bisphenol 

A on Maturation and Quality of Semen 

and Eggs in the Brown Trout, Salmo 

trutta f. fario. Aquatic Toxicology. Vol. 

75:213–224. 

13. EPA. 2010. List of References to BPARelated 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 

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16. Watts, M.M.; Pascoe, D.; and Carroll, K. 

2001. Chronic exposure to 17aethinylestradiol and bisphenol A-effects 

on development and reproduction in the 

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17. Sumpter, J.P.; Tyler, C.R.; Sherazi, A. 

2001. Bisphenol-A: Multigeneration 

study with the fathead minnow 

(Pimephales promelas). Brunel 

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18. Oehlmann, J.; Schulte-Oehlmann, U.; 

Werner, K.; Jagnytsch, O.; Lutz, I.; 

Kresten, K.; Wollenberger, L.; Santos, 

E.M.; Paull, G.C.; Van Look, K.J.W.; and 

Tyler, C.R. 2008. A Critical Analysis of 

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Aufderheide, J.; Warbritton, R.; Pounds, 

N.; Thompson, R.; van der Hoeven, N.; 

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induce superfeminization in Marisa 


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24. Heimeier, R.A.; Das, B.; Buchholz, D.R.; 

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32. Vinggaard, A.M.: Ko ̈rner, W.; Lund, K.H.; 

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other anthropogenic waste indicators in 

earthworms from agricultural soil 

amended with biosolid or swine manure. 

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51. Barnes, K.K.; Kolpin, D.W.; Focazio, M.J.; 

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E.M. 2008a. U. S. Geological Survey. 

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Septage, and Groundwater on Cape Cod, 

MA. Environmental Science & 

Technology. Vol. 32:861–869. 

55. Wilson, N.K.; Chuang, J.C.; Lyu, C.; 

Menton, R.; and Morgan, M.K. 2003. 

Aggregate exposures of nine preschool 

children to persistent organic pollutants 

at day care and home. Journal of 

Exposure Analysis and Environmental 

Epidemiology. Vol. 13:187–202. 

56. Stuart, J.D.; Capulong, C.P.; Launer, K.D.; 

and Pan, X. 2005. Analyses of phenolic 

endocrine disrupting chemicals in 

marine samples by both gas and liquid 

chromatography-mass spectrometry. 

Journal of Chromatography A. Vol. 

1079:136–145. 

57. Boyd, G.R.; Palmerib, J.M.; and 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. The 

Science of the Total Environment. Vol. 

333:137–48. 

58. Staples, C.A.; Dorn, P.B.; Klecka, G.M.; 

O’Block, S.T.; Branson, D.R.; and Harris, 

L.R. 2000. Bisphenol A Concentrations 

in Receiving Waters Near U.S. 

Manufacturing and Processing Facilities. 

Chemosphere. Vol. 40:521–525. 

59. Zhang, S.; Zhang, Q.; Darisaw, S.; Ehie, 

O.; and 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. Vol. 

66:1057–1069. 

60. Stackelberg, P.E.; Furlong, E.T.; Meyer, 

M.T.; Zaugg, S.D.; Henderson, A.K.; and 

Reissman, D.B. 2004. Persistence of 

Pharmaceutical Compounds and Other 

Organic Wastewater Contaminants in a 

Conventional Drinking-Water-Treatment 

Plant. The Science of the Total 

Environment. Vol. 329:99–113. 

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 Chemical Measurements. Water 

Environment Research. Vol. 77:12–23. 

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 http:// 

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

63. ASTM. 2004. ASTM D5730–04 Standard 

Guide for Site Characterization for 

Environmental Purposes With Emphasis 

on Soil, Rock, the Vadose Zone and 

Ground Water. Available on-line at 

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

D5730.htm. 

64. EPA. 1998. Method 8270D (SW–846), 

Semivolatile Organic Compounds by Gas 

Chromatography/Mass Spectrometry 

(GC/MS), Revision 4. Available on-line at 

http://www.epa.gov/sam/pdfs/EPA8270d.pdf. 

IV. Statutory and Executive Order 

Reviews 

Under Executive Order 12866, 

entitled ‘‘Regulatory Planning and 

Review’’ (58 FR 51735, October 4, 1993), 

this action was submitted to the Office 

of Management and Budget (OMB) for 

review. Any changes made to this 

document in response to OMB 

comments received by EPA during that 

review have been documented in the 

docket as required by the Executive 

Order. 

Since this document does not impose 

or propose any requirements, and 

instead seeks comments and suggestions 

for the Agency to consider in possibly 

developing a subsequent proposed rule, 

the various other review requirements 

that apply when an agency imposes 

requirements do not apply to this 

action. Nevertheless, as part of your 

comments on this ANPRM, you may 

include any comments or information 

that you have regarding this action. 

In particular, any comments or 

information that would help the Agency 

to assess the potential impact of a rule 

on small entities pursuant to the 

Regulatory Flexibility Act (RFA) (5 

U.S.C. 601 et seq.); to consider 

voluntary consensus standards pursuant 

to section 12(d) of the National 

Technology Transfer and Advancement 

Act of 1995 (NTTAA) (15 U.S.C. 272 

note); to consider environmental health 

or safety effects on children pursuant to 

Executive Order 13045, entitled 

‘‘Protection of Children from 

Environmental Health Risks and Safety 

Risks’’ (62 FR 19885, April 23, 1997); or 

to consider human health or 

environmental effects on minority or 

low-income populations pursuant to 

Executive Order 12898, entitled 

‘‘Federal Actions to Address 

Environmental Justice in Minority 

Populations and Low-Income 

Populations’’ (59 FR 7629, February 16, 

1994). 

The Agency will consider such 

comments during the development of 

any subsequent proposed rule as it takes 

appropriate steps to address any 

applicable requirements. 

List of Subjects in 40 CFR Part 799 

Environmental protection, Bisphenol 

A, BPA, Chemicals, Hazardous 

substances, Reporting and 

recordkeeping requirements. 

Dated: July 20, 2011. 

Stephen. A. Owens, 

Assistant Administrator, Office of Chemical 

Safety and Pollution Prevention. 

[FR Doc. 2011–18842 Filed 7–25–11; 8:45 am] 

BILLING CODE 6560–50–P 

DEPARTMENT OF THE INTERIOR 

Fish and Wildlife Service 

50 CFR Part 17 

[Docket No. FWS–R1–ES–2010–0023; MO 

92210–0–008–B2] 

Endangered and Threatened Wildlife 

and Plants; 12-Month Finding on a 

Petition To List the Giant Palouse 

Earthworm (Drilolerius americanus) as 

Threatened or Endangered 

AGENCY: Fish and Wildlife Service, 

Interior. 

ACTION: Notice of 12-month petition 

finding. 

SUMMARY: We, the U.S. Fish and 

Wildlife Service (Service), announce a 

12-month finding on a petition to list 

the giant Palouse earthworm (Driloleirus 

americanus) as threatened or 

endangered as petitioned, and to 

designate critical habitat under the 

Endangered Species Act of 1973, as 

amended (Act). After review of all 

available scientific and commercial 

information, we find that listing the 

giant Palouse earthworm is not 

warranted at this time. However, we ask 

the public to submit to us any new 

information that becomes available 

concerning the threats to the giant 

Palouse earthworm or its habitat at any 

time. 

DATES: The finding announced in this 

document was made on July 26, 2011. 

ADDRESSES: This finding is available on 

the Internet at http:// 

www.regulations.gov at Docket Number 

FWS–R1–ES–2010–0023. Supporting 

documentation we used in preparing 

this finding is available for public 

inspection, by appointment, during 

normal business hours at the U.S. Fish 

and Wildlife Service, Washington Fish 

and Wildlife Office, 510 Desmond Drive 

SE., Suite 102, Lacey, WA 98503–1263; 

telephone 360–753–9440; facsimile 

360–753–9008. Please submit any new 

information, materials, comments, or 

questions concerning this finding to the 

above street address. 

FOR FURTHER INFORMATION CONTACT: Ken 

Berg, Manager, Washington Fish and 

Wildlife Office (see ADDRESSES). If you 

use a telecommunications device for the 

deaf (TDD), please call the Federal 


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