U.S. Environmental Protection Agency Draft, 12/9/20092/25/2010

U.S. Government Internal Deliberative Document, Do Not Quote, Cite, or Release 

Bisphenol A Action Plan

(CASRN 80-05-7) 

[CA Index Name: Phenol, 4,4'-(1-methylethylidene)bis-] 

I. Overview

 Bisphenol A (BPA) is a high production volume (HPV) chemical widely used in 

manufacturing polycarbonate plastics and epoxy resins used in many industries. Humans appear 

to be exposed primarily through food packaging uses of products manufactured using BPA, 

although those products account for less than 5% of the BPA used in this country. Releases of 

BPA to the environment exceed one million pounds per year. 

 EPA intends to initiateconsider initiating immediate actions addressing BPA in the 

environment based on concerns for potential effects in aquatic species. At the same time, EPA 

will continue to work with the Food and Drug Administration (FDA), the Centers for Disease 

Control and Prevention (CDC), and the National Institute of Environmental Health Sciences 

(NIEHS) to better determine and evaluate the human health consequences of BPA exposures. 

Based on the results of those efforts, EPA will consider whether further action is needed to 

address human health risks resulting from non-food-packaging uses of BPA. 

 EPA intends to consider initiating rulemaking under section 5(b)(4) of the Toxic 

Substances Control Act (TSCA) to identify BPA on the Concern List as a substance that may 

present an unreasonable risk of injury to the environment on the basis of (1) itsits potential for 

long-term adverse effects on growth, reproduction and development in aquatic species, (2) its

substantial releases to and measured presence in the environment, and (3) studies that indicate

some concern for potential estrogenic effects on aquatic organisms at low dosesconcentrations

similar to levelsthose found in the environment. A notice of proposed rulemaking is intended to 

publish in autumn, 2010. In late 2010, EPA intends to consider also initiateing rulemaking under 

section 4(a) of TSCA to develop environmental effects data relevant to a further determination 

that BPA either does or does not present an unreasonable risk of injury to the environment. 

Beginning in JanuaryFebruary 2010, EPA intends to initiate collaborative alternatives 

assessment activities under its Design for the Environment (DfE) program to encourage 

reductions in BPA manufacturing and use to facilitate reductions in environmental releases and 

subsequent exposures. One of these activities will relate to thermal and carbonless paper 

coatings, including those on cash register receipts, which are uses where alternatives to BPA may 

be readily available. This DfE environmental and health assessment is expected to be completed 

in the latter half of 2011. Additionally, EPA intends to conduct alternatives analyses for BPA 

used in foundry castings since foundries are accountable for large releases of BPA as reported 

under the Toxic Release Inventory (TRI), and for BPA-based materials lining water and waste 

water pipes since this application may have a potential for human and environmental exposure. 

 EPA does not intend to initiate regulatory action under TSCA at this time on the basis of 

human health. EPA remains concerned withcommitted to protecting human health, but notes that 

most human exposure, including exposure to children, comes through food packaging materials 

under the jurisdiction of theFDA. Food, food additives, drugs, cosmetics, and Drug 

Administration (FDA). FDAmedical devices, all regulated by FDA, are specifically excluded 
U.S. Environmental Protection Agency Draft, 

12/9/20092/25/2010

U.S. Government Internal Deliberative Document, Do Not Quote, Cite, or Release

2

from the definition of chemical substance under TSCA. FDA, together with CDC and NIEHS, is 

currently performing aninvesting in-depth reassessment on important new health studies in both 

animals and humans to better determine and evaluate the potential riskshealth consequences of 

BPA to human health. The FDA reassessment is more comprehensive than the screening-level 

review undertaken by EPA during this action plan process, and 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 FDA 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. 

EPA will monitor the results of the $30 million research program on BPA recently 

funded by the National Institute of Environmental Health Sciences (NIEHS), and will reassess 

the potential for regulatory action as appropriate based on any new information from this and 

other research. As part of the Agency's efforts to address BPA, EPA also intends to evaluate the 

potential for disproportionate impact on children and other sub-populations. 

 Because BPA is a reproductive, developmental, and systemic toxicant in animal studies 

and is weakly estrogenic, there are questions about its potential impact particularly on children’s 

health and the environment. Most studies Studies employing standardized toxicity tests used 

globally for regulatory decision-making indicate that the levels of BPA in humans and the 

environment are below levels of potential concern for adverse effects. However, results of some 

non-guideline animalrecent studies have suggested the potential for endocrine-relatedusing novel 

low-dose approaches and examining different endpoints describe subtle effects in laboratory 

animals at much lower dose levels than those at which effects were seen in studies conducted 

under established guidelines. FDA is addressingvery low concentrations. Some of these studies 

in its human health assessment. Thesenovel low-dose studies in animals are also potentially of 

concern for the environment because the doseconcentration levels identified with effects are 

similar to some current environmental exposure levels. Regulatory authorities around the world 

that have reviewed these low-dose studies have generally concluded that they are insufficient for 

use in risk assessment because of a variety of flaws in some of the study designs, scientific 

uncertainty concerning the relevance to health and ecological hazard of the reported effects, and 

the inability of other researchers to reproduce the effects in more rigorousstandardized studies.

However, since guidelines for interpreting Although there is disagreement about the 

interpretation of these low-dose studies have not yet been established and , they do raise potential 

concerns for possiblelong-term effects at levels similar to those found in the environment, 

concentrations, and some authorities, including Canada and some U.S. state and county 

governments, have taken interim risk management action to protect certain sensitive populations. 

Due in part to these concerns, EPA intends to initiate, such as infants and toddlers. For example,

the risk management actions identified in this Plan to protect the environment while further 

research continues.Canadian government is taking steps to ban baby bottles that are 

manufactured with BPA.

II. Introduction
U.S. Environmental Protection Agency Draft, 

12/9/20092/25/2010

U.S. Government Internal Deliberative Document, Do Not Quote, Cite, or Release

3

 As part of EPA's efforts to enhance the existing chemicals program under the Toxic 

Substances Control Act (TSCA)1

, the Agency identified an initial list of widely recognized 

chemicals, including bisphenol A (BPA), for action plan development based on their presence in 

human blood; persistent, bioaccumulative, and toxic (PBT)2

 characteristics; use in consumer 

products; production volume; and other similar factors. This Action Plan is based on and 

encompasses EPA’s initial review of readily available use, exposure, and hazard information3 on 

BPA. EPA considered which of the various authorities provided under TSCA and other statutes 

might be appropriate to address potential concerns with BPA in developing the Action Plan. The 

Action Plan is intended to describe the courses of action the Agency plans to pursue in the near 

term to address its concerns. The Action Plan does not constitute a final Agency determination or 

other final Agency action. Regulatory proceedings indicated by the Action Plan will include 

appropriate opportunities for public and stakeholder input, including through notice and 

comment rulemaking processes.

III. Scope of Review

In conducting this review, EPA focused on the two areas with the most potential for 

environmental releases and exposures: manufacturing and processing. EPA also considered

potential human exposures to workers during the manufacturing process and to the general 

population from the presence of BPA in drinking water sources and systems. Because the 

principal concern is for potential reproductive and developmental effects in early life stages, 

EPA considered exposures to children from drinking water and from the use of BPA in consumer 

products. EPA also examined potential ecological impact from the presence of BPA in the 

environment.

Although most human exposure appears to come from food packaging materials (e.g.,

Willhite, 2008), less than 5% of the BPA produced is used in food contact applications. EPA’s 

review addresses the roughly 85-90% of BPA manufactured (includes imports) and used 

domestically that is subject to TSCA, including the manufacture of non-food-additive, nonmedical products.

 The FDA has jurisdiction over food additives, which include food contact substances 

such as food packaging. These substances are not regulated under TSCA. This review does not 

address potential risks from these food additive uses, which appear to comprise the bulk of 

human exposure. FDA is doing an assessment on those exposures.FDA and NIEHS are doing 

additional studies on the potential risks from these exposures, and the U.S. Department of Health 

 

1 15 U.S.C. §2601 et seq. 2

 Information on PBT chemicals can be found on the EPA website at http://www.epa.gov/pbt/. 3

 Information sources customarily employed include Inventory Update Reporting (IUR) submissions; Toxic Release 

Inventory (TRI) reporting; data submitted to the HPV Challenge Program; existing hazard and risk assessments 

performed by domestic and international authorities including but not limited to U.S. Federal government agencies, 

the Organization for Economic Cooperation and Development, the Stockholm Convention on Persistent Organic 

Pollutants, Health and Environment Canada, the European Union; and others. Action plans will reference

References to specific sources used in this Action Plan are provided in the individual sections discussing use, 

exposure, and hazard information. 
U.S. Environmental Protection Agency Draft, 

12/9/20092/25/2010

U.S. Government Internal Deliberative Document, Do Not Quote, Cite, or Release

4

and Human Services (HHS) has provided recommendations for parents and families to take 

reasonable steps to reduce exposures, especially for young children.4

Although most human exposure appears to come from food packaging materials (e.g., Willhite, 

2008), less than 5% of the BPA produced is used in food contact applications. EPA’s review 

addresses the roughly 85-90% of BPA manufactured (includes imports) and used domestically 

that is subject to TSCA, including the manufacture of non-food-additive, non-medical products. 

In conducting this review, EPA focused on the two areas with the most potential for 

environmental releases and exposures: manufacturing and processing. EPA also considered

potential human exposures to workers during the manufacturing process and to the general 

population from the presence of BPA in drinking water sources and systems. Because the 

principal concern is for potential reproductive and developmental effects in early life stages, 

EPA considered exposures to children from the use of BPA in consumer products and exposure 

of children to BPA from drinking water. EPA also examined potential ecological impact from 

the presence of BPA in the environment.

IV. Uses and Substitutes Summary

 

Bisphenol A (BPA) is a high production volume chemical with a U.S. volume estimated 

at 2.4 billion pounds in 2007, and an estimated value of almost $2 billion. It is a monomer used 

in manufacturing most or all polycarbonate plastics, the majority of epoxy resins, and certain 

other chemicalsproducts such as flame retardants (Mannsville, 2008a). Based on the nature of 

uses within product areas, EPA judges that the majority (possibly 85% to 90%) of BPA 

manufactured and used in the U.S.United States may fall within TSCA jurisdiction, as shown in 

Table 1, below. 

Table 1. BPA U.S. Consumption and Assumed Share Within TSCA Jurisdiction 

Product Percent of BPA U.S. 2007 

Consumption1 Assumed TSCA share2

Polycarbonate resins 74% 62 - 64 % 

Epoxy resins 20% 18 - 20 % 

Flame retardants; Polyetherimides/ 

Polyarylates; Polysulfone resins; Unsaturated 

polyester resins 

6% 5 - 6 % 

 Total 100% 85 - 90 % 

1

 Mannsville, 2008a 2

 EPA judgment, based on percentage of BPA consumption for each product area and use believed to fall within 

EPA jurisdiction under TSCA. Because the available data lack specific detail, these are “ballpark” estimates only 

and the range may under- or over-estimate the TSCA share. 

BPA-based materials are pervasive in the U.S. economy. Apart from food-related uses, 

they are used in automotive and other transportation equipment, optical media such as DVDs, 

electrical/electronics equipment, construction, linings inside drinking water pipes, thermal and 

carbonless paper coatings, foundry casting, and elsewhere. A handful of companies manufacture 

 

4

 Recommendations released by HHS on January 15, 2010 can be found at http://www.hhs.gov/safety/bpa/. 
U.S. Environmental Protection Agency Draft, 

12/9/20092/25/2010

U.S. Government Internal Deliberative Document, Do Not Quote, Cite, or Release

5

most BPA, as well as most BPA-based polycarbonate and epoxy resins, but numerous companies 

process BPA-based materials into final goods. 

 BPA-based materials tend to be chosen for their performance characteristics. For 

example, polycarbonates are lightweight and tough compared to glass. In uses subject to FDA 

jurisdiction, public concern has led industry to move toward non-BPA-based materials in such 

products as baby bottles, cups, and spoons and adult drink bottles, and to explore alternatives in 

food can linings. A vast number of other uses are subject to EPA jurisdiction. EPA is aware that 

substitutes for some of those uses include other epoxies, a wide variety of plastics (some of them 

blended with polycarbonate), glass, metals, and wood. However, EPA has not assessed the 

suitability and availability of substitutes for specific uses in this screening-level review. 

V. Hazard Identification Summary

Risk assessments for BPA have been conducted by numerous governmental bodies and 

review panels. OPPT reviewed the following assessments as well as numerous toxicological 

studies in assessing the hazard of BPA: 

 Government Assessments: 

o US (Federal) – Food and Drug Administration (FDA, 2008), National Toxicology 

Program/Center for Evaluation of Risks to Human Reproduction (NTP/-CERHR, 

2008) 

o US (State) - California Proposition 65 Developmental and Reproduction Toxicant 

Identification Committee (DARTIC) (California, 2009a)

o International – Japan, (AIST, 2007), European Union (EU) (EC, 2003, 2008), 

European Food Safety Administration (EFSA 2006, 2008a-b) and Canada

(Canada, 2008)

 Other Reviews: Harvard Panel (Gray et al., 2004 and; Goodman et al., 2006); Chapel 

Hill Group (vom Saal et al., 2007; Crain et al., 2007); NSF International (Willhite et al., 

2008) 

Human Health Hazard Summary 

There is general agreement 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); > 235 mg/kg-bw/day (reduced fetal or birth weight or growth early in life, effects on testis 

of male rats); and > 500 mg/kg-bw/day (possible decreased fertility in mice, altered estrous 

cycling in female rats, and reduced survival of fetuses). Systemic effects (reduction in body 

weight, changes in relative organ weights, and increases in liver toxicity) were observed at doses 

above 5 mg/kg-bw/day (identified as a NOAEL; LOAEL of 50 mg/kg-bw/day). There is 

controversy about whether effects seen at lower doses in animals (less than 1 mg/kg/day) are 

meaningful and relevant to humans. These low-dose effects are endocrine-related and include 

effects on puberty and developmental neurotoxicological effects (brain, behavior) at doses in 

animal studies as low as 2 μg/kg-bw/day. 

All of the government BPA assessments reviewed by EPA discuss these low-dose data 

and virtually all (the FDA, DARTIC, Japan, the EU, and2008; California, 2009a; AIST, 2007; 
U.S. Environmental Protection Agency Draft, 

12/9/20092/25/2010

U.S. Government Internal Deliberative Document, Do Not Quote, Cite, or Release

6

EC, 2003, 2008; EFSA, 2006, 2008a-b) have considered them insufficient for the purposes of 

hazard evaluation/risk assessment, the exceptions being Canada (Canada, 2008) and the NTP/-

CERHR. (NTP-CERHR, 2008). Canada acknowledged high uncertainty in the data, but took 

precautionary action to restrict BPA exposures to infants and young children. The NTP/-CERHR 

observed that the uncertainty led to a conclusion of “some concern”5 for potential effects. New 

information on these potential low-dose effects has been published on an almost monthly basis 

over the past year, with some studies supporting the concept and others finding no effects. For 

example, a recent study performed by EPA scientists comparing BPA with the oral contraceptive 

ethinyl estradiol (EE) found that low in utero doses of EE affected sexual differentiation in 

female rats, but low in utero doses of BPA produced no such effects (Ryan et al., 20109). The 

same investigators reported results in male rats in an earlier publication, also noting effects in 

males exposed in utero to EE, but not to BPA. (Howdeshell et al. 2008). (Howdeshell et al.,

2008). On the other hand, a different study reported that prenatal BPA exposure (again at low 

doses) in mice leads to adverse effects on the female reproductive tract later in life (Newbold et 

al., 2009). In addition, the NIEHS recently awarded $30 million dollars in grants for a two-year 

program of research on these issues. (NIEHS, 2009). FDA announced on January 15, 2010 that it 

shared the perspective of the NTP-CERHR and would undertake additional research in this area. 

(FDA, 2010).

MetabolismGiven the laboratory animal data, it is important to note that metabolism

studies have been performed in multiple species (rats, mice, monkeys, and humans) and show 

that humans and rodents metabolize BPA differently. Data in all four species indicate 

metabolism by conjugation in the liver with glucuronic acid to form the metabolite BPAglucuronide (BPAG). The relative amount of free-BPA and BPAG circulating in mammals is 

important because free-BPA (“parent”) is known to be weakly estrogenic and BPAG is not. Data 

indicate that BPAG is more prevalent in primates and free-BPA is more prevalent in rodents.

These differences in metabolism suggest that rodents may be more sensitive to effects from BPA 

than humans.

BPA has been found in human biological samples (serum, breast milk, urine, fetal blood) 

reported as, and umbilical cord blood). The literature reporting these results reflects both a 

variety of analytical techniques and the BPA forms measured (i.e., total BPA, or , free-BPA, or

and BPAG (except that BPAG has never been reported in fetal blood). ). In 2008, the National 

Report on Human Exposure to Environmental ChemicalsCDC reported that BPA was detected in 

the urine of 93% of the 2,517 people tested in 2003-4the 2003-4 National Health and Nutrition 

Examination Survey (NHANES) (Calafat et al., 2008). Recently, urinary BPA concentrations 

measured in premature infants from two separate intensive care facilities showed that mean 

urinary concentrations of total BPA were an order of magnitude higher in the infants than in the 

general population. Over >90% of the BPA found in the urine in that study was asin the form of

a glucuronide conjugate (Calafat et al., 2009), providing evidence of the ability for neonates to 

 

5 NTP’s possible levels of concern, from lowest to highest, are negligible concern, minimal concern, some concern, 

concern, and serious concern. “Some concern” thus represents the mid-point of a five-level scale of concern used by 

the NTP. In the case of BPA, the NTP stated it “expressed “some concern” for potential exposures to the fetus, 

infants and children. There are insufficient data from studies in humans to reach a conclusion on reproductive or 

developmental hazards presented by current exposures to bisphenol A, but there is limited evidence of 

developmental changes occurring in some animal studies at doses that are experienced by humans. It is uncertain if 

similar changes would occur in humans, but the possibility of adverse health effects cannot be dismissed.”
U.S. Environmental Protection Agency Draft, 

12/9/20092/25/2010

U.S. Government Internal Deliberative Document, Do Not Quote, Cite, or Release

7

conjugate BPA into its non-estrogenic form. The study authors noted, however, that this 

metabolic pathway would not be expected to be functional at adult rates until months after birth.

The authors also noted that the infants underwent intensive medical intervention, and that some 

of the BPA exposure may have been attributable to contact with medical devices.

 There was a recent report suggesting thatin which a cross-sectional study design was used 

to suggest an association between BPA levels in humans may be associated withand a higher risk 

of diabetes, heart disease, and elevation of certain liver enzyme activities (Lang et al., 2008). The 

authors examined the human data from a sub-sample of the National Report cohort (Calafat et 

al., 2008).2003-4 NHANES population. However, this report prompted an immediate review by 

the European Food Safety Authority (EFSA () (EFSA, 2008b) in late 2008 which concluded that 

the study did not provide sufficient proof for the stated associations. EPA notes that the same 

investigative group recently published an online research article repeating their original findings

for heart disease but not diabetes on a second NHANES population from 2005-6 (Melzer et al., 

2010).

Table 2 below is a list of each major assessment reviewed and the accompanying hazard 

valueintake limits chosen in their respective assessments. Some assessments did not derive a 

hazard valuean intake limit per se, but did make hazard/risk decisions: 

 The California Proposition 65 Developmental and Reproductive Toxicant Identification 

Committee (DARTIC) voted on 7/July 15/09, 2009 not to list BPA as a developmental 

toxicant, a female reproductive toxicant, or a male reproductive toxicant (each by 

separate, unanimous votes of 7-0) (California, 2009a). 

 Thirty-eight scientists (known as the “Chapel Hill Group”)”; vom Saal et al., 2007)

concluded that: (1) there is relevance of in vitro data to in vivo effects; (2) ecological 

studies are consistent with lab animal studies; (3) the low doses in animal studies are 

relevant to BPA levels found in humans; and (4) life stage is important in 

pharmacokinetics, exposure, &and effects in animals and humans. 

 A Harvard Panel (Gray et al., 2004) concluded that the low dose data are not relevant to 

humans (and reaffirmed this in an update reported in Goodman et al., 2006). 

 A National Toxicology Program (NTP) Center for Evaluation of Risks to Human 

Reproduction (CERHR) Panel (NTP-CERHR/NTP, 2008) concluded that rodent studies 

suggest that BPA causes “...neural and behavioral alterations related to disruptions in 

normal sex differences in rats and mice (0.01-0.2 mg/kg/day).” 

Table 2: BPA Hazard ValuesIntake Limits for Human Health Assessments 

Authors Hazard 

ValueIntake 

Limit

(mg/kg/day) 1

Endpoint (Animal dose in mg/kg/day) 

And Study 

USEPA (Integrated 

Risk Information 

System; IRIS (1993)) 

0.05 Reduced body weight (5) 

NTP 1982 two year cancer study in both rats and mice 

(1982) as cited in USEPA 1993)

FDA (2008) 

0.05 Systemic – reduced body wt and liver effects (5) 

Irreversible reproductive effects (50) 

Reversible reproductive effects (50) 

All based on both 2-generation mouse study (Tyl et al., 

2008) and 3-generation rat study (Tyl et al., 2002) 

0.05 

0.5 
U.S. Environmental Protection Agency Draft, 

12/9/20092/25/2010

U.S. Government Internal Deliberative Document, Do Not Quote, Cite, or Release

8

Table 2: BPA Hazard ValuesIntake Limits for Human Health Assessments 

Authors Hazard 

ValueIntake 

Limit

(mg/kg/day) 1

Endpoint (Animal dose in mg/kg/day) 

And Study 

EFSA (2006, 

20082008a-b) and 

EUEC (2003, 2008) 

0.05 Used 5 (lowest value in cited studies) 

Tyl et al.,. (2002 and, 2008) 

Japan (AIST, 2004) 

0.05 

0.5 

Body weight (5) 

Reproduction (50) 

Tyl et al., (2002, 2008) 

0.046 Liver effects (23) 

NTP (1985) – continuous breeding study in mice 

Canada (2008) Did not report 

any 

Body weight reduction (5) and dev/repro effects (50) 

Tyl et al., (2002, 2008) 

Cited numerous studies with effect levels ranging from 0.010 

to 0.100 mg/kg/day for a variety of effects in mice and/or rats 

including changes in: maternal behavior, gender-specific 

behaviors; sexual performance; novelty-seeking/impulse 

behaviors; avoidance response; maze performance. 

Willhite,et al., .

(2008)

(NSF International) 

0.016 Used 5 (lowest value in cited studies) 

Tyl et al., (2002 and, 2008) 

1

 Most risk assessments take an exposure value from an animal study (dose in mg/kg-bw/day) and divide it 

by several uncertainty factors to arrive at an acceptable dose in humans. This value is what is shown here 

andas an “intake limit” and is what is compared to an expected/estimated exposure value in a risk 

assessment. The uncertainty factors used by the various assessments are: EPA (IRIS) – 1000; FDA – either 

100 (systemic or reversible effects) or 1000 (irreversible effects); EFSA/EU – 100; Japan – either 100 or 

500; Canada – did not specify; and NSF Int.’l – 300. 

Environmental Hazard Summary 

Many studies have been conducted to determine potential effects of BPA exposure on 

invertebrates, fish, amphibians, reptiles, birds, and wild mammals, and a thorough review is 

provided by Crain et al. (2007). EPA’s screening-level ecological hazard review for this Action 

Plan focused on effects in freshwater aquatic species to provide a framework for determining 

whether toxicity may warrant further investigation or risk management action. A more robust 

review of effects in both terrestrial and aquatic (marine and freshwater) organisms will be 

conducted as the Agency proceeds with carrying out the activities identified in this Action Plan.

In general, studies have shown that BPA can affect growth, reproduction and 

development in aquatic organisms. Among freshwater organisms, fish appear to be the most 

sensitive species. Evidence of endocrine-related effects in fish, aquatic invertebrates, amphibians 

and reptiles has been reported at environmentally relevant exposure levels lower than those 

required for acute toxicity. There is a widespread variation in reported values for endocrinerelated effects, but many fall in the range of 1μg/L to 1 mg/L. (Canada, 2008). 

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

performed by the European Union (EUEC), Canada, and Japan as summarized below in Table 3. 

The different methodologies, endpoints and study results used by each country to derive these 
U.S. Environmental Protection Agency Draft, 

12/9/20092/25/2010

U.S. Government Internal Deliberative Document, Do Not Quote, Cite, or Release

9

values highlight the significant uncertainty in the estimated hazard values. Canada used a novel 

low-dose study (Lahnsteiner et al,., 2005) that reported reduced sperm quality and delayed 

ovulation in brown trout at a very low dose (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 or the induction of 

intersex or testes-ova in males were also reported in other studies referenced in the EU and 

Japanese hazard evaluations. However, because there were no standardized test guidelines or risk 

assessment guidance for evaluating some of these endocrine-related effects6 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. 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 lowdose exposure, particularly at sensitive developmental stages, with effects apparent later in the 

life cycle; (3) on filial generations following parental exposure; and (4) using more than one 

mode of action.” (Canada, 2008). 

Table 3: Summary of Bisphenol A Ecological Hazard Values 

Country 

Predicted No 

Effect 

Concentrations1 

(μg/L) 

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 (EUEC, 2008). 

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 published brown trout study 

(Lahnsteiner et al, 2005) and applying an uncertainty factor of 

10 (Canada, 2008). 

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 (AIST, 2007). 

 

6 As part of its endocrine disruptor screening program, EPA developed a two-tiered approach to implement statutory 

testing requirements. The purpose of Tier 1 screening is to identify substances that have the potential to interact with 

the estrogen, androgen, or thyroid hormone systems. The purpose of Tier 2 testing is to identify and establish a doseresponse relationship for any adverse effects that might result from the interactions identified through the Tier 1 

assays. EPA has established Tier 1 screening test guidelines. Tier 2 test guidelines will be developed after the 

completion of ongoing validation studies. 
U.S. Environmental Protection Agency Draft, 

12/9/20092/25/2010

U.S. Government Internal Deliberative Document, Do Not Quote, Cite, or Release

10

Table 3: Summary of Bisphenol A Ecological Hazard Values 

Country 

Predicted No 

Effect 

Concentrations1 

(μg/L) 

Endpoints 

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. 

VI. Fate Characterization Summary

 

BPA is a solid at room temperature. It has a low vapor pressure, moderate water 

solubility, and low volatility (HSDB, 2009). It has low to moderate mobility in soil. It is 

expected to biodegrade under environmental conditions, although conflicting results have been 

obtained using biodegradation screening tests. However, the weight of evidence suggests that it 

is not expected to be persistent in the environment, and degradation is expected to occur. The 

rate of atmospheric photooxidation is rapid. Hydrolysis is expected to be negligible under 

environmental conditions since BPA does not contain functional groups that are susceptible to 

hydrolysis. Based on the criteria set forth in EPA’s policy statement on Category for Persistent, 

Bioaccumulative, and Toxic New Chemical Substances (64 Fed. Reg. 60194, November 4, 1999), 

BPA is expected to have low persistence (P1) and low bioaccumulation potential (B1). (EUEC, 

2003 and EU, 2008) 

 Any residual, unreacted BPA remaining in polycarbonate products and epoxy resins can 

leach out into food or the environment. Polycarbonate is generally stable, but some BPA can be 

released from polycarbonate when it is exposed to strongly basic conditions, UV light, or high 

heat. Epoxy resins made with BPA are stable; only residual BPA is expected to be released from 

epoxy resins. 

VII. Exposure Characterization Summary

BPA may beis present in the environment as a result of direct releases from 

manufacturing or processing facilities, (USEPA, 2009a). BPA may also be present in the 

environment as a result of fugitive emissions during processing and handling, or release of 

unreacted monomer from products (NTP-CERHR/NTP, 2008). According to the Toxics Release 

Inventory (TRI) Database, total release of BPA in 2007 was 1,132,062 pounds7, with releases of 

122,965 pounds to air, 6,246 pounds to water (direct), 14,972 pounds released on-site to land, 

and 684,638 pounds transferred off-site to land (USEPA, 2009a). Sources of human exposure to 

BPA include dietary intake (e.g., migration from food packaging and from repeat-use 

polycarbonate containers, such as baby bottles), environmental media (ambient air, indoor air, 

drinking water, soil and dust), and use of consumer products. Given the tendency of young 

children to put inappropriate objects into their mouths, there is some minor potential for children 

to be exposed to BPA through their mouthing or accidental ingestion of suchconsumer products

 

7 This total does not include off-site water transfer to POTWs (Publicly Owned Treatment Works) wastewater 

treatment facilityies (32,928 pounds) or transfer to incineration (2,759,705 pounds). 
U.S. Environmental Protection Agency Draft, 

12/9/20092/25/2010

U.S. Government Internal Deliberative Document, Do Not Quote, Cite, or Release

11

as plastic toys, thermal paper, and possibly of toilet paper made from recycled materials. Dietary 

intake appears to be the primary source of human exposure. However, food packaging and food 

containers, such as baby bottles, are the purview of the Food and Drug Administration; therefore, 

OPPT’s human and environmental exposure characterization focuses on exposure from 

manufacturing; processing; industrial uses; commercial uses; selected consumer uses; ingestion 

of BPA in drinking water, including drinking water contaminated by wastewater releases to 

surface water, drinking water drawn from ground water contaminated by leachate from landfills, 

and drinking water distributed through BPA-based water pipes; and incidental ingestion of BPA 

from infants’ and children’s toys andcontact with consumer products. OPPT used release data, 

modeling, and information available in peer-reviewed articles and government publications to 

obtain information on exposure to BPA. 

Very little information is available on exposure from consumer products. While noting 

that the primary intake for children six months and older came through food, Miyamoto and 

Kotake (2006) also estimated exposure to BPA for Japanese infants from contact with consumer 

products such as toys. They estimated the mean intake of BPA from toys for male infants 0 to 5 

months of age to be 0.026 μg/kg bw per day and the mean intake for infants 6-11 months to be 

0.069 μg/kg per day. Current information posted by the HHS indicates that most plastic toys that 

children put in their mouths do not contain BPA4. No studies were identified measuring potential 

exposures to adults or children from contact with other consumer products.

Limited information is available for BPA concentrations in USU.S. water and other 

environmental media (Table 4, providing values from all of the studies cited in this discussion). 

Most environmental monitoring results show that the concentrations of BPA in water bodies are 

lower than 1 μg/L, mainly due to its partitioning and biodegradability properties (Tsai, 2006). 

BPA was detected at a median concentration of 0.14 μg/L and a maximum concentration of 12 

μg/L in 41.2% of 85 samples collected from USU.S. streams in 1999 and 2000 (Kolpin et al..,

2002). The maximum concentration of 12 μg/L is an outlier; the BPA concentration in other 

USU.S. waters was much lower (as indicated by the median concentration of 0.14 μg/L). In 

2001 and 2002, BPA was not detected (< 0.001 μg/L) in effluent from a wastewater treatment 

plant in Louisiana, and concentrations were not quantifiable in samples collected from surface 

waters in Louisiana and in drinking water at various stages of treatment at plants in Louisiana 

(Boyd et al.., 2003). 

In 2000, the U.S. Geological Survey collected samples from 47 ambient groundwater 

sites (not drinking water wells) in 18 states and analyzed them for 65 organic wastewater 

contaminants (Barnes et al., 2008; USGS, 20082008a-b). BPA was detected in 29.8% of the 

sampled groundwater sites, with a mean detected concentration of 1.78 μg/L and a range of 1.06 

to 2.55 μg/L (Barnes et al., 2008b). BPA was among the top five most frequently detected 

organic compounds (USGS, 2008Barnes, et al., 2008a). 

In the summer of 2001, the U.S. Geological Survey 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 
U.S. Environmental Protection Agency Draft, 

12/9/20092/25/2010

U.S. Government Internal Deliberative Document, Do Not Quote, Cite, or Release

12

was detected in 9.5% of these samples at a reporting level of 1 μg/L. The maximum 

concentration measured in these samples was 1.9 μg/L (USGS, 2008Barnes, et al., 2008a; 

Focazio et al., 2008). 

Landfill leachates from one U.S. study reported maximum BPA concentrations of 1.7 

μg/L in landfill leachate and 1.4 μg/L in the receiving groundwater plume at a landfill on Cape 

Cod that was known to be leaking (Crain et al., 2007). 2007). Data for other landfill sites in the 

United States were not available, and this single point may not be representative of the country.

Landfill leachate from other countries contained more than 500 μg/L of BPA, which is on the 

order of 500 times the BPA concentrations in water bodies (Tsai, 2006). Studies conducted at 

Japanese landfills resulted in maximum untreated leachate concentrations of 17,200 μg/L and 

treated leachate concentrations of 5.1 μg/L (Crain et al., 2007). 

Soil concentrations reported in by NTP-CERHR/NTP (2008) were for soil samples taken 

from outdoor play areas of homes and daycares; BPA concentrations ranged from 4-14 ppb dry 

weight, with means of 6-7 ppb dry weight. Klecka et al. (2009) reported a median concentration 

of 0.6 ppb BPA in North American freshwater sediments, including nondetected samples; BPA 

concentrations in samples from the USUnited States ranged from 1.4 to 140 ppb dry weight. 

USU.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 (Klecka et al.., 2009,; Tsai, 2006). 

Table 4: U.S. Reported Environmental Concentrations of BPA 

Location 

Mean or Range 

of Means (ppb) Range (ppb) 

Surface Water 0.012 to 0.14 0.0009 to 12 

Groundwater 0.0041 to 1.9 0.006 to 2.55 

Drinking Water 0.005 to <0.1 <0.1 to 0.42 

Wastewater <0.1 0.0036 to 50 

Soils 6 to 7 4 to 14 

Sediment, Fresh 0.6*† 1.4 to 140†

Sediment, Marine 3.5* 1.5 to 5.0 

* Value is median; mean values not reported 

†

 median value includes nondetected values below the MDL, while the reported range includes 

only detected values 

 

E-FAST28

 modeling of BPA releases in the 2007 TRI showed the most conservative 

estimates of the potential acute dose rate for ingestion of BPA in drinking water by children ages 

1-2 ranged from 0.0000531 to 16.5 μg/kg/day, and the most conservative estimates of the surface 

water concentration ranged from 0.000574 to 232 μg/L. The E-FAST2 model is intended to be 

used for screening level exposure characterization. E-FAST2 is based on numerous assumptions 

that are designed to be conservative; for example, E-FAST2 does not account for the half life of 

a chemical in surface water. The inputs selected for the E-FAST2 modeling of BPA were also 

selected to be conservative; for example, the bioconcentration factor was selected to be at the 

high end of the range of values reported for BPA in the literature. 

 

8

 Information on E-FAST2 can be found at http://www.epa.gov/opptintr/exposure/pubs/efastdl.htm.
U.S. Environmental Protection Agency Draft, 

12/9/20092/25/2010

U.S. Government Internal Deliberative Document, Do Not Quote, Cite, or Release

13

FDA estimated exposure to BPA from food contact uses to be 0.185 μg/kg bw/day for 

adults. The highest estimate by FDA is 2.42 μg/kg bw/day for female infants, 1-2 months of age 

(U.S. FDA, 2008). Human exposures from food contact uses are consistently estimated by 

researchers to be higher than exposures from all other sources (e.g., Willhite, 2008). 

Workers may be exposed to BPA by inhalation or skin contact during the manufacture of 

BPA and BPA-containing products. No data were available for dermal exposures, and limited 

data were available for inhalation exposures. Table 5 summarizes EPA’s estimates for 

occupational exposures that may occur during manufacturing. These estimates were derived 

using models developed by EPA/OPPT for use in preparing screening-level exposure 

assessments of chemicals. These models do not take into account the effect of any personal 

protective equipment that may be used. 

Table 5. Inhalation and Dermal Exposure Estimates to BPA 

During BPA Lifecycle Stages 

Lifecycle Stage Exposure Type BPA Exposure Dose (mg/day) 

Manufacturing Inhalation 0 – 9.6 

Dermal (liquids and solids) 882 – 3,100 a 

USE 1: Polycarbonates Inhalation 0.7 – 2.7 b 

Dermal (solids) 0.31 – 3,100 c 

USE 2: Epoxy Resins Inhalation 0 – 28 

Dermal (solids) 3,100 c 

USE 3: Flame Retardants Inhalation 0 d 

Dermal (solids) 3,100 c 

a – Exposure is in milligrams per event. Events can include sampling of solutions containing BPA or solid BPA and 

loading/unloading of BPA from containers. 

b – Exposure is to polycarbonate dust. 

c – Exposure is in milligrams per loading/unloading of BPA from containers, which is the only identified potential 

exposure during this stage of the lifecycle. 

d – Inhalation exposure to BPA during the production of flame retardants is not expected.

VIII. Risk Management Considerations

 

 BPA is not a heavily regulated chemical in the U.S., but has been identifiedevaluated as a 

chemical of potential concern by some U.S. agencies and other countries since the early 1980’s. 

U.S. EPA and State/Local Regulatory Reviews and Actions 

 BPA was included in the initial proposal of the Toxics Release Inventory (TRI) list 

published in 1987 (52 FRFed. Reg. 21001, June 4, 1987). That initial list was mandated by the 

Emergency Planning & Community Right-to-Know Act (EPCRA) section 313(c), 42 U.S.C. § 

11023(c), to include the substances specified by the Senate Environment and Public Works 

Committee Print 99-169, so there was no separate discussion of the justification for placing BPA 

on the initial TRI list. 
U.S. Environmental Protection Agency Draft, 

12/9/20092/25/2010

U.S. Government Internal Deliberative Document, Do Not Quote, Cite, or Release

14

 In 2009, the EPA Office of Water considered BPA during its development of the third 

Candidate Contaminant List (CCL3) of substances that might be appropriate candidates for 

future regulation. Although BPA appeared on the potential CCL (PCCL) list used during the 

screening process, BPA did not meet the combined screening criteria of potential to occur in 

public water systems and potential for public health concern because its measured presence in 

water was well below potential effect levels in guideline studies, and thus did not appear on the 

final CCL3 list. The notice publishing the final CCL3 list (74 FRFed. Reg. 51850, 10/October 8/, 

2009) does not specifically address BPA, but supporting materials available on the EPA website 

describe the process and criteria used in the development of the list, including the information on 

BPA (http://www.epa.gov/ogwdw000/ccl/ccl3.html).(USEPA, 2009b). 

 Connecticut, Minnesota, Wisconsin, Chicago and Suffolk County, N.Y., have banned the 

sale of polycarbonate baby bottles, food containers and cups that contain BPA. The Connecticut 

ban also applies to infant formula cans and all reusable food and beverage containers. The 

Suffolk County ban (County of Suffolk, 2009) went into effect in July 2009. The Minnesota ban 

will go(Minnesota, 2009) went into effect on 1/1/2010; the Chicago ban (Chicago, 2009) on 

1/31/2010; and the Connecticut ban (Connecticut, 2009) will take effect on 10/1/2011. The 

Wisconsin ban (Wisconsin, 2010) passed the state legislature on 2/17/2010, and will go into 

effect 90 days after it is published following signature by the governor. A California bill

(California, 2009) to ban the use of BPA in baby bottles and cups and infant formula cans failed 

to pass in September 2009 by six votes and was moved to the inactive file. It is eligible A similar 

bill failed to be raised again. pass in Oregon (Oregon, 2010) in February 2010.

International Regulatory Reviews and Actions 

 Numerous foreign governmental bodies and review panels have conducted human health 

risk assessments for BPA in the recent past. Japan (AIST, 2007), the European Union (EUEC, 

2008), and the European Food Safety Administration (EFSA, 2008) all concluded within the past 

two years that the novel studies indicating low dose, endocrine-related effects were insufficient 

for the purposes of hazard evaluation/risk assessment. Using hazard values derived by dividing 

the doses used in standardized animal studies by the respective uncertainty factors applied by the 

different regulatory bodies, theythese regulatory bodies concluded that expected exposures even 

from food contact uses, the largest expected source of exposure, did not present concern for risk 

to human health. 

 In contrast, on June 26, 2009, Canada became the first country to take regulatory action 

against BPA. Canada announced that it was moving forward with proposed regulations to 

prohibit the advertisement, sale and importation of polycarbonate plastic baby bottles that 

contain BPA, to reduce newborn and infant exposure to this substance. In announcing this 

decision, Canada noted “The Government has concluded that exposure levels for newborns and 

infants up to 18 months of age are below those that could cause health effects. However, due to 

the uncertainty raised in some studies relating to the potential effects of low levels of BPA, the 

Government wants to further limit exposure.” (Canada, 2009).

 Ecological risk for BPA has been evaluated by the European Union (EUEC, 2008), 

Canada (Canada, 2008), and Japan (AIST, 2007). Japan concluded that “the current exposure 

levels of BPA will not pose unacceptable risks to the local populations of aquatic life, 
U.S. Environmental Protection Agency Draft, 

12/9/20092/25/2010

U.S. Government Internal Deliberative Document, Do Not Quote, Cite, or Release

15

particularly fish.” 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. Based on a novel low-dose study (Lahnsteiner et al., 2005),

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.” 

On June 26, 2009, Canada became the first country to take regulatory action against 

BPA. Canada announced that it was moving forward with proposed regulations to prohibit the 

advertisement, sale and importation of polycarbonate plastic baby bottles that contain BPA, to 

reduce newborn and infant exposure to this substance. In making this decision, Canada indicated 

that its decision was grounded in the precautionary principle, noting “Science tells us that 

exposure levels are below those that could cause health effects; however, due to the uncertainty 

raised in some studies relating to the potential effects of low levels of bisphenol A, the 

Government of Canada is taking action to enhance the protection of infants and young children.” 

(http://www.chemicalsubstanceschimiques.gc.ca/challenge-defi/bisphenol-a_fs-fr_e.html) 

 In August 2009, Taiwan designated BPA as a Class 4 toxic substance under the Toxic 

Chemical Substances Control Act. (Taiwan, 2009). A Class 4 toxic substance is defined as a 

substance for which there is concern of pollution of the environment or the endangerment of 

human health. Handlers of Class 4 substances are required to keep and report records of the 

toxicity, production, release, and use of those chemicals, but the chemicals are not subject to 

other restrictions on handling, transportation, or use 

(http://law.epa.gov.tw/en/laws/788537580.html).(Taiwan, 2007). Class 4 is the lowest 

designation for a toxic substance in Taiwan. 

Ongoing Activities and Issues 

 The primary issue with regard to risk management approaches to BPA is the uncertainty 

surrounding the actual determination of risk, particularly from low dose exposures. There is 

agreement among international regulatory authorities using generally accepted approaches to 

human health assessment that human exposures to BPA are below levels that would be 

associated with health effects, leading to determinations that current uses of BPA do not present 

human health risks warranting further regulatory controls. Similarly, environmental exposures 

toconcentrations of BPA, apart from isolated hot spots, are estimated generally to be lower than 

the levels associated with effects in standardized toxicological studies done according to 

established guidelines, indicating low environmental risk from current uses of BPA on the basis 

of just those standard studies. The complicating factor, however, is the uncertainty surrounding 

the meaning and relevance both to humans and the environment of the effects seen in some novel 

low-dose studies, because some environmental exposuresconcentrations are similar to levels 

associated with observed effects reported in those low-dose studies. 
U.S. Environmental Protection Agency Draft, 

12/9/20092/25/2010

U.S. Government Internal Deliberative Document, Do Not Quote, Cite, or Release

16

 Reproductive and developmental toxicity are the most sensitive effects observed in the 

guideline studies, while controversial, non-guidelineand some novel studies suggest the potential 

for endocrine-related effects at much lower, environmentally-relevant levels than the effect 

levels identified in the guidelinestandardized studies. Accordingly, BPA exposures raise 

particular questions concerning children’s health. Children may be exposed to BPA before birth 

through their mothers’ exposures, and directly through the use of BPA in food packaging 

materials and child feeding products (such as baby bottles, sippy cups, and spoons) within FDA 

jurisdiction. FDA is assessingconducting further studies on potential health risks to both children 

and adults from exposure to BPA in food contact materials. (FDA, 2010), and HHS has provided 

recommendations on how parents and families can reduce their potential exposure to BPA while 

this investigation continues4. Children and adults may also be exposed to a lesser extent through 

contact with other consumer products such as toys and through contact with environmental 

media (e.g., air and water). Children’s exposures are greater than adults’ due to increased intakes 

of food, water, and air per pound of body weight, as well as child-specific exposure pathways 

such as mouthing of objects and ingestion of non-food items. 

 

 On October 28, 2009, the National Institute of Environmental Health Sciences (NIEHS), 

part of the National Institutes of Health under the U.S. Department of Health and Human 

Services, announced the award of $14 million in Recovery Act funds to support two-year 

research grants into the potential effects of BPA on human health. (NIEHS, 2009). Including 

these Recovery Act funds, NIEHS is investing approximately $30 million over two years on 

BPA research. The new two-year animal and human studies will focus on either developmental 

exposure or adult chronic exposures to low doses of BPA. Researchers will be looking at a 

number of health effects including behavior, obesity, diabetes, reproductive disorders, 

development of prostate, breast and uterine cancer, asthma, cardiovascular diseases and 

transgenerational or epigenetic effects (http://www.nih.gov/news/health/oct2009/niehs-28.htm)..

 Given that human exposures from TSCA uses of BPA are minor compared with human 

exposures from uses under FDA jurisdiction, EPA considers that FDA has the lead in making 

human health judgments on BPA. EPA does not consider that action under TSCA would be 

warranted at this time on the basis of potential human health concerns from exposures through 

TSCA uses of BPA.

EPA has jurisdiction over environmental exposures to BPA. Although there is 

controversydisagreement in interpreting some of the novel low-dose studies and some of the

effects observed in the many aquatic toxicity studies performed thus far with BPA, a comparison 

of the range of predicted no effect concentration (PNEC) values used in the three international 

regulatory risk assessments (0.175 to 1.6 μg/L, Table 3) with measured concentrations in U.S. 

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

(ground water), and 140 μg/kg sediment (freshwater sediment) (Table 4), raises concern about 

possible risk of injury to aquatic organisms. However, limited information is available for BPA 

concentrations in U.S. water, and most available environmental monitoring results show that the 

concentrations of BPA in water bodies are lower than 1 μg/L (median concentration of 0.14 

μg/L, below any calculated PNEC). These environmental measurements represent only isolated 

snapshots in time and do not provide an indication of how many areas may exceed PNEC values 
U.S. Environmental Protection Agency Draft, 

12/9/20092/25/2010

U.S. Government Internal Deliberative Document, Do Not Quote, Cite, or Release

17

or concentrations of concern, how often or how long such concentrations may be exceeded, or 

the pathways leading to BPA presence in the environment from manufacturing, processing, 

distribution in commerce, use, or disposal. Additional information would help to resolve these 

uncertainties. 

IX. Next Steps

 

 In conducting this review of bisphenol A, EPA considered a number of potential risk 

management actions, including regulatory actions under TSCA sections 4, 5 and 6; cooperative 

activities with other federal agencies; and voluntary actions through such programs as Design for 

the Environment (DfE). 

Based on EPA’s screening-level review of hazard and exposure information, including 

the uncertainties surrounding the low-dose studies, EPA intends to initiate risk management 

action to protect the environment while further research continues. Accordingly, EPA intends to::

1. InitiateConsider initiating rulemaking under section 5(b)(4) of the Toxic Substances 

Control Act (TSCA) to identify BPA on the Concern List as a substance that may 

present an unreasonable risk of injury to the environment on the basis of (1) itsits 

potential for long-term adverse effects on growth, reproduction and development in 

aquatic species, (2) its substantial releases to and measured presence in the 

environment, and (3) studies indicating some concern for potential estrogenic effects 

on aquatic organisms at low dosesconcentrations similar to levelsthose found in the 

environment. A notice of proposed rulemaking is intended to publish in autumn, 

2010. 

2. InitiateConsider initiating rulemaking under section 4(a) of TSCA to develop data 

with respect to environmental effects relevant to a further determination that BPA

either does or does not present an unreasonable risk of injury to the environment. This 

may include testing or monitoring data in the vicinity of landfills, manufacturing 

facilities, or similar locations to determine the potential for BPA to enter the 

environment, including surface water, ground water, and drinking water, at levels of 

potential concern particularly for environmental organisms, pregnant women, and 

children. EPA anticipates publishing an advance notice of proposed rulemaking in 

late 2010. 

3. Initiate collaborative alternatives assessment activities under its Design for the 

Environment (DfE) program to encourage reductions in BPA manufacturing and use 

to facilitate reductions in environmental releases and subsequent exposures. One of 

these activities, intended to be initiated in JanuaryFebruary 2010, will address thermal 

and carbonless paper coatings, a use where preferable alternatives to BPA may be 

readily available. This DfE environmental and healthalternatives assessment is 

expected to be completed in the latter half of 2011. Paper coatings are not a major use 

of BPA, but thermal paper has been reported to contain free BPA, which would be 

expected to be more available for exposure than BPA bound into resin or plastic. 

Popular uses of this paper include airline tickets, event and cinema tickets, labels, and 

point of sale applications (receipts). While there is little concern for dermal 
U.S. Environmental Protection Agency Draft, 

12/9/20092/25/2010

U.S. Government Internal Deliberative Document, Do Not Quote, Cite, or Release

18

absorption of BPA, free BPA can readily be transferred to skin and residues on hands 

can be ingested. There is some potential for incidental exposure of children since they 

are more likely than adults to mouth inappropriate objects. Use of BPA in paper also 

may contribute 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 since paper products are a major solid waste stream. Additionally, 

EPA intends to initiate alternatives analyses for BPA used in foundry castings since 

foundries are accountable for large releases of BPA as reported under TRI, and for 

BPA-based materials lining water and waste water pipes since this application may 

have a potential for human and environmental exposure. 

EPA does not intend to initiate regulatory action under TSCA at this time on the basis of 

human health. EPA remains concerned withcommitted 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). FDA, together with the 

Centers for Disease Control and Prevention (CDC) and the National Institute of Environmental 

Health Sciences (NIEHS), is currently performing aninvesting in-depth reassessment on

important new health studies in both animals and humans to better determine and evaluate the 

potential riskshealth consequences of BPA to human health, and 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 FDAthe 

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. 

A substantial program of research is underway through NIEHS to resolve the 

uncertainties in the human health hazard of BPA, and EPA will monitor the results of that and 

other research to determine whether they may change the risk picture for human and 

environmental exposures from uses within TSCA jurisdiction. 

As part of the Agency's efforts to address BPA, EPA also intends to evaluate the potential 

for disproportionate impact on children and other sub-populations through exposure from TSCA 

uses. 

X. References

AIST (Japan’s National Institute of Advanced Industrial Science and Technology). 2007. AIST Risk Assessment 

Document Series 4. Bisphenol A. 

Barnes, K.K., Kolpin, D.W., Furlong, E.T., Zaugg, S.D., Meyer, M.T., and Barber, L.B. 2008. A national 

reconnaissance of pharmaceuticals and other organic wastewater contaminants in the United States—I) 

Groundwater. Science of the Total Environment, v. 402, no. 2–3, p. 192–200. 

Boyd GR, Reemtsma H, Grimm DA, 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. 
U.S. Environmental Protection Agency Draft, 

12/9/20092/25/2010

U.S. Government Internal Deliberative Document, Do Not Quote, Cite, or Release

19

Calafat, A. M., Weuve, J., Ye, X., Jia, L. T., Hu, H., Ringer, S., Huttner, K. and R. Hauser. 2009. Exposure to 

Bisphenol A and Other Phenols in Neonatal Intensive Care Unit Premature Infants. Environ. Health Persp. 117(4): 

639-644. 

Calafat, AM, X Ye, Y-L Wong, JA Reidy, and LL Needham. 2008. Exposure of the U.S. Population to Bisphenol A 

and 4-tertiary-Octylphenol: 2003–2004 Environ Health Perspect 116:39–44 (2008).

California,. 2009a. California Proposition 65 Committee (see presentations/meeting materials for DARTIC decision 

meeting on July 15, 2009 http://www.oehha.ca.gov/prop65/public_meetings/dart071509ag.html ) 

California. 2009b. California Legislature Legislative Index. SB-797 Senate Bill History. Accessed at 

http://www.leginfo.ca.gov/pub/09-10/bill/sen/sb_0751-0800/sb_797_bill_20090911_history.html. (Text of bill as 

amended in Assembly July 15, 2009 accessed at http://www.leginfo.ca.gov/pub/09-10/bill/sen/sb_0751-

0800/sb_797_bill_20090715_amended_asm_v97.html.) 

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

Canada. 2009. Government of Canada Acts to Protect Newborns and Infants from Bisphenol A in Polycarbonate 

Plastic Baby Bottles. Accessed at http://hc-sc.gc.ca/ahc-asc/media/nr-cp/_2009/2009_106-eng.php. 

Caunter, J.E., Williams, T.D., Hetheridge, M.J., and Evans, M.R. 2000. Bisphenol A: Multigeneration study with the 

fathead minnow (Pimephales promelas). Brixham Environmental Laboratory, AstraZeneca UK Limited 

(unpublished). 

CERHR/NTP. 2008.Chicago. 2009. Substitute Ordinance. Municipal Code of Chicago, Section 7-28-637, BPA-Free 

Kids Ordinance. Accessed at 

http://egov.cityofchicago.org/webportal/COCWebPortal/COC_EDITORIAL/bpaordinance.pdf. 

Connecticut. 2009. Public Act No. 09-103, An Act Concerning Banning Bisphenol-A in Children’s Products and 

Food Products. Accessed at http://www.cga.ct.gov/2009/ACT/PA/2009PA-00103-R00HB-06572-PA.htm. 

County of Suffolk. 2009. Resolution No. 154-2009, Adopting Local Law No. 6-2009, A Local Law Establishing the 

Toxin Free Toddlers and Babies Act. Accessed at 

http://legis.suffolkcountyny.gov/clerk/legal_notices/2009/ln051409.pdf. 

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/chemicals/bisphenol/bisphenol.pdf.

Crain, D.A., Eriksen, M., Iguchi, T., Jobling, S., Laufer, H., LeBlanc, G.A. and L.J. Guillette, Jr. 2007. An 

ecological assessment of Bisphenol A: evidence from comparative biology. Reprod. Toxicology (24): 225-239. 

EPP. 2008. EPP Rapid Research. “Rehabilitating Home Water Pipes with Epoxy Coatings.” December 2008. 

Accessed October, 2009, at www.pprc.orghttp://www.pprc.org/research/epp/Epoxy-Lined_Pipes.pdf. 

EU (. 2003).. European Union 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. 

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. 
U.S. Environmental Protection Agency Draft, 

12/9/20092/25/2010

U.S. Government Internal Deliberative Document, Do Not Quote, Cite, or Release

20

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. 

European Food and Safety Authority (EFSA). 2008a. 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. 

European Food and Safety Authority (EFSA). 2008b. Statement of EFSA prepared by the Unit on food contact 

materials, enzymes, flavourings and processing aids (CEF) and the Unit on Assessment Methodology (AMU) on a 

study associating bisphenol A with medical disorders. The EFSA Journal (2008) 838, 1-3. 

Focazio, M.J., Kolpin, D.W., Barnes, K.K., Furlong, E.T., Meyer, M.T., Zaugg, S.D., Barber, L.B., and Thurman, 

E.M. 2008. A national reconnaissance for pharmaceuticals and other organic wastewater contaminants in the United 

States—II) Untreated drinking water sources. Science of the Total Environment, v. 402, no. 2–3, p. 201–216.

Gray, G. M., Joshua T. Cohen, Gerald Cunha, Claude Hughes, Ernest E.McConnell, Lorenz Rhomberg, I. Glenn 

Sipes, and Donald Mattison. 2004. Weight of the Evidence Evaluation of Low-Dose Reproductive and 

Developmental Effects of Bisphenol A. Human and Ecological Risk Assessment, 10: 875–921. 

Goodman JE, McConnell EE, Sipes IG, Witorsch RJ, Slayton TM, Yu CJ, Lewis AS, Rhomberg LR. 2006. An 

updated weight of the evidence evaluation of reproductive and developmental effects of low doses of bisphenol A. 

Crit Rev Toxicol 36:387–457. 

Howdeshell KL, Furr J, Lambright CR, Wilson VS, Ryan BC and Gray LE. 2008. Gestational and lactational 

exposure to ethinyl estradiol, but not bisphenol A, decreases androgen-dependent reproductive organ weights and 

epididymal sperm abundance in the male Long Evans hooded rat. Tox. Sci. (102)(2): 371-382. 

HSDB. 2009. Hazardous Substance Databank. National Library of Medicine. Available from: 

http://toxnet.nlm.nih.gov/cgi-bin/sis/htmlgen?HSDB as of June 22, 2009. 

ICIS. 2009. ISIS Chemical business, “Chemical Profile: Epoxy Resins,” July 13, 2009, page 35. 

Kirk-Othmer. 1996. Kirk-Othmer Encyclopedia of Chemical Technology, 4th Edition, “Polycarbonates,” 1996 

(pages 584-608). 

Klecka GM, Staples CA, Clark KE, van der Hoeven N, Thomas DE, Hentges SG. 2009. Exposure Analysis of 

Bisphenol A in Surface Water Systems in North America and Europe. Environ Sci Technol 43(16):6145-6150. 

Kolpin DW, Furlong ET, Meyer MT, Thurman EM, Zaugg SD, Barber LB, Buxton HT. 2002. Pharmaceuticals, 

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

Technol 36:1202–1211. 

Lahnsteiner, F., B. Berger, M. Kletzl and T. Weismann. 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. 

Lang, I., Galloway, T., Scarlet, A., Henley, W., Depledge, M., Wallace R. and Melzer, D. 

2008. Association of Urinary Bisphenol A Concentration With Medical Disorders and 

Laboratory Abnormalities in Adults. Journal of the American Medical Association. 2008; 

300(11):1303-1310 

Mannsville. 2006. Chemical Products Synopsis: Epoxy Resins, Mannsville Chemical Products Corp., August 2006. 

Mannsville. 2008a. Chemical Products Synopsis: Bisphenol A, Mannsville Chemical Products Corp., January 2008. 
U.S. Environmental Protection Agency Draft, 

12/9/20092/25/2010

U.S. Government Internal Deliberative Document, Do Not Quote, Cite, or Release

21

Mannsville. 2008b. Chemical Products Synopsis: Polycarbonate Resins, Mannsville Chemical Products Corp., 

January 2008. 

Melzer, D., Rice, N.E., Lewis, C. Henley, W.E., and Galloway, T.S. (2010). Association of Urinary Bisphenol A 

Concentration with Heart Disease: Evidence from NHANES 2003/06, PLoS One. Accessed at 

http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0008673. January 2010.

Minnesota. 2009. Minnesota Session Laws, 2009, Regular Session, Chapter 40--S.F.No. 247, An act

relating to public health; protecting the health of children; prohibiting bisphenol-A in products for young children. 

Office of the Revisor of Statutes. Accessed at 

https://www.revisor.mn.gov/laws/?id=40&doctype=chapter&year=2009&type=0.

 

Miyamoto, K. and Kotake, M.,. 2006. Estimation of Daily Bisphenol A Intake of Japanese Individuals with 

Emphasis on Uncertainty and Variability, Environmental Sciences, 13, 1 (2006) 015-029. 

Newbold, R, Jefferson W.N. and Padilla-Banks, E.. 2009. Prenatal Exposure to Bisphenol A at Environmentally 

Relevant Doses Adversely Affects the Murine Female Reproductive Tract Later in Life Env Health Persp (117)(6) 

879-885.

NIEHS. 2009. NIEHS Awards Recovery Act Funds to Address Bisphenol A Research Gaps. Accessed at 

http://www.niehs.nih.gov/news/releases/2009/bisphenol-research.cfm. 

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/chemicals/bisphenol/bisphenol.pdf.

Oregon. 2010. Oregon Senate Bill 1032 Relating to Containers Made with BPA, Measure Activity. Accessed at 

http://gov.oregonlive.com/bill/sb1032/. 

PlasticsEurope. 2009. American Chemistry Council, PlasticsEurope, and Japan Chemical Industry Assoc. Available 

at http://www.bisphenol-a.org. 

Ryan, B.C., Hotchkiss, A.K., Crofton, K.M., and Gray Jr., L.E. (20109). In Utero and Lactational Exposure to 

Bisphenol A, in contrast to Ethinyl Estradiol, Does not Alter Sexually Dimorphic Behavior, Puberty, Fertility and 

Anatomy of Female LE Rats. Toxicological Sciences, ToxSci Advance Access published on October 28, 2009. 

doi:10.1093/toxsci/kfp266. Accessed at http://toxsci.oxfordjournals.org/cgi/reprint/kfp266. 114(1), 133-148 (2010). 

 

Sohoni, P., C.R. Tyler, K. Hurd, J. Caunter, M. Hetheridge, T. Williams, C. Woods, M. Evans, R. Toy, M. Gargas, 

and J.P. Sumpter. 2001. Reproductive Effects of Long-Term Exposure to Bisphenol A in the Fathead Minnow 

(Pimephales promelas). Env. Sci. Technol. 35: 2917-2925. 

Sumpter, J. P., Tyler, C.R. and Sherazi A. 2001. Bisphenol-A: Multigeneration study with the fathead minnow 

(Pimephales promelas). Brunel University (unpublished). 

Taiwan. 2007. Toxic Chemical Substances Control Act. Accessed at http://law.epa.gov.tw/en/laws/788537580.html. 

Taiwan. 2009. Bisphenol A Added to List of Toxic Chemicals; New Restrictions on Mercury, Asbestos, and 

Dioxane. Environmental Protection Administration. Accessed at 

http://www.epa.gov.tw/en/NewsContent.aspx?NewsID=1417&path=426. 

Tsai, W. 2006. Human Health Risk on Environmental Exposure to Bisphenol-A: A Review. Journal of 

Environmental Science and Health Part C, 24:225-255. 
U.S. Environmental Protection Agency Draft, 

12/9/20092/25/2010

U.S. Government Internal Deliberative Document, Do Not Quote, Cite, or Release

22

Tyl RW, Myers CB, Marr MC, Thomas BF, Keimowitz AR, Brine DR, Veselica MM, Fail PA, Chang TY, Seely 

JC, Joiner RL, Butala JH, Dimond SS, Cagen SZ, Shiotsuka RN, Stropp GD, 

Tyl, R.W., Myers, C.B., Marr, M.C., Sloan, C.S., Castillo, N.P., Veselica, M.M., Seely, J.C., Dimond, S.S., Van 

Miller, J.P., Shiotsuka, R.N., Beyer, D., Hentges, S.G., Waechter, J.M.,Jr. (.. 2008). Two-generation reproductive 

toxicity study of dietary bisphenol A (BPA) in CD-1 (Swiss) mice. Toxicological Sciences 104(2): 362-384. 

USEPA, 2009.USEPA. 1993. Integrated Risk Information System (IRIS) (1993). Accessed at 

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

USEPA. 2009a. Toxic Release Inventory. 2007 Public Data Release, Released March 14, 2009. 

http://www.epa.gov/tri/tridata/index.htm#pdr

USEPA. 2009b. Drinking Water Contaminant Candidate List and Regulatory Determinations, Contaminant 

Candidate List 3, Accessed at http://www.epa.gov/ogwdw000/ccl/ccl3.html. 

US FDA,. 2008. U. S. Food and Drug Administration 

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

US 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. 

USGS. 2008. US 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. 

http://pubs.usgs.gov/of/2008/1293/. 

vom Saal FS, Akingbemi BT, Belcher SM, Birnbaum LS, Crain DA, Eriksen M, et al. 2007. Chapel Hill bisphenol 

A expert panel consensus statement: integration of mechanisms, effects in animals and potential to impact human 

health at current levels of exposure. Reprod Toxicol 24(2):131–138. 

Waechter JM (. 2002). Three-generation reproductive toxicity study of dietary bisphenol A in CD Sprague-Dawley 

rats. Toxicological Sciences 68(1): 121-146. 

Willhite, C.C., G.L. Ball and C.J. McLellan. 2008. Derivation of a bisphenol A oral reference dose (RfD) and 

drinking-water equivalent concentration. J. Toxicol. Environ. Health B Crit. Rev. 11: 69-146.

Wisconsin. 2010. History of Senate Bill 271. Accessed at http://www.legis.state.wi.us/2009/data/SB271hst.html.

Bill text accessed at http://www.legis.state.wi.us/2009/data/SB-271.pdf.