U.S. Environmental Protection Agency Draft, 12/9/2009 2/25/2010 U.S. Government Internal Deliberative Document, Do Not Quote, Cite, or Release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 vol ume (HPV) chemical widely used in manufacturing polycarbonate plas tics 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 initiat e consider initiating immediate actions addressing BPA in the environment based on concerns for potential eff ects 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) its its 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 indicat e some concern for potential estrogenic effects on aquatic organisms at low doses concentrations
similar to levels those found in the environment. A notice of proposed rulemaking is intended to publish in autumn, 2010. In late 2010, EPA intends to consider also initiat e ing rulemaking under section 4(a) of TSCA to develop envi ronmental 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 January February 2010, EPA intends to initiate collaborative alternatives assessment activities under its Design for th e Environment (DfE) program to encourage
reductions in BPA manufacturing and use to facilita te reductions in environmental releases and subsequent exposures. One of these activities will relate to thermal and carbonless paper coatings, including those on cash regist er 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. Add itionally, EPA intends to conduct alternatives analyses for BPA used in foundry castings since foundries are account able for large releases of BPA as reported under the Toxic Release Inventory (TRI), and fo r BPA-based materials lining water and waste water pipes since this applicati on may have a potential for human and environmental exposure.

EPA does not intend to initiate regulatory acti on under TSCA at this time on the basis of
human health. EPA remains concerned with committed to protecting human health, but notes that most human exposure, including exposure to ch ildren, comes through food packaging materials under the jurisdiction of the FDA. Food , food additives, drugs, cosmetics, and Drug Administration (FDA) . FDA medical devices, all regulated by FDA, are specifically excludedU.S. Environmental Protection Agency Draft,
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2 from the definition of chemical substance unde r TSCA. FDA, together with CDC and NIEHS, is currently performing an investing in

- depth reassessment on important new health studies in both
animals and humans to better determine and evaluate the potential risks health consequences of

BPA to human health

. The FDA reassessment is more comprehensive than t he 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 c ontact materials, EPA will work with FDA to identify and assess potential subs titutes. 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 Environmenta l 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 im pact 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 abou t its potential impact particularly on children’s
health and the environment. M ost studies Studies employing standardiz ed 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 animal recent studies have suggested the potential for endocrine

- related using novel low-dose approaches and examining different endpoints describe subtle effects in laboratory
animals at much low er dose levels than those at which effects were seen in studies conducted under established guidelines

. FDA is addressing very low concentrations. Some of these studies
in its human health assessment. These novel low-dose studies in animals are also potentially of
concern for the environment because the dose concentration levels identified with effects are similar to some current environmental exposur e levels. Regulatory aut horities around the world
that have reviewed the se low

- dose studies have generally conclude d that they are insufficient for
use in risk assessment because of a variety of flaws in some of the study design s , scientific uncertainty concerning the relevance to health an d ecological hazard of th e reported effects, and the inability of other research ers to reproduce the effects in more rigorous standardized studies. However, since guidelin es for interpreting Although there is disagreement about the interpretation of these low-dose studies ha ve not yet been established and

, they do raise potential
concerns for possible long-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 act ion to protect certai n sensitive populations

. Due in part to these concerns

, EPA intends to initiate

, such as infants and toddlers. For example,
the risk management action s 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. IntroductionU.S. Environmental Protection Agency Draft,
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3 As part of EPA's efforts to enhance th e 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 acti on 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 availabl e use, exposure, and hazard information 3 on BPA. EPA considered which of the various auth orities 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 proceedi ngs indicated by the Action Plan will include appropriate opportunities for public and stak eholder input, incl uding through notice and comment rulemaking processes.

III. Scope of Review

In conducting this review, EPA focused on th e two areas with the most potential for environmental releases and exposures: manuf acturing 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 drinki ng 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 drinki ng water and from the use of BPA in consumer products. EPA also examined potential ecologica l impact from the presence of BPA in the
environment.

Although most human exposure appears to co me 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 subjec t to TSCA, including the manu facture of non-food-additive, nonmedical products.

The FDA has jurisdiction over food additive s, which include food contact substances such as food packaging. These substances are no t 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 a n 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 includi ng 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,
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4 and Human Services (HHS) has provided recomm endations for parents and families to take reasonable steps to reduce exposur es, especially for young children. 4

Although most human exposure appears to co me from food packaging materials (e.g., Willhite, 2008) , less than 5% of the BPA produce d 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, in cluding the manufacture of non

- food

- additive , non

- medical products. In conducting this review, EPA focused on th e two areas with the most potential for
environmental releases and exposures: manufacturing and p rocessing. EPA also considered potential human exposures to workers during the manufacturing process and to the general population f rom the presence of BPA in drinking wa ter 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 exp osure of children to BPA fro m 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 plastic s, the majority of epoxy resins, and certain
other chemicals products 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 A ssumed Share Within TSCA Jurisdiction

Product Percent of BPA U.S. 2007 Consumption 1 Assumed TSCA share 2

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 l ack 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 transpor tation equipment, optical media such as DVDs, electrical/electronics equipment, construction, li nings inside drinking water pipes, thermal and carbonless paper coatings, foundry casting, and else where. A handful of companies manufacture

4 Recommendations released by HHS on January 15, 201 0 can be found at http://w ww.hhs.gov/safety/bpa/.U.S. Environmental Protection Agency Draft,
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5 most BPA, as well as most BPA-based polycarbo nate and epoxy resins, but numerous companies process BPA-based materials into final goods.

BPA-based materials tend to be chosen fo r their performance ch aracteristics. For example, polycarbonates are lightweight and tough compared to glass. In uses subject to FDA jurisdiction, public concern has le d industry to move toward non- BPA-based materials in such products as baby bottles, cups, and spoons and adult drink bottles, a nd to explore alternatives in food can linings. A vast number of other uses ar e 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 sp ecific uses in this screening-level review.

V. Hazard Identification Summary

Risk assessments for BPA have been c onducted by numerous governmental bodies and review panels. OPPT reviewed the following as sessments 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 ear ly 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 animal s (less than 1 mg/kg/day) are meaningful and relevant to humans. These low- dose effects are endocri ne-related and include effects on puberty and developmental neurotoxicol ogical effects (brain, behavior) at doses in
animal studies as low as 2 μ g/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, and 2008; California, 2009a; AIST, 2007;U.S. Environmental Protection Agency Draft,
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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 uncerta inty in the data, but took precautionary action to restrict BPA expos ures 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 scientis ts 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 su ch effects (Ryan et al., 20 1 0 9 ). The same investigators reported result s in male rats in an earlier pu blication, 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 fema le reproductive tract late r 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 w ould undertake additional research in this area. (FDA, 2010).

Metabolism Given 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 differ ently. Data in all four species indicate metabolism by conjugation in the liver with gl ucuronic acid to form the metabolite BPAglucuronide (BPAG). The relativ e 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 primat es and free-BPA is more prevalent in rodents. These differences in metabolism suggest that rode nts may be more sensitive to effects from BPA
than humans.

BPA has been found in human biological sample s (serum, breast milk, urine, fetal blood ) reported as , and umbilical cord blood). The literatu re 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 b een reported in fetal blood). ). In 2008, the National Report on Human Exposure to Environmental Chemicals CDC reported that BPA was detected in the urine of 93% of the 2,517 people tested in 2003

- 4 the 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 faciliti es showed that mean urinary concentrations of total BPA were an orde r of magnitude higher in the infants than in the general population. Over > 90% of the BPA found in the urine in that study was as in the form of a glucuronide conjugate (Calafat et al., 2009), providing eviden ce 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 NT P stated it “expressed “some concern” for potential exposures to the fetus,
infants and children. There are insufficie nt data from studies in humans to reach a conclusion on reproductive or developmental hazards presented by current exposure s to bisphenol A, but th ere 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,
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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 th e infants underwent intensive medi cal intervention, and that some of the BPA exposure may have been attri butable to contact with medical devices.

There was a recent report suggesting that in which a cross-sectional study design was used to suggest an association between BPA levels in humans may be associated with and a higher risk of diabetes, heart disease, and el evation of certain liver enzyme activities (Lang et al., 2008). The
authors examined the human data from a sub

- sample of the Nati onal 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 pr oof for the stated associations. EPA notes that the same investigative group recently publis hed an online research article repeating their original findings
for heart disease but not diab etes on a second NHANES populati on from 2005-6 (Melzer et al., 2010).

Table 2 below is a list of each major assessment reviewed and the accompanying hazard
value intake limits chosen in their respective assessmen ts. Some assessments did not derive a hazard value an 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) th ere is relevance of in vitro data to in vivo effects; (2) ecological
studies are consistent with la b 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 th at the low dose data are not relevant to humans (and reaffirmed this in an u pdate reported in Goodman et al., 2006).

 A National Toxicology Program (NTP) Cent er for Evaluation of Risks to Human Reproduction (CERHR) Panel ( NTP- CERHR /NTP , 2008) concluded that rodent studies suggest that BPA causes “...neur al 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 Values Intake Limits for Human Health Assessments
Authors Hazard
Value Intake
Limit (mg/kg/day) 1 Endpoint (Animal dose in mg/kg/day) And Study

US EPA (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 bod y 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

0.5U.S. Environmental Protection Agency Draft,
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8 Table 2: BPA Hazard Values Intake Limits for Human Health Assessments
Authors Hazard
Value Intake
Limit (mg/kg/day) 1 Endpoint (Animal dose in mg/kg/day) And Study

EFSA (2006,

2008 2008a-b ) and

EU EC (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 acceptabl e dose in humans. This value is what is shown here
and as an “intake limit” and is what is compared to an expected/e stimated exposure value in a risk assessment. The uncertainty factor s 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 determ ine potential effects of BPA exposure on invertebrates, fish, amphibians, reptil es, birds, and wild mammals, and a thorough review is provided by Crain et al. (2007). EPA’s screening-le vel 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 i nvestigation 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 show n that BPA can affect growth , reproduction and development in aquatic organisms. Among freshwat er organisms, fish appear to be the most sensitive species. Eviden ce of endocrine-related effects in fi sh, aquatic invertebrates, amphibians and reptiles has been reported at environmentally relevant exposure levels lower than those required for acute toxicity. Ther e 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 ( EU EC ), Canada, and Japan as summarized below in Table 3. The different methodologies, endpoints and study results used by each country to derive theseU.S. Environmental Protection Agency Draft,
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9 values highlight the significant uncertainty in the estimated hazard va lues. 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 st udies referenced in the EU and Japanese hazard evaluations. However, because there were no standardized test guidelines or risk assessment guidance for evaluating some of these endocrine-related effects 6 at the time of these assessments, the EU and Japan set ecotoxicologica l 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 str ong evidence that bisphenol A is capable of eliciting adverse e ffects: (1) following prolonged e xposure at levels below those usually seen to elicit effects in standard toxi city tests (i.e., tests based on recognized methods which evaluate endpoints such as survival, re production and growth); (2) following brief lowdose exposure, particularly at sensitive developmen tal 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
Concentrations 1
(μg/L) Endpoints

European
Union 1.5 The predicted no effect concentration (PNEC) for aquatic organisms (derived by using a stat istical analysis of data from
available data on freshwater a nd marine aquatic organisms (in this case, 16 different studie s, unpublished and published, from 10 different taxonomic groups) to ar rive at a value of 7.5 μg/L, which is divided by an uncertain ty factor of 5, resulting in a PNEC of 1.5 μg/L ( EU EC , 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 appl ying 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 withthe 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 re sult from the interactions identified through the Tier 1 assays. EPA has established Tier 1 screening test guidelin es. Tier 2 test guidelines will be developed after the completion of ongoing validation studies.U.S. Environmental Protection Agency Draft,
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10 Table 3: Summary of Bisphenol A Ecological Hazard Values

Country Predicted No
Effect
Concentrations 1
(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 concen tration to PNEC is less than one, the risk is generally considered acceptable. As noted in the table, countrie s 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 (H SDB, 2009). It has low to moderate mobility in soil. It is expected to biodegrade under environmental co nditions, although conflicting results have been obtained using biodegradation screen ing tests. However, the weight of evidence suggests that it is not expected to be persistent in the environment, and degrada tion is expected to occur. The rate of atmospheric photooxidation is rapid. Hydr olysis is expected to be negligible under
environmental conditions since BPA does not contai n 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). ( EU EC

, 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 cond itions, 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 be is present in the environment as a result of direct releases from manufacturing or pr ocessing facilities

, (USEPA, 2009a). BPA may al so be present in the
environment as a result of fugitive emissions during proces sing 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 pounds 7 , with releases of 122,965 pounds to air, 6,246 pounds to water (dir ect), 14,972 pounds released on-site to land, and 684,638 pounds transferred off- site to land (USEPA, 2009 a ). 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 m outhing or accident al ingestion of such consumer products

7 This total does not include off-site water transfer to PO TWs (Publicly Owned Treatme nt Works) wastewater
treatment facilit y ies (32,928 pounds) or transfer to incineration (2,759,705 pounds).U.S. Environmental Protection Agency Draft,
12/9/2009 2/25/2010 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 hum an 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; industr ial uses; commercial uses; sele cted consumer uses; ingestion of BPA in drinking water, incl uding drinking water contaminated by wastewater releases to surface water, drinking water drawn from ground water contaminated by leachate from landfills, and drinking water distributed th rough BPA-based water pipes; and incidental ingestion of BPA
from infants’ and c hildren’s toys and contact with consumer products. OPPT used release data, modeling, and information available in peer-revi ewed articles and government publications to obtain information on exposure to BPA.

Very little information is availabl e 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 in take of BPA from toys for male infants 0 to 5 months of age to be 0.026 μ g/kg bw per day and the mean intake for infants 6-11 months to be

0.069 μ g/kg per day. Current information posted by the HHS i ndicates that most plastic toys that children put in their mouths do not contain BPA 4 . No studies were identif ied measuring potential exposures to adults or children from contact with other consumer products.

Limited information is available for BPA concentrations in US U.S. water and other
environmental media (Table 4 , providing values from all of th e studies cited in this discussion ). Most environmental monitoring resu lts show that the concentrati ons of BPA in water bodies are
lower than 1 μ g/L, mainly due to its partitioning a nd biodegradability properties (Tsai

, 2006).
BPA was detected at a median concentration of 0.14 μ g/L and a maximum concentration of 12

μ g/L in 41.2% of 85 samples collected from US U.S. streams in 1999 and 2000 (Kolpin et al

. ., 2002). The maximum concentration of 12 μ g/L is an outlier; the BP A concentration in other

US U.S. waters was much lower (as indicated by the median concentration of 0.14 μ g/L). In 2001 and 2002, BPA was not detected (< 0.001 μ g/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 drinki ng water at various stages of tr eatment at plants in Louisiana (Boyd et al

. ., 2003).

In 2000, the U.S. Geological Survey collect ed 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

, 2008 2008a-b ). BPA was detected in 29.8% of the sampled groundwater sites, with a m ean detected concentration of 1.78 μ g/L and a range of 1.06

to 2.55 μ g/L (Barnes et al., 2008 b ). BPA was among the top five most frequently detected organic compounds ( USGS

, 2008 Barnes, 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 a nd Puerto Rico, in areas that were known or suspected to have at least so me human and/or animal wastew ater sources in upstream or upgradient areas. These sources comprise 25 gr oundwater and 49 surface water sources of drinking water serving populations ranging from one family to more than 8 million people. BPAU.S. Environmental Protection Agency Draft,
12/9/2009 2/25/2010 U.S. Government Internal Deliberative Document, Do Not Quote, Cite, or Release

12 was detected in 9.5% of these sa mples at a reporting level of 1 μ g/L. The maximum concentration measured in these samples was 1.9 μ g/L ( USGS , 2008 Barnes, et al., 2008a ; Focazio et al., 2008).

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

μ g/L in landfill leachate and 1.4 μ g/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 singl e point may not be representative of the country.
Landfill leachate from other count ries contained more than 500 μ g/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 μ g/L and
treated leachate concentrations of 5.1 μ g/L (Crain et al., 2007).

Soil concentrations reported in by NTP- CERHR /NTP ( 2008 ) were for soil samples taken from outdoor play areas of home s and daycares; BPA concentra tions 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 US United States ranged from 1.4 to 140 ppb dry weight.

US 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 (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 be low the MDL, while the reported range includes only detected values

E-FAST2 8 modeling of BPA releases in the 2007 TRI showed the most conservative estimates of the potential acute dose rate for inge stion of BPA in drinking water by children ages 1-2 ranged from 0.0000531 to 16.5 μg/kg/day, and the mo st 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 characterizatio n. E-FAST2 is based on numerous assumptions that are designed to be conservative; for exampl e, E-FAST2 does not account for the half life of a chemical in surface water. The inputs select ed for the E-FAST2 mode ling of BPA were also selected to be conservative; for example, the bi oconcentration factor was selected to be at the high end of the range of values re ported 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,
12/9/2009 2/25/2010 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 μ g/kg bw/day for adults. The highest estimate by FDA is 2.42 μ g/kg bw/day for female infants, 1-2 months of age ( U.S. FDA, 2008). Human exposures fr om food contact uses are consistently estimated by researchers to be higher than exposures fr om all other sources (e.g., Willhite, 2008).

Workers may be exposed to BPA by inhalation or skin contact duri ng 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 us e in preparing scr eening-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 BP A from containers, which is the only identified potential exposure during this st age 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 h eavily regulated chemical in the U.S., but has been identified evaluated 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 Regul atory Reviews and Actions

BPA was included in the ini tial proposal of the Toxics Release Inventory (TRI) list published in 1987 (52 FR Fed. 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,
12/9/2009 2/25/2010 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 substanc es that might be appropriate candidates for future regulation. Although BPA appeared on th e 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 eff ect levels in guideline studies , and thus did not appear on the final CCL3 list. The notice publishing the final CCL3 list (74 FR Fed. Reg. 51850, 10/ October 8 /

, 2009) does not specifically addr ess BPA, but supporting material s available on the EPA website describe the process and criteria used in the de velopment 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 al l reusable food and beverage containers. The Suffolk County ban (County of Suffolk, 2009) went into effect in July 2009. The Minnesota ban
wi ll 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 stat e legislature on 2/17/2010, and will go into effect 90 days after it is publishe d 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 Regulator y Reviews and Actions

Numerous foreign governmental bodies and re view panels have conducted human health risk assessments for BPA in the recent pa st. Japan (AIST, 2007), the European Union ( EU EC

, 2008), and the European Food Safety Administrati on (EFSA, 2008) all concluded within the past two years that the novel studies indicating low dos e, endocrine-related effects were insufficient for the purposes of hazard evaluation/risk asse ssment. Using hazard values derived by dividing
the doses used in standardized animal studies by the respective un certainty factors applied by the different regulatory bodies, they these regulatory bodies concluded that expected exposures even from food contact uses, the larges t expected source of exposure, di d not present concern for risk
to human health.

In contrast, on June 26, 2009, Canada became th e first country to take regulatory action against BPA. Canada announced that it was m oving forward with proposed regulations to prohibit the advertisement, sale and importati on of polycarbonate plas tic baby bottles that contain BPA, to reduce newborn and infant expo sure to this substance. In announcing this decision, Canada noted “The Government has conc luded 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 ( EU EC , 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,
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15 particularly fish.” The EU conc luded that although the predicte d 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 concen trations in water have the poten tial 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 avia n wildlife species in Cana da. In the conclusion of its risk assessment, Canada st ated that it is considered appr opriate 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 bi ological 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 polycarbona te plastic baby bottles that contain BPA, to reduce newborn and infant exposure to this substance. In making this decisi on, Canada indicated that its decision was grounded in the precautionary principle, noting “Science tells us that exposure levels are below those t hat could cause health effects; however, due to the uncertainty raised in some studies relating to the potential effects of lo w levels of bisphenol A, the Government of Canada is taking action to enha nce 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 c oncern of pollution of the enviro nment or the endangerment of
human health. Handlers of Class 4 substances are required to k eep and report records of the toxicity, production, release, and use of those chemicals, but th e chemicals are not subject to
other restrictions on hand ling, transportation, or use ( http://law.epa.gov.tw/en/l aws/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 mana gement approaches to BPA is the uncertainty surrounding the actual determinati on of risk, particularly from low dose exposures. There is agreement among international regu latory 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 determ inations that current us es of BPA do not present human health risks warranting further regu latory controls. Similarly, environmental exposures

to concentrations of BPA, apart from isolated hot spots, ar e estimated generally to be lower than
the levels associated with effects in standard ized 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 a nd the environment of the effects seen in some novel low-dose studies, because some environmental exposures concentrations are similar to levels
associated with observed effects reported in those low

- dose studies.U.S. Environmental Protection Agency Draft,
12/9/2009 2/25/2010 U.S. Government Internal Deliberative Document, Do Not Quote, Cite, or Release

16 Reproductive and developmental toxic ity are the most sensitive effects observed in the guideline studies, while controversial, non

- guideline and some novel studies suggest the potential
for endocrine-related effects at much lower , environmentally

- relevant levels than the effect
levels identified in the guideline standardized 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 us e of BPA in food packaging materials and child feeding products (such as ba by bottles, sippy cups, and spoons) within FDA jurisdiction. FDA is assessing conducting 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 continues 4

. 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 a dults’ 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 unde r 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 potenti al effects of BPA on human health

. (NIEHS, 2009). Including these Recovery Act funds, NIEHS is invest ing 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 in cluding behavior, obesity, diab etes, reproductive disorders, development of prostate, breast and uterine cancer, asthma, cardiovascular diseases and transgenerational or epigenetic effects ( http://www.nih.gov/news/h ealth/oct2009/niehs

- 28.htm ).

.

Given that human exposures from TSCA us es 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
controversy disagreement in interpreting some of the novel low-dose studies and some of the effects observed in the many aquatic toxicity stud ies performed thus far with BPA, a comparison of the range of predicted no eff ect concentration (PNEC) values used in the three international regulatory risk assessments (0.175 to 1.6 μ g/L, Table 3) with measured concentrations in U.S. waters and sediments, which included values as high as 12 μ g/L (surface water), 2.55 μ g/L (ground water), and 140 μ g/kg sediment (freshwater sediment) (Table 4), raises concern about possible risk of injury to aqua tic organisms. However, limited information is available for BPA concentrations in U.S. water, and most availabl e environmental monitoring results show that the
concentrations of BPA in wa ter bodies are lower than 1 μ g/L (median concentration of 0.14

μ g/L, below any calculated PNEC). These environm ental measurements represent only isolated snapshots in time and do not provide an indica tion of how many areas may exceed PNEC valuesU.S. Environmental Protection Agency Draft,
12/9/2009 2/25/2010 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 th e 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 ag encies; and voluntary actions thr ough 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 fu rther research con tinues. Accordingly, EP A intends to : :

1. I nitiate 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) its its 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 so me concern for potential estrogenic effects on aquatic organisms at low doses concentrations similar to levels those found in the environment. A notice of proposed rulema king is intended to publish in autumn,

2010.

2. I nitiate Consider initiating rulemaking under section 4(a) of TSCA to develop data with respect to environmen tal effects relevant to a further determination that BPA
either does or does not present an unreasonable ri sk of injury to the environment. This may include testing or monitoring data in the vicinity of landfills, manufacturing facilities, or similar locations to dete rmine the potential for BPA to enter the environment, including surface water, ground wa ter, and drinking water, at levels of potential concern particular ly for environmental organisms, pregnant women, and children. EPA anticipates publishing an adva nce notice of proposed rulemaking in
late 2010.

3. Initiate collaborative alte rnatives assessment activiti es 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 January February 2010, will address thermal and carbonless paper coatings, a use where preferable alternatives to BPA may be readily available. This DfE environmental and health alternatives assessment is expected to be completed in the latter ha lf of 2011. Paper coatings are not a major use of BPA, but thermal paper has been repor ted to contain free BPA, which would be expected to be more available for expos ure than BPA bound into resin or plastic. Popular uses of this paper include airline ti ckets, event and cinema tickets, labels, and point of sale applications (receipts). Wh ile there is little concern for dermalU.S. Environmental Protection Agency Draft,
12/9/2009 2/25/2010 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 anal yses 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 acti on under TSCA at this time on the basis of
human health. EPA remains concerned with committed to protecting human health, but notes that most human exposure, including exposure to ch ildren, 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 an investing in

- depth reassessment on important new health studies in both animal s and humans to better determine and evaluate the potential risks health 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 c ontact materials, EPA will work with FDA to identify and assess potential substitutes. Levels of exposure that may be identified by FDA the ongoing review as being of concern to human health, in cluding children’s health, will affect the
extent to which EPA would take additional actio n to address potential risks to human health resulting from uses within TSCA jurisdiction.

A substantial program of research is underway through NIEH S 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 BP A, 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 Tech nology). 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 wa stewater 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, M itra S. 2003. Pharmaceuticals and pers onal 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,
12/9/2009 2/25/2010 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

, . 2009 a . California Proposition 65 Committee (see presen tations/meeting materials for DARTIC decision meeting on July 15, 2009 http://www.oehha.ca.gov/prop65/public_meetings/dart071509ag.html )

California. 2009b. California Legisl ature 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 h ttp://www.leginfo.ca.gov/pu b/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/medi a/nr-cp/_2009/20 09_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/COCWe bPortal/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 Pot ential 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., Lauf er, H., LeBlanc, G.A. and L.J. Guillette, Jr. 2007. An ecological assessment of Bisphenol A: evidence from comp arative biology. Reprod. Toxicology (24): 225-239.

EPP

. 2008. EPP Rapid Research. “Rehabilitating Home Wa ter Pipes with Epoxy Co atings.” December 2008. Accessed October, 2009, at www.pprc.org http://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 Prior ity 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 Protectio n, European Chemicals Bureau, European Commission Joint Research Centre, 3rd Prior ity List, Luxembourg: Office for Official Publications of the European Communities.U.S. Environmental Protection Agency Draft,
12/9/2009 2/25/2010 U.S. Government Internal Deliberative Document, Do Not Quote, Cite, or Release

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