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Bisphenol A

(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 initiate rulemaking under section 5(b)(4) of the Toxic Substances Control 

Act (TSCA) to identify BPA as a substance that may present an unreasonable risk of injury to the 

environment on the basis of (1) its adverse effects on growth 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 doses similar 

to levels found in the environment. A notice of proposed rulemaking is intended to publish in 

autumn, 2010. In late 2010, EPA intends to also initiate rulemaking under section 4(a) of TSCA 

to develop environmental effects data relevant to a determination that BPA does or does not 

present an unreasonable risk of injury to the environment. Beginning in January 2010, EPA 

intends to initiate collaborative alternatives assessment activities under its Design for the 

Environment (DfE) program to encourage reductions in BPA releases and exposures. One of 

these activities will relate to thermal and carbonless paper coatings, uses where alternatives 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 exposure. 

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

human health. EPA remains concerned with 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 is currently performing an in-depth 

reassessment on the potential risks 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 EPA will continue to coordinate closely with FDA 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 
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2

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 indicate that the levels of BPA in humans and the 

environment are below levels of potential concern for adverse effects. However, some nonguideline animal studies have suggested the potential for endocrine-related effects at much lower 

dose levels than those at which effects were seen in studies conducted under established 

guidelines. FDA is addressing these studies in its human health assessment. These low-dose 

studies in animals are also potentially of concern for the environment because the dose levels 

identified with effects are similar to some current environmental exposure levels. Regulatory 

authorities around the world that have reviewed the low dose studies have generally concluded 

that they are insufficient for use in risk assessment because of a variety of flaws in study design, 

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 rigorous studies. 

However, since guidelines for interpreting these studies have not yet been established and they 

do raise concerns for possible effects at levels similar to those found in the environment, some 

authorities, including Canada, have taken interim risk management action to protect certain 

sensitive populations. Due in part to these concerns, EPA intends to initiate the risk management 

actions identified in this Plan to protect the environment while further research continues. 

II. Introduction

 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 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.

 

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 specific 

sources used. 
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III. Scope of Review

 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. 

 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. 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 chemicals 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. 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 
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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), National Toxicology 

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

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

Identification Committee (DARTIC) 

o International – Japan, European Union (EU), European Food Safety 

Administration (EFSA) and Canada 

 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 discuss these low-dose data and 

virtually all (the FDA, DARTIC, Japan, the EU, and EFSA) have considered them insufficient 

for the purposes of hazard evaluation/risk assessment, the exceptions being Canada and the 

NTP/CERHR. 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 
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uncertainty led to a conclusion of “some concern” 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., 2009). 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). In addition, the NIEHS 

recently awarded $30 million dollars in grants for a two-year program of research on these 

issues.

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 

BPA-glucuronide (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. 

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

reported as total BPA, or free-BPA, or BPAG (except that BPAG has never been reported in fetal 

blood). In 2008, the National Report on Human Exposure to Environmental Chemicals reported 

that BPA was detected in the urine of 93% of the 2,517 people tested in 2003-4 (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 

that study was as a glucuronide conjugate (Calafat et al., 2009), providing evidence of the ability 

for neonates to 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. 

 There was a recent report suggesting that BPA levels in humans may be associated with 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). However, this report prompted an immediate review by the EFSA (2008b) 

in late 2008 which concluded that the study did not provide sufficient proof for the stated 

associations. 

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

value chosen in their respective assessments. Some assessments did not derive a hazard value per 

se, but did make hazard/risk decisions: 

 The California Proposition 65 Developmental and Reproductive Toxicant Identification 

Committee (DARTIC) voted on 7/15/09 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). 
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 Thirty-eight scientists (known as the “Chapel Hill Group”) 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, & 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 (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 Values for Human Health Assessments 

Authors Hazard Value 

(mg/kg/day) 1

Endpoint (Animal dose in mg/kg/day) 

And Study 

EPA (Integrated Risk 

Information System; 

IRIS (1993)) 

0.05 Reduced body weight (5) 

NTP two year cancer study in both rats and mice (1982) 

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 

EFSA (2006, 2008) 

and EU (2003, 2008) 

0.05 Used 5 (lowest value in cited studies) 

Tyl et al., (2002 and 2008) 

Japan (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 

and what is compared to an expected/estimated exposure value in a risk assessment. The uncertainty factors 

used by the various assessments: 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 
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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 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 exposure levels lower than those required for acute toxicity. There is a widespread 

variation in reported values for endocrine-related 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), Canada, and Japan as summarized below in Table 3. 

The different methodologies, endpoints and study results used by each country to derive these 

values highlight the significant uncertainty in the estimated hazard values. Canada used a 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 decreased spermatogenesis, induction 

of vitellogenin, delayed or ceased ovulation, 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 effects4

 at the time of these 

assessments, the EU and Japan set ecotoxicological hazard values based on conventional effects 

(mortality and reproductive effects). Canada concluded in its hazard characterization that 

“[c]onsidered together, the data provide strong evidence that bisphenol A is capable of eliciting 

adverse effects: (1) following prolonged exposure at levels below those usually seen to elicit 

effects in standard toxicity tests (i.e., tests based on recognized methods which evaluate 

endpoints such as survival, reproduction and growth); (2) following brief low-dose exposure, 

particularly at sensitive developmental stages, with effects apparent later in the life cycle; (3) on 

filial generations following parental exposure; and (4) using more than one mode of action.” 

(Canada, 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 

 

4 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. 
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Table 3: Summary of Bisphenol A Ecological Hazard Values 

Country 

Predicted No 

Effect 

Concentrations1 

(μg/L) 

Endpoints 

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

(B1). (EU, 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 be present in the environment as a result of direct releases from manufacturing 

or processing facilities, fugitive emissions during processing and handling, or release of 
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unreacted monomer from products (CERHR/NTP, 2008). According to the Toxics Release 

Inventory (TRI) Database, total release of BPA in 2007 was 1,132,062 pounds5

, 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, 2009). 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 potential for children to be 

exposed to BPA through their mouthing or accidental ingestion of such products 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 ingestion of BPA from infants’ and 

children’s toys and 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. Miyamoto and 

Kotake (2006) 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. 

Limited information is available for BPA concentrations in US water (Table 4). 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 US streams in 1999 and 2000 (Kolpin et al. 2002). The 

maximum concentration of 12 μg/L is an outlier; the BPA concentration in other US 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, 2008). 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., 2008). BPA was among the top five most frequently detected organic 

compounds (USGS, 2008). 

 

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

facility (32,928 pounds) or transfer to incineration (2,759,705 pounds). 
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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 

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, 2008; 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). 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 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 US ranged from 1.4 to 140 ppb dry weight. US 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-FAST2 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 
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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. 

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 identified as a chemical 

of potential concern 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 FR 21001). 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. 
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 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, and thus did not appear on the final 

CCL3 list. The notice publishing the final CCL3 list (74 FR 51850, 10/8/2009) 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). 

 Connecticut, Minnesota, 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 went into effect in July 2009. The Minnesota ban will go into effect on 1/1/2010; the 

Chicago ban on 1/31/2010; and the Connecticut ban on 10/1/2011. A California bill 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 to be raised again. 

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 (EU, 

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

two years that the 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 animal studies by the respective uncertainty factors applied by the different 

regulatory bodies, they concluded that expected exposures even from food contact uses, the 

largest expected source of exposure, did not present concern for risk to human health. 

 Ecological risk for BPA has been evaluated by the European Union (EU, 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, 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. 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 
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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. 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). 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 to 

BPA, apart from isolated hot spots, are estimated generally to be lower than the levels associated 

with effects in standard 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 low-dose studies, because some 

environmental exposures are similar to levels associated with observed effects in those low-dose 

studies. 

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

studies, while controversial, non-guideline studies suggest the potential for endocrine-related 

effects at much lower, environmentally-relevant levels than identified in the guideline 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 assessing potential health risks to both 

children and adults from exposure to BPA in food contact materials. Children may also be 

exposed to a lesser extent through 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 
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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. 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). 

Although there is controversy in interpreting some of the studies and 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 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. 

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. Initiate rulemaking under section 5(b)(4) of the Toxic Substances Control Act 

(TSCA) to identify BPA as a substance that may present an unreasonable risk of 

injury to the environment on the basis of (1) its adverse effects on growth 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 doses similar to levels found in the environment. 

A notice of proposed rulemaking is intended to publish in autumn, 2010. 

2. Initiate rulemaking under section 4(a) of TSCA to develop data with respect to 

environmental effects relevant to a determination that BPA 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 
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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 releases and exposures. 

One of these activities, intended to be initiated in January 2010, will address thermal 

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

available. This DfE environmental and health 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 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. 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 exposure. 

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

human health. EPA remains concerned with 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 is currently performing an in-depth 

reassessment on the potential risks of BPA to human health, and EPA will continue to coordinate 

closely with FDA 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. 

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. 

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