Tuesday, July 3, 2012

Even China finds BPA Safety Concerns...

New study links widespread BPA chemical to brain cancer

Posted on: 1:42 pm, June 27, 2012, by updated on: 06:29pm, June 27, 2012

A newly published study, from China, is the first to report a link between brain cancer and exposure to bisphenol A (BPA), which is widely used in consumer products.
The study examined the relationship between BPA exposure and the common type of brain tumor called meningioma.
Researchers found a positive association between BPA concentrations in urine and a meningioma diagnosis. Those with the highest urine BPA levels were about 1.6 times more likely to be diagnosed with meningioma compared to those with lower concentrations.
Previous studies have shown that gender, Body Mass Index (BMI) and hormone replacement therapy all can influence the risk of meningioma. This new study showed that among all weight levels there was still a connection between high BPA urine levels and the disease.
Enivronmental Health news reports that 90% of diagnosed meningioma cases are benign, but the slow-growing tumors can still cause illness and death, as they push against the brain and spinal cord.

BPA shows up in many consumer products. The biggest push for awareness of BPA’s has been in regards to water bottles and food cans. The chemical, which behaves like estrogen, also shows up in plastics, dental sealants,  and water pipes.
BPAs have also been found in paper cash register receipts.
CBS reported that “extraordinarily high levels of BPA were found on two-fifths of the paper receipts tested recently by the Environmental Working Group, a nonprofit organization in Washington, D.C. “
CBS has also reported in the past that other studies have linked BPA to anxiety, hyperactivity, and individuals with heart disease.
Environmental Health News reports that “exposure in people is widespread and occurs mainly through eating or drinking contaminated food and beverages.”
On Tuesday, the Endocrine Society released a statement that the U.S. Environmental Protection Agency and other regulators are not using the best available science in their assessment of bisphenol-A’s (BPA) safety.
-  end  -
Bloggers note:  Google the letters "BPA" and the top sites returned are BPA ads with .org adresses.  This indicates that BPA needs significant counter-image marketing, which doesn't speak well for this chemical additive.  The amount of internet marketing suggests that a lot of money is behind the marketing effort, which might not be so if independent research corroborated that BPA was safe.   
BPA BACKGROUND from Wikipedia: 
Bisphenol A (BPA) is an organic compound with the chemical formula (CH3)2C(C6H4OH)2. It is a colorless solid that is soluble in organic solvents, but poorly soluble in water. Having two phenol functional groups, it is used to make polycarbonate polymers andepoxy resins, along with other materials used to make plastics.
BPA is controversial because it exerts weak, but detectable, hormone-like properties, raising concerns about its presence in consumer products and foods contained in such products. Starting in 2008, several governments questioned its safety, prompting some retailers to withdraw polycarbonate products. A 2010 report from the United States Food and Drug Administration (FDA) raised further concerns regarding exposure to fetuses, infants, and young children.[1] In September 2010, Canada became the first country to declare BPA a toxic substance.[2][3] In the European Union and Canada, BPA use is banned in baby bottles.[4] Bisphenol A has a vapor pressure of5*10-6 Pa.[5]  [snip]


Bisphenol A was discovered in 1891 by Russian chemist Aleksandr Dianin. In the early 1930s the British chemist Charles Edward Dodds recognized BPA as an artificial estrogen.[31] During that time BPA had two initial uses. The first use of BPA was to enhance the growth of cattle and poultry. The second use of BPA in the mid 1930s was as an estrogen replacement for women. BPA was only briefly used as an estrogen replacement and was replaced by diethylstilbestrol (DES).[32] Based on research by chemists at Bayer and General Electric, BPA has been used since the 1950s to harden polycarbonate plastics and make epoxy resin, and in the lining of food and beverage containers.[33][34] The first evidence of the estrogenicity of bisphenol A came from experiments on rats conducted in the 1930s,[35][36] but it was not until 1997 that adverse effects of low-dose exposure on laboratory animals were first proposed (hormesis).[22] Modern studies began finding possible connections to health issues caused by exposure to BPA during pregnancy and during development. See Government and industry response. Research is ongoing and the debate continues as to whether BPA should be banned or not, and to what extent, all over the world. In 2010 Canada's department of the environment declared BPA to be a "toxic substance".[37]

[edit]Health effects

Bisphenol A is a weak endocrine disruptor, which can mimic estrogen and may lead to negative health effects.[38][39][40][41] Early developmental stages appear to be the period of greatest sensitivity to its effects,[42] and some studies have linked prenatal exposure to later neurological difficulties. Regulatory bodies have determined safety levels for humans, but those safety levels are currently being questioned or are under review as a result of new scientific studies.[43][44] A 2011 study that investigated the number of chemicals pregnant women are exposed to in the U.S. found BPA in 96% of women.[45]
In 2009, The Endocrine Society released a statement citing the adverse effects of endocrine-disrupting chemicals, and the controversy surrounding BPA.[46]
In 2011, the chief scientist of the United Kingdom's Food Standards Agency commented on a study on dietary exposure of adult humans to BPA performed by the EPA,[47] saying, "This corroborates other independent studies and adds to the evidence that BPA is rapidly absorbed, detoxified, and eliminated from humans – therefore is not a health concern."[48]In the study 20 subjects were tested for BPA every hour for twenty-four hours while consuming three meals consisting of canned food.[47]
In 2012 a paper was written in response to this study, however, criticizing the study as lacking data and having flawed assumptions.[49]
Overall, empirical evidence supporting the negative health effects of BPA varies significantly across studies. Opinions vary greatly about the health effects of BPA. Some studies conclude that BPA poses no health risks while others state that BPA causes a number of adverse health effects. In general, the European’s Scientific Committee on Food, the EUs European Chemicals Bureau, the European Food Safety Authority, and the US Food and Drug Administration have concluded that current levels of BPA present no risk to the general population. However, experts in the field of endocrine disruptors have stated that the entire population may suffer adverse health effects from current BPA levels.[50] Experts advise readers of scientific studies to consider who conducted the study, what their affiliations are, and what the purpose of the study was.

[edit]Expert panel conclusions

In 2006, the US Government sponsored an assessment of the scientific literature on BPA. 38 opponents of bisphenol A gathered in Chapel Hill, North Carolina to review several hundred studies on BPA, many conducted by members of the group. At the end of the meeting, the group issued the Chapel Hill Consensus Statement, which stated “BPA at concentrations found in the human body is associated with organizational changes in the prostate, breast, testis, mammary glands, body size, brain structure and chemistry, and behavior of laboratory animals.”[51]
The Chapel Hill Consensus Statement claimed that average levels in people are above those that cause harm to many animals in laboratory experiments. They noted that while BPA is not persistent in the environment or in humans, biomonitoring surveys indicate that exposure is continuous, however, which is problematic because acute animal exposure studies are used to estimate daily human exposure to BPA, and no studies that had examined BPA pharmacokinetics in animal models had followed continuous low-level exposures. They added that measurement of BPA levels in serum and other body fluids suggests the possibilities that BPA intake is much higher than accounted for, and/or that BPA can bioaccumulate in some conditions (such as pregnancy).[52] A 2011 study, the first to examine BPA in a continuous low-level exposure throughout the day, did find an increased absorption and accumulation of BPA in the blood of mice.[53]
In 2007 studies indicating harm reported a variety of deleterious effects in rodent offspring exposed in the uterus: abnormal weight gain, insulin resistance, prostate cancer, and excessive mammary gland development.[54]
A panel convened by the U.S. National Institutes of Health in 2007 noted that many of the studies referenced by the Chapel Hill group had methodological problems. This panel could not rule out "some concern" about BPA's effects on fetal and infant brain development and behavior.[8] The concern over the effect of BPA on infants was also heightened by the fact that infants and children are estimated to have the highest daily intake of BPA.[55] A 2008 report by the U.S. National Toxicology Program (NTP) later agreed with the panel, expressing "some concern for effects on the brain, behavior, and prostate gland in fetuses, infants, and children at current human exposures to bisphenol A," and "minimal concern for effects on the mammary gland and an earlier age for puberty for females in fetuses, infants, and children at current human exposures to bisphenol A." The NTP had "negligibleconcern that exposure of pregnant women to bisphenol A will result in fetal or neonatal mortality, birth defects, or reduced birth weight and growth in their offspring."[56]


A 2008 review has concluded that obesity may be increased as a function of BPA exposure, which "...merits concern among scientists and public health officials."[57] A 2009 review of available studies has concluded that "perinatal BPA exposure acts to exert persistent effects on body weight and adiposity".[58] Another 2009 review has concluded that "Eliminating exposures to (BPA) and improving nutrition during development offer the potential for reducing obesity and associated diseases".[59] Other reviews have come with similar conclusions.[60][61] A later study on rats has suggested that perinatal exposure to drinking water containing 1 mg/L of BPA increased adipogenesis in females at weaning.[62] Another study suggested that larger size-for-age was due to a faster growth rate rather than obesity.[63]

[edit]Neurological issues

A panel convened by the U.S. National Institutes of Health determined that there was "some concern" about BPA's effects on fetal and infant brain development and behavior.[8] A 2008 report by the U.S. National Toxicology Program (NTP) later agreed with the panel, expressing "some concern for effects on the brain".[56] In January 2010 the FDA expressed the same level of concern.
A 2007 review has concluded that BPA, like other xenoestrogens, should be considered as a player within the nervous system that can regulate or alter its functions through multiple pathways.[64] A 2007 review has concluded that low doses of BPA during development have persistent effects on brain structure, function and behavior in rats and mice.[65]A 2008 review concluded that low-dose BPA maternal exposure causes long-term consequences at the level of neurobehavioral development in mice.[66] A 2008 review has concluded that neonatal exposure to Bisphenol-A (BPA) can affect sexually dimorphic brain morphology and neuronal adult phenotypes in mice.[67] A 2008 review has concluded that BPA altered long-term potentiation in the hippocampus and even nanomolar dosage could induce significant effects on memory processes.[68] A 2009 review raised concerns about BPA effect on anteroventral periventricular nucleus.[69]
A 2008 study by the Yale School of Medicine demonstrated that adverse neurological effects occur in non-human primates regularly exposed to bisphenol A at levels equal to theUnited States Environmental Protection Agency's (EPA) maximum safe dose of 50 µg/kg/day.[70][71] This research found a connection between BPA and interference with brain cell connections vital to memory, learning, and mood.
A 2010 study with rats prenatally exposed to 40 µg/kg bw BPA has concluded that corticosterone and its actions in the brain are sensitive to the programming effects of BPA.[72]

[edit]Disruption of the dopaminergic system

A 2005 review concluded that prenatal and neonatal exposure to BPA in mice can potentiate the central dopaminergic systems, resulting in the supersensitivity to the drugs-of-abuse-induced reward effects and hyperlocomotion.[73]
A 2008 review has concluded that BPA mimics estrogenic activity and impacts various dopaminergic processes to enhance mesolimbic dopamine activity resulting in hyperactivity, attention deficits, and a heightened sensitivity to drugs of abuse.[74]
A 2009 study on rats has concluded that prenatal and neonatal exposure to low-dose BPA causes deficits in development at dorsolateral striatum via altering the function of dopaminergic receptors.[75] Another 2009 study has found associated changes in the dopaminergic system.[76]

[edit]Thyroid function

A 2007 review has concluded that bisphenol-A has been shown to bind to thyroid hormone receptor and perhaps have selective effects on its functions.[77]
A 2009 review about environmental chemicals and thyroid function raised concerns about BPA effects on triiodothyronine and concluded that "available evidence suggests that governing agencies need to regulate the use of thyroid-disrupting chemicals, particularly as such uses relate exposures of pregnant women, neonates and small children to the agents".[78]
A 2009 review summarized BPA adverse effects on thyroid hormone action.[79]

[edit]Cancer research

According to the WHO's INFOSAN, carcinogenicity studies conducted under the US National Toxicology Program, have shown increases in leukaemia and testicular interstitial cell tumours in male rats.[80]
A 2010 review at Tufts University Medical School concluded that Bisphenol A may increase cancer risk.[81]

[edit]Breast cancer

A 2008 review stated that "evidence from animal models is accumulating that perinatal exposure to (...) low doses of (..) BPA, alters breast development and increases breast cancer risk".[82] Another 2008 review concluded that "animal experiments and epidemiological data strengthen the hypothesis that fetal exposure to xenoestrogens may be an underlying cause of the increased incidence of breast cancer observed over the last 50 years".[83]
A 2009 in vitro study has concluded that BPA is able to induce neoplastic transformation in human breast epithelial cells.[84] Another 2009 study concluded that maternal oral exposure to low concentrations of BPA during lactation increases mammary carcinogenesis in a rodent model.[85]
A 2010 study with the mammary glands of the offspring of pregnant rats treated orally with 0, 25 or 250 µg BPA/kg body weight has found that key proteins involved in signaling pathways such as cellular proliferation were regulated at the protein level by BPA.[86]
A 2010 study has found that BPA may reduce sensitivity to chemotherapy treatment of specific tumors.[87]


In vitro studies have suggested that BPA can promote the growth of neuroblastoma cells.[88][89] A 2010 in vitro study has concluded that BPA potently promotes invasion andmetastasis of neuroblastoma cells through overexpression of MMP-2 and MMP-9 as well as downregulation of TIMP2.[90]

[edit]Prostate development and cancer

A 1997 study in mice has found that neonatal BPA exposure of 2 μg/kg increased adult prostate weight.[91] A 2005 study in mice has found that neonatal BPA exposure at 10 μg/kg disrupted the development of the fetal mouse prostate.[92] A 2006 study in rats has shown that neonatal bisphenol A exposure at 10 μg/kg levels increases prostate gland susceptibility to adult-onset precancerous lesions and hormonal carcinogenesis.[93] A 2007 in vitro study has found that BPA within the range of concentrations currently measured in human serum is associated with permanent increases in prostate size.[94] A 2009 study has found that newborn rats exposed to a low-dose of BPA (10 µg/kg) showed increased prostate cancer susceptibility when adults.[95]

[edit]DNA methylation

At least one study has suggested that bisphenol A suppresses DNA methylation[96] which is linked to epigenetic changes.[97]

[edit]Reproductive system and sexual behavior research

A 2007 study using pregnant mice showed that BPA changes the expression of key developmental genes that form the uterus, which may impact female reproductive tract development and future fertility of female fetuses.[98]
A series of studies made in 2009 found:
  • Mouse ovary anomalies from exposure as low as 1 µg/kg, concluded that BPA exposure causes long-term adverse reproductive and carcinogenic effects if exposure occurs during prenatal critical periods of differentiation.[99]
  • Neonatal exposure of as low as 50 µg/kg disrupts ovarian development in mice.[100][101][102]
  • Neonatal BPA exposition of as low as 50 µg/kg permanently alters the hypothalamic estrogen-dependent mechanisms that govern sexual behavior in the adult female rat.[103]
  • Prenatal exposure to BPA at levels of (10 μg/kg/day) affects behavioral sexual differentiation in male monkeys.[104]
  • In placental JEG3 cells in vitro BPA may reduce estrogen synthesis.[105]
  • BPA exposure disrupted the blood-testis barrier when administered to immature, but not to adult, rats.[106]
  • Exposure to BPA in the workplace was associated with self-reported adult male sexual dysfunction.[107]
A 2009 rodent study, funded by EPA and conducted by some of its scientists, concluded that, compared with ethinyl estradiol, low-dose exposures of bisphenol A (BPA) showed no effects on several reproductive functions and behavioral activities measured in female rats.[108] That study was criticized as flawed for using polycarbonate cages in the experiment (since polycarbonate contains BPA) and the claimed resistance of the rats to estradiol,[109] but that claim was contested by the authors and others.[110] Another 2009 rodent study found that BPA exposure during pregnancy has a lasting effect on one of the genes that are responsible for uterine development and subsequent fertility in both mice and humans (HOXA10). The authors concluded, "We don't know what a safe level of BPA is, so pregnant women should avoid BPA exposure."[111]
In a 2010 study, mice were given BPA at doses thought to be equivalent to levels currently being experienced by humans. The research showed that BPA exposure affects the earliest stages of egg production in the ovaries of the developing mouse fetuses, thus suggesting that the next generation may suffer genetic defects in such biological processes as mitosis and DNA replication. In addition, the research team noted that their study "revealed a striking down-regulation of mitotic/cell cycle genes, raising the possibility that BPA exposure immediately before meiotic entry might act to shorten the reproductive lifespan of the female" by reducing the total pool of fetal oocytes.[112] Another 2010 study with mice concluded that BPA exposure in utero leads to permanent DNA alterations in sensitivity to estrogen.[113] Also in 2010, a rodent study found that by exposing fetal mice to BPA during pregnancy and examining gene expression and DNA in the uteruses of female fetuses, BPA exposure permanently affected the uterus by decreasing regulation of gene expression. The changes caused the mice to over-respond to estrogen throughout adulthood, long after the BPA exposure, thus suggesting that early exposure to BPA genetically "programmed" the uterus to be hyper-responsive to estrogen. Extreme estrogen sensitivity can lead to fertility problems, advanced puberty, altered mammary development and reproductive function, as well as a variety of hormone-related cancers. One of the authors concluded that BPA may be similar to diethylstilbestrol that caused birth defects and cancers in young women whose mothers were given the drug during pregnancy.[114]
A 2011 study using the rhesus monkey – a species that is very similar to humans in regard to pregnancy and fetal development – found that prenatal exposure to BPA causes changes in female primates' uterus development.[115] A 2011 rodent study found that male rats exposed to BPA had lower sperm counts and testosterone levels than those of unexposed males.[116] A 2011 mice study found that male mice exposed to BPA became demasculinized and behaved more like females in their spatial navigational abilities. They were also less desirable to female mice.[117]

[edit]General research

At an Endocrine Society meeting in 2009, new research reported data from animals experimentally treated with BPA.[118] Studies presented at the group's annual meeting show BPA can affect the hearts of women, can permanently damage the DNA of mice, and appears to be entering the human body from a variety of unknown sources.[119]
A 2009 in vitro study on cytotrophoblast cells has found cytotoxic effects in exposure of BPA doses from 0.0002 to 0.2 µg/ml and concluded this finding "suggests that exposure of placental cells to low doses of BPA may cause detrimental effects, leading in vivo to adverse pregnancy outcomes such as preeclampsia, intrauterine growth restriction, prematurity and pregnancy loss".[120]
A 2009 study in rats concluded that BPA, at the reference safe limit for human exposure, was found to impact intestinal permeability and may represent a risk factor in female offspring for developing severe colonic inflammation in adulthood.[121]
A 2010 study on mice has concluded that perinatal exposure to 10 µg/ml of BPA in drinking water enhances allergic sensitization and bronchial inflammation and responsiveness in an animal model of asthma,[122] and a 2011 study found that higher BPA concentrations in the urine of the pregnant women at 16 weeks were associated with wheezing, a symptom of asthma, in their babies.[123]

[edit]Studies on humans

[edit]Lang study and heart disease
The first large study of health effects on humans associated with bisphenol A exposure was published in September 2008 by Iain Lang and colleagues in the Journal of the American Medical Association.[124][125] The cross-sectional study of almost 1,500 people assessed exposure to bisphenol A by looking at levels of the chemical in urine. The authors found that higher bisphenol A levels were significantly associated with heart diseasediabetes, and abnormally high levels of certain liver enzymes. An editorial in the same issue concludes:
"Based on this background information, the study by Lang et al,1​ while preliminary with regard to these diseases in humans, should spur US regulatory agencies to follow the recent action taken by Canadian regulatory agencies, which have declared BPA a “toxic chemical” requiring aggressive action to limit human and environmental exposures.4 Alternatively, Congressional action could follow the precedent set with the recent passage of federal legislation designed to limit exposures to another family of compounds, phthalates, also used in plastic. Like BPA,5​ phthalates are detectable in virtually everyone in the United States.6 This bill moves US policy closer to the European model, in which industry must provide data on the safety of a chemical before it can be used in products."[41][126]
A later similar study performed by the same group of scientists, published in January 2010, confirmed, despite of lower concentrations of BPA in the second study sample, an associated increased risk for heart disease but not for diabetes or liver enzymes. Patients with the highest levels of BPA in their urine carried a 33% increased risk of coronary heart disease.[127]

[edit]Brain tumors

A Chinese human study links BPA to brain tumors. Those with higher urine BPA levels were about 1.6 times more likely to have meningioma compared to those with lower concentrations.[128]
[edit]Other studies
Studies have associated recurrent miscarriage with BPA serum concentrations,[129] oxidative stress and inflammation in postmenopausal women with urinary concentrations,[130]externalizing behaviors in two-year old children, especially among female children, with mother's urinary concentrations,[131] altered hormone levels in men[132][133] and declining male sexual function[134] with urinary concentrations. The Canadian Health Measures Survey, 2007 to 2009 published in 2010 found that teenagers carry 30 percent more l bisphenol A (BPA) in their bodies than older adults. The reason for this is not known.[135] A 2010 study that analyzed BPA urinary concentrations has concluded that for people under 18 years of age BPA may negatively impact human immune function.[136] A study done in 2010 reported the daily excretion levels of BPA among European adults in a large-scale and high-quality population-based sample, and it was shown that higher BPA daily excretion was associated with an increase in serum total testosterone concentration in men.[137] A 2011 study found higher BPA levels in women with polycystic ovary syndrome compared to controls. Furthermore, researchers found a statistically significant positive association between male sex hormones and BPA in these women, suggesting a potential role of BPA in ovarian dysfunction.[138] A 2010 study found that people over age 18 with higher levels of BPA exposure had higher CMV antibody levels, which suggests their cell-mediated immune system may not be functioning properly.[139]
[edit]Sexual difficulties
A 2009 study on Chinese workers in BPA factories found that workers were four times more likely to report erectile dysfunction, reduced sexual desire and overall dissatisfaction with their sex life than workers with no heightened BPA exposure.[140] BPA workers were also seven times more likely to have ejaculation difficulties. They were also more likely to report reduced sexual function within one year of beginning employment at the factory, and the higher the exposure, the more likely they were to have sexual difficulties.[141]

[edit]Historical studies

The first evidence of the estrogenicity of bisphenol A came from experiments on rats conducted in the 1930s,[36][142] but it was not until 1997 that adverse effects of low-dose exposure on laboratory animals were first reported.[22]

[edit]Low-dose exposure in animals

Dose (µg/kg/day)Effects (measured in studies of mice or rats,
descriptions (in quotes) are from Environmental Working Group)[143][144]
Study Year
0.025"Permanent changes to genital tract"2005[145]
0.025"Changes in breast tissue that predispose cells to hormones and carcinogens"2005[146]
1long-term adverse reproductive and carcinogenic effects2009[99]
2"increased prostate weight 30%"1997[147]
2"lower bodyweight, increase of anogenital distance in both genders, signs of early puberty and longer estrus."2002[148]
2.4"Decline in testicular testosterone"2004[149]
2.5"Breast cells predisposed to cancer"2007[150]
10"Prostate cells more sensitive to hormones and cancer"2006[151]
10"Decreased maternal behaviors"2002[152]
30"Reversed the normal sex differences in brain structure and behavior"2003[153]
50Adverse neurological effects occur in non-human primates2008[70]
50Disrupts ovarian development2009[100]
The current U.S. human exposure limit set by the EPA is 50 µg/kg/day.[154]


There is evidence that bisphenol A functions as a xenoestrogen by binding strongly to estrogen-related receptor γ (ERR-γ).[155] This orphan receptor (endogenous ligand unknown) behaves as a constitutive activator of transcription. BPA seems to bind strongly to ERR-γ (dissociation constant = 5.5 nM), but not to the estrogen receptor (ER).[155] BPA binding to ERR-γ preserves its basal constitutive activity.[155] It can also protect it from deactivation from the selective estrogen receptor modulator 4-hydroxytamoxifen.[155]
Different expression of ERR-γ in different parts of the body may account for variations in bisphenol A effects. For instance, ERR-γ has been found in high concentration in theplacenta, explaining reports of high bisphenol accumulation in this tissue.[156]

[edit]Human exposure sources

The major human exposure route to BPA is diet, including ingestion of contaminated food and water.[157] There is limited evidence on inhalation exposure and the body of research on dermal absorption continues to grow. (see below)
The problem is, BPA is also a synthetic estrogen, and plastics with BPA can break down, especially when they're washed, heated or stressed, allowing the chemical to leach into food and water and then enter the human body. That happens to nearly all of us; the CDC has found BPA in the urine of 93% of surveyed Americans over the age of 6. If you don't have BPA in your body, you're not living in the modern world.
Bisphenol A has been known to be leached from the plastic lining of canned foods[158] and polycarbonate plastics, especially those cleaned with harsh detergents or that contain acidic or high-temperature liquids. BPA is an ingredient in the internal coating of metal food and beverage cans used to protect the food from direct contact with the can. A recent Health Canada study found that the majority of canned soft drinks it tested had low, but measurable levels of bisphenol A.[159] Furthermore, a study conducted by the University of Texas School of Public Health in 2010, found BPA in 63 of 105 samples of fresh and canned foods, foods sold in plastic packaging, and in cat and dog foods in cans and plastic packaging. This included fresh turkey, canned green beans, and canned infant formula.[160] While most human exposure is through diet, exposure can also occur through air and through skin absorption.[161]
A 2011 study published in Environmental Health Perspectives, “Food Packaging and Bisphenol A and Bis(2-Ethyhexyl) Phthalate Exposure: Findings from a Dietary Intervention," selected 20 participants based on their self-reported use of canned and packaged foods to study BPA. Participants ate their usual diets, followed by three days of consuming foods that were not canned or packaged. The study's findings include: 1) evidence of BPA in participants’ urine decreased by 50% to 70% during the period of eating fresh foods; and 2), participants’ reports of their food practices suggested that consumption of canned foods and beverages and restaurant meals were the most likely sources of exposure to BPA in their usual diets. The researchers note that, even beyond these 20 participants, BPA exposure is widespread, with detectable levels in urine samples in more than an estimated 90% of the U.S. population.[162]
Free BPA is found in high concentration in thermal paper and carbonless copy paper, which would be expected to be more available for exposure than BPA bound into resin or plastic.[28][163][164] Popular uses of thermal paper include receipts, event and cinema tickets, labels, and airline tickets. A Swiss study found that 11 of 13 thermal printing papers contained 8 – 17 g/kg Bisphenol A (BPA). Upon dry finger contact with a thermal paper receipt, roughly 1 μg BPA (0.2 – 6 μg) was transferred to the forefinger and the middle finger. For wet or greasy fingers approximately 10 times more was transferred. Extraction of BPA from the fingers was possible up to 2 hours after exposure.[165] Further, it has been demonstrated that thermal receipts placed in contact with paper currency in a wallet for 24 hours cause a dramatic increase in the concentration of BPA in paper currency, making paper money a secondary source of exposure.[166] Also, other paper products, such as toilet paper, newspapers and napkins, become contaminated with BPA during the recycling process.[167] Free BPA can readily be transferred to skin, and residues on hands can be ingested.[9] Bodily intake through dermal absorption (99% of which comes from handling receipts) has been shown for the general population to be 0.219 ng/kg bw/day (occupationally exposed persons absorb higher amounts at 16.3 ng/kg bw/day)[167] whereas aggregate intake (food/beverage/environment) for adults is estimated at 0.36–0.43 μg/kg bw/day (estimated intake for occupationally exposed adults is 0.043–100 μg/kg bw/day).[168]
Studies conducted by the CDC found bisphenol A in the urine of 95% of adults sampled in 1988–1994[169] and in 93% of children and adults tested in 2003–04.[170] While the EPA considers exposures up to 50 µg/kg/day to be safe, the most sensitive animal studies show effects at much lower doses.[143][154]
In 2009, a study found that drinking from polycarbonate bottles increased urinary bisphenol A levels by two thirds, from 1.2 μg/g creatinine to 2 μg/g creatinine.[171] Consumer groups recommend that people wishing to lower their exposure to bisphenol A avoid canned food and polycarbonate plastic containers (which shares resin identification code 7 with many other plastics) unless the packaging indicates the plastic is bisphenol A-free.[172] To avoid the possibility of BPA leaching into food or drink, the National Toxicology Panel recommends avoiding microwaving food in plastic containers, putting plastics in the dishwasher, or using harsh detergents.[173]
In the U.S., consumption of soda, school lunches, and meals prepared outside the home was statistically significantly associated with higher urinary BPA.[174] This cannot be correlated with polycarbonate plastic, which is far too expensive to be used in packaging of such products, so it remains to be seen where this BPA is coming from.
BPA is also used to form epoxy resin coating of water pipes. In older buildings, such resin coatings are used to avoid replacement of deteriorating hot and cold water pipes.[175]

[edit]Fetal and early-childhood exposures

Children may be more susceptible to BPA exposure than adults. A recent study found higher urinary concentrations in young children than in adults under typical exposure scenarios.[176] In adults, BPA is eliminated from the body through a detoxification process in the liver. In infants and children, this pathway is not fully developed so they have a decreased ability to clear BPA from their systems. It is also estimated that from food consumption, infants and young children have higher BPA-exposure than adults.[177]
Studies have found that fetuses and young children exposed to BPA are at risk for secondary sexual developmental changes, brain and behavior changes and immune disorders.[178]
Infants fed with liquid formula are among the most exposed, and those fed formula from polycarbonate bottles can consume up to 13 micrograms of bisphenol A per kg of body weight per day (μg/kg/day; see table below).[179] In the US and Canada, BPA has been found in infant liquid formula in concentrations varying from 0.48 to 11 ng/g.[180][181] BPA has been rarely found in infant powder formula (only 1 of 14).[180] While breast milk is the optimal source of nutrition for infants, it is not always an option. The U.S. Department of Health & Human Services (HHS) states that "the benefit of a stable source of good nutrition from infant formula and food outweighs the potential risk of BPA exposure.".[182]
A 2010 study of people in Austria, Switzerland, and Germany has suggested polycarbonate (PC) baby bottles as the most prominent role of exposure for infants, and canned food for adults and teenagers.[183] In the United States, the growing concern over BPA exposure in infants in recent years has led the manufacturers of plastic baby bottles to stop using BPA in their bottles. However, babies may still be exposed if they are fed with old or hand-me-down bottles bought before the companies stopped using BPA.
One often overlooked source of exposure occurs when a pregnant woman is exposed, thereby exposing the fetus. Animal studies have shown that BPA can be found in both the placenta and the amniotic fluid of pregnant mice.[184] A small US study in 2009, funded by the EWG, detected an average of 2.8 ng/mL BPA in the blood of 9 out of the 10 umbilical cords tested.[185] A study of 244 mothers indicated that exposure to BPA before birth could affect the behavior of girls' at age 3. Girls whose mother's urine contained high levels of BPA during pregnancy scored worse on tests of anxiety and hyperactivity. Although these girls still scored within a normal range, for every 10-fold increase in the BPA of the mother, the girls scored at least six points lower on the tests. Boys did not seem to be affected by their mother's BPA levels during pregnancy.[186] After the baby is born, maternal exposure can continue to affect the infant through transfer of BPA to the infant via breast milk.[187][188] Because of these exposures that can occur both during and after pregnancy, mothers wishing to limit their child’s exposure to BPA should attempt to limit their own exposures during that time period.
While the majority of exposures have been shown to come through the diet, accidental ingestion can also be considered a source of exposure. One study conducted in Japan tested plastic baby books to look for possible leaching into saliva when babies chew on them.[189] While the results of this study have yet to be replicated, it gives reason to question whether exposure can also occur in infants through ingestion by chewing on certain books or toys.
PopulationEstimated daily bisphenol A intake, μg/kg/day.
Table adapted from the National Toxicology Program Expert Panel Report.
Infant (0–6 months)
Infant (0–6 months)
Infant (6–12 months)
Child (1.5–6 years)


There is no agreement between scientists of a physiologically based pharmacokinetic (PBPK) BPA model for humans. The effects of BPA on an organism depend on how much free BPA is available and for how long cells are exposed to it. Glucuronidation in the liver, by conjugation with glucuronic acid to form the metabolite BPA-glucuronide (BPAG),[9]reduces the amount of free BPA, however BPAG can be deconjugated by beta-glucuronidase, an enzyme present in high concentration in placenta and other tissues.[190][191] Free BPA can also be inactivated by sulfation, a process that can also be reverted by arylsulfatase C.[190]
A 2009 research study found that some drugs, like naproxensalicylic acidcarbamazepine and mefenamic acid can, in vitro, significantly inhibit BPA glucuronidation.[192] A 2010 study on rats embryos has found that genistein may enhance developmental toxicity of BPA,[193] and another 2010 vitro study has shown that placenta P-glycoprotein may efflux BPA from placenta.[194]
A 2010 review of 80+ biomonitoring studies concluded that the general population is internally exposed to significant amounts of unconjugated BPA (in the ng/ml blood range).[195]Using GC/MS on 20 samples, BPA was detected in 100% of urine samples with a median of 1.25 ng/ml, and 10% of blood samples (LOD 0.5 ng/ml).[196] In a 2011 study, researchers found that after a 5-day consumption of 1 serving of canned vegetarian soup, subjects exhibited a 1200% increase in urinary BPA concentrations compared to controls, suggesting that such a diet induces a peak of BPA elevation of unknown duration and of unknown biological safety.[197]
The best test methods for studying BPA effects are currently under discussion with scientists sharing different opinions.[198]

[edit]Environmental risk

In 2010 the EPA reported that over one million pounds of BPA are released into the environment annually.[31] BPA can enter the environment either directly or through degradation of products, such as ocean-borne plastic trash.[199] Leaching of BPA from plastic and metal waste in landfills is one potential source of environmental contamination. A 2009 meta-analysis of BPA in the surface water system reported that BPA is found in surface water and sediment in the United States and Europe.[200]
In general, studies have shown that BPA can affect growth, reproduction and development in aquatic organisms. Among freshwater organisms, fish appear to be the most sensitive species. Evidence of endocrine-related effects in fish, aquatic invertebrates, amphibians and reptiles has been reported at environmentally relevant exposure levels lower than those required for acute toxicity. There is a widespread variation in reported values for endocrine-related effects, but many fall in the range of 1μg/L to 1 mg/L.[9]
As an environmental contaminant, BPA interferes with nitrogen fixation at the roots of leguminous plants associated with the bacterial symbiont Sinorhizobium meliloti. Despite ahalf-life in the soil of only 1–10 days, its ubiquity makes it an important pollutant.[201] According to Environment Canada, "initial assessment shows that at low levels, bisphenol A can harm fish and organisms over time. Studies also indicate that it can currently be found in municipal wastewater."[202] However, a study conducted in the United States in 2005 found that 91-98% of BPA may be removed from water during treatment at municipal water treatment plants.[203]
A 2009 review of the biological impacts of plasticizers on wildlife published by the Royal Society with a focus on annelids (both aquatic and terrestrial), molluscscrustaceans, insects, fish and amphibians concluded that BPA has been shown to affect reproduction in all studied animal groups, to impair development in crustaceans and amphibians and to induce genetic aberrations.[204]
A large 2010 study of two rivers in Canada found that areas contaminated with hormone-like chemicals including bisphenol A showed females made up 85 per cent of the population of a certain fish, while females made up only 55 per cent in uncontaminated areas.[205]

[edit]Government and industry response

[edit]World Health Organization

Arguing uncertainty of possible adverse health effects of low dose BPA exposure, especially on the nervous system and on behaviour, and also the differences of exposure of very young children, the WHO announced in November 2009 that it would organize an expert consultation in 2010 to assess BPA safety.[80]
The WHO expert panel recommended no new regulations limiting or banning the use of Bisphenol-A, stating that "initiation of public health measures would be premature."[206]

[edit]Australia and New Zealand

The Australia and New Zealand Food Safety Authority (Food Standards Australia New Zealand) does not see any health risk with bisphenol A baby bottles if the manufacturer's instructions are followed. Levels of exposure are very low and do not pose a significant health risk. It added that “the move by overseas manufacturers to stop using BPA in baby bottles is a voluntary action and not the result of a specific action by regulators.”[207] It suggests the use of glass baby bottles if parents have any concerns.[208]


In April 2008, Health Canada concluded that, while adverse health effects were not expected, the margin of safety was too small for formula-fed infants[209] and proposed classifying the chemical as "'toxic' to human health and the environment."[210]
After the release of that assessment, Canadian Health Minister Tony Clement announced Canada's intent to ban the import, sale, and advertisement of polycarbonate baby bottles containing bisphenol A due to safety concerns, and investigate ways to reduce BPA contamination of baby formula packaged in metal cans. While the agency concluded that human exposures were less than levels believed unsafe, the margin of safety was not high enough for formula-fed infants.[42][211] Around the same time, Wal-Mart announced that it was immediately ceasing sales in all its Canadian stores of food containers, water and baby bottles, sippy cups, and pacifiers containing bisphenol A, and that it would phase out baby bottles made with it in U.S. stores by early 2009.[212] Nalgene also announced it will stop using the chemical in its products,[213] and Toys-R-Us said it too will cease selling baby bottles made from it.[214] Subsequent news reports showed many retailers removing polycarbonate drinking products from their shelves.[215]
The federal government proposed declaring Bisphenol A a hazardous substance in October 2008 and has since placed it on its list of toxic substances. Health officials wrote inCanada Gazette that "It is concluded that bisphenol A be considered as a substance that may be entering the environment in a quantity or concentration or under conditions that constitute or may constitute a danger in Canada to human life or health."[216] The federal ministries of health and the environment announced they would seek to restrict imports, sales and advertising of polycarbonate baby bottles containing BPA.[217]
In its statement released on 18 October 2008, Health Canada noted that “bisphenol A exposure to newborns and infants is below levels that cause effects” and that the “general public need not be concerned”.[218]
Environment Canada listed bisphenol A as a "toxic substance" in September 2010.[37]
The new plastic Canadian currency has been measured as having the highest levels of BPA from several international currencies measured.[219]

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