Bisphenol A, Commonly Abbreviated As BPA, Is an Organic Compound with Two Phenol Functional
Bisphenol A, commonly abbreviated as BPA, is an organic compound with two phenolfunctional groups. It is a difunctional building block of several important plastics and plastic additives.
Suspected of being hazardous to humans since the 1930s, concerns about the use of bisphenol A in consumer products were regularly reported in the news media in 2008 after several governments issued reports questioning its safety, thus prompting some retailers to remove products containing it from their shelves. A 2010 report from the United States Food and Drug Administration (FDA) raised further concerns regarding exposure of fetuses, infants, and young children.
Health Effects of Bisphenol A
Bisphenol A is an endocrine disruptor, which can mimic the body's own hormones and may lead to negative health effects. Early development appears to be the period of greatest sensitivity to its effects. Regulatory bodies have determined safety levels for humans, but those safety levels are currently being questioned or under review as a result of new scientific studies.
In 2009 the The Endocrine Society released a scientific statement expressing concern over current human exposure to BPA.
Previous studies
In 2007, a consensus statement by 38 experts on bisphenol A concluded that average levels in people are above those that cause harm to many animals in laboratory experiments. 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. 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 "negligible concern 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.
Obesity
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".A 2009 review of available studies has concluded that "perinatal BPA exposure acts to exert persistent effects on body weight and adiposity". Another 2009 review has concluded that "Eliminating exposures to (BPA) and improving nutrition during development offer the potential for reducing obesity and associated diseases".Other reviews have come with similar conclusions.
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. A 2008 report by the U.S. National Toxicology Program (NTP) later agreed with the panel, expressing "some concern for effects on the brain".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. 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. A 2008 review concluded that low-dose BPA maternal exposure causes long-term consequences at the level of neurobehavioral development in mice. A 2008 review has concluded that neonatal exposure to Bisphenol-A (BPA) can affect sexually dimorphic brain morphology and neuronal phenotypes in adulthood. 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. A 2009 review raised concerns about BPA effect on anteroventral periventricular nucleus.
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 the United States Environmental Protection Agency's (EPA) maximum safe dose of 50µg/kg/day. This research found a connection between BPA and interference with brain cell connections vital to memory, learning and mood.
Highly controversial claims have been made that BPA could be involved in attention-deficit hyperactivity disorder (ADHD)
A 2010 study with rats perinatal exposured to 40 microg/kg bw BPA has concluded that corticosterone and its actions in the brain are sensitive to the programming effects of BPA.
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.
A 2008 review has concluded that BPA, mimic estrogenic activity and impact various dopaminergic processes to enhance mesolimbic dopamine activity resulting in hyperactivity, attention deficits, and a heightened sensitivity to drugs of abuse.
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. Another 2009 study has found associated changes in the dopaminergic system.
Thyroid function
A 2007 review has concluded that bisphenol-A have been shown to bind to thyroid hormone receptor and perhaps have selective effects on its functions.
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".
A 2009 review summarized BPA adverse effects on thyroid hormone action.
Cancer research
According to the WHO's INFOSAN, "animal studies have not provided convincing evidence of risk of cancer from BPA exposure."
Neither the U.S. Environmental Protection Agency nor the International Agency for Research on Cancer has evaluated bisphenol A for possible carcinogenic activity.
Breast cancer
Further information: Risk factors of breast cancer#Bisphenol A
A 2008 review has concluded that "perinatal exposure to (...) low doses of (..) BPA, alters breast development and increases breast cancer risk".Another 2008 review concluded that " animal experiments and epidemiological data strengthen the hypothesis that foetal exposure to xenoestrogens may be an underlying cause of the increased incidence of breast cancer observed over the last 50 years".
A 2009 in vitro study has concluded that BPA is able to induce neoplastic transformation in human breast epithelial cells. Another 2009 study concluded that maternal oral exposure to low concentrations of BPA during lactation increases mammary carcinogenesis in a rodent model.
A 2010 study with the mammary glands of the offspring of pregnant rats treated orally with 0, 25 or 250µg 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.
A 2010 study has found that BPA may reduce sensitivity to chemotherapy treatment of specific tumors.
Neuroblastoma
In vitro studies have suggested that BPA can promote the growth of neuroblastoma cells. A 2010 in vitro study has concluded that BPA potently promote invasion and metastasis of neuroblastoma cells through overexpression of MMP-2 and MMP-9 as well as downregulation of TIMP2.
Prostate development and cancer
A 1997 study in mice has found that neonatal BPA exposure of 2 μg/kg increased adult prostate weight. A 2005 study in mice has found that neonatal BPA exposure at 10 μg/kg disrupted the development of the fetal mouse prostate. 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. A 2007 in vitro study has found that BPA within the range of concentrations currently measured in human serum is associated with permanently increase in prostate size. A 2009 study has found that newborn rats exposed to a low-dose of BPA (10µg/kg) increased prostate cancer susceptibility when adults.
Reproductive system and sexual behavior research
A series of studies made in 2009 found:
- Mouse ovary anomalies from exposure as low as 1µg/kg, concluded that BPA exposure causes long-term adverse reproductive and carcinogenic effects if exposure occurs during prenatal critical periods of differentiation.
- Neonatal exposure of as low as 50µg/kg disrupts ovarian development in mice.
- Neonatal BPA exposition of as low as 50µg/kg permanently alters the hypothalamic estrogen-dependent mechanisms that govern sexual behavior in the adult female rat.
- Prenatal exposure to BPA at levels of (10 μg/kg/day) affects behavioral sexual differentiation in male monkeys.
- In placental JEG3 cells in vitro BPA may reduce estrogen synthesis.
- BPA exposure disrupted the blood-testis barrier when administered to immature, but not to adult, rats.
- Exposure to BPA in the workplace was associated with self-reported adult male sexual dysfunction.
- A 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. That study was criticized as flawed for using polycabornate cages in the experiment and the claimed resistance of the rats to estradiol but that claim was contested by the authors and others.
A 2010 study with mice concluded that BPA exposure in utero leads to permanent DNA alterations in sensitivity to estrogen.
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