SAFETY
Health effects
According to the European Food Safety Authority "BPA poses no health risk to consumers of any age group (including unborn children, infants and adolescents) at current exposure levels".
In 2012, the United States' Food and Drug Administration (FDA) banned the use of BPA in baby bottles;however, the Environmental Working Group called the ban "purely cosmetic" and stated "If the agency truly wants to prevent people from being exposed to this toxic chemical associated with a variety of serious and chronic conditions it should ban its use in cans of infant formula, food and beverages. The Natural Resources Defense Council called the move inadequate, saying the FDA needed to ban BPA from all food packaging. The FDA maintains that the agency continues to support the safety of BPA for use in products that hold food.
The Environmental Protection Agency (EPA) also holds the position that BPA is not a health concern. In 2011, Andrew Wadge, the chief scientist of the United Kingdom's Food Standards Agency, commented on a 2011 US study on dietary exposure of adult humans to BPA,[49] 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.
The Endocrine Society said in 2015 that the results of ongoing laboratory research gave grounds for concern about the potential hazards of endocrine-disrupting chemicals – including BPA – in the environment, and that on the basis of the precautionary principle these substances should continue to be assessed and tightly regulated.
United States expert panel conclusions
In 2006, the US Government sponsored an assessment of the scientific literature on BPA. Thirty-eight experts in fields involved with 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. The Chapel Hill Consensus Statement stated that average BPA levels in people were above those that cause harm to many animals in laboratory experiments. It noted that while BPA is not persistent in the environment or in humans, biomonitoring surveys indicate that exposure is continuous. This 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. The authors added that measurement of BPA levels in serum and other body fluids suggests the possibilities that BPA intake is much higher than accounted for or that BPA can bioaccumulate in some conditions (such as pregnancy).
Metabolic disease
Numerous animal studies have demonstrated an association between endocrine disrupting chemicals (including BPA) and obesity. However, the relationship between bisphenol A exposure and obesity in humans is unclear. Proposed mechanisms for BPA exposure to increase the risk of obesity include BPA-induced thyroid dysfunction, activation of the PPAR-gamma receptor, and disruption of neural circuits that regulate feeding behavior. BPA works by imitating the natural hormone 17 B-estradiol. In the past BPA has been considered a weak mimicker of estrogen but newer evidence indicates that it is a potent mimicker. When it binds to estrogen receptors it triggers alternative estrogenic effects that begin outside of the nucleus. This different path induced by BPA has been shown to alter glucose and lipid metabolism in animal studies.
There are different effects of BPA exposure during different stages of development. During adulthood, BPA exposure modifies insulin sensitivity and insulin release without affecting weight.
Thyroid function
A 2007 review concluded that bisphenol-A has been shown to bind to thyroid hormone receptor and perhaps has selective effects on its functions.
A 2009 review about environmental chemicals and thyroid function raised concerns about BPA effects ontriiodothyronine 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.
Neurological effects
Limited epidemiological evidence suggests that exposure to BPA in the uterus and during childhood is associated with poor behavioral outcomes in humans. Exposure may be associated with higher levels of anxiety, depression, hyperactivity, and aggression in children. A panel convened by the National Toxicology Program (NTP) of 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. In January 2010, based on the NTP report, the FDA expressed the same level of concern.
A 2007 literature review concluded that BPA, like other chemicals that mimic estrogen (xenoestrogens), should be considered as a player within the nervous system that can regulate or alter its functions through multiple pathways. A 2008 review of animal research found that low-dose BPA maternal exposure can cause long-term consequences for the neurobehavioral development in mice. A 2009 review raised concerns about a BPA effect on the anteroventral periventricular nucleus.
Disruption of the dopaminergic system
A 2008 review of human participants has concluded that BPA mimics estrogenic activity and affects various dopaminergic processes to enhance mesolimbic dopamine activity resulting in hyperactivity, attention deficits, and a heightened sensitivity to drugs of abuse.
Cancer
According to the WHO's INFOSAN, carcinogenicity studies conducted under the US National Toxicology Program, have shown increases in leukemia and testicular interstitial cell tumors in male rats. However, according to the note "these studies have not been considered as convincing evidence of a potential cancer risk because of the doubtful statistical significance of the small differences in incidences from controls.
A 2010 review concluded that bisphenol A may increase cancer risk. At least one study suggested that bisphenol A suppresses DNA methylation, which is involved inepigenetic changes.
Breast cancer
Higher susceptibility to breast cancer has been found in many studies of rodents and primates exposed to BPA. However, the association between BPA and subsequent development of breast cancer in humans is unclear.
Neuroblastoma
BPA promotes the growth, invasiveness and metastasis of cells from a laboratory neuroblastoma cancer cell line, SK-N-SH.
Fertility
As of 2013, the evidence to support a link between BPA exposure and male infertility is weak though limited evidence does support an association with lower sperm quality. There is tentative evidence to support the idea that BPA exposure has negative effects on human fertility. Few studies have investigated whether recurrent miscarriage is associated with BPA levels. Exposure to BPA does not appear to be linked with higher rates of endometrial hyperplasia.
Sexual function
Higher BPA exposure has been associated with increased self-reporting of decreased male sexual function but few studies examining this relationship have been conducted.
Asthma
Studies in mice have found a link between BPA exposure and asthma; 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. A study published in JAMA pediatrics has found that prenatal exposure to BPA is also linked to lower lung capacity in some young children. This study had 398 mother-infant pairs and looked at their urine samples to detect concentrations of BPA. They study found that every 10-fold increase in BPA was tied to a 55% increase in the odds of wheezing. The higher the concentration of BPA during pregnancy were linked to decrease lung capacity in children under four years old but the link disappeared at age 5. Associate professor of pediatrics at the University of Maryland School of Medicine said, “Exposure during pregnancy, not after, appears to be the critical time for BPA, possibly because it’s affecting important pathways that help the lung develop.
In 2013, research from scientists at the Columbia Center for Children's Environmental Health also found a link between the compound and an increased risk for asthma. The research team reported that children with higher levels of BPA at ages 3, 5 and 7 had increased odds of developing asthma when they were between the ages of 5 and 12. The children in this study had about the same concentration of BPA exposure as the average U.S child. Dr. Kathleen Donohue, an instructor at Columbia University Medical Center said, “they saw an increased risk of asthma at fairly routine, low doses of BPA. Kim Harley, who studies environmental chemicals and children's health, commented in the Scientific Americanjournal saying while the study does not show that BPA causes asthma or wheezing, "it's an important study because we don't know a lot right now about how BPA affects immune response and asthma...They measured BPA at different ages, measured asthma and wheeze at multiple points, and still found consistent associations.
According to the European Food Safety Authority "BPA poses no health risk to consumers of any age group (including unborn children, infants and adolescents) at current exposure levels".
In 2012, the United States' Food and Drug Administration (FDA) banned the use of BPA in baby bottles;however, the Environmental Working Group called the ban "purely cosmetic" and stated "If the agency truly wants to prevent people from being exposed to this toxic chemical associated with a variety of serious and chronic conditions it should ban its use in cans of infant formula, food and beverages. The Natural Resources Defense Council called the move inadequate, saying the FDA needed to ban BPA from all food packaging. The FDA maintains that the agency continues to support the safety of BPA for use in products that hold food.
The Environmental Protection Agency (EPA) also holds the position that BPA is not a health concern. In 2011, Andrew Wadge, the chief scientist of the United Kingdom's Food Standards Agency, commented on a 2011 US study on dietary exposure of adult humans to BPA,[49] 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.
The Endocrine Society said in 2015 that the results of ongoing laboratory research gave grounds for concern about the potential hazards of endocrine-disrupting chemicals – including BPA – in the environment, and that on the basis of the precautionary principle these substances should continue to be assessed and tightly regulated.
United States expert panel conclusions
In 2006, the US Government sponsored an assessment of the scientific literature on BPA. Thirty-eight experts in fields involved with 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. The Chapel Hill Consensus Statement stated that average BPA levels in people were above those that cause harm to many animals in laboratory experiments. It noted that while BPA is not persistent in the environment or in humans, biomonitoring surveys indicate that exposure is continuous. This 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. The authors added that measurement of BPA levels in serum and other body fluids suggests the possibilities that BPA intake is much higher than accounted for or that BPA can bioaccumulate in some conditions (such as pregnancy).
Metabolic disease
Numerous animal studies have demonstrated an association between endocrine disrupting chemicals (including BPA) and obesity. However, the relationship between bisphenol A exposure and obesity in humans is unclear. Proposed mechanisms for BPA exposure to increase the risk of obesity include BPA-induced thyroid dysfunction, activation of the PPAR-gamma receptor, and disruption of neural circuits that regulate feeding behavior. BPA works by imitating the natural hormone 17 B-estradiol. In the past BPA has been considered a weak mimicker of estrogen but newer evidence indicates that it is a potent mimicker. When it binds to estrogen receptors it triggers alternative estrogenic effects that begin outside of the nucleus. This different path induced by BPA has been shown to alter glucose and lipid metabolism in animal studies.
There are different effects of BPA exposure during different stages of development. During adulthood, BPA exposure modifies insulin sensitivity and insulin release without affecting weight.
Thyroid function
A 2007 review concluded that bisphenol-A has been shown to bind to thyroid hormone receptor and perhaps has selective effects on its functions.
A 2009 review about environmental chemicals and thyroid function raised concerns about BPA effects ontriiodothyronine 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.
Neurological effects
Limited epidemiological evidence suggests that exposure to BPA in the uterus and during childhood is associated with poor behavioral outcomes in humans. Exposure may be associated with higher levels of anxiety, depression, hyperactivity, and aggression in children. A panel convened by the National Toxicology Program (NTP) of 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. In January 2010, based on the NTP report, the FDA expressed the same level of concern.
A 2007 literature review concluded that BPA, like other chemicals that mimic estrogen (xenoestrogens), should be considered as a player within the nervous system that can regulate or alter its functions through multiple pathways. A 2008 review of animal research found that low-dose BPA maternal exposure can cause long-term consequences for the neurobehavioral development in mice. A 2009 review raised concerns about a BPA effect on the anteroventral periventricular nucleus.
Disruption of the dopaminergic system
A 2008 review of human participants has concluded that BPA mimics estrogenic activity and affects various dopaminergic processes to enhance mesolimbic dopamine activity resulting in hyperactivity, attention deficits, and a heightened sensitivity to drugs of abuse.
Cancer
According to the WHO's INFOSAN, carcinogenicity studies conducted under the US National Toxicology Program, have shown increases in leukemia and testicular interstitial cell tumors in male rats. However, according to the note "these studies have not been considered as convincing evidence of a potential cancer risk because of the doubtful statistical significance of the small differences in incidences from controls.
A 2010 review concluded that bisphenol A may increase cancer risk. At least one study suggested that bisphenol A suppresses DNA methylation, which is involved inepigenetic changes.
Breast cancer
Higher susceptibility to breast cancer has been found in many studies of rodents and primates exposed to BPA. However, the association between BPA and subsequent development of breast cancer in humans is unclear.
Neuroblastoma
BPA promotes the growth, invasiveness and metastasis of cells from a laboratory neuroblastoma cancer cell line, SK-N-SH.
Fertility
As of 2013, the evidence to support a link between BPA exposure and male infertility is weak though limited evidence does support an association with lower sperm quality. There is tentative evidence to support the idea that BPA exposure has negative effects on human fertility. Few studies have investigated whether recurrent miscarriage is associated with BPA levels. Exposure to BPA does not appear to be linked with higher rates of endometrial hyperplasia.
Sexual function
Higher BPA exposure has been associated with increased self-reporting of decreased male sexual function but few studies examining this relationship have been conducted.
Asthma
Studies in mice have found a link between BPA exposure and asthma; 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. A study published in JAMA pediatrics has found that prenatal exposure to BPA is also linked to lower lung capacity in some young children. This study had 398 mother-infant pairs and looked at their urine samples to detect concentrations of BPA. They study found that every 10-fold increase in BPA was tied to a 55% increase in the odds of wheezing. The higher the concentration of BPA during pregnancy were linked to decrease lung capacity in children under four years old but the link disappeared at age 5. Associate professor of pediatrics at the University of Maryland School of Medicine said, “Exposure during pregnancy, not after, appears to be the critical time for BPA, possibly because it’s affecting important pathways that help the lung develop.
In 2013, research from scientists at the Columbia Center for Children's Environmental Health also found a link between the compound and an increased risk for asthma. The research team reported that children with higher levels of BPA at ages 3, 5 and 7 had increased odds of developing asthma when they were between the ages of 5 and 12. The children in this study had about the same concentration of BPA exposure as the average U.S child. Dr. Kathleen Donohue, an instructor at Columbia University Medical Center said, “they saw an increased risk of asthma at fairly routine, low doses of BPA. Kim Harley, who studies environmental chemicals and children's health, commented in the Scientific Americanjournal saying while the study does not show that BPA causes asthma or wheezing, "it's an important study because we don't know a lot right now about how BPA affects immune response and asthma...They measured BPA at different ages, measured asthma and wheeze at multiple points, and still found consistent associations.