After the stone age, bronze age, and the ice age,
we now have the plastic age
Global plastics consumption is estimated to reach 297.5 million tons by 2015
Our planet is literally poisoned by plastic. From the Great Pacific Garbage Patch till the Sahara, our planet is polluted by plastic and we are paying a lethal price for our throwaway society. Plastic never goes away. It fragments into millions of tiny toxic pieces that are ingested by wildlife and pollute everything.
The above picture is part of the «Out to Sea -- The Plastic Garbage Project» at the 'Exhibition Installation Museum für Gestaltung' at Zürich (Museum of Design Zürich)
6'400'000'000 kilograms of plastic garbage end up in the sea every year. This is equivalent to 17'500'000 kilograms per day or 12'000 kilograms per minute.
The garbage installed in the Museum weights 3'000 kilograms (see picture). It took 1,000 hours to pick up the garbage at different beaches (30 people, 4 days)
6'400'000'000 kilograms of plastic garbage end up in the sea every year. This is equivalent to 17'500'000 kilograms per day or 12'000 kilograms per minute.
The garbage installed in the Museum weights 3'000 kilograms (see picture). It took 1,000 hours to pick up the garbage at different beaches (30 people, 4 days)
Every 15 seconds the amount of plastic garbage
you see in the following video gets dumped into the sea
Plastic is dangerous!
|
Ever since mass-produced plastic products have made our lives easier, the sea has gradually begun to change into a gigantic soup of plastic – today not a single square kilometer of seawater is free of plastic particles.
As standard plastic is not biodegradable, these pieces are broken up into constantly smaller pieces and enter the food chain. And so the garbage ends up on our plates, with serious consequences for our health and the health of our marine life. WILD TIME talked to Christian Braendle from the "Plastic garbage Project" about awareness, education and more. More about his project here: http://www.plasticgarbageproject.org/... |
Plastic planet
From pantyhose to Porta Potties, plastic — the catch-all term for a wide variety of synthetic materials — has infiltrated virtually every aspect of modern life. For the Austrian filmmaker Werner Boote, it’s personal: plastic is, quite literally, in his blood. As we discover in “Plastic Planet,” it’s probably in ours, too.
And not just because of our addiction to Tupperware. Among the film’s many fascinating and ultimately alarming claims is that, for most of its roughly 500-year life expectancy, plastic slowly releases molecules of maleficence into the food chain, many of them linked to sexual abnormalities in fish and infertility in humans.
There’s more than enough material here for a meaty exposé, but Mr. Boote (the grandson of a plastics manufacturer, now deceased) is less focused than a kitten in a yarn store. Hugging a plastic globe from China, he zips through no fewer than 14 countries to interview plastic lovers and haters, scientists and citizens.
An appealingly eccentric guide, Mr. Boote trots from an environmental dispute in Venice to a rubbish dump in India, and meets a Japanese sculptor and an American plastic surgeon. Sniffing and licking as he goes, and pausing to rub his face vigorously with bioplastics, the director favors a peripatetic style that staves off boredom but is frustratingly shallow.
Sometimes things get a little weird, as Mr. Boote questions a woman on the sensations caused by her breast implants, and later — channeling Michael Moore — visits a trade show grasping a megaphone.
“You will get big breasts,” he warns the attendees, noting the possible hormonal disruptions caused by their products. And while these digressions lighten the film’s mood, “Plastic Planet” does little but raise an alarm, then leave it jangling.
Text: The New York Times
And not just because of our addiction to Tupperware. Among the film’s many fascinating and ultimately alarming claims is that, for most of its roughly 500-year life expectancy, plastic slowly releases molecules of maleficence into the food chain, many of them linked to sexual abnormalities in fish and infertility in humans.
There’s more than enough material here for a meaty exposé, but Mr. Boote (the grandson of a plastics manufacturer, now deceased) is less focused than a kitten in a yarn store. Hugging a plastic globe from China, he zips through no fewer than 14 countries to interview plastic lovers and haters, scientists and citizens.
An appealingly eccentric guide, Mr. Boote trots from an environmental dispute in Venice to a rubbish dump in India, and meets a Japanese sculptor and an American plastic surgeon. Sniffing and licking as he goes, and pausing to rub his face vigorously with bioplastics, the director favors a peripatetic style that staves off boredom but is frustratingly shallow.
Sometimes things get a little weird, as Mr. Boote questions a woman on the sensations caused by her breast implants, and later — channeling Michael Moore — visits a trade show grasping a megaphone.
“You will get big breasts,” he warns the attendees, noting the possible hormonal disruptions caused by their products. And while these digressions lighten the film’s mood, “Plastic Planet” does little but raise an alarm, then leave it jangling.
Text: The New York Times
Bisphenol A
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 and epoxy resins, along with other materials used to make plastics. Bisphenol A has a vapor pressure of 5*10-6 Pa.
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. In September 2010, Canada became the first country to declare BPA a toxic substance. The European Union, Canada, and recently the United States have banned BPA use in baby bottles.
History
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. 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). 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. The first evidence of the estrogenicity of bisphenol A came from experiments on rats conducted in the 1930s, but it was not until 1997 that adverse effects of low-dose exposure on laboratory animals were first proposed (hormesis). 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".
Health effects
Bisphenol A is a weak endocrine disruptor, which can mimic estrogen and may lead to negative health effects. Early developmental stages appear to be the period of greatest sensitivity to its effects, and some studies have linked prenatal exposure to later physical and 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. A 2011 study that investigated the number of chemicals pregnant women are exposed to in the U.S. found BPA in 96% of women.
In 2009, The Endocrine Society released a statement citing the adverse effects of endocrine-disrupting chemicals, and the controversy surrounding BPA.
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, 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." In the study 20 subjects were tested for BPA every hour for twenty-four hours while consuming three meals consisting of canned food.
In 2012 a paper was written in response to this study, however, criticizing the study as lacking data and having flawed assumptions.
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. Experts advise readers of scientific studies to consider who conducted the study, what their affiliations are, and what the purpose of the study was.
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."
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). 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.
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.
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. 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. 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. 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. Another study suggested that larger size-for-age was due to a faster growth rate rather than obesity.
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 adult phenotypes in mice. 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 50 µg/kg/day. 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.
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 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.
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 has 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, carcinogenicity studies conducted under the US National Toxicology Program, have shown increases in leukaemia and testicular interstitial cell tumours in male rats.
A 2010 review at Tufts University Medical School concluded that Bisphenol A may increase cancer risk.
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". 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".
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 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.
A 2010 study has found that BPA may reduce sensitivity to chemotherapy treatment of specific tumors.
NeuroblastomaIn vitro studies have suggested that BPA can promote the growth of neuroblastoma cells. A 2010 in vitro study has concluded that BPA potently promotes 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 permanent increases in prostate size. 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.
DNA methylation
At least one study has suggested that bisphenol A suppresses DNA methylation which is linked to epigenetic changes.
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.
A series of studies made in 2009 found:
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. 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, but that claim was contested by the authors and others. 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."
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. Another 2010 study with mice concluded that BPA exposure in utero leads to permanent DNA alterations in sensitivity to estrogen. 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.
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. A 2011 rodent study found that male rats exposed to BPA had lower sperm counts and testosterone levels than those of unexposed males. 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.
General research
At an Endocrine Society meeting in 2009, new research reported data from animals experimentally treated with BPA.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.
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".
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.
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, 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.[124]
Studies on humans
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. 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 disease, diabetes, 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." 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.
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.
Other studies
Studies have associated recurrent miscarriage with BPA serum concentrations, oxidative stress and inflammation in postmenopausal women with urinary concentrations, externalizing behaviors in two-year old children, especially among female children, with mother's urinary concentrations, altered hormone levels in men and declining male sexual function with urinary concentrations. The Canadian Health Measures Survey, 2007 to 2009 published in 2010 found that teenagers carry 30 percent more BPA in their bodies than older adults. The reason for this is not known. 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. 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. 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. 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.
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. 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.
Historical studies
The first evidence of the estrogenicity of bisphenol A came from experiments on rats conducted in the 1930s, but it was not until 1997 that adverse effects of low-dose exposure on laboratory animals were first reported.
The above information was taken from Wikipedia. To see the sources and references of this article, please go to Wikipedia
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. In September 2010, Canada became the first country to declare BPA a toxic substance. The European Union, Canada, and recently the United States have banned BPA use in baby bottles.
History
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. 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). 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. The first evidence of the estrogenicity of bisphenol A came from experiments on rats conducted in the 1930s, but it was not until 1997 that adverse effects of low-dose exposure on laboratory animals were first proposed (hormesis). 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".
Health effects
Bisphenol A is a weak endocrine disruptor, which can mimic estrogen and may lead to negative health effects. Early developmental stages appear to be the period of greatest sensitivity to its effects, and some studies have linked prenatal exposure to later physical and 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. A 2011 study that investigated the number of chemicals pregnant women are exposed to in the U.S. found BPA in 96% of women.
In 2009, The Endocrine Society released a statement citing the adverse effects of endocrine-disrupting chemicals, and the controversy surrounding BPA.
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, 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." In the study 20 subjects were tested for BPA every hour for twenty-four hours while consuming three meals consisting of canned food.
In 2012 a paper was written in response to this study, however, criticizing the study as lacking data and having flawed assumptions.
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. Experts advise readers of scientific studies to consider who conducted the study, what their affiliations are, and what the purpose of the study was.
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."
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). 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.
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.
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. 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. 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. 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. Another study suggested that larger size-for-age was due to a faster growth rate rather than obesity.
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 adult phenotypes in mice. 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 50 µg/kg/day. 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.
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 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.
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 has 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, carcinogenicity studies conducted under the US National Toxicology Program, have shown increases in leukaemia and testicular interstitial cell tumours in male rats.
A 2010 review at Tufts University Medical School concluded that Bisphenol A may increase cancer risk.
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". 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".
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 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.
A 2010 study has found that BPA may reduce sensitivity to chemotherapy treatment of specific tumors.
NeuroblastomaIn vitro studies have suggested that BPA can promote the growth of neuroblastoma cells. A 2010 in vitro study has concluded that BPA potently promotes 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 permanent increases in prostate size. 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.
DNA methylation
At least one study has suggested that bisphenol A suppresses DNA methylation which is linked to epigenetic changes.
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.
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.
- Neonatal exposure of as low as 50 µg/kg disrupts ovarian development in mice
- 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.
- 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 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. 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, but that claim was contested by the authors and others. 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."
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. Another 2010 study with mice concluded that BPA exposure in utero leads to permanent DNA alterations in sensitivity to estrogen. 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.
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. A 2011 rodent study found that male rats exposed to BPA had lower sperm counts and testosterone levels than those of unexposed males. 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.
General research
At an Endocrine Society meeting in 2009, new research reported data from animals experimentally treated with BPA.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.
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".
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.
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, 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.[124]
Studies on humans
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. 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 disease, diabetes, 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." 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.
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.
Other studies
Studies have associated recurrent miscarriage with BPA serum concentrations, oxidative stress and inflammation in postmenopausal women with urinary concentrations, externalizing behaviors in two-year old children, especially among female children, with mother's urinary concentrations, altered hormone levels in men and declining male sexual function with urinary concentrations. The Canadian Health Measures Survey, 2007 to 2009 published in 2010 found that teenagers carry 30 percent more BPA in their bodies than older adults. The reason for this is not known. 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. 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. 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. 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.
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. 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.
Historical studies
The first evidence of the estrogenicity of bisphenol A came from experiments on rats conducted in the 1930s, but it was not until 1997 that adverse effects of low-dose exposure on laboratory animals were first reported.
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