Unlucky #7 and which plastics contain BPA:
According to the American Chemistry Society, of the seven grades of commercial plastics available to manufactures on today’s market unlucky #7 has the worst track record for leeching the chemical known as BPA into liquids or foods likely to be consumed by humans or animals. The reason is because unlike the other six composites, containers bearing the number seven are made of a composite of leftover scraps that have been ‘repurposed’ and most likely purchased at a discount.
From the Nalgene BPA information center:
“Most plastic containers are marked (usually on the bottom) with a number within a triangle with arrows - commonly known as a recycling symbol. These numbers, known as the resin identification coding system, were created in 1988 to facilitate recycling programs across the country. These recycling numbers can range from #1 to #7, depending on the type of plastic. The #7 recycling label is a catchall indicator for plastics made with a resin other than those in the #1 to #6 designations, or made of more than one resin. The #7 category not only includes polycarbonate, but also includes compostable plastics made of organic material and other types of plastic that do not necessarily contain BPA (Bisphenol-A). For example, our new Everyday™ line manufactured with Eastman’s Tritan™ copolyester is a #7, but does not include BPA.”
From the American Chemistry’s Plastics index:
Other. Use of this code indicates that a package is made with a resin other than the six listed above, or is made of more than one resin and used in a multi-layer combination.
A Survey of Bisphenol A in U.S. Canned Foods:
March 5, 2007 Summary. Independent laboratory tests found a toxic food-can lining ingredient associated with birth defects of the male and female reproductive systems in over half of 97 cans of name-brand fruit, vegetables, soda, and other commonly eaten canned goods. The study was spearheaded by the Environmental Working Group (EWG) and targeted the chemical bisphenol A (BPA), a plastic and resin ingredient used to line metal food and drink cans. There are no government safety standards limiting the amount of BPA in canned food.
EWG’s tests found:
Of all foods tested, chicken soup, infant formula, and ravioli had BPA levels of highest concern. Just one to three servings of foods with these concentrations could expose a woman or child to BPA at levels that caused serious adverse effects in animal tests. For 1 in 10 cans of all food tested, and 1 in 3 cans of infant formula, a single serving contained enough BPA to expose a woman or infant to BPA levels more than 200 times the government’s traditional safe level of exposure for industrial chemicals. The government typically mandates a 1,000- to 3,000-fold margin of safety between human exposures and levels found to harm lab animals, but these servings contained levels of BPA less than 5 times lower than doses that harmed lab animals. BPA testing in canned food. We contracted with a national analytical laboratory to test 97 cans of food we purchased in March 2006 in three major, chain supermarkets in Atlanta, Georgia; Oakland, California; and Clinton, Connecticut. The lab tested 30 brands of food altogether, 27 national brands and 3 store brands. Among the foods we tested are 20 of the 40 canned foods most commonly consumed by women of childbearing age (NHANES, 2002), including soda, canned tuna, peaches, pineapples, green beans, corn, and tomato and chicken noodle soups. We also tested canned infant formula. The lab detected BPA in fifty-seven percent of all cans. BPA is a heavily produced industrial compound that has been detected in more than 2,000 people worldwide, including more than 95 percent of 400 people in the United States. More than 100 peer-reviewed studies have found BPA to be toxic at low doses, some similar to those found in people, yet not a single regulatory agency has updated safety standards to reflect this low-dose toxicity. FDA estimates that 17% of the U.S. diet comprises canned food; they last examined BPA exposures from food in 1996 but failed to set a safety standard.
Nalgene responds to consumer pressure about BPA in water bottles:
Nalgene to Phase Out Production of Consumer Bottles Containing BPA Nalgene to focus on existing non-BPA bottles and recently announced Everyday line; Ensures consumers get the bottle that fits their lifestyle ROCHESTER, N.Y. (April 18, 2008) – In response to consumer demand, Nalgene® will phase out production of its Outdoor line of polycarbonate containers that include the chemical Bisphenol-A (BPA) over the next several months, it announced today. Nalgene’s existing product mix, including the recently launched Everyday line, already features a number of containers made from materials that do not contain BPA. “We have always been focused on responding to the needs and concerns of our customers”, said Steven Silverman, general manager of the Nalgene business. “With 10 different product lines in several different materials, we have the largest bottle offering on the market today. By eliminating containers containing BPA from our consumer product mix, our customers can have confidence that their needs are being met.” The company recently unveiled its Everyday line, an assortment of bottles manufactured with Eastman’s Tritan™ copolyester. The line includes favorites such as the OTG (“On the Go”), the iconic 32-ounce Wide Mouth and the Grip-N-Gulp sippy cup. Tritan is impact resistant, withstands a wide range of temperatures and does not contain BPA. The new Everyday products are already available in stores and will be available through Nalgene-outdoor.com next month. To help consumers easily determine the bottle and material that is right for them, Nalgene also recently launched Nalgene Choice™, an online information resource at Nalgenechoice.com. Nalgene Choice provides consumers with information to help them understand the features and benefits of Nalgene’s wide assortment of products and materials. The result –individuals can choose the product that is right for them. “Today, everyone from hikers and outdoor enthusiasts to commuters and kids on the go are using Nalgene products to reduce the use of disposable bottles and containers,” said Silverman. “Based on all available scientific evidence, we continue to believe that Nalgene products containing BPA are safe for their intended use. However, our customers indicated they preferred BPA-free alternatives and we acted in response to those concerns.”
About NALGENE Outdoor
Nalgene Outdoor Products is based in Rochester, New York. Founded in 1949 as a manufacturer of the first plastic pipette holder, the company soon expanded its product line to include state-of-the-art polyethylene labware under the NALGENE brand. By the 1970s, outdoor enthusiasts had discovered the taste and odor-resistant, leakproof and rugged properties of NALGENE’s large selection of plastic containers. In response to this emerging demand, the NALGENE Consumer Products Division was formed.
What does the #7 represent?
Most plastic containers are marked (usually on the bottom) with a number within a triangle with arrows – commonly known as a recycling symbol. These numbers, known as the resin identification coding system, were created in 1988 to facilitate recycling programs across the country. These recycling numbers can range from #1 to #7, depending on the type of plastic. The #7 recycling label is a catchall indicator for plastics made with a resin other than those in the #1 to #6 designations, or made of more than one resin. The #7 category not only includes polycarbonate, but also includes compostable plastics made of organic material and other types of plastic that do not necessarily contain BPA (Bisphenol-A). For example, our new Everyday™ line manufactured with Eastman’s Tritan™ copolyester is a #7, but does not include BPA. For more information regarding types of plastics and recycling codes, please feel free to visit the following link: http://www.americanchemistry.com/s_plastics/bin.asp?CID=1102&DID=4645&DOC=FILE.PDF
What is Bisphenol A?
Bisphenol A is used primarily to make plastics, and products containing bisphenol A-based plastics have been in commerce for more than 50 years. At least 8 billion pounds of BPA are used by manufacturers yearly.It is a key monomer in production of epoxy resins and in the most common form of polycarbonate plastic. Polycarbonate plastic, which is clear and nearly shatter-proof, is used to make a variety of common products including baby and water bottles, sports equipment, medical and dental devices, dental fillings and sealants, eyeglass lenses, CDs and DVDs, and household electronics. BPA is also used in the synthesis of polysulfones and polyether ketones, as an antioxidant in some plasticizers, and as a polymerization inhibitor in PVC. Epoxy resins containing bisphenol A are used as coatings on the inside of almost all food and beverage cans, however, due to BPA health concerns, in Japan epoxy coating was mostly replaced by PET film. Bisphenol A is also a precursor to the flame retardant tetrabromobisphenol A, and was formerly used as a fungicide. Bisphenol A is a preferred color developer in carbonless copy paper and thermal paper, with the most common public exposure coming from some thermal point of sale receipt paper. BPA-based products are also used in foundry castings and for lining water pipes.
Global production of bisphenol A was estimated to be over 2 million tonnes in 2003, and more than 2.2 Mt in 2009. In the U.S., it is manufactured by Bayer MaterialScience, Dow Chemical Company, SABIC Innovative Plastics (formerly GE Plastics), Hexion Specialty Chemicals, and Sunoco Chemicals. In 2004, these companies produced just over 1 million t of bisphenol A, up from just 7,260 t in 1991. In 2003, annual U.S. consumption was 856,000 t, 72% of which was used to make polycarbonate plastic and 21% going into epoxy resins. In the US less than 5% of the BPA produced is used in food contact applications.
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 Endocrine Society released a scientific statement expressing concern over current human exposure to BPA.
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.”
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 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.
Highly controversial claims have been made that BPA could be involved in attention-deficit hyperactivity disorder (ADHD)
A 2010 study with rats prenatally exposed 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 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.
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.
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.
A 2010 review concluded that Bisphenol A may increase cancer risk.
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 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.
Research on mice and women has shown that exposure Bisphenol A during development has carcinogenic effects and produces precursors of breast cancer. Recent research has shown evidence that BPA remains more time in the body than previously thought.
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. The National Toxicology Panel recommends avoiding microwaving food in plastic containers, putting plastics in the dishwasher, or using harsh detergents on plastics, to avoid leaching.
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 (10 µg/kg) increased prostate cancer susceptibility when adults.
Bisphenol A suppress DNA methylation which is linked to epigenetic changes.
Reproductive System and Sexual behavior Research on Bisphenol A
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 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.
A 2010 study with mice concluded that BPA exposure in utero leads to permanent DNA alterations in sensitivity to estrogen.
General Research on Bisphenol A
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 appear to be entering the human body from a variety of unknown sources.
A 2009 in vitro study on cytotrophoblasts cells has found cytoxic effects in exposure of BPA doses from 0.0002 to 0.2 micrograms per millilitre 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 micrograms/mL of BPA in drinking water enhances allergic sensitization and bronchial inflammation and responsiveness in an animal model of asthma.
Studies on Humans of Bisphenol A Effects
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 notes that while this preliminary study needs to be confirmed and cannot prove causality, there is precedent for analogous effects in animal studies, which “add[s] biological plausibility to the results reported by Lang et al.”
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.
Other Studies of Bisphenol A
Studies have associated recurrent miscarriage with BPA serum concentrations, oxidative stress and inflamation 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.
Historical Studies of Bisphenol A
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.
Low Dose Exposure to Animals
Dose (µg/kg/day) Effects (measured in studies of mice or rats, descriptions (in quotes) are from Environmental Working Group) Study Year 0.025 “Permanent changes to genital tract” 2005 0.025 “Changes in breast tissue that predispose cells to hormones and carcinogens” 2005 1 long-term adverse reproductive and carcinogenic effects 2009 2 “increased prostate weight 30%” 1997 2 “lower bodyweight, increase of anogenital distance in both genders, signs of early puberty and longer estrus.” 2002 2.4 “Decline in testicular testosterone” 2004 2.5 “Breast cells predisposed to cancer” 2007 10 “Prostate cells more sensitive to hormones and cancer” 2006 10 “Decreased maternal behaviors” 2002 30 “Reversed the normal sex differences in brain structure and behavior” 2003 50 Adverse neurological effects occur in non-human primates 2008 50 Disrupts ovarian development 2009
The current U.S. human exposure limit set by the EPA is 50 µg/kg/day.
There is evidence that bisphenol A functions as a xenoestrogen by binding strongly to estrogen-related receptor γ (ERR-γ). 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). BPA binding to ERR-γ preserves its basal constitutive activity. It can also protect it from deactivation from the selective estrogen receptor modulator 4-hydroxytamoxifen.
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 the placenta, explaining reports of high bisphenol A accumulation in this tissue.
Human exposure sources
Bisphenol A has been known to be leached from the plastic lining of canned foods and, to a lesser degree, polycarbonate plastics, especially those that are cleaned with harsh detergents or used to contain acidic or high-temperature liquids. A recent Health Canada study found that the majority of canned soft drinks it tested had low, but measurable levels of bisphenol A. This exposure through metal cans is due to the fact that BPA is an ingredient in the internal coating of food and beverage metal cans used to protect the food from direct contact with metal. While most human exposure is through diet, exposure can also occur through air and through skin absorption.
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. Popular uses of thermal paper include airline tickets, event and cinema tickets, labels, and point of sale applications (receipts). While there is little concern for dermal absorption of BPA, free BPA can readily be transferred to skin and residues on hands can be ingested.
Studies by the CDC found bisphenol A in the urine of 95% of adults sampled in 1988–1994 and in 93% of children and adults tested in 2003–04. 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). The most sensitive animal studies show effects at much lower doses, while the EPA considers exposures up to 50 µg/kg/day to be safe. In 2009, a study found that drinking from polycarbonate bottles increased urinary bisphenol A levels by two thirds, from 1.2 micrograms/gram creatinine to 2 micrograms/gram creatinine.
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 were more transferred. Extraction of BPA from the fingers were possible up to 2 hours after exposure.
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. The National Toxicology Panel recommends avoiding microwaving food in plastic containers, putting plastics in the dishwasher, or using harsh detergents, to avoid leaching.
A 2009 small US study funded by the EWG has detected an average of 2.8 ng/mL BPA in the blood of 9 out of the 10 umbilical cords tested.
In the US and Canada, BPA has been found in infant liquid formula in concentrations varying from 0.48 to 11 ng/g. BPA has been rarely found in infant powder formula (only 1 of 14).
In the US consumption of soda, school lunches, and meals prepared outside the home was statistically significantly associated with higher urinary BPA.
A 2010 study of Austrian, Swiss and German population has suggested polycarbonate (PC) baby bottles as the most prominent role of exposure for infants, and canned food for adults and teenagers.
BPA is also used to form epoxy resin coating of water pipes. In older buildings, such resin coatings are used to avoid a replacement of deteriorating hot and cold water pipes.
Population Estimated daily bisphenol A intake, μg/kg/day. Table adapted from the National Toxicology Program Expert Panel Report. Infant (0–6 months) formula-fed 1–11 Infant (0–6 months) breast-fed 0.2–1 Infant (6–12 months) 1.65–13 Child (1.5–6 years) 0.043–14.7 Adult 0.008–1.5
There’s 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), 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. Free BPA can also be inactivated by sulfation, a process that can also be reverted by arylsulfatase C.
The best test methods for studying BPA effects are currently under discussion with scientists sharing different opinions.
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). 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).
A 2009 research has found that some drugs, like naproxen, salicylic acid, carbamazepine and mefenamic acid can, in vitro, significantly inhibit BPA glucuronidation.
A 2010 study on rats embryos has found that genistein may enhance developmental toxicity of BPA.
Environmental Risks of Bisphenol A
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.
BPA can contaminate the environment either directly or through degradation of products containing BPA, such as ocean-borne plastic trash.
As an environmental contaminant this compound interferes with nitrogen fixation at the roots of leguminous plants associated with the bacterial symbiont Sinorhizobium meliloti. Despite a half-life in the soil of only 1–10 days, its ubiquity makes it an important pollutant. 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.”
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), molluscs, crustaceans, insects, fish and amphibians concluded that BPA have been shown to affect reproduction in all studied animal groups, to impair development in crustaceans and amphibians and to induce genetic aberrations.
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.