BPA molecules are bound by "ester bonds” to form a polymer used to make polycarbonate plastic. As the building block of polycarbonate, BPA is the primary chemical in polycarbonate, and it thus does not exist in only trace amounts. While plastics are typically thought of as stable, scientists have known for many years that the chemical bond between BPA molecules is unstable. The bond is disrupted by heat and acidic or basic conditions that release BPA into food or beverages in contact with the plastics.
In brief, this summary reveals that there is extensive scientific literature reporting adverse effects of BPA at doses lower than the current level considered safe by U.S. EPA, a high rate of leaching of BPA from food and beverage containers, and evidence that the median BPA level in humans is higher than the level that causes adverse effects in lab studies.1
• Children are Most at Risk
Growing children are particularly at risk to chemicals in their environment because they face greater exposure per pound of body weight and are physiologically more susceptible to them.2 Children’s exposures begin at conception, as chemicals, including BPA, cross the placenta in a pregnant woman’s body3 and can affect the embryo or fetus during critical periods of development. Even after birth, children’s bodies remain immature, with underdeveloped detoxification mechanisms to protect them from BPA as well as drugs. Their brains and other organ systems are constantly developing, undergoing periods of particular sensitivity to damage or disruption. Especially because growing children are particularly at risk from BPA exposure and adverse effects on intellectual ability, social behaviors, fertility, and potential for disease may take decades to detect, precautionary measures must be taken to protect children from exposure to products containing BPA that they use everyday.
• BPA Levels in Humans are Above Harmful Levels Found in Studies
According to the U.S. Centers for Disease Control, 95% of Americans have detectable levels of bisphenol-A in their bodies.4 In a recent CDC study, the observed BPA levels detected—0.1 to 9 parts per billion (ppb)—were at and above the concentrations known to reliably cause adverse effects in laboratory experiments. Despite the fact that BPA is metabolized by the body, the findings provide strong evidence that exposure to BPA is very frequent or nearly continuous.
In fact, one recent study found significant increases in calcium inflow even at the lowest levels of BPA exposure in the parts per trillion (ppt) level.5 Increases in calcium within the cell initiate a wide array of processes within the cell such as regulating hormone secretion and controlling gene activity. The CDC data show that people contain BPA in the parts per billion (ppb) level—1,000 times higher than the lowest exposure at which an effect was seen on calcium influx. These CDC findings are confirmed by numerous studies conducted in other countries showing virtually identical levels of BPA in blood and tissues collected from human fetuses and adults.
• Dangers of BPA are Confirmed by Weight of the Science
Bisphenol-A can alter the expression of several hundred genes with effects varying among specific tissues and also depending upon the timing of exposure. More than 130 studies suggest that BPA exposure at very low doses is linked to a staggering number of health problems, including prostate and breast cancer, obesity, attention deficit and hyperactivity disorder, brain damage, altered immune system, lowered sperm counts, and early puberty.
Although the safe level of BPA exposure set by U.S. EPA based on experiments conducted prior to 1988 is 50 ppb, some examples of effects at significantly lower doses of BPA include:
Behavioral changes: Many laboratory studies show that low-dose exposure to BPA causes behavioral effects, including hyperactivity (at 30 ppb);6 increase in aggression (at 2 to 40 ppb);7 changes in response to painful or fear-provoking stimuli (at 40 ppb);8 impaired learning (at 100 ppb);9 reversal of normal sex differences in the brain structure and elimination of sex differences in behavior (at 30 ppb);10 decreased maternal behavior such as reductions in time spent nursing, increases in time resting away from offspring, and increases in time spent out of the nest (at 10 ppb);11 altered play and other socio-sexual behaviors (at 40 ppb);12 and increased susceptibility to drug addiction (at 40-300 ppb).13
Diabetes and obesity: Low-level, chronic exposure to BPA causes insulin resistance in adult mice.14 Such insulin resistance leads to Type II diabetes in people as well as hypertension and cardiovascular disease. A recent study shows that even a single dose of BPA at levels currently found in humans can result in altered levels of blood glucose and insulin, and twice-daily exposure for just four days results in insulin resistance. Several studies show an increased rate of postnatal growth in both males and females as a result of maternal doses between 2.4 and 500 ppb per day, and accelerated postnatal growth is associated with obesity, insulin-resistant diabetes, hypertension, and heart disease.15
Early puberty: Low-dose exposure to BPA can affect the timing of the onset of puberty. Several studies reveal the early onset of sexual maturation in females occurring at maternal doses between 2.4 and 50 ppb per day.16
Down Syndrome: BPA exposure is linked to an error in cell division called aneuploidy, which causes 10-20% of all birth defects in people, including Down Syndrome. In studies with mice, BPA causes aneuploidy even at extremely low doses.17
Reduced sperm count: Several studies show that low-dose developmental or adult exposure at levels between 0.2 and 20 ppb reduces daily sperm production and fertility in males.18 In one such study, low-dose exposure to male rats caused decreased sperm count and affected testicular weight and structure.19 The authors concluded that “BPA alter[s] spermatogenesis in a linear manner in a dose range which is perhaps relevant to the daily level of exposure in man." An important aspect of this finding is that BPA decreases the levels of testosterone in males.
Breast cancer: Studies show that low-dose BPA exposure stimulates mammary gland development.20 In one study, scientists exposed mouse fetuses to a daily dose of 250 nanograms per kilogram of their body weight—less than 1% the amount deemed safe for humans in the U.S—causing increased breast tissue development. Higher density breast tissue is a risk factor for cancer. One study author, Dr. Ana Soto, indicated the results lead her to believe that BPA likely increases the risk of breast cancer in humans.
Prostate disease and cancer: Low-dose exposure to BPA can significantly increase prostate size. Several studies show an increase in prostate size due to hyperplasia in male mouse offspring at very low maternal doses.21 Another study shows extremely low doses of BPA initiate the proliferation of human prostate cancer cells.22 In addition, exposure to a very low dose of BPA for just a few days after birth predisposes male rats to develop prostate cancer in adulthood.23
Impaired immune function: Studies show altered immune function occurring at BPA doses between 2.5 and 30 ppb.24
Decreased anti-oxidant enzyme levels: A decrease in antioxidant enzymes (required to protect against cell damage) occurred at the very low dose of 200 parts per trillion (ppt) in adult male rats.25
Brain damage: Low doses of BPA can disrupt important effects of estrogen in the developing brain, causing brain damage. In most studies, BPA has been found to mimic the actions of estrogen in developing neurons, but in specific areas of the brain, BPA can have the paradoxical effect of inhibiting the activity of estrogen, which normally increases the growth and regulates the viability of connections between neurons. The concern relating to this finding is that this type of disruption is associated with impaired learning and memory.26
Changes in brain chemistry: Low-dose exposure to BPA causes changes in the brain, including an increase in progesterone receptor mRNA levels at 400 ppb of BPA,27 increase in estrogen receptor alpha mRNA levels at 40 ppb of BPA,28 increase in estrogen receptor beta mRNA levels at 25 ppb of BPA,29 and a change in brain somatostatin receptors at 400 ppb of BPA.30 These receptors are involved in regulating the brain control systems that coordinate the functioning of the reproductive system as well as reproductive and other social behaviors.
The U.S. government has concluded that animal studies are a vital guide to identifying health risks for humans.31 Furthermore, there is extensive evidence that the sensitivity of tissues to BPA in the animals used in the experiments cited above is virtually identical to the sensitivity of human tissues to BPA. There are some strains of rat that are particularly insensitive to BPA as well as any other estrogenic chemical or drug, but these highly insensitive animals are considered by regulatory agencies to be inappropriate for use in toxicological studies aimed at predicting the potential risks to human health posed by exposure to low, environmentally relevant doses of BPA.
Miscarriage and polycystic ovarian disease in women: Low-dose BPA exposure is also associated with miscarriages in women.32 In one recent study, scientists found levels of BPA in women with a history of recurrent miscarriage three times higher than in women who had normal pregnancies.33 Specifically, the scientists examined patients who had suffered three or more consecutive miscarriages and compared the BPA levels of women who had subsequent successful pregnancies with women who miscarried again. In another study, women who had polycystic ovary syndrome (PCOS) had higher levels of BPA, were more obese, and had higher levels of male sex hormones, suggesting a range of physiological abnormalities, relative to normal, non-obese women without PCOS.34
• Polycarbonate Plastic Breaks Down and Leaches BPA
Numerous studies show that polycarbonate plastics break down and leach BPA into food or beverages in contact with the plastic.35 In one study, BPA leaching was detected in 12 polycarbonate baby bottles after dishwashing, brushing, and boiling. Levels of BPA detected in liquid held in these bottles exceeded 8 ppb.36
• Independent Science Shows Harmful Effects from BPA, while Industry Science Shows None
A recently-published review of scientific studies
shows that, in the last 7 years (through November 2005), 151 studies on the
low-dose effects of BPA have been published.37 None of the 12 studies funded by the chemical
industry reported adverse effects at low levels, whereas 128 of 139
government-funded studies found effects. These many studies were conducted in
academic laboratories in the U.S.
and abroad.
Even the 12 industry-funded studies have flaws, however. Of the industry studies, two had its positive control fail—an indication that the entire experiment had failed, not that BPA had not caused an effect.
|
|
Adverse effect |
No effect |
|
Industry Funded |
0 |
12 |
|
Government Funded |
128 |
11 |
Another industry study concluded BPA caused no effect, but an independent analysis of the experiment's data by scientists convened by the National Toxicology Program of the U.S. Department of Health & Human Services concluded that in fact there was an effect. Industry scientists had misreported their own results.
The chemical industry relies on an incomplete review of scientific studies by an effort funded by the American Plastics Council at the Harvard Center for Risk Analysis. The panel funded by the American Plastics Council only considered 19 studies in concluding in 2004 that the weight of the evidence for low-dose effects of BPA was weak.38 As of November 2005, there were 151 published studies on the low-dose effects of BPA.
• Massachusetts Must Lead the Way Due to Outdated Federal Government Action on BPA
The last U.S. EPA risk assessment for BPA was
based on research conducted in the 1980s and did not consider that BPA was a
chemical estrogen. The most recent risk assessment of BPA was based on a
comprehensive review of the scientific literature conducted in 1998 by the European
Union, with some selected articles added through 2001, at which time few of the
current 151 low-dose BPA studies had been published. The most recent review of
scientific studies shows effects from exposure to BPA at levels significantly
below the current “safe exposure” level established by the U.S. based on experiments conducted
prior to 1988.
In June 2006, San Francisco became the first jurisdiction
to enact a prohibition on the use of BPA in toys and child care articles
intended for use by children under the age of three.39
References:
1 Environment California Research & Policy Center & Environment Massachusetts Research & Policy Center would like to thank the authors of Our Stolen Future, Dr. Theo Colborn, Dianne Dumanoski, and Dr. Pete Myers, for their updates on the science of endocrine disruption found at www.ourstolenfuture.org from which we obtained much of the valuable information contained herein.
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17 Hunt, PA, KE Koehler, M Susiarjo, CA Hodges, A Ilagan, RC Voigt, S Thomas, BF Thomas and TJ Hassold. 2003. Bisphenol A exposure causes meiotic aneuploidy in the female mouse . Current Biology 13: 546-553 (2003).
18 Al-Hiyasat, A. S., H. Darmani and A. M. Elbetieha (2002). Effects of bisphenol A on adult male mouse fertility. Eur. J. Oral Sci. 110:163-167 (2002);
Chitra KC, Latchoumycandane C, Mathur PP. (2003). Induction of oxidative stress by bisphenol A in the epididymal sperm of rats. Toxicology. 185(1-2):119-127 (2003);
Sakaue, M, S Ohsako, R Ishimura, S Kurosawa, M Kurohmaru, Y Hayashi, Y Aoki, J Yonemoto and C Tohyama. 2001. Bisphenol-A Affects Spermatogenesis in the Adult Rat Even at a Low Dose. Journal of Occupational Health 43:185 -190 (2001);
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19 Sakaue, M, S Ohsako, R Ishimura, S Kurosawa, M Kurohmaru, Y Hayashi, Y Aoki, J Yonemoto and C Tohyama. 2001. Bisphenol-A Affects Spermatogenesis in the Adult Rat Even at a Low Dose. Journal of Occupational Health 43:185 -190 (2001).
20 Monica Muñoz-de-Toro, Caroline M. Markey, Perinaaz R. Wadia, Enrique H. Luque, Beverly S. Rubin, Carlos Sonnenschein and Ana M. Soto. Perinatal Exposure to Bisphenol-A Alters Peripubertal Mammary Gland Development in Mice. Endocrinology 2005; 146: 4138-4147 (2005);
Markey, CM, EH Luque, M Muñoz de Toro, C Sonnenschein and AM Soto. 2001. In Utero Exposure to Bisphenol A Alters the Development and Tissue Organization of the Mouse Mammary Gland. Biology of Reproduction 65: 1215–1223 (2001).
21 Gupta, Chhanda. 2000. Reproductive malformation of the male offspring following maternal exposure to estrogenic chemicals. Proceedings of the Society for Experimental Biology and Medicine, 224:61-68 (2000);
Nagel, SC, FS vom Saal, KA Thayer, MG Dhar, M Boechler and WV Welshons. 1997. Relative binding affinity-serum modified access (RBA-SMA) assay predicts the relative in vivo activity of the xenoestrogens bisphenol A and octylphenol. Environmental Health Perspectives 105(1):70-76 (1997);
Timms, BG, KL Howdeshell, L Barton, S Bradley, CA Richter and FS vom Saal. 2005. Estrogenic chemicals in plastic and oral contraceptives disrupt development of the fetal mouse prostate and urethra . Proceedings of the National Academy of Sciences , in press (2005).
22 Wetherill, YB, CE Petre, KR Monk, A Puga, and KE Knudsen. 2002. The Xenoestrogen Bisphenol A Induces Inappropriate Androgen Receptor Activation and Mitogenesis in Prostatic Adenocarcinoma Cells . Molecular Cancer Therapeutics, 1: 515–524 (2002).
23 Shuk-Mei Ho, Wan-Yee Tang, Jessica Belmonte de Frausto, and Gail S. Prins. Developmental Exposure to Estradiol and Bisphenol A Increases Susceptibility to Prostate Carcinogenesis and Epigenetically Regulates Phosphodiesterase Type 4 Variant 4, Cancer Research 66: (11), 5624-5632 (2006).
24 Sawai C, Anderson K, Walser-Kuntz D. 2003. Effect of bisphenol A on murine immune function: Modificattion of interferon-gamma, IgG2a, and disease symptoms in NZB x NZW F1 mice. Environ. Health Perspect. 111:1883-1887 (2003);
Yoshino S, Yamaki K, Yanagisawa R, Takano H, Hayashi H, Mori Y. 2003. Effects of bisphenol A on antigen-specific antibody production, proliferative responses of lymphoid cells, and TH1 and TH2 immune responses in mice. Br. J. Pharmacol. 138:1271-1276 (2003);
Yoshino S, Yamaki K, Li X, Sai T, Yanagisawa R, Takano H, Taneda S, Hayashi H, Mori Y. 2004. Prenatal exposure to bisphenol A up-regulates immune responses, including T helper 1 and T helper 2 responses, in mice. Immunol. 112:489-495 (2004).
25 Chitra KC, Latchoumycandane C, Mathur PP. (2003). Induction of oxidative stress by bisphenol A in the epididymal sperm of rats. Toxicology. 185(1-2):119-127 (2003).
26 MacLusky, NJ, T Hajszan, and C Leranth. 2005. The Environmental Estrogen Bisphenol-A Inhibits Estrogen-Induced Hippocampal Synaptogenesis . Environmental Health Perspectives 113:675-679 (2005);
Attila Zsarnovszky, Hoa H. Le, Hong-Sheng Wang, and Scott M. Belcher. Ontogeny of Rapid Estrogen-Mediated Extracellular Signal-Regulated Kinase Signaling in the Rat Cerebellar Cortex: Potent Nongenomic Agonist and Endocrine Disrupting Activity of the Xenoestrogen Bisphenol A. Endocrinology, 146 : 5388 – 5396 (2005).
27 Funabashi T, Sano A, Mitsushima D, Kimura F. 2003. Bisphenol A increases progesterone receptor immunoreactivity in the hypothalamus in a dose-dependent manner and affects sexual behaviour in adult ovariectomized rats. J. Neuroendocrinol. 15:134-140 (2003).
28 Aloisi AM, Della Seta D, Ceccarelli I, Farabollini F. 2001. Bisphenol-A differently affects estrogen receptors-alpha in estrous-cycling and lactating female rats. Neurosci. Lett. 310:49-52 (2001).
29 Ramos JG, Varayoud J, Kass L, Rodriguez H, Costabel L, Munoz-De-Toro M, Luque EH. 2003. Bisphenol a induces both transient and permanent histofunctional alterations of the hypothalamic-pituitary-gonadal axis in prenatally exposed male rats. Endocrinology 144:3206-3215 (2003).
30 Facciolo RM, Alo R, Madeo M, Canonaco M, Dessi-Fulgheri F. 2002. Early cerebral activities of the environmental estrogen bisphenol A appear to act via the somatostatin receptor subtype sst2. Environ. Health Perspect. 110 (Suppl 3):397-402 (2002).
31 U.S. National Research Council of the National Academy of Sciences, Committee on Hormonally Active Agents in the Environment (1999) (In August 1999, the National Research Council released its long awaited report on endocrine disruption, commissioned in 1995 by the U.S. EPA, the U.S. Department of the Interior, and Congress. The National Academy confirmed that human exposure to contaminants such as BPA and phthalates is widespread and that animal studies are a vital guide to identifying health risks for people. “Laboratory studies using male and female rats, mice, and guinea pigs and female rhesus monkeys have shown that exposure of these animals during development to a variety of concentrations of certain HAAs (e.g., DDT, methoxychlor, PCBs, dioxin, bisphenol A, octylphenol, butyl benzyl phthalate (BBP), dibutyl phthalate (DBP), chlordecone, and vinclozolin) can produce structural and functional abnormalities of the reproductive tract.”).
32 Hunt, PA, KE Koehler, M Susiarjo, CA Hodges, A Ilagan, RC Voigt, S Thomas, BF Thomas and TJ Hassold. 2003. Bisphenol A exposure causes meiotic aneuploidy in the female mouse . Current Biology 13: 546-553 (2003);
Sugiura-Ogasawara, M, Y Ozaki, S Sonta, T Makino and Kaoru Suzumori 2005. Exposure to bisphenol A is associated with recurrent miscarriage . Human Reproduction 20:2325-2329 (2005) .
33 Sugiura-Ogasawara, M, Y Ozaki, S Sonta, T Makino and Kaoru Suzumori 2005. Exposure to bisphenol A is associated with recurrent miscarriage . Human Reproduction 20:2325-2329 (2005) .
34 Takeuchi T, Tsutsumi O, Ikezuki Y, Takai Y, Taketani Y. 2004. Positive relationship between androgen and the endocrine disruptor, bisphenol A, in normal women and women with ovarian dysfunction. Endocrin. J. 51:165-169 (2004).
35 Brede, C., P. Fjeldal, I. Skjevrak and H. Herikstad (2003). Increased migration levels of bisphenol A from polycarbonate baby bottles after dishwashing, boiling and brushing. Food Addit. Contam. 20(7): 684-9 (2003);
Factor, A. (1996). Mechanisms of thermal and photodegradations of bisphenol A polycarbonate. Polymer Durability: Degradation, Stabilization, and Lifetime Prediction. R. L. Clough, N. C. Billingham and K. T. Gillen. Washington, D.C., American Chemistry Society: 59-76 (1996);
Howdeshell, K. L., P. H. Peterman, B. M. Judy, J. A. Taylor, C. E. Orazio, R. L. Ruhlen, F. S. vom Saal and W. V. Welshons (2003). Bisphenol A is released from used polycarbonate animal cages into water at room temperature. Environ. Health Perspect. 111:1180-1187 (2003);
Hunt, P. A., K. E. Koehler, M. Susiarjo, C. A. Hodges, A. Hagan, R. C. Voigt, S. Thomas, B. F. Thomas and T. J. Hassold (2003). Bisphenol A causes meiotic aneuploidy in the female mouse. Current Biol. 13:546-553 (2003).
Sajiki, J. and J. Yonekubo (2004). Leaching of bisphenol A (BPA) from polycarbonate plastic to water containing amino acids and its degradation by radical oxygen species. Chemosphere 55:861-7 (2004).
36 Brede, C., P. Fjeldal, I. Skjevrak and H. Herikstad (2003). Increased migration levels of bisphenol A from polycarbonate baby bottles after dishwashing, boiling and brushing. Food Addit. Contam. 20(7): 684-9 (2003).
37 vom Saal, F and C Hughes, An Extensive New Literature Concerning Low-Dose Effects of Bisphenol A Shows the Need for a New Risk Assessment . Environmental Health Perspectives 113:926-933 (2005).
38 vom Saal, F and C Hughes, An Extensive New Literature Concerning Low-Dose Effects of Bisphenol A Shows the Need for a New Risk Assessment . Environmental Health Perspectives 113:926-933 (2005) (“The charge to the HCRA panel, which was to perform a weight-of-the evidence evaluation of available data on the developmental and reproductive effects of exposure to BPA in laboratory animals, led to an analysis of only 19 of 47 available published studies on low-dose effects of BPA. The deliberations of the HCRA were in 2001–2002, and accordingly, a cut-off date of April 2002 was selected for consideration of the published literature. It is regrettable that the relevance of the analysis was further undermined by a delay of 2.5 years in publication of the report. During the intervening time, between April 2002 and the end of 2004, a large number of additional articles reporting low-dose effects of BPA in experimental animals have been published. The result is that by the end of 2004, a PubMed (National Library of Medicine, Bethesda, MD) search identified 115 published studies concerning effects of low doses of BPA in experimental animals.”).
39 San Francisco Ordinance no. 120-06 (2006).