18 Aug Harmful Toxins Bisphenol A (BPA)

Bisphenol A (BPA) is one of the most common chemicals to which we are exposed in everyday life. It is the building block of polycarbonate plastic and is also used in the manufacture of epoxy resins found in many common consumer products (Beronius, 2010). It is also prevalent in thermal receipts and other paper products, including in recycled paper products as a result of the recycling of thermal receipts (Liao, 2011).
Avoid canned foods; clear, shatterproof plastic food and drink containers; and thermal receipts. And even if a plastic is labeled as BPA-free, do not assume that it’s safe!
An estimated 5 million US tons of this endocrine-disrupting chemical were produced globally in 2008, and more than 2.4 million tons were produced in the United States in 2007 (CEPA, 2009). According to Global Industry Analysts, the global market is expected to reach 6 million tons by 2015 (GIA, 2010). Over 500 tons of BPA are released into the U.S. environment annually, according to an estimate by the U.S. Environmental Protection Agency (EPA, 2012). Significant levels of BPA have been measured in ambient air (Matsumoto, 2005), house dust (Rudel, 2003), and river and drinking water (Rodriguez-Mozaz, 2005).
Present in many common household products such as eyeglasses and compact discs, BPA is also commonly found in the epoxy lining of metal food cans; polycarbonate plastic food containers, including some baby bottles; microwave ovenware; and eating utensils. Because BPA is an unstable compound and is also lipophilic (fat-seeking), it can leach into food products, especially when heated (Brotons, 1995). Once in food, BPA can move quickly into people — a particular concern for women of childbearing age and young children. Two studies have explored the effects of increased ingestion of food and drink packaged in materials containing endocrine-disrupting compounds. Both found rapid increases (within a few days to a week) in BPA levels in urine and/or blood samples taken from subjects who intentionally increased their intake of common foods and drinks packaged in BPA-containing products (Carwile, 2009; Smith, 2009). Another study took the opposite approach and demonstrated that just a three-day period of limiting intake of packaged foods decreased the concentrations of BPA found in urine by an average 65 percent (Rudel, 2011).
Clearance of BPA from the body is quite rapid, with its urinary half-life on the order of hours to days. A recent study of samples taken from fasting people indicates that sources other than foods may also be responsible for the pervasive exposure to BPA, as levels of the chemical did not decrease as rapidly as would have been predicted were food the only source of contamination (Stahlhut, 2009), a finding supported by growing evidence of BPA’s presence in thermal receipts and other paper goods. Centers for Disease Control and Prevention researchers have measured BPA in 93 percent of about 2,500 urine samples from a broad national sample of adults through the NHANES study (Calafat, 2008). BPA has been found in the blood (Padmanabhan, 2008) and urine (Ye, 2009a) of pregnant women, and in breast milk soon after women gave birth (Kuruto-Niwa, 2006). BPA has also been found in blood samples from developing fetuses and the surrounding amniotic fluid (Ikezuki, 2002); it has also been measured in placental tissue and umbilical cord blood at birth (EWG, 2009; Schonfelder, 2002) as well as in the urine of premature infants housed in neonatal ICUs (Calafat, 2009).
That BPA is found so extensively in people, from prenatal to adult ages, is particularly impressive given the relatively short half-life of the chemical. Nevertheless, one of the big controversies in the field is related to the form of BPA that is measured in these human biomonitoring studies. The parent chemical, bisphenol A, is known to be weakly estrogenic (Markey, 2001; Wetherill, 2007). However BPA is rapidly metabolized (converted) by the gastrointestinal tract and the liver to a form of BPA (called conjugated BPA) that does not display known estrogenic activity (Matthews, 2001; Volkel, 2002). Analysis of human urine and blood samples has led some investigators to conclude that levels of the parent, estrogenic form of BPA are insignificant in both blood and urine samples of people, and that the conjugated metabolites being reported by most scientists have no known physiological activity (Teeguarden, 2011; Volkel 2008). Others recognize the importance of BPA conversion by metabolism, but conclude that the cumulative evidence from human biomonitoring studies indicates sufficient continued exposure of people to unconjugated (parent) BPA to explain its observed effects on physiological systems (Vandenberg, 2010b).
A further complication in understanding the data from human and animal studies is that, while adult rodents and mammals appear to have similar rates of metabolizing BPA, there may be important differences in metabolism of BPA between rodent and primate (including human) metabolism of the compound in very young animals, a factor that would influence the usefulness of using rodent models for understanding development effects of early BPA exposures in humans (Doerge, 2011; Taylor, 2010). Despite these important controversies over the form and amount of BPA to which developing and adult humans are exposed, considerable data indicate that exposure of humans to BPA is associated with increased risk for cardiovascular disease, miscarriages, decreased birth weight at term, breast and prostate cancer, reproductive and sexual dysfunctions, altered immune system activity, metabolic problems and diabetes in adults, and cognitive and behavioral development in young children (Braun, 2009, 2011; Rees-Clayton, 2011; Lang, 2008; Li, 2009; Miao, 2011; Sugiura-Ogasawara, 2005). These findings are entirely consistent with parallel research in rodent models demonstrating reproductive, metabolic and neurodevelopmental problems in animals exposed to environmentally relevant levels of BPA (e.g., Salian, 2011; Wei, 2011; Wolstenholme, 2011).
With regard to mammary development and increased risk for development of breast cancer, several studies using both rat and mouse models have demonstrated that even brief exposures to environmentally relevant doses of BPA during gestation or around the time of birth lead to changes in mammary tissue structure predictive of later development of tumors (Maffini, 2006; Markey, 2001; Muñoz-de-Toro, 2005). Exposure also increased sensitivity to estrogen at puberty (Wadia, 2007). Early exposure to BPA led to abnormalities in mammary tissue development that were observable even during gestation and were maintained into adulthood (Vandenberg, 2007; 2008). Prenatal exposure of rats to BPA resulted in increases in the number of pre-cancerous lesions and in situ tumors (carcinomas) (Murray, 2007a), as well as an increased number of mammary tumors following adulthood exposures to subthreshold doses (lower than that needed to induce tumors) of known carcinogens (Durando, 2007; Jenkins, 2009).
Another mechanism by which perinatal exposures to low levels of BPA may affect mammary tissue development at puberty and into adulthood is through increased synthesis of the progesterone receptor and activation of progesterone-regulated mammary-cell proliferation (Ayyanan, 2011).
Changes in mammary development comparable to those observed in rodent models were also observed when female rhesus monkeys were exposed to environmentally relevant doses of BPA during gestation (Tharp, 2012). Some of the long-term effects of neonatal exposures to BPA may be dose dependent, with low- and high-dose exposures resulting in different timing and profiles of changes in gene expression in cells of the mammary gland. In one study, low-dose exposures had the most profound effect on rat mammary glands during the period just prior to the animals’ reaching reproductive maturity, while higher doses had more delayed effects, altering gene expression in mammary tissues from mature adults (Moral, 2008). In a study of chronic exposure of adult mice to different concentrations of BPA, only low doses decreased the latency of tumor appearance and increased the number of mammary tumors as well as their rate of metastasis. All doses enhanced the rate of mammary cell proliferation, but only relatively higher doses counteracted this increased proliferation with parallel increases in programmed cell death (apoptosis) (Jenkins, 2011).
In addition to physical abnormalities in the developing mammary tissue of rodents treated around the time of birth with low levels of BPA (0.7 ug/kg body weight/day or 64 ug/kg body weight/day), there are also functional deficits. Female rats exposed to BPA during gestation and suckling had physical abnormalities in their adult mammary tissue as well as decreases in yield and different protein content of their own milk when as new mothers, they were feeding their pups. Observed differences following BPA exposure were similar to those found in rats that had been similarly exposed to diethylstilbestrol, a known breast tumor inducer (Kass, 2012).
Studies using cultures of human breast cancer cells demonstrate that BPA acts through the same cellular response pathways as the natural estrogen estradiol (Rivas, 2002; Welshons, 2006). BPA can interact weakly with the intracellular estrogen receptor, and it can also induce mammary cell proliferation in vitro and in vivo. It affects cellular functions through interactions with the membrane estrogen-receptor (Watson, 2005; Wozniak, 2005). Along with its many other effects on cell growth and proliferation, BPA has been shown to mimic estradiol in causing direct damage to the DNA of cultured human breast cancer cells (Iso, 2006). Exposure of normal and cancerous human breast cells to low levels of BPA leads to altered expression of hundreds of genes including many involved in hormone-receptor-mediated processes, cell proliferation and programmed cell death, and carcinogenesis (Goodson, 2011; Tilghman, 2012; Weng, 2010).
In the presence of BPA, cells from the non-cancerous breast of women diagnosed with breast cancer had a gene-response profile associated with the development of highly aggressive tumors (Dairkee, 2008). Studies indicate that BPA reduces the efficacy of common chemotherapy agents (cisplatin, doxirubicin and vinblastin) in their blocking the proliferation of breast cancer cells when tested in cell systems (LaPensee, 2009; 2010). Thus, not only does early exposure to BPA lead to an increased risk for development of breast tumors, but exposure to BPA during chemotherapy treatment for breast cancer may make the treatment less effective.
BPA’s history as a synthetic estrogen goes way back to the 1930’s where it was actually used as pharmaceutical hormone before being replaced with the more potent and way more horribly devastating chemical DES. But BPA found a new purpose in the 1940’s & 50’s in the manufacture of a new type of plastic – polycarbonate. Fast forward a bunch of decades, and look – we’ve got polycarbonate everywhere! In the late 1990’s it was determined that BPA was leaching from plastic baby bottles, yet thanks to industry pressure and government inaction, nothing was done. It wasn’t until the spring of 2008 that the shit hit the fan, so to speak, for the BPA/polycarbonate plastic industry, and since then state governments have been pushing for partial and outright bans of BPA in children’s products, including baby bottles, and the public has been demanding safer, non-toxic options.
In an attempt to appease the consumer demand, makers of polycarbonate plastic products rushed to create BPA-Free versions. And they did. Hundreds of hard, polycarbonate plastic containers started bearing stickers proclaiming they were BPA-FREE! And everyone bought them (and still are). People were tossing out their trusty Nalgene bottles and buying new ones – this time BPA-FREE. But we may have pushed too hard, too fast in our desire to be rid of this chemical and it’s hormone disrupting effects, because what we’re left with after the BPA-FREE parade left town, is a big public-perception mess to clean up. The BPA-FREE claim makes people feel good, safe, protected – even if they don’t know what BPA is to being with. “If the label is promoting that’s it’s “free” of something… I guess that something must have been bad, right? So now it’s better!”, the logic seems to flow. Turns out Bisphenol-A isn’t the only Bisphenol in the family… there are apparently 15 (bisphenol-F, bisphenol b/c/e/f/g, and so on). In the rush to be rid of BPA, many manufacturers simply swapped one bisphenol chemical for another, so rather than use BPA, they’re now using BPS, or BPF. These bisphenols, as well as other chemicals used in the production of plastics can exhibit what is called “estrogenic activity” – this is the indicator that it being a hormone disruptor, and this is what we want to test for – not whether it just has levels of BPA in it. A study published in the journal Environmental Health Perspectives in July of 2011 showed that almost all commercially available plastics (read: the kinds for sale in stores) showed levels of estrogenic activity, including items labeled BPA-free. In some cases, the BPA-free plastics had higher levels of estrogenic activity than plastics with BPA!
In 2012 the U.S. Food and Drug Administration banned the sale of baby bottles that contain bisphenol A (BPA), a compound frequently found in plastics. The ban came after manufacturers’ responded to consumer concerns of BPA’s safety after several studies found the chemical mimics estrogen and could harm brain and reproductive development in fetuses, infants and children.* Since then store shelves have been lined with BPA-free bottles for babies and adults alike. Yet, recent research reveals that a common BPA replacement, bisphenol S (BPS), may be just as harmful. BPA is the starting material for making polycarbonate plastics. Any leftover BPA that is not consumed in the reaction used to make a plastic container can leach into its contents. From there it can enter the body. BPS was a favored replacement because it was thought to be more resistant to leaching. If people consumed less of the chemical, the idea went, it would not cause any or only minimal harm.
Yet BPS is getting out. Nearly 81 percent of Americans have detectable levels of BPS in their urine. And once it enters the body it can affect cells in ways that parallel BPA. A 2013 study by Cheryl Watson at The University of Texas Medical Branch at Galveston found that even picomolar concentrations (less than one part per trillion) of BPS can disrupt a cell’s normal functioning, which could potentially lead to metabolic disorders such as diabetes and obesity, asthma, birth defects or even cancer. “[fusion_builder_container hundred_percent=”yes” overflow=”visible”][fusion_builder_row][fusion_builder_column type=”1_1″ background_position=”left top” background_color=”” border_size=”” border_color=”” border_style=”solid” spacing=”yes” background_image=”” background_repeat=”no-repeat” padding=”” margin_top=”0px” margin_bottom=”0px” class=”” id=”” animation_type=”” animation_speed=”0.3″ animation_direction=”left” hide_on_mobile=”no” center_content=”no” min_height=”none”][Manufacturers] put ‘BPA-free’ on the label, which is true. The thing they neglected to tell you is that what they’ve substituted for BPA has not been tested for the same kinds of problems that BPA has been shown to cause. That’s a little bit sneaky,” Watson says.
A 2011 study published in Environmental Health Perspectives found that almost all of the 455 commercially available plastics that were tested leached estrogenic chemicals. This study lead to a bitter legal battle between Eastman Chemical Co. and the study’s author, George Bittner, professor of neurobiology at The University of Texas at Austin and founder of CertiChem and PlastiPure, two companies designed to test and discover nonestrogenic plastics. Bittner claimed in the peer-reviewed report that Eastman’s product Tritan, marketed to be completely free of estrogenic leaching, showed such activity. Eastman claimed otherwise and filed a suit. A federal jury ruled in favor of the latter, saying Bittner’s testing methods were inadequate because the tests were done in vitro—in a petri dish rather than in vivo, in a live animal.
Since this episode, independent scientists have focused their efforts on in vivo testing. Deborah Kurrasch, from the University of Calgary, turned to zebra fish to study the effects of BPS on embryo development. Brain development in zebra fish is similar to that in humans but much easier to track. When the fish were dosed with BPS in similar concentrations to that found in a nearby river, neuronal growth exploded, rising 170 percent for fish exposed to BPA and a whopping 240 percent for those exposed to BPS. As the fish aged they began zipping around their tank much faster and more erratically than the unexposed fish. The researchers concluded that increased neural growth likely lead to hyperactivity. “Part of the problem with endocrine disruptors is they usually have a U-shaped dose response profile,” Kurrasch says. “At very low doses they have activity and then as you increase the dose it drops in activity. Then at higher doses it has activity again.” She found a very low dose—1,000-fold lower than the daily recommended amount for humans—can affect neural growth in zebra fish.
In another study, Hong-Sheng Wang, an associate professor at the University of Cincinnati, found that both BPA and BPS cause heart arrhythmia in rats. He tested almost 50 rats, giving them the chemicals in doses akin to concentrations found in humans. Even at such low concentrations the rats’ hearts began to race, but curiously only those of the females. They found that BPS blocked an estrogen receptor found only in female rats, which lead to the disruption of calcium channels—a common cause of heart arrhythmia in humans. These in vivo studies agree with in vitro studies claiming that BPS is a hazard. But the problem doesn’t stop with removing bisphenol S from the market as was done for bisphenol A. The problem, according to Kurrasch, lies in the lack of industry regulation. Currently, no federal agency tests the toxicity of new materials before they are allowed on the market. “We’re paying a premium for a ‘safer’ product that isn’t even safer,” Kurrasch says. There are many types of bisphenols out there, so part of the public’s responsibility “is making sure [manufacturers] don’t just go from BPA to BPS to BPF or whatever the next one is.”
So your new bpa free bottle, Vita-Mix Blender, or baby bottle might technically be BPA free, but that doesn’t exactly mean it’s not going to expose you to the synthetic estrogens you’re working to steer clear from. The whole reason we’re trying to avoid BPA is not because it’s BPA – but because of what BPA is capable of doing: blocking or mimicking our hormones.
How to Try Avoid these Toxins
1) We don’t get lulled into buying BPA-FREE labeled products. They’re no indication of safety.
2) We avoid all canned foods, heating foods in plastic, storing foods in plastic, or eating with plastic*
3) We treat the polycarbonate that we do have carefully. This means hand washing in warm (not hot) soapy water, using the soft side of the sponge, not using your Vitamix (BPA-Free or not) for hot, oily, acidic foods (like tomato soups – use a stainless steel immersion blender for those!).
4) We drink out of glass and stainless steel, not plastic
5) We take comfort that the healthy foods we’re putting into our Vitamix are going to keep us strong and healthy, and hopefully mitigate any of the impact of the estrogenic compounds that we are exposed to.
6) We, if we feel so compelled, buy a blender with a glass carafe
7) Plastic containers have recycle codes on the bottom. Some, but not all, plastics that are marked with recycle codes 3 or 7 may be made with BPA.
8) Employ a regular cleansing and detoxifying health strategy such as colonics, sauna, exercise, green juice, wheatgrass,medicinal mushrooms and herbs and include daily probiotic food and drinks such as yogurt, kombucha and kimchi. Increasing the Gut flora is a great protection against all harmfull toxins.
 
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