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===Endocrine disruption===
===Endocrine disruption===
The first evidence of the estrogenicity of bisphenol A came from experiments in the 1930s in which it was fed to ovariectomized rats,<ref>E. C. Dodds and Wilfrid Lawson, "Synthetic Œstrogenic Agents without the Phenanthrene Nucleus", ''Nature'', 137 (1936), 996.</ref><ref>E. C. Dodds and W. Lawson, ''Proceedings of the Royal Society of London, Series B, Biological Sciences'', 125, #839 (27-IV-1938), pp. 222–232.</ref> but it was not until 1997 that adverse effects of low-dose exposure on laboratory animals were first reported.<ref name=C&ENews/> Since then, its endocrine disrupting properties have been extensively investigated, and more than 100 studies have been published "rais[ing] health concerns" about the chemical.<ref name="WaPo">{{Citation | last = Layton | first = Lyndsey | title = Studies on Chemical In Plastics Questioned Congress Examines Role Of Industry in Regulation | newspaper = Washington Post | pages = A1 | year = 2008 | date = April 27, 2008 | url = http://www.washingtonpost.com/wp-dyn/content/article/2008/04/26/AR2008042602126.html}}.</ref> Early development appears to be the period of greatest sensitivity to its effects,<ref name=HealthCanada>[http://www.ec.gc.ca/substances/ese/eng/challenge/batch2/batch2_80-05-7.cfm Draft Screening Assessment for The Challenge Phenol, 4,4' -(1-methylethylidene)bis- (Bisphenol A)Chemical Abstracts Service Registry Number 80-05-7.] [[Health Canada]], 2008.</ref> and studies have demonstrated developmental toxicity, carcinogenic effects, and possible neurotoxicity at low doses in animal models (see [[#Selected studies on low dose bisphenol A exposure in animals|table]] below).<ref>{{cite journal |author=Lee YM, Seong MJ, Lee JW, ''et al'' |title=Estrogen receptor independent neurotoxic mechanism of bisphenol A, an environmental estrogen |journal=J. Vet. Sci. |volume=8 |issue=1 |pages=27–38 |year=2007 |month=Mar |pmid=17322771 |doi= |url=http://www.vetsci.org/2007/abstract/27a.html}}</ref><ref>{{cite journal | last =Zsarnovszky A, Le HH, Wang HS, Belcher SM. | title = 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 | journal = Endocrinology. | volume = 146 | issue = 12 | pages = 5388–96 |date=2005 | doi = 10.1210/en.2005-0565 | pmid = 16123166}}</ref> Recent studies suggest it may also be linked to obesity<ref>{{cite news |title=Bisphenol A linked to obesity in mice, study says |url=http://www.ctv.ca/servlet/ArticleNews/story/CTVNews/20080515/BPA_obesity_080515/20080515?hub=Health |work=CTV News |date=2008-05-15 |accessdate=2008-05-16 }}</ref> by triggering fat-cell activity<ref>{{cite journal | last =Grossman, Elizabeth. | title = Chemicals May Play Role in Rise in Obesity | journal = Washington Post. |date=March 12, 2007 | url = http://www.washingtonpost.com/wp-dyn/content/article/2007/03/11/AR2007031100918.html?referrer%3Demailarticlepg&sub=AR}}</ref> and have confirmed that bisphenol A exposure during development has [[carcinogenic]] effects and produce precursors of [[breast cancer]].<ref>{{cite journal |author=Murray TJ, Maffini MV, Ucci AA, Sonnenschein C, Soto AM |title=Induction of mammary gland ductal hyperplasias and carcinoma in situ following fetal bisphenol A exposure |journal=Reprod. Toxicol. |volume=23 |issue=3 |pages=383–90 |year=2007 |pmid=17123778 |pmc=1987322 |doi=10.1016/j.reprotox.2006.10.002 |url=}}</ref><ref name=pmid_18226065>{{cite journal |author=Soto AM, Vandenberg LN, Maffini MV, Sonnenschein C |title=Does breast cancer start in the womb? |journal=Basic Clin. Pharmacol. Toxicol. |volume=102 |issue=2 |pages=125–33 |year=2008 |pmid=18226065 |doi=10.1111/j.1742-7843.2007.00165.x |doi_brokendate=2008-06-22}}</ref> However, neither the U.S. [[Environmental Protection Agency]]<ref>[http://www.epa.gov/iris/subst/0356.htm U.S.EPA, IRIS: Bisphenol A]</ref> nor the [[International Agency for Research on Cancer]]<ref>[http://monographs.iarc.fr/ENG/Classification/ListagentsCASnos.pdf AGENTS REVIEWED BY THE IARC MONOGRAPHS Volumes 1–99]</ref> have evaluated Bisphenol A for possible carcinogenic activity.
The first evidence of the estrogenicity of bisphenol A came from experiments in the 1930s in which it was fed to ovariectomized rats,<ref>E. C. Dodds and Wilfrid Lawson, "Synthetic Œstrogenic Agents without the Phenanthrene Nucleus", ''Nature'', 137 (1936), 996.</ref><ref>E. C. Dodds and W. Lawson, ''Proceedings of the Royal Society of London, Series B, Biological Sciences'', 125, #839 (27-IV-1938), pp. 222–232.</ref> but it was not until 1997 that adverse effects of low-dose exposure on laboratory animals were first reported.<ref name=C&ENews/> Since then, its endocrine disrupting properties have been extensively investigated, and more than 100 studies have been published "rais[ing] health concerns" about the chemical.<ref name="WaPo">{{Citation | last = Layton | first = Lyndsey | title = Studies on Chemical In Plastics Questioned Congress Examines Role Of Industry in Regulation | newspaper = Washington Post | pages = A1 | year = 2008 | date = April 27, 2008 | url = http://www.washingtonpost.com/wp-dyn/content/article/2008/04/26/AR2008042602126.html}}.</ref> Early development appears to be the period of greatest sensitivity to its effects,<ref name=HealthCanada>[http://www.ec.gc.ca/substances/ese/eng/challenge/batch2/batch2_80-05-7.cfm Draft Screening Assessment for The Challenge Phenol, 4,4' -(1-methylethylidene)bis- (Bisphenol A)Chemical Abstracts Service Registry Number 80-05-7.] [[Health Canada]], 2008.</ref> and studies have demonstrated developmental toxicity, carcinogenic effects, and possible neurotoxicity at low doses in animal models (see [[#Selected studies on low dose bisphenol A exposure in animals|table]] below).<ref>{{cite journal |author=Lee YM, Seong MJ, Lee JW, ''et al'' |title=Estrogen receptor independent neurotoxic mechanism of bisphenol A, an environmental estrogen |journal=J. Vet. Sci. |volume=8 |issue=1 |pages=27–38 |year=2007 |month=Mar |pmid=17322771 |doi= |url=http://www.vetsci.org/2007/abstract/27a.html}}</ref><ref>{{cite journal | last =Zsarnovszky A, Le HH, Wang HS, Belcher SM. | title = 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 | journal = Endocrinology. | volume = 146 | issue = 12 | pages = 5388–96 |date=2005 | doi = 10.1210/en.2005-0565 | pmid = 16123166}}</ref> Recent studies suggest it may also be linked to obesity<ref>{{cite news |title=Bisphenol A linked to obesity in mice, study says |url=http://www.ctv.ca/servlet/ArticleNews/story/CTVNews/20080515/BPA_obesity_080515/20080515?hub=Health |work=CTV News |date=2008-05-15 |accessdate=2008-05-16 }}</ref> by triggering fat-cell activity<ref>{{cite journal | last =Grossman, Elizabeth. | title = Chemicals May Play Role in Rise in Obesity | journal = Washington Post. |date=March 12, 2007 | url = http://www.washingtonpost.com/wp-dyn/content/article/2007/03/11/AR2007031100918.html?referrer%3Demailarticlepg&sub=AR}}</ref> and have confirmed that bisphenol A exposure during development has [[carcinogenic]] effects and produce precursors of [[breast cancer]].<ref>{{cite journal |author=Murray TJ, Maffini MV, Ucci AA, Sonnenschein C, Soto AM |title=Induction of mammary gland ductal hyperplasias and carcinoma in situ following fetal bisphenol A exposure |journal=Reprod. Toxicol. |volume=23 |issue=3 |pages=383–90 |year=2007 |pmid=17123778 |pmc=1987322 |doi=10.1016/j.reprotox.2006.10.002 |url=}}</ref><ref name=pmid_18226065>{{cite journal |author=Soto AM, Vandenberg LN, Maffini MV, Sonnenschein C |title=Does breast cancer start in the womb? |journal=Basic Clin. Pharmacol. Toxicol. |volume=102 |issue=2 |pages=125–33 |year=2008 |pmid=18226065 |doi=10.1111/j.1742-7843.2007.00165.x |doi_brokendate=2008-06-22}}</ref> However, neither the U.S. [[Environmental Protection Agency]]<ref>[http://www.epa.gov/iris/subst/0356.htm U.S.EPA, IRIS: Bisphenol A]</ref> nor the [[International Agency for Research on Cancer]]<ref>[http://monographs.iarc.fr/ENG/Classification/ListagentsCASnos.pdf AGENTS REVIEWED BY THE IARC MONOGRAPHS Volumes 1–99]</ref> have evaluated Bisphenol A for possible carcinogenic activity. Most recently, a study by the [[Yale School of Medicine]] demonstrated that adverse neurological effects occur in [[monkeys|non-human primates]] regularly exposed to bisphenol A at levels equal the EPA's maximum safe dose of 50 µg/kg/day.<ref name="pmid18768812">{{cite journal |author=Leranth C, Hajszan T, Szigeti-Buck K, Bober J, Maclusky NJ |title=Bisphenol A prevents the synaptogenic response to estradiol in hippocampus and prefrontal cortex of ovariectomized nonhuman primates |journal=Proc. Natl. Acad. Sci. U.S.A. |volume= |issue= |pages= |year=2008 |month=September |pmid=18768812 |doi=10.1073/pnas.0806139105 |url=}}</ref><ref name="Layton2">{{cite news|url=http://www.washingtonpost.com/wp-dyn/content/article/2008/09/03/AR2008090303397.html?hpid=topnews|title=Chemical in Plastic Is Connected to Health Problems in Monkeys|last=Layton|first=Lindsey|date=Sept. 4, 2008|publisher=Washington Post|pages=A02|accessdate=2008-09-06}}</ref>
In 2007, a consensus statement by 38 experts on bisphenol A concluded that average levels in people are above those that cause harm to animals in laboratory experiments,<ref>{{cite journal |author=vom Saal FS, Akingbemi BT, Belcher SM, ''et al'' |title=Chapel Hill bisphenol A expert panel consensus statement: integration of mechanisms, effects in animals and potential to impact human health at current levels of exposure |journal=Reprod. Toxicol. |volume=24 |issue=2 |pages=131–8 |year=2007 |pmid=17768031 |doi=10.1016/j.reprotox.2007.07.005 |url=}}</ref> and 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.<ref name="CERHR"/> A 2008 report by the U.S. [[National Toxicology Program]] (NTP) 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."<ref>[http://www.niehs.nih.gov/news/media/questions/sya-bpa.cfm Since you asked - Bisphenol A: Questions and Answers about the Draft National Toxicology Program Brief on Bisphenol A], National Institute of Environmental Health Sciences website.</ref>
In 2007, a consensus statement by 38 experts on bisphenol A concluded that average levels in people are above those that cause harm to animals in laboratory experiments,<ref>{{cite journal |author=vom Saal FS, Akingbemi BT, Belcher SM, ''et al'' |title=Chapel Hill bisphenol A expert panel consensus statement: integration of mechanisms, effects in animals and potential to impact human health at current levels of exposure |journal=Reprod. Toxicol. |volume=24 |issue=2 |pages=131–8 |year=2007 |pmid=17768031 |doi=10.1016/j.reprotox.2007.07.005 |url=}}</ref> and 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.<ref name="CERHR"/> A 2008 report by the U.S. [[National Toxicology Program]] (NTP) 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."<ref>[http://www.niehs.nih.gov/news/media/questions/sya-bpa.cfm Since you asked - Bisphenol A: Questions and Answers about the Draft National Toxicology Program Brief on Bisphenol A], National Institute of Environmental Health Sciences website.</ref>
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Dr. Maida Galvez, a pediatrician studying BPA, recommends parents stay away from bottles containing the chemical and says, "We know the animal studies raise concerns, but there aren't human studies showing effects yet ... so, when we don't have the evidence, what we recommend is that parents try to err on the side of caution."<ref name="ABC">[http://www.abcnews.go.com/WN/story?id=4259036&page=1 Parents Concerned Over Potentially Toxic Baby Bottles] ABC News, Feb. 7, 2008.</ref>
Dr. Maida Galvez, a pediatrician studying BPA, recommends parents stay away from bottles containing the chemical and says, "We know the animal studies raise concerns, but there aren't human studies showing effects yet ... so, when we don't have the evidence, what we recommend is that parents try to err on the side of caution."<ref name="ABC">[http://www.abcnews.go.com/WN/story?id=4259036&page=1 Parents Concerned Over Potentially Toxic Baby Bottles] ABC News, Feb. 7, 2008.</ref>

Further tests, by a Yale University team presented to the National Acadmey of Sciences reported in September 2008, on primates with BPA to approximate human trials, suggest that exposure to low-dose BPA may have widespread effects on brain structure and function by interfering with brain-cell connections vital to memory, learning and mood.<ref>Layton, L., 'BPA linked to primate health issues', ''The Washington Post'', September 4, 2008. [http://seattletimes.nwsource.com/html/nationworld/2008157592_bpa04.html]</ref>


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Revision as of 01:29, 6 September 2008

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Bisphenol A, commonly abbreviated as BPA, is an organic compound with two phenol functional groups. It is a difunctional building block of several important polymers and polymer additives. With an annual production of approximately 3 million tonnes, it is an important monomer in the production of polycarbonate.

Suspected of being hazardous to humans since the 1930s, concerns about the use of Bisphenol A in consumer products grabbed headlines in 2008 when several governments issued reports questioning its safety, and some retailers pulled products made from it off their shelves.

Synthesis

Bisphenol A was first reported by A.P. Dianin in 1891.[1][2] It is prepared by the condensation of acetone (hence the suffix A in the name)[3] with two equivalents of phenol. The reaction is catalyzed by an acid, such as hydrochloric acid (HCl) or a sulfonated polystyrene resin. Typically, a large excess of phenol is used to ensure full condensation:

(CH3)2CO + 2 C6H5OH → (CH3)2C(C6H4OH)2 + H2O

A large number of ketones undergo analogous condensation reactions. The method is efficient and the only by-product is water.[4]

Use

Further information: [[:Polycarbonate]]

Products containing or made from Bisphenol A have been in commerce for more than 50 years, and its current uses are numerous. It is used in the synthesis of polyesters, polysulfones, and polyether ketones, as an antioxidant in some plasticizers, and as a polymerization inhibitor in PVC. It is a key monomer in production of polycarbonate plastic and epoxy resins.[4] 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 devices, CDs, and household electronics.[5] Epoxy resins are used as coatings on the inside of almost all food and beverage cans.[6] It is also a precursor to the flame retardant, tetrabromobisphenol A, and was formerly used as a fungicide.[7]

Global production of bisphenol A in 2003 was estimated to be about 3 million metric tonnes (t).[8] In the U.S., it is manufactured by Bayer MaterialScience, Dow Chemical Company, General Electric, 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.[5]

Health effects

Bisphenol A has low acute toxicity, with an oral LD50 of 3250 mg/kg in rats.[9] However, bisphenol A is an endocrine disruptor: it is an estrogen receptor agonist,[10] and such agonists can act like the body's own hormones, leading to similar physiological effects on the body.[11] There is thus concern that long term low dose exposure to bisphenol A may induce chronic toxicity in humans.[12][13][14]

Endocrine disruption

The first evidence of the estrogenicity of bisphenol A came from experiments in the 1930s in which it was fed to ovariectomized rats,[15][16] but it was not until 1997 that adverse effects of low-dose exposure on laboratory animals were first reported.[6] Since then, its endocrine disrupting properties have been extensively investigated, and more than 100 studies have been published "rais[ing] health concerns" about the chemical.[17] Early development appears to be the period of greatest sensitivity to its effects,[18] and studies have demonstrated developmental toxicity, carcinogenic effects, and possible neurotoxicity at low doses in animal models (see table below).[19][20] Recent studies suggest it may also be linked to obesity[21] by triggering fat-cell activity[22] and have confirmed that bisphenol A exposure during development has carcinogenic effects and produce precursors of breast cancer.[23][24] However, neither the U.S. Environmental Protection Agency[25] nor the International Agency for Research on Cancer[26] have evaluated Bisphenol A for possible carcinogenic activity. Most recently, a 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 the EPA's maximum safe dose of 50 µg/kg/day.[27][28]

In 2007, a consensus statement by 38 experts on bisphenol A concluded that average levels in people are above those that cause harm to animals in laboratory experiments,[29] and 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.[5] A 2008 report by the U.S. National Toxicology Program (NTP) 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."[30]

In April 2008, the Health Canada released its Draft Screening Assessment for bisphenol A, which concluded that the chemical may pose some risk to infants[31] and proposed classifying the chemical as "'toxic' to human health and the environment."[32] This action follows Canadian regulators selection of bisphenol A in 2006 as one of 200 substances deserving of thorough safety assessments because preliminary studies had found it to be "inherently toxic"; the chemical had not previously been studied by them in depth, having been accepted under grandfather clauses when stricter regulations were passed in the 1980s.[33]

In contrast to the recent actions in North America, in January 2006 the German Federal Institute for Risk Assessment announced that polycarbonate baby bottles are safe and stated that published research on the health effects of Bisphenol A is "difficult to interpret and [is] occasionally contradictory".[34] An assessment released later that year by the European Union’s Food Safety Authority reached a similar conclusion, expressing "considerable reservations" about the biological significance and robustness of the low-dose exposure studies on rodents.[35] In 2007 Japan also concluded that for individuals in that country, "the current exposure levels of BPA will not pose any unacceptable risk to human health [and] that a ban is not needed."[36]

Some toxicologists and regulatory agencies have criticized low-dose toxicity studies, especially those that involved injecting bisphenol A directly into animals, since human exposures typically involve ingestion and subsequent metabolism in the liver, and the experimental design of a few of these early studies has also been questioned.[37][38] On the other hand, studies have also appeared pointing out flaws in chemical industry funded studies that found no evidence of adverse effects from low dose exposure,[39] and a study from 2008 concluded that blood levels of bisphenol A in neonatal mice are the same whether it is injected or ingested.[40]

Selected studies on low dose bisphenol A exposure in animals

Dose (µg/kg/day) Effects (measured in studies of mice or rats,
descriptions are from Environmental Working Group)[41][33] 		Study Year
0.025 Permanent changes to genital tract 2005[42]
0.025 Changes in breast tissue that predispose cells to hormones and carcinogens 2005[43]
2 increased prostate weight 30% 1997[44]
2 lower bodyweight, increase of anogenital distance in both genders, signs of early puberty and longer estrus. 2002[45]
2.4 Decline in testicular testosterone 2004[46]
2.5 Breast cells predisposed to cancer 2007[47]
10 Prostate cells more sensitive to hormones and cancer 2006[48]
10 Decreased maternal behaviors 2002[49]
30 Reversed the normal sex differences in brain structure and behavior 2003[50]
50 U.S. human exposure limit (not a result from an animal study, but a guideline set by EPA) 1998[51]

Human exposure to bisphenol A

Bisphenol A has been known to leach from the plastic lining of canned foods[52] and, to a lesser degree, polycarbonate plastics that are cleaned with harsh detergents or used to contain acidic or high-temperature liquids. Studies by the CDC found bisphenol A in the urine of 95% of adults sampled in 1988–1994[53] and in 93% of children and adults tested in 2003–04.[54] Almost all exposure is through diet, and infants fed with liquid formula are among the most exposed. Infants fed canned formula with polycarbonate bottles can consume quantities of bisphenol A up to 13 µg/kg/day (see table below),[55] while the most sensitive animal studies show effects at much lower concentrations. Debate continues on what the safe limit of this compound is. Within the United States, an exposure of up to 50 µg/kg/day (50 ppb/day) is considered safe[33] by the United States Environmental Protection Agency.[56]

Dr. Maida Galvez, a pediatrician studying BPA, recommends parents stay away from bottles containing the chemical and says, "We know the animal studies raise concerns, but there aren't human studies showing effects yet ... so, when we don't have the evidence, what we recommend is that parents try to err on the side of caution."[57]

Population Estimated daily bisphenol A intake, μg/kg/day.
Table adapted from the National Toxicology Program Expert Panel Report.[5]
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

Government and industry response

On April 18, 2008 Canadian Health Minister Tony Clement announced that Canada intends to ban the import, sale, and advertising of polycarbonate baby bottles containing bisphenol A over concerns about the safety of bisphenol A. While Health Canada concluded that human exposures are less than the levels deemed to be potentially unsafe, the margin of safety was considered too low for formula-fed infants.[18][58] Around the same time, Wal-Mart announced that it was immediately ceasing sales in all its Canadian stores of food containers, water and baby bottles, sippy cups, and pacifiers containing bisphenol A, and that it would phase out baby bottles made with it in U.S. stores by early 2009.[59] Nalgene also announced it will stop using the chemical in its products,[60] and Toys-R-Us said it too will cease selling baby bottles made from it.[61] Subsequent news reports showed many retailers removing polycarbonate drinking products from their shelves.[62]

As of the release of NTP and Health Canada reports, 10 U.S. states, including California,[63] Maryland,[17] Connecticut[64] and New Jersey,[65] already had legislation pending that would affect the use of BPA, and in the wake of these reports, U.S. Senator Charles Schumer (D–N.Y.) introduced legislation that would ban bisphenol A nationally from products for infants.[17] In addition, the U.S. Congress is investigating the Weinberg Group, a chemical industry consulting firm, for its role in downplaying the health effects of bisphenol A and other chemicals,[66] and the Energy and Commerce Committee in the House of Representatives is investigating the use of BPA in baby products as well as the FDA's approval of the chemical. In asking the FDA to reassess its approval of bisphenol A, committee chairman Bart Stupak (D–Mich.) said "We would expect the FDA to make decisions based on the best available science…Yet the FDA relied on only two industry-funded studies, while other respected authorities used all available data to reach vastly different conclusions." The FDA maintains that bisphenol A is safe and is not recommending that people avoid using products made from it. The Consumer Product Safety Commission agrees, and its deputy director has stressed that use of bisphenol A based plastics has many practical benefits, and that "a ban could result in less effective protection of children from head, eye, or bodily injury."[6] FDA has set up a task force to address these concerns, and in August it released a draft finding[67] concurring with its initial position that the chemical is safe. The agency will make its final decision after an advisory panel on the issues is convened in September.[68]

In response to the recent events, an American Chemistry Council (ACC)/BPA Global Group spokesman said, “The weight of scientific evidence, as assessed by Health Canada and other agencies around the world, provides reassurance that consumers can continue to safely use products made from bisphenol A."[69] The ACC says that bisphenol A does not pose a risk to consumers and has called on the Food and Drug Administration to review the chemical. The ACC also called the media coverage of the controversy "unnecessarily confusing and frightening the public."[64] The Grocery Manufacturers Association also insists that bisphenol A is safe, and argues that "Data purporting to demonstrate 'low' dose effects on the male reproductive system by BPA have not been successfully replicated and, therefore, are not credible to estimate human health risks and safety in light of the weight of a large body of evidence to the contrary."[70] A spokesman for the tin can industry has said that without lining cans with bisphenol A based resins, E. coli and botulism poisoning would be "rampant."[6] An industry website Bisphenol-a.org also carries a number of articles dated as recently as February 2008 claiming the use of Polycarbonate water bottles is safe.

The chemical industry has been criticized over bisphenol A by Democrats and their allies. David Michaels, who served in the Clinton Administration, told the Washington Post that "Tobacco figured this out, and essentially it's the same model … If you fight the science, you're able to postpone regulation and victim compensation, as well. As in this case, eventually the science becomes overwhelming. But if you can get five or 10 years of avoiding pollution control or production of chemicals, you've greatly increased your product."[17]

In the U.S. retail sector, growing concern over bisphenol A exposure had already led a number of retailers to stop using bisphenol A, particularly chains promoting healthy food and lifestyles. In 2005, Patagonia Inc. ceased selling polycarbonate bottles, and in 2006, Whole Foods Markets ceased selling baby bottles as did Mountain Equipment Co-op in 2007.[71]

Environmental risk

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.[72] According to Health 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."[73]

Identification in plastics

Some type 7 plastics may leach bisphenol A
Some type 3 plastics may leach bisphenol A

There are seven classes of plastics used in packaging applications. Type 7 is the catch-all "other" class, and some type 7 plastics, such as polycarbonate (sometimes identified with the letters "PC" near the recycling symbol) and epoxy resins, are made from bisphenol A monomer.[4] When such plastics are exposed to hot liquids, bisphenol A leaches out 55 times faster than it does under normal conditions, at up to 32 ng/hour.[74] Type 3 (PVC) can also contain bisphenol A as antioxidant in plasticizers.[4] Types 1 (PET), 2 (HDPE), 4 (LDPE), 5 (polypropylene), and 6 (polystyrene) do not use bisphenol A during polymerization or package forming,[75] and thus will not leach bisphenol A into food or beverages.

References

  1. ^ Dianin (1891). "Zhurnal russkogo fiziko-khimicheskogo obshchestva". 23: pp. 492–. {{cite journal}}: |pages= has extra text (help); Cite journal requires |journal= (help)CS1 maint: extra punctuation (link)
  2. ^ Zincke, Theodor (1905). "Ueber die Einwirkung von Brom und von Chlor auf Phenole: Substitutionsprodukte, Pseudobromide und Pseudochloride". Justus Liebigs Annalen der Chemie. 343: 75–99. doi:10.1002/jlac.19053430106.
  3. ^ Uglea, Constantin V. (1991). Synthesis and Characterization of Oligomers. CRC Press. pp. page 103. {{cite book}}: |pages= has extra text (help); Unknown parameter |coauthors= ignored (|author= suggested) (help)
  4. ^ a b c d Fiege, Helmut (2002), Phenol Derivatives, Ullmann's Encyclopedia of Industrial Chemistry, Weinheim: Wiley-VCH, doi:10.1002/14356007.a19_313 {{citation}}: Unknown parameter |coauthors= ignored (|author= suggested) (help)
  5. ^ a b c d National Toxicology Program, U.S. Department of Health and Human Services (2007-11-26). "CERHR Expert Panel Report for Bisphenol A" (PDF). Retrieved 2008-04-18. {{cite news}}: Check date values in: |accessdate= (help)
  6. ^ a b c d Erickson, Britt E. (June 2, 2008). "Bisphenol A under scrutiny". Chemical and Engineering News. 86 (22). American Chemical Society: 36–39.
  7. ^ Pesticideinfo.org: Bisphenol A
  8. ^ Draft Screening Assessment for The Challenge Phenol, 4,4' -(1-methylethylidene)bis- (Bisphenol A) Chemical Abstracts Service Registry Number 80-05-7, Environment Canada.
  9. ^ MSDS: Bisphenol A 99+%
  10. ^ Okada H, Tokunaga T, Liu X, Takayanagi S, Matsushima A, Shimohigashi Y (2008). "Direct evidence revealing structural elements essential for the high binding ability of bisphenol A to human estrogen-related receptor-gamma". Environ. Health Perspect. 116 (1): 32–8. doi:10.1289/ehp.10587. PMC 2199305. PMID 18197296. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  11. ^ O’Connor, Chapin (2003). "Critical evaluation of observed adverse effects of endocrine active substances on reproduction and development, the immune system, and the nervous system" (Full Article). Pure Appl. Chem. 75 (11–12): 2099–2123. doi:10.1351/pac200375112099. Retrieved 2007-02-28.
  12. ^ vom Saal FS, Hughes C (2005). "An extensive new literature concerning low-dose effects of bisphenol A shows the need for a new risk assessment". Environ. Health Perspect. 113 (8): 926–33. PMID 16079060.
  13. ^ Hot liquids release potentially harmful chemicals in polycarbonate plastic bottles
  14. ^ Le HH, Carlson EM, Chua JP, Belcher SM (2008). "Bisphenol A is released from polycarbonate drinking bottles and mimics the neurotoxic actions of estrogen in developing cerebellar neurons". Toxicol. Lett. 176 (2): 149–56. doi:10.1016/j.toxlet.2007.11.001. PMID 18155859.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  15. ^ E. C. Dodds and Wilfrid Lawson, "Synthetic Œstrogenic Agents without the Phenanthrene Nucleus", Nature, 137 (1936), 996.
  16. ^ E. C. Dodds and W. Lawson, Proceedings of the Royal Society of London, Series B, Biological Sciences, 125, #839 (27-IV-1938), pp. 222–232.
  17. ^ a b c d Layton, Lyndsey (April 27, 2008), "Studies on Chemical In Plastics Questioned Congress Examines Role Of Industry in Regulation", Washington Post, pp. A1{{citation}}: CS1 maint: date and year (link).
  18. ^ a b Draft Screening Assessment for The Challenge Phenol, 4,4' -(1-methylethylidene)bis- (Bisphenol A)Chemical Abstracts Service Registry Number 80-05-7. Health Canada, 2008.
  19. ^ Lee YM, Seong MJ, Lee JW; et al. (2007). "Estrogen receptor independent neurotoxic mechanism of bisphenol A, an environmental estrogen". J. Vet. Sci. 8 (1): 27–38. PMID 17322771. {{cite journal}}: Explicit use of et al. in: |author= (help); Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  20. ^ Zsarnovszky A, Le HH, Wang HS, Belcher SM. (2005). "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 (12): 5388–96. doi:10.1210/en.2005-0565. PMID 16123166.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  21. ^ "Bisphenol A linked to obesity in mice, study says". CTV News. 2008-05-15. Retrieved 2008-05-16.
  22. ^ Grossman, Elizabeth. (March 12, 2007). "Chemicals May Play Role in Rise in Obesity". Washington Post.
  23. ^ Murray TJ, Maffini MV, Ucci AA, Sonnenschein C, Soto AM (2007). "Induction of mammary gland ductal hyperplasias and carcinoma in situ following fetal bisphenol A exposure". Reprod. Toxicol. 23 (3): 383–90. doi:10.1016/j.reprotox.2006.10.002. PMC 1987322. PMID 17123778.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  24. ^ Soto AM, Vandenberg LN, Maffini MV, Sonnenschein C (2008). "Does breast cancer start in the womb?". Basic Clin. Pharmacol. Toxicol. 102 (2): 125–33. doi:10.1111/j.1742-7843.2007.00165.x. PMID 18226065. {{cite journal}}: Unknown parameter |doi_brokendate= ignored (|doi-broken-date= suggested) (help)CS1 maint: multiple names: authors list (link)
  25. ^ U.S.EPA, IRIS: Bisphenol A
  26. ^ AGENTS REVIEWED BY THE IARC MONOGRAPHS Volumes 1–99
  27. ^ Leranth C, Hajszan T, Szigeti-Buck K, Bober J, Maclusky NJ (2008). "Bisphenol A prevents the synaptogenic response to estradiol in hippocampus and prefrontal cortex of ovariectomized nonhuman primates". Proc. Natl. Acad. Sci. U.S.A. doi:10.1073/pnas.0806139105. PMID 18768812. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  28. ^ Layton, Lindsey (Sept. 4, 2008). "Chemical in Plastic Is Connected to Health Problems in Monkeys". Washington Post. pp. A02. Retrieved 2008-09-06. {{cite news}}: Check date values in: |date= (help)
  29. ^ vom Saal FS, Akingbemi BT, Belcher SM; et al. (2007). "Chapel Hill bisphenol A expert panel consensus statement: integration of mechanisms, effects in animals and potential to impact human health at current levels of exposure". Reprod. Toxicol. 24 (2): 131–8. doi:10.1016/j.reprotox.2007.07.005. PMID 17768031. {{cite journal}}: Explicit use of et al. in: |author= (help)CS1 maint: multiple names: authors list (link)
  30. ^ Since you asked - Bisphenol A: Questions and Answers about the Draft National Toxicology Program Brief on Bisphenol A, National Institute of Environmental Health Sciences website.
  31. ^ Morrissey, Susan R. (April 23, 2008), "Banning Bisphenol A In Baby Bottles: Canada moves toward restricting the chemical; Congress proposes similar legislation", Chemical and Engineering News{{citation}}: CS1 maint: date and year (link).
  32. ^ Government of Canada Takes Action on Another Chemical of Concern: Bisphenol A, Chemical Substances, Health Canada. Accessed April 19, 2008.
  33. ^ a b c Mittelstaedt, Martin (2007-04-07). "'Inherently toxic' chemical faces its future". Globe & Mail. Retrieved 2007-04-07. {{cite news}}: Check date values in: |date= (help)
  34. ^ Selected questions and answers relating to bisphenol A in baby bottles- Federal Institute for Risk Assessment
  35. ^ Opinion of the Scientific Panel on food additives, flavourings, processing aids and materials in contact with food (AFC) related to 2,2-BIS(4-HYDROXYPHENYL)PROPANE, European Food Safety Authority, November 29, 2006. Accessed April 19, 2008
  36. ^ Bisphenol A Risk Assessment Document (AIST Risk Assessment Document Series No. 4) Summary, New Energy and Industrial Technology Development Organization, Research Center for Chemical Risk Management, National Institute of Advanced Industrial Science and Technology, November 2007.
  37. ^ Goodman JE, McConnell EE, Sipes IG; et al. (2006). "An updated weight of the evidence evaluation of reproductive and developmental effects of low doses of bisphenol A". Crit. Rev. Toxicol. 36 (5): 387–457. doi:10.1080/10408440600758317. PMID 16954066. {{cite journal}}: Cite has empty unknown parameters: |1= and |unused_data= (help); Explicit use of et al. in: |author= (help); Text "1B69BA326FFE69C3F0A8F227DF8201D0" ignored (help)CS1 maint: multiple names: authors list (link)
  38. ^ Weight of the Evidence Evaluation of Low-Dose Reproductive and Developmental Effects of Bisphenol A, George M. Gray, Joshua T. Cohen, Gerald Cunha, Claude Hughes, Ernest E. McConnell, Lorenz Rhomberg, I. Glenn Sipes, and Donald Mattison7Human and Ecological Risk Assessment, 10: 875–921, 2004.
  39. ^ vom Saal FS, Welshons WV (2006). "Large effects from small exposures. II. The importance of positive controls in low-dose research on bisphenol A". Environ. Res. 100 (1): 50–76. doi:10.1016/j.envres.2005.09.001. PMID 16256977. {{cite journal}}: Unknown parameter |month= ignored (help)
  40. ^ Taylor JA, Welshons WV, Vom Saal FS (2008). "No effect of route of exposure (oral; subcutaneous injection) on plasma bisphenol A throughout 24h after administration in neonatal female mice". Reprod. Toxicol. 25 (2): 169–76. doi:10.1016/j.reprotox.2008.01.001. PMID 18295446. Retrieved 2008-05-05. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  41. ^ This table is adapted from: EWG, 2007. "Many studies confirm BPA's low-dose toxicity across a diverse range of toxic effects," Environmental Working Group Report: A Survey of Bisphenol A in U.S. Canned Foods. Accessed November 4th, 2007 at http://www.ewg.org/node/20941. All studies included in this table where judged by the CEHRH panel to be at least of moderate usefulness for assessing the risk of BPA to human reproduction.
  42. ^ Markey CM, Wadia PR, Rubin BS, Sonnenschein C, Soto AM (2005). "Long-term effects of fetal exposure to low doses of the xenoestrogen bisphenol-A in the female mouse genital tract". Biol. Reprod. 72 (6): 1344–51. doi:10.1095/biolreprod.104.036301. PMID 15689538.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  43. ^ Muñoz-de-Toro M, Markey CM, Wadia PR; et al. (2005). "Perinatal exposure to bisphenol-A alters peripubertal mammary gland development in mice". Endocrinology. 146 (9): 4138–47. doi:10.1210/en.2005-0340. PMID 15919749. {{cite journal}}: Explicit use of et al. in: |author= (help)CS1 maint: multiple names: authors list (link)
  44. ^ Nagel SC, vom Saal FS, Thayer KA, Dhar MG, Boechler M, Welshons WV (1997). "Relative binding affinity-serum modified access (RBA-SMA) assay predicts the relative in vivo bioactivity of the xenoestrogens bisphenol A and octylphenol". Environ. Health Perspect. 105 (1): 70–6. PMID 9074884.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  45. ^ Honma S, Suzuki A, Buchanan DL, Katsu Y, Watanabe H, Iguchi T (2002). "Low dose effect of in utero exposure to bisphenol A and diethylstilbestrol on female mouse reproduction". Reprod. Toxicol. 16 (2): 117–22. PMID 11955942.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  46. ^ Akingbemi BT, Sottas CM, Koulova AI, Klinefelter GR, Hardy MP (2004). "Inhibition of testicular steroidogenesis by the xenoestrogen bisphenol A is associated with reduced pituitary luteinizing hormone secretion and decreased steroidogenic enzyme gene expression in rat Leydig cells". Endocrinology. 145 (2): 592–603. doi:10.1210/en.2003-1174. PMID 14605012.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  47. ^ Murray TJ, Maffini MV, Ucci AA, Sonnenschein C, Soto AM (2007). "Induction of mammary gland ductal hyperplasias and carcinoma in situ following fetal bisphenol A exposure". Reprod. Toxicol. 23 (3): 383–90. doi:10.1016/j.reprotox.2006.10.002. PMID 17123778.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  48. ^ Ho SM, Tang WY, Belmonte de Frausto J, Prins GS (2006). "Developmental exposure to estradiol and bisphenol A increases susceptibility to prostate carcinogenesis and epigenetically regulates phosphodiesterase type 4 variant 4". Cancer Res. 66 (11): 5624–32. doi:10.1158/0008-5472.CAN-06-0516. PMID 16740699.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  49. ^ Palanza PL, Howdeshell KL, Parmigiani S, vom Saal FS (2002). "Exposure to a low dose of bisphenol A during fetal life or in adulthood alters maternal behavior in mice". Environ. Health Perspect. 110 Suppl 3: 415–22. PMID 12060838.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  50. ^ Kubo K, Arai O, Omura M, Watanabe R, Ogata R, Aou S (2003). "Low dose effects of bisphenol A on sexual differentiation of the brain and behavior in rats". Neurosci. Res. 45 (3): 345–56. PMID 12631470.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  51. ^ EPA (Environmental Protection Agency). 1988. Oral RfD Assessment: Bisphenol A. Integrated Risk Information System.
  52. ^ "Environmental Working Group". Retrieved 2007-03-07.
  53. ^ Calafat AM, Kuklenyik Z, Reidy JA, Caudill SP, Ekong J, Needham LL (2005). "Urinary concentrations of bisphenol A and 4-nonylphenol in a human reference population". Environ. Health Perspect. 113 (4): 391–5. PMID 15811827.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  54. ^ Calafat AM, Ye X, Wong LY, Reidy JA, Needham LL (2008). "Exposure of the U.S. population to bisphenol A and 4-tertiary-octylphenol: 2003–2004". Environ. Health Perspect. 116 (1): 39–44. doi:10.1289/ehp.10753. PMID 18197297.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  55. ^ "European Food Safety Authority Opinion" (Abstract). Retrieved 2007-02-28.
  56. ^ Bisphenol A - United States Environmental Protection Agency
  57. ^ Parents Concerned Over Potentially Toxic Baby Bottles ABC News, Feb. 7, 2008.
  58. ^ The government has given the public 60 days to comment on the proposed ban starting April 19, 2008 and will evaluate whether the ban will become law in October 2008. "Government of Canada Takes Action on Another Chemical of Concern: Bisphenol A". Retrieved 2008-04-18.
  59. ^ Wal-Mart to pull baby bottles made with chemical BPA: Washington Post, Market Watch, April 18, 2008.
  60. ^ Bottle Maker to Stop Using Plastic Linked to Health Concerns, New York Times, April 18, 2008.
  61. ^ "Toys 'R' Us to phase out bisphenol A baby bottles". CBC News. 2008-04-22. Retrieved 2008-04-22.
  62. ^ CANOE - CNEWS - Politics: Bisphenol A water-bottle removal expanding among Canadian retailers
  63. ^ Bill List
  64. ^ a b Weil, William (April 23, 2008), "Debate In A Bottle" ([dead link] – Scholar search), Hartford Courant {{citation}}: External link in |format= (help)CS1 maint: date and year (link).
  65. ^ "Momentum Builds to End BPA in Plastics", NewsInferno.com, April 22, 2008.
  66. ^ Congressional Probe Targets Consulting Group, Integrity in Science Watch, Center for Science in the Public Interest, 02/11/2008.
  67. ^ [http://www.fda.gov/ohrms/dockets/ac/08/briefing/2008-0038b1_01_02_FDA%20BPA%20Draft%20Assessment.pdf DRAFT ASSESSMENT OF BISPHENOL A FOR USE IN FOOD CONTACT APPLICATIONS], US Food and Drug Administration, undated.
  68. ^ "Health Highlights: Aug. 16, 2008". Washington Post. Aug. 16, 2008. Retrieved 2008-08-17. {{cite news}}: Check date values in: |date= (help)
  69. ^ Canada bans BPA plastic from baby bottles, Kansas City Star, Apr. 18, 2008 .
  70. ^ "Canada Could Ban Baby Bottles Containing Bisphenol A". Environment News Service. 2008-04-22. Retrieved 2008-04-24.
  71. ^ "Polycarbonate bottles raise questions". Associated Press. 2007-12-23. {{cite news}}: Check date values in: |date= (help)
  72. ^ Fox, J.E., J. Gulledge, E. Engelhaupt, M.E. Burrow & J.A. McLachlan (2007). "Pesticides reduce symbiotic efficiency of nitrogen-fixing rhizobia and host plants". Proc. Nat. Acad. Sci. 104: 10282–7. doi:10.1073/pnas.0611710104. PMID 17548832.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  73. ^ Bisphenol A Fact Sheet, Health Canada. Assessed April 19, 2008.
  74. ^ Biello D (2008-02-19). "Plastic (not) fantastic: Food containers leach a potentially harmful chemical". Scientific American. 2. Retrieved 2008-04-09.
  75. ^ http://www.ehponline.org/docs/2006/8804/letter.html Environmental Health Perspectives Volume 114, Number 2, February 2006
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