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Some [[endocrine disruptor|hormone disrupting]] effects in studies on animals and human [[cancer]] cells have been shown to occur at levels as low as 2–5 ppb (parts per billion). It has been claimed that these effects lead to health problems such as, in men, lowered [[Spermatozoon|sperm]] count and infertile sperm. Recent studies have confirmed that bisphenol A exposure during development has [[carcinogenic]] effects and produce precursors of [[breast cancer]].<ref>{{cite journal | last =Murray TJ | title = Induction of mammary gland ductal hyperplasias and carcinoma in situ following fetal bisphenol A exposure.| journal = Reproductive Toxicology |date=2007 | url = http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=17123778 | format = Abstract | accessdate = 2007-02-28}}</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}}</ref> Bisphenol A has been shown to have developmental toxicity, carcinogenic effects, and possible neurotoxicity.<ref>{{cite journal | last =Lee Ym, 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 |date=2007 | url = http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=AbstractPlus&list_uids=17322771&query_hl=2&itool=pubmed_docsum | format = Abstract | accessdate = 2007-02-28}}</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 | url = http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=16123166 | format = Abstract | accessdate = 2007-02-28}}</ref> Recent studies suggest it may also be linked to obesity 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> [[Schizophrenia]] research indicates [[endocrine disruptor]]s like BPA may be involved in [[schizophrenia]] [[pathogenesis]].<ref name=pmid_18245062>{{cite journal |author=Brown JS |title=Effects of Bisphenol-A and Other Endocrine Disruptors Compared With Abnormalities of Schizophrenia: An Endocrine-Disruption Theory of Schizophrenia |journal=[[Schizophrenia Bulletin]] |volume= |issue= |pages= |year=2008 |pmid=18245062 |doi=10.1093/schbul/sbm147}}</ref>
Some [[endocrine disruptor|hormone disrupting]] effects in studies on animals and human [[cancer]] cells have been shown to occur at levels as low as 2–5 ppb (parts per billion). It has been claimed that these effects lead to health problems such as, in men, lowered [[Spermatozoon|sperm]] count and infertile sperm. Recent studies have confirmed that bisphenol A exposure during development has [[carcinogenic]] effects and produce precursors of [[breast cancer]].<ref>{{cite journal | last =Murray TJ | title = Induction of mammary gland ductal hyperplasias and carcinoma in situ following fetal bisphenol A exposure.| journal = Reproductive Toxicology |date=2007 | url = http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=17123778 | format = Abstract | accessdate = 2007-02-28}}</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}}</ref> Bisphenol A has been shown to have developmental toxicity, carcinogenic effects, and possible neurotoxicity.<ref>{{cite journal | last =Lee Ym, 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 |date=2007 | url = http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=AbstractPlus&list_uids=17322771&query_hl=2&itool=pubmed_docsum | format = Abstract | accessdate = 2007-02-28}}</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 | url = http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=16123166 | format = Abstract | accessdate = 2007-02-28}}</ref> Recent studies suggest it may also be linked to obesity 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> [[Schizophrenia]] research indicates [[endocrine disruptor]]s like BPA may be involved in [[schizophrenia]] [[pathogenesis]].<ref name=pmid_18245062>{{cite journal |author=Brown JS |title=Effects of Bisphenol-A and Other Endocrine Disruptors Compared With Abnormalities of Schizophrenia: An Endocrine-Disruption Theory of Schizophrenia |journal=[[Schizophrenia Bulletin]] |volume= |issue= |pages= |year=2008 |pmid=18245062 |doi=10.1093/schbul/sbm147}}</ref>


A consensus statement by 38 BPA experts concluded that average levels in people are above those that cause harm to animals in laboratory experiments,<ref>{{cite journal | last =vom Saal, Fred. | 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. |date=July 27, 2007 | url = http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=ShowDetailView&TermToSearch=17768031&ordinalpos=2&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum}}</ref> and a NIH-sponsored panel in the U.S. determined that there was 'some concern' about BPA's effect on fetal and infant brain and behavior.<ref>{{cite news | title = CERHR Expert Panel Report for Bisphenol A | url = http://cerhr.niehs.nih.gov/chemicals/bisphenol/BPAFinalEPVF112607.pdf | accessdate = 2007-12-07}}</ref> A draft report by the U.S. [[National Toxicology Program]] agreed with the panel, concluding that "there is some concern for neural and behavioral effects in fetuses, infants, and children at current human exposures," and that there is "some concern for bisphenol A exposure in these populations based on effects in the prostate gland, mammary gland, and an earlier age for puberty in females."<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>
A consensus statement by 38 BPA experts concluded that average levels in people are above those that cause harm to animals in laboratory experiments,<ref>{{cite journal | last =vom Saal, Fred. | 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. |date=July 27, 2007 | url = http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=ShowDetailView&TermToSearch=17768031&ordinalpos=2&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum}}</ref> and a NIH-sponsored panel in the U.S. determined that there was 'some concern' about BPA's effect on fetal and infant brain and behavior.<ref>{{cite news | title = CERHR Expert Panel Report for Bisphenol A | url = http://cerhr.niehs.nih.gov/chemicals/bisphenol/BPAFinalEPVF112607.pdf | accessdate = 2007-12-07}}</ref> A draft report by the U.S. [[National Toxicology Program]] (NPT) agreed with the panel, concluding that "there is some concern for neural and behavioral effects in fetuses, infants, and children at current human exposures," and that there is "some concern for bisphenol A exposure in these populations based on effects in the prostate gland, mammary gland, and an earlier age for puberty in females." The NPT also concluded that there is 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" or that it causes adverse effects in exposed adults.<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 2006, Canadian regulators selected bisphenol A as one of 200 substances deserving of thorough safety assessments after preliminary studies found it to be 'inherently toxic'; the chemical had not previously been studied by them in depth, having been accepted under [[grandfather clause]]s when stricter regulations were passed in the 1980s.<ref name="globemittelstaedt">{{cite news | last=Mittelstaedt | first=Martin | title='Inherently toxic' chemical faces its future | date=[[2007-04-07]] | url=http://www.theglobeandmail.com/servlet/story/RTGAM.20070406.wbisphenolA0407/BNStory/National/ | accessdate=2007-04-07 | publisher=Globe & Mail}}</ref>
In 2006, Canadian regulators selected bisphenol A as one of 200 substances deserving of thorough safety assessments after preliminary studies found it to be 'inherently toxic'; the chemical had not previously been studied by them in depth, having been accepted under [[grandfather clause]]s when stricter regulations were passed in the 1980s.<ref name="globemittelstaedt">{{cite news | last=Mittelstaedt | first=Martin | title='Inherently toxic' chemical faces its future | date=[[2007-04-07]] | url=http://www.theglobeandmail.com/servlet/story/RTGAM.20070406.wbisphenolA0407/BNStory/National/ | accessdate=2007-04-07 | publisher=Globe & Mail}}</ref>

Revision as of 04:39, 18 April 2008

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Bisphenol A (abbreviated BPA) is an organic compound with the formula (CH3)2C(C6H4OH)2. Containing two phenol functional groups, it is a difunctional building block to several important polymers and polymer additives.[1] Bisphenol A has become controversial because it mimics estrogen and thus could induce hormonal responses.[2][3]

Synthesis

Bisphenol A is prepared by the reaction of two equivalents of phenol with one equivalent of acetone. Hydrochloric acid (HCl) and or sulfonated polystyrene is used as a catalyst. 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.[1]

History and use

Further information: [[:Polycarbonate]]

Bisphenol A was first reported by A.P. Dianin in 1891.[4][5] Bisphenol A current uses are numerous. It is a key monomer in production of polycarbonate plastic and epoxy resins and is also used in the following polymer types: polyesters, polysulfones, and polyether ketones. Bisphenol A is also used as an antioxidant in plasticizers and as a polymerization inhibitor in PVC.[1]

It is a precursor to the flame retardant tetrabromobisphenol A, and was formerly used as a fungicide.[6]

Health effects

Bisphenol A has a low acute toxicity (oral LD50 = 3250 mg/kg)[7] and has been widely used as antioxidants in cosmetics and foods.[1] However, bisphenol A is an endocrine disruptor, and there is growing concern that long term low dose exposure to bisphenol A may induce chronic toxicity in humans.[8]

Early studies of bisphenol A's hormonal activity

Bisphenol A was investigated in the 1930s during the search for estrogen mimics. From this study the synthetic compound diethylstilbestrol was shown to be a better competitor with estrogen.[citation needed] Bisphenol A, like many other compounds, is known to be an estrogen receptor agonist.[9] Such agonists can activate estrogen receptors, leading to similar physiological effects as the body's own estrogens.[10] The first evidence of the estrogenicity of bisphenol A came from experiments in the 1930s in which it was fed to ovariectomized rats.[11][12]

Recent Studies

Some hormone disrupting effects in studies on animals and human cancer cells have been shown to occur at levels as low as 2–5 ppb (parts per billion). It has been claimed that these effects lead to health problems such as, in men, lowered sperm count and infertile sperm. Recent studies have confirmed that bisphenol A exposure during development has carcinogenic effects and produce precursors of breast cancer.[13][14] Bisphenol A has been shown to have developmental toxicity, carcinogenic effects, and possible neurotoxicity.[15][16] Recent studies suggest it may also be linked to obesity by triggering fat-cell activity.[17] Schizophrenia research indicates endocrine disruptors like BPA may be involved in schizophrenia pathogenesis.[18]

A consensus statement by 38 BPA experts concluded that average levels in people are above those that cause harm to animals in laboratory experiments,[19] and a NIH-sponsored panel in the U.S. determined that there was 'some concern' about BPA's effect on fetal and infant brain and behavior.[20] A draft report by the U.S. National Toxicology Program (NPT) agreed with the panel, concluding that "there is some concern for neural and behavioral effects in fetuses, infants, and children at current human exposures," and that there is "some concern for bisphenol A exposure in these populations based on effects in the prostate gland, mammary gland, and an earlier age for puberty in females." The NPT also concluded that there is 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" or that it causes adverse effects in exposed adults.[21]

In 2006, Canadian regulators selected bisphenol A as one of 200 substances deserving of thorough safety assessments after preliminary studies 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.[22] On April 16th, 2008 the New York Times quoted an anonymous insider source saying that Health Canada had finished the research and was "said to be ready to declare [Bisphenol A] as 'toxic'".[23]

Peer reviewed publications have appeared pointing out flaws within the chemical industry funded studies that report bisphenol A safety.[24] The U.S. Congress is currently investigating the Weinberg Group, a chemical industry consulting group, for its role in downplaying the health effects of bisphenol A and other chemicals.[25]

Human exposure to bisphenol A

Bisphenol A has been known to leach from the plastic lining of canned foods and, to a lesser degree, polycarbonate plastics that are cleaned with harsh detergents or used to contain acidic or high-temperature liquids.[26] The chemical is found in almost everyone that lives in developed countries at low concentrations. Infants fed with liquid infant formula have among the highest exposures of anyone eating canned foods. Infants fed canned formula with polycarbonate bottles can consume quantities of bisphenol A up to 13 µg/kg/day,[27] while the most sensitive animal studies show effects at much lower concentrations. Debate continues on what is the safe limit of this compound. Within the United States, an exposure of up to 50 µg/kg/day (50 ppb/day) is considered safe[22] by the United States Environmental Protection Agency[28] - well above the levels found to have caused negative health effects in studies (see table below).

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."[29]

Dose (µg/kg/day) Effects (measured in studies of laboratory animals) Study Year[30][22]
0.025 Permanent changes to genital tract 2005
0.025 Changes in breast tissue that predispose cells to hormones and carcinogens 2005
2 30% increase in prostate mass 1997
2.4 Signs of early puberty 2002
2.4 Decline in testicular testosterone 2004
2.5 Breast cells predisposed to cancer 2006
10 Prostate cells more sensitive to hormones and cancer 2006
10 Insulin resistance 2006
10 Decreased maternal behavior 2002
20 Damage to eggs and chromosomes 2003
25 Health Canada provisional human exposure limit 1999
30 Hyperactivity 2004
30 Reversal of normal sex difference in brain structure 2001
50 U.S. human exposure limit 1998
50 European Food Safety Authority tolerable daily intake level[31] 2007

Restrictions on bisphenol A

The city of San Francisco, California, banned the sale of baby bottles and other products for young children containing bisphenol A effective December 2006, and was, at the time, the only jurisdiction in the world to outright forbid the substance.[32] The ban was never enforced, and in May 2007 the city repealed the ban. In January 2006, the German Federal Institute for Risk Assessment announced that polycarbonate baby bottles are safe, stating that published research is "difficult to interpret and [is] occasionally contradictory".[33] A subsequent study by the European Union’s Food Safety Authority reached a similar conclusion, and sharply criticized the methodology used in many of the low-dose exposure studies on rodents.[34] Japan has also concluded that normal use of these products is safe.[35] Currently 9 U.S. states have legislation pending that would affect the use of BPA in containers.[29]

Growing awareness of health concerns in the U.S. retail sector, particularly in chains promoting healthy food and lifestyles, has led to a number of classes of products containing bisphenol A to be withdrawn. In 2005, Patagonia Inc., a retailer of outdoor gear, ceased selling polycarbonate bottles. In 2006, Whole Foods Markets ceased selling baby bottles. In 2007, Mountain Equipment Co-op ceased selling bottles containing BPA.[36]

The results of a Health Canada investigation into the chemical are likely to cause the department to declare bisphenol A a dangerous chemical. The official report is expected to be released on Wednesday, April 16th, 2008. This decision could lead to restrictions on the use of the chemical in Canada.[37][23]

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.[38]

Identification in plastics

There are seven groups of plastic polymers,[39] each with specific properties that are used worldwide for many packaging applications (see table below). Each group of plastic polymer can be identified by its Plastic Identification code (PIC) - usually a number or a letter abbreviation. For instance, Low-Density Polyethylene can be identified by the number "4" and/or the letters "LDPE". The PIC appears inside a three-chasing arrow symbol. The symbol is used to indicate the type of plastic the product is made from.

Types 2, 4 and 5 highlighted green in the table below are believed not to leach chemicals in any significant amount. Type 1 (PET) and Type 6 (PS) have unreacted phthalate monomer in PET and unreacted styrene monomer in PS which could be leached to packed contents in certain conditions [39], but those resins do not use Bisphenol A (BPA) during polymerization and package forming.

Some type 7 plastics, such as polycarbonate plastic and epoxy resins, are made from BPA monomer.[1] When such plastics are exposed to hot liquids, BPA leaches out 55 times faster than it does under normal conditions, at up to 32 ng/hour.[40] Also, Type 3 (PVC) could have BPA as antioxidant in plasticizers, if BPA is used during package forming.[1]

Plastic Identification Code Type of plastic polymer Common Packaging Applications
1 Polyethylene Terephthalate (PET, PETE) Soft drink, water and salad dressing bottles; peanut butter and jam jars
2 High Density Polyethylene (HDPE) Milk, juice and water bottles; yogurt and margarine tubs; trash and retail bags.
3 Polyvinyl Chloride (PVC) Juice bottles; cling films
4 Low Density Polyethylene (LDPE) Frozen food bags; squeezable bottles, e.g. honey, mustard; cling films; flexible container lids.
5 Polypropylene (PP) Reusable microwaveable ware; kitchenware; yogurt containers; margarine tubs; microwaveable disposable take-away containers; disposable cups and plates.
6 Polystyrene (PS) Egg cartons; disposable cups, plates, trays and cutlery; disposable take-away containers; yogurt and margarine containers
7 Other (Including polycarbonate) Beverage bottles; baby milk bottles.

References

  1. ^ a b c d e f Helmut Fiege, Heinz-Werner Voges, Toshikazu Hamamoto, Sumio Umemura, Tadao Iwata, Hisaya Miki, Yasuhiro Fujita, Hans-Josef Buysch, Dorothea Garbe, Wilfried Paulus "Phenol Derivatives" in Ullmann's Encyclopedia of Industrial Chemistry Wiley-VCH: Weinheim, 2002. DOI: 10.1002/14356007.a19_313.
  2. ^ Hot liquids release potentially harmful chemicals in polycarbonate plastic bottles
  3. ^ 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)
  4. ^ Dianin, Zhurnal russkogo fiziko-khimicheskogo obshchestva, 23 (1891), pp. 492 ff.
  5. ^ Theodor Zincke (1905). "Ueber die Einwirkung von Brom und von Chlor auf Phenole: Substitutionsproducte, Pseudobromide und Pseudochloride". Justus Liebigs Annalen der Chemie (343): 75–99. doi:10.1002/jlac.19053430106.
  6. ^ http://pesticideinfo.org/Detail_Chemical.jsp?Rec_Id=PC33756 Pesticideinfo.org: Bisphenol A
  7. ^ MSDS: Bisphenol A 99+%
  8. ^ 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.
  9. ^ Okada, H; et al. (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): 32–38, PMID: 18197296 {{citation}}: Explicit use of et al. in: |last2= (help)CS1 maint: date and year (link)
  10. ^ 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. Retrieved 2007-02-28.
  11. ^ E. C. Dodds and Wilfrid Lawson, "Synthetic Œstrogenic Agents without the Phenanthrene Nucleus", Nature, 137 (1936), 996.
  12. ^ 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.
  13. ^ Murray TJ (2007). "Induction of mammary gland ductal hyperplasias and carcinoma in situ following fetal bisphenol A exposure" (Abstract). Reproductive Toxicology. Retrieved 2007-02-28.
  14. ^ 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}}: CS1 maint: multiple names: authors list (link)
  15. ^ Lee Ym; et al. (2007). "Estrogen receptor independent neurotoxic mechanism of bisphenol A, an environmental estrogen" (Abstract). J Vet Sci. 8 (1): 27–38. Retrieved 2007-02-28. {{cite journal}}: Explicit use of et al. in: |last= (help)
  16. ^ 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" (Abstract). Endocrinology. 146 (12): 5388–96. Retrieved 2007-02-28.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  17. ^ Grossman, Elizabeth. (March 12, 2007). "Chemicals May Play Role in Rise in Obesity". Washington Post.
  18. ^ Brown JS (2008). "Effects of Bisphenol-A and Other Endocrine Disruptors Compared With Abnormalities of Schizophrenia: An Endocrine-Disruption Theory of Schizophrenia". Schizophrenia Bulletin. doi:10.1093/schbul/sbm147. PMID 18245062.
  19. ^ vom Saal, Fred. (July 27, 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.
  20. ^ "CERHR Expert Panel Report for Bisphenol A" (PDF). Retrieved 2007-12-07.
  21. ^ 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.
  22. ^ 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)
  23. ^ a b "Canada Likely to Label Plastic Ingredient 'Toxic'". New York Times Online. 2008-04-16. Retrieved 2008-04-17. {{cite news}}: Check date values in: |date= (help)
  24. ^ Frederick S. vom Saal (2006). "Large effects from small exposures. II. The importance of positive controls in low-dose research on bisphenol A." (Abstract). Environmental Research. 100 (1): 50–76. Retrieved 2007-02-28.
  25. ^ Congressional Probe Targets Consulting Group, Integrity in Science Watch, Center for Science in the Public Interest, 02/11/2008.
  26. ^ "Environmental Working Group". Retrieved 2007-03-07.
  27. ^ "European Food Safety Authority Opinion" (Abstract). Retrieved 2007-02-28.
  28. ^ Bisphenol A - United States Environmental Protection Agency
  29. ^ a b Parents Concerned Over Potentially Toxic Baby Bottles ABC News, Feb. 7, 2008.
  30. ^ Adapated 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.
  31. ^ "EFSA publishes opinion on bisphenol A". Retrieved 2008-04-12.
  32. ^ "Anxieties about toxics". San Francisco Chronicle. 2006-11-22. {{cite news}}: Check date values in: |date= (help)
  33. ^ Selected questions and answers relating to bisphenol A in baby bottles- Federal Institute for Risk Assessment
  34. ^ European Safety Review: No Risk from Bisphenol A Exposure
  35. ^ Why has bisphenol A not been banned? - Federal Institute for Risk Assessment
  36. ^ "Polycarbonate bottles raise questions". Associated Press. 2007-12-23. {{cite news}}: Check date values in: |date= (help)
  37. ^ Health Canada bisphenol A announcement imminent
  38. ^ 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.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  39. ^ a b "Safe Use Of Plastic Food Packaging And Containers".
  40. ^ Biello D (2008-02-19). "Plastic (not) fantastic: Food containers leach a potentially harmful chemical". Scientific American. 2. Retrieved 2008-04-09.

External links

Retrieved from "https://en.wikipedia.org/w/index.php?title=Bisphenol_A&oldid=206427486"