Bisphenol A

From Wikipedia, the free encyclopedia

Bisphenol A
Bisphenol-A-Skeletal.svg
Bisphenol A.png
Names
Preferred IUPAC name
4,4′-(Propane-2,2-diyl)diphenol
Other names
BPA, p,p-Isopropylidenebisphenol,
2,2-Bis(4-hydroxyphenyl)propane
Identifiers
CAS Number
  • 80-05-7 checkY
3D model (JSmol)
ChEBI
ChEMBL
ChemSpider
DrugBank
ECHA InfoCard 100.001.133 Edit this at Wikidata
EC Number
  • 201-245-8
IUPHAR/BPS
KEGG
PubChem CID
RTECS number
  • SL6300000
UNII
UN number 2924 2430
CompTox Dashboard (EPA)
InChI
SMILES
Properties
Chemical formula
 C15H16O2
Molar mass 228.291 g·mol−1
Appearance White solid
Density 1.20 g/cm³
Melting point 158 to 159 °C (316 to 318 °F; 431 to 432 K)
Boiling point 360 °C (680 °F; 633 K)
Solubility in water
 120–300 ppm (21.5 °C)
Vapor pressure 5×10−6 Pa (25 °C)[1]
Hazards
GHS pictograms GHS05: CorrosiveGHS07: HarmfulGHS08: Health hazard
GHS Signal word Danger
GHS hazard statements
 H317, H318, H335, H360
GHS precautionary statements
 P201, P202, P261, P271, P272, P280, P281, P302+352, P304+340, P305+351+338, P308+313, P310, P312, P321, P333+313, P363, P403+233, P405, P501
NFPA 704 (fire diamond)
2
1
0
Flash point 227 °C (441 °F; 500 K)
Autoignition
temperature
 600 °C (1,112 °F; 873 K)
Related compounds
Related phenols
 Bisphenol S
Except where otherwise noted, data are given for materials in their standard state (at 25 °C [77 °F], 100 kPa).
checkY  (what is checkY☒N ?)
Infobox references

Bisphenol A (BPA) is an organic synthetic compound with the chemical formula (CH3)2C(C6H4OH)2 belonging to the group of diphenylmethane derivatives and bisphenols, with two hydroxyphenyl groups. It is a colorless solid that is soluble in organic solvents, but poorly soluble in water (0.344 wt % at 83 °C).[2]

BPA is a precursor to important plastics, primarily certain polycarbonates and epoxy resins, as well as some polysulfones and certain niche materials. BPA-based plastic is clear, tough, and flame resistant. Major areas of application include electronics (e.g., housing for electrical gear), construction materials (e.g. windows), automotive (headlight covers), data storage (e.g. CDs). In 2015, an estimated 4 million tonnes of BPA-derived chemical were produced, making it one of the highest volume organic chemicals produced worldwide.[3]

BPA is a xenoestrogen, exhibiting estrogen-mimicking, hormone-like properties.[4] Although the effect is very weak, the pervasiveness of BPA-containing materials raises concerns. Since 2008, several governments have investigated its safety, which prompted some retailers to withdraw polycarbonate products. Since then, BPA-free plastics have been manufactured using alternative bisphenols such as bisphenol S and bisphenol F, but there is controversy around whether these are actually safer.[5]

History[]

Bisphenol A was reported in 1891 by Russian chemist Aleksandr Dianin.[6]

In 1934 workers at I.G. Farbenindustrie reported the coupling of BPA and epichlorohydrin. Over the following decade, coatings and resins derived from similar materials were described by workers at the companies of DeTrey Freres in Switzerland and DeVoe and Raynolds in the US. This early work underpinned the development of epoxy resins, which in turn motivated production of BPA.[7] The utilization of BPA further expanded with discoveries at Bayer and General Electric on polycarbonate plastics. These plastics first appeared in 1958, being produced by Mobay and General Electric, and Bayer.[8]

In terms of the endocrine disruption controversy, the British biochemist Edward Charles Dodds tested BPA as an artificial estrogen in the early 1930s. He found BPA to be 1 / 37,000 as effective as estradiol.[9][10][11] Dodds eventually developed a structurally similar compound, diethylstilbestrol (DES), which was used as a synthetic estrogen drug in women and animals until it was banned due to its risk of causing cancer; the ban on use of DES in humans came in 1971 and in animals, in 1979.[9] BPA was never used as a drug.[9]

Uses[]

Bisphenol A is primarily used to make plastics, such as this polycarbonate water bottle.

In 2003, U.S. consumption was 856,000 tons, of which 75% was used to make polycarbonate plastic and 21% for epoxy resins.[12]

Human contact[]

Epoxy resins derived from BPA are used to line water pipes and as coatings on the inside of many food and beverage cans. BPA is also used in making thermal paper such as that used in sales receipts.[13] In the U.S., less than 5% of the BPA produced is used in food contact applications,[14] but remains in the canned food industry and printing applications, such as sales receipts.[15][16]

Polycarbonates[]

Further information: Polycarbonate

Bisphenol A is a precursor to polycarbonate plastics. Its reaction with phosgene is conducted under biphasic conditions; the hydrochloric acid is scavenged with aqueous base:[17]

Polycarbonatsynthese.svg

An estimated 3.6 million tonnes (8 billion pounds) of BPA are consumed for this purpose yearly. These polymers do not contain BPA, but esters derived from it.[17]

Epoxy and vinyl ester resins[]

BPA is a precursor in production of major classes of resins, specifically the vinyl ester resins. This application usually begins with alkylation of BPA with epichlorohydrin.[18]

Typical "vinyl ester" derived from bisphenol A diglycidyl ether, sometimes called BADGE. Free-radical polymerization gives a highly crosslinked polymer.[7]

Specialized derivatives[]

BPA is a versatile building block from which many derivatives have been prepared. Nitration gives dinitrobisphenol A. Bromination gives tetrabromobisphenol A (TBBPA), which exhibits fire retardant properties.[19]

Several drug candidates have been developed from bisphenol A, including Ralaniten, Ralaniten acetate, and EPI-001.[citation needed]

Health effects[]

Main article: BPA controversy
The largest exposure humans have had to BPA is by mouth from sources such as food packaging, the epoxy lining of metal food and beverage cans, and plastic bottles.[20][21]

BPA's ability to mimic the effects of natural estrogen derive from the similarity of phenol groups on both BPA and estradiol, which enable this synthetic molecule to trigger estrogenic pathways in the body.[22] Typically phenol-containing molecules similar to BPA are known to exert weak estrogenic activities, thus it is also considered an endocrine disruptor (ED) and estrogenic chemical.[23] Xenoestrogens is another category the chemical BPA fits under because of its capability to interrupt the network that regulates the signals which control the reproductive development in humans and animals.[24]

BPA has been found to bind to both of the nuclear estrogen receptors (ERs), ERα and ERβ. It is 1000- to 2000-fold less potent than estradiol. BPA can both mimic the action of estrogen and antagonize estrogen, indicating that it is a selective estrogen receptor modulator (SERM) or partial agonist of the ER. At high concentrations, BPA also binds to and acts as an antagonist of the androgen receptor (AR). In addition to receptor binding, the compound has been found to affect Leydig cell steroidogenesis, including affecting 17α-hydroxylase/17,20 lyase and aromatase expression and interfering with LH receptor-ligand binding.[citation needed]

In 1997, adverse effects of low-dose BPA exposure in laboratory animals were first proposed.[25] Some studies have found that BPA increases anxiety in rats.[26][27] Modern studies began finding possible connections to health issues caused by exposure to BPA during pregnancy and during development. As of 2014, research and debates are ongoing as to whether BPA should be banned or not.

A 2007 study investigated the interaction between bisphenol A's and estrogen-related receptor γ (ERR-γ). This orphan receptor (endogenous ligand unknown) behaves as a constitutive activator of transcription. BPA seems to bind strongly to ERR-γ (dissociation constant = 5.5 nM), but only weakly to the ER.[28] BPA binding to ERR-γ preserves its basal constitutive activity.[28] It can also protect it from deactivation from the SERM 4-hydroxytamoxifen (afimoxifene).[28] This may be the mechanism by which BPA acts as a xenoestrogen.[28] Different expression of ERR-γ in different parts of the body may account for variations in bisphenol A effects. BPA has also been found to act as an agonist of the GPER (GPR30).[29]

According to the European Food Safety Authority "BPA poses no health risk to consumers of any age group (including unborn children, infants and adolescents) at current exposure levels".[30] But in 2017 the European Chemicals Agency concluded that BPA should be listed as a substance of very high concern due to its properties as an endocrine disruptor.[31]

In 2012, the United States' Food and Drug Administration (FDA) banned the use of BPA in baby bottles.[32]

The U.S. Environmental Protection Agency (EPA) holds the position that BPA is not a health concern. In 2011, Andrew Wadge, the chief scientist of the United Kingdom's Food Standards Agency, commented on a 2011 U.S. study on dietary exposure of adult humans to BPA,[33] saying, "This corroborates other independent studies and adds to the evidence that BPA is rapidly absorbed, detoxified, and eliminated from humans – therefore is not a health concern."[34]

The Endocrine Society said in 2015 that the results of ongoing laboratory research gave grounds for concern about the potential hazards of endocrine-disrupting chemicals – including BPA – in the environment, and that on the basis of the precautionary principle these substances should continue to be assessed and tightly regulated.[35] A 2016 review of the literature said that the potential harms caused by BPA were a topic of scientific debate and that further investigation was a priority because of the association between BPA exposure and adverse human health effects including reproductive and developmental effects and metabolic disease.[36]

In July 2019, the European Union upheld a decision by the European Chemicals Agency to list BPA as a substance of very high concern, the first step in the procedure for restrictions of its use. The decision is based on concerns about BPA's toxicity for human reproduction.[37]

Environmental effects[]

In 2010, the U.S. Environmental Protection Agency reported that over one million pounds of BPA are released into the environment annually.[38] BPA can be released into the environment by both pre-consumer and post-consumer leaching. Common routes of introduction from the pre-consumer perspective into the environment are directly from plastics, coat and staining manufacturers, foundries who use BPA in casting sand, or transport of BPA and BPA-containing products.[39][40] Post-consumer BPA waste comes from effluent discharge from municipal wastewater treatment plants, irrigation pipes used in agriculture, ocean-borne plastic trash, indirect leaching from plastic, paper, and metal waste in landfills, and paper or material recycling companies.[39][40][41] Despite a rapid soil and water half-life of 4.5 days, and an air half-life of less than one day, BPA's ubiquity makes it an important pollutant. BPA has a low rate of evaporation from water and soil, which presents issues, despite its biodegradability and low concern for bio-accumulation. BPA has low volatility in the atmosphere and a low vapor pressure between 5.00 and 5.32 Pascals. Aqueous solutions of BPA absorbs at wavelengths greater than 250 nm.[42]

BPA interferes with nitrogen fixation at the roots of leguminous plants associated with the bacterial symbiont Sinorhizobium meliloti.[43] BPA affects soybean seedlings with respect to root growth, nitrate production, ammonium production, and the activities of nitrate reductase and nitrite reductase. At low doses of BPA, the growth of roots were improved, the amount of nitrate in roots increased, the amount of ammonium in roots decreased, and the nitrate and nitrite reductase activities remained unchanged. However, at considerably higher concentrations of BPA, the opposite effects were seen for all but an increase in nitrate concentration and a decrease in nitrite and nitrate reductase activities.[44] Nitrogen is both a plant nutritional substance, but also the basis of growth and development in plants.

A 2005 study conducted in the United States had found that 91–98% of BPA may be removed from water during treatment at municipal water treatment plants.[45] Nevertheless, a 2009 meta-analysis of BPA in the surface water system showed BPA present in surface water and sediment in the U.S. and Europe.[46] According to Environment Canada in 2011, "BPA can currently be found in municipal wastewater. … initial assessment shows that at low levels, bisphenol A can harm fish and organisms over time."[47]

BPA affects growth, reproduction, and development in aquatic organisms. Among freshwater organisms, fish appear to be the most sensitive species. Evidence of endocrine-related effects in fish, aquatic invertebrates, amphibians, and reptiles has been reported at environmentally relevant exposure levels lower than those required for acute toxicity. There is a widespread variation in reported values for endocrine-related effects, but many fall in the range of 1μg/L to 1 mg/L.[14]

A 2009 review of the biological impacts of plasticizers on wildlife published by the Royal Society with a focus on aquatic and terrestrial annelids, molluscs, crustaceans, insects, fish and amphibians concluded that BPA affects reproduction in all studied animal groups, impairs development in crustaceans and amphibians and induces genetic aberrations.[48]

Toxicity[]

BPA exhibits very low acute toxicity as indicated by its LD50 of 4 g/kg (mouse). In those mice, weight gain was reduced and exhibited estrogen-like properties. Reports indicate that it is a minor skin irritator as well, although less so than phenol.[2]

The FDA's National Center for Toxicology Research conducted its own research studies. In rodent studies, the amount of BPA passed from the mother to the unborn offspring after oral administration was found to be insignificant. The BPA administration dose for the rodents was 100-1000 times higher than human exposure.[49]

Production[]

World production capacity of BPA was 1 million tons in the 1980s,[2] and more than 2.2 million tons in 2009.[50] It is a high production volume chemical. This compound is synthesized by the condensation of acetone (hence the suffix A in the name)[51] with two equivalents of phenol. The reaction is catalyzed by a strong acid, such as hydrochloric acid (HCl) or a sulfonated polystyrene resin. Industrially, a large excess of phenol is used to ensure full condensation; the product mixture of the cumene process (acetone and phenol) may also be used as starting material:[2]

Synthesis of bisphenol A from phenol and acetone

Numerous ketones undergo analogous condensation reactions.[2]

BPA substitutes[]

Concerns about the health effects of BPA have led many manufacturers to replace BPA with substitutes such as bisphenol S (BPS) and diphenyl sulfone. However, health concerns have been raised about these substitutes as well.[52]

Reactions[]

Nitration yields Dinitrobisphenol A. Bromination yields Tetrabromobisphenol A that has been used in flame retardant epoxy materials but is becoming more generally avoided due to restrictions on using halogenated species in general.

Identification in plastics[]

Main article: Resin identification code
Some type 7 plastics may contain bisphenol A.

In the U.S., plastic packaging is split into seven broad classes for identification purposes by a resin identification code. As of 2014 there are no BPA labeling requirements for plastics in the U.S. "In general, plastics that are marked with Resin Identification Codes 1, 2, 4, 5, and 6 are very unlikely to contain BPA. Some, but not all, plastics that are marked with the Resin Identification Code 7 may be made with BPA."[53] 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.[2][54] Type 3 (PVC) may contain bisphenol A as an antioxidant (not a plasticizer) in "flexible PVC" softened by plasticizers,[2] but not rigid PVC such as pipe, window frames, and siding.

Legislation[]

The U.S. Food and Drug Administration (FDA) has ended its authorization of the use of BPA in baby bottles and infant formula packaging, based on market abandonment, not safety.[55] The European Union and Canada have banned BPA use in baby bottles.

Currently in the United States, there are 12 states, in addition to Washington, D.C., that have restrictions in place against BPA. These states include California, Connecticut, Delaware, Maine, Maryland, Massachusetts, Minnesota, Nevada, New York, Vermont, Washington, and Wisconsin. Each state's restrictions differ slightly, but all restrict the use of BPA in some way.[56]

The following are some examples of legislation in place in these states:

  • California - Assembly Bill 1319 (2011) prohibits the manufacture and sale of bottles and cups with BPA at detectable levels above 0.1 parts per billion if these items are meant to be used by children 3 years old or younger. It requires manufacturers to use alternative non-toxic materials that are not categorized as carcinogenic or reproductive toxicants.[57]
  • Delaware - Senate Bill 70 (2011) prohibits the sale of bottles and cups containing BPA if the items are designed to be used by children 4 years old or younger.[58]
  • Illinois - Senate Bill 2950 (2011) prohibits the sale of empty containers like bottles or cups designed to store food and beverage for children that contain BPA.[59]
  • Maine - House Bill 330 (2011) helped process BPA to be recognized as a priority chemical under Title 38, §1691, Maine's law on toxic chemicals in products designed to be used by children. BPA was formally designated as a substance that must pass through certain reporting requirements for manufactureres of products that contain BPA, as well as authorize the prohibition of sale of products that are reported to contain BPA.[60]

See also[]

  • Tetramethyl bisphenol F
  • Bisphenol S
  • Para tertiary butyl phenol

References[]

  1. ^ "Chemical Fact Sheet – Cas #80057 CASRN 80-05-7". speclab.com. 1 April 2012. Archived from the original on 12 February 2012. Retrieved 14 June 2012.
  2. ^ Jump up to: a b c d e f g Fiege H, Voges HW, Hamamoto T, Umemura S, Iwata T, Miki H, Fujita Y, Buysch HJ, Garbe D, Paulus W (2000). "Phenol Derivatives". Ullmann's Encyclopedia of Industrial Chemistry. Weinheim: Wiley-VCH. doi:10.1002/14356007.a19_313.
  3. ^ "Archived copy". Archived from the original on 19 March 2017. Retrieved 24 January 2017.CS1 maint: archived copy as title (link)
  4. ^ Egan, Michael (2013). "Sarah A. Vogel. Is It Safe? BPA and the Struggle to Define the Safety of Chemicals". Isis. Berkeley: University of California Press. 105 (1): 254. doi:10.1086/676809. ISSN 0021-1753.
  5. ^ Thoene M, Dzika E, Gonkowski S, Wojtkiewicz J (February 2020). "Bisphenol S in Food Causes Hormonal and Obesogenic Effects Comparable to or Worse than Bisphenol A: A Literature Review". Nutrients. 12 (2): 532. doi:10.3390/nu12020532. PMC 7071457. PMID 32092919.
  6. ^ See:
  7. ^ Jump up to: a b Pham HQ, Marks MJ (2012). Ullmann's Encyclopedia of Industrial Chemistry. Weinheim: Wiley-VCH. doi:10.1002/14356007.a09_547.pub2.
  8. ^ Volker Serini (2000). Ullmann's Encyclopedia of Industrial Chemistry. Weinheim: Wiley-VCH. doi:10.1002/14356007.a21_207.
  9. ^ Jump up to: a b c Vogel SA (2009). "The Politics of Plastics: The Making and Unmaking of Bisphenol A "Safety". Am J Public Health. 99 (S3): S559–S566. doi:10.2105/AJPH.2008.159228. PMC 2774166. PMID 19890158.
  10. ^ Dodds EC, Lawson W (1936). "Synthetic Œstrogenic Agents without the Phenanthrene Nucleus". Nature. 137 (3476): 996. Bibcode:1936Natur.137..996D. doi:10.1038/137996a0. S2CID 4171635.
  11. ^ Dodds EC, Lawson W (1938). "Molecular Structure in Relation to Oestrogenic Activity. Compounds without a Phenanthrene Nucleus". Proceedings of the Royal Society of London B: Biological Sciences. 125 (839): 222–232. Bibcode:1938RSPSB.125..222D. doi:10.1098/rspb.1938.0023.
  12. ^ Chapin RE, Adams J, Boekelheide K, Gray LE Jr, Hayward SW, Lees PS, McIntyre BS, Portier KM, Schnorr TM, Selevan SG, Vandenbergh JG, Woskie SR (June 2008). "NTP-CERHR Expert Panel Report on the Reproductive and Developmental Toxicity of Bisphenol A". Birth Defects Research Part B: Developmental and Reproductive Toxicology. 83 (3): 157–395. doi:10.1002/bdrb.20147. PMID 18613034.
  13. ^ Pivnenko K, Pedersen GA, Eriksson E, Astrup TF (October 2015). "Bisphenol A and its structural analogues in household waste paper" (PDF). Waste Management. 44: 39–47. doi:10.1016/j.wasman.2015.07.017. PMID 26194879.
  14. ^ Jump up to: a b "Bisphenol A Action Plan" (PDF). U.S. Environmental Protection Agency. 29 March 2010. Retrieved 12 April 2010.
  15. ^ "Concern over canned foods". Consumer Reports. December 2009. Retrieved 2 February 2012.
  16. ^ "Soaring BPA Levels Found in People Who Eat Canned Foods". Fox News. 23 November 2011.
  17. ^ Jump up to: a b Serini, Volker (2000). "Polycarbonates". Ullmann's Encyclopedia of Industrial Chemistry. Weinheim: Wiley-VCH. doi:10.1002/14356007.a21_207.
  18. ^ Kroschwitz, Jacqueline I. (1998). Kirk-Othmer Encyclopedia of Chemical Technology. 5 (5 ed.). p. 8. ISBN 978-0-471-52695-7.
  19. ^ Dagani MJ, Barda HJ, Benya TJ, Sanders DC. "Bromine Compounds". Ullmann's Encyclopedia of Industrial Chemistry. Weinheim: Wiley-VCH. doi:10.1002/14356007.a04_405.
  20. ^ Heather Caliendo for PlasticsToday – Packaging Digest, 20 June 2012 History of BPA Archived 12 June 2013 at the Wayback Machine
  21. ^ Walsh B (1 April 2010). "The Perils of Plastic – Environmental Toxins". Time. Archived from the original on 4 April 2010. Retrieved 2 July 2010.
  22. ^ Kwon JH, Katz LE, Liljestrand HM (2007). "Modeling Binding Equilibrium in a Competitive Estrogen Receptor Binding Assay". Chemosphere. 69 (7): 1025–1031. Bibcode:2007Chmsp..69.1025K. doi:10.1016/j.chemosphere.2007.04.047. PMID 17559906.
  23. ^ Ahmed, R. A. M. (2014). "Effect of Prenatal Exposure to Bisphenol A on the Vagina of Albino Rats: immunohistochemical and ultrastructural study". Folia Morphologica. 73 (4): 399–408. doi:10.5603/FM.2014.0061. PMID 25448896.
  24. ^ Ramos, J.G. (2003). "Bisphenol A induces both transient and permanent histofunctional alterations of the hypothalamic-pituitary-gonadal axis in prenatally exposed male rats". Endocrinology. 144 (7): 3206–3215. doi:10.1210/en.2002-0198. PMID 12810577.
  25. ^ Erickson BE (2 June 2008). "Bisphenol A under scrutiny". Chemical and Engineering News. 86 (22): 36–39. doi:10.1021/cen-v086n022.p036.
  26. ^ Hicks, Kimani D.; Sullivan, Alana W.; Cao, Jinyan; Sluzas, Emily; Rebuli, Meghan; Patisaul, Heather B. (August 2016). "Interaction of Bisphenol A (BPA) and soy phytoestrogens on sexually dimorphic sociosexual behaviors in male and female rats". Hormones and Behavior. 84: 121–126. doi:10.1016/j.yhbeh.2016.06.010. ISSN 0018-506X. PMC 4996731. PMID 27373758.
  27. ^ Shipman, Matt (7 September 2012). "Study Finds How BPA Affects Gene Expression, Anxiety; Soy Mitigates Effects". NC State News. Retrieved 4 February 2021.
  28. ^ Jump up to: a b c d Matsushima A, Kakuta Y, Teramoto T, Koshiba T, Liu X, Okada H, Tokunaga T, Kawabata S, Kimura M, Shimohigashi Y (October 2007). "Structural evidence for endocrine disruptor bisphenol A binding to human nuclear receptor ERR gamma". J. Biochem. 142 (4): 517–24. doi:10.1093/jb/mvm158. PMID 17761695.
  29. ^ Prossnitz ER, Barton M (May 2014). "Estrogen biology: new insights into GPER function and clinical opportunities". Molecular and Cellular Endocrinology. 389 (1–2): 71–83. doi:10.1016/j.mce.2014.02.002. PMC 4040308. PMID 24530924.
  30. ^ "Bisphenol A". European Food Safety Authority. 2015. Lay summary.
  31. ^ "MSC unanimously agrees that Bisphenol A is an endocrine disruptor - All news - ECHA". echa.europa.eu. Retrieved 19 June 2017.
  32. ^ Mirmira P, Evans-Molina C (July 2014). "Bisphenol A, obesity, and type 2 diabetes mellitus: genuine concern or unnecessary preoccupation?". Translational Research (Review). 164 (1): 13–21. doi:10.1016/j.trsl.2014.03.003. hdl:1805/8373. PMC 4058392. PMID 24686036.
  33. ^ Teeguarden JG, Calafat AM, Ye X, Doerge DR, Churchwell MI, Gunawan R, Graham MK (September 2011). "Twenty-four-hour human urine and serum profiles of bisphenol A during high-dietary exposure". Toxicological Sciences. 123 (1): 48–57. doi:10.1093/toxsci/kfr160. PMID 21705716.
  34. ^ Wage, Andrew (27 July 2011). "Small pond, same big issues". FSA. Archived from the original on 10 September 2011. Retrieved 3 August 2011.
  35. ^ Gore AC, Chappell VA, Fenton SE, Flaws JA, Nadal A, Prins GS, Toppari J, Zoeller RT (2015). "Executive Summary to EDC-2: The Endocrine Society's Second Scientific Statement on Endocrine-Disrupting Chemicals". Endocr. Rev. 36 (6): 593–602. doi:10.1210/er.2015-1093. PMC 4702495. PMID 26414233.
  36. ^ Giulivo M, Lopez de Alda M, Capri E, Barceló D (2016). "Human exposure to endocrine disrupting compounds: Their role in reproductive systems, metabolic syndrome and breast cancer. A review". Environ. Res. (Review). 151: 251–264. Bibcode:2016ER....151..251G. doi:10.1016/j.envres.2016.07.011. PMID 27504873.
  37. ^ Fisher, Douglas (12 July 2019). "EU court confirms BPA as substance of 'very high concern'". Environmental Health News. Retrieved 21 July 2020.
  38. ^ Erler C, Novak J (October 2010). "Bisphenol a exposure: human risk and health policy". Journal of Pediatric Nursing. 25 (5): 400–7. doi:10.1016/j.pedn.2009.05.006. PMID 20816563.
  39. ^ Jump up to: a b Corrales J, Kristofco LA, Steele WB, Yates BS, Breed CS, Williams ES, Brooks BW (29 July 2015). "Global Assessment of Bisphenol A in the Environment: Review and Analysis of Its Occurrence and Bioaccumulation". Dose-Response. 13 (3): 1559325815598308. doi:10.1177/1559325815598308. PMC 4674187. PMID 26674671.
  40. ^ Jump up to: a b EPA (26 July 2011). "Testing of Bisphenol A, Advance notice of proposed rulemaking (ANPRM)". Federal Register /Vol. 76, No. 143 / Proposed Rules. Federal Register. Retrieved 8 May 2017.
  41. ^ "Plastic Breaks Down in Ocean, After All -- And Fast". news.nationalgeographic.com. 20 August 2009. Retrieved 27 November 2017.
  42. ^ Abo R (September 2016). "Optimized photodegradation of Bisphenol A in water using ZnO, TiO2, and SnO2 and photocatalysts under ultraviolet radiation as a decontamination procedure". Drinking Water Engineering and Science. 9 (2): 27–35. doi:10.5194/dwes-9-27-2016.
  43. ^ Fox JE, Gulledge J, Engelhaupt E, Burow ME, McLachlan JA (June 2007). "Pesticides reduce symbiotic efficiency of nitrogen-fixing rhizobia and host plants". Proceedings of the National Academy of Sciences of the United States of America. 104 (24): 10282–7. Bibcode:2007PNAS..10410282F. doi:10.1073/pnas.0611710104. PMC 1885820. PMID 17548832.
  44. ^ Sun H, Wang L, Zhou Q (January 2013). "Effects of bisphenol A on growth and nitrogen nutrition of roots of soybean seedlings". Environmental Toxicology and Chemistry. 32 (1): 174–80. doi:10.1002/etc.2042. PMID 23109293.
  45. ^ Drewes JE, Hemming J, Ladenburger SJ, Schauer J, Sonzogni W (2005). "An assessment of endocrine disrupting activity changes during wastewater treatment through the use of bioassays and chemical measurements". Water Environment Research. 77 (1): 12–23. doi:10.2175/106143005x41573. PMID 15765931.
  46. ^ Klecka GM, Staples CA, Clark KE, Van der Hoeven N, Thomas DE, Hentges SG (August 2009). "Exposure analysis of bisphenol A in surface water systems in North America and Europe". Environmental Science & Technology. 43 (16): 6145–50. Bibcode:2009EnST...43.6145K. doi:10.1021/es900598e. PMID 19746705.
  47. ^ "Bisphenol A Fact Sheet". Government of Canada. Archived from the original on 23 April 2011. Retrieved 1 February 2012.
  48. ^ Oehlmann J, Schulte-Oehlmann U, Kloas W, Jagnytsch O, Lutz I, Kusk KO, Wollenberger L, Santos EM, Paull GC, Van Look KJ, Tyler CR (2009). "A critical analysis of the biological impacts of plasticizers on wildlife". Philosophical Transactions of the Royal Society B: Biological Sciences. 364 (1526): 2047–62. doi:10.1098/rstb.2008.0242. PMC 2873012. PMID 19528055.
  49. ^ Churchwell MI (May 2014). "Comparison of life-stage-dependent internal dosimetry for bisphenol A, ethinyl estradiol, a reference estrogen, and endogenous estradiol to test an estrogenic mode of action in Sprague Dawley rats". Toxicological Sciences. 139 (1): 4–20. doi:10.1093/toxsci/kfu021. PMC 4038784. PMID 24496641.
  50. ^ "Experts demand European action on plastics chemical". Reuters. 22 June 2010.
  51. ^ Uglea CV, Negulescu II (1991). Synthesis and Characterization of Oligomers. CRC Press. p. 103. ISBN 978-0-8493-4954-6.
  52. ^ "BPA substitutes may be just as bad as the popular consumer plastic". 13 September 2018.
  53. ^ "Bisphenol A (BPA) Information for Parents". Hhs.gov. 15 January 2010. Retrieved 23 October 2011.
  54. ^ Biello D (19 February 2008). "Plastic (not) fantastic: Food containers leach a potentially harmful chemical". Scientific American. 2. Retrieved 9 April 2008.
  55. ^ "Bisphenol A (BPA): Use in Food Contact Application". FDA.gov. Food and Drug Administration. November 2014. Retrieved 21 June 2018.
  56. ^ "NCSL Policy Update: State Restrictions on Bisphenol A (BPA) in Consumer Products". NCSL.org.
  57. ^ "NCSL Policy Update: State Restrictions on Bisphenol A (BPA) in Consumer Products". NCSL. Retrieved 20 November 2019.
  58. ^ "Senate Bill 70". Delaware General Assembly. Retrieved 19 November 2019.
  59. ^ "NCSL Policy Update: State Restrictions on Bisphenol A (BPA) in Consumer Products". ncsl.org. Retrieved 20 November 2019.
  60. ^ "NCSL Policy Update: State Restrictions on Bisphenol A (BPA) in Consumer Products". NCSL.org. Retrieved 20 November 2019.

Further reading[]

Retrieved from ""