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Synthesis

Bisphenol A was first reported by A.P. Dianin in 1891.

It is prepared by the condensation of acetone (hence the suffix A in the name) 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.

Use

Further information: Polycarbonate

Repeating chemical structure unit of polycarbonate made from bisphenol A

Bisphenol A is used primarily to make plastics, and products containing bisphenol A-based plastics have been in commerce for more than 50 years. It is a key monomer in production of epoxy resins and in the most common form of polycarbonate plastic. 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 and dental devices, dental fillings and sealants, eyeglass lenses, CDs and DVDs, and household electronics. BPA is also used in the synthesis of polysulfones and polyether ketones, as an antioxidant in some plasticizers, and as a polymerization inhibitor in PVC. Epoxy resins containing bisphenol A are used as coatings on the inside of nearly all food and beverage cans, but, due to BPA health concerns, in Japan epoxy coating was mostly replaced by PET film. Bisphenol A is also a precursor to the flame retardant, tetrabromobisphenol A, and was formerly used as a fungicide. Bisphenol A is a preferred color developer in thermal paper and in carbonless copy paper.

Global production of bisphenol A in 2003 was estimated to be over 2 million tonnes. In the U.S., it is manufactured by Bayer MaterialScience, Dow Chemical Company, SABIC Innovative Plastics (formerly GE Plastics), 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.

Identification in plastics

Main article: Resin identification code

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.

Type 3 (PVC) can also contain bisphenol A as an antioxidant in plasticizers.

Types 1 (PET), 2 (HDPE), 4 (LDPE), 5 (polypropylene), and 6 (polystyrene) do not use bisphenol A during polymerization or package forming.[citation needed]
Health effects

Bisphenol A is an endocrine disruptor, which can mimic the body’s own hormones and may lead to negative health effects. Early development appears to be the period of greatest sensitivity to its effects. Regulatory bodies have determined safety levels for humans, but those safety levels are currently being questioned or under review as a result of new scientific studies.
In 2009 the The Endocrine Society released a scientific statement expressing concern over current human exposure to BPA.

Previous studies

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. 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. A 2008 report by the U.S. National Toxicology Program (NTP) later 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.”

Obesity

A 2008 review has concluded that obesity may be increased as a function of BPA exposure, which “merits concern among scientists and public health officials”. A 2009 review of available studies has concluded that “perinatal BPA exposure acts to exert persistent effects on body weight and adiposity”. Another 2009 review has concluded that “Eliminating exposures to (BPA) and improving nutrition during development offer the potential for reducing obesity and associated diseases”. Other reviews have come with similar conclusions. A later study on rats has suggested that perinatal exposure to drinking water containing 1 mg/L of BPA increased adipogenesis in females at weaning.

Neurological issues

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. A 2008 report by the U.S. National Toxicology Program (NTP) later agreed with the panel, expressing “some concern for effects on the brain”. In January 2010 the FDA expressed the same level of concern.

A 2007 review has concluded that BPA, like other xenoestrogens, should be considered as a player within the nervous system that can regulate or alter its functions through multiple pathways. A 2007 review has concluded that low doses of BPA during development have persistent effects on brain structure, function and behavior in rats and mice. A 2008 review concluded that low-dose BPA maternal exposure causes long-term consequences at the level of neurobehavioral development in mice. A 2008 review has concluded that neonatal exposure to Bisphenol-A (BPA) can affect sexually dimorphic brain morphology and neuronal phenotypes in adulthood. A 2008 review has concluded that BPA altered long-term potentiation in the hippocampus and even nanomolar dosage could induce significant effects on memory processes. A 2009 review raised concerns about BPA effect on anteroventral periventricular nucleus.

A 2008 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 to the United States Environmental Protection Agency’s (EPA) maximum safe dose of 50 g/kg/day. This research found a connection between BPA and interference with brain cell connections vital to memory, learning and mood.

Highly controversial claims have been made that BPA could be involved in attention-deficit hyperactivity disorder (ADHD)

Disruption of the dopaminergic system

A 2005 review concluded that prenatal and neonatal exposure to BPA in mice can potentiate the central dopaminergic systems, resulting in the supersensitivity to the drugs-of-abuse-induced reward effects and hyperlocomotion.

A 2008 review has concluded that BPA, mimic estrogenic activity and impact various dopaminergic processes to enhance mesolimbic dopamine activity resulting in hyperactivity, attention deficits, and a heightened sensitivity to drugs of abuse.

A 2009 study on rats has concluded that prenatal and neonatal exposure to low-dose BPA causes deficits in development at dorsolateral striatum via altering the function of dopaminergic receptors. Another 2009 study has found associated changes in the dopaminergic system.

Thyroid function

A 2007 review has concluded that bisphenol-A have been shown to bind to thyroid hormone receptor and perhaps have selective effects on its functions.

A 2009 review about environmental chemicals and thyroid function, raised concerns about BPA effects on triiodothyronine and concluded that “available evidence suggests that governing agencies need to regulate the use of thyroid-disrupting chemicals, particularly as such uses relate exposures of pregnant women, neonates and small children to the agents”.

A 2009 review summarized BPA adverse effects on thyroid hormone action.

Cancer research

According to the WHO’s INFOSAN, “animal studies have not provided convincing evidence of risk of cancer from BPA exposure.”

Neither the U.S. Environmental Protection Agency nor the International Agency for Research on Cancer has evaluated bisphenol A for possible carcinogenic activity.

Breast cancer

Further information: Risk factors of breast cancer#Bisphenol A

A 2008 review has concluded that “perinatal exposure to (…) low doses of (..) BPA, alters breast development and increases breast cancer risk”. Another 2008 review concluded that ” animal experiments and epidemiological data strengthen the hypothesis that foetal exposure to xenoestrogens may be an underlying cause of the increased incidence of breast cancer observed over the last 50 years”.

A 2009 in vitro study has concluded that BPA is able to induce neoplastic transformation in human breast epithelial cells. Another 2009 study concluded that maternal oral exposure to low concentrations of BPA during lactation increases mammary carcinogenesis in a rodent model.

Neuroblastoma

In vitro studies have suggested that BPA can promote the growth of neuroblastoma cells. A 2010 in vitro study has concluded that BPA potently promote invasion and metastasis of neuroblastoma cells through overexpression of MMP-2 and MMP-9 as well as downregulation of TIMP2.

Prostate development and cancer

A 1997 study in mice has found that neonatal BPA exposure of 2 g/kg increased adult prostate weight. A 2005 study in mice has found that neonatal BPA exposure at 10 g/kg disrupted the development of the fetal mouse prostate. A 2006 study in rats has shown that neonatal bisphenol A exposure at 10 g/kg levels increases prostate gland susceptibility to adult-onset precancerous lesions and hormonal carcinogenesis. A 2007 in vitro study has found that BPA within the range of concentrations currently measured in human serum is associated with permanently increase in prostate size. A 2009 study has found that newborn rats exposed to a low-dose of BPA (10 g/kg) increased prostate cancer susceptibility when adults.

Reproductive system and sexual behavior research

A series of studies made in 2009 found:

Mouse ovary anomalies from exposition as low as 1 g/kg, concluded that BPA exposure causes long-term adverse reproductive and carcinogenic effects if exposure occurs during prenatal critical periods of differentiation.

Neonatal exposure of as low as 50 g/kg disrupts ovarian development in mice.

Neonatal BPA exposition of as low as 50 g/kg permanently alters the hypothalamic estrogen-dependent mechanisms that govern sexual behavior in the adult female rat.

Prenatal exposure to BPA at levels of (10 g/kg/day) affects behavioral sexual differentiation in male monkeys.

In placental JEG3 cells in vitro BPA may reduce estrogen synthesis.

BPA exposure disrupted the blood-testis barrier when administered to immature, but not to adult, rats.

Exposure to BPA in the workplace could produce sexual dysfunction in male adult humans.

General research

In 2009, at an Endocrine Society meeting new research reported data from animals experimentally treated with BPA. Studies presented at the group’s annual meeting show BPA can affect the hearts of women, can permanently hurt the DNA of mice, and appear to be entering the human body from a variety of unknown sources.

A 2009 in vitro study on cytotrophoblasts cells has found cytoxic effects in exposure of BPA doses from 0.0002 to 0.2 micrograms per millilitre and concluded this finding “suggests that exposure of placental cells to low doses of BPA may cause detrimental effects, leading in vivo to adverse pregnancy outcomes such as preeclampsia, intrauterine growth restriction, prematurity and pregnancy loss”

A 2009 study in rats concluded that BPA, at the reference safe limit for human exposure, was found to impact intestinal permeability and may represent a risk factor in female offspring for developing severe colonic inflammation in adulthood.

A 2010 study on mice has concluded that perinatal exposure to 10 micrograms/mL of BPA in drinking water enhances allergic sensitization and bronchial inflammation and responsiveness in an animal model of asthma.

Studies on humans

Lang study and heart disease

The first large study of health effects on humans associated with bisphenol A exposure was published in September 2008 by Iain Lang and colleagues in the Journal of the American Medical Association. The cross-sectional study of nearly 1,500 people assessed exposure to bisphenol A by looking at levels of the chemical in urine. The authors found that higher bisphenol A levels were significantly associated with heart disease, diabetes, and abnormally high levels of certain liver enzymes. An editorial in the same issue notes that while this preliminary study needs to be confirmed and cannot prove causality, there is precedent for analogous effects in animal studies, which “add[s] biological plausibility to the results reported by Lang et al.”

A later similar study performed by the same group of scientists, published in January 2010, confirmed, despite of lower concentrations of BPA in the second study sample, an associated increased risk for heart disease but not for diabetes or liver enzymes.

Other studies

Studies have associated recurrent miscarriage with BPA serum concentrations, oxidative stress and inflamattion in postmenopausal women with urinary concentrations, externalizing behaviors in two-year ancient children, especially among female children, with mother’s urinary concentrations, and altered hormone levels in men with urinary concentrations.

Historical studies

The first evidence of the estrogenicity of bisphenol A came from experiments on rats conducted in the 1930s, but it was not until 1997 that adverse effects of low-dose exposure on laboratory animals were first reported.

Low dose exposure in animals

Dose (g/kg/day)

Effects (measured in studies of mice or rats,

descriptions (in quotes) are from Environmental Working Group)

Study Year

0.025

“Permanent changes to genital tract”

2005

0.025

“Changes in breast tissue that predispose cells to hormones and carcinogens”

2005

1

long-term adverse reproductive and carcinogenic effects

2009

2

“increased prostate weight 30%”

1997

2

“lower bodyweight, increase of anogenital distance in both genders, signs of early puberty and longer estrus.”

2002

2.4

“Decline in testicular testosterone”

2004

2.5

“Breast cells predisposed to cancer”

2007

10

“Prostate cells more sensitive to hormones and cancer”

2006

10

“Decreased maternal behaviors”

2002

30

“Reversed the normal sex differences in brain structure and behavior”

2003

50

Adverse neurological effects occur in non-human primates

2008

50

Disrupts ovarian development

2009

A study from 2008 concluded that blood levels of bisphenol A in neonatal mice are the same whether it is injected or ingested. The current U.S. human exposure limit set by the EPA is 50 g/kg/day.

Xenoestrogen

There is evidence that bisphenol A functions as a xenoestrogen by binding strongly to estrogen-related receptor (ERR-). This orphan receptor (endogenous ligand unknown) behaves as a constitutive activator of transcription. BPA seems to bind strongly to ERR- (dissociation constant = 5.5 nM), but not to the estrogen receptor (ER). BPA binding to ERR- preserves its basal constitutive activity. It can also protect it from deactivation from the selective estrogen receptor modulator 4-hydroxytamoxifen.

Different expression of ERR- in different parts of the body may account for variations in bisphenol A effects. For instance, ERR- has been found in high concentration in the placenta, explaining reports of high bisphenol A accumulation in this tissue.

Human exposure sources

Bisphenol A has been known to leach from the plastic lining of canned foods and, to a lesser degree,[citation needed] polycarbonate plastics, especially those that are cleaned with harsh detergents or used to contain acidic or high-temperature liquids. A recent Health Canada study found that the majority of canned soft drinks it tested had low, but measurable levels of bisphenol A. This exposure through metal cans is due to the fact that BPA is an ingredient in the internal coating of food and beverage metal cans used to protect the food from direct contact with metal. While most human exposure is through diet, exposure can also occur through air and through skin absorption.

BPA is found in high concentration in thermal paper, which is commonly used to print receipts in automated machines, and carbonless copy paper.

Studies by the CDC found bisphenol A in the urine of 95% of adults sampled in 19881994 and in 93% of children and adults tested in 200304. Infants fed with liquid formula are among the most exposed, and those fed formula from polycarbonate bottles can consume up to 13 micrograms of bisphenol A per kg of body weight per day (g/kg/day; see table below). The most sensitive animal studies show effects at much lower doses, while the EPA considers exposures up to 50 g/kg/day to be safe. In 2009, a study found that drinking from polycarbonate bottles increased urinary bisphenol A levels by two thirds, from 1.2 micrograms/gram creatinine to 2 micrograms/gram creatinine.

Consumer groups recommend that people wishing to lower their exposure to bisphenol A avoid canned food and polycarbonate plastic containers (which shares resin identification code 7 with many other plastics) unless the packaging indicates the plastic is bisphenol A-free. The National Toxicology Panel recommends avoiding microwaving food in plastic containers, putting plastics in the dishwasher, or using harsh detergents, to avoid leaching.

A 2009 small US study funded by the EWG has detected an average of 2.8 ng/mL BPA in the blood of 9 out of the 10 umbilical cords tested.

In the US and Canada, BPA has been found in infant liquid formula in concentrations varying from 0.48 to 11 ng/g. BPA has been rarely found in infant powder formula (only 1 of 14).

Population

Estimated daily bisphenol A intake, g/kg/day.

Table adapted from the National Toxicology Program Expert Panel Report.

Infant (06 months)

formula-fed

111

Infant (06 months)

breast-fed

0.21

Infant (612 months)

1.6513

Child (1.56 years)

0.04314.7

Adult

0.0081.5

Pharmacokinetics

There’s no agreement between scientists of a PBPK BPA model for humans. The effects of BPA on an organism depends on how much free BPA is available and for how long cells are exposed to it. Glucuronidation in the organism reduces the amount of free BPA, but BPA glucuronide can be deconjugated by beta-glucuronidase, an enzyme present in high concentration in placenta and other tissues. Free BPA can also be inactivated by sulfation, a process that can also be reverted by arylsulfatase C.

A 2009 research has found that some drugs, like naproxen, salicylic acid, carbamazepine and mefenamic acid can, in vitro, significantly inhibit BPA glucuronidation.

Environmental risk

BPA can contaminate the environment either directly or through degradation of products containing BPA, such as ocean-borne plastic trash.

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 110 days, its ubiquity makes it an vital pollutant. According to Environment 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.”

A 2009 review of the biological impacts of plasticizers on wildlife published by the Royal Society with a focus on annelids (both aquatic and terrestrial), molluscs, crustaceans, insects, fish and amphibians concluded that BPA have been shown to affect reproduction in all studied animal groups, to impair development in crustaceans and amphibians and to induce genetic aberrations.

Government and industry response

World Health Organization

Arguing uncertainty of possible adverse health effects of low dose BPA exposure, especially on the nervous system and on behaviour, and also the differences of exposure of very young children, the WHO announced in November 2009 that it would organize an expert consultation in 2010 to assess BPA safety.

Australia and New Zealand

The Australia and New Zealand Food Safety Authority (Food Standards Australia New Zealand) does not see any health risk with bisphenol A baby bottles if the manufacturers instructions are followed. Levels of exposure are very low and do not pose a significant health risk. It added that he go by overseas manufacturers to stop using BPA in baby bottles is a voluntary action and not the result of a specific action by regulators.1] It suggests the use of glass baby bottles if parents have any concerns.

Canada

In April 2008, Health Canada assessed that the chemical may pose some risk to infants and proposed classifying the chemical as “‘toxic’ to human health and the environment.”

After the release of that assessment, Canadian Health Minister Tony Clement announced Canada’s intent to ban the import, sale, and advertisement of polycarbonate baby bottles containing bisphenol A due to safety concerns, and investigate ways to reduce BPA contamination of baby formula packaged in metal cans. While the agency concluded that human exposures were less than levels believed to be unsafe, the margin of safety was not high enough for formula-fed infants. Around the same time, Wal-Mart announced that it was immediately stopping 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. Nalgene also announced it will stop using the chemical in its products, and Toys-R-Us said it too will stop selling baby bottles made from it. Subsequent news reports showed many retailers removing polycarbonate drinking products from their shelves.

In 2006, Canadian regulators selected bisphenol A 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.

The federal government has formally declared bisphenol A a hazardous substance as of October 2008 and is now placed on its list of toxic substances. Health officials wrote in Canada Gazette that “It is concluded that bisphenol A be considered as a substance that may be entering the environment in a quantity or concentration or under conditions that constitute or may constitute a danger in Canada to human life or health.” The federal ministries of health and the environment announced they would seek to restrict imports, sales and advertising of polycarbonate baby bottles containing BPA.

In its statement Gc.ca released on 18 October 2008, Health Canada noted that isphenol A exposure to newborns and infants is below levels that cause effects and that the eneral public need not be concerned.

Europe

European Union

The updated 2008 European Union Risk Assessment Report on bisphenol A, published in June 2008 by the European Commission and European Food Safety Authority (EFSA) concluded that bisphenol A-based products, such as polycarbonate plastic and epoxy resins, are safe for consumers and the environment when used as intended. By October 2008, after the Lang Study was published, the EFSA issued a statement concluding that the study provided no grounds to revise the current TDI (Tolerable Daily Intake) level for BPA of 0.05 mg/kg bodyweight.

A 2009 scientific study criticized the European risk assessment processes of endocrine disruptors, including BPA.

On 22 December 2009 the EU Environment ministers released a statement expressing concerns over recent studies showing adverse effects of exposure to endocrine disrupters.

The EFSA is scheduled to release another opinion on BPA by May 2010.

Denmark

In May 2009, the Danish parliament passed a resolution to ban the use of BPA in baby bottles. But, this has yet to be enacted as of December 2009, because the Danish Minister of Public Health seeks further evidence of the hazardous effect of BPA.

France

On 27 July 2009, French senator members of the RDSE proposed legislation to ban BPA of plastics used as food containers.

On 5 February 2010, the French Food Safety Agency (AFSSA) questioned the previous assessments of the health risks of BPA, especially in regard to behavioral effects observed in rat pups following exposure in utero and during the first months of life.

Germany

On 19 September 2008, the German Federal Institute for Risk Assessment (Bundesinstitut fr Risikobewertung, BfR) stated that there was no reason to change the current risk assessment for bisphenol A on the basis of the Lang Study.

In October, 2009, the German environmental organization Bund fr Umwelt und Naturschutz Deutschland requested a ban on BPA for childrens’ products, especially pacifiers, and products that make contact with food. In response, some manufacturers voluntarily removed the problematic pacifiers from the market.

Netherlands

On 6 November 2008, the Dutch Food and Consumer Product Safety Authority (VWA), stated in a newsletter that baby bottles made from polycarbonate plastic do not release measurable concentrations of bisphenol A and therefore are safe to use.

Switzerland

In February 2009 the Swiss Federal Office for Public Health, based on reports of other health agencies, stated that the intake of bisphenol A from food represents no risk to the consumer, including newborns and infants. But, in the same statement it advised for proper use of polycarbonate baby bottles and listed alternatives.

UK

In December 2009 responding to a letter from a group of seven scientists that urged the UK Government to dopt a standpoint consistent with the approach taken by other Governments who have finished the use of BPA in food contact products marketed at children150] the UK Food Standards Agency reaffirmed in January 2009 their view that xposure of UK consumers to BPA from all sources, including food contact materials, was well below levels considered harmful.

United States

September 2008

In September, the National Toxicology Program finalized their report on bisphenol A, finding “some concern”, mid-point of a five-level scale, that infants were at risk from exposure to the chemical.

At that time, the FDA reassured consumers that current limits were safe, but convened an outside panel of experts to review the issue. The Lang study was also released that month, and David Melzer, a co-author of the study, presented the results of the study before the FDA panel.

The editorial accompanying the Lang study’s publication in JAMA criticized the FDA’s assessment of bisphenol A: “A fundamental problem is that the current ADI [acceptable daily intake] for BPA is based on experiments conducted in the early 1980s using outdated methods (only very high doses were tested) and insensitive assays. More recent findings from independent scientists were rejected by the FDA, apparently because those investigators did not follow the outdated testing guidelines for environmental chemicals, whereas studies using the outdated, insensitive assays (predominantly involving studies funded by the chemical industry) are given more weight in arriving at the conclusion that BPA is not harmful at current exposure levels.”

The Union of Concerned Scientists similarly criticized the agency saying, “We’re concerned that the FDA is basing its conclusion on two studies while downplaying the results of hundreds of other studies…. This appears to be a case of cherry-picking data with potentially high cost to human health.”

In contrast, the American Chemistry Council, the manufacturing industry’s lobby group, was skeptical of the latest study.

March 2009

Sunoco, a producer of gasoline and chemicals, is now refusing to sell the chemical to companies for use in food and water containers for children younger than 3, saying it can’t be certain of the compound’s safety. Sunoco plans to require its customers to guarantee that the chemical will not be used in children’s food products.

The six largest US companies which commercialize baby bottles chose to stop using bisphenol A in their products. Suffolk County, New York banned baby beverage containers made with bisphenol A.

On March 13 leaders from the House and Senate proposed legislation to ban bisphenol A.

In the same month, Rochelle Tyl, author of two studies used by FDA to assert BPA safety in August 2008, said those studies didn’t claim that BPA is safe since they weren’t designed to cover all aspects of the chemical’s effects.

May 2009

Among the first US jurisdictions to pass regulations limiting or banning BPA were Minnesota and Chicago. Minnesota’s regulation takes effect in 2010, “manufacturers of … children’s products containing BPA may not sell them in the state after Jan. 1, 2010. The ban extends to all retailers in the state a year later.” The products impacted are known as sippy cups and baby bottles. The City of Chicago adopted a similar ban shortly thereafter. Coverage of Chicago’s ban in the news showed a relentless opposition by the industry. A Chicago Tribune article noted an up-hill battle while passing legislation, “[industry officials] used FDA position on the issue when they tried to block the city measure.” It further notes that,

he FDA continues to be recalcitrant and very slow about taking any action on BPA, said Ald. Manny Flores (1st), who co-sponsored the Chicago measure with Ald. Edward Burke.

Chicago bans the sale after 2010 of any empty food or drink container containing BPA that is intended for use by children less than 3 years ancient.

Burke and Flores pushed the measure through after backing down from a more aggressive version that would have outlawed nearly any product for children that was made with the chemical. Still, the chemical industry fought hard to thwart the scaled-back ban, including hiring former Ald. Terry Gabinski to lobby against it. The American Chemistry Council trade group responded with a written statement that called [the] vote nwarranted..

In May 2009 the Washington Post accused the manufacturers of food and beverage containers and some of their largest customers of trying to devise a public relations and lobbying strategy to block government BPA bans.

June 2009

In June 2009, the FDA announced the choice to reconsider the BPA safety levels.

Connecticut was the first US state to ban bisphenol A from infant formula and baby food containers, as well from any reusable food or beverage container.

July 2009

The California Environmental Protection Agency’s Developmental and Reproductive Toxicant Identification Committee unanimously voted against placing Bisphenol A on the state’s list of chemicals that are believed to cause reproductive harm. The panel, although concerned over the growing scientific research showing BPA’s reproductive harm in animals, found that there was insufficient data of the effects in humans. Critics point out that the same panel failed to add second-hand smoke to the list until 2006, and only one chemical was added to the list in the last three years.

August 2009

On August 3, Massachusetts’ Department of Public Health advised mothers to take certain actions to prevent possible health impact in children. Mothers with children up to two years ancient were advised to limit exposure by avoiding products that might contain BPA, such as plastic drinking bottles and other plastic materials with recycling codes of 7 or 3.

The Milwaukee Journal Sentinel, as part of an ongoing investigative series into BPA and its effects, revealed plans by the Society of the Plastics Industry to do a major public relations blitz to promote BPA, including plans to attack and discredit those who report or comment negatively on the monomer and its effects.

September 2009

On September 29, the U.S. Environmental Protection Agency announced that it is evaluating BPA, and another five chemicals, for action plot development.

October 2009

On October 28, the NIH announced $30,000,000 in stimulus grants to study the health effects of BPA. This money is expected to result in many peer-reviewed publications.

November 2009

The Consumer Reports magazine published an analysis of BPA content in some canned foods and beverages, where in specific cases the content of a single can of food could exceed the current FDA Cumulative Exposure Daily Intake.

January 2010

On January 15 the FDA expressed “some concern”, the middle level in the scale of concerns, about the potential effects of BPA on the brain, behavior, and prostate gland in fetuses, infants, and young children and announced it was taking reasonable steps to reduce human exposure to BPA in the food supply. But, the FDA is not recommending that families change the use of infant formula or foods, as it sees the benefit of a stable source of excellent nutrition to outweigh the potential risk from BPA exposure.

On the same date the U.S. Department of Health & Human Services released information for parents to reduce children’s BPA exposure.

February 2010

According with the Milwaukee Journal Sentinel, which supports BPA ban, after lobbyists for the chemical industry met with administration officials, the EPA delayed BPA regulation and not included the chemical in action plot released December 30, 2009.

Many US states are considering some sort of BPA ban.

See also

Look up bisphenol a in Wiktionary, the free dictionary.

Food contact materials

Bisphenol A diglycidyl ether (BADGE)

References

^ “Update on Bisphenol A for Use in Food Contact Applications: January 2010″. U.S. Food and Drug Administration. 15 January 2010. http://www.fda.gov/NewsEvents/PublicHealthFocus/ucm197739.htm. Retrieved 15 January 2010. 

^ Dianin (1891). Zhurnal russkogo fiziko-khimicheskogo obshchestva. 23. pp.  492. 

^ Zincke, Theodor (1905). “Ueber die Einwirkung von Brom und von Chlor auf Phenole: Substitutionsprodukte, Pseudobromide und Pseudochloride”. Justus Liebigs Annalen der Chemie 343: 7599. doi:10.1002/jlac.19053430106. 

^ Uglea, Constantin V.; Ioan I. Negulescu (1991). Synthesis and Characterization of Oligomers. CRC Press. p. 103. 

^ a b c d Fiege, Helmut; Heinz-Werner Voges, Toshikazu Hamamoto, Sumio Umemura, Tadao Iwata, Hisaya Miki, Yasuhiro Fujita, Hans-Josef Buysch, Dorothea Garbe, Wilfried Paulus (2002). Phenol Derivatives. Ullmann’s Encyclopedia of Industrial Chemistry. Weinheim: Wiley-VCH. doi:10.1002/14356007.a19_313. 

^ Replogle, Jill (2009-07-17). “Lawmakers to press for BPA regulation”. California Progress Report. http://www.californiaprogressreport.com/2009/07/committee_succe.html. Retrieved 2009-08-02. 

^ Ubelacker, Sheryl (2008-04-16). “Ridding life of bisphenol A a challenge”. Toronto Star. http://www.thestar.com/article/415296. Retrieved 2009-08-02. 

^ Kroschwitz, Jacqueline I.. Kirk-Othmer encyclopedia of chemical technology. 5 (5 ed.). pp. 8. 

^ “Polycarbonate (PC) Polymer Resin”. Alliance Polymers, Inc. http://www.alliancepoly.com/polycarbonate.asp. Retrieved 2009-08-02. 

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^ a b Erickson, Britt E. (June 2, 2008). “Bisphenol A under scrutiny”. Chemical and Engineering News (American Chemical Society) 86 (22): 3639. http://pubs.acs.org/isubscribe/journals/cen/86/i22/html/8622gov1.html. 

^ Byrne, Jane (22 September 2008). “Consumers dread the packaging – a BPA alternative is needed now”. http://www.foodnavigator.com/Financial-Industry/Consumers-dread-the-packaging-a-BPA-alternative-is-needed-now. Retrieved 5 January 2010. 

^ Pesticideinfo.org: Bisphenol A

^ US patent 6562755

^ Fukazawa, H.; Hoshino, K.; Shiozawa, T.; Matsushita, H.; Terao, Y. (2001). “Identification and quantification of chlorinated bisphenol a in wastewater from wastepaper recycling plants”. Chemosphere 44 (5): 973979. doi:10.1016/S0045-6535(00)00507-5. PMID 11513431.  edit

^ a b Lang IA, Galloway TS, Scarlett A, Henley WE, Depledge M, Wallace RB, Melzer D (2008). “Association of Urinary Bisphenol A Concentration With Medical Disorders and Laboratory Abnormalities in Adults”. JAMA 300 (300): 1303. doi:10.1001/jama.300.11.1303. PMID 18799442. http://jama.ama-assn.org/cgi/content/full/300.11.1303. 

^ Biello D (2008-02-19). “Plastic (not) fantastic: Food containers leach a potentially harmful chemical”. Scientific American 2. http://www.sciam.com/article.cfm?id=plastic-not-fantastic-with-bisphenol-a. Retrieved 2008-04-09. 

^ Jack Snyder (2009-08-24). “Styrene Not a Human Carcinogen, Does Not Contain BPA”. Styrene Information and Research Center (SIRC), Arlington, Va.. http://www.styrene.org/news_styrene_human_health/not_carcinogen_no_bpa_statement.html. Retrieved 2009-12-28. 

^ Gore, Andrea C. (June 8, 2007). Endocrine-Disrupting Chemicals: From Basic Research to Clinical Practice. Contemporary Endocrinology. Humana Press. ISBN 978-1588298300. 

^ Oonnor, JC; Chapin, RE (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 (1112): 20992123. doi:10.1351/pac200375112099. http://www.iupac.org/publications/pac/2003/pdf/7511×2099.pdf. Retrieved 2007-02-28. 

^ Okada H, Tokunaga T, Liu X, Takayanagi S, Matsushima A, Shimohigashi Y (January 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): 328. doi:10.1289/ehp.10587. PMID 18197296. 

^ a b c vom Saal FS, Myers JP (2008). “Bisphenol A and Risk of Metabolic Disorders”. JAMA 300 (300): 1353. doi:10.1001/jama.300.11.1353. PMID 18799451. http://jama.ama-assn.org/cgi/content/full/300.11.1353. 

^ 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.

^ Ginsberg G, Rice DC (2009). “Does Rapid Metabolism Ensure Negligible Risk from Bisphenol A?”. EPH 117 (11): 16391643. doi:10.1289/ehp.0901010. http://www.ehponline.org/members/2009/0901010/0901010.html. 

^ Beronius, A.; Rudn, C.; Hkansson, H.; Hanberg, A. (2009). “Risk to all or none?-A comparative analysis of controversies in the health risk assessment of Bisphenol A”. Reproductive toxicology (Elmsford, N.Y.). doi:10.1016/j.reprotox.2009.11.007. PMID 19931376.  edit

^ Endocrine Society released scientific statement on endocrine-disrupting chemicals

^ 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): 1318. doi:10.1016/j.reprotox.2007.07.005. PMID 17768031. 

^ a b c Since you questioned – Bisphenol A: Questions and Answers about the Draft National Toxicology Program Brief on Bisphenol A, National Institute of Environmental Health Sciences website.

^ Elobeid, M.; Allison, D. (Oct 2008). “Putative environmental-endocrine disruptors and obesity: a review”. Current opinion in endocrinology, diabetes, and obesity 15 (5): 403408. doi:10.1097/MED.0b013e32830ce95c. ISSN 1752-296X. PMID 18769210.  edit

^ Rubin, B.; Soto, A. (May 2009). “Bisphenol A: Perinatal exposure and body weight”. Molecular and cellular endocrinology 304 (1-2): 5562. doi:10.1016/j.mce.2009.02.023. ISSN 0303-7207. PMID 19433248.  edit

^ Heindel, J.; Vom Saal, F. (May 2009). “Role of nutrition and environmental endocrine disrupting chemicals during the perinatal period on the aetiology of obesity”. Molecular and cellular endocrinology 304 (1-2): 9096. doi:10.1016/j.mce.2009.02.025. ISSN 0303-7207. PMID 19433253.  edit

^ Newbold, R.; Padilla-Banks, E.; Jefferson, W. (May 2009). “Environmental estrogens and obesity”. Molecular and cellular endocrinology 304 (1-2): 8489. doi:10.1016/j.mce.2009.02.024. ISSN 0303-7207. PMID 19433252.  edit

^ Grn, F.; Blumberg, B. (May 2009). “Endocrine disrupters as obesogens”. Molecular and cellular endocrinology 304 (1-2): 1929. doi:10.1016/j.mce.2009.02.018. ISSN 0303-7207. PMID 19433244.  edit

^ Somm, E. (2009). “Perinatal Exposure to Bisphenol a Alters Early Adipogenesis in the Rat (PDF)”. Environmental Health Perspectives. doi:10.1289/ehp.11342.  edit

^ Panzica, G.; Viglietti-Panzica, C.; Mura, E.; Quinn Mj, J.; Lavoie, E.; Palanza, P.; Ottinger, M. (2007). “Effects of xenoestrogens on the differentiation of behaviorally-relevant neural circuits”. Frontiers in neuroendocrinology 28 (4): 179200. doi:10.1016/j.yfrne.2007.07.001. PMID 17868795.  edit

^ Richter, C.; Birnbaum, L.; Farabollini, F.; Newbold, R.; Rubin, B.; Talsness, C.; Vandenbergh, J.; Walser-Kuntz, D. et al. (2007). “In vivo effects of bisphenol a in laboratory rodent studies”. Reproductive toxicology (Elmsford, N.Y.) 24 (2): 199224. doi:10.1016/j.reprotox.2007.06.004. PMID 17683900.  edit

^ Palanza, P; Gioiosa; Vom Saal; Parmigiani (2008). “Effects of developmental exposure to bisphenol a on brain and behavior in mice”. Environmental research 108 (2): 1507. doi:10.1016/j.envres.2008.07.023. PMID 18949834.  edit

^ Patisaul, H.; Polston, E. (2008). “Influence of endocrine active compounds on the developing rodent brain”. Brain research reviews 57 (2): 352362. doi:10.1016/j.brainresrev.2007.06.008. PMID 17822772.  edit

^ Ogiue-Ikeda, M.; Tanabe, N.; Mukai, H.; Hojo, Y.; Murakami, G.; Tsurugizawa, T.; Takata, N.; Kimoto, T. et al. (2008). “Rapid modulation of synaptic plasticity by estrogens as well as endocrine disrupters in hippocampal neurons”. Brain research reviews 57 (2): 363375. doi:10.1016/j.brainresrev.2007.06.010. PMID 17822775.  edit

^ 10.1016/j.yfrne.2008.02.002

^ a b Leranth C, Hajszan T, Szigeti-Buck K, Bober J, Maclusky NJ (September 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. 105 (37): 14187. doi:10.1073/pnas.0806139105. PMID 18768812. 

^ Layton, Lindsey (September 4, 2008). “Chemical in Plastic Is Connected to Health Problems in Monkeys”. Washington Post. pp. A02. http://www.washingtonpost.com/wp-dyn/content/article/2008/09/03/AR2008090303397.html?hpid=topnews. Retrieved 2008-09-06. 

^ Brown, J. S.; Jr, (2009). “Effects of Bisphenol-A and Other Endocrine Disruptors Compared with Abnormalities of Schizophrenia: an Endocrine-Disruption Theory of Schizophrenia”. Schizophrenia Bulletin 35: 256. doi:10.1093/schbul/sbm147. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2643957/.  edit

^ Kiguchi, M.; Fujita, S.; Oki, H.; Shimizu, N.; Cools, A. R.; Koshikawa, N. (2008). “Behavioural characterisation of rats exposed neonatally to bisphenol-A: responses to a novel environment and to methylphenidate challenge in a putative model of attention-deficit hyperactivity disorder”. Journal of Neural Transmission 115 (7): 1079. doi:10.1007/s00702-008-0044-5. PMID 18368283.  edit

^ a b Tanida, T.; Warita, K.; Ishihara, K.; Fukui, S.; Mitsuhashi, T.; Sugawara, T.; Tabuchi, Y.; Nanmori, T. et al. (2009). “Fetal and neonatal exposure to three typical environmental chemicals with different mechanisms of action: mixed exposure to phenol, phthalate, and dioxin cancels the effects of sole exposure on mouse midbrain dopaminergic nuclei.”. Toxicology letters 189 (1): 4047. doi:10.1016/j.toxlet.2009.04.005. PMID 19481886.  edit

^ Suzuki; Mizuo, K; Miyagawa, K; Narita, M (2005). “Exposure to bisphenol-A affects the rewarding system in mice”. Nihon shinkei seishin yakurigaku zasshi = Japanese journal of psychopharmacology 25 (3): 1258. PMID 16045194.  edit

^ Jones, D.; Miller, G. (2008). “The effects of environmental neurotoxicants on the dopaminergic system: A possible role in drug addiction”. Biochemical pharmacology 76 (5): 569581. doi:10.1016/j.bcp.2008.05.010. PMID 18555207.  edit

^ Zhou, R.; Zhang, Z.; Zhu, Y.; Chen, L.; Sokabe, M.; Chen, L. (2009). “Deficits in development of synaptic plasticity in rat dorsal striatum following prenatal and neonatal exposure to low-dose bisphenol A”. Neuroscience 159 (1): 161171. doi:10.1016/j.neuroscience.2008.12.028. PMID 19162132.  edit

^ Zoeller, R. (2007). “Environmental chemicals impacting the thyroid: targets and consequences”. Thyroid : official journal of the American Thyroid Association 17 (9): 811817. doi:10.1089/thy.2007.0107. PMID 17956155.  edit

^ Boas, M.; Main, K.; Feldt-Rasmussen, U. (Oct 2009). “Environmental chemicals and thyroid function: an update”. Current opinion in endocrinology, diabetes, and obesity 16 (5): 385391. doi:10.1097/MED.0b013e3283305af7. ISSN 1752-296X. PMID 19625957.  edit

^ Kashiwagi, K.; Furuno; Kitamura; Ohta; Sugihara; Utsumi; Hanada; Taniguchi et al. (2009). “Disruption of Thyroid Hormone Function by Environmental Pollutants”. Journal of Health Science 55: 147. doi:10.1248/jhs.55.147. http://jhs.pharm.or.jp/data/55(2)/55_147.pdf.  edit

^ a b “BISPHENOL A (BPA) – Current state of knowledge and future actions by WHO and FAO”. 27 November 2009. http://www.who.int/entity/foodsafety/publications/fs_management/No_05_Bisphenol_A_Nov09_en.pdf. Retrieved 02 December 2009. 

^ U.S.EPA, IRIS: Bisphenol A

^ Agents Reviewed by the Monographs Volumes 199

^ Brisken, C. (2008). “Endocrine Disruptors and Breast Cancer”. CHIMIA International Journal for Chemistry 62: 406409. doi:10.2533/chimia.2008.406.  edit

^ Soto, A.; Vandenberg, L.; Maffini, M.; Sonnenschein, C. (2008). “Does breast cancer start in the womb?”. Basic & clinical pharmacology & toxicology 102 (2): 125133. doi:10.1111/j.1742-7843.2007.00165.x. PMID 18226065.  edit

^ Fernandez, S. V.; Russo, J. (2009). “Estrogen and Xenoestrogens in Breast Cancer”. Toxicologic Pathology. doi:10.1177/0192623309354108.  edit

^ Jenkins, S.; Raghuraman, N.; Eltoum, I.; Carpenter, M.; Russo, J.; Lamartiniere, C. A. (2009). “Oral Exposure to Bisphenol a Increases Dimethylbenzanthracene-Induced Mammary Cancer in Rats” (Free full text). Environmental Health Perspectives. doi:10.1289/ehp.11751. http://ehp.niehs.nih.gov/members/2009/11751/11751.html.  edit

^ Zhu, H.; Xiao, X.; Zheng, J.; Zheng, S.; Dong, K.; Yu, Y. (2009). “Growth-promoting effect of bisphenol a on neuroblastoma in vitro and in vivo”. Journal of Pediatric Surgery 44 (4): 672680. doi:10.1016/j.jpedsurg.2008.10.067. PMID 19361625.  edit

^ Zheng, J.; Xiao, X.; Liu, J.; Zheng, S.; Yin, Q.; Yu, Y. (2007). “Growth-promoting effect of environmental endocrine disruptors on human neuroblastoma SK-N-SH cells”. Environmental Toxicology and Pharmacology 24: 189193. doi:10.1016/j.etap.2007.05.003.  edit

^ Zhu, H; Zheng, J; Xiao, X; Zheng, S; Dong, K; Liu, J; Wang, Y (2010). “Environmental endocrine disruptors promote invasion and metastasis of SK-N-SH human neuroblastoma cells”. Oncology reports 23 (1): 12939. PMID 19956873.  edit

^ Nagel, SC; Vom Saal; Thayer; Dhar; Boechler; Welshons (1997). “Relative binding affinity-serum modified access (RBA-SMA) assay predicts the relative in vivo bioactivity of the xenoestrogens bisphenol a and octylphenol”. Environmental health perspectives 105 (1): 706. doi:10.2307/3433065. PMID 9074884.  edit

^ Timms, B.; Howdeshell, K.; Barton, L.; Bradley, S.; Richter, C.; Vom Saal, F. (2005). “Estrogenic chemicals in plastic and oral contraceptives disrupt development of the fetal mouse prostate and urethra”. Proceedings of the National Academy of Sciences of the United States of America 102 (19): 70147019. doi:10.1073/pnas.0502544102. PMID 15867144.  edit

^ Ho, S.; Tang, W.; Belmonte De Frausto, J.; Prins, G. (2006). “Developmental exposure to estradiol and bisphenol a increases susceptibility to prostate carcinogenesis and epigenetically regulates phosphodiesterase type 4 variant 4″. Cancer research 66 (11): 56245632. doi:10.1158/0008-5472.CAN-06-0516. PMID 16740699.  edit

^ Richter, C.; Taylor, J.; Ruhlen, R.; Welshons, W.; Vom Saal, F. (2007). “Estradiol and Bisphenol a stimulate androgen receptor and estrogen receptor gene expression in fetal mouse prostate mesenchyme cells”. Environmental health perspectives 115 (6): 902908. doi:10.1289/ehp.9804. PMID 17589598.  edit

^ Prins, G. (2008). “Developmental exposure to bisphenol a increases prostate cancer susceptibility in adult rats: epigenetic mode of action is implicated”. Fertility and Sterility 89: e41-e41. doi:10.1016/j.fertnstert.2007.12.023.  edit

^ a b Newbold, R.; Jefferson, N.; Padilla-Banks, E. (Jun 2009). “Prenatal exposure to bisphenol a at environmentally relevant doses adversely affects the murine female reproductive tract later in life”. Environmental health perspectives 117 (6): 879885. doi:10.1289/ehp.0800045. ISSN 0091-6765. PMID 19590677.  edit

^ a b Adewale, B.; Jefferson, N.; Newbold, R.; Patisaul, B. (Jun 2009). “Neonatal Bisphenol-A Exposure Alters Rat Reproductive Development and Ovarian Morphology Without Impairing Activation of Gonadotropin Releasing Hormone Neurons” (Free full text). Biology of reproduction 81 (4): 690699. doi:10.1095/biolreprod.109.078261. ISSN 0006-3363. PMID 19535786. http://www.biolreprod.org/cgi/pmidlookup?view=long&pmid=19535786.  edit

^ Study Finds Reproductive Health Effects From Low Doses of Bisphenol-A

^ Bosquiazzo, L.; Varayoud, J.; Muoz-De-Toro, M.; Luque, H.; Ramos, G. (Aug 2009). “Effects of Neonatal Exposure to Bisphenol a on Steroid Regulation of Vascular Endothelial Growth Factor Expression and Endothelial Cell Proliferation in the Adult Rat Uterus” (Free full text). Biology of reproduction. doi:10.1095/biolreprod.109.078543. ISSN 0006-3363. PMID 19696011. http://www.biolreprod.org/cgi/pmidlookup?view=long&pmid=19696011.  edit

^ Monje, L.; Varayoud, J.; Muoz-De-Toro, M.; Luque, H.; Ramos, G. (Jul 2009). “Neonatal exposure to bisphenol a alters estrogen-dependent mechanisms governing sexual behavior in the adult female rat”. Reproductive toxicology (Elmsford, N.Y.) 28 (4): 435442. doi:10.1016/j.reprotox.2009.06.012. ISSN 0890-6238. PMID 19577632.  edit

^ Nakagami, A.; Negishi, T.; Kawasaki, K.; Imai, N.; Nishida, Y.; Ihara, T.; Kuroda, Y.; Yoshikawa, Y. et al. (Sep 2009). “Alterations in male infant behaviors towards its mother by prenatal exposure to bisphenol a in cynomolgus monkeys (Macaca fascicularis) during early suckling period”. Psychoneuroendocrinology 34 (8): 11891197. doi:10.1016/j.psyneuen.2009.03.005. ISSN 0306-4530. PMID 19345509.  edit

^ Huang, H.; Leung, K. (Sep 2009). “Bisphenol a downregulates CYP19 transcription in JEG-3 cells”. Toxicology letters 189 (3): 248252. doi:10.1016/j.toxlet.2009.06.853. ISSN 0378-4274. PMID 19539015.  edit

^ Li; Mruk, D.; Lee, W.; Cheng, C. (2009). “Disruption of the blood-testis barrier integrity by bisphenol a in vitro: is this a suitable model for studying blood-testis barrier dynamics?”. The international journal of biochemistry & cell biology 41 (11): 23022314. doi:10.1016/j.biocel.2009.05.016. PMID 19497385.  edit

^ http://dx.doi.org/10.1093/humrep/dep381

^ “More Troubling News About BPA / Science News”. www.sciencenews.org. http://www.sciencenews.org/view/generic/id/44577/title/More_troubling_news_about_BPA. Retrieved 2009-06-11. 

^ “Hormone experts worried about plastics, chemicals – Yahoo! News”. news.yahoo.com. http://news.yahoo.com/s/nm/20090611/hl_nm/us_bisphenol_2. Retrieved 2009-06-11. 

^ Benachour, N.; Aris, A. (2009). “Toxic effects of low doses of Bisphenol-A on human placental cells.”. Toxicology and applied pharmacology 241 (3): 322328. doi:10.1016/j.taap.2009.09.005. PMID 19769995. Lay summary.  edit

^ Braniste, V.; Jouault, A.; Gaultier, E.; Polizzi, A.; Buisson-Brenac, C.; Leveque, M.; Martin, P.; Theodorou, V. et al. (2009). “Impact of oral bisphenol a at reference doses on intestinal barrier function and sex differences after perinatal exposure in rats” (PDF). Proceedings of the National Academy of Sciences of the United States of America. doi:10.1073/pnas.0907697107. PMID 20018722. http://www.pnas.org/content/early/2009/12/10/0907697107.full.pdf.  edit

^ Midoro-Horiuti, T.; Tiwari, R.; Watson, C.; Goldblum, R. (2010). “Maternal bisphenol a exposure promotes the development of experimental asthma in mouse pups”. Environmental health perspectives 118 (2): 273277. doi:10.1289/ehp.0901259. PMID 20123615.  edit

^ Newscientist.com Plastic bottle chemical linked to heart disease

^ Melzer, D.; Rice, N. E.; Lewis, C.; Henley, W. E.; Galloway, T. S.; Zhang, B. (2010). “Association of Urinary Bisphenol a Concentration with Heart Disease: Evidence from NHANES 2003/06″ (pdf). PLoS ONE 5: e8673. doi:10.1371/journal.pone.0008673. http://www.plosone.org/article/fetchObjectAttachment.action?uri=info:doi/10.1371/journal.pone.0008673&representation=PDF. Lay summary.  edit

^ Sugiura-ogasawara, M.; Ozaki, Y.; Sonta, S. -I.; Makino, T.; Suzumori, K. (2005). “Exposure to bisphenol a is associated with recurrent miscarriage”. Human reproduction (Oxford, England) 20 (8): 23252329. doi:10.1093/humrep/deh888. PMID 15947000.  edit

^ Yang, J.; Hong, C.; Oh, Y.; Park, S.; Kim, H.; Leem, H.; Ha, H. (Aug 2009). “Bisphenol a exposure is associated with oxidative stress and inflammation in postmenopausal women”. Environmental research 109 (6): 797801. doi:10.1016/j.envres.2009.04.014. ISSN 0013-9351. PMID 19464675.  edit

^ Braun, J.; Yolton, K.; Dietrich, K.; Hornung, R.; Ye, X.; Calafat, A.; Lanphear, B. (2009). “Prenatal Bisphenol a Exposure and Early Childhood Behavior”. Environmental Health Perspectives. doi:10.1289/ehp.0900979.  edit

^ Meeker, J. D.; Calafat, A. M.; Hauser, R. (2009). “Urinary Bisphenol a Concentrations in Relation to Serum Thyroid and Reproductive Hormone Levels in Men from an Infertility Clinic”. Environmental Science & Technology: 091223134144053. doi:10.1021/es9028292.  edit

^ E. C. Dodds and Wilfrid Lawson, “Synthetic strogenic Agents without the Phenanthrene Nucleus”, Nature, 137 (1936), 996.

^ E. C. Dodds and W. Lawson, Proceedings of the Royal Society of London, Series B, Biological Sciences, 125, #839 (27-IV-1938), pp. 222232.

^ a b c Mittelstaedt, Martin (2007-04-07). “‘Inherently toxic’ chemical faces its future”. Globe & Mail. http://www.theglobeandmail.com/servlet/tale/RTGAM.20070406.wbisphenolA0407/BNStory/National/. Retrieved 2007-04-07. 

^ 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.

^ 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): 134451. doi:10.1095/biolreprod.104.036301. PMID 15689538. http://www.biolreprod.org/cgi/pmidlookup?view=long&pmid=15689538. 

^ Muoz-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): 413847. doi:10.1210/en.2005-0340. PMID 15919749. http://endo.endojournals.org/cgi/pmidlookup?view=long&pmid=15919749. 

^ 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): 706. doi:10.2307/3433065. PMID 9074884. 

^ 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): 11722. doi:10.1016/S0890-6238(02)00006-0. PMID 11955942. http://linkinghub.elsevier.com/retrieve/pii/S0890623802000060. 

^ 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): 592603. doi:10.1210/en.2003-1174. PMID 14605012. http://endo.endojournals.org/cgi/pmidlookup?view=long&pmid=14605012. 

^ 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): 38390. doi:10.1016/j.reprotox.2006.10.002. PMID 17123778. PMC 1987322. http://linkinghub.elsevier.com/retrieve/pii/S0890-6238(06)00263-2. 

^ 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): 562432. doi:10.1158/0008-5472.CAN-06-0516. PMID 16740699. PMC 2276876. http://cancerres.aacrjournals.org/cgi/pmidlookup?view=long&pmid=16740699. 

^ 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: 41522. PMID 12060838. PMC 1241192. http://ehpnet1.niehs.nih.gov/docs/2002/suppl-3/415-422palanza/abstract.html. 

^ 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): 34556. doi:10.1016/S0168-0102(02)00251-1. PMID 12631470. http://linkinghub.elsevier.com/retrieve/pii/S0168010202002511. 

^ Taylor JA, Welshons WV, Vom Saal FS (February 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): 16976. doi:10.1016/j.reprotox.2008.01.001. PMID 18295446. http://linkinghub.elsevier.com/retrieve/pii/S0890-6238(08)00002-6. Retrieved 2008-05-05. 

^ EPA (Environmental Protection Agency). 1988. Oral RfD Assessment: Bisphenol A. Integrated Risk Information System.

^ 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): 51724. doi:10.1093/jb/mvm158. PMID 17761695. 

^ Takeda Y, Liu X, Sumiyoshi M, Matsushima A, Shimohigashi M, Shimohigashi Y (July 2009). “Placenta expressing the greatest quantity of bisphenol A receptor ERR{gamma} among the human reproductive tissues: Predominant expression of type-1 ERRgamma isoform”. J. Biochem. 146 (1): 11322. doi:10.1093/jb/mvp049. PMID 19304792. 

^ “Environmental Working Group”. http://www.ewg.org/reports/bisphenola. Retrieved 2007-03-07. 

^ Health Canada. “Survey of Bisphenol A in Canned Drink Products”. http://www.hc-sc.gc.ca/fn-an/securit/packag-emball/bpa/bpa_survey-enquete-can-eng.php. Retrieved 2009-03-13. 

^ Lang IA Galloway TS, Scarlett A, Henley WE, Depledge M, Wallace, Robert B, Melzer, D (2008). “Association of Urinary Bisphenol A Concentration With Medical Disorders and Laboratory Abnormalities in Adults”. JAMA 300 (300): 1303. doi:10.1001/jama.300.11.1303. PMID 18799442. http://jama.ama-assn.org/cgi/content/full/300.11.1303. 

^ Fukazawa, H.; Hoshino, K.; Shiozawa, T.; Matsushita, H.; Terao, Y. (2001). “Identification and quantification of chlorinated bisphenol a in wastewater from wastepaper recycling plants”. Chemosphere 44 (5): 973979. doi:10.1016/S0045-6535(00)00507-5. PMID 11513431.  edit

^ Raloff, Janet (2009-10-07). “Concerned About BPA: Check Your Receipts”. Society for Science and the Public. http://www.sciencenews.org/view/generic/id/48084/title/Concerned_about_BPA_Check_your_receipts. Retrieved 2009-10-07. 

^ Gehring, Martin; Tennhardt, L., Vogel, D., Weltin, D., Bilitewski, B. (2004) (PDF). Bisphenol A Contamination of Wastepaper, Cellulose and Recycled Paper Products. Waste Management and the Environment II. WIT Transactions on Ecology and the Environment, vol. 78. WIT Press. http://rcswww.urz.tu-dresden.de/~gehring/deutsch/dt/vortr/040929ge.pdf. Retrieved 2009-10-15. Lay summary. 

^ Calafat AM, Kuklenyi…

I am Frbiz Site writer, reports some information about mosquito repellent deet , preventive pest control.

“At the start of last week, we reported on the very strong demand response from the physical market due to the drop in the gold price below $1,180. This demand has continued unabated. The gold price decline comes at a excellent time, especially for the Indian market but also other markets such as Turkey where price elasticity is being helped by a very strong seasonal demand reaction”

Standard Bank, Gold Physical Flow Index, 8/3/10

 

“The pace and severity of financial crises has taken an ominous turn for the worse….

With one crisis seemingly begetting another, and the fuse between crises now getting shorter and shorter, the world economy is on a very treacherous course.”

Stephen Roach, Morgan Stanley, May, 2010

 

“Washington is not helping.

The massive permanent expansion in federal spending and regulatory oversight built into President Obama’s budget is discouraging private hiring by raising fears of higher taxes and regulation. Simply, higher taxes discourage buys of non-essentials and high-line durable goods…

All that spending will require higher taxes, and raising taxes on families earning $250,000 simply won’t be enough finance it…

Much of the $787 Billion stimulus money was squandered on pet projects that made few jobs…

The largest banks received more than $2 trillion in TARP and Federal Reserve help to clean up their balance sheets and recapitalize securities trading, while the 8000 regional banks got small help and remain burdened by toxic real estate loans. Consequently, more than 230 regional banks have failed, and small and medium sized businesses cannot get credit to expand.”

“Morici: Friday’s Jobs Report: Outlook Darkens for Economy, Obama”
Peter Morici, CNBC Guest Blog, 8/4/10

 

 

‘Black Swans’ are Phenomena which are Statistical Outliers – Phenomena ostensibly so improbable  that they are not typically be taken into account when determining probabilities, even though, if and when they do occur, their consequences typically have a very high, and often very negative, impact. [All Swans were thought to be White, until a 1697 Dutch Expedition to Australia found Black ones.]

The BP Oil Disaster is arguably such a Black Swan event, given the hundreds of Deep Water Wells which have been drilled safely (although an advance look at BP’s safety record might well have dramatically increased the forecast likelihood of a Disaster).

In the world of Finance and Investment, Black Swan Events are those surprise events which (defective) Analytical Models deem so unlikely that one may relatively “safely” risk their occurrence, until, of course they occur, with catastrophic results.

One such Congeries of Events is the Counterparty Failures which characterized the AIG, Lehman Brothers, and Bear Stearns debacles. These debacles show that high leverage coupled with a Black Swan event/s often has lethal consequences.

Black Swan phenomena were noted by the Latin Poet Juvenal and John Stuart Mill, but, to his credit, were recently applied to finance and investing, by Nassim Taleb in his 2007 Book The Black Swan.

Our main point here is that what are apparently ‘White Swan’ Phenomena sometimes really are, or will metamorphose into being, threatening Black Swan Phenomena. Indeed, some of these (ostensibly White) Swan Phenomena are threatening to reveal their inherent Blackness now, and that Investors need to be aware of these lest they be blindsided. As well, Investors need to buy “Antidotes” in advance, several of which we identify here.

Thus, in what follows, we list some apparent White Swans that are really Black (and some that are immediately threatening), and suggest Antidotes.

One of the Most Visible White Swans which is really Black is the Recent Eurozone Non-Solution to the Euro-Sovereign-Debt Crisis. Mega-Bank Creditors of the PIIGS were bailed out, but the PIIGS Sovereign Debt problems were by no means solved, just extended. Investors world-wide were, and are, being “invited” by Mainstream Media spin to pretend that the Black Swan Sovereign Debt Threat is now solved, and thus is now transformed into a financial ‘White Swan’.

In fact the “Sovereign Debt Can” was just kicked down the Road a few months and will surely arise again in ever more threatening form as a Gigantic Black Swan.

Now we change our focus from that very public White/Black Swan issue of the PIIGS Bailout to one quite Hidden, but no less Threatening.

Consider the Black Swan (covered in opaque White) of ongoing Covert Fed Monetization (known euphemistically as QE, or Quantitative Easing), which is quite vital because if it were Overt it would immediately make hyperinflationary pressures (which QE does make in the long run in any event).

Jim Willie cogently comments:

“…the USFed and USDept Treasury are using the United Kingdom as a ledger item for their mammoth USTreasury monetization, all barely hidden, with the TIC data used as a tiny fig leaf… At end 2009, as of the December tally, the UK owned $180.3B in USTBonds, yet somehow managed to accumulate in the new year, up to the current $350.0B. THE UK SUPPOSEDLY HAS Nearly DOUBLED THEIR HOLDINGS IN A MERE FIVE MONTHS!!

Bear witness to the shadow USFed debt monetization operation, operating out of the United Kingdom, or at least its accounting…

Bear in mind that we are talking about crippled England here, or the United Kingdom more generally. The UKGovt just announced spending cuts to reach 40% of budget, not the previous 20%. Britain could not cope with an extended episode in the credit crisis, according to the Bank For Intl Settlements. Yet this nation gobbled up $170 billion in USTreasurys from ripe savings in five months?? Hardly… Newly ordained Prime Minister David Cameron ordered the officials to draw up 40% cuts, the largest in history. He has ordered cabinet ministers to draw up a Doomsday budget whose essential service spending cuts could see tens of thousands given pink slips. Yet this nation gobbled up $170 billion in USTreasurys from ripe savings in five months?? Hardly. This is a smoking gun…”

“Smoking Guns of U.S. Treasury Monetization”
Jim Willie, GoldenJackass.com, 7/22/10

 

And then there are the U.S. Treasury Reports themselves showing which Categories of ‘Investors’ bought U.S. Treasury Securities.

Consider again Jim Willie and Eric Sprott and Bill Yucky:

“…Eric Sprott of Sprott Asset Mgmt casts a suspicious eye at the USTreasurys for the so-called Household category in their accounting. It is a blatant ledger item for illicit monetization, a veritable crime scene without the cordoned zone and yellow tape. Sprott directs his accusations like a skilled prosecutor. He reinforces the claim of Ponzi Scheme cited by Bill Yucky of PIMCO. Sprott calls the solution to finance the mammoth USGovt deficits to be the actual problem, namely hidden monetization…

… The remainder was bought by a category called loosely “Other Investors” as a catch-all. This other group bought $90 billion in 2008, but then turned up into hyper-drive its buys to $510.1 billion of freshly minted USTreasury securities so far in the first three quarters of fiscal 2009…

Go to the source. The USDept Treasury Bulletin identifies “Other Investors” as consisting of Individuals, Government Sponsored Enterprises (GSE, as in Fannie Mae & Freddie Mac et al), Brokers & Dealers (who sell as intermediaries), Bank Personal Trusts & Estates, Corporate & Non-Corporate Businesses, Individuals, and Other Investors. It is far-fetched to believe parties in these groups had $700 spare billion to invest in the USTreasury market in fiscal 2009…

This category supposedly bought $15 billion worth of USTreasurys in 2008, then jumped with ink jet help (printing press) in 3Q2009 to a staggering $528.7 billion in buys, a 35-fold increase. The Household is on track to buy $704 billion worth in all fiscal 2009. The bottom line is a shocker! What is the Household Sector? It is a combination of miscellaneous, ledger adjustments, and blatant monetization. Sprott calls it a PHANTOM that does not exist, but serves the purpose to balance the ledger in the US Federal Reserve Flow of Funds report…

BY THE END OCTOBER 2009, THE “HOUSEHOLD” ACCOUNTING CATEGORY OWNED MORE USTREASURYS THAN THE US FEDERAL RESERVE ITSELF. THAT IS Right. MONETIZED USTREASURY BONDS ACCOUNT FOR MORE THAN WHAT THE USFED HOLDS. THE USTBONDS ARE HIDING IN ENGLAND.”

“Smoking Guns of U.S. Treasury Monetization”
Jim Willie, GoldenJackass.com, 7/22/10

 

Zhu Min, deputy governor of the Peoples Bank of China is understandably worried:

“The world does not have so much money to buy more USTreasurys. The United States cannot force foreign governments to increase their holdings of Treasuries… Double the holdings? It is certainly impossible.”

“Smoking Guns of U.S. Treasury Monetization”
Jim Willie, GoldenJackass.com, 7/22/10

 

Unfortunately, the ostensible White Swan of Fed Policy is quite threateningly Black.

“…With foreign sources unwilling or unable to support USGovt debt, the monetization card will be used repeatedly and powerfully inside the desperate US-UK quarters. When the process is more widely recognized and publicized, the USDollar will be denigrated further, and rejected as quickly as any reasonable alternative can be produced by consensus. It is that simple…

No creditor nation whose leaders are in their right mind would continue to support the USDollar as the global reserve currency when its debt securities are the object of such open fraud and high volume monetization…”

“Smoking Guns of U.S. Treasury Monetization”
Jim Willie, GoldenJackass.com, 7/22/10

 

This Covert Monetization, when widely understood, will likely have catastrophe consequences for the U.S. Dollar, and will launch hyperinflation. It could happen anytime.

A third ‘White Swan’ which is really Black is the effect of the Bailout and stimulus Bills on the U.S. Economy. The Obama administration says they have catalyzed a Recovery with their Stimulus Bill. The Realities as presented by Peter Morici above, by Deepcaster, and by many others, say otherwise. ‘Nuff said.

Yet a fourth apparent ‘White Swan’ is the somewhat rosy picture Official U.S. Statistics give us of the U.S. Economy.

Looking at these somewhat rosy recent Official Reports leads Observers to believe that there is virtually no Inflation, that GDP growth is slow but solid, and therefore, that a Recovery is underway.

The very real Positive Investor Sentiment generated by this somewhat positive picture has, along with Cartel Intervention, helped impel the markets into rally mode beginning Monday this week.

The only problem is that if the Official Numbers are Bogus, the Market Rally is built on sand and can be expected to collapse as easily as a sand castle, and sooner rather than later. (See Deepcaster’s latest Alert in the ‘Alerts Cache’ at Deepcaster’s website.)

In fact, the Official Numbers are Bogus and the Real Numbers paint a very different picture.

Our regular Readers are quite familiar with the work of Shadowstats.com, and several have questioned that we continue to provide updated ones in our articles. (Shadowstats calculates statistics the way they were calculated in the 1980’s and 1990’s, before data manipulation started in earnest) So here they are:

Official Numbers vs.      Real Numbers (per Shadowstats.com)

Annual U.S. Consumer Price Inflation reported July 16, 2010
1.05%                  /                     8.37% (annualized June 2010 Rate)

U.S. Unemployment reported July 2, 2010
9.5%                /               21.6%

U.S. GDP Annual Growth/Decline reported July 30th, 2010
3.17%                    /                   -1.25%

U.S. M3 reported July 22, 2010 (Month of June, Y.O.Y.)
No Official Report      /       – 5.90%

 

Clearly the White Swan of an Apparent Economic Recovery is a Delusion. The Reality is a Black Swan of Negative Economic prospects, which will inevitably have negative consequences for the equities Markets.

So what are Antidotes to these “White Swan into Black” Realities and Threats?

Our immediate answer is the Precious Monetary Metals, Gold and Silver, plus the Category of High Yield Investments whose Yields exceed Real Inflation.

Gold is a hedge against the Current Realities of both the economic contraction/deflation pressures we see today, as well as the hyperinflationary pressures (which Jim Willie’s and other’s Revelations about Covert Monetization reveal) which are on the horizon.

Until recent months, our positive Recommendation regarding Gold and Silver acquisition, would have had to be severely qualified (as to timing) by the Reality of ongoing Cartel* Intervention to suppress Gold and Silver Prices.

In recent months, but, thanks to GATA and others, certain Revelations (as e.g. that not all Precious Metals repositories have all the actual metal they lead people to believe they have, including the Spectacular Allegation that the LBMA has sold some 45 ounces of Gold for every ounce they really hold), have led to a weakening of Cartel* ability to cap prices. (See Deepcaster’s Alert for the week April 16, 2010: “Cartel Failing? Precious Metal Buy Reco! Forecasts: Gold, Silver, Equities, Crude Oil, U.S. Dollar & U.S. T-Notes & Bonds” in the ‘Alerts Cache’ at Deepcaster’s website)

*We encourage those who doubt the scope and power of Overt and Covert Interventions by a Fed-led Cartel of Key Central Bankers and Favored Financial Institutions to read Deepcaster’s December, 2009, Special Alert containing a summary overview of Intervention entitled “Forecasts and December, 2009 Special Alert: Profiting From The Cartel’s Dark Interventions – III” and Deepcaster’s July, 2010 Letter entitled “Profit from a Weakening Cartel; Buy Reco; Forecasts: Gold, Silver, Equities, Crude Oil, U.S. Dollar & U.S. T-Notes & T-Bonds” in the ‘Alerts Cache’ and ‘Latest Letter’ Cache at Deepcaster’s website. Also consider the substantial evidence collected by the Gold AntiTrust Action Committee at www.gata.org, including testimony before the CFTC, for information on precious metals price manipulation. Virtually all of the evidence for Intervention has been gleaned from publicly available records. Deepcaster’s profitable recommendations showed at Deepcaster’s website have been facilitated by attention to these “Interventionals.” Attention to The Interventionals facilitated Deepcaster’s recommending five small positions prior to the Fall, 2008 Market Crash all of which were subsequently liquidated profitably.

Nonetheless, The Cartel still remains Potent (if they were not, Precious Metals prices would doubtless be much higher than they are now).

Thus as practical Antidotes we strongly recommend acquisition of physical Gold and Silver with the Timing and in the Form of those Acquisition described in our latest Alert, as well as employing the Strategy laid out in “Defeating the Cartel… With Profit, Part 2″ (6/19/2009) and “Defeating the Cartel… With Profit, Part 1″ (3/28/2008) in the ‘Articles by Deepcaster’ Cache at Deepcaster’s website. We also recommend the acquisition of Securities whose yields are higher than Real Inflation. (See Deepcaster’s Alert for the week ending July 23, 2010: “NEW HIGH YIELD PORTFOLIO: 15.6%, 26%, 18.5% & 10.6% Recent Yields” for Specific Recommendations, located in the ‘Alerts Cache’ at Deepcaster’s website.)

In sum, to Identify Ostensible White Swans which are, or are likely to become, Black Swans. We recommend employing the following Guidelines.

-      Get the Real Data from sources such as Shadowstats.com and GATA.

-      Assume the Mainstream Media is not providing the Full Tale on Key Issues, and Search for Alternative Sources, and/or Additional Facts

-      Consider whether a particular Mainstream Tale is Reliable, or whether it is likely it is “Manufactured News”

-      Consider The Interventionals as well as the Fundamentals and Technicals.

Following these Guidelines can help ensure that one does not, in making Investing and Trading decisions, rely on a White Swan which later turns out to be a Black, much to Investors and Traders detriment.