About 2.8m tons of Bisphenol A are produced every year worldwide. BPA has been used in babies' drinks bottles and teats in addition to food packaging. The largest producers are Sunoco, Dow, Bayer and GE.
Please see two recent articles on risks related to Bisphenol A:

Medical Research News, 2. Dec 2005

Bisphenol A (BPA) has been linked to damage in developing brain tissue

The chemical bisphenol A (BPA), widely used in products such as food cans, milk container linings, water pipes and even dental sealants, has now been found to disrupt important effects of estrogen in the developing brain. A University of Cincinnati (UC) research team, headed by Scott Belcher, PhD, reports in two articles in the December 2005 edition of the journal Endocrinology that BPA shows negative effects in brain tissue "at surprisingly low doses."

The research was supported by funding from the National Institutes of Health and the Pediatric Brain Tumor Foundation.

"These new studies are also the first to show that estrogen's rapid signaling mechanisms are active in the developing and maturing brain in regions not thought to be involved with sexual differences or reproductive functions," Dr. Belcher said.

BPA has often been implicated in disease or developmental problems.

Long known to act as an artificial estrogen, the primary hormone involved in female sexual development, BPA has already been shown to increase breast cancer cell growth, and in the January 2005 edition of the journal Cancer Research, another UC research team reported that it increased the growth of some prostate cancer cells as well. Warnings about other possible long-term health risks associated with fetal exposures to BPA have also been discussed in recent scientific literature.

"BPA molecules are linked into polymers used to create polycarbonate plastics and epoxy resins that are widely used in many products," said Dr. Belcher, an associate professor in the pharmacology and cell biophysics department at UC College of Medicine. "While plastics are typically thought of as being stable, scientists have known for many years that the chemical linkage between BPA molecules was unstable, and that BPA leaches into food or beverages in contact with the plastics."

Dr. Belcher and his colleagues worked with rats at a period in their development equivalent to the third trimester of human fetal development through to the first few years of childhood.

Although best known for its function as a female sex hormone, Dr. Belcher explained, estrogen also has very important roles in the developing brain of both males and females.

In the absence of estrogen, Dr. Belcher said, BPA alone was found to mimic the actions of estrogen in developing neurons, and very low doses of BPA completely inhibited the activity of estrogen. Because estrogen normally increases the growth and regulates viability of developing neurons, he said, these results support the idea that BPA may harm developing brain cells.

In fact, Dr. Belcher said, while high doses cause little effect, analysis of cellular and molecular markers of estrogen signaling revealed that near-maximal effects of BPA on rat brain neurons not only occurred "at surprisingly low" doses of 0.23 parts per trillion, they also happened in a matter of minutes.

"From other studies it's clear that these low concentrations are in line with human fetal exposures, and at levels one might even see in the water supply," said Dr. Belcher.

This "low-dose" effect of BPA is troubling, Dr. Belcher points out, since its maximal effects occur at the level typical of human exposure. This means that the harmful effects of BPA could easily be missed using standard approaches for determining the risks of chemical exposure.

"These are important considerations in view of the widespread presence of low concentrations of BPA in the environment," said Dr. Belcher

In earlier research, which showed estrogens could control the survival of maturing neurons in the brain region involved in movement and coordination, Dr. Belcher and his co-workers found the effects of estrogen were the same in both males and females.

"Estrogen's actions on these neurons appear to be a double-edged sword," he said. "During certain periods of development estrogen can kill specific subsets of neurons, but at a later developmental stage it actually appears to increase their viability." Disruption of either of these actions of estrogen could be considered potentially harmful, he added.

"We have now shown that environmental estrogens like BPA appear to alter, in a very complicated fashion, the normal way estrogen communicates with immature nerve cells," Dr. Belcher explained. "The developmental effects that we studied are known to be important for brain development and also for normal function of the adult brain," he said.

What remains unclear, he said, is how inappropriate hormone signaling, or blocking the normal signaling at a critical time during development, will influence later life.

In the face of more than 100 studies published in peer-reviewed journals showing the detrimental effects of BPA, Dr. Belcher said, the chemical industry and federal regulatory agencies have resisted banning BPA from plastics used as food and beverage containers, despite the fact that plastics free of BPA and other toxic chemicals are available. (

Environmental Health Perspectives Volume 114, Number 1, January 2006
Exploring the Roots of Diabetes

Bisphenol A May Promote Insulin Resistance

Poor diet and lack of exercise are known contributors to the epidemic of type 2 diabetes spreading around the world. Now researchers have implicated another possible culprit in the rise of the disease EHP 114:106-112. A team of Spanish and Mexican researchers reports discovering that the endocrine-disrupting chemical bisphenol A (BPA) causes insulin resistance in mice similar to that seen just before the onset of type 2 diabetes.
Type 2 diabetes occurs when insulin receptors throughout the body fail; this is known as insulin resistance. Complications of diabetes include heart disease, kidney failure, blindness, and nerve damage. The World Health Organization estimates that at least 154 million people around the world have type 2 diabetes, and predicts that number will more than double within 25 years.
Endocrine disruptors mimic the natural sex hormone 17β-estradiol (E2), which is involved in the development of sexual traits. Scientists have known for years that BPA and other endocrine disruptors can diminish sperm production, accelerate the onset of puberty, and damage sexual organs. But they had not studied a link between the chemicals and glucose metabolism, even though increases in E2 are known to cause insulin resistance.
The researchers chose to study BPA because its use is so widespread. Since the 1950s, it has been used in plastics for water bottles and jugs, baby bottles, toys, and the linings of food and beverage cans. People ingest BPA that leaches from containers into foods and drinks. Studies in the United States showed that BPA appeared in the blood and urine of 95% of people tested.
The researchers tested BPA's effect on glucose regulation by measuring glucose and insulin levels in adult male mice treated with BPA injections, then comparing them with levels in mice treated with E2 and a control group treated with corn oil. BPA caused oversecretion of insulin in mice at a dose of 10 micrograms per kilogram body weight per day (µg/kg/day) via a rapid mechanism, taking only 15 to 30 minutes. Treatment over a course of four days with 100 µg/kg/day induced the insulin resistance that precedes type 2 diabetes. E2 had the same effects at the same doses. Glucose metabolism remained stable in the control rats.
These results are novel because the mechanism reported is the lesser known of the two major pathways used by estrogens and other steroids. It involves signaling rapidly initiated from the plasma membrane rather than the nuclear transcription pathway depicted in most textbooks.
The BPA dose high enough to cause insulin resistance in mice was in the same range as the 50 µg/kg/day reference dose established by the U.S. Environmental Protection Agency, which is based on a lowest-observed-adverse-effect level of 50 milligrams per kilogram per day. The researchers see the newly discovered link between BPA and insulin resistance as one more reason the agency should at least consider lowering the lowest-observed-adverse-effect level. They further suspect that because other endocrine disruptors mimic E2, they too may hinder glucose metabolism.
Cynthia Washam