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Americans are exposed to far more of a controversial chemical than previously thought — levels that likely surpass the government's current safety standard and which have been shown to cause harm in animals, according to a joint statement issued 2 August 2007 by 38 leading scientists.

While the chemical, bisphenol A, is hardly a household word, it is found in nearly every home — and nearly everybody.

Government tests have found bisphenol A — used in plastic baby bottles, dental sealants and linings of metal cans — in 95% of people studied.

Bisphenol A (BPA) is an intermediate used in the manufacture of epoxy, polycarbonate, and polyester-styrene resins; flame retardants, and rubber chemicals, and fungicides.

While scientists haven't yet conducted definitive studies in people, animal tests have linked bisphenol A — which acts like a hormone — to problems such as obesity, early puberty, hyperactivity, and abnormal sexual behavior and reproductive cycles.

In their joint statement, however, scientists say they took a conservative approach, including only statements backed by many strong studies.
Scientists agreed that even very low doses cause profound effects on laboratory animals, particularly during pregnancy and infancy.

The chemical can permanently rewire genetic programming before birth, potentially predisposing exposed animals to cancer. Bisphenol A also changes brain structure, body size and behavior in animals studied, scientists said.

Researchers issued their statement, published in Reproductive Toxicology, after reviewing about 700 animal studies.

The Environmental Protection Agency says bisphenol A is safe in doses of up to 50 micrograms per kilogram of body weight, per day. But a paper presented 2Aug concludes that the high levels of bisphenol A in human blood and tissue suggest people are actually exposed to 10 times that amount.

One of the scientists, Retha Newbold of the National Institute of Environmental Health Sciences, says researchers need to find ways to measure whether people have been exposed to bisphenol A before or after birth, and if exposure increases their disease risk.

Researchers agree many questions remain, such as: Does bisphenol A, like mercury, build up as it moves through the food chain? Could that explain why there's so much of it in our bodies?

The scientists' findings are at odds with other recent analyses, according to a statement released by the American Chemistry Council, which notes that the European Food Safety Authority has concluded that consumers are not at risk from the chemical.

A report on bisphenol A being prepared by the National Toxicology Program's reproductive health center — which will hold a hearing on the issue Monday — will provide a more balanced and accurate picture, said the council's Steven Hentges.

In the past two years, lawmakers in California, Maryland and Minnesota have introduced bills to ban bisphenol A in children's products. None succeeded. California is still considering a bill to ban similar chemicals from children's products.

Frederick vom Saal, a professor of reproductive biology and neurobiology at the University of Missouri-Columbia who signed the joint statement, says manufacturers should voluntarily get rid of bisphenol A. He asks, "Why would you subject your baby to something that you know is a sex hormone?"  [Reproductive Toxicology; 2Aug07, USA Today,  Liz Szabo]




Bisphenol A is an intermediate used in the manufacture of epoxy, polycarbonate, and polyester-styrene resins; flame retardants, and rubber chemicals, fungicide (HSDB 1990).

Bisphenol A: (CAS No. 80-05-7) Reproduction and Fertility Assessment in CD-1 Mice When Administered in the Feed
Molecular Formula:  C15H16O2

NTP Report # RACB84080
Bisphenol A (BPA), used in the manufacture of epoxy resins and polycarbonates, was tested for its effects on reproduction and fertility in CD-1 mice, following the standard NTP protocol. Data on body weights, clinical signs, and food and water consumptions were collected during the dose-range-finding phase (Task 1), and used to set exposure concentrations for Task 2 at 0.0, 0.25, 0.5, and 1.0% in feed. For females, feed consumption dropped by 19% for the medium dose group and by 23% for the high dose group. These concentrations produced estimated daily intakes of nearly equal to 437, 875, and 1750 mg/kg/day.

For the continuous cohabitation phase (Task 2), the mean number of litters/pair dropped by 5% ( at 0.5% BPA) and by 9% (at 1.0% BPA), while the number of live pups/litter dropped by 20% at the medium dose and by 48% at the high dose. Pup weight adjusted for litter size was unchanged. Postpartum dam weights were reduced only at the high dose, by nearly equal to 8-9%. Interestingly, cumulative days to litter increased by up to 10% for the high dose group.

Mice from the last litter in all three dose groups and controls were reared by their dams until weaning, when they were fed BPA at the same concentration received by their parents.

The reductions in litter size spurred the conduct of a Task 3 crossover mating trial of the F0 mice to determine the affected sex. In the treated male X control female group, there were 25% fewer pups (compared to the control X control group). The number of live pups in the treated female X control male group was reduced by 51%. Pup weight and viability were not affected.

After the Task 3 litters were delivered and evaluated, the F0 mice from the control and 1% BPA groups were killed and necropsied. Male body weight was unchanged, while liver and kidney weights increased by 29% and 16%. Seminal vesicle weight was reduced by 19%, while sperm motility dropped by 39% in the high dose animals.

Female body weights in the 1% BPA group were reduced by 4%, while adjusted liver and kidney weights were reduced by 27% and 10%, respectively.

For the second generation animals, weaning weights were equivalent across groups, but pup mortality before weaning was significantly increased at 1% BPA. Adult body weight at the time of mating was unaffected at any dose
in either sex. F1 mice were mated within treatment levels. There was no effect on mating or fertility indices, or on the number of live pups/litter, the proportion born alive, or the adjusted live pup weight.

After the F2 pups had been evaluated and discarded, the F1 adults were killed and necropsied. Male body weight was not affected, while adjusted liver weights were increased by 7%, 7%, and 29% (low to high doses, respectively). Male kidney weights adjusted for body weight were increased by 16%, 20%, and 20%. Right epididymal weight was reduced by 7%, 16%, and 18%. Seminal vesicles weight was reduced by 11% and 28% at the low and high dose levels, respectively. The 10% reduction at the middle dose level did not reach statistical significance. For females, body weight was not affected, while body-weight-adjusted liver weights were increased by 6%, 13%, and 20%, and kidney weights were increased by 13%, 15%, and 13%. None of the sperm endpoints measured were significantly affected in a dose-dependent manner. Although sperm count was reduced dose-dependently, to a maximum of 18% less than controls, this reduction did not reach statistical significance.

In summary, exposure of the first generation mice to 0.5% or 1.0% resulted in a reduction in number of litters per pair, live pups per litter, and live pup weight. At the high dose, this occurred in the presence of increases in liver and kidney weights. The second generation did not appear more sensitive than the first to the reproductive toxicity of Bisphenol A.

Report Date: May 1985


National Toxicology Program (NTP)