TCS Daily


Frisco's Folly Trolley

By John Luik - July 13, 2006 12:00 AM

The San Francisco city council apparently knows something that health safety regulators around the world don't. If the city council there is to be believed, American parents need to worry about the plastic baby bottles they give their children and dental sealants used on kids' teeth.

Specifically, they need to fear a common ingredient found in baby bottles and hundreds of other everyday products called Bisphenol-A, or BPA for short. So, to protect them, the San Francisco council recently -- without much examination of the scientific evidence -- outlawed as of Dec.1 the manufacture, distribution and sale of any toys or child care products intended for use by children under the age of three if those products have been made with, or contain, any level of BPA.

Why this sudden concern? After all, BPA has been around and used for making plastic and epoxy resins for the last half century. And while humans exposures to BPA occur mainly through food contact in water bottles, baby bottles and through food containers -- with virtually all metal cans having e BPA in the epoxy resin coatings on the interior surfaces -- BPA was thought to be fully excreted and not collect in human tissues.

Until recently, when some activists, including Greenpeace, Environment California and others began making claims that BPA is linked to a variety of health problems, including low sperm counts, early onset of puberty, impaired immune function and perhaps most seriously, prostate cancer.

Amid their clamor, California State Assemblywoman Wilma Chan last year introduced a bill that would have made California the first state to ban the manufacture and sale of any toy or child care product that contained BPA. Similar legislation was introduced in Maryland and Minnesota.

All the bills have failed when confronted by science, thus far. But with the San Francisco ban, that might change, which would be a victory for the ramped up rhetoric of BPA's critics.

SF city supervisor, Fiona Ma who authored the BPA ban bill, argued, "When you look at the science behind these chemicals, there is no question that they ought to be banned from baby products." Greenpeace described BPA as a "toxic pollutant."

So just what does the research evidence as opposed to activist rhetoric about BPA really say? Fortunately, BPA has a large research base about its effects on animals and humans thanks to its being around for over 70 years and in active commercial use for more than 50. The debate over BPA centers on three areas:

  1. The science from animal and human studies about BPA and human health and safety in general.

  2. The relevant regulatory authorities' conclusions about the risks of BPA.

  3. The evidence about low dose exposure to BPA and risks of hormonal disruption and prostate cancer.

First, the weight of the scientific evidence says BPA is not carcinogenic.

Lois Haighton et al, in "An Evaluation of the Possible Carcinogenicity of Bisphenol A to Humans," April, 2002, Regulatory Toxicology and Pharmacology, for instance, concluded in an extensive review of the relevant science on both animal and human populations that "BPA is not likely to be carcinogenic to humans." Equally important, Haighton et al found that the exposure data suggested that at current levels of use humans were exposed to only "trivial" amounts of BPA. Given that -- as with any chemical -- the dose makes the poison, this is particularly important.

A number of other studies have found that the average human intake of BPA is 0.000118 milligrams per kilogram of body weight a day, which is more than 400 times below the Environmental Protection Agency's reference dose for an acceptably safe level of BPA of 0.05 mg/kg per day. The reference dose is itself calculated by dividing the lowest dose at which any effect was found of 50 mg/kg by a safety factor of 1,000. To put that a different way, a person would have to eat more than a ton and a half of food and beverages per day for 70 years to exceed the safe level of BPA set by the U.S. EPA. (See: A. Goodson et al, "Survey of bisphenol A and bisphenol F in canned foods," Food Additives and Contaminants, 19: 796-802, 2002, S. Howe et al, "Potential Exposure to Bisphenol A from Food-Contact use of Polycarbonate Resins," Food Additives and Contaminants, 15: 370-375, 1998, S. Howe et al, "Potential Exposure to Bisphenol A From Food-Contact use of Epoxy Can Coatings," Journal of Coatings Technology, 70: 69-74, 1998.)

Again, a number of studies have examined the question of whether even exceptionally small doses of BPA -- less than the EPA's reference dose -- might cause reproductive and developmental problems. These studies were reviewed in 2000 by the U.S. National Toxicology Program, which issued a final report on low-dose endocrine disruptors, including BPA in August 2001. The report conceded that some studies had shown low-dose effects. But the review concluded that "due to the inability of other credible studies in several different laboratories to observe low dose effects of BPA, and the consistency of these negative studies, the Subpanel is not persuaded that a low dose effect of BPA has been conclusively established as a general or reproducible finding."

Regarding regulatory assessments of BPA, none support the claim that it is hazardous to humans. For instance, a comprehensive risk assessment by the European Union's Joint Research Centre found no convincing evidence that BPA affected development or was carcinogenic. Last year the Japanese Ministry of Environment, after extensive tests of BPA, including on animals, concluded that there was no clear evidence that BPA at low doses had endocrine disrupting consequences. In January of this year Germany's Institute for Risk Assessment concluded that it did not "recognize any health risk for babies that are fed from baby bottles" with BPA. And in November of last year, Dr. George Pauli of FDA wrote Greg Aghazarian of the California State Assembly that "based on all the evidence available at this time, FDA sees no reason to change its long-held position that current uses with food are safe."

Finally, the most controversial aspect of the BPA debate involves the low-dose hypothesis. According to the controversial claim, estrogen-like chemicals such as BPA, even at levels well below those considered hazardous, can disrupt human hormonal processes possibly causing prostate cancer. Critics of BPA have argued that low doses of BPA can change the genes of a fetus' prostate cells in such a way that cancer in adulthood is more likely. Indeed, some anti-BPA activists have claimed that prostate cancer is increasing due to in vitro exposure to BPA and other estrogen-like chemicals. A just published study by Gail Prins and Shuk-Mei Ho at the University of Illinois at Chicago, for instance, claims to show a link between low-doses of BPA and prostate cancer.

Counting against the low-dose hypothesis is a general problem about generalizing from animal studies to humans based on the fact that animal studies appear to show no consistent relation between changes in the size of the prostate and prostate cancer. Compounding this problem is that rodents have low rates of prostate cancer. Most of the animals studies have not found developmental effects from BPA or prostatic pathology. For example, the most comprehensive animal study by Rochelle Tyl, where rats were fed a diet containing BPA, found no evidence of a low dose BPA effect even in adults of the third generation. A 2001 study for the Japanese National Institute of Health Sciences, "Rat two-generation reproductive toxicity study of bisphenol A," in Reproductive Toxicology, had similar results.

In addition, two comprehensive risk evaluations of the low dose effects of BPA, one from the Harvard Center for Risk Analysis in 2004, and the other just published by Rhomberg et al in Critical Reviews in Toxicology, both found no compelling evidence in either human or animal studies of a link between low-doses of BPA and reproductive effects.

More importantly, the claim that BPA is the cause of the increase in prostate cancer is undermined by the fact that prostate cancer rates in the United States, contra the claims of the BPA activists, are not increasing. While there was an uptake of prostate cancer incidence in the early 1990s this was a result of increased PSA screening. Since then, rates have returned to their historic levels. Given that long period for prostate cancer to develop, and given that BPA was first widely used in the 1950s, any effects of BPA on prostate cancer levels should have resulted in significant and sustained incidence levels.

Finally, the recent animal study by Ho fails to establish that the same effects found in animals are plausible or predictive of harm in humans. As noted earlier, there are general problems about the applicability of animal findings about prostate development and pathology to humans. Furthermore, Prins's animals developed precancerous lesions -- not cancer. There is no other experimental evidence of BPA producing prostate cancer. And, as a matter of perspective, Prins's rats received BPA doses ranging from 100-1,000 times higher than the acceptable exposure levels set by the government.

So, despite San Francisco's craziness and the anti-BPA activists' rhetoric, safety regulators here and abroad still have found no reason for parents to place BPA high on their lists of things to worry about.

John Luik is a TCS Daily contributing writer and is writing a book on health policy.

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