STATS ARTICLES 2008

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Should You Be Worried About Toxic Baby Bottles?
Trevor Butterworth, February 9, 2008
European scientific assessments and new studies challenge latest scare claims about risk to children, but they are ignored by the media.

Many environmental activists in the U.S. today look to Europe as a model for how chemicals should be regulated. The European Union has enshrined the precautionary principle into its regulatory process, which means that chemicals can be banned when the evidence for a risk is less strong than a similar ban in the U.S. would require. Some media organizations have editorialized in favor of precautionary thinking, because, intuitively, caution seems like a good thing.

But what happens when European risk assessments say the evidence doesn’t merit being precautious - and non-industry sponsored Japanese and American risk assessments also say the same thing? Is there a balanced discussion of the science? Does the media accurately reflect why there is such a dramatic disagreement? In general, no.

This is amply illustrated by headlines on the latest scare over the chemical bisphenol a (BPA), a component of polycarbonate bottles, driven by a new study Baby’s Toxic Bottle: “Toxic Baby Bottles?” “Report Shows Dangerous Chemical Can Leach From Baby Bottles” and “Parents Concerned Over Potentially Toxic Baby Bottles” - are just three out of dozens echoing the same message.

The study, by a coalition of activist groups under the umbrella “The Work Group for Safe Markets”, in fact, says nothing that isn’t already well-known, either by virtue of an essentially similar “study” published last year by environmental activists in California, or through more rigorous studies. But it raises several red flags, which were missed in the press coverage.

First of all, this study wasn’t peer-reviewed. It has not, in other words, been vetted for accuracy by independent scientists prior to publication in a scientific journal. Second, it required extreme methods to produce a tiny amount of BPA.. Finding no BPA migration from plastic bottles filled with liquid and left standing at room temperature for 24 hours, the test was repeated by raising the temperature to 80 degrees centigrade (176 degrees Fahrenheit) for 24 hours. From this second test, BPA levels of five to seven parts per billion were found.

The European Union sets a specific migration limit (SML) rate of 600 parts per billion per day for children when it comes to BPA migrating from plastic contact to food. As the European Food Safety Agency recently raised the Tolerable Daily Intake (TDI) of BPA by a factor of five, this SML is now effectively 3000 parts per billion.

In other words, environmental activists are claiming BPA is more toxic than once thought at the very same time as Europe’s regulatory body for food has decided that BPA is less toxic than previously thought.

There is also a more robust European analysis of migration rates of BPA from plastic bottles under normal and extreme circumstances, which was conducted by Norwegian and Swiss researchers for Norway’s Food Safety Authority (a pdf file in English is available at the bottom of the page).

The maximum amounts of BPA these researchers managed to extract from bottles under normal washing conditions was between 1 and 7 micrograms per liter (μg/l) of fluid. The European Union’s Tolerable Daily Intake of BPA for infants is 250 micrograms per liter of fluid. This led the researchers to conclude:

“the amount of BPA contained in the polycarbonate is so small that BPA migration in the proper sense is below 1 μg/l; also liquids with a strong extraction power do not extract much BPA.

BPA is formed and transferred into the beverage when alkali aqueous solutions are “baked” onto the polycarbonate during the drying process, as it occurs when the washing liquid is poured out, but rinsing with water fails. However, the BPA still amounted to less than 10 μg/l when referred to a 100 ml filling

With this understanding of the mechanisms of BPA formation and transfer into beverages it seems possible to confirm that even under extreme conditions and scenarios the amount of BPA released from polycarbonate baby bottles is clearly below the TDI for babies. In particular it can be ruled out that the observed increase of BPA release with aging of the bottle may extend to levels which could be of health concern.”

There has been no media coverage of the Norwegian study.

Have the risks of BPA been widely exaggerated?
BPA has been extensively studied, but it has produced a dramatic disagreement between regulatory bodies around the world and a small group of scientists, centered around Frederick Vom Saal and Wade Welshons at the University of Missouri. Both were involved in creating and proofing the Work Group for Safe Markets study on baby bottles.

Because this disagreement involves massive amounts of data and fundamentally different understandings of toxicology, STATS is conducting an in-depth survey of the evidence, what independent toxicologists think of the competing interpretations of the data, and how the media has covered this controversy. This has yet to be completed, but in light of the media coverage of "Baby's Toxic Bottle," a rough overview of the controversy is still possible.

Determining who is right – or has the most persuasive evidence – in this dispute, however, is of vital importance to public health as BPA is ubiquitous in plastic, and news reports have linked BPA to all manner of health problems from prostate and breast cancer, early onset of puberty, obesity, hyperactivity, lowered sperm counts, miscarriage, diabetes, and an altered immune system. This new study by the Work Group for Safe Markets calls for a moratorium on the use of BPA in food and beverage containers.

Lying behind this is a hypothesis, largely formulated by Vom Saal, that trace amounts of BPA can have the kind of estrogenic impact that one might, intuitively, say could only occur at much higher doses.

Paradigm Shift or Weak Hypothesis?
Ten years ago on PBS Frontline, Vom Saal described his theory as “a  paradigm inversion.”

“The paradigm is the way people are doing things, and then periodically information comes along that says it's upside down, it's backwards, and if you ask the question a different way you get a totally different outcome. And whenever this happens, there is a convulsion in the field that is being turned upside down and there's a very documented series of responses because this has happened over and over through science. It's not the first time that the fundamental tenets of a field of science have been shown to be wrong, and the first thing is absolute denial. The second is a feeling that it may be true, but it's only true in very limited circumstances. The third is, it's true but the economic consequences are so great that we can't do anything about it.”

Ten years on, this paradigm inversion has not happened in toxicology. In fact, in the past couple of years there have two major independent risk assessments in America and Europe which have specifically rejected the evidence Vom Saal et al have marshaled in support of their theory that BPA poses a risk to infants.

The one in Europe, conducted by the European Food Safety Agency and published in 2006, was specifically focused on infant risk and endocrine and reproductive system-related effects. The researchers said that while low-dose effects are theoretically possible, they rejected the relevance to human risk assessments of studies looking at low-effects of BPA in rodents. A risk assessment by the Center for the Evaluation of Risks to Human Reproduction (CERHR) published in the U.S. in the summer of 2007 came to the same conclusion.

But the reasons for  rejecting Vom Saal’s scientific evidence are important, but rarely, if ever, discussed in the media. At best it is reported as one group of scientists says this, and another says that. Understanding how both camps are so diametrically opposed requires beginning with what happends to BPA when it is absorbed through food or drink.

Metabolic pathways
Humans are exposed to BPA through oral ingestion. The chemical is rapidly broken down first in the gastrointestinal tract (GI) and then in the liver by enzymes which add a sugar molecule to BPA, transforming it into a water soluble BPA-glucuronide. Being water soluble, BPA-glucuronide is easily excreted in urine. This happens very quickly. The half life of BPA-glucuronide is six hours. There is a minor metabolic pathway in which some BPA is converted to a sulfate, but this is also water soluble and quickly excreted as a metabolite.

In adult human volunteer studies, no free or parent BPA is found in blood. There is 100 percent conversion to a metabolite.

Crucially, given that BPA is routinely described in the media and by environmental activists as being a weak estrogen and thus a possible endocrine disruptor, BPA-glucuronide is, as the European report notes, “devoid of endocrine activity.” In other words, once BPA is broken down, it is not estrogenic in the body.

But different things happen to rodents when BPA is orally ingested. The process of converting BPA into BPA-glucuronide largely begins in the liver but then it goes back into the gut, where it is broken down into BPA and glucuronic acid. The BPA is reabsorbed back into the bloodstream. This process, known as enterohepatic recirculation, means that BPA is slow to be excreted from rats and it is available as free BPA for much longer.

This, the European researchers note, “has important implications for the relevance of observations on the effects of BPA in sensitive strains of rodents, including low-dose effects, for human health risk assessment.

In studies on mice, low dose exposure to BPA has been associated with the creation of different metabolites through oxidation, which may have more estrogenic or toxic potential. As a species, mice are significantly more sensitivity to estrogens than humans, and thus may be predisposed to react to BPA in different ways to humans.

To add another complicating factor, many studies showing low-dose effects from BPA were a result of intravenous injection of BPA directly into rodents. This can also lead to the creation of different metabolites, which in turn may have toxic effects on the rodents that simply do not occur through oral exposure.

The European researchers also noted other limitations in the studies on rodents:

“The effects of BPA reported in some studies at low doses in sensitive animal systems were small changes in organ weight or changes in tissue architecture, increased or decreased receptor expression, changes in hormone concentrations in plasma or tissues, small changes in the time required to attain puberty landmarks, and behavioural effects. The Panel noted that the changes observed were often not sustained through adulthood. The biological consequences of many of the changes in the affected animals are unknown and some, such as small increases in prostate weight, are not considered as precursors of pathological change. While some of the changes may be indicative of biomarkers of effect in very sensitive species and strains, in the light of present knowledge, they cannot be readily interpreted as adverse effects.

The Panel also noted that in some studies reporting low-dose effects, only a single dose level was investigated, or there was absence of a dose-response relationship where several dose levels had been used. Many studies also used only small numbers of animals per dose group. There are also a number of other potential confounding factors in these types of study that may contribute to the lack of consistency in the database...”

The panel concluded that “the low-dose effects in rodents have not been demonstrated in a robust and reproducible way such as they could be used as pivotal studies for risk assessment.” And based on “an extensive database of repeated-dose toxicity, reproductive and developmental toxicity of BPA in rodents and on the comparison of toxokinetics in primates, including humans, and rodents,” the panel then raised the Tolerable Daily Intake of BPA from 0.01 mg per kg to 0.05 mg per kg. This included a “conservative” uncertainty factor of 100.

The European Food Safety Authority report on BPA was almost entirely ignored by the American media.

Further problems with low-dose exposures
Vom Saal has claimed that there are over 700 studies showing low dose effects on rodents, but there are significant limitations to this claim in terms of weight of evidence: to put it simply, any study finding an endpoint suggesting a low-dose effect is included in this number, while any study and/or endpoint that showed no effect was excluded. In the literature on BPA, the number of studies and endpoints which find no effect is vastly higher than those which do. Studies which find no change are just as important than studies that find change; if the former outnumber the latter, the causes of this inconsistency needs to be addressed.

More importantly, many studies which have reported low-dose effects have not been conducted using the internationally-recognized protocols within toxicology for testing structure and reproductive function in parents and offspring. Instead of accounting for these weaknesses, Vom Saal and environmental activists have tried to portray the recent U.S. risk assessment as compromised by virtue that the panel members were not “experts” in BPA and that the toxicology report was compiled by a contractor that had done work for the chemical industry. The European risk assessment is rarely if ever mentioned.

Given that the CERHR’s reasons for rejecting the evidence cited by Vom Saal were similar to the European Food Safety Authority, an earlier risk assessment in Japan, and two industry-sponsored risk assessments conducted by Harvard and the Gradient Corporation, the charge of a lack of expertise in BPA has less the quality of a scientific criticism and more the ring of an ad hominem. Either way, the claim that a paradigm inversion is happening or is needed has remained a minority viewpoint, at least with respect to BPA.

To put it another way, non-industry affiliated scientists have systematically evaluated and rejected Vom Saal et al’s evidence on scientific grounds; there appears to be no such systematic evaluation and rejection on the part of Vom Saal et al.

Meanwhile new, robust studies are continuing to challenge the low-dose risks of BPA. A new study by EPA scientists published online in December 2007 in the pre-eminent toxicological journal Toxicological Sciences found that gestational and lactational exposure to ethinyl estradiol, a sex hormone used in the contraceptive pill did produce low dose effects in rats, such as decreased sperm counts, while similar low-dose exposures to BPA had no effects whatsoever.

This study has also not been reported by the media.

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