By the time the NTP panel drew its conclusions, BPA was already a $3 billion industry unto itself. BPA was used in an infinite variety of products, from baby bottles and food and beverage cans to dental sealants and football helmets. And, in some cases at least, it had no obvious substitute. That made employing the precautionary principle or resetting the exposure limits almost impossible. “Makers of plastic bottles had other things they could substitute BPA with,” says Aaron L. Brody, a food scientist at the University of Georgia. “But what about cans?” Food manufacturers have long used BPA to create epoxy linings for steel cans. This coating makes the cans extremely durable; it protects the contents of canned goods without affecting taste, and, most importantly, the coatings are integral to reducing the incidence of bacterial contamination and foodborne illness. “BPA-based plastic is among the few materials so far that can withstand the high temperatures and pressures used to kill bacteria,” says Brody. “It’s not a perfect plastic, but without it, you’d probably have a lot more food preservation and safety issues.”

As scientists debated and regulatory agencies struggled, people were left to decide for themselves whether the risk posed by continued exposure to BPA warranted the hassle of trying to purge it from their lives or at least from their baby bottles. “Sometimes, if there’s enough momentum from the public, regulatory change will follow,” says Vogel. “But more often than not, because of the way the system works, it really has to start with individual consumers deciding for themselves that they won’t purchase or use certain items.”

To make such decisions, we need to know two things: whether a given chemical has the potential to harm us and how great that harm might be. It’s crucial to consider both. Say, for example, a new study reports that BPA exposure doubles one’s chances of developing a particular disease. Before hitting the panic button, we must first ask what the chances are of getting the disease in the first place, without BPA exposure. If it’s a rare condition, with a 1% probability, then BPA increases our chances to a mere 2%. If it is more common, with, say, a 20% probability, then BPA doubles our chances to 40%—a significantly greater risk. How important that increase is, and thus what we should do in light of it, depends on the seriousness of the disease.

So, what to do about BPA? Let’s take a look at what we’ve learned so far: We know that chemicals like BPA can have effects at low doses. We know that the fetuses and young offspring of many mammal species, including humans, are particularly susceptible to these low-dose effects. We know that BPA is, in fact, leaching into our systems from food and beverage containers and that it can indeed cross the human placental barrier.

But we also know that BPA is water soluble and can be excreted in our urine. This means that, in most cases, it may not be building up, or bioaccumulating, in our tissues.

What we don’t know—and what we may never know—is how well the effects seen in mice correspond to the risks faced by humans. And because of all the additive and synergistic effects BPA is likely to have with all the countless other chemicals we encounter, it will be difficult to tell, even in the future, how much of any given health condition can be specifically attributed to BPA. The bane of risk assessment is that we can’t really wait for those facts to come in.

Over the past few years, the public has employed a de facto precautionary principle. With the scientific jury still out, consumer and environmental groups took matters into their own hands. They issued dozens of public statements, advising consumers to avoid using food and beverage containers made with BPA. They also lobbied Congress for a full, nationwide ban. The public response to those campaigns led Walmart to say that it would no longer stock its shelves with any bottles or containers made with BPA. Facing hundreds of millions of dollars in lost sales, Nalgene, a leading plastic bottle maker, finally conceded, promising that it would phase out BPA over the next 5 years. Other companies quickly followed suit.

By 2011, both Canada and the European Union banned BPA; the United States followed in late 2012, with an official ban on BPA in baby bottles and “sippy” cups. Even before the U.S. ban, more and more companies had stopped using the chemical. In fact, many plastic bottles now tout their BPA-free status. What replaced it? A very similar chemical known as BPS (bisphenol S).

A century hence, such drastic measures may prove unwarranted. Even vom Saal concedes that it is possible that the long-term studies on BPA will not yield conclusions nearly as horrendous as those on, say, DES. It’s possible that BPA will prove to be relatively harmless. But in the meantime, he insists, we’re much better safe than sorry.

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Select References:

Bohannon, J. (2013). Who’s afraid of peer review? Science 4(6154): 66–65.

Ishido, M., & J. Suzuki. (2010). Quantitative analyses of inhibitory effects of bisphenol A on neural stem-cell migration using a neurosphere assay in vitro. Journal of Health Science, 56(2): 175–181.

Lang, I. A., et al. (2008). Association of urinary bisphenol A concentration with medical disorders and laboratory abnormalities in adults. Journal of the American Medical Association, 300(11): 1303–1310.

Nagel, S. C., et al. (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): 70–76.

Schönfelder, G., et al. (2002). Parent bisphenol A accumulation in the human maternal–fetal–placental unit. Environmental Health Perspectives, 110: 703–707.

vom Saal, F. S., & C. Hughes. (2005). An extensive new literature concerning low-dose effects of bisphenol a shows the need for a new risk assessment. Environmental Health Perspectives, 113(8): 926–933.

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