Skeptical Tuesdays: The Muddy Waters of BPA Reporting | Vol. 2 / No. 12.1

Don't try this at home, kids. Photo: A href="">Flickr user Traci Lawson, CC BY 2.0
Don’t try this at home, kids. Photo: Flickr user Traci Lawson, CC BY 2.0

Everyone’s favourite kickaround chemical BPA is back in the news this week because of a recent study that has otherwise rational people quaking in their boots (and melting down their water bottles). Yes, it turns out that some of the replacements for bisphenol-a (BPA) are “just as bad for you.” Now, normally I love Gizmodo. They’re great. But there are days when I don’t, and when I read this article last week, well, that was one of those days. Read the following and we’ll keep talking.

“‘Bisphenol A,’ aka, BPA is a compound found in many polycarbonate plastics, like your old Nalgene water bottle from summer camp. It’s everywhere, and it’s been linked, as the authors point out, to obesity, cancer, and childhood neurological disorders. Study after study showed the chemical was harmful and so eventually, manufacturers relented and started using ‘bisphenol S,’ aka BPS, as a substitute. If you buy something that says ‘BPA-free’ on it, there’s a pretty good chance the manufacturer just swapped out BPS for BPA.


I’ve always maintained that the worst truths are half-truths, because they’re believable to people who aren’t, well, skeptical by nature. Let’s look at the claims.

We’ll start with why BPA was banned: “study after study shower the chemical was harmful, and so eventually, manufacturers relented” and stopped using the stuff. Unfortunately, studies showing BPA was harmful were in very short supply when BPA was removed and/or replaced. In fact, when the US FDA stopped authorizing its use in certain circumstances (in infant formula packaging) it was still so lacking in science that it stated unequivocally that the “action is based solely on a determination of [market] abandonment and is not related to the safety of BPA. The agency’s current safety review supports the safety of BPA for use in the manufacture of food contact articles as authorized in the food additive regulations.”

As I said, half-truths: “manufacturers relented,” sure, but not because of safety issues, but because of perceived safety issues. Back in 2008, there were some concerns that it could do bad things to you. There wasn’t much evidence, but news media sources got their hands on the story, it blew up, and everyone stopped buying BPA-based plastics. Because of all the attention, a lot of funding has gone toward the study of BPA, because, as I said, there really wasn’t much evidence.

What about the potential health effects? The article says it’s been “linked… to obesity, cancer, and childhood neurological disorders.” Has it? Yes and no.  The article is here, and I’d suggest you go read it yourself, but I’ve already done that part for you, because you love me (I know). The link with cancer is not footnoted in the article, which is always a warning sign, but probably refers to the fears that the chemical aids in the growth of breast cancer. The science isn’t there yet to defend that claim with much certainty, though, and it’s the same with the obesity claim. Let’s be clear: I’m not saying BPA doesn’t do these things, but the case is yet to be made that it does do them outside of a petri dish. (Remember, a lot of things work in a petri dish that don’t in the body — like killing cancer cells with bullets).

Anyway, let’s step back and actually ask: does BPA actually pose risks to humans?

The Washington Post (why is it always WaPo writing about BPA?) reported in December that “BPA is still everywhere, and mounting evidence suggests harmful effects.” And those are both accurate statements, if incredibly misleading ones.

The research that’s come out shows that BPA may well act as an endocrine disruptor — a class of chemicals that aren’t hormones, but act enough like hormones to possibly get in the way. But the science isn’t there yet to prove they cause much harm in the real world, and the science there is isn’t exactly damning: on the link between endocrine disruptors and breast cancer, for instance, Peter Lipson over at Science-Based Medicine says “while [the link] is not implausible, it’s pretty damned tenuous.”

But as I said, we’ve done a lot of research on BPA since 2008, and some of the reviews show that it can have some pretty negative effects. A review of studies on BPA’s reproductive effects carried out between 2007 and 2013 concluded that “strong evidence exists that… BPA is an ovarian toxicant in animal models and women… BPA is a uterine toxicant in animal models… BPA is a prostate toxicant in animal models… [and that] The effects of BPA on the reproductive system are variable and evident at doses below the LOAEL [lowest observed adverse affect level] of 50 mg/kg and the proposed safe level of 50 μg/kg/day.” (In some places it’s lower, around 25μg/kg/day, but 50 is the recommended maximum allowable exposure in the US).

It sure sounds scary. So if that’s true, then why does the US FDA say it’s safe?

“Is BPA safe? Yes. Based on FDA’s ongoing safety review of scientific evidence, the available information continues to support the safety of BPA for the currently approved uses in food containers and packaging. People are exposed to low levels of BPA because, like many packaging components, very small amounts of BPA may migrate from the food packaging into foods or beverages.” 

Well, like all things, the dose makes the poison.

The lowest observed adverse affect level is 50mg/kg, and the EPA’s current maximum “safe” dose is 50 µg/kg/day. But wait, the studies said there were even effects below those! Well, worry not, because the average exposure to BPA is 0.026 µg/kg/day and falling. Moreover, the studies that found plausible effects at below the “safe” limit also fail to take into account some other important factors: namely, how our bodies deal with BPA.

Number one, we take BPA in orally, and we break it down pretty quickly. As the FDA reports: “BPA is rapidly metabolized and eliminated through feces and urine.” Even pregnant and nursing mothers have little to fear: “The level of BPA from food that could be passed from pregnant mothers to the fetus is so low that it could not be measured. Researchers fed pregnant rodents 100 to 1,000 times more BPA than people are exposed to through food, and could not detect the active form of BPA in the fetus eight hours after the mother’s exposure.”

Here’s the thing: if you take a long, hard look at most of the chemicals we interact with on a daily basis, most of them are toxic in the right (or wrong) doses. Which returns us to WaPo’s comment that BPA is “still everywhere,” and “mounting evidence suggests harmful effects.” They’re absurd claims, because they’re true of pretty much everything. Both statements are equally true of cyanide, for instance: it’s present in everything from lima beans to broccoli to almonds, and goddamn if that stuff won’t kill you dead.

But with endocrine disruptors, apparently, it’s not that simple. According to the study Gizmodo was citing, the one about BPA and its replacement BPS, there’s something called a “U-shaped dose response curve” we have to deal with. It’s a bit crazy sounding, but for a moment let’s follow the logic:

“…many endocrine-disrupting compounds follow alternative U-shaped dose–response curves, whereby exposure to midrange concentrations activates physiological defense mechanisms against the compound, but at low-range concentrations, the compound mimics endogenous hormones (10). Thus, our finding that BPA at a very low dose (0.0068 μM) alters neurogenesis and that a moderate BPA (1 μM) dose did not affect neurogenesis significantly calls for change in government-sanctioned methods of assessing human tolerable daily intake levels.”

Basically, the idea is that unlike every other class of chemicals, they’re saying sometimes less is worse than more. In their study they found that zebrafish embryos developing in two different concentrations of BPA-laced water developed cells in one part of their brain faster than they normally would, but mostly it was in the ones with the lower doses, which they’re attributing to this U-shaped curve. It sounds a little weird but it’s not totally unbelievable, but there is something odd about the logic.

They picked the two concentrations, 0.0068μM and 1μM, because they represent the amount in the water of a local river on the one hand, and the amount in the human placenta on the other (which they equate to 12μg/kg). The problem in the logic seems to be that the amount showing adverse effects is the one found in the river water, not the one found in the placenta, while the study calls for worry over effects seen in gestational exposure. Based on this study, then, it’s very unclear what the changes in human tolerable daily intake levels should be: should we make sure that everyone gets more BPA, but not too much? If we’re talking doses in the thousandths of a microgram per kg, it’s going to be almost impossible to eliminate from the environment.

In any case, the article found a similar response (in zebrafish brains exposed to less-but-not-more BPA and its replacement BPS) that may cause hyperactivity or depression (but they’re not totally sure of the mechanism) if the developing brain is exposed at a very specific time in gestation. It also said nothing about the migration of BPA to the brain of a developing fetus (which is where the link with the placental amount would come in), so we have no idea of what exposure fetuses might have. Literally nothing about this makes for a clear policy recommendation, which is why when I read the following in the Gizmodo article, it bothered me:

Well, it’s clear that BPS hasn’t been tested nearly enough. According to the authors, “These findings suggest that BPA-free products are not necessarily safe and support a societal push to remove all structurally similar bisphenol analogues and other compounds with endocrine-disruptive activity from consumer goods.” In other words, let’s switch to something else. Yeah, that seems reasonable.”

Except it doesn’t seem reasonable to switch to something else, because as we’ve just seen with BPS being substituted in for BPA, we don’t know what the effects of the “something else” might end up being. The only thing that’s “clear” is that we need a better understanding of the peculiarities of “endocrine disruptors” before we can say anything for sure — whether we think it’s even possible to eliminate hormone-like chemicals from our bodies (or if we even should) and whether it will cause more harm to reduce the amounts if it turns out we’re incapable of eliminating them entirely.

But that doesn’t make a catchy headline, does it?