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Of BPA and Men

by Bill Chameides | August 31st, 2010
posted by Erica Rowell (Editor)

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New studies suggest that the synthetic chemical BPA may be messing with men.

If you had to give an award for the bad consumer chemical of the decade, bisphenol A (BPA) would have to be a candidate. Most of us were shocked to learn that BPA, a known endocrine disruptor, is commonly found in blood and urine samples of people throughout the developed world. Where is the BPA coming from? From the chemical industry by way of the marketplace. (See related posts in our series The Chemical Marketplace.)

Despite some concern over its safety in recent years (in fact Canada has just announced intentions to label it toxic), BPA is produced worldwide at a whopping clip. In 2008 worldwide production capacity for BPA was estimated at 5.1 million metric tons with a projected annual increase of as much as five percent.

Most of that BPA is used in the manufacture of polycarbonate plastic and epoxy resins and thusly shows up in various bottles and food containers. From there it’s a small hop to our mouths, our bodies (specifically our blood and tissue), and eventually our urine.

The consumer push in response to this information has been strong and clear, so much so that many companies have now gone to selling “BPA-free” bottles and other related products. But BPA remains in the marketplace, for example, in canned foods, soft drinks and beers. And that may only be the tip of the BPA iceberg. According to the U.S. Food and Drug Administration:

“Current BPA food contact uses were approved under food additive regulations issued more than 40 years ago. This regulatory structure limits the oversight and flexibility of FDA. Once a food additive is approved, any manufacturer of food or food packaging may use the food additive. … There is no requirement to notify FDA of that use. For example, today there exist hundreds of different formulations for BPA-containing epoxy linings, which have varying characteristics. As currently regulated, manufacturers are not required to disclose to FDA the existence or nature of these formulations.”

The bottom line: We have virtually no way of knowing whether a product contains BPA.

And so even with the new “BPA-free” movement, we still need to know how dangerous the stuff is. Two new papers shed some light.

BPA and Testosterone Levels

In a paper published in Environmental Health Perspectives, authors Tamara Galloway of the University of Exeter, UK, and colleagues used a cohort of 715 Italian adults to look for an association between BPA urine concentrations and sex hormones in blood. The report had some good news for women: no evidence of any effects. For men the results were not as encouraging: higher levels of BPA in the urine (taken over a 24-hour period) were correlated with higher testosterone concentrations in the blood (sampled after the same 24-hour period).

What could cause such a correlation? One possibility advanced by Galloway et al is that BPA slows the ability of the body to metabolize testosterone in men. Another is that BPA interferes with sites that naturally regulate testosterone thereby increasing its circulation in the body. But still another that the authors cannot rule out is “reverse causation”: that is, BPA is not causing higher testosterone levels but that higher levels of testosterone slow down the processes that metabolize BPA, leading to more of it in the blood.

BPA and Semen Quality

Now, I can’t speak for all men, but it is my general impression that we guys are concerned about our testosterone levels, but when you start messing with our semen, things get pretty serious. (It’s a male thing, obviously.) And so, the stakes get a wee bit (no pun intended) higher when you consider the recent paper by John Meeker of the University of Michigan and co-authors on the possible effects of BPA on semen quality and sperm DNA damage.

The study, published in Reproductive Toxicology, though preliminary, is fascinating. The authors recruited 190 men from couples being treated for infertility. While this group is clearly a subset of the general population, not all the men were subfertile (because some of their partners were), so, the authors argue, the study was not biased by only considering subfertile men. Unlike the Galloway et al study, the BPA determinations were based on spot urine samples instead of 24-hour samples, although some of the men provided additional urine samples from three days to two and a half months later.

The analyses didn’t produce a slam-dunk conclusive result, but the authors did find evidence for a decline in semen quality and increased sperm DNA damage with elevated BPA urine concentrations. For reasons not well understood the effect was most pronounced among men who had low semen quality — the semen quality of men whose semen were normal did not seem to be effected by BPA.


One of the compelling aspects of these two studies is that they were based on actual people, you know, human beings, as opposed to rats, guinea pigs, etc. That adds a lot of weight to the findings of the Galloway team’s study that even low “background” levels of BPA are associated with changes in testosterone levels in the general population. At the same time, it throws some wild cards into the deck. You can’t control all the factors that might influence your subjects when they are people, and you can’t be sure that your subjects are representative of the general population.

That is certainly a concern for the Meeker et al study — can we be certain that semen taken from a cohort of men in subfertile couples is truly representative of men in general?

Another major issue (and an issue fully recognized by both sets of authors) is the possibility of reverse causation. The authors in these studies have found a statistical link between BPA and a health outcome. But statistical correlation does not establish cause and effect. As already noted, it is possible that BPA is not the cause of the correlation but the result. If that’s the case, the whole issue is moot.

The other part of these studies that I find a bit cautionary is the use of urine BPA as a measure of BPA exposure. BPA levels in urine can be quite variable. For example, Meeker et al found that “repeated urine samples collected from the same man weeks to months apart … were weakly correlated.” This suggests that Meeker and c
oauthors might have gotten a different result if they took their urine samples at a different time or collected composite samples as opposed to spot samples.

I also found the variability of BPA urine levels across the studies curious. In the Galloway et al study, the geometric mean (mean) urinary BPA concentrations were 3.59 nanograms per milliliter (with a 95 percent confidence interval from 3.42 to 3.77). By comparison, the mean urinary BPA concentrations in the Meeker et al study was 1.4 nanograms per milliliter. And the mean for American men based on data collected from 2005 to 2006 was 2.3 nanograms per milliliter. Why these variations? Are they real or just reflective of different sampling/measuring protocols? If they are real and BPA is a causative in reproductive health outcomes, shouldn’t this mean that the reproductive health of the Galloway et al cohort is worse than the Meeker et al cohort? That in itself would suggest that at least one of the cohorts was not representative.

Lots of questions to be sure, but … guys like us, we’d prefer not to mess with BPA.

Related Posts on BPA

  • The Chemical Marketplace: BPAF – Introducing bisphenol AF, BPA’s more toxic sibling. (August 17, 2010)
  • Update: BPA Now Bigger on EPA’s Radar – A chemical once common, now slightly less common in plastics might soon be even less common. Or not. (March 30, 2010)
  • Oh That Chemical Feeling – Congress is (finally) looking into the persistent and growing problem of persistent and bioaccumulating pollutants. (February 11, 2010)
  • Science Update: BPA – A couple of new studies warrant serious consideration by the federal government. They support a growing body of research that shows risks to human health from bisphenol A (BPA), a common ingredient in many plastic bottles and tin cans. (September 18, 2008)
  • The Link Between Environmental Toxins and Disease – Is the ever-growing list of chemicals we are introducing into our environment, putting in our foods, and adding to our drinking water messing with our epigenome? (June 11, 2008)
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