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The FDA’s new report on the safety of endocrine-disrupting chemical bisphenol A is months overdue and there is still no sign of when or if the agency will release the report. Perhaps they are waiting for that piece of “smoking gun” evidence that BPA represents a clear and present danger to human health? Well, thanks to researchers from Peninsula College of Medicine in Britain, we just may have it.

In 2008, the group looked at data from the 2003-2004 US National Health and Nutrition Examination Survey (NHANES) which included urinary BPA levels for the first time. The results:

[A] quarter of the population with the highest levels of BPA were more than twice as likely to report having heart disease or diabetes, compared to the quarter with the lowest BPA levels. They also found that higher BPA levels were associated with clinically abnormal liver enzyme concentrations.

At the time, even the researchers admitted the possibility that it was a statistical fluke. But the same team has now analyzed the 2005-2006 NHANES, which used an entirely different group of people, and guess what? The association between BPA exposure and heart disease in humans is as strong as ever (via Toronto’s Globe and Mail):

According to the new research, 60-year-old American males with the highest amounts of bisphenol A in their urine had about a 45 per cent greater risk of cardiovascular disease than men the same age with lower exposures, confirming the results of a previous study on the topic released in 2008 and based on a different sample of people.

This comes despite the fact that median BPA levels dropped by 30 percent between 2004 and 2006 to around 2 parts per billion. Even with the lower exposure, however, odds of heart disease were still significantly higher. Note that the researchers performed rigorous calculations to ensure that they isolated the effect of bisphenol A and weren’t getting correlations with other factors (you can dig into the statistics here).

It’s true that the earlier relationship between BPA and diabetes and BPA and liver function were less present in the new data. But Dr. David Melzer, the lead author on the study, believes this is a result of the lower human BPA levels measured. As he put it to me:

The 2005/6 data for the liver enzymes and diabetes are also statistically consistent with the 2003/4, although not significant on their own, probably because of the fall in BPA levels. Note that the new data do not statistically contradict the 2003/4 data on diabetes or liver enzymes: overall they add to it although the sample size is too small at these lower BPA levels to get a definitive result for 2005/6 on its own. Overall this clearly takes the hypothesis of a BPA — adult heart disease association through to the level of evidence. Given the obvious concern that BPA might be directly driving these health effects, we now need to urgently clarify the mechanisms behind these associations.

Indeed, Dr. Melzer believes his study is underestimating the effect of BPA due to the relatively small sample size — he believes further study will revise the effect of BPA on heart disease upward.

The Globe and Mail article offered this response from a spokesman for industry lobbying group the American Chemistry Council:

“The study itself does not establish a cause-and-effect relationship between BPA exposure and heart disease,” commented Steven Hentges, a spokesman for the group.

But what he doesn’t say is that the only way to “prove” that cause-and-effect, in other words to isolate BPA’s role beyond doubt, would involve conducting a controlled clinical trial, i.e. exposing humans to BPA and seeing who dies. That, of course, isn’t science, it’s homicide, which is why toxic chemical research is mostly performed on rats. And the evidence from rats on BPA, despite industry attempts at obfuscation, is already overwhelming.

These kind of population studies — analysis in effect of the natural experiment industry is performing on us — represents the best evidence we could reasonably hope to get. These results go far beyond what’s required by any meaningful precautionary principle. This is now about saving lives. Yes, as the scientists observe, more research is needed to understand the precise physiology through which BPA causes heart disease and to determine the risk factor with greater accuracy. But whether that increased risk end up at 30 percent or 60 percent or somewhere inbetween, the FDA now knows all it needs to know to conclude that even low exposure to BPA represents a serious risk to human health.