Anti-chemical
activists opened a new front in their jihad against the plastics chemical
bisphenol-A (BPA) this week.
A first-of-its-kind study, published in the prominent Journal of the
American Medical Association (Sept. 17) claimed that exposure to BPA, used in
food and beverage containers, was associated with increased rates of heart
disease and diabetes in humans.
Using data collected by the Centers for Disease Control and Prevention in
2003-2004, the researchers compared urinary concentrations of BPA with a
variety of health outcomes in 1,455 adults.
They claimed to have found statistically significant correlations between
higher BPA urinary concentrations and increases in heart disease and diabetes.
No correlations were reported for arthritis, cancer, liver disease, respiratory
disease, stroke or thyroid disease.
The researchers concluded that "[t]hese findings add to the evidence
suggesting adverse effects of low-dose BPA in animals" — and the media
unquestioningly reported in numerous headlines that the study
"linked" or "tied" BPA with heart disease and diabetes.
This column has
already debunked the BPA animal studies the researchers referred to so
we'll focus on the new study's claims.
For both the heart-disease and diabetes correlations, the researchers
reported that disease rates more than doubled between those in the highest
quartile versus the lowest quartile of BPA urinary concentration.
The correlations, however, are of doubtful reliability since their margins
of error are so large — 355 percent for heart disease and 211 percent for
diabetes.
This unreliability is precisely what one might expect from the slipshod
manner in which the data were collected by the CDC and analyzed by the
researchers.
None of the health data collected was verified. Survey respondents were
simply asked "Has a doctor or other health provider ever told you that you
have [fill in the disease]?"
Such self-reported data are notoriously unreliable. A 1995 study, for
example, reported that 40 percent of self-reported heart attacks were false
positives — people confusing angina (pain) with a real heart attack.
Next, the researchers didn't compare the timing, duration or level of
exposure with the onset of disease — in effect, they simply assumed that the
occurrence of disease was BPA-related.
BPA, however, is metabolized and excreted from the body pretty quickly,
usually within 24 hours. Without more information on exposure to BPA and
disease origins, there is absolutely no basis for linking the two.
The researchers failed to rule out many competing or confounding risk
factors for heart disease and diabetes, including family history of the
diseases, high cholesterol, high blood pressure, physical activity levels,
stress and alcohol intake, to name a few.
Moreover, diabetes is a risk factor for heart disease and heart disease is a
risk factor for diabetes — neither of which the researchers considered.
Nor were lipid and glucose blood chemistry irregularities correlated with
BPA urinary concentrations, further detracting from the case that BPA was truly
associated with increased heart disease and diabetes risk, respectively.
Finally, the numbers of heart disease cases (79) and diabetes cases (136)
are inadequate for drawing reliable conclusions.
By dividing these relatively few cases over four exposure categories, the
researchers relied on even fewer cases of disease in the highest exposure
categories.
Although the researchers tried to imagine how BPA might act to cause heart
disease and diabetes, they offer no evidence or ideas that would qualify their
speculation as more than simply "idle."
It's also important to keep in mind that plastics industry workers have been
occupationally exposed to BPA for more than 40 years, likely with much higher
exposures than those of the study's subjects.
Yet there are no reports of higher rates of heart disease and diabetes among
these workers.
It's hardly surprising, then, that the FDA told the Washington Post this
week that it has no reason to think that BPA in food packaging and liquid
containers is unsafe.
So who's making all the fuss and why? This column has previously spotlighted
some of the more outspoken activists behind the BPA scare — we'll get to them
(again) in a minute.
The new study features less well-known personalities. Co-author Michael
Depledge, described as responsible for the "supervision" of the
study, sits on the board of the U.K. anti-chemical group Natural England.
Another co-author, Tamara Galloway, has written of her conviction that
"pollution is a major threat to human and environment health."
The smoking gun indicating that this study is little more than rank
anti-chemical fear-mongering is that the study was accompanied in JAMA by an
editorial penned by Frederick vom Saal and John Peterson Myers.
Readers of this column will recall that vom Saal is behind much of the dubious
animal study work on BPA and Myers is a co-author of the debunked 1996
chemical-scare book "Our Stolen Future."
Vom Saal and Myers advocate in their editorial that U.S. regulators abandon
science and risk assessment as a standard for regulating chemicals, and instead
move to the European model of regulation that requires that substances be
proven not to cause harm under any conditions — knowing full well that "proving
a negative" is impossible to do.
This so-called "precautionary principle" would essentially provide
regulators with arbitrary power to ban virtually any chemical, regardless of
its risks, benefits or realities.
It's appalling that the editors of JAMA — the official voice of the American
Medical Association whose physician-members rely on the benefits of chemicals
to treat patients — would lend their credibility to activists advocating the
abandonment of science and risk analysis in favor of Luddite anti-chemical
hysteria and politics.