Ever see a headline that forces you to read what follows against your better judgment? Headlines like "Misplaced focus on experimental detail" work on me. This sounds very "please, pay no attention to the man behind the curtain." I spend a lot of my working day worrying about experimental details.
This letter was a reply to another letter by a lawyer named Robert Mathews. Mathews' questions whether the method used to give bisphenol A (BPA) to green monkeys in Leranth et al. 2008 simulates a realistic physiologic exposure to BPA that corresponds to the EPA oral reference dose (RfD). For the record, I know next to nothing about the details of the BPA debate, but, as you shall see, my ignorance is not relevant to this discussion.
Lernath et al. composed the awkwardly, yet irresistibly, headlined (PNAS editors, did you know what you were doing?) reply letter mentioned at the top. In what follows, remember that the question at hand is whether the method used by Leranth et al. to simulate BPA exposure is a reasonable way to experimentally reproduce BPA exposure, which appears to be a reasonable and not thoroughly answered question.
Instead of crushing Mathews' concern with their method and the resulting results under the weight of accumulated data and testing, the authors mention his employment.
But, finally, having completely poisoned Mathews' well and bayoneted his straw man, Leranth et al. describe the challenges to the assumption that there is no threat to human health, which as you might recall was not the central question.
#3 follows as a hypothesis from #1 and #2. This raises two questions that need to be answered: does BPA exposure vary and is variance in BPA exposure significantly correlated with diabetes or cardiovascular disease?
#4 is confusing. Are they conceding the industry "spin" position that oral exposure to BPA does not lead to harmful levels of blood BPA? Or, are blood BPA levels (#1) higher than can be explained by oral exposure alone? #4 certainly does not follow from #1, #2, or #3. The "thus" is unwarranted and is probably just lazy scientific writing. Perhaps they meant something about the probability of non-oral exposure.
So, it has only been suggested that their method is the best? They only reference provided is to the paper in question, demonstrating that they did indeed use this technique. Neither the letters nor the paper provide any previous evidence that using continuous release capsules recreate physiological BPA levels.
They end like they began, by poisoning the well.
Mathews a shill for the plastics industry. His letter is questioning the methods of a research paper with results that his clients would not be happy with. Pointing these things out, however, does not constitute evidence that the question is invalid. This exchange in PNAS merely provides fodder for both extremes of the BPA debate and polarizes rather than illuminates. When discussing the products of the scientific method, scientists need to hold themselves to the highest standards, not the standards of the media and politicians. Our tools are data and logic, not cheap rhetoric.
This letter was a reply to another letter by a lawyer named Robert Mathews. Mathews' questions whether the method used to give bisphenol A (BPA) to green monkeys in Leranth et al. 2008 simulates a realistic physiologic exposure to BPA that corresponds to the EPA oral reference dose (RfD). For the record, I know next to nothing about the details of the BPA debate, but, as you shall see, my ignorance is not relevant to this discussion.
Lernath et al. composed the awkwardly, yet irresistibly, headlined (PNAS editors, did you know what you were doing?) reply letter mentioned at the top. In what follows, remember that the question at hand is whether the method used by Leranth et al. to simulate BPA exposure is a reasonable way to experimentally reproduce BPA exposure, which appears to be a reasonable and not thoroughly answered question.
Instead of crushing Mathews' concern with their method and the resulting results under the weight of accumulated data and testing, the authors mention his employment.
Mathews, who represents the plastic industry. . .So, we have established that Mathews is getting paid to raise this question. This fact has nothing to do with the legitimacy of his position and is a logical fallacy known as poisoning the well , where one provides information not directly related to the debate about the other party in order to affect the way the audience perceives the other party's actual arguments. This serves only to undermine Mathews argument by appealing to distrust (not necessarily ill-founded) of corporate interests without actually addressing its merits.
. . .presents the industry ‘‘spin’’ on the issue of human bisphenol A (BPA) exposure (1), stating that BPA is subject to very rapid firstpass metabolism with the implication that there should be no BPA detected in human biomonitoring studies and thus that no threat to human health is posed by BPA.Unfortunately, nothing is shown to state whether this view of oral exposure is correct or not. The fact that the information comes from the "industry spin" tells us nothing about the quality of the information and is only intended to discredit the argument via rhetoric, not data.
The evidence from science not funded by the chemical industry challenges this assumption (2, 3).Is there really a true dichotomy here? Is all industry funded research negative and all non-industry funded research positive? Why is the science funded by the chemical industry flawed? What were the errors in experimental design? Unfortunately, there are no references to the industry funded science. So, we cannot know to which studies they refer, which makes this a straw man argument.
But, finally, having completely poisoned Mathews' well and bayoneted his straw man, Leranth et al. describe the challenges to the assumption that there is no threat to human health, which as you might recall was not the central question.
- Human blood BPA levels are in the low parts per billion range
- Animal and human cell culture and tissue culture have adverse responses to BPA levels below low parts per billion
- Translation of ex vivo results to humans predicts a relationship between BPA exposure and diabetes as well as cardiovascular disease
- "There are thus potentially many non-oral sources of BPA exposure"
- It has been suggested that the best way to simulate continuous exposure to BPA is by a continuous release capsule
#3 follows as a hypothesis from #1 and #2. This raises two questions that need to be answered: does BPA exposure vary and is variance in BPA exposure significantly correlated with diabetes or cardiovascular disease?
#4 is confusing. Are they conceding the industry "spin" position that oral exposure to BPA does not lead to harmful levels of blood BPA? Or, are blood BPA levels (#1) higher than can be explained by oral exposure alone? #4 certainly does not follow from #1, #2, or #3. The "thus" is unwarranted and is probably just lazy scientific writing. Perhaps they meant something about the probability of non-oral exposure.
So, it has only been suggested that their method is the best? They only reference provided is to the paper in question, demonstrating that they did indeed use this technique. Neither the letters nor the paper provide any previous evidence that using continuous release capsules recreate physiological BPA levels.
They end like they began, by poisoning the well.
The focus of Mathews on our method of administering a very low dose of BPA rather thanAs an aside, it appears that the tobacco industry is to environmental toxin research as Nazis are to political discourse. If one questions research showing that a chemical could be harming people, one gets compared to the tobacco industry. The tobacco industry denied the relationship between smoking and cancer despite overwhelming evidence. Mathews raised a methodological question about a study in a field that, to date, has had mixed results (as documented in the introduction of Leranth et al. 2008).
on the significant damage to the brain is reminiscent of the response of tobacco industry product protection firms to scientific publications showing harm from cigarettes.
Mathews a shill for the plastics industry. His letter is questioning the methods of a research paper with results that his clients would not be happy with. Pointing these things out, however, does not constitute evidence that the question is invalid. This exchange in PNAS merely provides fodder for both extremes of the BPA debate and polarizes rather than illuminates. When discussing the products of the scientific method, scientists need to hold themselves to the highest standards, not the standards of the media and politicians. Our tools are data and logic, not cheap rhetoric.
