Skip to content

The mercury zombie rises again…this time, in the grandchildren of Pink disease (infantile acrodynia) sufferers

August 10, 2011

Category: Antivaccination lunacyAutismMedicine
Posted on: August 10, 2011 11:30 AM, by Orac

Here we go again.

Starting sometime in 2007, back when the idea that mercury in vaccines was the cause of the “autism epidemic” of the late 1990s and into the new century, I started referring to the “mercury/autism” hypothesis as being dead, dead, dead, as in pining for the fjords dead. Then, depending on what kind of mood I was in, I’d start liberally quoting more from Monty Python’s famous Dead Parrot Sketch, including pointing out that the mercury/autism hypothesis passed on! This hypothesis is no more! It has ceased to be! It’s expired and gone to meet its maker! It’s a stiff! Bereft of life, it rests in peace! Its metabolic processes are now history! It’s off the twig! It’s kicked the bucket, it’s shuffled off its mortal coil, run down the curtain and joined the bleedin’ choir invisibile!! THIS IS AN EX-HYPOTHESIS!!

I know, I know. I use that bit perhaps more than I should, but if there’s a bit that’s appropriate to describe the state of the mercury/autism–particularly the claim that it was mercury in the thimerosal preservative that used to be in vaccines in the U.S. until around 2001–it’s the most appropriate one I can think of. Well, not quite, there’s always the Black Knight sketch, in which each time the Black Knight and King Arthur engage in combat Arthur lops off one of the Black Knight’s limbs, after which the Black Knight brushes off the injury, proclaiming things like, “It’s just a flesh wound.” With each new scientific and epidemiological study published that’s inconsistent with the mercury/autism hypothesis, the Black Knight of the Mercury Militia brushes it off as though it’s a flesh wound, even as he sits on the stumps of his amputated legs telling scientists to come back and fight so that he can bleed on them some more.

So it is again with the mercury militia’s embrace of a rather curious, puzzling, and not-so-impressive study hot off the presses.

Worse, even the mainstream media is getting it wrong. Rachael Dunlop (a.k.a. Dr. Rachie) herself sent me a link to an article in the Australian press that pretty much takes the story at face value entitled Mercury link backs autism cause theory, which proclaims:

A FAMILY history of mercury poisoning has emerged as a significant risk factor for developing autism, researchers say.A survey by Swinburne University in Melbourne of 522 Australian survivors of Pink disease – a form of mercury poisoning common in the early 20th century – found one in 25 of their 398 grandchildren aged six to 12 had an autism spectrum disorder.

The prevalence is six times higher than the one-in-160 diagnosed in the general population.

The study, published this week in the Journal of Toxicology and Environmental Health, found the grandchildren did not have elevated rates of other conditions such as epilepsy, Down syndrome or attention deficit hyperactivity disorder.

Before I get into the study itself, let me just point out that that particular journal looks very, very, familiar. Very familiar indeed. So I invoked the “search” function of my blog to see if I had blogged about any studies before that appeared in this particular journal. Surprise! Surprise! I have. And–surprise! surprise!–the papers I’ve blogged about were–shall we say?–not of the best quality and–shall we say?–supportive of the vaccine-autism hypothesis. For instance, the Journal of Toxicological and Environmental Health has published at least one paper by incompetent mercury-autism quack Mark Geier (who is currently in the process of having his medical licenses suspended in more than one state) and a truly awful paper by Gayle DeLong trying to link vaccines with autism. So, right off the bat I knew I was probably dealing with badness. Then I dug into the paper itself, entitled Ancestry of Pink Disease (Infantile Acrodynia) Identified as a Risk Factor for Autism Spectrum Disorders by Kerrie Shandley and David W. Austin. Here’s the abstract:

Pink disease (infantile acrodynia) was especially prevalent in the first half of the 20th century. Primarily attributed to exposure to mercury (Hg) commonly found in teething powders, the condition was developed by approximately 1 in 500 exposed children. The differential risk factor was identified as an idiosyncratic sensitivity to Hg. Autism spectrum disorders (ASD) have also been postulated to be produced by Hg. Analogous to the pink disease experience, Hg exposure is widespread yet only a fraction of exposed children develop an ASD, suggesting sensitivity to Hg may also be present in children with an ASD. The objective of this study was to test the hypothesis that individuals with a known hypersensitivity to Hg (pink disease survivors) may be more likely to have descendants with an ASD. Five hundred and twenty-two participants who had previously been diagnosed with pink disease completed a survey on the health outcomes of their descendants. The prevalence rates of ASD and a variety of other clinical conditions diagnosed in childhood (attention deficit hyperactivity disorder, epilepsy, Fragile X syndrome, and Down syndrome) were compared to well-established general population prevalence rates. The results showed the prevalence rate of ASD among the grandchildren of pink disease survivors (1 in 25) to be significantly higher than the comparable general population prevalence rate (1 in 160). The results support the hypothesis that Hg sensitivity may be a heritable/genetic risk factor for ASD.

Whenever I see a study like this, I ask a couple of questions. Well, I ask more than a couple of questions, but chief among the questions I ask are three. First, what’s the hypothesis being tested? Second, are the methods adequate for testing the hypothesis? And, third, do the authors demonstrate a background knowledge of their topic adequate to give me some confidence that they know what they’re doing? Regarding the hypothesis, it is not, as at least one anti-vaccine commenter has claimed, a “beautifully thought out hypothesis.” I’ll show you what I mean from the authors themselves:

Mercury contained in vaccines (as a preservative under the tradename Merthiolate, but more commonly known as thiomersal/thimerosal), dental amalgams (silver fillings), seafood, and the atmosphere is argued to be the primary set of sources of Hg exposure for infants both in utero and in their early years (Austin 2008). However, not all children exposed to such sources of Hg develop an ASD, suggesting, as was the case with pink disease, that a hypersensitivity to the adverse effects of Hg needs to be present in addition to the Hg exposure for the condition to manifest. Therefore, the Hg-autism hypothesis is, in reality, a two-part hypothesis that states that Hg exposure combined with a genetic/physiological sensitivity to Hg or a predisposition to impaired Hg excretion capacity leads to a chronic elevation of Hg in the brain and body (Bernard et al. 2001).The purpose of the present study was to test the Hg-autism hypothesis. If the hypothesis is indeed correct, and a sensitivity to Hg is heritable (genetic), the prevalence of ASD among the descendants of a cohort confirmed as having a hypersensitivity to Hg (pink disease survivors) should be higher than a comparable general population prevalence.

Let’s take a look at this. First, note how the authors cite “studies” from anti-vaccine stalwarts like Sallie Bernard and the infamous paper she published in Medical Hypotheses back in 2001. This is not an isolated citation, either. The authors copiously cite Mark and David Geier’s “work,” a paper by Mark Blaxill and Boyd Haley, Bradstreet’s paper from the infamous Ayn Randian rag of pseudoscience and quackery, the Journal of American Physicians and Surgeons, the Windham’s paper trying to correlate air pollution near freeways with autism, Palmer’s paper trying to relate autism prevalence to proximity to coal-fired power plants, and a wide variety of other really bad studies performed and/or promoted by the anti-vaccine movement. Right away, these citations tell me that the authors don’t know enough about the background of what they’re studying to be credible, nor do they understand good research methodology. If they did, they would never credulously cite such dreck in support of their “hypothesis.”

What about their hypothesis? A good hypothesis should be based on good data and sound observations. The authors propose a “two-hit” model of autism causation: genetic susceptibility coupled with mercury exposure. The idea is clearly to support the vaccine-autism hypothesis, even though they aren’t studying vaccines in this study. One problem, of course, is that the amount of mercury to which infants were exposed in vaccines, even at the height of the use of thimerosal as a vaccine preservative in the 1990s, is nowhere near what babies who developed Pink disease were exposed to. The difference is many orders of magnitude; so even if the authors did find a result in which the offspring of parents with Pink disease had a higher prevalence of autism or autism-spectrum disorder (ASD), it would not be particularly strong evidence that thimerosal causes autism. True, the authors don’t state that this is what they are testing, but their choice of citations makes it pretty clear that that’s what they’re interested in. Moreover, the fact that the mercury exposure associated with Pink disease was not even the same chemical form as thimerosal, the mercury being mercurous chloride in the case of Pink disease and thimerosal in the case of vaccines also makes the comparison tenuous at best. Finally, as has been pointed out time and time and time again, they symptoms of mercury poisoning do not resemble the symptoms of autism, except on a very superficial level.

It’s obvious that the authors’ hypothesis is not well supported, either by scientific observation or by reason. Nor does the observation that only a relatively small subset of children exposed to mercury-containing teething powders developed infantile acrodynia necessarily support the argument for a genetic susceptibility of some kind to mercury. It might, but it might not. Absent some background evidence demonstrating that dose doesn’t matter that much in children who developed Pink disease, it’s difficult to have much enthusiasum for a hypothesis of genetic susceptibility. It’s not entirely implausible, true, but it is for the most part unsupported. Remember again that the dose makes the poison, and the doses of mercury that we are dealing with in infantile acrodynia are very high. More importantly, no reliable study has ever truly correlated mercury dose with probability of developing Pink disease. As pointed out by Sullivan, it is very possible that the children who developed Pink disease could well be the children whose exposure to mercury was the highest. We really don’t know. The association between mercury-containing teething powders and infantile acrodynia wasn’t figured out until 60 years ago, and epidemiological methods and lab-based assays were much cruder then than they are now. It’s also not as though we could “repeat the experiment” now; mercury-containing teething powders are, fortunately, no longer manufactured or used.

So let’s look at the methodology of this paper. First, it’s impossible not to note that this study relied solely on questionnaires distributed to the Pink disease survivors, all of whom are now old enough to be grandparents, given how long ago mercury-containing teething powders were identified as the culprit in Pink disease. In other words, the diagnoses of ASD reported by the elderly respondents to the survey were not verified. Second, there was no real effort to control for potential confounding factors, such as urbanicity, socioeconomic status, etc. that can affect the rate of diagnosis of ASD. Indeed, all we really have are ages, where the respondents live, gender, how they responded (mail, telephone, or online). Moreover, even though the investigators managed to garner 522 responses, that was only a 23% return rate for the surveys. The authors tried to minimize the possibility of response bias, in which responders respond to a survey because they believe that the hypothesis is likely to be true (as in vaccine-autism studies, where parents of children with autism are far more likely to respond than other parents if the survey is about vaccines and autism), but I don’t know that they really did:

The PDSG maintains a membership database and sent out the survey to all of its past and present members, in addition to advertising the study on its website ( In order to minimize response bias, the true purpose of the study was not included on recruitment materials sent out to potential participants; instead, recruitment materials indicated that the purpose of the study was to investigate the general health outcomes of the descendants of pink disease survivors.

How is this “hiding the purpose of the study”? It’s not, except only partially. Pink disease survivors who believe that Pink disease left them or their descendents with health problems would be more likely to respond. Why would that not include people with children or grandchildren with ASD? It wouldn’t. We can therefore answer question two rather confidently: The methods used were poor methods to test the hypothesis of the study.

Then there are the results.

The authors do veritable backflips of logic to try to explain how a “genetic susceptibility” to the effects of mercury that led to Pink disease could manifest itself as an increased autism prevalence not in the children of Pink disease survivors but only in their grandchildren. The authors don’t state specifically, but the answer is implied: It’s the mercury in the vaccines that the grandchildren got. Of course, arguably the children of the Pink disease cohort would have been exposed to more mercury from products of daily living (remember mercurochrome solution for cuts and scrapes?), from pollution, and from laxer standards in manufacturing that allowed more mercury exposure. But the real elephant in the room is the question of why there wasn’t a higher prevalance of autism or ASD in the actual Pink disease cohort itself. After all, this group received a very high dose of mercury. If the same “genetic susceptibility” that led to Pink disease in response to mercury exposure also leads to autism (which is part of the authors’ hypothesis, by the way), then why don’t we see higher levels of ASD in the people who had Pink disease?

The authors drop some more howlers in trying to overcome the logical lapses in their very own hypothesis:

As identified earlier, numerous studies demonstrated a relationship between ASD and Hg (Agency for Toxic Substances and Disease Registry 1999; Austin and Shandley 2008; Bradstreet et al. 2003; Geier and Geier 2006a; 2007; Nataf et al. 2007; Adams et al. 2009; Geier et al. 2009; Holmes et al. 2003; Gallagher and Goodman 2010; Palmer et al. 2006; 2009; Windham et al. 2006), and our results add further compelling evidence in support of this relationship. The unique contribution of this study is that, to our knowledge, it is the first to examine the “individual susceptibility” variable inherent in the Hg-autism hypothesis. Our results suggest that this variable may have a heritable component and therefore, of course, a genetic basis. What our results do not do, however, is enable an understanding of the degree to which the susceptibility is inheritable and the mechanism by which this may occur.

That last statement wins the award for understatement of the year, if not the decade. Also note the multiple studies by the Geiers, Bradstreet, and other luminaries of the anti-vaccine movement. Again.

Near the end, the authors plop another howler into their discussion:

The Hg-autism hypothesis engenders passionate debate on both sides; however, the cumulative science in this field is now of such depth and breadth that it is difficult, if not impossible, to be completely dismissive of the Hg-autism link. Furthermore, our findings clearly suggest that individuals with a family history of pink disease are at significantly greater risk of having a grandchild with an ASD than the general population.

Uh, no. It is not difficult, much less impossible, to be dismissive of the autism-mercury hypothesis. There is copious evidence refuting the hypothesis, and the only evidence supporting it these days comes from cranks like the Geiers. As for the authors’ conclusion, I’m not even sure they can say that a family history of Pink disease is associated with autism, given that the authors never verified the cases of ASD reported and there isn’t yet a solid estimate of ASD prevalence in Australia. In other words, the study says…nothing!

Unfortunately, I doubt this will be the last we hear of this nonsense. A press release tells us that Shandley and Austin are “are now extending their research by examining cellular and genetic characteristics of Pink Disease survivors and people with autism” and that the results are likely to be published in 2012.

Oh, goody. I can hardly wait. No doubt it will be published in the Journal of Toxicology and Environmental Health, and no doubt the merry band of science-challenged anti-vaccine propagandists at Age of Autism will be ignorantly trumpeting it as “yet another study” that will “add to the growing list of research showing that autism can be connected with exposure to mercury.”

ADDENDUM: Oh, dear. It’s been pointed out to me that one of the authors has in the past published even worse dreck than this current study.


Source :


From → Pro - Kontra

Leave a Comment

Leave a Reply

Fill in your details below or click an icon to log in: Logo

You are commenting using your account. Log Out / Change )

Twitter picture

You are commenting using your Twitter account. Log Out / Change )

Facebook photo

You are commenting using your Facebook account. Log Out / Change )

Google+ photo

You are commenting using your Google+ account. Log Out / Change )

Connecting to %s

%d bloggers like this: