Yet another dubious study has been making the rounds of mercury militia websites and discussion forums. The study is being played up and touted by certain very excitable and scientifically not-too-bright militia members and woo-meisters like Mike Adams as some sort of vindication of the scientifically discredited hypothesis that mercury in vaccines somehow causes autism.
It doesn’t.
It is, however, somewhat interesting in that their embrace of this bit of questionable research shows how desperate the mercury militia is to grasp to any bit of peer-reviewed published research that they can spin to their cause. It’s also interesting in that it shows how easy it is to stretch research findings too far to justify a hypothesis, given that the study has so many limitations that its conclusions are, at best, tenuous and not particularly convincing. Before I look at the actual scientific paper itself, let’s look at how it’s being spun in the press. After that, I will show why this study’s conclusions do not follow from its methodology. First, a press release published on Science Daily:
A newly published study of Texas school district data and industrial mercury-release data, conducted by researchers at The University of Texas Health Science Center at San Antonio, indeed shows a statistically significant link between pounds of industrial release of mercury and increased autism rates. It also shows–for the first time in scientific literature–a statistically significant association between autism risk and distance from the mercury source.
“This is not a definitive study, but just one more that furthers the association between environmental mercury and autism,” said lead author Raymond F. Palmer, Ph.D., associate professor of family and community medicine at the UT Health Science Center San Antonio. The article is in the journal Health & Place.
Dr. Palmer, Stephen Blanchard, Ph.D., of Our Lady of the Lake University in San Antonio and Robert Wood of the UT Health Science Center found that community autism prevalence is reduced by 1 percent to 2 percent with each 10 miles of distance from the pollution source.“This study was not designed to understand which individuals in the population are at risk due to mercury exposure,” Dr. Palmer said. “However, it does suggest generally that there is greater autism risk closer to the polluting source.”
The study should encourage further investigations designed to determine the multiple routes of mercury exposure. “The effects of persistent, low-dose exposure to mercury pollution, in addition to fish consumption, deserve attention,” Dr. Palmer said. “Ultimately, we will want to know who in the general population is at greatest risk based on genetic susceptibilities such as subtle deficits in the ability to detoxify heavy metals.”The new study findings are consistent with a host of other studies that confirm higher amounts of mercury in plants, animals and humans the closer they are to the pollution source. The price on children may be the highest.
It sounds to me as though the article is just quoting whatever the scientists say without looking at the soundness of the research, an aspect of Science Daily that has driven me crazy on more than one occasion. However, that’s pretty much how the study is being reported, with headlines such as Emissions, autism are linked, study says; New Study Says Autism Linked To Coal Power Plants; and Health Science Center discovers new link between autism, power plants.
But does the study actually provide good evidence for such a link? I’ve already said that it does not. Let’s take a look at the reasons why.
The study itself is a followup to a widely-criticized study that the principal investigator, Dr. Raymond F. Palmer in the Department of Family and Community Medicine at the University of Texas Health Science Center in San Antonio published in 20061. That study purported to show the same thing but was viewed as uninterpretable for a variety of reasons, with its most glaring flaw being that it failed to control for urbanicity of the populations being studied. Particularly harsh was Thomas A. Lewandowski:
Lastly, the authors found that the most important determining factor for autism prevalence in their study was whether the child lived in an urban, suburban, or rural area. For example, residence in an urban school district resulted in a 473% higher rate of autism compared to rural districts. Similar findings have been reported by others (e.g., Deb and Prasad, 1994). The urbanization effect is nearly 8 times stronger than the effect suggested for mercury but is given relatively little discussion and is not even noted in the abstract. Since levels of many pollutants (including mercury) would be strongly correlated with urbanization/industrialization, this also leads one to question the mercury-autism association the authors report. More detail on the impact of residence would have been helpful. Was one particular urban area (e.g., Dallas, Houston, San Antonio) responsible for the effect? Did the authors explore how data for other chemicals correlated with autism incidence? Certainly a host of environmental and social variables associated with urbanization could be investigated as possible factors in autism. Alternatively, an increased tendency for diagnosis in urban localities could explain at least part of the increased incidence.
From Dr. Palmer’s 2006 study, which was so full of holes that even antivaccinationists had a hard time defending it, I got the impression that Palmer was a man with an axe to grind. This new study2, clearly done to answer that major criticism, does nothing to change my mind. Indeed, when I see that Dr. Palmer approvingly cites the infamous “baby hair mercury study” (Holmes et al) in the introduction of the manuscript, I know right away where he is probably coming from, given that that paper was a load of poorly designed garbage bordering on, if not actually, pseudoscience. He also approvingly and uncritically cites the even worse Bradstreet et al study claiming to show that autistic children excrete more mercury in the urine. If you want to get an idea just how bad this study is, consider that it was published in the Journal of American Physicians and Surgeons and that it was co-authored with Mark and David Geier. (Say no more.) Where on earth were the peer-reviewers?
Whenever looking at a study, it’s very useful to look at the hypothesis and then decide whether the methods are appropriate and adequate to answer the question asked in the hypothesis. Indeed, whenever I write a research paper or a grant, I almost always include a paragraph starting “we hypothesized that,” followed by a statement and justification of the hypothesis being tested (or, in the case of a grant, to be tested). The closest I could find to a statement of hypothesis in this study was this:
The objective of the current study is to determine if proximity to major sources of mercury pollution is related to autism prevalence rates.
Fair enough, as far as it goes. However, embedded in the methodology are assumptions that the methodology must account for. First, consider how the study was done. Data for 39 coal-fired power plants and 56 industrial facilities in Texas were examined in 1998 and modeled to see if the distance from these plants of various school districts correlated autism rates in 2002, with this being the rationale:
…it is plausible to postulate that releases during 1998 would have exposure potential for a cohort who was in utero in 1997. If an effect was present, this would be reflected in the 2002 school district records–the age (5 years old) this cohort would be entering the system.
So the real hypothesis being studied, although not stated explicitly, appears to be that exposure to mercury in utero contributes to autism, not that infant or childhood exposure to mercury is related to autism prevalence. Thus, even if this were a good study, how this relates to antivaccinationist claims that mercury in the thimerosal preservative in vaccines causes autism is as tenuous as most antivaccinationists’s grasp of science. Be that as it may, the next step is to see if the methodology tests the hypothesis. There are a number of problems. First among these is that it is quite unclear exactly what data from the Texas Education Agency were used. Apparently Dr. Palmer used some sort of special data set provided by the TEA that is not publicly available. Another really glaring error is this:
Total number of students reflects all enrolled students in the districts 2002 school year and was used as the denominator in calculating autism rates.
Later, under the Statistical Methods section, Palmer states:
District autism data in 2002 were treated as event counts and used as the outcome in a Poisson regression model predicted by pounds of environmental mercury release in 1998, distance to sources of the release, and the relevant covariates. Total number of students enrolled in each district for 2002 defined the rates for each district
Wait a minute! How could this be? I thought that the model assumed that in utero exposure to mercury in 1997 would correlate with autism prevalence in the five year old cohort in 2002. Yet it appears that autism prevalence in 2002 was calculated using the total number of students enrolled, not the number of students entering kindergarten; i.e., the number of students who were exposed to the levels of pollution in utero in 1997. If this statement is accurate, it tells us that Palmer was using autism prevalence in 2002 for all students, K through 12. Since this includes children up to age 18 and since autism is usually diagnosed by age 5, this methodology would necessarily include a large number of autistic children who would already have been diagnosed with autism in 1997, the year for which mercury emissions from power plants and industrial sources was measured. In other words, Palmer included in his dataset far more children whose autism, using his own hypothesis, could not possibly have been related to mercury emissions than he did children who might have been susceptible.
This flaw alone, pointed out by Michelle Dawson, if I have not missed something, makes the results of this study completely uninterpretable. The correct methodology would have been to compare autism prevalence in the kindergarten (or, if using loose criteria, perhaps the kindergarten through third grade cohort) with mercury emissions. Moreover, the perils of using special educational services data as a surrogate for true prevalence are well known.
There are also numerous other deficiencies in the design and methodology of the study, as one might expect. Another glaring flaw is that Palmer appears not to have done any tests to see if distance from power plants correlates with some other confounding variable other than urbanicity and wealth. True, he did try to control for urbanicity, mainly because urbanicity correlates so strongly with autism awareness and access to resources, making it not surprising at all that in his earlier study autism prevalence correlated far more strongly with urbanicity than with mercury emissions. It also correlates with population density, many other forms of pollutants such as auto exhaust, and many other potentially confounding variables. Other serious flaws that I found include:
- The method for calculating distance from power plants. Basically, Palmer took the geographic center of each school district, measured the distance from that to the nearest power plant, and then used that distance for every child in the district. Remember, this is Texas we’re talking about. Some of these school districts are quite large, but Palmer’s methodology averages the distance out for every child in the district.
- Moves. The authors appear to assume that no one moves in or out of the district.
- No examination of wind effects. The underlying hypothesis here appears to be that mercury carried on the wind is what correlates with autism prevalence. If that were the case, then it would be expected that the effect would be much stronger in school districts that, based on the general direction of the prevailing winds, are downwind from a power plant. Palmer didn’t even consider this variable.
- No comparison to other regions. The EPA has a very nice map showing the distribution of deposition of mercury on a global basis. Texas has few “hot spots,” while in the U.S. the Northeast and Midwest have many and China is one continuous hotspot. If Palmer’s hypothesis is true, it would have been nice of him to include a spot check of autism prevalence rates in a state with a lot of coal burning power plants, such as West Virginia.
In the end, Palmer has only answered one of Lewandowski’s criticisms of his 2006 study. The others stand:
Palmer et al. used county-level (and school district-level) TRI data for mercury as a surrogate measure of mercury exposure. The authors note in their introduction that mercury emitted into the air may be carried many miles before being deposited to soil or water. This is critical. Air modeling analyses indicate that mercury deposition that occurs in the west of the nation (including Texas) is overwhelmingly attributable to Asian or other non-US sources (Seigneur et al., 2004). Texas is a significant source of mercury emissions, but the mercury from these emissions is largely deposited hundreds to thousands of miles to the east. It is therefore highly unlikely that mercury emitted in a particular county or school district can be correlated with air mercury exposures in that locality.
TRI data also do not specify mercury species or the environmental medium to which the mercury is released. The likelihood of human exposure (and resulting toxicity) is highly influenced by these factors. For example, community exposure to inorganic mercury present in coal fly ash shipped to an off-site disposal facility will be zero. Releases to surface water bodies may also have a very different exposure potential than releases to air.
The authors also acknowledge that fish consumption is the primary source of human exposure to mercury. Fish mercury exposures in the general population are primarily associated with ocean caught fish, such as tuna or swordfish (Carrington and Bolger, 2002; Dabeka et al., 2004). Mercury levels in ocean fish are impacted by releases on a continental rather than a county-wide scale. Even for freshwater fish, which may be sources of mercury intake for a limited number of individuals, the mercury will most likely be attributable to distant sources. Local mercury releases (as described by the TRI data) should therefore not be used as a surrogate variable for actual mercury exposure. Because TRI-mercury releases on the county or school-district level are unlikely to be correlated with actual mercury exposures in the same geographic regions, it seems implausible that the observed association between mercury release rates and autism prevalence represents a real biological phenomenon.
It’s entirely possible that some environmental factor, or factors, may contribute to the development of autism, either on their own or by acting with some genetic susceptibility, but if that is the case with mercury this study is thin gruel to use to support such a hypothesis. In fact, it’s not even that good as a hypothesis-generating study. There’s just too much potential interference from confounding variables that hasn’t been accounted for.
Finally, it is important to note that Dr. Palmer may well be biased. For example, yesterday he spoke at a demonstration promoted by Safeminds and Autism United, both boosters of the “vaccines cause autism” lie. I tried to find an account that describes what he said there, but the best that I could find was this, which didn’t say much. Given the poor quality of this study and his cozying up to antivaccination groups, one has to wonder. If he has an obvious source of bias, it may well explain much; if he does not I’m left with the less satisfying conclusion that he is just not a very good scientist at all. I also have to wonder about the quality of the peer review of this particular journal. After all, if I, who am not an epidemiologist, can spot the glaring flaws in this study, why couldn’t the peer reviewers?
REFERENCES:
- PALMER, R., BLANCHARD, S., STEIN, Z., MANDELL, D., MILLER, C. (2006). Environmental mercury release, special education rates, and autism disorder: an ecological study of Texas. Health & Place, 12(2), 203-209. DOI: 10.1016/j.healthplace.2004.11.005
- PALMER, R., BLANCHARD, S., WOOD, R. (2008). Proximity to point sources of environmental mercury release as a predictor of autism prevalence. Health & Place DOI: 10.1016/j.healthplace.2008.02.001
