Archive for the ‘The Pretzel’ Category
Unequal distributions of scary chemicals and (possible) implications for autism clusters, a static rate of autism, and why some of us may be more doomed than others
Posted March 12, 2010on:
Hello friends –
Recently there have been a few studies that tackled the issue of apparent autism clusters in California, The spatial structure of autism in California, 1993-2001, and Geographic distribution of autism in California: A retrospective birth cohort analysis. A nice overview and some discussion of these papers can be found at LBRB, here, and here. One of the arguments we see made there is that the rates of autism diagnosis are, in fact, a reflection of the available services in an area, as opposed to an actual difference in the number of children with autism; essentially that an undiagnosed child with autism who lives far from a center of autism services will not get a diagnosis, but a child born relatively close to such services, will be appropriately diagnosed. We are measuring diagnosis, as opposed to autism. I have no doubt that there is some validity to this, but have many doubts that we can, or should, assign all of our observed increases in autism as consequences of this type of artifact.
There have been several other studies that looked at things like mercury emissions, or airborne pollutants, or Superfund sites and autism rates at larger scales. However, on a macro level, these types of studies have, so far, been unable to design around a feature of reality; the likelihood that things like Superfund sites or airborne pollution are situated in relative proximity to an urban center, and as such, autism diagnosis services. In effect, the argument that these observations are diagnostic only is the same; without a controlling factor for diagnostic availability, we can not assume that other parameters are actually responsible. And again, I have no doubt that this is a force that contributes to the findings of these studies.
At the end of the day, I’m just not satisfied with a God of the Gaps explanation; what we seem to be seeing is just too goddamned important to explain away with the spongy soft and ultimately unmeasurable forces of greater awareness et all. (The Fairytale, 20##).
Anyways, the other day pubmed alerted me to the publication of this interesting study:
BACKGROUND: Levels of brominated flame retardants are increasing in US populations, yet little data are available on body burdens of these and other persistent hormonally active agents (HAAs) in school-aged children. Exposures to such chemicals may affect a number of health outcomes related to development and reproductive function. OBJECTIVE: Determine the distribution of biomarkers of polybrominated diphenyl ethers (PBDEs), polychlorinated biphenyls (PCBs), and organo-chlorinated pesticides (OCPs), such as DDT/DDE, in children, and their variation by key descriptor variables. METHODS: Ethnically diverse cohorts of girls 6-8y old at baseline are being followed for growth and pubertal development in a multi-site, longitudinal study. Nearly 600 serum samples from the California and Ohio sites were analyzed for lipids, 36 PCB congeners, 11 PBDE congeners, and 9 OCPs. The biomarker distributions were examined and geometric means compared for selected analytes across categories of age, race, site, body mass index (BMI), parental education, maternal age at delivery, and breast feeding in adjusted models. RESULTS: Six PBDE congeners were detected among greater than 70% of samples, with BDE-47 having the highest concentration (median 42.2, range 4.9-855ng/g lipid). Girls in California had adjusted geometric mean (GM) PBDE levels significantly higher than girls in Ohio. Furthermore, Blacks had significantly higher adjusted GMs of all six PBDE congeners than Whites, and Hispanics had intermediate values. GMs tended to be lower among more obese girls, while other variables were not strongly associated. In contrast, GMs of the six PCB congeners most frequently detected were significantly lower among Blacks and Hispanics than Whites. PCBs and the three pesticides most frequently detected were also consistently lower among girls with high BMI, who were not breast-fed, whose mothers were younger, or whose care-givers (usually parents) were less educated. Girls in California had higher GMs than in Ohio for the pesticides and most PCB congeners, but the opposite for CB-99 and -118. CONCLUSIONS: Several of these potential HAAs were detected in nearly all of these young girls, some at relatively high levels, with variation by geographic location and other demographic factors that may reflect exposure pathways. The higher PBDE levels in California likely reflect differences in fire regulation and safety codes, with potential policy implications.
The environmental impact argument usually focuses on vaccines, or in some instances, similarly widespread environmental pollutants (i.e., mercury emissions); external forces which tend to operate more or less evenly across large geographic swaths, and also largely independent of things like culture or race. But with this paper we can observe the counter-intuitive opposite, chemicals that have achieved widespread distribution in society and the environment, seem to be bioaccumulating differentially according to factors such as geography, race, body type, and education levels. The paper here mentions fire regulation as a possible factor in state by state differences, but taking things a bit further, it can quickly be seen how socio-economic factors might play a role in why we might observe different levels of chemicals. It takes a lot of crazy chemistry to make a baby onesie not catch on fire, but at a high level, it involves dousing the material with a bunch of exotic chemicals. Politically correct or not the facts on the ground are that the well to do white woman has baby showers where she gets a bewildering array of freshly minted, ‘extra safe’ baby clothes more often than, say, the not so well to do Latina woman. We have already established a connection between having older parents and a diagnosis of autism, it would seem, there is also a correlation between having older parents and your bodies burden of these molecular mimics; and again, white women tend to have babies at later stages in life than their Black or Latina counterparts; especially the ones that happen to be residing near the trendy autism diagnosis hubs (i.e., the wealthier white women). The ability for these types of chemicals to cause a variety of difficult to predict developmental trajectories is too long, and terrifying to go into detail in this post; for purposes of this discussion, it is sufficient to understand that we have a growing body of evidence that endocrine disrupting compounds can have wide ranging effects; including epigenetic changes, changes in immune profiles, altered behaviors and neuroanatomical structures known to be abnormal in autism.
I found the finding of BDE-47 particularly intriguing, considering it was used as a primer for immunological response measurement by Ashwood, who found in vitro differences in immune responses in the autism population (an exaggerated innate immune response was observed).
Of course, this study does not present sufficient evidence for us to draw conclusions about the geographic distribution of autism rates in the two California studies above; but it should give us enough to pause before we take the comforting road out and assume that our observation are the result of diagnostic artifact alone; such assumptions feel good (except for the guilt), but ultimately require that we ignore our growing knowledge of how unpredictable endocrine disruptors affect the body, and how much more we have to learn.