International Meeting for Autism Research (London, May 15-17, 2008): LINKING TOXICOLOGY LITERATURE TO AUTISM RESEARCH: A BIBLIOMETRIC CONTRIBUTION TO A TRANSLATIONAL RESEARCH CHALLENGE

LINKING TOXICOLOGY LITERATURE TO AUTISM RESEARCH: A BIBLIOMETRIC CONTRIBUTION TO A TRANSLATIONAL RESEARCH CHALLENGE

Friday, May 16, 2008
Champagne Terrace/Bordeaux (Novotel London West)
10:30 AM
M. Herbert , Neurology, Mass Gen Hosp/Harvard Med School, Charlestown, MA
A. P. Ringer , School of Public Health, University of California, Berkeley, Berkeley, CA
M. A. Corrales , US Environmental Protection Agency, Washington, DC
Background: While autism spectrum disorders likely arise from gene-environment interactions, environmental risk factors are greatly underrepresented in ASD literature, with the possible exception of articles on thimerosal and vaccines.

Objectives: To quantify the share of autism research literature devoted to various types of chemical substances, such as endogenous biological substances, exogenous potential risk factors, and medications. Furthermore, to present a tabular and graphical overview of chemicals in toxicology or epidemiology literature that have been associated with biological effects relevant to autism.

Methods: 1) All autism literature indexed in PubMed was searched for publications relating autism to chemical substances, and substances were classified as medications, pollutants, or other, and then subclassified. 2) Literature in toxicology and epidemiology potentially relevant to autism was identified, based on a) risk factors for behavioral or cognitive symptoms of autism, and b) risk factors for physiological or molecular features of autism.

Results: Most autism literature that focuses on the molecular level addresses pharmaceuticals or genetics. There is almost no investigation of potential chemical risk factors beyond thimerosal and vaccines. Conversely, although substantial toxicology and epidemiology literature identifies chemical risk factors for features found in autism, (e.g. altered monoamine levels, PPI deficit, hyperactivity, anxiety) almost none of this literature is explicitly focused on autism. For example, since the 1980s, endosulfan has been known to affect serotonin, GABA receptors, and dopamine, but it has been investigated in connection with autism only very recently in one small study. Similar observations relate to the immune system.

Conclusions: Translational linkage of knowledge about exogenous substances that may cause or contribute to autism-pertinent endpoints will require expansion of substance-related research in autism guided by existing literatures in toxicology and epidemiology, as well as inclusion of more specifically autism-related endpoints in toxicology and epidemiology.

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