Mercury is a ubiquitous environmental toxin. Exposure to all three of its forms, organic, inorganic, or elemental, can have adverse effects on the developing nervous system. Medical science has known of potentially grave effects of high dose mercury exposure since the
Mercury is a ubiquitous environmental toxin. Exposure to all three of its forms, organic, inorganic, or elemental, can have adverse effects on the developing nervous system. Medical science has known of potentially grave effects of high dose mercury exposure since the late 19th century. Only recently, however, have questions arisen regarding possible associations between mercury exposure and autism.
The debate over mercury and autism escalated quickly because of thimerosal, a synthetic form of organic mercury used as a preservative and antimicrobial agent in vaccines. Thimerosal has been an ingredient in vaccines and biologicals since the 1930s but, with increases in recommended childhood immunization doses, by the 1990s it became possible for a six month old infant to have been exposed to a cumulative dose of organic mercury that exceeded certain limits set by government health agencies. This, paired with the immense growth in numbers of children diagnosed with autism in the 1990s prompted many in and out of the autism community to wonder if there could be a connection.
The body of evidence gathered through epidemiologic research to date does not currently support a causal relationship between thimerosal in childhood vaccines and autism risk. However, it is very difficult for even the best epidemiologic study to rule out the existence of small susceptible subgroups of children with autism in whom thimerosal exposure may have played a causal role. Unfortunately, there are currently no means of identifying individuals with increased mercury susceptibility nor are there proven methods allowing researchers to separate individuals with autism into groups more or less likely to have different sets of causes.
The thimerosal question has highlighted a number of points whose further consideration should significantly advance autism research. First, although genes are believed to play a major role in autism, more attention needs to be paid to mechanisms where genes exert their influence by altering susceptibility to environmental exposures and mechanisms by which environmental exposures may alter gene expression. Second, there is a great need, when studying environmental exposures, to find ways of identifying highly susceptible individuals. And, third, because autism is a complex condition possibly having multiple causes, researchers need to find reliable ways to distinguish autism subgroups with distinct etiologies.
Autism Speaks plans to strongly support a multidisciplinary research agenda on environmental exposures and autism. We believe that projects acknowledging the role of gene-environment interaction and incorporating markers of exposure susceptibility and etiologic heterogeneity will be the most productive in the long-term. Given present knowledge, there is a fairly broad array of neurotoxic environmental exposures worthy of further study but, moving forward, the type and timing of exposures under investigation should continue to comport with emerging developments in autism neurobiology.
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