Toxic Overload: Assessing the Role of Mercury in Autism

By Boyd E. Haley
Issue 115, November - December 2002

From 1996 to 1997, J. Curtis Pendergrass, PhD, did some experiments in my research laboratory at the University of Kentucky that confirmed the toxicity of thimerosal in vaccines. The results appeared on our website (www.altcorp.com), where they attracted the attention of some parents of autistic children.

These parents informed me that increased mandatory vaccination of infants was, in their opinion, the cause of an apparent epidemic of autism. This was the first time I had heard of this situation. The rationale for considering vaccinations as the cause of their children's problems seemed sensible and worth an investigation. I would like to state here that I am a very strong supporter of the national vaccine program, and that nothing in this article should be construed to imply that parents should avoid getting their children vaccinated. But I do recommend avoiding vaccines that contain thimerosal.

My laboratory was well experienced in mercury research. We had earlier demonstrated that mercury, when exposed to normal human brain tissue homogenates, is capable of causing many of the same biochemical aberrancies found in Alzheimer's diseased (AD) brains.1-4 Also, rats exposed to mercury vapor show the same major protein aberrancy as AD brains. Specifically, the rapid inactivation of important brain enzymes occurs following the addition of low levels of mercury or exposure to mercury vapor, and these same enzymes are significantly inhibited in AD brains.5 Also, mercury exposure to neurons in culture by other researchers, at a concentration lower than that found in many human brains, has now been shown to produce three of the widely accepted pathological diagnostic hallmarks of AD.6,7

Therefore, we hypothesized that exposure to mercury is involved in the etiology of AD, or at least would exacerbate this disease. We also proposed that other heavy metals, such as lead and cadmium, which act synergistically to enhance the toxicity of mercury, could be involved. Additionally, we proposed that exposure to organic-mercury compounds like methyl mercury from fish and ethyl mercury from thimerosal would also enhance the toxicity of any exposure to mercury. The early work of Dr. Pendergrass confirmed this with pure thimerosal, with some interesting additional observations. First, in human brain samples the exposure to mercury dramatically reduced the viability of a major brain protein called tubulin, but had little if any effect on another major protein, actin. Both tubulin and actin are critically important for the growth of dendrites or maintenance of axon structures of neurons. Exposing neurons to mercury rapidly results in the stripping of tubulin from the axon structure, leaving bare neurofibrils that form the tangles that are the diagnostic hallmark of AD. Thimerosal, like mercury, also rapidly reduces the viability of tubulin; in addition, however, it abolishes the viability of actin. This likely represents a major difference in the mechanism of mercury versus organic-mercury (more neurotoxic) toxicity. However, both mercury and organic-mercury inhibit tubulin viability and would work in concert to damage neurons of the central nervous system.

We therefore decided to investigate vaccines with and without thimerosal present as a preservative, using human brain tissues. To date the data have been very consistent: the toxicity of the vaccines is primarily dependent on the presence of thimerosal and, in my opinion, would be classified as severely toxic to numerous brain proteins. In the spring of 2001 these data were presented to the Institute of Medicine Immunization Safety Review Committee, which concluded its analysis by suggesting that thimerosal involvement in autism was a plausible hypothesis. Since then I have formed a collaboration with one of my colleagues, Mark Lovell, PhD, who uses cultured neurons in some of his experiments. Using his cultured neuron system, we studied the extent of neurotoxicity of pure thimerosal and of vaccines with and without thimerosal present. The experiments were done as follows: Neurons were grown in culture for 24 hours. Then pure thimerosal or vaccines were added to test cultures. The death of neurons was observed for the next 24 hours and compared to the death of neurons in the absence of toxicant.

The results were almost identical to the results observed with brain tissues: vaccines with thimerosal present were much more toxic than thimerosal-free vaccines. Pure thimerosal was toxic at the low nanomolar level--an extremely low concentration, about 10,000 times less than the thimerosal concentration found in most vaccines. These results leave little doubt about thimerosal being the toxic agent in the vaccines. However, many vaccines contain aluminum ions that have neurotoxic properties, and aluminum was once considered a factor in AD etiology. So we tested aluminum in the same system.

Aluminum is not nearly as toxic to neurons in culture as is thimerosal. However, we had earlier observed with mercury that the presence of other metals would enhance toxicity. Experiments were done to determine if aluminum would increase the toxicity of very low levels of thimerosal. The results were unequivocal: the presence of aluminum dramatically increased the rate of neuronal death caused by thimerosal. Therefore, the aluminum and thimerosal combination found in vaccines produces a toxic mixture that cannot be compared to situations where thimerosal alone is the toxic exposure.