There have been several diaries on this topic already today, and it is clear that people have their minds made up. This diary is not expected to change anyone's mind at this point, merely to point out a few things that were missed in the discussions.
Prior to 2000, many childhood vaccines contained 25 micrograms of mercury in the form of the preservative thiomersol. For an infant of 10 lbs this represents 50X the EPA's daily limit for mercury. This is not a negligible amount, as is often asserted.
Mercury is a neurotoxin and the EPA limits exist for a reason. It is true that the limits were set using methyl mercury, and there are studies that demonstrate methyl mercury is more dangerous than ethyl and visa versa - scientists always cite studies that support their own conclusions, and there are many areas that do not achieve consensus.
But if you begin looking up some of the more upbeat studies, and looking at the affiliation of their authors as I did 7 years ago when I was investigating this, you will find something startling... they are nearly all sponsored by large pharmaceutical companies. This calls their objectivity into question. I know you'll want me to cite examples, but I am not going to call out scientists in this diary. I urge you, the reader, to look up a study on thiomersol, google the principle investigator, and read the names of his or her sponsors.
To address the claims that there is no evidence of links between thiomersol and autism, and to refute cries that any such studies are "junk science", please read on....
Below are abstracts of several recent studies detailing possible links between autism and the preservative thiomersol, which was widely used in childhood vaccines until its phase out (in the US) began in 2000. These are not quacks, people, as those so intent on being mainstream would assert. Please read these... they are just a drop in the bucket. There are dozens of studies reaching similar conclusion, suggesting that the issue is far from dead.
Neurotoxic Effects of Postnatal Thimerosal are Mouse Strain Dependant, Mady Hornig, MD, PhD, Columbia University
The developing brain is uniquely susceptible to the neurotoxic hazard posed by mercurials. Host differences in maturation, metabolism, nutrition, sex, and autoimmunity influence outcomes. How population-based variability affects the safety of the ethylmercury-containing vaccine preservative, thimerosal, is unknown. Reported increases in the prevalence of autism, a highly heritable neuropsychiatric condition, are intensifying public focus on environmental exposures such as thimerosal. Immune profiles and family history in autism are frequently consistent with autoimmunity. We hypothesized that autoimmune propensity influences outcomes in mice following thimerosal challenges that mimic routine childhood immunizations. Autoimmune disease-sensitive SJL J mice showed growth delay; reduced locomotion; exaggerated response to novelty; and densely packed, hyperchromic hippocampal neurons with altered glutamate receptors and transporters. Strains resistant to autoimmunity, C57BL 6J and BALB /cJ, were not susceptible. These findings implicate genetic influences and provide a model for investigating thimerosal-related neurotoxicity.
Influence of Thimerosal on Phospholipid Methylation in Lymphoblasts, Richard C. Deth, PhD, Northeastern University
It has been proposed that the ethylmercury-containing vaccine preservative thimerosal may contribute to autism, and our earlier studies demonstrated the ability of thimerosal to inhibit methionine synthase-dependent phospholipid methylation (PLM) in cultured human neuroblastoma cells. To investigate the possible contribution of this action of thimerosal to autism, we compared its ability to inhibit PLM measured with [ 14C]-formate, which labels the cellular pool of 5-methyltetrahydrofolate and therefore selectively measures methionine synthase-dependent PLM. PLM was measured in immortalized lymphoblasts from same-sex siblings who were discordant for autism, as obtained from the Autism Genetic Resource Exchange (AGRE). Basal PLM was not significantly different between lymphoblasts from autistic and non-autistic siblings. Thimerosal (100 nM) did not significantly affect PLM in lymphoblasts from non-autistic siblings, but significantly reduced PLM in lymphoblasts from autistic subjects (p < 0.05). Analysis of MTHFR and transcobalamin polymorphisms in a sample of 18 sib-pairs did not reveal a significant genetic pattern of association with autism. Preliminary studies indicate a trend for autistic subjects to exhibit higher rates of mitochondrial oxygen consumption. Taken together, our results to date provide evidence that methionine synthase-dependent methylation is more sensitive to thimerosal in cells from autistic children, consistent with a potential role of thimerosal in causing autism.
Mechanisms of Thimerosal Toxicity, Jill James, PhD, University of Arkansas
Children with autism have increased vulnerability to pro-oxidant exposures such as ethyl mercury in Thimerosal as a result of increased frequency of genetic polymorphisms that reduce the synthesis of cysteine and glutathione, the major metabolites involved in the detoxification and excretion of mercury. Dr. James will extend preliminary data on plasma levels in children with autism by measuring intracellular levels of thiol metabolites and selected enzyme activities in lymphoblastoid cell lines derived from children with autism and unrelated control children. Iintracellular metabolic profiles will be correlated with genetic profiles of specific polymorphisms that negatively affect methionine, cysteine, and glutathione synthesis. These experiments will allow us to determine whether intracellular metabolites and related enzyme activities are abnormal in children with autism compared to controls and whether the intracellular metabolic profile reflects the profile previously observed in plasma (see preliminary data). If the observed metabolic profiles are associated with increased frequency of polymorphisms in the same metabolic pathway, it will provide support for our hypothesis that children with autism have a genetic vulnerability to heavy metal toxicity. In addition, we will expose lymphoblastoid cells derived from autistic children and unrelated controls to increasing doses of thimerosal (nanomolar to micromolar levels) and define individual dose-response curves in terms of cytotoxicity, glutathione depletion, and DNA damage. In addition, we will determine whether subtoxic doses of ethylmercury in the presence of subtoxic levels of an additional pro-oxidant heavy metal such as lead, will interact synergistically to reach a threshold of toxicity. If lymphocytes from autistic children exhibit increased sensitivity to Thimerosal toxicity in culture compared to cells from normal children, the dose-response curve should be shifted to the left. An interaction between subtoxic doses of thimerosal and other heavy metals in autistic children, but not normal children, would further support the hypothesis that autistic children have an increased vulnerability to pro-oxidant exposures. In addition, we will be able to determine whether an increase in thimerosal sensitivity is associated with abnormal genetic and metabolic profiles and glutathione depletion. If confirmed, these results would support for the hypothesis that children with autism have an increased sensitivity to thimerosal as a result of reduced intracellular levels of cysteine and glutathione, and consequently, reduced capacity to detoxify and excrete ethylmercury.
This issue is not dead as a research topic and a court ruling is not a scientific conclusion. Today's ruling was simply about liability. Period.