TLDR: The brain is useful in cleaning vaccine mercury out of the blood.

The large difference in the blood Hg half-life compared to the brain half-life for the thimerosal-exposed infants (6.9 days vs 24 days) indicates that blood Hg may not be a good indicator of risk of adverse effects on the brain, particularly under conditions of rapidly changing blood levels such as those observed following vaccinations. The blood concentrations of the thimerosal-exposed infants in the current study are within the range of those reported for human infants following vaccination (Stajich et al 2000).

Data from the current study predicts that while little accumulation of Hg in the blood occurs over time with repeated vaccinations, accumulation of Hg in the brain of infants will occur. Thus, conclusion regarding the safety of thimerosl drawn from blood Hg clearance data in human infants receiving vaccines may not be valid, given the significantly slower half- life of Hg in the brain as observed in the infant macaques.

There was a much higher proportion of inorganic Hg in the brain of thimerosal infants than MeHg infants (up to 71% vs. 10%). Absolute inorganic Hg concentrations in the brains of the thimerosal-exposed infants were approximately twice that of the MeHg infants. Interestingly, the inorganic fraction in the kidneys of the same cohort of infants was also significantly higher following i.m. thimerosal than oral MeHg exposure (0.71±0.04 vs. 0.40±0.03). This suggest that the dealkylation of ethylmercury is much more extensive than that of MeHg.

Previous reports have indicated that the dealkylation of mercury is a detoxification process that helps to protect the CNS (Magos et al. 1985; Magos 2003). These reports are largely based on histology and histochemistry studies of adult rodents exposed to mercury for a short period of time.

The results of these studies indicated that damage to the cerebellum was only observed in MeHg treated animals who had much lower levels of inorganic mercury in the brain than animals comparably treated with ethylmercury. Moreover, the results did not indicate the presence of inorganic mercury deposits in the area where the cerebellar damage was localized (granular layer).

In contrast, previous studies of adult M. fascicularis monkeys exposed chronically to MeHg have indicated that demethylation of mercury occurs in the brain over a long period of time following MeHg exposure and that this is not a detoxification process (Vahter et al. 1994, 1995; Charleston et al. 1994, 1995, 1996).

Results from these studies indicated higher inorganic Hg concentrations in the brain 6 months after MeHg exposure had ended while organic Hg had cleared from the brain. The estimated half-life of organic Hg in the brain of these adult monkeys was consistent across various brain regions at approximately 37days (similar to the brain half-life in the present infant monkeys).
The estimated half-life of inorganic Hg in the brain in the same adult cohort varied greatly across some regions of the brain, from 227 days to 540 days. In other regions, the concentrations of inorganic Hg remained the same (thalamus) or doubled (pituitary) 6 months after exposure to MeHg had ended (Vahter et al. 1994, 1995).

Stereologic and autometallographic studies on the brains of these adult monkeys indicated that the persistence of inorganic Hg in the brain was associated with a significant increase in the number of microglia in the brain, while the number of astrocytes declined. Notably, these effects were observed 6 months after exposure to methymercury ended, when inorganic Hg concentrations were at their highest levels, or in animals solely exposed to inorganic Hg (Charleston et al. 1994, 1995, 1996).

The effects in the adult macaques were associated with brain inorganic Hg levels approximately 5 times higher than those observed in the present group of infant macaques. The longer-term effects (greater than 6 months) of inorganic Hg in the brain have not been examined.

In addition, whether similar effects are observed at lower levels in the developing brain is not known. It is important to note that a recent publication has demonstrated “an active neuroinflammatory process” in brains of autistic patients, including a marked activation of microglia (Vargas et al. 2005).