I have recently reformulated the definition of aluminium’s body burden placing it into the context of what I have called aluminium’s exposome [13]. https://doi.org/10.1038/jes.2009.64, Environmental Research Relationship between tightness of binding and immunogenicity in an aluminum-containing adjuvant-adsorbed hepatitis B vaccine.
Everyone is exposed to low levels of aluminum from food, air, and water. Although vaccine safety is constantly reaffirmed in regard to its immunogenicity and rare adverse events, it is assumed that low doses of preservative (thimerosal) and adjuvant (aluminum salts) have the same innocuous effects across the large spectrum of those vaccinated — adults, children, infants, newborns, and unborn fetuses — and for the ever-increasing number of them given to young children. Current immunization schedules with vaccines containing aluminum (as adjuvant) are given to infants, but thimerosal (as preservative) is found mostly in vaccines used in non-industrialized countries. Pragmatic vaccine safety needs to embrace conventional toxicology, addressing especial characteristics of unborn fetuses, neonates and infants exposed to low levels of aluminum, and ethylmercury traditionally considered innocuous to the central nervous system. The potency with which aluminium acts as an adjuvant and additionally as an antigen is testimony to its potential role in autoimmunity and specifically aluminium-related conditions such as multiple sclerosis [10].

A report by Gallagher and Goodman (2008) suggested an association of HB vaccines and a higher risk of receiving special education services. In the meantime, to ensure continued support, we are displaying the site without styles Correspondence to The research protocol of the original study was approved by the ethics committee of studies for humans of the Universidade Federal de Rondonia and details appeared elsewhere (Marques et al., 2007a). The likely principal antagonist in all such events is Al3+ (aq) and its mechanism of action will involve numbers of different agents or intermediates. At present, because of the universal coverage of vaccines, the child population can be exposed to a combination of Hg and Al at very early ages. In this regard, aluminum-adsorbed vaccines caused a transient rise in brain tissue of mice (Redhead et al., 1992).

There are simply myriad opportunities for aluminium to exert neurotoxicity and when one considers that Al3+ is an effective substituent and, often, potent antagonist for Mg2+ then one begins to wonder how neuronal biochemistry persists in the face of an attack by aluminium [6]. In neither of these cases is aluminium necessarily the cause of the disease, but to discount its likely role in the etiology of disease is to significantly misunderstand the neurotoxicity of aluminium. For example, aluminium sinks such as the extracellular senile plaques of Aβ42 and the intracellular chromatin of neuronal nuclei are both likely targets of aluminium-driven oxidative damage. Google Scholar.
This work was supported by United Nations Educational, Scientific and Cultural Organization — UNESCO, Ministério da Saúde do Brasil (SC27824/2005/914BRA2000 Decit PRODOC) and the National Research Council of Brazil-CNPq (PNOPG project-55.0882/01-4; PPG7, project-556985/2005-2). Virtually all food, water, air, and soil contain some aluminum. The Hg concentration of the doses delivered through vaccines was respectively 12.5 μg/0. Aluminium-adjuvanted vaccines transiently increase aluminium levels in murine brain tissue. Breast-fed infants ingest about 7 milligrams, formula-fed infants ingest about 38 milligrams, and infants who are fed soy formula ingest almost 117 … While aluminium’s neurotoxicity is incontrovertible, it is much more difficult to understand the risk that this neurotoxin poses to human health. The American Academy of Pediatrics' revision of 1996 discussed aluminum in infant feeding but did not address the additional higher and acute exposure to aluminum in commonly used infants' vaccines . This suggested that approximately 70% of the brain donors (aged 70–103) were potentially combating some form of aluminium-related neurodegenerative condition. Studies show that toxic metals contribute to brain diseases by producing oxidative stress and aluminum is one of the worst offenders. The latter are not expected to achieve levels responsible for overt toxicity, such as were found for dialysis encephalopathy [11], but do they approach or exceed those required for covert toxicity, including exacerbation of an ongoing disease state? The authors have no relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript. Marques R.C., Bernardi J.V., Dórea J.G., Bastos W.R., and Malm O.