This study reveals that iatrogenic exposure to acute dose of aluminum occurs in newborns and in infants at greater amounts than through breastfeeding. The estimated amount of Al available after absorption from breastfeeding contrasts with the non-enteral high adjuvant-Al doses in serial vaccination schedules. Environmental aluminum through breastfeeding, as a consequence of dietary intake of mothers, encounters several physiological barriers (maternal gut → mammary-gland → infant gut). These barriers are absent in non-enteral adjuvant-Al exposure; the high acute doses of adjuvant-Al (250 to 1,500 μg) constitute a neurological challenge to neonates and are never encountered by young humans even when exposed to high Al infant formulas.

It is often noted that infants are exposed to Al in breast milk (40 μg/l) and in infant formulas at levels of 225 μg/l and that this approaches Al concentrations of some vaccines (Keith et al., 2002; Offit and Jew, 2003). Although the half-life of enterally absorbed Al elimination from the body is short (approximately 24 h), the same cannot be assumed for adjuvant-Al; because of “depot effect” a longer elimination is one of the very functions of adjuvants. Indeed a tightness of bonding between the aluminum adjuvant and the antigen is a desired feature that can be used to predict immunogenicity of vaccines (Egan et al., 2009).

The HB vaccine has both Hg and Al at lowest concentration. However, given the special characteristics of the first dose, the variability in dose can be substantial. Recently, we showed that on a body mass basis neonates can have a wide variation in the dose of thimerosal-Hg (from 2.1 to 21.1 μg/kg) depending on the vaccine manufacturer (Dórea et al., 2009); this amplitude in variability is extended to aluminum. Therefore, Keith et al. (2002)'s model of first-year body burden of Al (from vaccines and feeding) is insufficient to show low risk of brain-Al derived from acute high exposure to adjuvant-Al in vaccinated neonates.

Furthermore, the 1-day neonate has anatomical and functional differences crucial for toxicokinetis and toxicodynamics of neuro-toxic metals: an immature renal system and a developing blood-brain barrier; these and other modifying circumstances can be aggravated by shorter gestational age, pre-maturity, or low birth weight (Dórea et al., 2009). In addition, neonates (<24 h and >2,000 g) may receive a dose of adjuvant-Al (250 μg) in HB vaccine that is equivalent to a >6 month exposure to absorbed Al in breast milk. Therefore, safety assumptions derived from feeding (high quantities) of aluminum to experimental animals may not be an appropriate proxy for non-enteral exposure (frequently in combination with thimerosal-Hg) in neonates as it is currently accepted (Offit and Jew, 2003).

In relation to vaccine adverse events, the track record established in the past 70 years is a convincing argument for the safety of adjuvant-Al (Offit and Jew, 2003) for non-susceptible individuals. However, neuro-behavioral, cognitive and learning impairment effects of small doses of toxic metals took place in the last 40 years; neuro-developmental studies of toxic metals as preservatives and adjuvants in vaccines are starting to appear (Marques et al., 2009). A report by Gallagher and Goodman (2008) suggested an association of HB vaccines and a higher risk of receiving special education services. Although HB vaccines have aluminum hydroxide as adjuvant (Baylor et al., 2002) the paper by Gallagher and Goodman (2008) draws attention only to thimerosal-Hg.

Mild post-vaccine symptoms in young infants, especially neonates, are non-specific and considered tolerable; rare (neurologic) adverse effects are unlikely to occur as a result of adjuvant-Al per se or in combination with thimerosal-Hg. As a descriptive study it is only possible to make clear that future research is needed to ascertain neuro-toxic effects and risks of non-enteral binary exposure to preservatives and adjuvants in vaccines destined for young infants. To date, we have no clue as to the effects of combined ethylmercury and aluminum dose unlikely to be encountered through environmental exposure in breastfed (or even formula fed babies) and as such do not understand its low-dose effect on brain function regarding cognitive and learning impairments occurring later.