Although milk based infant formulas generally contain less manganese than soy based formulas, the concentration is still many more times the manganese of breast milk. The following report from the U.S. EPA gives a good overview of why infants are more susceptible to manganese toxicity than adults. It also addresses the issue of the type of manganese used in formulas and the manganese content of the water used to prepare the formula. These quotes were taken from the U.S. Environmental Protection Agency; Integrated Risk Information System website, from the section entitled: I.A.3. Uncertainty and Modifying Factors (Oral RfD).

“Third, although toxicity has not been demonstrated, there is concern for infants fed formula that typically has a much higher concentration of manganese than does human milk. If powdered formula is made with drinking water, the manganese in the water would represent an additional source of intake. Finally, there is some evidence that neonates absorb more manganese from the gastrointestinal tract, that neonates are less able to excrete absorbed manganese, and that in the neonate the absorbed manganese more easily passes the blood-brain barrier. These findings may be related to the fact that manganese in formula is in a different ionic form and a different physical state than in human milk. These considerations concerning increased exposure in an important population group, in addition to the likelihood that any adverse neurological effects of manganese are likely to be irreversible and not manifested for many years after exposure, warrant caution until more definitive data are available.”

In another part of this same section it says:

“An additional concern for infants has been expressed because of the often high levels of manganese in infant formulas, particularly compared with breast milk. Also, manganese in human milk is in the trivalent form bound to lactoferrin, the major iron-binding protein. Lactoferrin receptors are located in the brush border membranes of epithelial cells throughout the length of the small intestine, thus allowing for regulation of the uptake of manganese. In infant formulas, however, because manganese is in the divalent state, absorption through the GI tract cannot be regulated by lactoferrin receptors. Collipp et al. (1983) found that hair manganese levels in newborn infants increased significantly from birth (0.19 ug/g) to 6 weeks of age (0.865 ug/g) and 4 months of age (0.685 ug/g) when the infants were given formula, but that the increase was not significant in babies who were breast- fed (0.330 ug/g at 4 months). While human breast milk is relatively low in manganese (7-15 ug/L), levels in infant formulas are much higher (50-300 ug/L). It was further reported in this study that the level of manganese in the hair of learning-disabled children (0.434 ug/g) was significantly increased in comparison with that of normal children (0.268 ug/g). Other investigators also have reported an association between elevated levels of manganese in hair and learning disabilities in children (Barlow and Kapel, 1979; Pihl and Parkes, 1977). Although no causal relationship has been determined for learning disabilities and manganese intake, further research in this area is warranted. High levels of manganese in infant formulas may be of concern because of the increased absorption and retention of manganese that has been reported in neonatal animals (Lonnerdal et al., 1987). Also, manganese has been shown to cross the blood-brain barrier, with the rate of penetration in animal experiments being 4 times higher in neonates than in adults (Mena, 1974).”