Aluminum bone toxicity in infants may be promoted by iron deficiency.

Aluminum has adverse effects on human health. Aluminum is poorly transported from the gastrointestinal tract, but if the load is high, a significant level of aluminum may be absorbed. There are two main sources of aluminum in infants - adapted formulas (when an infant is predominantly fed with it), and vaccines. After aluminum enters the circulation, it binds to transferrin and remains mainly in the skeleton for a longer period of time. Transferrin receptor 1 (TfR1) is highly expressed on osteoblast-like cells whereas the number of TfR1 may additionally rise in case of iron deficiency. Since iron deficiency can induce the additional expression of TfR1, a larger quantities of aluminum may be uptaken by osteoblasts and consequently aluminum may decrease the number of osteoblasts and lead peak bone mass (PBM) closer to the osteoporotic threshold. Iron deficiency may potentiate aluminum-induced toxicity to bones. Aluminum burden in infants has always been considered as harmless whereas a potential increased toxicity of aluminum in high-sensitive infants caused by iron deficiency has not been evaluated.