Nanotechnology has been applied in consumer products and commercial applications, showing a significant impact on almost all industries and all areas of society. Significant evidence indicates that manufactured nanomaterials and combustion-derived nanomaterials elicit toxicity in humans exposed to these nanomaterials. The interaction of the engineered nanomaterials with the nervous system has received much attention in the nanotoxicology field. In this review, the biological effects of metal, metal oxide, and carbon-based nanomaterials on the nervous system are discussed from both in vitro and in vivo studies. The translocation of the nanoparticles through the blood-brain barrier or nose to brain via the olfactory bulb route, oxidative stress, and inflammatory mechanisms of nanomaterials are also reviewed.

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Alumina nanoparticles (AlNP) have been shown to accumulate in organs and penetrate biological barriers which lead to toxic effects in many organ systems. However, it is not known whether AlNP exposure to female mice during pregnancy can affect the development of the central nervous system or induce neurodevelopmental toxicity in the offspring. The present study aims to examine the effect of AlNP on neurodevelopment and associated underlying mechanism. ICR strain adult female mice were randomly divided into four groups, which were treated with normal saline (control), 10 μm particle size of alumina (bulk-Al), and 50 and 13 nm AlNP during entire pregnancy period. Aluminum contents in the hippocampus of newborns were measured and neurodevelopmental behaviors were tracked in the offspring from birth to 1 month of age. Furthermore, oxidative stress and neurotransmitter levels were measured in the cerebral cortex of the adolescents. Our results showed that aluminum contents in the hippocampus of newborns in AlNP-treated groups were significantly higher than those in bulk-Al and controls. Moreover, the offspring delivered by AlNP-treated female mice displayed stunted neurodevelopmental behaviors. Finally, the offspring of AlNP-treated mice demonstrated significantly increased anxiety-like behavior with impaired learning and memory performance at 1 month of age. The underlying mechanism could be related to increased oxidative stress and decreased neurotransmitter levels in the cerebral cortex. We therefore conclude that AlNP exposure of female mice during pregnancy can induce neurodevelopmental toxicity in offspring.

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