Nanopolystyrene (NPs), a common byproduct of plastic degradation, and bisphenol A (BPA), an industrial chemical widely used in the production of polycarbonate plastics and epoxy resins, can co-exist in the environment as NPs-carried BPA (NPs-BPA) complexes. This is especially relevant in the ocean, where the breakdown of plastic waste generates NPs that adsorb BPA and other organic pollutants present in seawater. As a result, such complexes may become widely distributed along coastal areas and throughout marine ecosystems, raising concern about their effects on ecological health. Despite this, most studies have examined NPs or BPA separately, and few have investigated the toxicity of NPs-BPA, particularly its effects on neurodevelopment. To address this gap, we investigated the neurotoxic effects of NPs-BPA using both in vitro and in vivo models. NPs-BPA exposure caused pronounced amoeboid changes in primary microglia, an effect not observed with NPs or BPA alone. In mice, maternal NPs-BPA exposure similarly increased blood-brain barrier permeability and raised the number of microglia and astrocytes in the hippocampus and cortex. These changes were accompanied by amoeboid microglial transformation and reactive astrogliosis. At the mechanistic level, NPs-BPA exposure activated NF-κB signaling, which led to a marked increase in pro-inflammatory cytokines. Furthermore, adult offspring maternally exposed to NPs-BPA showed significant deficits in recognition and spatial memory, along with increased depressive-like behavior. Collectively, these findings suggest that maternal NPs-BPA exposure disrupts normal brain development and triggers lasting neuroinflammation, raising concerns about the neurodevelopmental risks of nanoplastic-adsorbed endocrine disruptors amid ongoing marine plastic pollution.

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