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Human Health Effects of Environmental Micro and Nanoplastic (MNP) Exposure: Linking Hippocampal Memory and Neurodegenerative Mechanisms
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This planned study will compare memory test scores between plastic factory workers with high and low plastic particle exposure, and will expose lab-grown human brain cells to microplastics and nanoplastics to measure stress and damage. Researchers expect highly exposed workers to show weaker memory and exposed cells to show signs of stress and impaired function.
Microplastics and nanoplastics (MNPs) have become a serious matter because of their widespread prevalence in the environment and accumulation in human tissues, including the brain. Animal studies indicated that MNP exposure impaired hippocampal learning and memory through oxidative stress, neuroinflammation, mitochondrial dysfunction, and blood-brain barrier (BBB) disruption, but evidence in humans remains inadequate. This proposed study will investigate the relationship among MNP exposure, hippocampal memory, and potential neurodegenerative mechanisms using complementary behavioral and cellular approaches. A cross-sectional behavioral study will compare hippocampus-dependent memory between plastic factory workers with high occupational MNP exposure and matched workers with lower exposure using the Mnemonic Similarity Task (MST). The Montreal Cognitive Assessment (MoCA) will be used as a measure of cognitive function. A human induced pluripotent stem cell (iPSC)-derived BBB model containing brain microvascular endothelial cells, astrocytes, pericytes, and hippocampal neurons will be exposed to MNPs to evaluate oxidative stress, mitochondrial dysfunction, neuroinflammation, synaptic impairment, apoptosis, and neuronal viability. The behavioral arm is expected to determine whether occupational exposure is associated with differences in hippocampus-dependent memory, while the cell culture arm is expected to characterize cellular responses to controlled MNP exposure. We expect highly exposed workers to demonstrate lower memory performance than matched controls. We also expect MNP-treated cell cultures to show changes consistent with cellular stress, impaired neuronal function, and neurodegenerative processes. Because the two study arms use different samples, their findings will be interpreted as complementary evidence rather than as a direct individual-level relationship between cellular changes and memory performance. By combining human behavioral assessment with evidence from human-derived cell culture models, this study aims to reduce the gap between existing animal research and human health. The findings may contribute to understanding the potential neurological effects of chronic MNP exposure and provide a basis for future studies of exposure reduction and neurological health.
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