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Microplastics and neurotoxicity: could prenatal exposure to microplastics boost congenital enteric neuropathies?

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This review examined how microplastic neurotoxicity during fetal development could contribute to congenital enteric neuropathies, noting that microplastics can cross the placenta and accumulate in fetal organs, potentially disrupting neuronal migration in the gut. The authors proposed that prenatal microplastic exposure may be an underrecognized aggravating factor in disorders like Hirschsprung's disease and recommended reducing pregnant women's exposure as a preventive measure.

Microplastics (MPs) pollution represents an increasing worldwide problem and a real global challenge for human health, which also affects unborn children. Specifically, during their degradation, they can release a broad range of toxic and hormonally active agents, such as plasticizers. Thus, microplastics alone are pernicious, but they often also carry other harmful chemicals and even problematic bacteria on their surface and within their structure (heavy metals, pesticides, parabens, etc.), which amplifies their toxic potential. Due to their induction of oxidative damage, inflammation, mitochondrial apoptosis, and microbiota dysbiosis, and more, microplastics act as neurotoxic agents. Periods particularly sensitive to this neurotoxicity include fetal development and childhood, during which microplastics can negatively affect proper neuronal development. When expecting mothers are exposed, microplastics can cross the placenta barrier, reach the developing embryo, and accumulate in its organs. During fetal development, even minor interferences in neuronal migration can result in deficient neuronal innervation in the gut, potentially leading to congenital enteric neuropathy. Although an accurate estimation of human exposure is still pending, this may produce serious intestinal motility disorders and compromise the long-term quality of life of newborns. In this review, we analyze how microplastic neurotoxicity could be an aggravating factor in the development of congenital enteric aganglionosis and, consequently, postnatal motility disorders. Finally, we propose reducing pregnant women’s exposure to microplastics as an important preventive measure to protect the fetus from neurotoxicity.

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