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Can exposure to micro- and nanoplastics disrupt neural crest development? Evidence and a testable model for MNP-associated environmental neurocristopathies
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This review paper summarizes existing research on whether micro- and nanoplastics could affect "neural crest cells," special embryonic cells that form facial, heart, and nerve structures. It discusses evidence from chick embryo studies showing links between plastic particles and cell abnormalities, but states this remains an unproven framework, not an established cause-and-effect relationship in humans.
Micro- and nanoplastics (MNPs) have been detected in human placenta, amniotic fluid, umbilical cord blood, and fetal tissues, raising concern that maternal exposure may reach the embryonic milieu during sensitive developmental windows. Neural crest cells (NCCs) are migratory, multipotent embryonic cells that contribute to craniofacial and cardiac structures, the peripheral nervous system and its enteric division, and melanocytes. Whether disruption of this lineage could connect gestational MNP exposure to developmental phenotypes across organs has not been evaluated within an integrated developmental framework. This review traces evidence from maternal uptake and transbarrier transport to potential embryonic exposure, and then evaluates direct and indirect mechanisms by which MNPs may perturb NCC development. Direct effects may involve particle contact or uptake, lysosomal and autophagic dysfunction, mitochondrial injury, oxidative stress, cytoskeletal remodeling, and impaired survival or delamination, with downstream consequences for migration and target-site colonization. Indirect effects may arise from particle uptake by macrophages at the maternal-fetal interface or in embryonic tissues, leading to immunometabolic reprogramming and altered inflammatory, chemotactic, and extracellular-matrix cues. Chick embryo studies currently provide the most direct evidence, linking particle-associated signals and NCC retention in the dorsal neural tube with deficient pharyngeal arch colonization, regional cell death, and craniofacial and cardiovascular abnormalities. Embryo, organoid, and maternal-exposure models provide additional, but mostly indirect, evidence involving neural tube morphogenesis, the enteric nervous system, and pigment lineages. Across this literature, tissue-level particle detection does not establish intracellular NCC exposure, and organ phenotypes do not establish lineage-specific causation. Human-relevant internal dosimetry and direct comparisons between NCCs and non-NCC lineages remain major gaps. We propose MNP-associated environmental neurocristopathies as a testable framework in which NCC perturbation may represent a shared upstream event in a subset of cross-organ developmental phenotypes. This concept should not yet be interpreted as an established causal relationship in humans. Validation will require intact-particle localization, dynamic NCC lineage tracing, non-NCC controls, human-relevant dose-response analysis, and mechanistic rescue experiments.
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