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Micro- and nanoplastic exposure as an emerging risk factor for depressive-like phenotypes across species: a systematic review
Summary
This review of animal and early human studies found that exposure to microplastics and nanoplastics (tiny plastic particles that can travel through the body and reach the brain) is consistently linked to depression-like symptoms, likely by triggering brain inflammation and cell damage. While the human evidence is still preliminary, the pattern across multiple animal studies suggests these ubiquitous plastic particles—found in food, water, and air—could be an overlooked contributor to mental health problems. More rigorous, long-term human research is needed to confirm this link and understand what it means for everyday exposure.
The pervasive environmental presence of micro- and nanoplastics (MNPs), combined with their ability to cross biological barriers and accumulate in the brain, has raised significant concerns regarding their neurotoxic potential. While neuroinflammatory and neurodegenerative effects are increasingly documented, a focused synthesis of their impact on depression-relevant behaviors is lacking. This systematic review evaluates the evidence linking MNPs exposure to depressive-like phenotypes across species. Following PRISMA guidelines, nine animal studies and one human cross-sectional study met the inclusion criteria. Rodent models exposed to MNPs, primarily polystyrene, showed consistent induction of depressive-like behaviors, whereas aquatic models exhibited neurobehavioral alterations compatible with depression-relevant phenotypes. Effects were dose-dependent and influenced by particle characteristics, exposure window, and sex. Preliminary human data suggest a positive association between estimated environmental MNPs exposure and depressive symptoms. Although evidence remains limited and methodologically heterogeneous, converging findings across experimental models indicate that MNPs exposure may represent a potential emerging risk factor for depression-related outcomes, possibly mediated by neuroinflammatory processes and neuronal damage. Future research requires standardized behavioral assessments, environmentally relevant exposure models, and longitudinal human studies with direct exposure biomonitoring to establish causality and public health relevance.