Microplastics in the Female Genital Tract and Fetoplacental Continuum: A Lesion-Based Framework for...

Background/Objectives: Microplastics (MPs) are increasingly reported in human reproductive tissues and fluids, but detection alone does not establish tissue injury or disease. Recent reviews have synthesised occurrence, reproductive toxicity, placental transfer, fertility, and pregnancy outcomes. The unresolved problem is that occurrence, model-response, lesion-comparison, clinical-association, and causal evidence are not interchangeable. This review asks what minimum evidence is required for an MP finding in the female genital tract (FGT) or fetoplacental continuum to become lesion-relevant and where inference must stop. Methods: We performed a critical narrative search of PubMed, Scopus, Web of Science, ScienceDirect, and Google Scholar from database inception through 10 July 2026. The final synthesis comprised 59 sources: 28 primary studies, 24 reviews or systematic syntheses, and 7 regulatory, consensus, or professional-guidance documents.. Methodological recommendations were graded as claim-essential, context-dependent, or exploratory and as routine, specialised, or research-intensive. Results: The distinct contribution is an FGT-specific mechanistic and claim-to-evidence architecture rather than another environmental or reproductive-toxicity catalogue. We propose an ordered, claim-calibrated evidence ladder linking external exposure, internal dose, reproductive-fluid burden, spatial localisation, lesion response, and clinically annotated phenotype. The framework specifies the minimum evidence for occurrence, localisation, lesion, clinical, and causal claims and provides explicit stopping and downgrading rules rather than treating all desirable measurements as mandatory. The FGT Lesion Atlas is a compartment-by-compartment map of prioritised, non-exhaustive endpoints and sampling requirements. The FGT Lesionome is a cross-compartment synthesis of recurring barrier-receptivity, stromal-fibrotic, vascular-perfusion, immune-microbiome, endocrine-steroidogenic, and particle-cargo axes. An integrated hypothesis-generating pathway links systemic or local exposure, internal and target-compartment burden, physicochemical conditioning in reproductive-fluid microenvironments, particle or particle-associated-constituent interaction with compartment-specific cells and matrices, the six response axes, physiological dysfunction, and clinically annotated outcomes. A reproductive-fluid model, an assisted-reproductive-technology sentinel sequence, and an FGT Microplastic Pathology Reporting Checklist rank study elements by evidentiary necessity, feasibility, and interpretive consequence. Conclusions: The framework is hypothesis-generating, not a validated causal map or a universal core outcome set. It separates essential validity safeguards from context-dependent best practices and exploratory endpoints. Human reproductive and fetoplacental disease causation remains unproven without contamination-controlled sampling, polymer confirmation, spatial co-localisation with lesions, temporality, exposure-response assessment, confounder control, replication, and appropriately powered, temporally informative clinical outcomes.