UTTAR PRADESH JOURNAL OF ZOOLOGY

Microplastic pollution is now documented across freshwater, estuarine, coastal and oceanic systems, yet the implications of widespread occurrence remain difficult to interpret because particles differ in size, shape, polymer, density, weathering state and associated chemicals, while analytical and toxicological methods remain poorly harmonised. This critical narrative review integrates evidence on sources, transport, transformation, ecological effects and human-health implications, with emphasis on where inference is robust and where it remains constrained. Literature published from 1 January 2004 to 19 July 2026 was considered, supplemented by authoritative institutional assessments and citation searching. The evidence consistently identifies land-based waste leakage, wastewater, textile fibres, tyre wear and atmospheric deposition as important pathways, but source contributions are strongly context dependent. Hydrodynamics, particle density and morphology, biofouling, aggregation and resuspension redistribute particles among surface waters, the water column and sediments, making surface measurements an incomplete proxy for ecosystem exposure. Laboratory and field studies establish ingestion, retention and trophic transfer in diverse taxa and provide credible evidence for effects on feeding, energy balance, oxidative status, tissue responses, growth and reproduction under some conditions. Ecological risk, however, cannot be inferred from hazard demonstrations alone because many experiments use particle types and doses that differ from environmental mixtures, and effect thresholds vary among organisms and particle traits. Sorbed contaminants and additives can contribute to toxicity, but microplastics are not universally dominant chemical vectors relative to food and other environmental media. Seafood and drinking water provide plausible human exposure routes, and plastic particles have been detected in human tissues and fluids, but the fraction attributable to aquatic sources and the causal significance of internal exposure remain unresolved. Recent human observational evidence justifies stronger exposure assessment rather than definitive disease attribution. The most consequential research priorities are harmonised metrology, environmentally realistic mixtures, coupled field–laboratory designs, quantitative source-to-receptor models, longitudinal human studies and intervention evaluation.