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Microplastics as an Emerging Human Health Risk: Mechanisms, Exposure, and Clinical Evidence
Summary
This review examines the growing body of evidence on how microplastics enter the human body through ingestion, inhalation, and skin contact, and have now been detected in blood, lung tissue, placenta, and cardiovascular tissue. Evidence indicates that microplastics may cause harm through oxidative stress, inflammation, and cellular damage, though a direct causal link to specific health conditions has not yet been fully established.
Microplastics (MPs) refer to plastic particles <5 mm in size, have gained growing attention pervasive across environmental compartments such as air, soil, and aquatic systems. Human exposure primarily occurs via ingestion, inhalation, and dermal contact with MPs now detected in various biological specimens such as blood, placenta, lung tissue, and cardiovascular tissue. Evidence indicates that MPs can move across biological membranes, undergo systemic distribution, and build up within tissues, raising concern for organ-specific toxicity. Mechanisms implicated in microplastic-induced pathology include oxidative stress, inflammation, epithelial barrier disruption, cellular injury, mitochondrial dysfunction, autophagy dysregulation, and thrombogenic effects. Emerging clinical observations link microplastic burden with cardiovascular disease severity, respiratory disorders, and inflammatory conditions, though causality remains incompletely defined. Advances in detection methodologies, including microscopy, spectroscopy, and mass spectrometric techniques, have supported identification and characterization of MPs in human samples. Prevention strategies focus on reducing plastic use, modifying dietary and personal habits, and improving water treatment and filtration systems. Overall, the growing evidence underscores microplastics as a pressing environmental health concern requiring further mechanistic, epidemiological, and regulatory investigation. Keywords: Microplastics; Human health; Exposure pathways; Cardiovascular toxicity; Respiratory toxicity; Oxidative stress; Autophagy; Inflammation; Nanoplastics
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