ScholarWorks@중앙대학교

초록

Purpose of review This review summarizes (i) major human exposure sources and routes, (ii) penetration andtranslocation pathways across biological barriers, and (iii) recent evidence regarding MNP excretion, internaldistribution/accumulation, and associated health eff ects. Recent findings Recent studies have detected MNPs in multiple human tissues and biofl uids (e.g., blood, placenta,stool, and breast milk), supporting the possibility of barrier penetration and systemic distribution. Emerging evidencelinks internal MNP burdens with infl ammatory and cardiometabolic outcomes and suggests potential reproductiveand immune eff ects, but diff erences in particle characterization and analytical methods still limit comparability andcausal interpretation. Background Environmental contamination by micro- and nanoplastics (MNPs) is increasing worldwide, raising concerns about chronic human exposure and potential adverse effects on ecosystems and human health. These particles originate from industrial activities, improper waste management, and the degradation of larger plastics, and have been detected across air, water, soil, food, and medical environments. Objective This review synthesizes current knowledge on (i) major human exposure sources and routes, (ii) penetration and translocation pathways across biological barriers, and (iii) recent evidence regarding MNP excretion, internal distribution/accumulation, and associated health effects. Results Humans may be exposed to MNPs through ingestion, inhalation, dermal contact, and medical interventions. Emerging analytical evidence has detected MNPs in human tissues and fluids, including blood, atherosclerotic plaque, stool, breast milk, and semen, supporting the possibility of systemic distribution following barrier penetration. Recent observational findings have linked internal MNP burdens with outcomes related to immunotoxicity, inflammatory bowel disease, cardiovascular disease, and reproductive dysfunction. Complementary experimental studies suggest that MNP exposure can elevate inflammatory markers, impair sperm quality, and modulate the tumor microenvironment. However, differences in particle properties, analytical workflows, and exposure assessment approaches limit cross-study comparability and prevent definitive causal inference for specific diseases. Conclusions Although a clear causal relationship between MNP exposure and human disease remains unconfirmed, converging evidence from detection studies, epidemiological observations, and experimental models underscores the need for standardized methodologies and mechanistic investigations. Consolidating recent data on MNP presence, distribution, and health outcomes, this review highlights the importance of incorporating MNP risk assessment into public health strategies and developing targeted interventions to reduce exposure from environmental and medical sources.

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