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Pulmonary accumulation and immune modulation by intravenously administered environmentally relevant microplastics in mice

Journal of Hazardous Materials 2025 1 citation ? Citation count from OpenAlex, updated daily. May differ slightly from the publisher's own count.
Yujeong Lee, Dong-Seon Kim, Hee-Kyung Kim, Min Kyung Sung, Soo‐Eun Sung, Kyung Ho Kang, Dongmin Kim, Sunjong Lee, Sijoon Lee

Summary

Researchers intravenously administered environmentally relevant oxidized polyethylene microplastics to mice and tracked their distribution using fluorescent labeling. The particles primarily accumulated in the lungs and induced inflammatory cell infiltration, demonstrating that microplastics entering the bloodstream can concentrate in pulmonary tissue and trigger immune responses.

Polymers
Models
Study Type In vivo

Microplastics (MPs), especially those formed via environmental degradation, are emerging health concerns. While oral and inhalation exposures have been widely studied, the systemic effects of intravenously introduced MPs remain poorly understood. This study aimed to assess the biodistribution and immune responses induced by intravenously administered oxidized polyethylene microplastics (Ox-PE-MPs) in mice. Environmentally mimicking Ox-PE-MPs were synthesized and labeled with Cy5.5 for in vivo tracking. Following a single intravenous injection (100 mg/kg), biodistribution was examined via IVIS imaging and Raman spectroscopy, while histopathology and molecular analyses were performed on lung and lymphoid tissues. The particles primarily accumulated in the lungs, inducing inflammatory cell infiltration and fibrin-like exudates with demonstrated a 2.8-fold increase in pulmonary inflammation score compared to the control, and increased tingible body macrophages in lymph nodes. ELISA revealed a 1.6-fold and 1.7-fold reduction in pulmonary TGF-β and IL-10 levels, respectively, and western blot showed a 1.5-fold decrease in COX-2 expression. These findings highlight that even short-term systemic exposure to MPs may disrupt pulmonary immune homeostasis, emphasizing the importance of evaluating non-oral routes of microplastic exposure.

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