OROPHARYNGEAL ADMINISTRATION OF POLYSTYRENE MICROPLASTICS INDUCES PROFIBROTIC AND OXIDATIVE CHANGES IN MURINE LUNG TISSUE

Aim: This study investigated the early pulmonary effects of intratracheally administered polystyrene microplastics (PS-MPs) in mice. Recognizing the emerging health concern of atmospheric microplastic inhalation, the research focused on identifying fibrotic remodeling markers, assessing immune cell activity, and analyzing oxidative stress-related molecular signaling to clarify the pathophysiological consequences and provide mechanistic insights into the initial stages of pulmonary fibrosis development. Materials and Methods: A controlled experimental design was used involving healthy BALB/c mice that were oropharyngeally exposed to 1.5 µm polystyrene microplastic particles or a saline control over 21 days. Following exposure, lung tissue samples were collected for comprehensive analysis. The key methodologies included determining the hydroxyproline content, detailed histopathological examinations to observe tissue changes, and immunohistochemistry for Nrf2 and STAT1 expression. Macrophage infiltration and active phagocytosis of microplastic particles within the lung tissue were also evaluated. All data underwent appropriate statistical analysis. Results: Despite the short exposure period, hydroxyproline levels and macroscopic fibrosis scores showed no statistically significant differences between the groups. However, the PS-MP-treated mice exhibited significant alveolar macrophage infiltration and robust intra-alveolar particle phagocytosis, indicating an active cellular response. A mild increase in Nrf2 expression suggested early antioxidant activation. In contrast, STAT1 expression was notably decreased in the PS-MP group, strongly suggesting immune dysregulation and increased susceptibility to pro-fibrotic remodeling processes within the pulmonary system. Conclusions: This study demonstrates that even short-term intratracheal PS-MP exposure induces early molecular and immunological changes in lung tissue. Characterized by STAT1 downregulation, mild Nrf2 upregulation, and significant activation of particle phagocytosis by macrophages, these changes collectively indicate a shift toward pro-fibrotic conditions, even in the absence of substantial collagen accumulation during this acute phase. These findings highlight the potential health risks associated with airborne microplastic exposure and emphasize the urgent need for further long-term research to fully understand their chronic effects on the lungs and develop comprehensive mitigation strategies for safeguarding respiratory health.