The Effect of Subchronic Polyethylene Microplastic Exposure on Pulmonary Fibrosis Through Pro-Inflammatory Cytokines TNF-α and IL-1β in Wistar Rats

The lungs function as the organs responsible for the respiratory system and they are essential for breathing, where any dysfunction can impair the respiratory processes. Pulmonary fibrosis is a lung disease that progresses slowly and is not contagious. The purpose of this study was to analyze the effect of airborne microplastic exposure on the expression of TNF-α and IL-1β cytokines, and on fibroblast cell formation in Rattus norvegicus Wistar strain rats. This research was a quantitative analytical study with a laboratory experimental approach that used experimental animals as research subjects. The research design was a true experimental design with a randomized posttest-only group design. The research was conducted at the molecular level, and the indicators measured were molecular biomarkers. This design involved dividing the experimental animals into six groups: a control group (X0) and five treatment groups (X1, X2, X3, X4, and X5), which received doses of 0.025, 0.5, 1, 2, and 4 mg/L, respectively. Biomarkers and microscopic changes were then measured after 90 days of treatment. In Wistar rats, microplastic exposure significantly increased the expression of TNF-α and IL-1β cytokines, which play an important role in the early phase of the inflammatory response in the lungs, as well as the formation of fibroblast cells as indicators of pulmonary fibrosis. Subchronic inhalation exposure to polyethylene microplastics significantly increased the expression of TNF-α and IL-1β cytokines, and the formation of fibroblast cells, leading to pulmonary fibrosis.