Cytological and biochemical changes in bronchoalveolar lavage fluid in female rats during acute exposure to polystyrene microparticles

Microplastics are considered a potentially hazardous environmental pollutant. However, their impact on the respiratory system remains poorly understood. Evaluation of the cytological and biochemical parameters of bronchoalveolar lavage fluid can be used to describe the early local airway response in rats. The aim of the study is to evaluate the changes in cytological and biochemical parameters of bronchoalveolar lavage fluid during acute single exposure to 300 nm polystyrene microparticles in an experiment. Materials and Methods. The effects of a single intratracheal administration of polystyrene microparticles were studied in two groups of female rats (n=14). Bronchoalveolar lavage was performed 24 hours later, followed by the evaluation of the cytological composition and biochemical parameters of the lavage fluid (enzyme activity and total protein concentration). The estrous cycle stage was not determined; all manipulations were performed at the same time of the day to minimize circadian variability. Results. A single intratracheal instillation of polystyrene particles was shown to cause a statistically significant neutrophil-lymphocyte shift in the bronchoalveolar lavage fluid without signs of massive cytolysis. These changes are consistent with the patterns of early nonspecific airway response to inert particles, as described in experimental models for other types of submicron particles. Conclusions. The data obtained characterize the early local airway response to particle exposure in an experimental model. The absence of pronounced signs of cytotoxicity should not be considered evidence of the complete safety of polystyrene microparticles during acute exposure. Further studies incorporating an expanded range of markers, long-term observation, and assessment of combined effects with environmentally relevant toxicants are required to objectively evaluate plastic microparticles as a factor in lung tissue damage.