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Aggregation and deposition kinetics of polystyrene nanoplastics in lung fluids: Influence of particle property, fluid condition, and surfactant protein
Summary
Researchers investigated how tiny polystyrene nanoplastics behave after being inhaled into the lungs by simulating their interactions with lung fluids in the lab. They found that the particles rapidly clump together and settle out of acidic lung fluid much faster than neutral fluid, with particle size and surface charge playing key roles. The findings suggest that once inhaled, nanoplastics may accumulate in lung tissue rather than being easily cleared.
Nanoplastics (NPs) are emerging atmospheric contaminants that aggregate and deposit in lung fluids post-inhalation, affecting their migration and health risks. This study investigated the aggregation and deposition kinetics of six polystyrene NPs (PSNPs): NP50, NP100, NP500, A-NP50 and A-NP100 (amino-modified), and C-NP100 (carboxyl-modified), in artificial lysosomal fluid (ALF) and Gamble's solution (GMB). In ALF, PSNPs aggregated within 20 min to 132-1066 nm, with rates ranking A-NP50 > NP100 > A-NP100 > C-NP100 > NP50 > NP500. After 24 h, most exceeded 5000 nm, except NP500 (1473 nm). In GMB, only positively charged A-NP50 aggregated substantially (> 5000 nm), while negatively charged PSNPs remained stable. All PSNPs exhibited higher deposition rates in ALF than GMB. Higher particle concentrations promoted aggregation for all PSNPs in ALF, but only A-NP50 in GMB. Opposite pH effects on A-NP50 and NP50 were observed. NaHPO, NaHCO, sodium pyruvate, and trisodium citrate promoted A-NP50 aggregation via electrostatic interactions and adsorption. BSA modulated aggregation in a concentration- and fluid-dependent manner: low levels (< 260 mg/L) enhanced NP50 aggregation via charge screening, while higher levels stabilized it via steric hindrance. For A-NP50, BSA consistently reduced aggregation. These findings provide insights into NP transport and health risks in pulmonary environments.
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