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Nanoplastics inSimulated Human Lung Fluids: AggregationKinetics, Theoretical Model Simulation, and Effects on Pulmonary Bacteria
Summary
Researchers studied how polystyrene nanoplastics of different sizes and surface charges behave in simulated lung fluids, finding that all particles aggregated in inflammatory fluid while charge-modified particles remained stable in healthy fluid. Aggregation followed classical colloidal theory and exposure to nanoplastics significantly inhibited the growth of key pulmonary bacteria.
The widespread presence of nanoplastics poses serious threats to public health with inhalation emerging as a crucial exposure pathway. However, their behavior and toxicity in the pulmonary microenvironment are largely unknown. In this study, polystyrene nanoplastics (PSNPs) with different diameters and surface modifications were employed to investigate the aggregation kinetics, interaction mechanisms, and effects on pulmonary bacteria in different lung fluids. All PSNPs aggregated in inflammatory artificial lysosomal fluid (ALF), whereas bare- and carboxyl-modified PSNPs remained stable in healthy Gamble’s solution (GS) and modified GS (MGS). Aggregation of PSNPs in ALF and GS followed the classical Derjaguin–Landau–Verwey–Overbeek theory, while steric hindrance and hydrogen bonding between PSNPs and the lung surfactant governed the aggregation in MGS. Furthermore, redundancy analysis indicated that the aggregation of PSNPs reduced oxidative stress and membrane damage to bacteria in lung fluids. Specifically, amino-modified PSNPs, which aggregated in GS, could induce sustained oxidative stress, damage the cell membrane of native pulmonary bacteria, and promote the release of pyoverdine from pathogenic bacteria up to 2.16 times. Moreover, the aging process significantly enhanced the toxicity of PSNPs on pulmonary bacteria. These findings enhance our understanding of the behavior and toxic effects of nanoplastics on humans.
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