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Nanoplastic-induced Disruption of DPPC and Palmitic Acid Monolayers: Implications for Membrane Integrity
Summary
Polystyrene nanoplastics were found to disrupt DPPC and palmitic acid lipid monolayers—models of lung alveolar and cell membranes—suggesting that inhaled or ingested nanoplastics could compromise lung alveolar stability, cell signaling, nutrient delivery, and potentially cause neurotoxicity through membrane disruption.
Nanoplastics are generated from the fragmentation of microplastics under various environmental conditions in the atmosphere. These tiny pollutants are widespread and can enter the human body through the air we breathe and the food and water we consume. Understanding how nanoplastics interact with different membrane lipids is paramount to discerning the kind of threat they pose in terms of lung alveolar destabilization, impaired cell communication, cell wall disruption, diminished nutrient delivery, and neurotoxicity. In this research, we examined the interaction of polystyrene nanoplastics with palmitic acid and phosphatidylcholine at the air-aqueous interface to identify individual lipid response. Employing a comprehensive experimental approach that includes infrared-reflection absorption spectroscopy (IRRAS), Langmuir isotherms and Brewster angle microscopy (BAM), we investigated chemical and physical changes of lipid monolayer systems with nanoplastics dispersed within the water solution phase. Increasing concentration of the polystyrene nanoplastics in the solution phase led to enhanced interfacial activity; the nanoplastics were observed to incorporate into the monolayer driven by lipid adsorption/complexation to the nanoplastics. The findings in this research aid in understanding the physical mechanisms through which nanoplastics may alter and impact biophysical interfaces.