Academic Projects

The widespread environmental presence of nanoplastics (NPs) has raised significant concerns regarding their potential health impacts, particularly through inhalation exposure. The human respiratory system, with its extensive surface area and direct contact with the external environment, is a key route for NP entry. Once inhaled, these NPs interact with lung surfactant (LS), a substance present in the alveoli. The LS monolayer, made up of proteins and lipids, forms an important air-liquid interface in the lungs. Its main role is to lower surface tension, which is vital for normal lung function during breathing. Understanding the molecular interactions between plastic particles and biological interfaces within human systems is essential for predicting potential health effects. While a lot is known about LS, the exact molecular mechanisms that control the interaction, attachment, and movement of nanoplastics, particularly polyethylene, within the LS monolayer are still not fully understood. Therefore, a thorough investigation is needed to be conducted to understand the impact of nano-plastics on alveolar fluid. In this work, coarse-grained molecular dynamics simulation technique was employed to investigate the interaction mechanisms of polyethylene nano-plastics and their effects on the lung surfactant monolayer film. When inhaled, nanoplastics, including those found in environmental pollutants, come into contact with the LS monolayer, potentially affecting lung function.The simulations reveal that nanoplastics exhibit distinct translocation profiles depending on their surface chemistry, size, and hydrophobicity. Hydrophobic PS nanoparticles demonstrate strong adsorption to the surfactant layer, inducing local disruption in lipid packing, while PE nanoparticles penetrate more readily into the monolayer without causing immediate destabilization. The energy landscape analysis indicates a lower free energy barrier for PE translocation compared to PS, suggesting easier incorporation into the surfactant interface. Furthermore, the presence of NPs alters the lateral diffusion and order parameters of lipid molecules, potentially compromising the surfactant’s biophysical function.

Our findings suggest that nanoplastics can significantly perturb the structure and dynamics of lung surfactant monolayers, potentially impairing their ability to maintain alveolar stability. These interactions are modulated by NP physicochemical properties, highlighting the importance of surface characteristics in assessing respiratory toxicity. The study provides atomic-scale insights into NP-lung surfactant interactions, offering a foundational understanding that can guide future experimental studies and inform risk assessments for airborne nanoplastic exposure. Ultimately, this work underscores the need for stringent evaluation of airborne nanomaterials and supports the development of safer plastic alternatives and mitigation strategies.