Airborne nanoparticles (NPs) can be harmful to health when they act as pollutants, potentially causing various negative effects on the body. However, recent advancements in nanotechnology have enabled the development of NPs with carefully designed properties, allowing them to be used in a wide range of biomedical applications. For example, gold nanoparticles (AuNPs) are commonly found in exhaust fumes and mining dust, where they can contribute to serious respiratory issues, particularly lung diseases. Despite this potential danger, AuNPs are also utilized in medical research and treatments as nanocarriers, helping improve the delivery of drugs directly to target cells. This dual nature of NPs demonstrates the complex balance between their environmental risks and their significant benefits in medical applications. The lungs serve as the main pathway for airborne nanoparticles (NPs) to enter the body. 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. While a lot is known about LS, the exact molecular mechanisms that control the interaction, attachment, and movement of bare nanoparticles, particularly gold nanoparticles (AuNPs), within the LS monolayer are still not fully understood. These bare AuNPs, commonly found in sources of pollution like vehicle exhaust, can potentially disrupt lung function if they interact with the LS. Understanding these interactions is crucial because, despite significant research, we still lack complete knowledge of how these bare NPs influence the LS on a molecular level, including their adsorption, movement within the monolayer, and possible effects on surface tension and the overall function of the LS.

In this Thesis, a series of coarse-grained molecular dynamics simulations were performed to investigate how bare gold nanoparticles (AuNPs) interact with lung surfactant (LS) monolayers. LS is essential for regulating surface tension in the alveoli, ensuring lung stability during breathing. When inhaled, nanoparticles, including those found in environmental pollutants, come into contact with the LS monolayer, potentially affecting lung function. The simulations revealed that bare AuNPs cause structural deformation in the LS monolayer in a concentration-dependent manner. As the concentration of AuNPs increased, the deformation became more pronounced, creating pores in the monolayer. These structural changes significantly alter the biophysical properties of the monolayer, which could interfere with its ability to reduce surface tension in the lungs. Since surface tension regulation is crucial for efficient breathing and lung function, the disruption of the LS monolayer by bare AuNPs could lead to respiratory complications, making it difficult for the lungs to function properly. Understanding how bare AuNPs interact with the LS monolayer is crucial for assessing the health risks associated with inhaling nanoparticles, particularly those in air pollution. These findings highlight the importance of studying nanoparticle-LS interactions to design safer nanoparticles, particularly in pulmonary drug delivery applications. The insights from this study will also help evaluate AuNPs as pollutants and contribute to identifying potential health risks in individuals exposed to bare AuNPs.

In summary, these simulation studies provide valuable molecular-level insights into the structure and dynamics of the LS monolayer and the interaction of bare AuNPs with it. This understanding will guide the future design of safer nanocarriers for drug delivery and help assess the impact of AuNPs as environmental pollutants, ultimately advancing public health safety.