Plastic pollution is one of the main environmental problems of our time. Due to mismanagement or inadequate recycling practices, up to 300 million tons of plastic end up annually in landfills or are discharged into ecosystems, posing potential threats to aquatic and terrestrial life. Once discharged to the environment, plastic waste undergoes degradation processes due to UV irradiation and mechanical abrasion, which produce an array of particles of widely varying size and shape. Among these, microplastic particles (MPs, size 0.1-5 mm) have been the focus of many recent studies focusing on their fate, transport, and environmental interactions. In contrast, nanoplastic particles (NPs), the smallest fraction of plastic debris (< 100 nm), have received far less attention. Unlike microplastics, NPs are able to interact with, damage, and translocate through, biological membranes, given their small size, heterogeneous morphology, and enhanced surface reactivity. Studies at different trophic levels have shown that NP exposure can result in disrupted cell function and cell death. However, the underlying toxicology of NPs remains poorly understood. The lack of fundamental understanding of nanoplastic biological interactions hinders the formulation of measures to mitigate NP environmental impact.
Studies with engineered nanomaterials (ENMs) such as nanocarbons and metal(-oxide) nanoparticles have revealed two paradigms to explain how nanoscale materials break down the bacterial cell membrane. First, membrane stress posits that short-range interactions (e.g., van der Waals, hydrogen bond, or hydrophobic interactions) between cell membrane constituents and the ENM may result in piercing of the cell membrane and the destructive extraction of phospholipids. An alternative explanation invokes the formation of reactive oxygen species (ROS) induced by the nanomaterial; oxidative stress ensues when ROS concentration exceeds that of cellular antioxidants, resulting in oxidation of the cell membrane. Certain ENMs may also directly oxidize the cell membrane without intervention of ROS. Recent experimental evidence suggests that both oxidative and membrane stress may be at play during cell inactivation derived from NP exposure; however, the dominant pathway and molecular level mechanisms have yet to be established. The paucity in our understanding of NP interactions at the nano-bio interface obscures the potential negative environmental impacts of this family of contaminants.
Specific Objectives. The overall objective of this PhD project is to elucidate the mechanisms underlying nanoplastic (NP) toxicity, by examining the extent to which membrane stress versus oxidative stress underlies the bactericidal activity of nanoscale plastics. Our studies will focus on bacterial cells, as bacteria form the base of trophic chains, and play key roles in nutrient cycling.
The objectives of this PhD research project are as follows:
· To develop new AFM experimental protocols to provide direct, real-time quantitative measurements of the interactions between bacterial cell membranes and NPs in aqueous media.
· To systematically investigate the effects of NP length scale and morphology, by synthesizing NPs with well-defined edge asperities.
· To evaluate the relevance of oxidative pathways in NP-induced cell membrane damage.
· To develop computational tools (i.e., Matlab or Python scripts) for the high-throughput analysis of experimental AFM data.