Internalization and toxicity: A preliminary study of effects of nanoplastic particles on human lung epithelial cell

As a kind of newly emerging pollutant, nanoplastics are easily to be ingested by organisms, and cause severe damage to biological functions because of their small size, high specific surface area, and strong biological penetration. Recently, there are increasing reports of numerous airborne microplastics, including polystyrene (PS), being detected in atmospheric samples, which implies a potential risk to the human respiratory system. In this work, we evaluated the effects of polystyrene nanoparticles of two different sizes (PS-NP25: 25 nm diameter and PS-NP70: 70 nm diameter) on the human alveolar epithelial A549 cell line including internalization, cell viability, cell cycle, apoptosis, and associated gene transcription and protein expression. Results showed that PS-NP25 was internalized more rapidly and efficiently into the cytoplasm of A549 than PS-NP70. PS-NPs significantly affected the cell viability, caused cell cycle S phrase arrest, activated inflammatory gene transcription, and changed the expression of proteins associated with cell cycle and pro-apoptosis. PS-NPs induced significant up-regulation of pro-inflammatory cytokines such as IL-8, NF-κB, and TNF-α, as well as pro-apoptotic proteins such as DR5, caspase-3, caspase-8, caspase-9, and cytochrome c, which revealed that PS-NPs triggered a TNF-α-associated apoptosis pathway. This study suggests that exposure duration, diameter, and concentration are the key factors for evaluating the toxicological effects of PS-NPs on alveolar epithelial cells. More attention must be focused on the risk of nanoplastic-related air pollution and the environmental toxicological effects of nanoplastics on humans and other terrestrial mammals.