Polycyclic aromatic hydrocarbons bound to microplastics enhance their bioaccumulation and toxicity, inducing mitochondrial damage and apoptosis in lung epithelium.

As the co-exposure of microplastics (MPs) and hydrophobic organic contaminants (HOCs) in the environment poses potential adverse effects on ecosystems and human health, the combined toxicity of MPs and HOCs has caused growing concerns. In the present study, we evaluated the toxicity and bioaccumulation of polystyrene microbeads (micro-PS, Φ < 1 μm) bound various polycyclic aromatic hydrocarbons (PAHs) to lung epithelial cells. Our results indicated that PAH-loaded MPs had significantly greater cytotoxicity than MPs alone, due to PAH's ability to induce epithelial cellular changes and cause more MP to accumulate intracellularly. The observed reduction in surface negative charge following PAH adsorption suggests a potential alteration in the interfacial properties of the particles, which may facilitate their adhesion and subsequent internalization by lung epithelial cells. PAH-loaded made PS cause more severe oxidative stress and further induced mitochondrial damage and apoptosis, as a result, increasing the health risk of MPs exposure in the environment. Our findings provide new insight into the combined toxicity of MPs loading HOCs and highlight the implication of the environmental contaminants for altering the toxicological profiles of MPs.