microplastics

toxic effects

air pouch

micro nanoplastics

air-liquid interface

zno nps

Ecotoxicology and Environmental Safety

Awareness of risks posed by widespread presence of nanoplastics (NPs) and bioavailability and potential to interact with organic pollutants has been increasing. Inhalation is one of the more important pathways of exposure of humans to NPs. In this study, combined toxicity of concentrations of polystyrene NPs and various phthalate esters (PAEs), some of the most common plasticizers, including dibutyl phthalate (DBP) and di-(2-ethyl hexyl) phthalate (DEHP) on human lung epithelial A549 cells were investigated. When co-exposed, 20 μg NPs/mL increased viabilities of cells exposed to either DBP or DEHP and the modulation of toxic potency of DEHP was greater than that of DBP, while the 200 μg NPs/mL resulted in lesser viability of cells. PAEs sorbed to NPs decreased free phase concentrations ( C free ) of PAEs, which resulted in a corresponding lesser bioavailability and joint toxicity at the lesser concentration of NPs. The opposite effect was observed at the greater concentration of NPs, which may result from the dominated role of NPs in the combined toxicity. Furthermore, our data showed that oxidative stress and inflammatory reactions were mechanisms for combined cytotoxicities of PAEs and NPs on A549 cells. Results of this study emphasized the combined toxic effects and mechanisms on human lung cells, which are helpful for assessing the risk of the co-exposure of NPs and organic contaminants in humans. • Assessment of human cells co-exposed to nanoplastics (NPs) and phthalate esters (PAEs) were conducted. • A lesser concentration of NPs reduced toxicity of PAEs by decreasing free concentrations of PAEs. • The PAEs with greater adsorption capacity to NPs showed greater reduction in combined cytotoxicity. • NPs dominated the cytotoxicity at the co-exposure of a greater concentration of NPs and PAEs.

Combined cytotoxicity of polystyrene nanoplastics and phthalate esters on human lung epithelial A549 cells and its mechanism