Objective Studies investigating toxicity of airborne micro- and nanoplastics (MNPs) are mostly based on conventional submerged cell cultures while limited studies utilize air-liquid interface (ALI) systems. Inherent differences in these culture/exposure modalities, such as particle behavior and deposited dose, likely affect cellular responses. To investigate this, we exposed submerged human bronchial epithelial cells (BEAS-2B) to polystyrene (PS) MNPs vs. aerosol exposure of ALI cultures.Methods First, submerged bronchial epithelial cells (BEAS-2B) were exposed to suspensions of PS particles (50 nm or 1 µm) in four different applied concentrations (0.79–50 µg/cm2; 24 h). Second, BEAS-2B cells were cultured at ALI and exposed in a cloud system to PS 1 µm particles (deposited dose: 55.4 µg/cm2; 24 h). Toxicity readouts focused on cytotoxicity (LDH release), inflammation (IL-8 release and transcriptional activation of inflammatory genes), and oxidative stress (DCFH-DA assay, antioxidant gene expression, and assessment of reduced/oxidized glutathione).Results In both models, PS exposure did not induce cell death, or an antioxidant response. However, NF-κB transcriptional activity was strongly upregulated in submerged cells in response to both sizes of PS particles in a dose-dependent manner. Gene expression of CXCL1, CXCL2, and CXCL8 increased up to 7-fold after PS microplastic exposure (50 µg/cm2) in the submerged model (which was less pronounced in response to PS nanoplastics) and 2-fold in the ALI model. In contrast, IL-8 secretion increased 1.6-fold for the ALI, but not the submerged model.Conclusions Overall, both exposure modalities revealed an inflammatory response toward PS MNPs although with differences, likely due to significant differences in deposited dose.
Gosselink et al. (Wed,) studied this question.