We can't find the internet
Attempting to reconnect
Something went wrong!
Hang in there while we get back on track
Evaluating the toxicity of polystyrene micro- and nanoplastics in human bronchial epithelial cells: differences and challenges using aerosol and suspension exposures
Summary
Scientists exposed human lung cells to tiny plastic particles (the kind found in air pollution) using two different lab methods, and both showed signs of inflammation in the cells—though the cells didn't die or show classic damage signals. This matters because it adds to growing evidence that breathing in microplastics may trigger low-level lung inflammation, but it also shows that how scientists test these effects in the lab can change the results, so more consistent research is needed before we know exactly how risky everyday plastic exposure really is.
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.