Evaluation of the pulmonary toxicity of PSNPs using a Transwell-based normal human bronchial epithelial cell culture system

To reduce the nanoplastics (NPs) toxicity assessment error, we established a Transwell-based bronchial epithelial cell exposure system to assess the pulmonary toxicity of polystyrene NPs (PSNPs). Transwell exposure system was more sensitive than submerged culture for toxicity detection of PSNPs. PSNPs adhered to the BEAS-2B cell surface, were ingested by the cell, and accumulated in the cytoplasm. PSNPs induced oxidative stress and inhibited cell growth through apoptosis and autophagy. A noncytotoxic dose of PSNPs (1 ng/cm2) increased the expression levels of inflammatory factors (ROCK-1, NF-& kappa;B, NLRP3, ICAM-1, etc) in BEAS-2B cells, whereas a cytotoxic dose (1000 ng/cm2) induced apoptosis and autophagy, which might inhibit the activation of ROCK-1 and contribute to reducing inflammation. In addition, the noncytotoxic dose increased the expression levels of zonula occludens-2 (ZO-2) and & alpha;1-antitrypsin (& alpha;-AT) proteins in BEAS-2B cells. Therefore, in response to PSNP exposure, a compensatory increase in the activities of inflammatory factors, ZO-2, and & alpha;-AT may be triggered at low doses as a mechanism to preserve the survival of BEAS-2B cells. In contrast, exposure to a high dose of PSNPs elicits a noncompensatory response in BEAS-2B cells. Overall, these findings suggest that PSNPs may be harmful to human pulmonary health even at an ultralow concentration.

Automated summary

To assess the pulmonary toxicity of polystyrene nanoparticles (PSNPs) and reduce assessment error, a Transwell-based bronchial epithelial cell exposure system was established. The system was more sensitive than submerged culture in detecting PSNPs toxicity. PSNP adhesion, ingestion, and accumulation in the cytoplasm of BEAS-2B cells induced oxidative stress, inhibited cell growth, and triggered apoptosis and autophagy. PSNPs also increased the expression of inflammatory factors in noncytotoxic doses and induced apoptosis and autophagy in cytotoxic doses, suggesting their harmful effects on human pulmonary health.