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Updated: Jul 3, 2026

An Air-liquid Interface Bronchial Epithelial Model for Realistic, Repeated Inhalation Exposure to Airborne Particles for Toxicity Testing
Published on: May 13, 2020
Artificial stone dust affects oxidative stress and epithelial barrier in CALU 3 cells
Noa Ophir1,2, Elizabeth Fireman1,2,3, Mordechai Reuven Kramer2,4
1Laboratory for Pulmonary and Allergic Diseases, Tel Aviv Medical Center.
Abstract:
Aim: Artificial Stone Dust (ASD) exposure has been identified as a significant health risk for workers, leading to oxidative stress, inflammatory responses, and potential systemic autoimmune diseases due to its high crystalline silica content. The aim of this study is to identify the impact of ASD on the permeability of alveolar epithelial cells and the mechanisms underlying particle translocation across the alveolar membrane remain unexplored. Methods: The acute toxicological effects of ASD on human bronchial submucosal gland cells CALU-3 cells in vitro were investigated to assess its impact on epithelial barrier integrity, in comparison to crystalline silica particles (Min-U-Sil®5). Results: Exposure to ASD increased oxidative stress, evidenced by heightened Reactive Oxygen Species (ROS) levels and Heme Oxygenase-1 (HO-1) gene expression in CALU-3 cells, exceeding effects observed with Min-U-Sil®5. Notably, ASD exposure resulted in a significant decrease in Transepithelial Electrical Resistance (TEER), indicating compromised epithelial barrier integrity, especially at higher concentrations (3.7 mg,18.5 mg and 37 mg) after 24, 48 and 72 h. These findings were not paralleled by a decrease in cell viability, underscoring a specific effect on cellular barrier function rather than cytotoxicity. Conclusions: Our study reveals that ASD induces oxidative stress and disrupts epithelial barrier integrity in vitro, potentially contributing to systemic translocation of particles and subsequent health effects. These findings underscore the need for a rigorous protective measure for workers and highlight potential biomarkers of ASD-induced cellular damage.
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