Effect of Cadmium on Human Middle Ear Epithelial Cells.

OBJECTIVE

Cadmium (Cd(2+)) exposure can occur through passive smoking, ambient air pollution, and food. Even low exposure can affect hearing and cause lung disease. Here we investigated whether cadmium causes cytotoxicity, induces inflammation, or increases mucin gene expression in immortalized human middle ear epithelial cells (HMEECs).

MATERIALS AND

METHODS

Cell viability was investigated using the MTT assay following Cd(2+) treatment. Increases in apoptosis and necrosis were determined, and the production of reactive oxygen species (ROS) was measured. We analyzed the expression of an inflammatory cytokine (COX-2) gene and a mucin gene (MUC5AC) using RT-PCR.

RESULTS

Exposure to >20 µM Cd(2+) caused a significant decrease in cell viability. Hoechst 33258 staining showed apoptotic morphology of heterogeneous intensity, condensation, and fragmentation after Cd(2+) exposure. Cd(2+) was shown to increase cell death by apoptosis and necrosis by annexin V-FITC/PI double staining. Cd(2+) exposure increased ROS production and COX-2 and MUC5AC expressions.

CONCLUSION

Our findings suggest that environmental cadmium exposure is related to the development of otitis media.