Effect of Cadmium on Human Middle Ear Epithelial Cells

J Int Adv Otol. 2015 Dec;11(3):183-7. doi: 10.5152/iao.2015.756.


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.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Apoptosis / drug effects
  • Cadmium / pharmacology*
  • Cell Survival / drug effects
  • Cells, Cultured
  • Cyclooxygenase 2 / genetics
  • Cyclooxygenase 2 / metabolism
  • Ear, Middle / cytology*
  • Epithelial Cells / drug effects*
  • Humans
  • Mucin 5AC / genetics
  • Mucin 5AC / metabolism
  • Necrosis
  • Otitis Media / etiology*
  • Otitis Media / pathology*
  • Reactive Oxygen Species / metabolism
  • Up-Regulation


  • MUC5AC protein, human
  • Mucin 5AC
  • Reactive Oxygen Species
  • Cadmium
  • Cyclooxygenase 2
  • PTGS2 protein, human