Cerium oxide nanoparticle-induced pulmonary inflammation and alveolar macrophage functional change in rats

Abstract

The use of cerium compounds as diesel fuel catalyst results in the emission of cerium oxide nanoparticles (CeO₂) in the exhaust. This study characterized the potential effects of CeO₂ exposure on lung toxicity. Male Sprague Dawley rats were exposed to CeO₂ by a single intratracheal instillation at 0.15, 0.5, 1, 3.5 or 7 mg/kg body weight. At 1 day after exposure, CeO₂ significantly reduced NO production, but increased IL-12 production, by alveolar macrophages (AM) in response to ex vivo lipopolysacchride (LPS) challenge, and caused AM apoptosis, through activation of caspases 9 and 3. CeO₂ exposure markedly increased suppressor of cytokine signaling-1 at 1-day and elevated arginase-1 at 28-day post exposure in lung cells, while osteopontin was significantly elevated in lung tissue at both time points. CeO₂ induced inflammation, cytotoxicity, air/blood barrier damage, and phospholipidosis with enlarged AM. Thus, CeO₂ induced lung inflammation and injury in lungs which may lead to fibrosis.

Keywords::

• Cerium oxide
• nanoparticle
• lung injury
• alveolar macrophages
• pulmonary fibrosis

Declaration of interest: The authors report no conflicts of interest. The authors alone are responsible for the content and writing of the paper.