Formaldehyde exposure induces airway inflammation by increasing eosinophil infiltrations through the regulation of reactive oxygen species production

Woon Won Jung, Eun Mi Kim, Eun Hee Lee, Hee Jung Yun, Hyang Ran Ju, Moon Jin Jeong, Kwang Woo Hwang, Dong Geun Sul, Hyung Sik Kang

Research output: Contribution to journalArticle

37 Citations (Scopus)


Formaldehyde (FA) is a well-known cytotoxic irritant to the airways, but the mechanism of airway inflammation due to FA has not been clarified. In the present study, C57BL/6 mice were exposed to two concentrations (5 and 10 ppm) of FA for 6 h/day, 5 days/week, for 2 weeks. The FA-exposed mice had much higher number of CCR3+ eosinophils than control mice, and showed upregulated gene expression of CC-chemokine receptor-3 (CCR3), eotaxin and intercellular adhesion molecules-1 (ICAM-1) as well as an increased expression of proinflammatory and Th2 cytokines, such as interleukin (IL)-1β, IL-4 and IL-5. In addition, FA exposure revealed a considerable increase in the serum levels of IgG1, IgG3, IgA and IgE compared to controls. Histopathological analysis of the lung tissues demonstrated eosinophils and mononuclear cell infiltration of the alveolar cell walls and alveolar spaces. Gene expression of thioredoxin (TRX), redox-regulating antioxidant proteins, was markedly suppressed in FA-exposed mice, and thereby intracellular ROS levels were increased along with increased FA concentration. These results were consistent with an increase in the number of CCR3-expressing eosinophils, and indicate that FA-induced ROS was generated from eosinophils recruited to the inflammatory sites of the airways.

Original languageEnglish
Pages (from-to)174-182
Number of pages9
JournalEnvironmental Toxicology and Pharmacology
Issue number2
Publication statusPublished - 2007 Sep 1



  • Airway inflammation
  • Eosinophil
  • Formaldehyde
  • Reactive oxygen species

ASJC Scopus subject areas

  • Toxicology
  • Health, Toxicology and Mutagenesis
  • Pharmacology

Cite this