Formaldehyde interferes with airway epithelium integrity and functions in a dose- and time-dependent manner.

Formaldehyde (HCHO) is a common indoor air pollutant. To assess its potential role and mechanism of action in asthma, we exposed the bronchial epithelial cell lines Calu-3 and 16HBE to HCHO (70-7000 μM) according to two exposure schedules (30 min and 24 h), before measuring cell viability, necrosis and apoptosis, reactive oxygen species production, cytokine release, as well as trans-epithelial electrical resistance (TEER) of cell monolayers. Whereas exposure to HCHO for 30 min had a limited effect on cell viability, exposure for 24h to 1400-7000 μM HCHO induced a pronounced dose-dependent cell death. The important decrease in cell viability observed after 24h exposure to the highest concentrations of HCHO (1400-7000 μM) was accompanied by important LDH release and ROS production, whereas a 4h exposure to lower HCHO concentrations (350 μM) induced cell apoptosis. Also, exposure to HCHO for 30 min dose-dependently inhibited basal and lipopolysaccharide-induced interleukin-6 (IL-6) and IL-8 production by bronchial epithelial cells. As well, HCHO triggered a dose- and time-dependent decrease in TEER of Calu-3 cell monolayers. The present work demonstrates that HCHO interferes with airway epithelium integrity and functions, and may thus modulate the onset and the severity of asthma. However, importantly, conditions of exposure to HCHO, e.g. level and duration, are determinant in the nature of the effects triggered by the pollutant.