Inflammatory effects of acrolein, crotonaldehyde and hexanal vapors on human primary bronchial epithelial cells cultured at air-liquid interface.

The cytotoxicity of aldehydes was studied using human primary bronchial epithelial cells (PBEC) cultured at the air-liquid interface (ALI) or under submerged conditions. PBEC were exposed for 30min via the air phase to acrolein (0.1-1mg/m3), crotonaldehyde (1.5-15mg/m3) or hexanal (22-221mg/m3) or under submerged conditions to acrolein (0.1 and 0.2mg/L), crotonaldehyde (1 and 2mg/L) or hexanal (10 and 20mg/L). Cell culture medium was collected 8h and 24h post-exposure and analyzed for interleukin-8 (IL-8) and matrix metalloprotein-9 (MMP-9). The gene expression of inflammatory and oxidative stress markers were measured 6h post-exposure. In the ALI setup, all three aldehydes caused increased secretion of IL-8, acrolein and crotonaldehyde also increased the gene expression of inflammatory and oxidative stress markers. In contrast, exposure under submerged conditions resulted in significantly reduced IL-8 secretion. The inflammatory response seen in the air phase exposures correspond well with previous in vivo studies. This indicates that lung models cultured at ALI are more suitable than submerged cell cultures in toxicity assessment studies of inhaled agents.