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

- Using PBEC-ALI, a more realistic in vivo situation is established.
- We found increased inflammatory mediators and upregulated mRNA at PBEC-ALI.
- PBEC-ALI system exposed to aldehydes, correspond well with in vivo studies.
- PBEC-ALI system with exposure via air represents a novel approach.
- This study could be used in future toxicity assessment studies of inhaled agents.

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 30 min via the air phase to acrolein (0.1-1 mg/m3), crotonaldehyde (1.5-15 mg/m3) or hexanal (22-221 mg/m3) or under submerged conditions to acrolein (0.1 and 0.2 mg/L), crotonaldehyde (1 and 2 mg/L) or hexanal (10 and 20 mg/L). Cell culture medium was collected 8 h and 24 h 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 6 h 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.