Background: Soot particles are a major component of the particle matter (PM) in polluted ambient air, exposure to which has been linked to chronic lung disorders - especially COPD. Toxicity assessment of PM is typically based on mass concentration rather than the physicochemical properties of the constituents. This study aimed to identify correlations between exposure to soot particles and cytotoxicity pathways associated with adverse health effects.

Methods: Human bronchial epithelial cells (BEAS-2B), alveolar epithelial cells (H441 and A549), human lung fibroblasts (HFL-1) and rat precision cut lung slices (PCLS) were exposed to uncoated soot particles (90 nm; 1-100 ?g/mL) for 5-72 hours. Changes in cytotoxicity, metabolic activity, reactive oxygen species (ROS) and immune responses were measured. 

Results: Soot exposure was found to induce concentration-dependent cytotoxic responses in BEAS-2B and H441 cells and increase oxidative stress and reduce metabolic activity in BEAS-2B, H441, A549 and HFL-1 cells. Reduced viability was most pronounced after 48 and 72 hours of soot exposure. Soot exposure reduced the release of IL-6, MCP-1, RANTES, PFGF-bb and VEGF from A549 but not from BEAS-2B cells.

Conclusions: Soot exposure induced cellular responses linked to adverse health effects. Alveolar cells were in general more responsive to soot than bronchial cells. Increased ROS generation and mitochondrial dysfunction are well known in COPD. Measurements of the toxicity of individual PM components such as soot particles can be used to better understand adverse health effects and improve targeted air quality guidelines.