Late Breaking Abstract - Differential toxicities of particulate matter components linked to air pollution and adverse health effects

Background: Particulate matter (PM) is a major component of ambient air pollution that has been linked to chronic lung disorders, especially COPD. Toxicity assessment of PM is currently typically based on mass concentration rather than the physicochemical properties of the constituents. The aim of this study was to identify correlations between PM components and pathways that are associated with the induction of adverse health effects. Methods: Toxicity of uncoated soot particles (80 nm; 10-100 μg/mL), ammonium nitrate (10‑1000 μg/mL), ammonium sulphate (10-1000 μg/mL) and Copper Oxide (CuO) ( Results: The highest toxicity score was obtained for CuO followed by soot that both induced cytotoxic responses (increased LDH release) in H441 and reduced metabolic activity/mitochondrial function in both H441, A549 and HFL-1. ROS generation was induced by both CuO and soot in H441 and HFL-1. Ammonium nitrate and ammonium sulphate did not induce any significant cytotoxic effect. Conclusions: There are significant differences in toxicity of PM components and cellular responses that can be linked to adverse health effects. Increased ROS generation and mitochondrial dysfunctions are well known in COPD. The toxicity of individual particles can be used to better understand the adverse health effects and improve air quality guidelines.