Signalling Pathways of Inflammation and Cancer in Human Mononuclear Cells: Effect of Nanoparticle Air Pollutants.

Fine inhalable particulate matter (PM) triggers an inflammatory response in the airways and activates mononuclear cells, mediators of tissue homeostasis, and tumour-promoting inflammation. We have assessed ex vivo responses of human monocytes and monocyte-derived macrophages to standardised air pollutants: carbon black, urban dust, and nanoparticulate carbon black, focusing on their pro-inflammatory and DNA-damaging properties. None of the PM (100 μg/mL/24 h) was significantly toxic to the cells, aside from inducing oxidative stress, fractional DNA damage, and inhibiting phagocytosis.

Cell cycle-specific phosphorylation of p53 protein in A549 cells exposed to cisplatin and standardized air pollutants.

Exposure to particulate matter is associated with DNA damage and the risk of lung cancer. Protein p53 is activated by multi-site phosphorylation in the early stages of DNA damage and affects cell outcome. Our study aimed to assess the effect of (100 µg/mL/24 h) standardized air pollutants: carbon black (CB), urban dust (UD), and nanoparticle carbon black (NPCB) on cell cycle, DNA damage and 53 phosphorylation at Ser 9, Ser 20, Ser 46, and Ser 392 in proliferating and quiescent A549 cells and in cells that survived cisplatin (CisPT) exposure.