Printing devices such as photocopiers and printers emit predominantly nanoparticles, which may aggregate with time to form PM0.25-2.0 particles. To date, there are no reports on cytotoxic or genotoxic effects of PM0.25-2.0 particles emitted from photocopiers. To investigate the ability of PM0.25-2 fraction emitted from photocopiers, induce pro-inflammatory cytokines, DNA damage and apoptosis in different human-derived cell lines. Three cell types, i.e. a THP-1 line, primary human nasal and small airway epithelial cells, were used. The airborne PM0.25-2.0 size fraction collected from a photocopy center was characterized for its physicochemical and morphological properties, dispersed in culture media and cells were treated with 30, 100 or 300 µg/ml doses. Levels of 13 cytokines and chemokines in the culture medium harvested at 6 and 24 h of treatment were measured using Luminex cytokine kits. In cells harvested at the same timepoints, DNA damage in cells was studied by a Comet assay, and apoptosis was measured by cytofluorimetry using an Annexin V staining kit. The results indicate that in THP-1 cells, several cytokines (IL-6, IL-8, TNFα and IL-1β) were significantly elevated. Only IL-8 was significantly elevated in the primary nasal and small airway cells. Cells exposed to PM0.25-2.0 underwent apoptosis in a dose-dependent manner, but no significant differences were found in the extent of DNA damage at either timepoint. Airborne PM0.25-2.0 collected at one photocopier center was capable of inducing several pro-inflammatory cytokines and apoptosis, but no genotoxicity, in all cell lines suggesting a role for PM0.25-2.0 in our previously documented airway inflammation in human volunteers. Further toxicological evaluations of these particles across different toner manufacturers are warranted.