The interactions of fly ash aerosol with lung cells were tested in vitro via exposure at the air– liquid interface or via suspension in medium. The experimental set-up for aerosol generation, dilution and exposure of cells under conditions that do not affect the cell viability by the treatment procedure was shown to work in principle. First experiments showed only low effects concerning metabolic activity and release of pro-inflammatory mediators in NR8383 alveolar macrophages and BEAS-2B epithelial cells. Exposure to fly ash resuspended in culture medium neither reduced the viability nor induced the release of tumor necrosis factor α (TNFα), macrophage inflammatory protein-2 (MIP-2) and nitrite in NR8383 macrophages at the indicated concentrations. These conditions, however, enhanced the production of the lipopolysaccharide (LPS)-induced cytokines and inhibited the LPS-induced nitrite release considerably. BEAS-2B cells produced interleukin-6 (IL-6) and IL-8 after fly ash exposure, and this could be further amplified by TNFα. The results support the hypothesis that ambient particulate matter may contribute to the aggravation of lung diseases.