We have previously examined the ability of air pollution particles (PM₁₀) to promote release of the pro-inflammatory cytokine tumour necrosis factor alpha (TNF-) from human peripheral blood mononuclear cells and demonstrated a role for calcium as a signalling molecule in this process. We have now studied the ability of oxidative stress induced by a synthetic oxidant tert-butylhydroperoxide (tBHP) to induce TNF production via calcium signalling in the mouse macrophage cell line (J774). The oxidant tBHP significantly increased intracellular calcium and the release of TNF- in J774 cells, an effect which was reduced to control levels by inhibition of calcium signalling with verapamil, BAPTA-AM and W7. This study also investigated interactions between PM₁₀ treated macrophages and epithelial cells by using conditioned medium (CM) from PM₁₀ treated mononuclear cells to stimulate the release of the neutrophil chemoattractant chemokine IL-8 from A549 lung epithelial cells. TNF- protein release was demonstrated in human mononuclear cells after PM₁₀ treatment, an effect which was inhibited by calcium antagonists. Treatment of A549 cells with monocyte/PM₁₀ CM produced increased IL-8 release which was reduced with CM from monocyte/PM₁₀/calcium antagonist treatments. The expression of ICAM-1 was increased after incubation with CM from monocyte/PM₁₀ treatment and this increase was prevented by treatment with CM from monocyte/PM₁₀/calcium antagonist. These data demonstrate a link between oxidative stress, calcium and inflammatory mediator production in macrophages and lung epithelial cells.