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Experimental studies have shown that rats exposed to ultrafine particles of, for example, titanium dioxide or carbon black, sustain more lung injury and pathology than rats exposed to the same deposited mass of fine respirable particles composed of the same material. Epidemiological studies have shown a correlation between environmental particulate air pollution (PM₁₀) and a range of endpoints of lung morbidity and also mortality, and an ultrafine fraction of the PM₁₀ particles is considered to be the principal mediator of these effects. A sequence of events following pulmonary deposition of ultrafine particles can be hypothesised, based on studies to date. The large number of deposited particles per unit mass may exceed the ability of macrophages to phagocytose them, and the prolonged interaction between the particles and epithelial cells that this allows may be an important factor in stimulating inflammation …