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 articulate 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 and interstitial transfer of the particles. The large surface area provided by ultrafine particles in contact with the lung provides the opportunity for surface chemistry of the particles to have a profound effect. Free radicals, such as hydroxyl radical, may be generated via transition metals associated with PM10 particles leading to oxidative damage and cell stimulation; stable radicals at the particle surface may also be important in the interactions of other types of ultrafine particles with cells. Ultrafine particles that penetrate to the interstitium will make contact with interstitial macrophages and other sensitive cell populations and this is likely to have a powerful inflammogenic effect that underlies development of subsequent disease.