How can ultrafine particles be responsible for increased mortality?

The link between particulate air pollution at relatively low levels and adverse effects both in the lungs and of the cardiovascular system remains a puzzling event. The authors have developed a hypothesis which suggests that ultrafine components of particulate air pollution may result in local and systemic oxidative stress, which produces lung inflammation, but also the systemic effects, resulting in mortality in susceptible individuals from cerebrovascular disease. Preliminary data in vitro and in vivo suggest that both local and systemic oxidative stress occur in response to ultrafine particles and that the effects of such oxidative stress on pro-inflammatory gene regulation and changes in blood coagulation may result in the adverse effects of particulate air pollution. In this article, the evidence which supports this hypothesis is reviewed.