A strong and consistent association has been observed between adjusted mort
ality rates and ambient particle concentration. The strongest associations
are seen for respiratory and cardiac deaths, particularly among the elderly
. Particulate air pollution is also associated with asthma exacerbations, i
ncreased respiratory symptoms, decreased lung function, increased medicatio
n use, and increased hospital admissions. The U.S. Environmental Protection
Agency (EPA) has recently promulgated a new national ambient air quality s
tandard for fine particles, and yet the mechanisms for health effects at su
ch low particle mass concentrations remain unclear. Hypotheses to identify
the responsible particles have focused on particle acidity, particle conten
t of transition metals, bioaerosols, and ultrafine particles. Because ultra
fine particles are efficiently deposited in the respiratory tract and may b
e important in initiating airway inflammation, we have initiated clinical s
tudies with ultrafine carbon particles in healthy subjects. These studies e
xamine the role of ultrafines in: (1) the induction of airway inflammation;
(2) expression of leukocyte and endothelial adhesion molecules in blood; (
3) the alteration of blood coagulability; and (4) alteration in cardiac ele
ctrical activity. These events could lead to exacerbation of underlying car
diorespiratory disease. For example, airway inflammation may activate endot
helium and circulating leukocytes, and induce a systemic acute phase respon
se with transient hypercoagulability; this could explain the epidemiologic
linkages between pollutant exposures and cardiovascular events. These appro
aches should be useful in identifying mechanisms for pollutant-induced resp
iratory and systemic effects, and in providing data for determining appropr
iate air quality standards.