Acute health effects of ambient air pollution: The ultrafine particle hypothesis

Citation
Mj. Utell et Mw. Frampton, Acute health effects of ambient air pollution: The ultrafine particle hypothesis, J AEROSOL M, 13(4), 2000, pp. 355-359
Citations number
22
Categorie Soggetti
Envirnomentale Medicine & Public Health
Journal title
JOURNAL OF AEROSOL MEDICINE-DEPOSITION CLEARANCE AND EFFECTS IN THE LUNG
ISSN journal
08942684 → ACNP
Volume
13
Issue
4
Year of publication
2000
Pages
355 - 359
Database
ISI
SICI code
0894-2684(200024)13:4<355:AHEOAA>2.0.ZU;2-3
Abstract
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.