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Responses to Fresh Aerosol in Susceptible Subjects

Howard Kipen1,2, Robert Laumbach1,2, Deborah Laskin3, Paul Lioy1,2, Tina Fan1,2,
Claire Philipp1,Daniel Shindler1, Jim Zhang4, and Pamela Ohman-Strickland4
1University of Medicine and Dentistry of New Jersey Robert Wood Johnson Medical School,
Piscataway, NJ; 2University of Medicine and Dentistry of New Jersey Environmental
and Occupational Health Sciences Institute, Piscataway, NJ; 3Rutgers University,
Piscataway, NJ; 4University of Medicineand Dentistry of New Jersey School
of Public Health, Piscataway, NJ

EPA Grant Number: R832144

Project Description:

Increased occurrence of unstable angina and myocardial infarction, particularly in individuals vulnerable from preexisting atherosclerotic cardiovascular disease (ASCVD), follow even hourly increases in particulate air pollution. The mechanisms underlying these acute cardiovascular effects are unknown. Thrombosis, closely related to endothelial cell dysfunction and platelet activation, is now widely recognized to play an important role in acute exacerbations of cardiovascular disease. In experimental studies, endothelial changes are observed within minutes following a 2-hour exposure of humans to inhaled particulate air pollution. Similarly, platelet activation and thrombosis are observed in rodents within 30 minutes of intratracheal instillation of various ultrafine particles. In these models, both the endothelial and platelet responses appear to be independent of lung inflammation, suggesting an immediate and direct effect of ultrafine particles on these cells. The overall objective of our studies is to explore mechanisms mediating particle-induced cardiovascular effects. We hypothesize that the acute increase in risk of cardiac events following inhalation of ultrafine and fine particles is mediated by a rapid and direct passage of the particles from the lung into the blood, leading immediately to platelet activation and endothelial dysfunction. Moreover individuals with genetically increased risk for ASCVD and endothelial dysfunction will be more sensitive to the effects of ultrafine and fine particles on the endothelium. To test this hypothesis we will use pollutant models of freshly generated diesel exhaust or a sec-ondary organic aerosol both of which consist predominately of particles less than one micron in diameter. The effects of the two fine and ultra fine aerosols will be compared in healthy individuals and individuals with and without a genetic predisposition to endothelial cell dysfunction and ASCVD.



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