Scientists Probe Air Pollution-Heart Disease Link: The Environmental Protection Agency awarded the University of Rochester Medical Center $8 million in 2005 to study the link between cardiovascular health and the harmful ambient air particles we breathe every day. The initiative was part of a nationwide effort, with this Medical Center being named one of five EPA Particulate Matter (PM) Centers. The grants to each institution are funded through the EPA’s Science to Achieve Results (STAR) competitive grants program.... [The EPA’s other PM Centers are located at the University of California at Los Angeles, Harvard University, the University of California at Davis, and Johns Hopkins University.] [more]

The award described above represents the result of an open competition. This university was successful once again in being chosen to have an EPA Star Particulate Matter Center.

The initial grant also provided support to study the role of airborne particulate matter, especially ultrafine particles, in causing health problems. A multidisciplinary team of experienced investigators is testing the hypothesis that ultrafine particles occurring in the urban atmosphere cause adverse health effects.

Epidemiological studies have consistently found an association between small increases in urban particulates and health effects, including increased morbidity and mortality in people with respiratory and cardiac disease. The elderly are especially susceptible. These effects are associated with fine rather than coarse particles.

Some epidemiological studies found that particle number—reflecting ambient ultrafine particles—correlated with increased symptoms in people with compromised respirtory and cardiovascular symptoms. Moreover, animal studies have shown that ultrafine particles have a significantly greater pulmonary inflammatory potency than larger submicronic particles of the same chemical composition. These results form the basis for the ultrafine particle hypothesis.

The following describes the studies addressed by our interactive Research Cores:

• Studies will identify health hazards of source-specific physicochemical components of fine PM (e.g., UFP; organics) in epidemiological, controlled clinical, animal, and in vitro studies; a main focus is on sources and on pathophysiological mechanisms by which ambient ultrafine (UF)/fine PM trigger cardiovascular adverse health effects, with specific emphasis on events leading to endothelial dysfunction. Results will be crucial for risk assessment and will strengthen risk management decisions with respect to regulatory actions.
• The Center is comprised of five Research Cores, thus representing a highly integrated approach linking measurement and physicochemical characterization of ambient ultrafine and fine PM (Core 1) with
1. epidemiological findings (Core 2) from panel studies in susceptible populations, including diabetics, MI patients and patients with genetic susceptibility;
2. results of controlled clinical exposures (Core 3) of healthy and diabetic subjects exposed to concentrated ambient UF/fine PM;
3. outcomes of acute and subchronic studies in diabetic rats and a mouse model of neurodegeneration (Core 4) following exposures to concentrated ambient UF/fine PM and on-road highway aerosols;
4. findings from in vitro studies (Core 5) to evaluate underlying mechanisms of injury that will explain in vivo findings.
• The Research Cores are supported by four Facility Cores: Aerosol Generation and Analysis, Vascular and Inflammation, Cardiac, and Biostatistics, which are essential elements in our coordinated research approach. Our central hypothesis is based on particle-induced oxidative stress – potentially involving reactive oxygen species (ROS) on ambient UF/fine PM as well as cellular ROS production resulting from particle-cell interactions following UFP deposition in the respiratory tract and translocation to the cardiovascular system with subsequent target cell activation and inflammation.
• A major focus is on mechanisms of vascular events involving activation of endothelial cells and blood platelets, resulting in thrombus formation with potential fatal consequences in susceptible subjects with predisposing cardiovascular disease.
• Pathophysiological mechanisms of neurodegenerative effects of inhaled UFP will also be studied based on the hypothesis that UFP translocating to the CNS induce oxidative stress at sensitive target sites.
• Our integrated approach to perform the proposed research by a highly experienced multidisciplinary team of atmospheric scientists, chemists, epidemiologists, pulmonary, vascular and cardiac physicians and scientists, inhalation-, neuro-, cellular- and molecular- toxicologists, diabetologists, and immunologists should result in important novel findings to be used in protecting public health and regulatory decision-making.