Research Reports

Research Report 138, Health Effects of Real-World Exposure to Diesel Exhaust in Persons with Asthma, is one part of HEI's larger program on the role of particles in exacerbating asthma and other allergic diseases. This report describes a study to evaluate how inhaling air with a high concentration of diesel exhaust from vehicular traffic while walking on a busy street in Central London might affect people who had either mild or moderate asthma. Dr.

Research Report 135 describes a study to determine whether the biologic response to inhaled ultrafine particles depends on particle composition. Neonatal and young adult rats were exposed to laboratory-generated ultrafine metal particles, either alone or in combination with soot, and their lungs examined for oxidative stress, inflammation, and injury.

The RIOPA project comprised three studies, one funded by the Mickey Leland National Urban Air Toxics Research Center (NUATRC) and two funded by HEI, that investigated seasonal concentrations of 16 VOCs, 10 carbonyls, and PM_2.5 in homes in Los Angeles CA, Houston TX, and Elizabeth NJ. The project was jointly funded and reviewed by a Special Review Panel of the two organizations. It generated a rich database on concentrations of air toxics and PM2.5 in the personal breathing zone of 100 adults in each city as well as inside and outside their homes.

Dr. Koutrakis and his colleagues assessed the correlations between personal exposure to PM_2.5 and gaseous copollutants and compare these measurements with those taken at central-site monitors. Three groups of possibly susceptible individuals (children, seniors, and individuals with chronic obstructive pulmonary disease) were recruited in two cities (Boston and Baltimore) in two seasons (summer and winter).

Dr. Hahn and colleagues systematically examined lung inflammation in young adult and old rats after inhalation of fine particles (< 2.5 µm in aerodynamic diameter) and ultrafine particles (< 0.1 µm in aerodynamic diameter) of different composition: relatively inert carbon and vanadium pentoxide (V₂O₅), which contains the transition metal vanadium, known to cause toxic effects upon inhalation in humans in occupational settings. In addition, they examined the effect of a short-term increase (spike) in particle exposure concentration on inflammatory response.

This report contains two studies, by Drs. Annette Peters and Douglas Dockery. Dr. Peters and her colleagues evaluated the association between nonfatal myocardial infarction (MI) and exposure to particulate matter just prior to the event. She asked 691 patients in hospitals in Augsburg, Germany who survived an MI to provide hourly details about their activities 4 days before MI onset. The investigators used a case-crossover analysis to determine whether exposure to pollutants was associated with onset of MI. Dr. Dockery and colleagues assessed the correlation between short-term increases in ambient concentrations of particulate matter and the risk of possibly life-threatening arrhythmias in patients with implanted cardioverter defibrillators (ICDs). The investigators studied 195 patients from Boston, MA who had either single or dual-chamber ICD's and used logistic regression models to determine whether exposure to air pollutants was associated with arrhythmias.

Dr. Brunekreef and his colleagues assessed the correlation between personal, indoor, and outdoor PM_2.5 concentrations for elderly people with cardiovascular disease living in Amsterdam, The Netherlands, and Helsinki, Finland. Measurements were taken between November 1998 and June 1999 using fixed monitoring sites near the subjects' residences and inside their homes using the same type of monitor. Personal exposures were monitored with a different type of sampler that the subjects kept with them at all times.

Dr. Frampton and his colleagues evaluated the effects of exposing healthy and mildly asthmatic men and women to laboratory-generated ultrafine carbon particles. They hypothesized that ultrafine particle exposure would activate leukocytes and endothelial cells and lead to an inflammatory response in the airway and in the blood; and that it also might affect respiration and cardiac electrophysiologic function. They further hypothesized that effects would be greater in people with asthma than in healthy people.