Publications

In a follow-up study to previous research, Dr. Mercer and colleagues at Duke University exposed three groups of rats continuously for six weeks to 2 or 6 ppm nitric oxide (NO) or to filtered air to learn more about the toxicity of NO so as to compare it with two other important oxidants, ozone and nitrogen dioxide (NO₂). At the end of the exposure period he used an electron microscope to measure the number of holes in the alveolar septa and to observe other structural changes, such as in the surface area and the number and type of other abnormalities in the alveolar septa.

A Special Report of the Institute's Diesel Epidemiology Expert Panel. Although epidemiologic data have been used generally to identify the hazards associated with exposure to diesel exhaust, questions remain as to whether the human data can be used to develop reliable estimates of the magnitude of any risk for lung cancer (that is, through quantitative risk assessment [QRA]), and whether new research efforts could provide any additional data needed. In response to such issues, the Health Effects Institute initiated the Diesel Epidemiology Project in 1998.

Dr. Kleeberger and colleagues at Johns Hopkins University compared ozone-induced inflammation, epithelial cell injury, and epithelial cell proliferation (a marker of cell injury) in three types of mice: mice with a normal content of mast cells, mutant mice without mast cells, and mutant mice whose mast cells were repleted by a bone marrow transplant from normal mice. Each group of mice was exposed to clean air or to ozone for varying lengths of time.

Drs. Douglas Dockery at the Harvard School of Public Health and C. Arden Pope III at Brigham Young University speculated that exposure to PM might lead to a transient drop in blood oxygenation, which might have serious consequences in humans with heart or lung problems. The investigators designed a study to increase the possibility of observing PM effects by testing a potentially at-risk group (the elderly) at a time of year that historically had experienced relatively high levels of PM (the winter).

Daniel L. Albritton and Daniel S. Greenbaum, cochairs. Report of the PM Measurements Research Workshop, Chapel Hill NC, July 22 and 23, 1998. Aeronomy Laboratory of the National Oceanic and Atmospheric Administration, Boulder, CO, and Health Effects Institute, Cambridge, MA.

Dr. John Peters and colleagues of the University of Southern California School of Medicine compared the lung function, respiratory symptoms, activity levels, and bronchodilator use of 10- to 12-year-old healthy, asthmatic, and wheezy children. They conducted the study in Southern California during mid-spring (when ozone levels were expected to be low) and late summer (when ozone levels were expected to be high).

Dr. Thom and Dr. Ischiropoulos at the University of Pennsylvania Medical Center examined the effects of low concentrations of carbon monoxide on platelets and cells isolated from blood vessels. The investigators exposed blood platelets (taken from rats) and endothelial cells (isolated from bovine blood vessels) to varying concentrations of carbon monoxide and measured how much nitric oxide was released. To determine if exposure to carbon monoxide causes endothelial cells to produce peroxynitrite, the investigators looked for markers of its presence in the culture medium and in the cells.

Communication 5 contains proceedings of a workshop held in Cambridge, MA, December 3–4 1996. Presentations included: Current Understanding of the Health Effects of Particles and the Characteristics That Determine Dose or Effect; Particle Formation in Combustion; The EPA Particle Emissions Testing Procedure; Characterizing Particulate Matter in Motor Vehicle Exhaust; Atmospheric Aerosol Transformation; Generating Particles for Laboratory Studies; and Issues and Research Needs for Particle Characterization.

Dr. John Balmes and colleagues of the University of California, San Francisco, and Dr. Mark Frampton and associates of the University of Rochester characterized ozone-induced responses in two different study populations: normal and asthmatic men and women in the Balmes study (Part I), and male and female nonsmokers and smokers in the Frampton study (Part II). The investigators addressed three issues: (1) Is an individual's reactivity to inhaled methacholine related to changes in lung function after exposure to ozone? (2) What is the relation between ozone-induced airway inflammation and changes in lung function? and (3) Do the changes in lung function and markers of inflammation in response to ozone exposure differ between normal people and people with asthma?

The Phase I.B Report of the Particle Epidemiology Evaluation Project. The Health Effects Institute began the Particle Epidemiology Evaluation Project in 1994 to evaluate the emerging epidemiologic evidence of a relation between particulate air pollution and daily mortality. In Phase I.B, Drs. Jonathan M. Samet and Scott L. Zeger and their colleagues at the Johns Hopkins University School of Hygiene and Public Health (1) compared approaches for controlling the effects of weather variables when analyzing the connection between air pollution and daily mortality, primarily focusing on Synoptic Weather Categories, an approach newly proposed by Dr. Laurence S. Kalkstein of the University of Delaware; and (2) evaluated the association between particulate air pollution and daily mortality in the Philadelphia metropolitan area using statistical models that included data for five pollutants regulated under the Clean Air Act Amendments of 1990 (referred to as criteria pollutants).

Dr. Loomis and colleagues at the University of North Carolina and Dr. Víctor Borja-Aburto of the Instituto Nacional de Salud Pública in Cuernavaca, Mexico, collected mortality, air quality, and weather data from records and monitoring stations in Mexico City from 1990 through 1992. Using statistical techniques, the investigators evaluated the association between mortality and ambient levels of ozone, sulfur dioxide, and total suspended particles, both individually and in a model that included all three pollutants.

Drs. Pollack and Brouwer at the University of North Carolina determined the relationship between methanol exposure and its uptake into and elimination from the blood of nonpregnant and pregnant rodents. The investigators exposed rats and mice at several different stages of gestation to methanol intravenously or orally (doses ranged from 100 mg/kg of body weight to 2,500 mg/kg) or by inhalation (1,000 to 20,000 ppm for 8 hours). They measured blood, urine, and amniotic fluid concentrations of methanol and used the data to develop a model of methanol distribution in rodents.