Publications

This page is a list of publications in reverse chronological order. Please use search or the filters to browse by research areas, publication types, and content types.

Displaying 231 - 240 of 347. Show 10 | 25 | 50 | 100 results per page.


Statistical Methods for Epidemiologic Studies of the Health Effects of Air Pollution

William Navidi
Duncan Thomas
Bryan Langholz
Daniel Stram
1999
Research Report 86

Dr. Navidi and colleagues at the University of Southern California discussed the development of three sophisticated statistical methods that would improve the estimates of the health effects of air pollution obtained from epidemiologic studies. First, they took a standard case-crossover design and introduced a bidirectional element where control data were obtained both before and after the health event of interest.

Mechanisms of Response to Ozone Exposure: The Role of Mast Cells in Mice

Steven R Kleeberger
Malinda Longphre
Clarke G Tankersley
1999
Research Report 85

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.

Evaluation of The Potential Health Effects of the Atmospheric Reaction Products of Polycyclic Aromatic Hydrocarbons

Andrew J Grosovsky
Jennifer C Sasaki
Janet Arey
David Eastmond
Karyn K Parks
Roger Atkinson
1999
Research Report 84

Dr. Arey and colleagues of the University of California, Riverside, examined the genotoxic potential of two PAHs (naphthalene and phenanthrene) that are common air pollutants, and a subset of their atmospheric transformation products. The investigators evaluated the genotoxicity of these compounds using a variety of human cell lines with a range of metabolic capabilities. They examined the ability of these compounds to produce small-scale (damage to genes) and large-scale (damage to chromosomes) genetic damage.

Daily Changes in Oxygen Saturation and Pulse Rate Associated with Particulate Air Pollution and Barometric Pressure

Douglas W. Dockery
C Arden Pope III
Richard E Kanner
G Martin Villegas
Joel Schwartz
1999
Research Report 83

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).

A Partnership to Examine Emerging Health Effects: EC/HEI Workshop on 1,3-Butadiene

Health Effects Institute
1999
Communication 6
Communication 6 contains proceedings from a workshop held in Brussels, Belgium, June 29–30 1998. Presentations focused on butadiene ambient concentrations, metabolism, mutagenicity, epidemiology, and a panel discussion on Butadiene Risk Assessment in the Regulatory Framework.

Atmospheric Observations: Helping Build the Scientific Basis for Decisions Related to Airborne Particulate Matter

National Oceanic & Atmospheric Administration
Health Effects Institute
1998
Workshop Report

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.

Consequences of Prolonged Inhalation of Ozone on F344/N Rats: Collaborative Studies. Part XIII: A Comparison of Changes in the Tracheobronchial Epithelium and Pulmonary Acinus in Male Rats at 3 and 20 Months

Kent E Pinkerton
Barbara L Weller
Margaret G Ménache
Charles G Plopper
1998
Research Report 65-XIII

Ozone, a common outdoor air pollutant, is a highly reactive gas and a major component of smog. A public health concern is that prolonged exposure to ozone might damage the airways and contribute to the development of noncancerous respiratory diseases. To examine this issue, the Health Effects Institute collaborated with the NTP to provide HEI-funded investigators access to animals that underwent the same rigorously controlled ozone exposure and quality assurance processes along with the animals used for NTP studies. One of the NTP/HEI investigator groups, Dr.

Acute Effects of Ambient Ozone on Asthmatic, Wheezy, and Healthy Children

Edward L Avol
William Navidi
Edward B Rappaport
John M Peters
1998
Research Report 82

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).

Methods Development for Epidemiologic Investigations of the Health Effects of Prolonged Ozone Exposure

Ira B Tager
Patrick L Kinney
1998
Research Report 81

Dr. Ira Tager and colleagues at the University of California at Berkeley (UCB), and Dr. Patrick Kinney and colleagues at the School of Public Health, Columbia University objectives were to develop new methods for estimating an individual's past exposure to ozone.

Mechanism of Oxidative Stress from Low Levels of Carbon Monoxide

Stephen R Thom
Harry Ischiropoulos
1997
Research Report 80

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.