Lawrence J. Folinsbee
University of North Carolina at Chapel Hill
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Featured researches published by Lawrence J. Folinsbee.
J. Air Pollut. Control Assoc.; (United States) | 1988
Lawrence J. Folinsbee; William F. McDonnell; Donald Horstman
Episodes occasionally occur when ambient ozone (O3) levels remain at or near 0.12 ppm for more than 6 h. Small decrements In lung function have been reported following 2-h exposures to 0.12 ppm O3. For short exposures to higher O3 concentrations, lung function decrements are a function of exposure duration. Thus, we investigated the hypothesis that prolonged exposure to 0.12 ppm O3 would result in progressively larger changes in respiratory function and symptoms over time. Ten nonsmoking males (18-33 yr) were exposed once to clean air and once to 0.12 ppm O3 for 6.6 h. Exposures consisted of six 50-min exercise periods, each followed by 10-min rest and measurement; a 35-min lunch period followed the third exercise period. Exercise ventilation averaged approximately 40 L/min. Forced expiratory and inspiratory spirometry and respiratory symptoms were measured prior to exposure and after each exercise. Airway reactivity to methachollne was determined after each exposure. After correcting for the air exposure...
Toxicology and Industrial Health | 1995
Donald H. Horstman; Beth A. Ball; James S. Brown; Timothy R. Gerrity; Lawrence J. Folinsbee
To determine if asthmatic subjects (ASTH, n = 17) experience greater O3 induced pulmonary decrements than nonasthmatic subjects (NONA, n = 13), both groups were exposed for 7.6 h to both clean air and 0.16 ppm 03. Exposures consisted of seven 50-min periods of light exercise (VE = 14.2 and 15.3 l/min/m2 for ASTH and NONA, respectively), each followed by 10 min rest. A 35-min lunch period followed the third exercise. Following 03 exposure, decrements in forced expiratory volume in one second (FEV1) and FEV1 divided by forced vital capacity (FVC), corrected for air exposure, for ASTH
American Industrial Hygiene Association Journal | 1988
Donald H. Horstman; Elston Seal; Lawrence J. Folinsbee; Phillip Ives; L. Jack Roger
The purpose of this study was to determine the shortest duration of exposure to 1.0 ppm sulfur dioxide (SO2) sufficient to induce bronchoconstriction significantly greater than that observed with exposure to clean air (CA) in exercising SO2-sensitive asthmatics. Asymptomatic, nonmedicated, male asthmatics (n = 12) with airway hyperresponsiveness to both methacholine and SO2 were exposed in a chamber (20 degrees C, 40% relative humidity) for 0.0, 0.5, 1.0, 2.0 and 5.0 min to both CA and 1.0 ppm SO2 on separate days (10 exposures). Just prior to each exposure, subjects walked on a treadmill in CA for 5 min at a predetermined speed/elevation to elicit a target ventilation of about 40 L/min, i.e., a brisk pace up a slight incline. After this walk, subjects rapidly entered an adjoining exposure chamber containing either CA or SO2 and immediately walked at the same speed/elevation for the specified exposure duration. Subjects then rapidly exited the chamber. Specific airway resistance (SRaw) and ratings of respiratory symptoms associated with asthma [shortness of breath/chest discomfort (SB/CD) and wheezing (WHZ)] were measured prior to any exercise and following each exposure. Postexposure SRaw and symptom ratings increased with increased exposure duration in SO2; postexposure SRaw also was increased with increased exposure duration in CA but to a lesser extent. After adjusting for the CA response, significantly greater SO2-induced bronchoconstriction was observed for the 2.0 and 5.0 min exposures as indicated by substantially greater increases in SRaw and substantially higher ratings of respiratory symptoms. The authors conclude that with the above exposure conditions, on average, SO2-sensitive asthmatics exhibit significant bronchoconstriction at exposure durations of 2.0 min or more.
Journal of The Air & Waste Management Association | 1991
Ralph I. Larsen; William F. McDonnell; Donald Horstman; Lawrence J. Folinsbee
Forced expiratory volume in 1 second (FEV1) was measured in 21 men exercising while exposed to four O3 concentrations (0.0,0.08,0.10, and 0.12 ppm). A lognormal multiple linear regression model was fitted to their mean FEV1 measurements to predict FEV1 percent decrease as a function of O3 concentration and exposure duration. The exercise level used was probably comparable to heavy manual labor. The longest O3, exposure studied was 6 h. Extrapolating cautiously to an 8-h workday of heavy manual labor, the model predicts that O3 concentrations of 0.08, 0.10, and 0.12 ppm would decrease FEV1 by 9,15, and 20 percent, respectively.
The American review of respiratory disease | 1990
Donald H. Horstman; Lawrence J. Folinsbee; Phillip Ives; Sa'id Abdul-Salaam; William F. McDonnell
The American review of respiratory disease | 2015
Steven M. Horvath; Jeffrey A. Gliner; Lawrence J. Folinsbee
American Journal of Respiratory and Critical Care Medicine | 1994
Lawrence J. Folinsbee; Donald H. Horstman; Howard Kehrl; S Harder; S Abdul-Salaam; P J Ives
American Journal of Respiratory and Critical Care Medicine | 1997
William F. McDonnell; Paul W. Stewart; Solange Andreoni; Elston Seal; Howard Kehrl; Donald H. Horstman; Lawrence J. Folinsbee; Marjo V. Smith
The American review of respiratory disease | 2015
Jeffrey A. Gliner; Steven M. Horvath; Lawrence J. Folinsbee
Inhalation Toxicology | 1997
Robert B. Devlin; Lawrence J. Folinsbee; Frank Biscardi; Gary E. Hatch; Susanne Becker; Michael C. Madden; Mark Robbins; Hillel S. Koren