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L J Folinsbee

Publications and source records attributed to L J Folinsbee.

16 recordsLinked to original sources
PubMed1992

Effects of steady-state and variable ozone concentration profiles on pulmonary function.

Measurements of ambient ozone (O2) concentration during daylight hours have shown a spectrum of concentration profiles, from a relatively stable to a variable pattern usually reaching a peak level in the early afternoon. Several recent studies have suggested that in estimating exposure dose (O3 concentration [C] x exposure time [T] x ventilation [V]), O3 concentration needs to be weighted more heavily than either ventilation or duration of exposure in the estimates. In this study we tested the hypothesis that regardless of concentration pattern and exposure rate the same exposure dose of O3 will induce the same spirometric response. We exposed 23 healthy male volunteers (20 to 35 yr of age) for 8 h to air, 0.12 ppm O3 (steady-state), and a triangular exposure pattern (concentration increased steadily from zero to 0.24 ppm over the first 4 h and decreased back to zero by 8 h). During the first 30 min of each hour, subjects exercised for 30 min at minute ventilation (VE) approximately 40 L/min. The order of the exposures was randomized, and the exposures were separated by at least 7 days. The response patterns over the 8-h periods for spirometric variables in both O3 exposures were statistically different from air exposure changes and from each other. For FEV1 the p values were 0.017 between air and steady-state profile, 0.002 between air and triangular profile, and 0.037 between steady-state and triangular profiles. Although in the triangular pattern of exposure the maximal O3 concentration was reached at 4 h, the maximum FEV1 decrement (10.2%) was observed at 6 h of exposure.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1991

An air quality data analysis system for interrelating effects, standards, and needed source reductions: Part 11. A lognormal model relating human lung function decrease to O3 exposure.

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.

Adult↗
PubMed1990

Ozone concentration and pulmonary response relationships for 6.6-hour exposures with five hours of moderate exercise to 0.08, 0.10, and 0.12 ppm.

The magnitudes of pulmonary responses we previously observed (1) following 6.6-h exposures to 0.12 ppm ozone (O3) suggested that responses would also occur with similar exposures at lower O3 concentrations. The objective of this study was to determine the extent of pulmonary function decrements, respiratory discomfort, and increased airway reactivity to methacholine induced by exposure to O3 below 0.12 ppm. Separate 6.6-h chamber exposures to 0.00, 0.08, 0.10, and 0.12 ppm O3 included six 50-min periods of moderate exercise (VE approximately equal to 39 L/min, HR approximately equal to 115 bpm, and VO2 approximately equal to 1.5 L/min). Each exercise period was followed by 10 min of rest. A 35-min lunch break was included midway through the exposure. Although not intended as an exact simulation, the overall duration, intensity, and metabolic requirements of the exercise performed were representative of a day of moderate to heavy work or play. Preexposure FEV1 averaged 4.39 L, and essentially no change (+0.03 L) occurred with exposure to 0.00 ppm O3. Significant decreases (p less than 0.01) of -0.31, -0.30, and -0.54 L were observed with exposures to 0.08, 0.10, and 0.12 ppm, respectively. The provocative dose of methacholine required to increase airway resistance by 100% (PD100) was 58 cumulative inhalation units (CIU) following exposure to 0.00 ppm and was significantly reduced (p less than 0.01) to 37 CIU at 0.08, 31 CIU at 0.10, and 26 CIU at 0.12 ppm O3; reductions in PD100 are considered indicative of increases in nonspecific airway responsiveness.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1989

Human health effects of exposure to airborne acid.

This paper summarizes and critiques a series of reports on the health effects of acid aerosol exposure, presented at the Symposium on the Health Effects of Acid Aerosols and compares these data to selected previous studies. The role of the two major defenses against acid aerosols, the conversion of acid to the ammonium salts by respiratory ammonia and buffering of acid by airway surface liquid are discussed in relation to airway acid burdens expected from typical inhalation exposures. The roles of particle size and hygroscopicity on airway deposition of aerosol are also included. The major health effects studied were the effects of acid aerosol on mucociliary clearance in healthy individuals and changes in lung function in asthmatics, an important sensitive subpopulation. The broad range of response in asthmatics suggests the need for further study.

Acid Rain↗
PubMed1988

The relationship between exposure duration and sulfur dioxide-induced bronchoconstriction in asthmatic subjects.

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.

Adult↗
PubMed1987

Combined effect of ozone and sulfuric acid on pulmonary function in man.

A potential effect of the combination of ozone and sulfuric acid mist (H2SO4) on respiratory function has been postulated for humans simultaneously exposed to these two pollutants. Nine young men were exposed to 0.25 ppm ozone (O3), 1200-1600 micrograms/m3 sulfuric acid aerosol (H2SO4), and a combination of O3 and H2SO4. During the 2-hr exposures, the subjects exercised (ventilation = 30 L/min) three times for 20 min each. Air temperature was 35 degrees C and relative humidity 83%. Pulmonary function changes after exposure to ozone alone were not expected and were not demonstrated. If a reaction between the combination of O3 and H2SO4 and pulmonary function occurred, pulmonary function responses may have been anticipated following the combination exposure, but no significant changes were seen. It was concluded that the combination of ozone and sulfuric acid aerosol at levels in excess of Threshold Limit Values (TLV) levels do not cause pulmonary dysfunction.

Adolescent↗
PubMed1979

Response of women mountaineers to maximal exercise during hypoxia.

Eight members of the American Women's Himalayan Expedition, ranging in age from 20-49, performed maximal exercise on a treadmill under normoxic and acute hypoxic (12.58% O2) conditions. Normoxic values for VO2 max were above average for all subjects and did not decline with age. The mean decrease in VO2 max (26.7%) during hypoxia was equivalent to that reported for younger males, which suggests that age was not a factor in response to hypoxia. Maximal heart rate, respiratory exchange ratio, oxygen pulse, and walk time were lower in hypoxia while ventilatory equivalent and blood lactate were higher. VEmax BTPS, was the same under both conditions. The combination of laboratory results and field observations by the Expedition physician suggest that women are capable of performing hard work at high altitude if they are in good condition and properly acclimatized.

Adult↗
PubMed1977

Decrease of maximum work performance following ozone exposure.

A bicycle ergometer was used to measure maximum exercise oxygen consumption following 2 h of intermittent exercise in an environmental chamber ventilated with air (FA test) or filtered air plus 0.75 ppm ozone (PO test). Thirteen adult males performed both tests according to a random sequence. The maximum attained VO2 declined 10% (P less than 0.01), maximum attained work load was reduced by 10% (P less than 0.01), maximum ventilation decreased 16% (P less than 0.01), and maximum heart rate dropped 6% (P less than 0.05) in the PO test. At the highest common work load, heart rate and oxygen consumption were similar and ventilation was slightly higher (P less than 0.05); however, frequency of respiration increased 45% (P less than 0.01) and tidal voluem fell by 29% (P less than 0.01) following ozone exposure. During maximum exercise, the respiratory frequency was similar in both tests, but tidal volume was 21% lower (P less than 0.01) in PO experiments. Decreases in vital capacity and FEV1.0 as well as cough and chest discomfort were also noted following ozone exposure. We conclude that the reduction of maximum attained VO2 is a consequence of ventilatory limitation of maximum effort, probably related to respiratory discomfort.

Adult↗
PubMed1977

Influence of exercise and heat stress on pulmonary function during ozone exposure.

We studied the effects of a 2-h exposure to ozone (0.5 ppm) in 14 nonsmoking males under four environmental conditions (WBGT (wet bulb-globe temperature index) = 64.4, 80.0, 85.2, and 92.0 degrees F). The subjects were divided into two groups, A (n = 8) and B (n = 6). Thirty minutes of exercise at 40% Vo2 max was performed from 60 to 90 min for group A and 30 to 60 min for group B. Pulmonary function changes, determined throughout exposure, were greatest immediately after exercise in both groups. Few changes occurred before the exercise period. However, the decrease in FVC (826 ml) and FEV1.0 (937 ml) following exercise was more than twice as large as the decrement seen at end exosure (388 and 423 ml, respectively). Measures of maximum expiratory flow (FEF 25-75%, FEF 50% FEF 75%) showed similar reductions. In many cases, reversal of these changes occurred during the remainder of the exposure period. The greatest decrease in FVC occurred when heat and ozone exposures were combined (WBGT = 92.0 degrees F). We conclude that the effects of ozone are most severe immediately after exercise and that heat stress may modify the overall effect of ozone on pulmonary function.

Adult↗
PubMed1976

Pulmonary function changes in ozone-interaction of concentration and ventilation.

A total of 28 healthy young subjects have been exposed for 2 h to ozone (0.37-0.75 ppm) under conditions of either rest or intermittent light exercise (sufficient to increase the respiratory minute volume by a factor of 2.5). All pulmonary function tests (vital capacity, forced expiratory volume, maximum expiratory flow-volume curve, slope of phase III of alveolar nitrogen plateau) showed a significant deterioration relative to parallel control experiments. Responses were related to the dose of ozone as calculated from the product of concentration, exposure time, and respiratory minute volume during exposure, changes at 1 h averaging approximately one-half those seen at 2 h.

Adult↗
PubMed1975

Exercise responses following ozone exposure.

We have tested the response of 28 subjects to a three-stage ergometer test, with loads adjusted to 45, 60, and 75% of maximum aerobic power following ozone exposure. The subjects were exposed to one of 0.37, 0.50, or 0.75 ppm O3 for 2 h either at rest (R) or while exercising intermittently (IE) (15 min rest alternated with 15 min exercise at approximately 50 W. sufficient to increase VE by a factor of 2.5). Also, all subjects completed a mock exposure VE, respiratory frequency (fR), mixed expired PO2 and PCO2, and electrocardiogram were monitored continuously during the exercise test. Neither submaximal exercise oxygen consumption nor minute ventilation was significantly altered following any level of ozone exposure. The major response noted was an increase in respiratory frequency during exercise following ozone exposure. The increase in fR was closely correlated with the total dose of ozone (r = 0.98) and was accompanied by a decrease in tidal volume (r = 0.91) so that minute volume was unchanged. It is concluded that through its irritant properties, ozone modifies the normal ventilatory response to exercise, and that this effect is dose dependent.

Adult↗
PubMedDate not supplied

Human exposure to sulfur dioxide and ozone: absence of a synergistic effect.

Studies of the human health effects of exposure to a combination of ozone and sulfur dioxide have produced somewhat conflicting results; the possibility of a synergistic enhancement of toxicity when the two gases are present simultaneously remains equivocal. We evaluated the effects of 0.40 ppm sulfur dioxide, 0.40 ppm ozone, and the combination of these two under one environmental condition (25 degrees C and 45% relative humidity). Subjects alternately walked and rested during a 2-hr exposure. Subjects exposed to filtered air or to 0.40 ppm sulfur dioxide showed no significant changes in pulmonary function. When exposed to either ozone or ozone plus sulfur dioxide, significant decreases in maximum expiratory flow, forced vital capacity, and inspiratory capacity were observed. There were no significant differences in response between ozone alone and ozone plus sulfur dioxide exposures, thus, in our subjects on synergistic effects were discernible.

Adolescent↗
PubMedDate not supplied

Respiratory response of humans exposed to low levels of ozone for 6.6 hours.

Recent evidence suggests that prolonged exposures of exercising men to 0.08 ppm ozone (O3) result in significant decrements in lung function, induction of respiratory symptoms, and increases in nonspecific airway reactivity. The purpose of this study was to confirm or refute these findings by exposing 38 healthy young men to 0.08 ppm O3 for 6.6 h. During exposure, subjects performed exercise for a total of 5 h, which required a minute ventilation of 40 l/min. Significant O3-induced decrements were observed for forced vital capacity (FVC, -0.25 l), forced expiratory volume in 1 s (FEV1.0, -0.35 l), and mean expiratory flow rate between 25% and 75% of FVC (FEF25-75, -0.57 l/s), and significant increases were observed in airway reactivity (35%), specific airway resistance (0.77 cm H2O/s), and respiratory symptoms. These results essentially confirm previous findings. A large range in individual responses was noted (e.g., percentage change in FEV1.0; 4% increase to 38% decrease). Responses also appeared to be nonlinear in time under these experimental conditions.

Adolescent↗
PubMedDate not supplied

Does nitrogen dioxide exposure increase airways responsiveness?

A number of reports have suggested that exposure to nitrogen dioxide (NO2) may cause increased airways responsiveness (AR). Twenty studies of asthmatics and five studies of healthy subjects exposed to NO2 were used to test this hypothesis using a simple method of meta-analysis. Individual data were obtained for the above studies and the direction of change in AR was determined for each subject. Only studies with available individual data were used. Subjects from these studies whose directional change in AR could not be determined were excluded. The fraction of positive responses (i.e. increased AR) was determined for all subjects within a group and tested for significance using a sign test. Data were also grouped according to NO2 concentration and by whether the exposure included exercise. There was an overall trend among asthmatics for AR to increase (60%) but this was primarily due to increased AR seen in resting exposures (70%). Among healthy subjects AR also increased with NO2 exposure but only at concentrations above 1.0 ppm. This analysis suggests that NO2 exposure causes increased airway responsiveness in healthy and asthmatic subjects but that exercise during exposure may modify this response in asthmatics.

Asthma↗