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D H Horstman

Publications and source records attributed to D H Horstman.

At least 19 recordsLinked to original sources
PubMed1997

Prediction of ozone-induced FEV1 changes. Effects of concentration, duration, and ventilation.

The purpose of this analysis of previously published data was to identify a model that accurately predicts the mean ozone-induced FEV1 response of humans as a function of concentration (C), minute ventilation (VE), duration of exposure (T), and age. Healthy young adults (n = 485) were exposed for 2 h to one of six ozone concentrations while exercising at one of three levels. Candidate models were fitted to portions of the data and evaluated on the basis of their ability to predict the mean response of independent samples. A sigmoid-shaped model that is consistent with previous observations of ozone exposure-response (E-R) characteristics was identified and found to accurately predict the mean response with independent data. This model in a more general form may allow the prediction of responses under conditions of changing C and VE. We did not find that response was more sensitive to changes in C than in VE, nor did we find convincing evidence of an effect of body size upon response. We did find that response to ozone decreases with age. In summary, we have identified a biologically plausible, predictive model that quantifies the relationship between the ozone-induced change in FEV1, and C, VE, T, and age.

Adolescent↗
PubMed1994

Respiratory responses to repeated prolonged exposure to 0.12 ppm ozone.

Repeated exposure to high concentrations of ozone results first in augmentation (typically on the second day) and then attenuation of pulmonary response in humans. To determine the effects of repeated prolonged low-concentration ozone exposure, we exposed 17 healthy nonsmoking male subjects to 0.12 ppm ozone for 6.6 h on 5 consecutive days. Subjects were also exposed once to filtered air. Volunteers exercised at a ventilation of approximately 39 L/min for 50 min of each hour during the exposure. Spirometry, plethysmography, and symptom responses were obtained before, during, and after each exposure. Nasal lavage and aerosol bolus dispersion were obtained before and after exposure. Spirometry decreased and symptoms increased on the first day. Responses were less on the second day compared with those on the first day, and they were absent compared with control values on the subsequent 3 days of ozone exposure. Percent change in FEV1 after ozone exposure compared with that after air exposure averaged -12.79, -8.73, -2.54, -0.6, +0.18% for Days 1 to 5 of ozone exposure, respectively. FEV1 responses ranged from a zero to 34% decrease on Days 1 and 2. After each exposure, we determined the ratio of SRaw after inhaling a fixed dose of methacholine to SRaw after inhaling saline aerosol, as an index of airway responsiveness. Airway responsiveness was significantly increased after each ozone exposure. The mean ratios were 2.22, 3.67, 4.55, 3.99, 3.24, and 3.74 for filtered air and ozone Days 1 to 5, respectively. Symptoms of cough and pain on deep inspiration increased significantly on ozone Day 1 only.(ABSTRACT TRUNCATED AT 250 WORDS)

Analysis of Variance↗
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↗
PubMed1990

Pulmonary function, airway responsiveness, and respiratory symptoms in asthmatics following exercise in NO2.

Two experiments were conducted to determine respiratory responses of persons with asthma performing intermittent moderate exercise while exposed to low concentrations of NO2. In the first, preliminary experiment, 13 male subjects, aged 19-35, with mild asthma were exposed on separate days in a chamber (natural breathing, 20 degrees C, 40% RH) to 0.30 ppm NO2 and to a control or "clean air" exposure (0.0 ppm NO2). Exposure included three 10-min periods of moderate treadmill exercise (VE = 44.5 liter/min), each followed by symptom measurement and pulmonary function testing. The average decrease in FEV1 following the initial 10 min exercise in 0.30 ppm was 11% which was significantly greater (p less than 0.05) than that observed in clean air (7%). Differences in FVC and SRaw were not significantly different at this time. Slight cough and dry mouth and throat were apparent only after the first exercise in NO2. After the second and third exercises, decreases in FEV1 and FVC and increases in SRaw were significantly greater in 0.30 than in 0.0 ppm NO2. Individual subject responses were variable. These results suggested that some asthmatics who perform moderate exercise while exposed to 0.30 ppm NO2 may experience bronchoconstriction and reduction in spirometric performance. Because of these preliminary findings, a more comprehensive, concentration-response experiment was conducted. Twenty-one male volunteers with mild asthma were exposed for 75 min with natural breathing to 0.0, 0.15, 0.30, and 0.60 ppm NO2. Exposure included three 10-min periods of moderate treadmill exercise (VE = 43 liter/min), each exercise followed by symptoms measurement and pulmonary function testing. In addition, airway responsiveness was measured two hr after each exposure by methacholine bronchial challenge testing. In the control exposures (0.0 ppm NO2), the exercise alone caused substantial decrements in pulmonary function. These decrements (as measured by decreases in FEV1 and FVC, and increases in SRaw) were not increased relative to the control exposure after any exercise session in any concentration of NO2. Furthermore, there was no overall group-averaged indication of a concentration-related effect of the NO2 on pulmonary function. Likewise, symptoms reported after NO2 exposure were not significantly different from those reported in clean air. Group-averaged airway responsiveness after exercise in NO2 was also not different from responsiveness after exercise in clean air. For only two subjects was there any indication of a concentration-related increase in airway responsiveness due to exposure to NO2.(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗
PubMed1989

Ozone-induced inflammation in the lower airways of human subjects.

Although ozone (O3) has been shown to induce inflammation in the lungs of animals, very little is known about its inflammatory effects on humans. In this study, 11 healthy nonsmoking men, 18 to 35 yr of age (mean, 25.4 +/- 3.5), were exposed once to 0.4 ppm O3 and once to filtered air for 2 h with intermittent exercise. Eighteen hours later, bronchoalveolar lavage (BAL) was performed and the cells and fluid were analyzed for various indicators of inflammation. There was an 8.2-fold increase in the percentage of polymorphonuclear leukocytes (PMN) in the total cell population, and a small but significant decrease in the percentage of macrophages after exposure to O3. Immunoreactive neutrophil elastase often associated with inflammation and lung damage increased by 3.8-fold in the fluid while its activity increased 20.6-fold in the lavaged cells. A 2-fold increase in the levels of protein, albumin, and IgG suggested increased vascular permeability of the lung. Several biochemical markers that could act as chemotactic or regulatory factors in an inflammatory response were examined in the BAL fluid (BALF). The level of complement fragment C3 alpha was increased by 1.7-fold. The chemotactic leukotriene B4 was unchanged while prostaglandin E2 increased 2-fold. In contrast, three enzyme systems of phagocytes with potentially damaging effects on tissues and microbes, namely, NADPH-oxidase and the lysosomal enzymes acid phosphatase and beta-glucuronidase, were increased neither in the lavaged fluid nor cells. In addition, the amounts of fibrogenic-related molecules were assessed in BALF.(ABSTRACT TRUNCATED AT 250 WORDS)

Acute Disease↗
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

Differing response of asthmatics to sulfur dioxide exposure with continuous and intermittent exercise.

Ten subjects with mild asthma were initially exposed in an environmental chamber (26 degrees C 70% relative humidity) to clean air and 1.0 ppm SO2 while performing 3 sets of 10-min treadmill exercises (ventilation, 41 L/min) broken by 15-min rest periods. To evaluate the effects of the pattern and duration of exercise on the response to SO2 exposure, the subjects were then exposed to the same environmental conditions while exercising continuously for 30 min. Specific airway resistance (SRaw) was measured by body plethysmography before each exposure and after each exercise. All SO2 responses were significantly greater than the clean air responses. With intermittent exercise and SO2 exposure, mean SRaw measurements (preexposure and after 10, 20, and 30 min of exercise) were 5.4, 14.7, 12.8, and 11.1 cm H2O/s. After SO2 exposure with continuous exercise, the mean SRaw showed an increase from 5.2 to 17.3 cm H2O/s. This increase was significantly (p = 0.018) greater than the response after the third exercise in the intermittent protocol. It appears that asthmatics show an attenuated response to repetitive exercise in an atmosphere of 1.00 ppm SO2 and that the response to SO2 exposure develops rapidly and is maintained during 30 min of continuous exercise.

Adult↗
PubMed1987

Ozone exposure increases respiratory epithelial permeability in humans.

Ozone is a respiratory irritant that has been shown to cause an increase in the permeability of the respiratory epithelium in animals. We used inhaled aerosolized 99mTc-labeled diethylene triamine pentacetic acid (99mTc-DTPA) to investigate whether human respiratory epithelial permeability is similarly affected by exposure to ozone. In a randomized, crossover double-blinded study, 8 healthy, nonsmoking young men were exposed for 2 h to purified air and 0.4 ppm ozone while performing intermittent high intensity treadmill exercise (minute ventilation = 66.8 L/min). SRaw and FVC were measured before and at the end of exposures. Seventy-five minutes after the exposures, the pulmonary clearance of 99mTc-DTPA was measured by sequential posterior lung imaging with a computer-assisted gamma camera. Ozone exposure caused respiratory symptoms in all 8 subjects and was associated with a 14 +/- 2.8% (mean +/- SEM) decrement in FVC (p less than 0.001) and a 71 +/- 22% increase in SRaw (p = 0.04). Compared with the air exposure day, 7 of the 8 subjects showed increased 99mTc-DTPA clearance after the ozone exposure, with the mean value increasing from 0.59 +/- 0.08 to 1.75 +/- 0.43%/min (p = 0.03). These data show that ozone exposure sufficient to produce decrements in the pulmonary function of human subjects also causes an increase in 99mTc-DTPA clearance.

Adult↗
PubMed1987

The respiratory responses of subjects with allergic rhinitis to ozone exposure and their relationship to nonspecific airway reactivity.

Ozone exposure in man produces changes in respiratory function and symptoms. There is a large degree of unexplained intersubject variability in the magnitude of these responses. There is concern that individuals with chronic respiratory diseases may also be more responsive to ozone than normal individuals. The purpose of this study was to describe the responses of subjects with allergic rhinitis to ozone exposure and to compare these responses to those previously observed in normal individuals. A further purpose was to measure the association of baseline nonspecific airway reactivity with changes in lung function and respiratory symptoms following ozone exposure. A group of 26 nonasthmatic subjects with allergic rhinitis performed a bronchial inhalation challenge with histamine and subsequently underwent two hour exposures to both clean air and to 0.18 part per million ozone with alternating periods of rest and heavy exercise. The airway reactivity of this group of subjects was no greater than that of a comparable group of subjects without allergic rhinitis. The respiratory responses of these subjects to ozone exposure were similar to those previously reported for subjects without allergic rhinitis with the exception that the allergic rhinitis subjects appeared to have a modestly increased bronchoconstrictor response compared to normals. Furthermore, we observed no significant relationships between nonspecific airway reactivity and response to ozone as measured by changes in lung function or the induction of symptoms.

Adolescent↗
PubMed1985

Bronchoconstriction in asthmatics exposed to sulfur dioxide during repeated exercise.

Young male volunteers with mild asthma and hypersensitivity to methacholine were exposed for 75 min with natural breathing to 0.0, 0.25, 0.5, and 1.0 ppm SO2. Each exposure included three 10-min periods of moderate treadmill exercise (minute ventilation 21 l . m-2 . min-1, O2 consumption 25 ml . kg-1, and heart rate 120/min). Specific airway resistance (sRaw) was not significantly increased after exercise in 0.25 ppm SO2, relative to the control exposure (clean air). In 0.5 and 1.0 ppm SO2, sRaw was increased twofold and threefold above preexposure levels, respectively, corresponding to increases of 3.2 and 9.2 cmH2O . s in excess over the increases seen in clean air (P less than 0.001). There was a broad range of responses to exercise and SO2. The increases in sRaw after the second and third exercises were significantly less than after the first exercise. Respiratory impedance measured by forced random noise suggests that the induced bronchoconstriction was primarily associated with peripheral airways. These results confirm that mild asthmatics selected for methacholine sensitivity have as a group significant bronchoconstriction in response to short-term moderate exercise with natural breathing in 1.0 and 0.5 ppm SO2. In addition, the induced bronchoconstriction is decreased after short-term repeated exercise in SO2.

Adult↗
PubMed1985

Role of the parasympathetic nervous system in acute lung response to ozone.

We conducted an ozone (O3) exposure study using atropine, a muscarinic receptor blocker, to determine the role of the parasympathetic nervous system in the acute response to O3. Eight normal subjects with predetermined O3 responsiveness were randomly assigned an order for four experimental exposures. For each exposure a subject inhaled either buffered saline or atropine aerosol followed by exposure either to clean air or 0.4 ppm O3. Measurements of lung mechanics, ventilatory response to exercise, and symptoms were obtained before and after exposure. O3 exposure alone resulted in significant changes in specific airway resistance, forced vital capacity (FVC), forced expiratory flow rates, tidal volume (VT), and respiratory rate (f). Atropine pretreatment prevented the significant increase in airway resistance with O3 exposure and partially blocked the decrease in forced expiratory flow rates but did not prevent a significant fall in FVC, changes in f and VT, or the frequency of reported respiratory symptoms after O3. These results suggest that the increase in pulmonary resistance during O3 exposure is mediated by a parasympathetic mechanism and that changes in other measured variables are mediated, at least partially, by mechanisms not dependent on muscarinic cholinergic receptors of the parasympathetic nervous system.

Adolescent↗
PubMed1985

Reproducibility of individual responses to ozone exposure.

Because large intersubject differences in the magnitudes of response to a single ozone (O3) exposure have been observed, we undertook to determine if this variability were due to differences in intrinsic responsiveness to O3 or to other factors. Thirty-two subjects were exposed to 1 of 5 O3 concentrations (0.12, 0.18, 0.24, 0.30, or 0.40 ppm), and each underwent one or more repeat exposures separated by from 3 wk to 14 months. Magnitudes of change for pulmonary function variables, respiratory rate and tidal volume, and for reported symptoms were compared for the repeated exposures. Changes induced in forced expiratory spirometric measurements were highly reproducible for as long as 10 months and for all tested O3 concentrations of 0.18 ppm or greater. This high degree of reproducibility indicates that the magnitude of response to a single exposure is a precise estimate of that subject's intrinsic O3 responsiveness. We conclude that the previously observed intersubject variability in magnitude of O3-induced effects is the result of large differences in intrinsic responsiveness to O3.

Adolescent↗
PubMed1983

Effects of acute plasma volume expansion on altering exercise-heat performance.

To determine the effect an acute plasma volume expansion has on body temperature responses and exercise performance in the heat, seven unacclimatized male volunteers attempted to complete two 90-min walks (45% of VO2 max) in a hot/dry (45 degrees C/20% rh) environment. The experimental walk was preceded by an infusion of human albumin (50 g in a 200-ml solution) and the control walk was preceded by an infusion of isotonic saline (200 ml). Saline infusion did not alter the plasma volume. The albumin infusion was found to significantly (p less than 0.01) increase plasma volume approximately 13% over control levels. No significant differences were found for performance time, final heart rate or final rectal temperature values between the two walks. In general, significant differences were not found for systolic blood pressure, rectal temperature, mean skin temperature, heat storage, sweat rate, plasma lactate, plasma osmolality, or plasma protein content values between the two walks. However, heart rate responses were found to be significantly lower (p less 0.05; approximately 13 bt x min-1) during the 25-min and 40-min measurements of the experimental walk. These data suggest that plasma volume expansion may be a supportive adaptation to enable lowered heart rate responses but does not improve thermoregulatory function or performance time in the heat.

Adult↗
PubMed1983

Pulmonary effects of ozone exposure during exercise: dose-response characteristics.

Because minimal data are available regarding the pulmonary effects of ozone (O3) at levels less than 0.27 ppm, six groups of healthy young males were exposed for 2.5 h to one of the following O3 concentrations: 0.0, 0.12, 0.18, 0.24, 0.30, or 0.40 ppm. Fifteen-minute periods of rest and exercise (65 l/min minute ventilation) were alternated during the first 2 h of exposure. Coughing was observed at all levels of O3 exposure. Small changes in forced-expiratory spirometric variables [forced vital capacity (FVC), forced expiratory volume in 1 s, and mean expiratory flow rate between 25 and 75% FVC] were observed at 0.12 and 0.18 ppm O3, and larger changes were found at O3 levels greater than or equal to 0.24 ppm. Changes in tidal volume and respiratory frequency during exercise, specific airway resistance, the presence of pain on deep inspiration, and shortness of breath occurred at O3 levels greater than or equal to 0.24 ppm. In conclusion, pulmonary effects of O3 were observed at levels much lower than that for which these effects have been previously described. Stimulation of airway receptors is probably the mechanism responsible for the majority of observed changes; however, the existence of a second mechanism of action is postulated.

Adolescent↗
PubMed1982

Acclimatization to dry heat: active men vs. active women.

Physiological responses to exercise in dry heat were compared between six active men [maximum O2 consumption (VO2max), 51.4 +/- 1.2 ml . kg-1 . min-1] and four active women (VO2max, 47.2 +/- 1.3 ml . kg-1 . min-1) before, during, and after heat acclimatization. Subjects cycled a maximum of 2 h at 40% VO2max at 45 degrees C dry-bulb temperature, 23 degrees C wet-bulb temperature for 11 days. Prior to acclimatization there were no sexual differences for performance time, rate of increase of rectal temperature (delta Tre), or sweat rate per degree C increase of rectal temperature (msw/delta Tre). Sweat rate (msw) was greater for the men than for the women. Although there was no difference in the rate of increase of heart rate (delta HR), HR for the women was maintained 15-20 beats . min-1 higher than for the men. Acclimatization occurred for both sexes as indicated by reduced Tre and HR and increased msw and performance time. With acclimatization the women had longer performance times than the men. Even though the men still had greater msw, delta Tre was also greater; therefore msw/delta Tre for the men was less than for the women. Neither HR nor delta HR was different between the sexes. Throughout, resting hematocrit for the women was less than for the men; no changes in hematocrit were observed during exercise or with acclimatization. Plasma protein concentration increased during exercise on all days; no changes in plasma osmolality were observed. It is concluded that active women perform exercise of equal relative intensity in dry heat as well as active men. Moreover active women acclimatized to heat at a faster rate or to a greater extent than did active men.

Acclimatization↗
PubMed1979

Perception of effort during constant work to self-imposed exhaustion.

The purpose of this study was to describe the pattern of change in effort sense and the value of this pattern in predicting work end-point at relatively high work intensity (80% VO2 max). The patterns of change of various physiological functions were also observed. Two modes of work (walking and running) were compared to ascertain generalizability of results. 26 healthy male volunteers served as subjects. Time to exhaustion (ET) did not differ between walking and running. As work continued during both tasks, significant increases of VE, VE/VO2, VE/VCO2 and HR and a significant decrease of ETCO2 were observed; while VO2 and R remained fairly constant. VO2 and VE during the run were about 5% greater than during the walk; there were no differences in other measures. Ratings of perceived exertion (RPE) from the Borg Scale were identical for both conditions, increasing in a near linear fashion from a value of 12.9 at 25% of total work time to 18.9 at exhaustion. Ratings obtained at 25 and 50% ET were extrapolated to time of exhaustion; the point of intercept corresponded to ratings of perceived exertion for maximal work. At exhaustion, subjects rated perception of respiratory exertion for the walk as less than that for the run; perception of leg exertion was not different for the two conditions. Plasma lactate, epinephrine and norepinephrine concentrations following exercise did not differ between the two conditions. The findings for the walking experiment were essentially replicated in a second investigation involving another 28 subjects. It is concluded that, with the exception of VO2 and some ventilatory parameters, walking and running at the same relative work intensity resulted in comparable perceptual and physiological responses. Psychophysical judgments made early during work were reasonably accurate predictors of exhaustion time.

Adult↗