Biomedical subjects

E S Schelegle

Publications and source records attributed to E S Schelegle.

42 records · Page 3Linked to original sources

PubMed1987

Effects of NO2 alone and in combination with O3 on young men and women.

Previous studies of 2 h of exposure to NO2 at high urban atmospheric levels (i.e., 0.50-1.0 ppm), utilizing light-to-moderate exercise for up to 1 h have failed to demonstrate significant pulmonary dysfunction in healthy humans. To test the hypothesis that heavy sustained exercise would elicit pulmonary dysfunction on exposure to 0.60 ppm NO2 and/or enhance the effects of exposure to 0.30 ppm O3, 40 aerobically trained young adults (20 males and 20 females) completed 1 h of continuous exercise at work rates eliciting a mean minute ventilation of 70 and 50 l/min for the males and females, respectively. Exposures to filtered air, 0.60 ppm NO2, 0.30 ppm O3, and 0.60 ppm NO2 plus 0.30 ppm O3 were randomly delivered via an obligatory mouthpiece inhalation system. Treatment effects were assessed by standard pulmonary function tests and exercise ventilatory and subjective symptoms response. Two-way analysis of variance with repeated measures and post hoc analyses revealed a statistically significant (P less than 0.05) effect of O3 on forced expiratory parameters, specific airway resistance, exercise ventilatory response, and reported subjective symptoms of respiratory discomfort. In contrast, no significant effect of NO2 was observed nor was there any significant interaction of NO2 and O3 in combination. There were no significant differences between male and female responses to gas mixture treatments. It was concluded that inhalation of 0.60 ppm NO2 for 1 h while engaged in heavy sustained exercise does not elicit effects evidenced by measurement techniques used in this study nor evoke additive effects beyond those induced by 0.30 ppm O3 in healthy young adults.

Adult↗

PubMed1987

Indomethacin pretreatment reduces ozone-induced pulmonary function decrements in human subjects.

We studied whether O3-induced pulmonary function decrements could be inhibited by the prostaglandin synthetase inhibitor, indomethacin, in healthy human subjects. Fourteen college-age males completed six 1-h exposure protocols consisting of no drug, placebo, and indomethacin (Indocin SR 75 mg every 12 h for 5 days) pretreatments, with filtered air and O3 (0.35 ppm) exposures within each pretreatment. Pretreatments were delivered weekly in random order in a double-blind fashion. Ozone and filtered air exposures, separated by 72 h, were delivered in random order in a single-blind fashion. Exposures consisted of 1-h exercise on a bicycle ergometer with work loads set to elicit a mean minute ventilation of 60 L/min. Statistical analysis revealed significant (p less than 0.05) across pretreatment effects for FVC and FEV1, with no drug versus indomethacin and placebo versus indomethacin comparisons being significant. These findings suggest that cyclooxygenase products of arachidonic acid, which are sensitive to indomethacin inhibition, play a prominent role in the development of pulmonary function decrements consequent to acute O3 exposure.

Adult↗

PubMed1986

Reduced exercise time in competitive simulations consequent to low level ozone exposure.

Ten highly trained endurance athletes were studied to determine the effects of exposure to low ozone (O3) concentrations on simulated competitive endurance performance and associated physiological and subjective symptom responses. Each subject was randomly exposed to filtered air (FA), and to 0.12, 0.18, and 0.24 ppm O3 while performing a 1 h competitive simulation protocol on a bicycle ergometer. Endurance performance was evaluated by the number of subjects unable to complete rides (last 30 min at an intense work load of approximately 86% VO2max). All subjects completed the FA exposure, whereas one, five, and seven subjects did not complete the 0.12, 0.18, and 0.24 ppm O3 exposures, respectively. Statistical analysis indicated a significant (P less than 0.05) increase in the inability of subjects to complete the competitive simulations with increasing O3 concentration, including a significant difference between the 0.24 ppm O3 and FA exposure. Significant decreases (P less than 0.05) were also observed following the 0.18 and 0.24 ppm O3 exposures, respectively, in forced vital capacity (-7.8 and -9.9%), and forced expiratory volume in 1 s (-5.8 and -10.5%). No significant O3 effect was observed for exercise respiratory metabolism or ventilatory pattern responses. However, the number of reported subjective symptoms increased significantly following the 0.18 and 0.24 ppm O3 protocols. These data demonstrate significant decrements in simulated competitive endurance performance and in pulmonary function, with accompanying enhanced subjective symptoms, following exposure to low O3 levels commonly observed in numerous metropolitan environments during the summer months.

Adult↗

PubMed1983

Ozone and high ventilation effects on pulmonary function and endurance performance.

Ozone (O3) toxicity is potentiated by exercise-induced expired minute ventilation (VE) for a given exposure, which may also impair endurance performance. Ten healthy, well-trained long-distance runners were exposed on six occasions for 1 h to O3 concentrations of 0, 0.20, or 0.35 parts per million (ppm), during exercise simulating either training or competition, with mean VE = 77.5 1 X min -1. Standard pulmonary function tests, subjective symptoms, and periodic observations of exercise ventilatory response and respiratory metabolism were obtained. Statistical analyses revealed no significant exercise mode effect for pulmonary function, but a significant O3 effect for forced vital capacity and expiratory volume at 1 s was observed. Altered exercise ventilatory pattern response was noted, but there was no significant O3 effect on exercise oxygen uptake, heart rate, VE, or alveolar ventilation. Subjective symptoms increased with O3 concentration. Statistically significant pulmonary function impairment observed at 0.20 ppm O3 suggests that endurance athletes may be more susceptible to the effects of a given O3 concentration than normal young adult males as a result of sustained high mean VE incurred during training and competition. Three subjects were unable to complete both the training and competitive simulations at 0.35 ppm O3. Performance decrements appeared to be the result of physiologically induced respiratory discomfort rather than decrements in pulmonary gas exchange and/or oxygen transport and delivery.

Adult↗

PubMedDate not supplied

Duration of enhanced responsiveness upon re-exposure to ozone.

It has been repeatedly observed that ozone (O3) re-exposure within 24 h elicits enhanced pulmonary function responses. However, there are only limited observations concerning re-exposure to O3 at intervals between 24 h and several days. The present study was designed to assess the effects of re-exposure to 0.35 ppm O3 at intervals of 24, 48, 72, and 120 h. Forty young adult male subjects were assigned randomly to one of four groups in ascending order of time to re-exposure (groups 1-4). Each exercised on a bicycle ergometer for 60 min at a workload that elicited a mean ventilation of 60 l/min on three occasions: protocol 1 (P1), filtered air (FA); protocol 2 (P2), 0.35 ppm O3; and protocol 3 (P3), 0.35 ppm O3. In addition to standard pulmonary function measures, specific airway resistance (SRaw); exercise ventilatory pattern, i.e., respiratory frequency (fR) and tidal volume (VT); and subjective symptoms (SS) were assessed. Statistical analysis revealed significant differences (p less than .05) for all groups between the FA (P1) responses and those for the two O3 exposures (P2, P3) for forced vital capacity (FVC), forced expiratory volume in 1 s (FEV1.0), SRaw, fR, VT, and SS. When the two O3 exposures (P2 and P3) were compared, only group 1 (24 h) responses were statistically significant upon re-exposure: FEV1.0, -16.1 vs. -30.4% (p less than .003); SRaw, 20.5 vs. 34.5% (p less than .05); fR, 44.2 vs. 65.3% (p less than .001); and SS (p less than .015).(ABSTRACT TRUNCATED AT 250 WORDS)

Adaptation, Physiological↗

PubMedDate not supplied

Oral and oronasal breathing during continuous exercise produce similar responses to ozone inhalation.

Breathing route has a profound effect on sulfur dioxide-induced pulmonary function response in human subjects. There is comparatively little evidence of the effects of oral, nasal, and oronasal breathing on ozone (O3)-induced responses in humans. In this study, six young adult males were exposed on five occasions to 0.40 parts per million (ppm) O3 while exercising continuously at one of two workloads (minute ventilation, VE, of approximately 30 and 75 l/min). The VE exposure time product was similar for all protocols. Four exposures were delivered randomly with a Hans-Rudolph respiratory valve attached to a silicone facemask, with breathing route effected with and without noseclip. A 2 x 2 analysis of variance revealed no statistically significant differences (p less than .05) across conditions in pulmonary function, exercise ventilatory pattern, or subjective symptoms responses. The fifth exposure, delivered via the same respiratory valve with mouthpiece, but without facemask, revealed significantly greater forced expiratory volume in 1 s (FEV1.0) impairment than that observed for the respiratory valve, facemask with noseclip exposure (-20.4% and -15.9%, respectively). The latter suggests partial O3 reactivity to the facemask and clean shaven facial surface of the subjects, although reduced oral scrubbing by mouthpiece-induced bypassing of the oral vestibule might account, in part, for this difference. Recent O3 uptake evidence from another laboratory, however, supports our conclusion that breathing route during moderate and heavy continuous exercise does not affect acute physiologic responses to 0.40 ppm O3.

Adult↗