0.35 ppm O3 exposure induces hyperresponsiveness on 24-h reexposure to 0.20 ppm O3

K. A. Brookes, W. C. Adams, Edward S Schelegle

Research output: Contribution to journalArticle

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Abstract

Pulmonary function hyperresponsiveness, defined as enhanced response on reexposure to O3, compared with initial O3 exposure, has been previously noted in consecutive day exposures to high ambient O3 concentrations (i.e., 0.32-0.42 ppm). Effects of consecutive-day exposure to lower O3 concentrations (0.20-0.25 ppm) have yielded equivocal results. To examine the occurrence of hyperresponsiveness at two levels of O3 exposure, 15 aerobically trained males completed seven 1-h exposures of continuous exercise at work rates eliciting a mean minute ventilation of 60 l/min. Three sets of consecutive-day exposures, involving day 1/day 2 exposures to 0.20/0.20 ppm O3, 0.35/0.20 ppm O3, and 0.35/0.35 ppm O3, were randomly delivered via an obligatory mouthpiece inhalation system. A filtered-air exposure was randomly placed 24 h before one of the three sets. Treatment effects were assessed by standard pulmonary function tests, exercise ventilatory pattern (i.e., respiratory frequency, f; and tidal volume, V(T)) changes and subjective symptom (SS) response. Initial O3 exposures to 0.35 and 0.20 ppm had a statistically significant effect, compared with filtered air, on all measurements. On reexposure to 0.35 ppm O3 24 h after an initial 0.35 ppm O3 exposure, significant hyperresponsiveness was demonstrated for forced vital capacity (FVC), forced expiratory volume in 1 s (FEV1), f, V(T), and total SS score. Exposure to 0.20 ppm O3 24 h after 0.35 ppm O3 exposure, however, resulted in significantly enhanced responses (compared with initial 0.20 ppm O3 exposure) only for FEV1, f, and V(T). Reexposure to 0.20 ppm O3 24 h after initial exposure to 0.20 ppm O3 did not result in significantly enhanced f, V(T), or SS responses, but a trend toward an enhanced FEV1 was observed. These data indicate that exposure to high ambient O3 concentrations can induce a sensitized airway state such that enhanced responses, compared with initial exposure effects, are observed on reexposure 24 h later to moderate, as well as to high, ambient O3 concentrations.

Original languageEnglish (US)
Pages (from-to)2756-2762
Number of pages7
JournalJournal of Applied Physiology
Volume66
Issue number6
StatePublished - 1989

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Forced Expiratory Volume
Air
Respiratory Function Tests
Tidal Volume
Vital Capacity
Inhalation
Ventilation
Lung

ASJC Scopus subject areas

  • Endocrinology
  • Physiology
  • Orthopedics and Sports Medicine
  • Physical Therapy, Sports Therapy and Rehabilitation

Cite this

0.35 ppm O3 exposure induces hyperresponsiveness on 24-h reexposure to 0.20 ppm O3 . / Brookes, K. A.; Adams, W. C.; Schelegle, Edward S.

In: Journal of Applied Physiology, Vol. 66, No. 6, 1989, p. 2756-2762.

Research output: Contribution to journalArticle

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abstract = "Pulmonary function hyperresponsiveness, defined as enhanced response on reexposure to O3, compared with initial O3 exposure, has been previously noted in consecutive day exposures to high ambient O3 concentrations (i.e., 0.32-0.42 ppm). Effects of consecutive-day exposure to lower O3 concentrations (0.20-0.25 ppm) have yielded equivocal results. To examine the occurrence of hyperresponsiveness at two levels of O3 exposure, 15 aerobically trained males completed seven 1-h exposures of continuous exercise at work rates eliciting a mean minute ventilation of 60 l/min. Three sets of consecutive-day exposures, involving day 1/day 2 exposures to 0.20/0.20 ppm O3, 0.35/0.20 ppm O3, and 0.35/0.35 ppm O3, were randomly delivered via an obligatory mouthpiece inhalation system. A filtered-air exposure was randomly placed 24 h before one of the three sets. Treatment effects were assessed by standard pulmonary function tests, exercise ventilatory pattern (i.e., respiratory frequency, f; and tidal volume, V(T)) changes and subjective symptom (SS) response. Initial O3 exposures to 0.35 and 0.20 ppm had a statistically significant effect, compared with filtered air, on all measurements. On reexposure to 0.35 ppm O3 24 h after an initial 0.35 ppm O3 exposure, significant hyperresponsiveness was demonstrated for forced vital capacity (FVC), forced expiratory volume in 1 s (FEV1), f, V(T), and total SS score. Exposure to 0.20 ppm O3 24 h after 0.35 ppm O3 exposure, however, resulted in significantly enhanced responses (compared with initial 0.20 ppm O3 exposure) only for FEV1, f, and V(T). Reexposure to 0.20 ppm O3 24 h after initial exposure to 0.20 ppm O3 did not result in significantly enhanced f, V(T), or SS responses, but a trend toward an enhanced FEV1 was observed. These data indicate that exposure to high ambient O3 concentrations can induce a sensitized airway state such that enhanced responses, compared with initial exposure effects, are observed on reexposure 24 h later to moderate, as well as to high, ambient O3 concentrations.",
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N2 - Pulmonary function hyperresponsiveness, defined as enhanced response on reexposure to O3, compared with initial O3 exposure, has been previously noted in consecutive day exposures to high ambient O3 concentrations (i.e., 0.32-0.42 ppm). Effects of consecutive-day exposure to lower O3 concentrations (0.20-0.25 ppm) have yielded equivocal results. To examine the occurrence of hyperresponsiveness at two levels of O3 exposure, 15 aerobically trained males completed seven 1-h exposures of continuous exercise at work rates eliciting a mean minute ventilation of 60 l/min. Three sets of consecutive-day exposures, involving day 1/day 2 exposures to 0.20/0.20 ppm O3, 0.35/0.20 ppm O3, and 0.35/0.35 ppm O3, were randomly delivered via an obligatory mouthpiece inhalation system. A filtered-air exposure was randomly placed 24 h before one of the three sets. Treatment effects were assessed by standard pulmonary function tests, exercise ventilatory pattern (i.e., respiratory frequency, f; and tidal volume, V(T)) changes and subjective symptom (SS) response. Initial O3 exposures to 0.35 and 0.20 ppm had a statistically significant effect, compared with filtered air, on all measurements. On reexposure to 0.35 ppm O3 24 h after an initial 0.35 ppm O3 exposure, significant hyperresponsiveness was demonstrated for forced vital capacity (FVC), forced expiratory volume in 1 s (FEV1), f, V(T), and total SS score. Exposure to 0.20 ppm O3 24 h after 0.35 ppm O3 exposure, however, resulted in significantly enhanced responses (compared with initial 0.20 ppm O3 exposure) only for FEV1, f, and V(T). Reexposure to 0.20 ppm O3 24 h after initial exposure to 0.20 ppm O3 did not result in significantly enhanced f, V(T), or SS responses, but a trend toward an enhanced FEV1 was observed. These data indicate that exposure to high ambient O3 concentrations can induce a sensitized airway state such that enhanced responses, compared with initial exposure effects, are observed on reexposure 24 h later to moderate, as well as to high, ambient O3 concentrations.

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