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Nociceptive mechanisms modulate ozone-induced human lung function decrements

A N Passannante1, M J Hazucha, P A Bromberg

  • 1Department of Anesthesiology, School of Medicine, University of North Carolina at Chapel Hill, USA.

Journal of Applied Physiology (Bethesda, Md. : 1985)
|November 6, 1998
PubMed
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Ozone exposure causes pain and breathing difficulty by stimulating airway C fibers. Opioid drugs can reverse these ozone-induced effects in strong responders, indicating pain

Area of Science:

  • Respiratory Physiology
  • Environmental Health
  • Pain Perception

Background:

  • Ozone (O3) exposure can cause pain and limit maximal inspiration, potentially via airway C-fiber stimulation.
  • Endogenous opioids may modulate the physiological responses to inhaled ozone.

Purpose of the Study:

  • To investigate if ozone-induced pain limits maximal inspiration.
  • To determine the role of endogenous opioids in modulating ozone's effects on lung function.

Main Methods:

  • Double-blind crossover study with healthy volunteers categorized as weak (WR) or strong (SR) ozone responders.
  • Participants underwent controlled ozone exposure with moderate exercise.
  • Pharmacological interventions (naloxone or sufentanil) were administered post-exposure to assess opioid receptor involvement.

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Main Results:

  • Ozone exposure significantly impaired lung function (P < 0.001).
  • Sufentanil reversed ozone-induced chest pain and spirometric changes (forced expiratory volume in 1 s; P < 0.0001) in strong responders.
  • Naloxone or saline had no significant effect on weak responders.

Conclusions:

  • Nociceptive mechanisms are crucial for ozone-induced inspiratory inhibition.
  • Endogenous opioids modulate ozone's effects on lung function, particularly in strong responders.
  • Pain does not appear to be the primary driver of spirometric impairment in weak responders.