{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,3,6]],"date-time":"2026-03-06T16:47:54Z","timestamp":1772815674996,"version":"3.50.1"},"reference-count":22,"publisher":"American Physiological Society","issue":"5","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Journal of Applied Physiology"],"published-print":{"date-parts":[[1998,11,1]]},"abstract":"<jats:p> We have previously suggested that ozone (O<jats:sub>3<\/jats:sub>)-induced pain-related symptoms and inhibition of maximal inspiration are due to stimulation of airway C fibers (M. J. Hazucha, D. V. Bates, and P. A. Bromberg. J. Appl. Physiol. 67: 1535\u20131541, 1989). If this were so, pain suppression or inhibition by opioid-receptor agonists should partially or fully reverse O<jats:sub>3<\/jats:sub>-induced symptomatic and lung functional responses. The objectives of this study were to determine whether O<jats:sub>3<\/jats:sub>-induced pain limits maximal inspiration and whether endogenous opioids contribute to modulation of the effects of inhaled O<jats:sub>3<\/jats:sub> on lung function. The participants in this double-blind crossover study were healthy volunteers (18\u201359 yr) known to be \u201cweak\u201d (WR; n = 20) and \u201cstrong\u201d O<jats:sub>3<\/jats:sub> responders (SR; n = 42). They underwent either two 2-h exposures to air or two 2-h exposures to 0.42 parts\/million O<jats:sub>3<\/jats:sub> with moderate intermittent exercise. Immediately after post-O<jats:sub>3<\/jats:sub> spirometry, the WR were randomly given either naloxone (0.15 mg\/kg iv) or saline, whereas SR randomly received either sufentanil (0.2 \u03bcg\/kg iv) or saline. O<jats:sub>3<\/jats:sub> exposure significantly ( P &lt; 0.001) impaired lung function. In SR, sufentanil rapidly, although not completely, reversed both the chest pain and spirometric effects (forced expiratory volume in 1 s; P &lt; 0.0001) compared with saline. Immediate postexposure administration of saline or naloxone had no significant effect on WR. Plasma \u03b2-endorphin levels were not related to an individual\u2019s O<jats:sub>3<\/jats:sub>responsiveness. Cutaneous pain variables showed a nonsignificant weak association with O<jats:sub>3<\/jats:sub>responsiveness. These observations demonstrate that nociceptive mechanisms play a key role in modulating O<jats:sub>3<\/jats:sub>-induced inhibition of inspiration but not in causing lack of spirometric response to O<jats:sub>3<\/jats:sub> exposure in WR. <\/jats:p>","DOI":"10.1152\/jappl.1998.85.5.1863","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T15:33:15Z","timestamp":1513956795000},"page":"1863-1870","source":"Crossref","is-referenced-by-count":39,"title":["Nociceptive mechanisms modulate ozone-induced  human lung function decrements"],"prefix":"10.1152","volume":"85","author":[{"given":"Anthony N.","family":"Passannante","sequence":"first","affiliation":[{"name":"Departments ofAnesthesiology and"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Milan J.","family":"Hazucha","sequence":"additional","affiliation":[{"name":"Medicine, School of Medicine, University of North Carolina at Chapel Hill, Chapel Hill 27599-7010; Center for Environmental Medicine and Lung Biology, University of North Carolina at Chapel Hill, Chapel Hill 27599-7310;"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Philip A.","family":"Bromberg","sequence":"additional","affiliation":[{"name":"Medicine, School of Medicine, University of North Carolina at Chapel Hill, Chapel Hill 27599-7010; Center for Environmental Medicine and Lung Biology, University of North Carolina at Chapel Hill, Chapel Hill 27599-7310;"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Elston","family":"Seal","sequence":"additional","affiliation":[{"name":"Clinical Research Branch, Human Studies Division, National Health and Environmental Effects Research Laboratory and"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Larry","family":"Folinsbee","sequence":"additional","affiliation":[{"name":"National Center for Environment Assessment, US Environmental Protection Agency, Research Triangle Park 27711; and"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Gary","family":"Koch","sequence":"additional","affiliation":[{"name":"Department of Biostatistics, School of Public Health, University of North Carolina, Chapel Hill, North Carolina 27599-7400"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"24","reference":[{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1183\/09031936.97.10081892"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1213\/00000539-199001000-00003"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1007\/BF00175710"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1152\/jappl.1992.72.3.1096"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1093\/bja\/68.4.370"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1152\/jappl.1993.74.5.2345"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.ph.56.030194.000441"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1016\/0304-3959(86)90030-8"},{"key":"B11","first-page":"28","volume":"38","author":"Folinsbee L. 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