Ozone differentially modulates airway responsiveness in atopic versus nonatopic guinea pigs

Richard B. Schlesinger, Mitchell D. Cohen, Terry Gordon, Christine Nadziejko, Judith T. Zelikoff, Maureen Sisco, Jean F. Regal, Margaret G. Ménache

Research output: Contribution to journalArticlepeer-review

8 Scopus citations


While acute exposures to ozone (O3) can alter airway responsiveness, effects from long-term exposures at low concentrations are less clear. This study assessed whether such exposures could induce nonspecific hyperresponsiveness in nonatopic (nonsensitized) guinea pigs and/or could exacerbate the pre-existing hyperresponsive state in atopic (sensitized) animals, and whether gender was a factor modulating any effect of O3. Responsiveness was measured during and following exposures to 0.1 and 0.3 ppm O3 for 4 h/day, 4 days/wk for 24 wk in male and female nonsensitized animals, those sensitized to allergen (ovalbumin) prior to initiation of O3 exposures, and those sensitized concurrently with exposures. Ozone did not produce hyperresponsiveness in nonsensitized animals, but did exacerbate hyperresponsiveness to both specific and nonspecific bronchoprovocation challenges in sensitized animals, an effect that persisted through at least 4 wk after exposures ended. Gender was not a factor modulating response to O3. Induced effects on responsiveness were not associated with numbers of eosinophils in the lungs nor with any chronic pulmonary inflammatory response, but were correlated with antigen-specific antibodies in blood. This study supports a role for chronic O3 exposure in the exacerbation of airways dysfunction in a certain segment of the general population, namely, those demonstrating atopy.

Original languageEnglish (US)
Pages (from-to)431-457
Number of pages27
JournalInhalation Toxicology
Issue number5
StatePublished - 2002

Bibliographical note

Funding Information:
Received 1 October 2001; sent for revision 31 October 2001; revision received 9 November 2001; accepted 12 November 2001. This study was supported by a research contract (94-12) from the Health Effects Institute and is part of a Center Program (ES00260) supported by NIEHS. Address correspondence to Mitchell D. Cohen, Department of Environmental Medicine, New York UniveyrSchosolioftMedicine, 57 Old ForegRo Tuaxedo, dN,10Y8,9U 7ESa-Acmiohl.:m e@ n env.med.nyu.edu

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