Low-level ozone exposure induces airways inflammation and modifies cell surface phenotypes in healthy humans

Abstract

The effects of low-level ozone exposure (0.08 ppm) on pulmonary function in healthy young adults are well known; however, much less is known about the inflammatory and immunomodulatory effects of low-level ozone in the airways. Techniques such as induced sputum and flow cytometry make it possible to examine airways inflammatory responses and changes in immune cell surface phenotypes following low-level ozone exposure. The purpose of this study was to determine if exposure to 0.08 parts per million ozone for 6.6 h induces inflammation and modifies immune cell surface phenotypes in the airways of healthy adult subjects. Fifteen normal volunteers underwent an established 0.08 part per million ozone exposure protocol to characterize the effect of ozone on airways inflammation and immune cell surface phenotypes. Induced sputum and flow cytometry were used to assess these endpoints 24 h before and 18 h after exposure. The results showed that exposure to 0.08 ppm ozone for 6.6 h induced increased airway neutrophils, monocytes, and dendritic cells and modified the expression of CD14, HLA-DR, CD80, and CD86 on monocytes 18 h following exposure. Exposure to 0.08 parts per million ozone is associated with increased airways inflammation and promotion of antigen-presenting cell phenotypes 18 hours following exposure. These findings need to be replicated in a similar experiment that includes a control air exposure.

Keywords::

• Antigen-presenting cells
• dendritic cell
• inflammation
• macrophage
• ozone
• pollution
• polymorphonuclear neutrophil

Acknowledgments

The authors gratefully acknowledge the skillful assistance of Martha Almond, Aline Kala, Margaret Herbst, Carole Robinette, Heather Wells, Fernando Dimeo, Danuta Sujkowski, Lynne Newlin-Clapp, and Nolan Sweeny from the University of North Carolina Center for Environmental Medicine, Asthma and Lung Biology, and Maryann Bassett, Tracy Montilla, and Martin Case of the Environmental Public Health Division of the US Environmental Protection Agency in the completion of this project.

Declaration of interest

This work was supported by NIEHS grant R01ES012706 and US EPA Cooperative Agreement CR 83346301. The authors have no competing financial or nonfinancial interests to disclose.

Disclaimer: Although the research described in this article has been funded wholly or in part by the United States Environmental Protection Agency through cooperative agreement CR-83346301 with the Center for Environmental Medicine and Lung Biology at the University of North Carolina at Chapel Hill, it has not been subjected to the Agency’s required peer and policy review, and therefore does not necessarily reflect the views of the Agency and no official endorsement should be inferred.