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James S. Brown,¹ Thomas F. Bateson,² and William F. McDonnell³

¹National Center for Environmental Assessment, U.S. Environmental Protection Agency, Research Triangle Park, North Carolina, USA; ²National Center for Environmental Assessment, U.S. Environmental Protection Agency, Washington, DC, USA; ³William F. McDonnell Consulting, Chapel Hill, North Carolina, USA

Abstract
Background: Ozone is a potent photochemical oxidant that produces transient, reversible decrements in the lung function of acutely exposed individuals. A recent study provided previously unavailable clinical data for 30 healthy young adults exposed to O₃ at 0.06 ppm. That study showed significant effects of 0.08 ppm on lung function, confirming the findings of others. However, exposure to 0.06 ppm O₃ was not reported to significantly affect lung function.

Objectives: We conducted this analysis to reevaluate the existing lung function data of the volunteers previously exposed to 0.06 ppm O₃.

Methods: We obtained pre- and postexposure data on forced expiratory volume in 1 sec (FEV₁) for all subjects who were previously exposed for 6.6 hr to filtered air or to 0.06 ppm or 0.08 ppm O₃. We used standard statistical methods appropriate for paired comparisons to reanalyze FEV₁ responses after exposure to 0.06 ppm O₃ relative to filtered air.

Results: Controlling for filtered air responses, 24 of the 30 subjects experienced an O₃-induced decrement in FEV₁. On average, 0.06 ppm O₃ exposure caused a 2.85% reduction in FEV₁ (p < 0.002) , which was consistent with the predicted FEV₁ response from existing models. Although the average response was small, two subjects had > 10% FEV₁ decrements.

Conclusions: Exposure to 0.06 ppm O₃ causes a biologically small but highly statistically significant decrease in mean FEV₁ responses of young healthy adults.

Key words: air pollutants, photochemical oxidants, spirometry. Environ Health Perspect 116:1023–1026 (2008) . doi:10.1289/ehp.11396 available via http://dx.doi.org/ [Online 21 April 2008]

Address correspondence to J.S. Brown, U.S. Environmental Protection Agency, Office of Research and Development, National Center for Environmental Assessment, B243-01, Research Triangle Park, NC 27711 USA. Telephone: (919) 541-0765. Fax: (919) 541-1818. E-mail: Brown.James@epa.gov

W.F.M. was funded by U.S. EPA contract EP07H001352.

This document has been reviewed in accordance with U.S. Environmental Protection Agency (EPA) policy and approved for publication. Mention of trade names or commercial products does not constitute endorsement or recommendation for use. The views expressed in this article are those of the authors and do not necessarily reflect the views or policies of the U.S. EPA.

Unrelated to the production of this article, W.F.M. received funding from the American Petroleum Institute to evaluate new ozone health effects data and to conduct research related to a human ozone exposure–response model. The other authors declare they have no competing financial interests.

Received 20 February 2008 ; accepted 21 April 2008.