In previous studies exposure to ozone (O₃), a common outdoor air pollutant, is shown to cause a decrement in spirometry parameters. This decrement has been shown to be attenuated in smokers. We hypothesize that hypersecretion of respiratory mucus due to smoking reduces the absorbance of O₃ in the conducting airways of smokers, resulting in decreased responsiveness to exposure to O₃. Due to the reduced amount of O₃ absorbed in the conducting airways, the amount of O₃ absorbed in the deeper respiratory airways of the lung is expected to be increased in smoking subjects when compared to non-smoking subjects.

In this study, subjects participate in three research sessions: bolus, air and ozone. In the bolus research session, measurements of flow and O₃ concentration are used in the determination of longitudinal distribution of O₃ uptake in human lungs. During the air and ozone research sessions the subject will exercise on a cycle ergometer for one hour while breathing either room air or ozone mixed with room air. In these sessions measurements of flow, ozone concentration and carbon dioxide (CO₂) concentration are recorded.

Ozone bolus measurements have been preformed in previous studies to determine flow effects and subject variability on non-smoking subjects. The objective of the present study is to determine uptake using the bolus inhalation apparatus on a population of smoking and non-smoking subjects, allowing for a comparison between these two populations. Fractional uptake (Λ) is expressed as the amount of O₃ absorbed during a single breath relative to the amount of O₃ in the inhaled bolus. Uptake is related to the penetration volume (V_P) of the bolus into the respiratory tract.

From the flow and ozone concentration data, the Λ-V_P distribution will be determined from a series of 60-80 test breaths that are collected at a fixed flow of 60 L/min for each subject using the bolus apparatus. Comparing the Λ-V_P profiles of the smoking and non-smoking populations shows a small distal shift of the absorption profile for the smoking subjects. However, this result may be due to differences in population respiratory system sizes. To minimize the effects of differences in lung size among the individuals in this study, the V_P is normalized by the anatomical dead space (V_D) obtained from carbon dioxide expirometry. V_D is a measurement of the volume of the lung that does not take part in gas exchange, and can therefore also be used as an estimate of the conducting airway volume of each subject. Comparing the Λ-V_P/V_D profiles show that there are no significant differences between the two populations in terms of ozone absorption.

For the air and ozone sessions changes were made to the equipment and data collection process from previous studies for the inclusion of CO₂ monitoring. The goal of the inclusion of the CO₂ data in the air and ozone sessions is to show the dynamic changes in lung function during ozone exposure. Data from CO₂ expirography has been used to determine anatomic information non-invasively. The CO₂ expirogram can be divided into three regions, the pure dead space, the transition region, and the alveolar plateau. V_D can be determined from the pure dead space and transition regions of the expirogram, while the normalized slope (S_N) can be computed from the alveolar plateau.

The following results are for thirty healthy non-smoking subjects (17 men, 13 women) that participated in these two research sessions (air and ozone). The value of V_D decreases during the O₃ exposure session at a rate of 0.067 ± 0.035 mL/min (P = 0.06). The value of S_N increases during the O₃ exposure session at a rate of 0.57 ± 0.094 E^-3 L^-1min^-1 (P < 0.001). During the course of the air exposure, the value of V_D does not change significantly with time (P = 0.72). However, the value of S_N is seen to also increase with air exposure at a rate of 0.29 ± 0.11 E^-3 L^-1min^-1 (P = 0.011). The results of the air session suggest that exercise alone can lead to an increase in S_N. The larger and more significant increase in S_N during O₃ exposure indicates there is a loss of gas exchange efficiency in addition to the exercise-induced effect. However, there was a systematic change in tidal volume observed during the one-hour exposure period. The changes in breathing pattern may have contributed to changes in S_N during the dynamic measurements.

Future work in this study will focus in the following area: 1) Establish a model that will enable parameters determined from the absorption data in the bolus session to partition the absorbed ozone during the ozone session into distinct respiratory compartments; 2) Develop methods in which anatomic information can be obtained independent of exhaled tidal volume from CO₂ measurements during the air and ozone sessions; and 3) Determine if uptake of ozone in the respiratory system can account for difference in responsiveness to zone exposure between smoking and non-smoking subjects.