Ozone (O₃) is an urban outdoor pollutant primarily generated by a photochemical reaction of atmospheric oxygen with oxides of nitrogen and unburned hydrocarbons from automobile emissions. The inhalation of O₃ is associated with health effects that include decrements in pulmonary function, pulmonary inflammation, and alterations in lung development. The purpose of the current research was to determine the influence of smoking on the retention of O₃ in the adult human lung.

Thirty smokers and thirty nonsmokers each participated in two research sessions. During an O₃ exposure session, subjects exercised on a cycle ergometer for one hour while breathing room air containing 0.3 ppm O₃. By making periodic adjustments in the ergometer workload, the experimenter targeted a minute ventilation (MV) of 15 L/min/m² of body surface. During a control session, carried out at least one week prior to the O₃ exposure session, the subject followed the same procedure while breathing room air not containing O₃. During both sessions, the subject breathed through an oral mask fitted with sensors that monitored respiratory flow and O₃ concentration throughout the one-hour session.

The fractional uptake efficiency (UE), defined as the ratio of retained amount of O₃ to inhaled amount of O₃, was determined for each breath and averaged at five minute increments. UE decreased for both smokers and nonsmokers during the one-hour exposure, and the smoking subjects had a somewhat higher UE than the nonsmoking subjects. An ANCOVA of UE using time as the covariate and smoking status as the fixed variable revealed that smoking status was indeed a significant predictor of uptake efficiency (p=0.02).

Respiratory flow data was processed to obtain MV, frequency (FR), and tidal volume (VT). Minute-by-minute values of the MV exhibited minimal variation within either the control or O₃ exposure sessions, and the session-averaged MV values were not significantly different between the control and exposure sessions or between the smokers and nonsmokers. Relative to the control session, there was an increase in FR and a decrease in TV associated with O₃ exposure for both smokers and nonsmokers. Smokers breathed at a slightly higher VT and lower FR than the nonsmokers. We hypothesized it was these variations in breathing pattern that were responsible for the observed variations in UE.

In previous work, the UE values observed in health nonsmoking subjects during a one-hour O₃ exposure were simulated with a single-path respiratory transport model. Simulations were performed for individual subjects by incorporating a square wave respiratory flow pattern with VT and FR varying in accordance with their observed minute-by-minute values. By adjusting the rate constant for O₃ reaction in the mucous layer (k_r) on a subject-by-subject basis, these simulations closely matched the measured UE for all subjects.

To test our hypothesis, the single-path model was employed to separately simulate the current data grouped into four subpopulations: male nonsmokers, female nonsmokers, male smokers, and female smokers. The squared error between the observed and simulated UE was minimized by adjustment of k_r for each subpopulation. The final values of k_r were 1.06E6 s^-1 for female nonsmokers, 2.25E6 s^-1 for male nonsmokers, 2.55E6 s^-1 for female smokers, and 2.60E6 s^-1 for male smokers. Thus, by taking breathing pattern alone into account, it was possible to simulate differences in the observed UE between the smokers and nonsmokers.