Effects of Ozone Exposure at Ambient Air Pollution Episode Levels on Exercise Performance

Ozone is a principal component of photochemical air pollution endogenous to numerous metropolitan areas, which may induce irritant effects on the respiratory tract which impair pulmonary function, result in subjective symptoms of respiratory discomfort, including cough and shortness of breath, and can limit exercise performance. The effects of moderate ambient photochemical air pollution observed in a mobile laboratory have also been shown to be similar to those induced in laboratory chamber exposures to the same level of ozone alone. The metabolic demand of exercise increases minute ventilation VE and thus, the rate of ozone inhalation over that at rest. Potentially, exercise can also enhance the effects of ozone by: (a) reducing nasal passage absorption; (b) increasing the uniformity of ventilation throughout the lungs; and (c) replacing reacted ozone at a faster rate. However, results from 2-hour intermittent exercise and 1-hour continuous exercise exposures at the same total ventilation and ozone concentration have been shown to yield similar pulmonary function effects. It has been shown via significant variation in exercise intensity, and thus VE, that the simple product of ozone concentration, VE and exposure time (termed the ozone effective dose) predicts pulmonary function and exercise ventilatory pattern (induced rapid, shallow breathing) effects more precisely than ozone concentration alone. Better prediction of pulmonary function effects has been achieved via multiple regression analysis in which ozone concentration is given a greater weighting than VE and exposure time. Light intermittent exercise was first studied in 2-hour laboratory exposures to ozone at concentrations rarely seen in the ambient environment. In recent studies, heavy continuous exercise has been used in 1-hour exposures to ozone at levels routinely observed in photochemical episodes (≤ 0.35 ppm). Statistically significant impairment of exercise performance has been observed at 0.18 ppm, a level reached for 1 hour, or more, on about 180 days per year in the Los Angeles basin. Responses of subpopulation groups, such as children, young adult females, older adults, and those with pre-existing pulmonary disease are not notably different from those of young adult males provided that the ozone effective dose is proportional to body size. Conversely, highly trained endurance athletes demonstrate significant responses at rather low ozone concentrations due to their ability to sustain very high VE over prolonged periods. Numerous investigators have observed a wide range of individual subject’s pulmonary function responses to a given ozone exposure, although mechanisms accounting for this disparate individual responsiveness have not been identified. In recent studies, decreases in exercise performance and greater respiratory subjective symptom severity have been observed in those with greater pulmonary function impairment. Repeated exposure to high ambient levels of ozone within 24 hours results in greater response than upon initial exposure, if 72 hours or longer intervenes before re-exposure. However, with several consecutive daily exposures, pulmonary function and subjective symptom responses are greatly reduced. Exercise performance is also much less affected than that incurred upon initial exposure. Photochemical smog episodes also include air pollutants other than ozone and usually coincide with high ambient temperatures, which can significantly reduce endurance exercise performance. There is no appreciable additive impact with carbon monoxide, nitrogen dioxide or sulphur dioxide, but peroxyacetyl nitrate appears to induce an additive effect with ozone. The combination of heat and ozone exposure has been shown to accentuate ozone-induced effects although the mechanism remains unclear. Only a few studies have been designed to investigate maximum exercise performance and VE max impairment following ozone exposure sufficient to induce significant pulmonary function and respiratory discomfort response. With the increasing use of high intensity (≥ 65% of V2max) 1-hour continuous exercise protocols, especially in the presence of ambient heat (Tdb > 31°C), numerous instances of subjects unable to complete the full hour at the workload prescribed, or only upon reducing the workload, have been reported. Mechanisms accounting for reduced maximum exercise performance upon significant ozone exposure have not been well elucidated. Although significant pulmonary function impairment has been routinely observed, as well as enhanced subjective symptoms of res-piratory discomfort, no consistent objective evidence of effect on oxygen diffusion, transport and delivery has been observed. Hence, it appears that factors associated with ventilatory limitation impair both VO2max and prolonged heavy exercise (> 65% VO2max) performance. The observation that ozone exposure, which induces significant pulmonary function impairment, also incurs an increased perceived exertion during submaximal exercise strongly supports this contention. The hypothesis of subjective respiratory discomfort as the principal factor accounting for reduced exercise performance is further substantiated by several notable occurrences of discordance with pulmonary function impairment.