Health and pollution control professionals and the general public need to develop a more complete understanding of the health effects of ozone (O3) because: 1) we have been unable to significantly reduce ambient O3 levels using current strategies and controls; 2) in areas occupied by more than half of the U.S. population, current peak ambient O3 concentrations are sufficient to elicit measurable transient changes in lung function, respiratory symptoms, and airway inflammation in healthy people engaged in normal outdoor exercise and recreational activities; 3) the effects of O3 on transient functional changes are sometimes greatly potentiated by the presence of other environmental variables; and 4) cumulative structural damage occurs in rats and monkeys exposed repetitively to O3 at levels within currently occurring ambient peaks, and initial evidence from dosimetry models and interspecies comparisons indicate that humans are likely to be more sensitive to O3 than rats. The extent and significance of these effects, and the multibillion dollar costs of ambient O3 controls need to be considered in any future revisions of ambient standards and the Clean Air Act. The transient effects of O3 are more closely related to cumulative daily exposure than to one hour peak concentrations, and future revisions of the ambient standard for O3 should take this into account. The effects of long-term chronic exposure to O3 remain poorly defined, but recent epidemiologic and animal inhalation studies suggest that current ambient levels are sufficient to cause premature aging of the lungs. More research is needed to determine the need for a standard with a seasonal or annual average concentration limit.

The relation between the concentrations and characteristics of air contaminants in the work place and the resultant toxic doses and potential hazards after their inhalation depends greatly on their patterns of deposition and the rates and pathways for their clearance from the deposition sites. The distribution of the deposition sites of inhaled particles is strongly dependent on their aerodynamic diameters. For normal man, inhaled non-hygroscopic particles > 2 ,um that deposit in the conducting airways by impaction are concentrated on to a small fraction of the surface. Cigarette smoking and bronchitis produce a proximal shift in the deposition pattern. The major factor affecting the deposition of smaller particles is their transfer from tidal to reserve air.For particles soluble in respiratory tract fluid, systemic uptake may be relatively complete for all deposition patterns, and there may be local toxic or irritant effects or both. On the other hand, slowly soluble particles depositing in the conducting airways are carried on the surface to the glottis and are swallowed within one day. Mucociliary transport rates are highly variable, both along the ciliated airways of a given individual and between individuals. The changes in clearance rates produced by drugs, cigarette smoke, and other environmental pollutants can greatly increase or decrease these rates. Particles deposited in non-ciliated airways have large surface-to-volume ratios, and clearance by dissolution can occur for materials generally considered insoluble. They may also be cleared as free particles either by passive transport along surface liquids or, after phagocytosis, by transport within alveolar macrophages. If the particles penetrate the epithelium, either bare or within macrophages, they may be sequestered within cells or enter the lymphatic circulation and be carried to pleural, hilar, and more distant lymph nodes. Non-toxic insoluble particles are cleared from the alveolar region in a series of temporal phases. The earliest, lasting several weeks, appears to include the clearance of phagocytosed particles via the bronchial tree. The terminal phases appear to be related to solubility at interstitial sites. While the mechanisms and dynamics of particle deposition and clearance are reasonably well established in broad outline, reliable quantitative data are lacking in many specific areas. More information is needed on: (1) normal behaviour, (2) the extent of the reserve capacity of the system to cope with occupational exposures, and (3) the role of compensatory changes in airway sizes and in secretory and transport rates in providing protection against occupational exposures, and in relation to the development and progression of dysfunction and disease.

Overall, the results suggest short-term associations between ozone and daily mortality in the majority of the cities, although the estimates appear to be heterogeneous across cities.