inhalation. These interesting findings must be interpreted with caution, especially because high pollutant concentrations were used in the initial study. In addition, it is not clear whether the findings represent an independent carcinogenic effect of sulfur dioxide in addition to benzopyrene or a potentiation of benzopyrene carcinogenesis by an otherwise unrelated consequence of sulfur dioxide exposure. Recent preliminary studies by this group appear to indicate that combined exposure to nitrogen dioxide and benzopyrene also results in lung carcinogenesis. If this is confirmed, it would tend to support the hypothesis that sulfur dioxide promotes benzopyrene carcinogenesis through its action as a nospecific irritant. However, whatever biomedical mechanisms are involved, further animal inhalation studies with lower pollutant concentrations are definitely warranted.

Despite the biochemical and animal inhalation studies cited, there appears to be insufficient epidemiologic evidence to assign a definite risk to the possibility that ambient sulfur oxides are a factor in the production of human lung cancer.

There have been a number of attempts to quantify the damage caused by air pollutants. To do so, it is necessary to assign some numerical value to the expected health effects in relation to given degrees of air pollution. In the preceding sections of this review, where permitted by the data, quantitative estimates of morbidity and mortality in association with air pollution have been cited from individual papers. It would be possible to graph these estimates and analyze them statistically to arrive at some quantitative estimate of the amount of morbidity and mortality associated with measured concentrations of individual pollutants. However, such an exercise would be grossly misleading and would undoubtedly lead to erroneous conclusions. Each of the studies cited earlier must be considered in relation to