Ozone chronic

P[Pg.540]

The most important health effects, in terms of economic damages that can be assigned monetary values, are premature mortality and increased incidence of chronic heart and lung disease. The air pollutants that have shown the strongest association with premature mortality and heart and lung disease are PM and airborne lead. PM has also been associated with hospital admissions, respiratory infections, and asthma attacks. Ozone has also been associated with mortality, hospital admissions, asthma attacks and respiratory restricted activity days (RADs), days on which a person cuts back on his or her normal activities, but does not necessarily miss work or stay in bed. S02 and NOx do not have such significant direct effects, though they do have... 

The Clean Air Act recognizes a number of so-called primary air pollutants, and the EPA has established standards for these substances. Ozone, nitrogen oxides, and sulfur dioxide are among these (the others are carbon monoxide and lead, discussed below, and total suspended particulates ). The EPA s standard for ozone is 0.08 parts of the gas per million parts of air (0.08 ppm), averaged over eight hours. Standards also exist for the oxides of sulfur and nitrogen. These are designed to prevent chronic respiratory toxicity of any kind. 

Recent studies involving repeated or prolonged exposures of laboratory animals to ozone have suggested that changes indicative of chronic lung disease (such as decreased elasticity of the lungs) also require concentrations of 0.2-0.5 ppm. 

With various tests of ventilatory function, it has been shown that healthy male college students experienced no effect of sulfur dioxide at 0.37 ppm, a 10% decline in function with ozone at 0.37 ppm, and a 20-40% decline in function with a combination of sulfur dioxide at 0.37 ppm and ozone at 0.37 ppm. Other experiments have suggested an adaptation of southern Californians to chronic exposure to ambient ozone. 

Oxidants reduce yields of many plants, especially sensitive cultivars. Chronic exposures to concentrations between 0.05 and 0.15 ppm will reduce soybean, com, and radish yields. The threshold appears to be between 0.05 and 0.1 ppm for some sensitive cultivars—well within values monitored in the eastern United States. Growth or flowering effects on carnation, geranium, radish, and pinto bean have been found at chronic exposures to ozone at 0.05-0.15 ppm. Estimated costs to consumers of agricultural losses from oxidant damage are several hundred million dollars a year. 

A few definitive experiments are needed to complete our knowledge of acute dose-response relationships for ozone. Research is necessary in the case of PAN and other oxidants. More important is the need for studies of crop and native species over growing seasons with chronic oxidant exposures. At the same time, additional work with field chambers, filtered or nonfiltered, is needed. 

According to Stokinger, at least three effects of long-term exposure to ozone have been recc ized effects on morphology and function of the lung, lung-tumor acceleration, and aging. An additional effect, the development of tolerance after exposure to low concentrations of ozone, may also be related to chronic toxicity. 

Stokinger et reported that chronic bronchitis, bronchiolitis, and emphysematous and fibrotic changes in the lung tissues occur in mice, hamsters, and guinea pigs exposed daily to ozone at a concentration slightly above 1 ppm. These irreversible changes also develop in animals that have developed tolerance to acute inflammatory effects. 

As described elsewhere in this chapter, alterations in the activity of a number of lung enzymes have been described after acute and chronic ozone exposure. With the possible exceptions of the sulfhydryl-containing enzyme succinic dehydrogenase and the cytochrome P-4 en me benzopyrene hydroxylase, it is difficult to determine whether these findings are due to a direct oxidative effect of ozone or are secondary to changes in protein synthesis, concentrations of intermediates, or destruction of cells or organelles. 

As discussed in detail by Dillard et al. and by Mittman et al. the possible relationship of lysosomal proteases to chronic lung disease has been inferred from the finding of an increased incidence of emphysema in subjects deficient in serum ai>antitrypsin factor, an -globulin that can inhibit lysosomal proteases. (No effect of ozone on serum aj-antitrypsin inhibitor was noted in rabbits chronically exposed to ozone. ) Thus, an ozone-induced increase in concentrations of such enzymes in the lung might produce excess proteolysis and result in eventual chronic lung disease. However, the available evidence is inadequate to support the belief that such a process occurs in humans intermittently exposed to ozone. Further studies of this potential hazard would be of value. 

In a recent abstract, Hussain et al presented evidence that exposure of rats to ozone at 0.8 ppm for up to a week resulted in an increased rate of collagen thesis. Such a finding might be relevant to ozone-induced fibrosis. Obviously, further study of the biochemical effects of ozone on lung collagen and elastin are in order, particularly in conjunction with chronic-exposure experiments. 

Biochemical changes in animal central nervous sterns have been reported by Skillen et who noted a decrease in brain 5-hydroxytiypt-amine (serotonin) in rats exposed to ozone at 6 ppm for 4 h, and by Trams et who observed decreases in catecholamines and catechol-O-methyl-transferase in dogs chronically exposed to ozone at 1,2, or 3 ppm. Electro-encephalographic (eeg) measurements in the same dogs were recently presented by Johnson et who noted alterations in eeg patterns at 9 months of ozone exposure, but not after 18 months of exposure. Previously, Xintaras et o/. had observed alterations in the visual evoked electric response in rats acutely exposed to 0.5-1.0 ppm. As pointed out by Johnson et it is not clear whether these findings indicate a direct neurotoxic action of ozone or are secondary to damage in other organs. 

An interesting report by P an and Jegier noted an increase in serum trypsin protein esterase in association with pulmonaiy vascular lesions in rabbits chronically exposed to ozone at 0.4 ppm. This serum a,-macroglobulin, which is synthesized in the liver, has been reported to be increased in human vascular disorders, but its physiologic significance is unknown. 

Bartlett, D., Jr., C. S. Faulkner, II, and K. Cook. Effect of chronic ozone exposure on lung elasticity in young rats. J. Appl. Physiol. 37 92-%, 1974. 

Trams, E. G., C. J. Lauter, E. A. B. Brown, and O. Young. Cerebral cortical metabolism after chronic exposure to ozone. Arch. Environ. Health 24 153-159,... 

Werthamer, S., P. D. Penha, and L. Amaral. Pulmonary lesions induced by chronic exposure to ozone. I. Biochemical alterations. Arch. Environ. Health 29 164-166, 1974. 

Many workers have used controlled additions of ozone in acute or chronic studies to determine effects on a variety of growth measures. These studies suggest results attributable to ambient oxidants in field... 

Heagle and associates found a reduction in yield of sweet com and soybean after exposure to ozone at 0.10 ppm for 6 h/day over much of the growing season. These exposures were carried out in field chambers set over soybean plots in the field. They suggested that a threshold for measurable effects on these crops would lie between ozone (oxidant) concentrations of 0.05 and 0.10 ppm for 6 h/day. These values are realistic in terms of growing-season averages in the eastern United States. More of these studies could help to clarify dose-response relationships for economically important crops. Table 11-5 summarizes these long-term, chronic studies. 

---