Doesn't mean I want to be breathing it to kill a deer.
What are the effects of recurrent or long-term exposure to ozone?
One of the major unanswered questions about the health effects of ozone is whether repeated episodes of damage, inflammation, and repair induced by years of recurrent short-term ozone exposures result in adverse health effects beyond the acute effects themselves.
Daily ozone exposure for a period of 4 days results in an attenuation of some of the acute, neurally-mediated effects (e.g., lung function changes and symptoms) for subsequent exposures occurring within 1 to 2 weeks. Some health experts have, therefore, suggested that individuals living in high ozone areas may be protected from any harmful effects of long-term ozone exposure. Others suggest, however, that the attenuation of the ozone-induced tendency to take rapid and shallow breaths may blunt a protective mechanism, resulting in greater delivery and deposition of ozone deeper in the respiratory tract and other airway responses described below.
Studies including bronchoalveolar lavage and bronchial mucosal biopsies indicate that, unlike the neurally-mediated lung function changes, the processes of airway injury, inflammation, and repair continue to occur during repeated exposure. After either 4 or 5 days of exposure, markers of cell injury and increased epithelial permeability remain elevated, and an increase in airway mucosal PMN, which was not present following a single exposure, has been noted. Also, unlike the neurally-mediated effects, small airway function has been observed to remain depressed over the course of exposures and is thought to be related to the ongoing inflammation.
Studies of laboratory animals have consistently demonstrated that long-term exposure to ozone concentrations above ambient levels results in persistent morphological changes that could be a marker of chronic respiratory disease. Exposed animals experience mucous cell metaplasia and epithelial cell hyperplasia in the upper airway as well as structural changes in the lower airway including an increase in fibrous tissue in the basement membrane area and a remodeling of the distal conducting airways. In addition to airway remodeling and basement membrane changes, concurrent long-term exposure of very young primates to ozone and house dust mite allergen has been observed to result in changes in the innervation of the airways as well as an accumulation of eosinophils in the distal airways suggesting induction of an allergic phenotype. Other studies indicate that sensitization of animals to antigen occurs more easily during ongoing ozone exposures. Based on traditional measures, there is little evidence that long-term exposure in animals results in substantial changes in airway function. However, these morphological findings suggest that long-term ozone exposure might play a role in the development or progression of chronic lung disease and/or asthma.
The epidemiologic evidence is inconclusive with regard to whether long-term exposure of humans is related to chronic respiratory health effects in humans. Several cross-sectional studies have found that young adults who spent their childhoods in locales with high ozone concentrations had lower measures of lung function than those from locales with lower ozone. Similar results have not been observed, however, in a recent well-conducted longitudinal study of lung function in children or in other cross-sectional studies. Two longitudinal studies have observed associations between development of asthma and long-term ozone concentrations in subgroups of the population. These findings have not been confirmed in other longitudinal or cross-sectional studies, but they are consistent with the animal toxicological literature. Part of the difficulty in evaluating such associations has been the small number of longitudinal epidemiologic studies specifically designed to evaluate respiratory health in samples with differing ozone exposures. The mobility of the population as well as the inability to precisely estimate exposure to ozone and other potential confounders over a period of many years degrades the power of, and leads to bias in, both longitudinal and cross-sectional studies.
In spite of the inconclusive nature of the epidemiologic literature, the repeated cycles of damage, inflammation, and repair in humans and the morphological findings from the animal toxicological studies suggest that it would be prudent to avoid repeated short-term exposures, particularly in young children, until more is known about the effects of long-term ozone exposure.
