This is the first study examining the effects of ozone levels on spontaneous pneumothorax occurrences. Some previous studies have proposed that seasonality and especially atmospheric pressure may be precipitating factors for SP. Bense and Scott et al. had previously shown the link between SP and changes in atmospheric pressure [5, 11]. However, more recent studies in different regions have failed to show an association between SP and climate changes [12–14]. Recently, the first large nationwide population based study did not support the premise that seasonality is a precipitating factor for SP [8]. In all these studies, humidity, atmospheric pressure changes and temperatures were under consideration in relation to the spontaneous pneumothorax occurrences. Many studies have demonstrated no association of changes in atmospheric pressure in different regions and SP. Also with regard to SP and variations in ambient temperature, some studies have revealed no relationships. The results from these studies are controversial, but they have consistently failed to show a significant association.
The most important finding of our study was the increased number of patients with SP during periods of high ozone levels. The increased SP frequency may be due to the oxidative stress effect of ozone. Ozone is known to cause damage to the lung interstitium by way of oxidative stress [15]. Ozone has also been known as a protoplasmic poison causing damage to lung tissue during lung exposure to chlorine [16]. Studies of the noxious effects of ozone on lung tissues are limited but it is known that ozone can cause damage in lung tissue. Previously, acute ozone exposure has been shown to decrease lung volume per unit of distending pressure. This effect may be potentially caused by a change of lung tissue elasticity or by changes in surface tension forces of the alveoli [10]. The lungs are constantly exposed to oxidants which are present in the air inhaled. The oxidants in inhaled air include cigarette smoke and ozone, or those released from inflammatory leukocytes. These oxidants, including ozone, cause direct damage to the lung interstitium. These oxidative stressors have been shown to contribute to the pathogenesis of SP in some studies [15]. An increase in interstitial mass and a proliferation of epithelial cells has been reported as a response to pulmonary stress and insult including exposure to ozone [9]. By way of these effects on lung tissue, increased levels of ozone in the inhaled air may contribute to the pathogenesis and occurrence of SP.
The other important finding of our study was the increased SP frequency in the spring. There was also a positive correlation between SP frequency and average ozone values for the seasons. The average ozone value was higher in spring, and in spring there was an increased SP frequency. In the literature there is no consensus regarding the causes of the apparent increase in the rate of SP. There is also no agreement about factors causing the occurrence of SP. Some studies have proposed that changes in atmospheric pressure cause alterations of the volume of air-holding lung cysts, and that this may cause weakening of the walls [3]. However, both weakening of the walls due to atmospheric changes and contributions from other seasonal factors including temperature, humidity and storms as an explanation for the occurrence of SP do not provide strong explanations for the SP occurrence from the point of view of pathophysiology.
In our study, we found that SP was more often seen in high ozone levels. Ozone itself is known to have some destructive effects on lung tissue. This has been shown by both biochemical studies and by electron microscopical studies [10, 15, 17]. It is also interesting that similar ultrastructural changes are seen in lungs both in response to acute ozone exposure and in the occurrence of spontaneous pneumo thorax. These changes include proliferation of epithelial cells and an increase in the intersitial mass and edema [9, 10]. As certain climatic parameters have shown weak and controversial associations with the incidence of SP, there is a need to invesitigate possible other associations. From our findings and from the potential pathophysiological mechanisms of ozone acting on lung tissue, a high level of ozone may be a precipitating factor in the alteration of lung tissue elasticity and may also be a factor in the rupture of blebs/bullae in SP. In our study a high level of ozone in the spring may explain the more frequent occurrence of SP in this season.