Pulmonary Epithelial Integrity in Children: Relationship to Ambient Ozone Exposure and Swimming Pool Attendance

Abstract

Airway irritants such as ozone are known to impair lung function and induce airway inflammation. Clara cell protein (CC16) is a small anti-inflammatory protein secreted by the nonciliated bronchiolar Clara cells. CC16 in serum has been proposed as a noninvasive and sensitive marker of lung epithelial injury. In this study, we used lung function and serum CC16 concentration to examine the pulmonary responses to ambient O3 exposure and swimming pool attendance. The measurements were made on 57 children 10–11 years of age before and after outdoor exercise for 2 hr. Individual O3 exposure was estimated as the total exposure dose between 0700 hr until the second blood sample was obtained (mean O3 concentration/m3 × hours). The maximal 1-hr value was 118 μg/m3 (59 ppb), and the individual exposure dose ranged between 352 and 914 μg/m3hr. These O3 levels did not cause any significant changes in mean serum CC16 concentrations before or after outdoor exercise, nor was any decrease in lung function detected. However, children who regularly visited chlorinated indoor swimming pools had significantly lower CC16 levels in serum than did nonswimming children both before and after exercise (respectively, 57 ± 2.4 and 53 ± 1.7 μg/L vs. 8.2 ± 2.8 and 8.0 ± 2.6 μg/L; p < 0.002). These results indicate that repeated exposure to chlorination by-products in the air of indoor swimming pools has adverse effects on the Clara cell function in children. A possible relation between such damage to Clara cells and pulmonary morbidity (e.g., asthma) should be further investigated.

Swimming pool, respiratory health, and childhood asthma: Should we change our beliefs?

“…CC16 was also positively associated with cumulated pool attendance, but no clear dose-effect relationship emerged. On the other hand, Lagerkvist et al 41 reported that repeated exposure to chlorination by-products was associated with lower levels of CC16. To explain these contradictory results, it has been suggested that CC16 serum levels reflect both epithelial permeability and Clara cell damage 41 .…”

“…On the other hand, Lagerkvist et al 41 reported that repeated exposure to chlorination by-products was associated with lower levels of CC16. To explain these contradictory results, it has been suggested that CC16 serum levels reflect both epithelial permeability and Clara cell damage 41 . In their study, Bernard et al 1 also described a correlation between lung hyperpermeability and total IgE levels, as well as an association between asthma prevalence and cumulated pool attendance.…”

Upper Airway Mucosal Inflammation : Proteomic Studies after Exposure to Irritants and Microbial Agents

“…However, some studies have instead linked the increase of CC16 in serum and urine to high intensity training, generating higher permeability in the lung epithelium, thereby enabling leakage to the blood stream [59,61]. When CC16 was measured in children regularly attending swimming pool facilities, not necessarily under intense training, the levels were instead lowered [62]. One in vitro study showed higher release of interleukin 6 (IL-6) and interleukin 8 (IL-8) from human lung cells exposed to swimming pool air, as compared to cells stimulated with trichloramine alone.…”

Asthma, allergy, the athlete and the Olympics

“…Larsson showed that cold air inhalation increased the number of inflammatory cells in broncho alveaveolar lavage (17). In children, Bernard et al found a relationship between the time spent in swimming pools during early childhood and the development of asthma as well as signs of lung involvement by increased serum levels of surfactant proteins (18) and reduced levels of Clara cell protein (19). Also, respiratory tract infections increase bronchial responsiveness in actively training athletes (20).…”