Changes in serum pneumoproteins caused by short-term exposures to nitrogen trichloride in indoor chlorinated swimming pools

Abstract

Nitrogen trichloride (NCl(3)) is an irritant gas released in the air of indoor pools sanitized with chlorine-based disinfectants. In the present study we investigated the effects of NCl(3) on the pulmonary epithelium of pool attendees by measuring the leakage into serum of three lung-specific proteins (pneumoproteins): the alveolar surfactant-associated proteins A and B (SP-A and SP-B) and the bronchiolar 16 kDa Clara cell protein (CC16). These pneumoproteins were measured in the serum of 29 recreational swimmers (16 children and 13 adults) before and after attending a chlorinated pool with a mean NCl(3) concentration of 490 microg m(-3). Pneumoprotein changes in serum were also studied in 14 trained swimmers performing an intensive 45 min standardized swimming session in a chlorinated pool (mean NCl(3) concentration of 355 microg m(-3)) and for the purposes of comparison in a non-chlorinated pool sanitized by the copper/silver method. Serum CC16 was not increased in recreational swimmers, but in trained swimmers serum levels of this protein peaked immediately after strenuous exercise, both in the copper/silver pool and in the chlorinated pool. This acute increase in airway permeability is probably the consequence of the mechanical stress on the epithelial barrier caused by overinflation and/or hyperventilation during intense exercise. Serum levels of SP-A and SP-B were unaffected by strenuous exercise in the copper/silver pool. The two proteins were, however, significantly increased in a time-dependent manner in recreational and trained swimmers attending the chlorinated pool. The intravascular leakage of SP-A and SP-B was already statistically significant after only 1 h of exposure to pool air without exercising and remained elevated for 12 h after. These changes were not associated with decrements in lung function. The ability of NCl(3) to acutely disrupt the lung epithelium barrier was confirmed in mice using serum CC16 and plasma proteins in bronchoalveolar lavage fluid as permeability markers. The significance of these permeability changes induced by NCl(3) in the deep lung is presently unknown. In view of the increasing and widespread human exposure to this gas not only in indoor pools but also in a variety of other situations, these findings warrant further study.

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

“…Club (Clara) cell secretory protein 16 (CC16) and pulmonary surfactant-associated protein A and B (SP-A and SP-B) are typical airway proteins that often are measured in serum. Augmented serum levels of SP-A and SP-B have been shown after swimming in chlorinated pools, suggesting increased permeability of the lung barrier [59]. In line, increased plasma levels of CC16, associated with disinfection by-products from the chlorinated water, are shown among swimmers, especially after short-term training [40,60].…”

“…In line, increased plasma levels of CC16, associated with disinfection by-products from the chlorinated water, are shown among swimmers, especially after short-term training [40,60]. 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].…”

Swimming pool attendance and risk of asthma and allergic symptoms in children

“…Eczema (or atopic dermatitis) is a chronic inflammatory skin disease characterised by the formation of specific antibodies (IgE) to environmental allergens, which frequently starts early in infancy and affects 15-30% of children in industrialised countries [25]. Although IgE blood levels were unrelated to both cumulative and acute pool exposure in two studies [26,27], a semi-experimental study suggested that dermal pool exposure may play a role in the exacerbation of atopic dermatitis [28]. Furthermore, it has been described that workers engaged in wet-works are at risk for suffering irritant dermatitis [29], which in turn may enhance the atopic dermatitis [30].…”

Airway irritation among indoor swimming pool personnel: trichloramine exposure, exhaled NO and protein profiling of nasal lavage fluids

“…Thus, increased serum levels of surfactant proteins (SP-A and SP-B) have been found after swimming in chlorinated pools (Carbonnelle et al 2002) and associated to pool attendance in children (Bernard et al 2005). Furthermore, increased serum levels of Clara cell secretory protein 16 (CC16) have been suggested as a short-term marker after swimming in chlorinated pools , although other results indicates CC16 being a marker of exercise rather than exposure to chlorinated irritants (Carbonnelle et al 2002). Both SP-A/SP-B and CC16 are typical airway proteins and increased levels in serum are believed to reflect increased epithelial permeability, e.g.…”