Infant swimming practice, pulmonary epithelium integrity, and the risk of allergic and respiratory diseases later in childhood

Unit of Toxicology, Faculty of Medicine, Catholic University of Louvain, Avenue E Mounier 53, Box 53.02, B-1200 Brussels, Belgium.
PEDIATRICS (Impact Factor: 5.47). 07/2007; 119(6):1095-103. DOI: 10.1542/peds.2006-3333
Source: PubMed


Irritant gases and aerosols contaminating the air of indoor swimming pools can affect the lung epithelium and increase asthma risk in children. We evaluated the impact of infant swimming practice on allergic status and respiratory health later in childhood.
Clara cell protein, surfactant-associated protein D, and total and aeroallergen-specific immunoglobulin E were measured in the serum of 341 schoolchildren aged 10 to 13 years, among whom 43 had followed an infant swimming program. Asthma was defined as doctor-diagnosed asthma and/or positive exercise-induced bronchoconstriction (15% decrease in postexercise forced expiratory volume).
There were no significant differences between the infant swimming group and the other children regarding the levels of exhaled nitric oxide and total or aeroallergen-specific serum immunoglobulin E. Children who swam as infants showed, by contrast, a significant decrease of serum Clara cell protein and of the serum Clara cell protein/surfactant-associated protein D ratio integrating Clara cell damage and permeability changes of the lung epithelial barrier. These effects were associated with higher risks of asthma and of recurrent bronchitis. Passive exposure to tobacco alone had no effect on these outcomes but seemed to interact with infant swimming practice to increase the risk of asthma or of recurrent bronchitis.
Our data suggest that infant swimming practice in chlorinated indoor swimming pools is associated with airways changes that, along with other factors, seem to predispose children to the development of asthma and recurrent bronchitis.

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    • "This study documents that serum CC16 concentrations are significantly lower in top athletes than in control subjects from the general population. Decreased serum CC16 concentrations were reported in infants and children regularly visiting indoor pools [22,23] but other studies brought conflicting results regarding the effect of single and repeated training session on serum CC16 [24,25]. Discrepancies are believed to be due to intensity of exertion and breathing pattern employed during various types of athletic activity (reviewed by LaKind et al. [11]). "
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    ABSTRACT: Respiratory epithelium integrity impairment caused by intensive exercise may lead to exercise-induced bronchoconstriction. Clara cell protein (CC16) has anti-inflammatory properties and its serum level reflects changes in epithelium integrity and airway inflammation. This study aimed to investigate serum CC16 in elite athletes and to seek associations of CC16 with asthma or allergy, respiratory tract infections (RTIs) and immune response to respiratory pathogens. The study was performed in 203 Olympic athletes. Control groups comprised 53 healthy subjects and 49 mild allergic asthmatics. Serum levels of CC16 and IgG against respiratory viruses and Mycoplasma pneumoniae were assessed. Allergy questionnaire for athletes was used to determine symptoms and exercise pattern. Current versions of ARIA and GINA guidelines were used when diagnosing allergic rhinitis and asthma, respectively. Asthma was diagnosed in 13.3% athletes, of whom 55.6% had concomitant allergic rhinitis. Allergic rhinitis without asthma was diagnosed in 14.8% of athletes. Mean CC16 concentration was significantly lower in athletes versus healthy controls and mild asthmatics. Athletes reporting frequent RTIs had significantly lower serum CC16 and the risk of frequent RTIs was more than 2-fold higher in athletes with low serum CC16 (defined as equal to or less than 4.99 ng/ml) . Athletes had significantly higher anti-adenovirus IgG than healthy controls while only non-atopic athletes had anti-parainfluenza virus IgG significantly lower than controls. In all athletes weak correlation of serum CC16 and anti-parainfluenza virus IgG was present (R = 0.20, p < 0.01). In atopic athletes a weak positive correlations of CC16 with IgG specific for respiratory syncytial virus (R = 0.29, p = 0.009), parainfluenza virus (R = 0.31, p = 0.01) and adenovirus (R = 0.27, p = 0.02) were seen as well. Regular high-load exercise is associated with decrease in serum CC16 levels. Athletes with decreased CC16 are more susceptible to respiratory infections. Atopy may be an additional factor modifying susceptibility to infections in subjects performing regular high-load exercise.
    Respiratory research 04/2014; 15(1):45. DOI:10.1186/1465-9921-15-45 · 3.09 Impact Factor
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    • "In other studies, differences in serum concentrations of other surfactant proteins (SP-A, and SP-B) were found after a short exposure in a chlorinated swimming pool in recreational and trained swimmers, but not in a pool with copper-silver disinfection method [22], [23]. On the contrary, a significant increase in serum SP-A and SP-B concentrations in adults after one hour of pool side presence without swimming was previously found [21]despite no significant differences being found in serum SP-D levels between children who swan in a chlorinated pool during lactation and children who did not [33]. Moreover, there are other suitable biomarkers (i.e. "
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    ABSTRACT: Swimming in indoor pools treated with combined chemical treatments (e.g. ozone) may reduce direct exposure to disinfection byproducts and thus have less negative effects on respiratory function compared to chlorinated pools. The aim of this study is to analyze the effects of a short-term training intervention on respiratory function and lung epithelial damage in adults exercising in indoor swimming pool waters treated with different disinfection methods (chlorine vs. ozone with bromine). Lung permeability biomakers [surfactant protein D (SP-D) and Clara cell secretory protein (CC16) in plasma] and forced expiratory volumes and flow (FEV1, FVC and FEF25-75) were measured in 39 healthy adults. Thirteen participants swam during 20 sessions in a chlorinated pool (CP), 13 performed and equivolumic intervention in an ozone pool (OP) and 13 were included in a control group (CG) without exposition. Median plasma CC16 levels increased in CP swimmers (4.27±3.29 and 6.62±5.51 µg/L, p = 0.01, pre and post intervention respectively) while no significant changes in OP and CG participants were found. No significant changes in median plasma SP-D levels were found in any of the groups after the training period. FVC increased in OP (4.26±0.86 and 4.43±0.92 L, p<0.01) and CP swimmers (4.25±0.86 and 4.35±0.85 L, p<0.01). FEV1 only increased in OP swimmers (3.50±0.65 and 3.59±0.67, p = 0.02) and FEF25-75 decreased in CP swimmers (3.70±0.87 and 3.37±0.67, p = 0.02). Despite lung function being similar in both groups, a higher lung permeability in CP compared to OP swimmers was found after a short-term swimming program. Combined chemical treatments for swimming pools such as ozone seem to have less impact on lung epithelial of swimmers compared to chlorinated treated pools.
    PLoS ONE 07/2013; 8(7):e68447. DOI:10.1371/journal.pone.0068447 · 3.23 Impact Factor
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    • "Another effect of DBPs on swimmers is irritation of the respiratory passage and trichloramine has been suggested as the causative compound. Several studies on the association of NCl 3 with respiratory irritation or asthma have been carried out (Bernard et al., 2007; Goodman and Hays, 2008; Hery et al., 1995; Massin et al., 1998; Thickett et al., 2002) however there is still a lack of evidence with which to make a definite conclusion. A recent study performed an in vitro air exposure test using the human alveolar epithelial carcinoma cell line A-549 to conclude that the concentration of NCl 3 alone could not explain the inflammatory effect of air from an indoor swimming pool and that other volatile DBPs must also be contributing to the observed effects (Schmalz et al., 2011). "
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    ABSTRACT: Medium pressure UV is used for controlling the concentration of combined chlorine (chloramines) in many public swimming pools. Little is known about the fate of other disinfection by-products (DBPs) in UV treatment. Photolysis by medium pressure UV treatment was investigated for 12 DBPs reported to be found in swimming pool water: chloroform, bromodichloromethane, dibromochloromethane, bromoform, dichloroacetonitrile, bromochloroacetonitrile, dibromoacetronitrile, trichloroacetonitrile, trichloronitromethane, dichloropropanone, trichloropropanone, and chloral hydrate. First order photolysis constants ranged 26-fold from 0.020min(-1) for chloroform to 0.523min(-1) for trichloronitromethane. The rate constants generally increased with bromine substitution. Using the UV removal of combined chlorine as an actinometer, the rate constants were recalculated to actual treatment doses of UV applied in a swimming pool. In an investigated public pool the UV dose was equivalent to an applied electrical energy of 1.34kWhm(-3)d(-1) and the UV dose required to removed 90% of trichloronitromethane was 0.4kWhm(-3)d(-1), while 2.6kWhm(-3)d(-1) was required for chloral hydrate and the bromine containing haloacetonitriles and trihalomethanes ranged from 0.6 to 3.1kWhm(-3)d(-1). It was predicted thus that a beneficial side-effect of applying UV for removing combined chlorine from the pool water could be a significant removal of trichloronitromethane, chloral hydrate and the bromine containing haloacetonitriles and trihalomethanes.
    Science of The Total Environment 01/2013; 443C:850-856. DOI:10.1016/j.scitotenv.2012.11.064 · 4.10 Impact Factor
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