Respiratory health and baby swimming

Although baby swimming programmes are very popular, there are no reliable data on the potential advantages and risks of this practice for the child's development.¹ In particular, no study has evaluated the possible effects of exposing babies to the volatile chlorination products of indoor pools that recently have been found to affect the lung epithelium and to increase asthma risks.²,³,⁴

We examined a total of 341 schoolchildren aged 10–13 years who were recruited from 10 primary schools in the same area of Brussels, after informed consent was obtained from their parents. The institutional ethics committee approved the study protocol. Among participants, 43 had followed a baby swimming programme before the age of 2 years. Levels of active and combined chlorine in the attended swimming pool were within recommended limits (below 1.5 and 2 mg/l, respectively). Concentrations of trichloramine in pool air ranged from 170 to 540 μg/m³ (mean 325 μg/m³, n = 7) and were probably in the same range 10 years ago since operating conditions had remained unchanged. Information about the health of children and their exposure to risk factors of asthma and allergy was obtained from a questionnaire completed by the parents. Lung epithelium integrity was assessed by measuring serum Clara cell protein (CC16) and surfactant associated protein D (SP‐D).⁵ Total and aeroallergens specific IgE in serum were also measured (DPC, LA). Asthma was defined as doctor diagnosed asthma and/or a positive exercise induced bronchoconstriction test (based on a 15% fall of FEV₁).³ Backyard multiple and logistic regression analyses were used to further assess associations between baby swimming practice and the outcomes by testing a total of 23 potential predictors, including classical risk factors (for example, gender, serum IgE, and family history of allergic diseases).

There were no statistically significant differences between the swimming baby group and the other children regarding the proportion of children whose mother or father had asthma, the mean levels of total serum IgE, and the prevalence of aeroallergen specific serum IgE (table 1). Children who had been swimming as babies showed a significant decrease of serum CC16 and an even more significant decrease of the serum CC16/SP‐D ratio, adjusting serum CC16 for the permeability of the alveolar‐capillary barrier.⁵ In multivariate analyses, baby swimming emerged as the only statistically significant predictor of serum CC16 (partial r = −0.14, p = 0.01); this practice was the strongest determinant of the CC16/SP‐D ratio (log transformed values, partial r = −0.15, p = 0.006). These effects were associated with higher risks of asthma and recurrent bronchitis, as confirmed by logistic regression analyses (adjusted odds ratio for asthma 3.0, p = 0.01; adjusted odds ratio for recurrent bronchitis 2.6, p = 0.006).

Table 1 Lung epithelium integrity and respiratory health of children having followed a swimming baby programme.

	Swimming baby (n = 43)	Other children (n = 298)	p value
Age (mean, SD), years*	11.5 (0.6)	11.5 (0.6)	0.98
Boys, n (%)†	22 (51.1)	150 (50.3)	0.92
Mother and/or father with asthma, n (%)†	6 (14.0)	58 (19.5)	0.39
Aeroallergen specific serum IgE, n (%)†	13 (30.2)	95 (31.9)	0.83
Total serum IgE (median, IQR), kUI/l‡	54.7 (24.6–162)	55.8 (21.9–175)	0.96
Serum CC16 (mean, SD), μg/l*	8.0 (3.3)	10.4 (4.2)	0.01
Serum SP‐D (mean, SD), μg/l*	113 (42)	100 (45)	0.08
Serum CC16/SP‐D ratio (median, IQR)‡	0.07 (0.05–0.12)	0.10 (0.07–0.16)	0.003
Asthma†	10 (23.3)	33 (11.1)	0.025
Recurrent bronchitis†	26 (60.5)	110 (36.9)	0.006

CC16, Clara cell protein; SP‐D, surfactant associated protein D; IQR, interquartile range.

*Two sided unpaired t test; †χ² test; ‡two sided Mann‐Whitney U test.

Our data suggest that swimming baby practice in chlorinated indoor pools can be associated with distal airways alterations predisposing children to the development of asthma and recurrent bronchitis. While an increase of serum SP‐D reflects an increased permeability of the alveolar‐capillary barrier, the reduction of serum CC16 means a loss of the Clara cells lining the terminal airways.⁵ These effects might result from repeated inhalation of chlorination products, in particular of trichloramine, the irritant gas formed when chlorine reacts with organic matter brought by swimmers and that gives indoor swimming pools their typical chlorine smell.²,³ A link between swimming as a baby and more frequent recurrent respiratory diseases has also been observed in a recent study.⁶ Although these findings need to be confirmed by prospective studies, we recommend caution before regularly taking babies to poorly ventilated indoor pools where there is a strong chlorine smell.