The recently proposed chlorine hypothesis postulates that childhood asthma rise could be linked to the increasing attendance of chlorinated pools by increasingly younger children. The culprit would be trichloramine, an irritant gas building up in the air of indoor chlorinated pools. To further test this hypothesis, we have explored the relationships between asthma, atopy and cumulated pool attendance (CPA) in 342 children (10-12 yr), 90% of them having attended the same pool in Brussels (trichloramine in air, 0.3-0.5 mg/m3).
The pool chlorine hypothesis postulates that the rise in childhood asthma in the developed world could result at least partly from the increasing exposure of children to toxic gases and aerosols contaminating the air of indoor chlorinated pools. To further assess this hypothesis, we explored the relationships between childhood asthma, atopy, and cumulated pool attendance (CPA). We studied 341 schoolchildren 10–13 years of age who attended at a variable rate the same public pool in Brussels (trichloramine in air, 0.3–0.5 mg/m3). Examination of the children included a questionnaire, an exercise-induced bronchoconstriction (EIB) test, and the measurement of exhaled nitric oxide (eNO) and total and aeroallergen-specific serum IgE. CPA by children (range, 0–1,818 hr) emerged among the most consistent predictors of asthma (doctor diagnosed or screened with the EIB test) and of elevated eNO, ranking immediately after atopy and family history of asthma or hay fever. Although the risk of elevated eNO increased with CPA [odds ratio (OR) = 1.30; 95% confidence interval (CI), 1.10–1.43] independently of total or specific serum IgE, the probability of developing asthma increased with CPA only in children with serum IgE > 100 kIU/L (OR for each 100-hr increase in CPA = 1.79; 95% CI, 1.07–2.72). All these effects were dose related and most strongly linked to pool attendance before 6–7 years of age. Use of indoor chlorinated pools especially by young children interacts with atopic status to promote the development of childhood asthma. These findings further support the hypothesis implicating pool chlorine in the rise of childhood asthma in industrialized countries.
The prevalence of allergic diseases such as atopic asthma and eczema has dramatically increased in the developed world over the past decades. In the United States, as in most industrialized countries, asthma has become the most common chronic childhood disease. Intriguingly, countries the most affected by this rise are English-speaking countries such as the United Kingdom, Ireland, Australia, and New Zealand, where prevalence rates of childhood asthma are up to 10-fold higher than in most southern and eastern countries (American Lung Association 2004; Johnsson et al. 2002).
The causes of both the rise and international disparities in childhood asthma prevalence are largely unknown. Given the rapidity of the rise, genetic factors alone cannot explain this phenomenon, and research has thus turned its attention to changes in environment and, more recently, in lifestyle. One of the hypotheses, which generated most interest, is the “hygiene hypothesis” postulating that the rise of allergic diseases in industrialized countries could be caused by the declining exposure of children to infections during early infancy (Strachan 1989). Although the T-helper types 1–2 (TH1–TH2) paradigm provides a convincing mechanistic support to the hygiene hypothesis (McGeady 2004), epidemiologic studies still generate conflicting results and, despite intense research, have not yet succeeded in causally linking the asthma rise to specific risk factors that might serve as a basis for preventive actions (Kramer et al. 2004; Liu and Murphy 2003; Sheikh et al. 2003; Strachan 2000). The hygiene hypothesis has also been challenged by some recent experimental data, which suggest that, if at all protective, the effects of infections could be limited to a handful of pathogens (e.g., parasites) and operate only within narrow windows of opportunity during early life (Umetsu 2004).
Recently, a hitherto unsuspected factor, so deeply rooted in our hygienic Western way of life that it had never been investigated, has come to light with the finding that the attendance at indoor chlorinated pools correlated with lung epithelium hyperpermeability and asthma prevalence in children (Bernard et al. 2003). This finding led to the pool chlorine hypothesis, proposing that the increasing attendance at indoor chlorinated pools by increasingly younger children could be implicated in the childhood asthma rise, most probably by interacting with other risk factors (Bernard et al. 2003). The main culprit might be trichloramine (or nitrogen trichloride), an irritant gas released in pool air when chlorine reacts with organic matter brought by swimmers (Massin et al. 1998). Trichloramine has the same irritating potency as chlorine and formaldehyde (Gagnaire et al. 1994) and can cause eye and upper respiratory tract irritation in lifeguards and other pool attendees (Massin et al. 1998). Concentrations of trichloramine in public indoor pools vary greatly depending on pool occupancy and ventilation. Levels of trichloramine typically fluctuate between 0.2 and 0.9 mg/m3, with mean values around 0.5 mg/m3 (Bernard et al. 2003; Massin et al. 1998), making this gas one of the most concentrated air pollutants to which children of industrialized countries are regularly exposed (mean concentrations of other indoor or outdoor air pollutants seldom exceed 0.3 mg/m3; World Health Organization 2000). For many years, trichloramine was believed to be an upper respiratory tract irritant only, clearly a wrong premise for this water-insoluble irritant that can cause asthma in lifeguards (Thickett et al. 2002) and epithelial damage in the deep lung of rodents and recreational swimmers (Bernard et al. 2003; Carbonnelle et al. 2002; Lagerkvist et al. 2004).
In this study focused on schoolchildren, we examined the relationships between asthma, atopy, and chlorinated pool attendance by using different outcome measures and studying age-related variations in exposure and susceptibility.