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\begin{document}

\title{Health effects of exposure to chlorination by-products in swimming
pools: Position Paper}



\author[1]{Mariana Couto}%
\author[2]{Alfred Bernard}%
\author[3]{Luís Delgado}%
\author[4]{Franchek Drobnic}%
\author[5]{Marcin Kurowski}%
\author[3]{André Moreira}%
\author[6]{Rodrigo Rodrigues-Alves}%
\author[7]{Maia Rukhadze}%
\author[8]{Sven Seys}%
\author[9]{Marta Wiszniewska}%
\author[10]{Santiago Quirce}%
\affil[1]{Hospital CUF Descobertas}%
\affil[2]{Louvain Center for Toxicology and Applied Pharmacology (LTAP)}%
\affil[3]{University of Porto Faculty of  Medicine}%
\affil[4]{Olympic Training Center}%
\affil[5]{Medical University of Lodz}%
\affil[6]{Hospital do Divino Espírito Santo de Ponta Delgada EPE}%
\affil[7]{Center of Allergy and Immunology}%
\affil[8]{KU Leuven}%
\affil[9]{Nofer Institute of Occupational Medicine}%
\affil[10]{Hospital LA Paz Health Research Institute (IdiPaz)}%


\vspace{-1em}



  
  \date{May 18, 2024}


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\selectlanguage{english}
\begin{abstract}
Concerns have been raised regarding the potential negative effects on
human health of water disinfectants used in swimming-pools. Among the
disinfection options, the approaches using chlorine-based products have
been typically preferred. Chlorine readily reacts with natural organic
matter that are introduced in the water mainly through the bathers,
leading to the formation of potentially harmful chlorination by-products
(CBPs). The formation of CBPs is of particular concern since they have
been epidemiologically associated with the development of various
clinical manifestations. The higher the concentration of these volatile
CBPs in the water, the higher their concentration in the air above the
pool, and different routes of exposure to chemicals in swimming-pools
(water ingestion, skin absorption and inhalation) contribute to the
individual exposome. CBPs may affect the respiratory and skin health of
those who stay indoor for long periods, such as swimming instructors,
pool staff, and competitive swimmers. Whether those who use
chlorinated-pools as customers, particularly children, may also be
affected has been a matter of debate. In this article, the EAACI Joint
Task Force of the Working Group of Allergy, Asthma \& Sports and the
Interest Groupf of Environmental \& Occupational Allergy discusses the
current evidence regarding the health effects of both acute and chronic
exposures in different populations (work-related exposures, intensive
sports and recreational attendance) and identify the main
recommendations and unmet needs for research in this area.%
\end{abstract}%



\sloppy


\textbf{INTRODUCTION}

The quality of the water and the air of swimming-pools is currently a
topic of interest in occupational and environmental health. Even though
the beneficial effects of swimming on increasing physical activity,
cardiopulmonary fitness and improving lung function are
undeniable\textsuperscript{1}, concerns have been raised regarding the
potential negative effects on human health of water disinfectants used
in swimming-pools.

The World Health Organization (WHO) highlights the need of adequate
water disinfection of swimming-pools to prevent microbial proliferation.
Disinfectants are the principal management-derived chemicals added to
minimize the risk of microbial contaminants, and although several
options are available (bromine, ozone, copper-silver, UV irradiation,
electrochemically generated mixed oxidants, UV/hydrogen peroxide, etc)
chlorine-based products have been typically preferred due to their
effectiveness and lower overall relative cost, in spite of possibly
leading to unwanted effects.

Indoor swimming-pools are of particular concern since they are used
regularly all year round, and volatile chlorination by-products (CBPs)
can become trapped within the swimming-pool complexes indoor air. The
higher the concentration of these volatile CBPs in the water, the higher
their concentration in the air above the pool\textsuperscript{2}.
Besides inhalation of volatile or aerosolized solutes, there are two
other main routes of exposure to chemicals in swimming-pools: water
ingestion, and skin absorption (which may represent a source of
muco-cutaneous symptoms). These several routes add to the individual
``exposome'', which comprises all environmental exposures that a person
experiences from conception throughout the lifespan\textsuperscript{3}.

CBPs may affect the respiratory and skin health of those who stay indoor
for long periods, such as swimming instructors, pool staff, and
competitive swimmers. Whether those who use chlorinated-pools as
customers, particularly children, may also be affected has been a matter
of debate. We aimed to review this topic, by describing the chemical and
toxicity of these compounds given the types of exposure and reviewing
health effects of such exposures in different populations considering
also personal and environmental risk factors, in order to propose
recommendations and to identify unmet needs in this area.

\textbf{THE SWIMMING POOL ENVIRONMENT}

Swimming-pool environment is a complex and dynamic ecosystem that can be
affected by the type of swimming-pool (indoor, outdoor,\ldots{}) and by
other factors, including water temperature, ventilation, climate,
location, purpose of use (competition, relaxation, recreational
activities) and swimming habits, particularly swimmer\selectlanguage{ngerman}´s
hygiene\textsuperscript{4-6}. In the case of an indoor swimming-pool,
the environment consists of the water in the pool, the air above the
pool within the natatorium, and the people in the pool
(biota)\textsuperscript{2}.

Both organic and inorganic compounds are continuously entering this
ecosystem via filling waters (tap water, seawater, thermal
water\ldots{}), disinfectant addition (chlorine, bromine, ozone,
UV\ldots{}), pharmaceuticals and personal care products (analgesics,
antibiotics, sunscreens, lotions, cosmetics, soaps\ldots{}) and human
body excretions (urine, sweat, saliva\ldots{}). Interactions between all
these compounds generates CBPs, some of which are of health
concern\textsuperscript{7}.

The addition of chlorine-based disinfectants (chlorine gas, sodium or
calcium hypochlorite, di- or trichloroisocyanurates) to the
swimming-pools water releases hypochlorous acid (HClO), which is the
active biocide. HClO is a weak acid with a pKa of 7.5 at 25°C that
reversely dissociates into hypochlorite (ClO\selectlanguage{english}\textsuperscript{-}) and
hydrogen ion. The sum of HClO and ClO\selectlanguage{english}\textsuperscript{-} is referred to
as free chlorine. HClO is a non-specific biocide that inactivates most
waterborne pathogens but also reacts with organic matter to produce a
wide range of CBPs\textsuperscript{8}. Compared to tap water, CBPs
formation in pools is much more important due to the higher input of
organic matter and the constant addition of
disinfectants\textsuperscript{9}. In chlorinated-pools, major groups of
CBPs include chloramines, trihalomethanes (THMs), haloacetics acids
(HAAs), haloacetaldehydes (HALs) and haloacetonitriles (HANs)
(\textbf{Figure 1} ).

Chloramines are formed as a result of the reaction of HClO with urea and
other nitrogenous compounds brought by swimmers. This group comprises
monochloramine (chloramide, NH\textsubscript{2}Cl), dichloramine
(chlorimide, NHCl\textsubscript{2}) and trichloramine (nitrogen
trichloride, NCl\textsubscript{3}). Monochloramine and dichloramine (the
sum of which is referred to as combined chlorine) are mainly found in
water. Trichloramine, which is 400 times more volatile than its two
congeners, is mainly found in the air at levels that are inversely
proportional to the ventilation rate of indoor
swimming-pools\textsuperscript{10,11}. The odour and taste of water are
mainly affected by the monochloramine/dichloramine ratio and the
trichloramine concentration. This last compound is also responsible for
the distinctive odour of indoor pools, wrongly attributed to
chlorine\textsuperscript{9}.

THMs represent between 5 to 10\% of total organohalogens in
swimming-pool water and air, with chloroform (CHCl\textsubscript{3})
being the dominant species\textsuperscript{8}. THMs are generated from
the complex reaction between active chlorine and naturally present or
imported carbonaceous organic matter. Parameters influencing the
formation of THMs include: organic matter concentration, chlorine
concentration, contact time, water pH, temperature, and bromine ion
concentrations\textsuperscript{12}. THMs are generally well absorbed by
inhalation, ingestion or skin contact.

Haloacetics acids (HAAs), haloacetaldehydes (HALs) and haloacetonitriles
(HANs) are less frequent CBPs and therefore described in the\emph{online
supplementary material} .

\textbf{EFFECTS OF ACUTE EXPOSURES}

Pool chemical--associated health events result in \textgreater{}4.500
emergency department visits annually during 2008-2017 in US, as reported
by the CDC, and over one-third were children or teenagers. Irritated
eye, nose and throat symptoms, and asthma, are the most frequent
symptoms in swimmers and workers of indoor swimming-pools caused by
CBPs; particularly NCl\textsubscript{3} causes the most irritative
symptoms\textsuperscript{13,14}. A significant concentration-response
relation was found between NCl\textsubscript{3} exposure concentrations
and irritant eye, nasal, and throat symptoms\textsuperscript{15}.

\emph{Respiratory symptoms}

Cold and sneezing are the most frequent self-reported complaints (65.4\%
and 52.6\%, respectively) while only 7.5\% of the total indoor
swimming-pools workers reported an asthmatic
condition\textsuperscript{13}. It is discussed whether recreational
swimming or working in indoor swimming-pools may aggravate asthma or
actually cause it\textsuperscript{16}. Irritant-induced asthma (IIA) is
defined as development of asthma, nonspecific bronchial
hyperresponsiveness (BHR), and airway inflammation induced by irritant
mechanisms, as opposed to occupational asthma (OA) caused by immunologic
mechanisms\textsuperscript{17}. Three cases of OA in swimming-pool
workers have been documented\textsuperscript{18}, two of them had a
positive bronchial provocation test to chloramine. Another study with a
large sample of swimming-pool workers (n=624) also showed increased risk
of respiratory symptoms indicative of asthma upon
NCl\textsubscript{3}exposure\textsuperscript{14}.

\emph{Short-term changes in respiratory biomarkers}

CBPs have a strong oxidizing potential and may contribute to airway
damage through opening tight junctions, causing barrier
disruption\textsuperscript{19,20}. A summary of the studies describing
short-term changes in respiratory biomarkers is presented
in\textbf{Table 1} . It is important to note that some of these studies
did not measure NCl\textsubscript{3} and/or did not compare with a
non-chlorinated-pool, which precludes drawing clear conclusions. The
role of physical activity should not be neglected in this type of
studies measuring biomarkers before and after swimming.

\emph{Non-respiratory symptoms}

Concerning self-reported ocular symptoms, indoor swimming-pools
employees declared frequently having red (48.9\%) and itchy (44.4\%)
eyes, mostly lifeguards and trainers\textsuperscript{13}.

Regarding the skin, both water itself and CBPs have negative effects due
to a dilution or flushing out of the natural moisturizing. An increasing
risk of irritative skin symptoms was demonstrated dependent on the
NCl\textsubscript{3} concentrations\textsuperscript{21}. Recreational
swimming leads to transient but significant changes in skin surface
properties of women with healthy skin\textsuperscript{22}; skin dryness,
itch and erythema are non-specific complains in swimming-pool
attendants\textsuperscript{23,24}. Additionally, both allergic contact
dermatitis and contact urticaria due to chlorinated-pool water have been
identified\textsuperscript{20,23,25,26}. Swimming in public pools/spas
in the current or previous week has been associated with dermal symptoms
(rash, generalized itching, dermal infection)\textsuperscript{27}.
Besides, more verrucas, mycosis, eczema and rash have been identified in
lifeguards and trainers compared to other workers at swimming
pools\textsuperscript{13}.

Three different disinfection systems (chlorine, chlorine/ozone and
bromine/ozone) were investigated to assess adverse skin and eye
effects\textsuperscript{28}: compared with the bromine/ozone pool, the
odds ratio (OR) of having a rash \textless{}24 h after pool use was 1.91
(CI 0.71-5.10) for the chlorine-pool and 1.88 (CI 0.61-5.81) for the
chlorine/ozone pool. Goma et al.\textsuperscript{29} reported the
efficacy of a new disinfection method (based upon on replacement of the
strong HCl by CO\textsubscript{2}, inclusion of a low concentration salt
electrolysis system, and ultraviolet radiation phase) to markedly reduce
the irritant substances levels in the pool atmosphere and significantly
reduce eye, nose, skin and cough complaints, both in recreational and
competitive swimmers.

\textbf{EFFECTS OF CHRONIC EXPOSURES}

Studies based on serum pneumoproteins show that not only acute but also
chronic exposure to NCl\textsubscript{3} can increase the lung
epithelium permeability and thereby perhaps facilitate the
transepithelial delivery of allergens to dendritic
cells\textsuperscript{30} and contribute to a T2-dependent immune
response\textsuperscript{31,32}. Recent experimental evidence in mice
has shown that chronic chlorine inhalation contributes to exacerbate
airways inflammation in asthma by mobilizing pro-inflammatory
macrophages into the lung as well as stimulating group 2 and 3
ILCs\textsuperscript{33}.

The barrier disruption effect may occur also on the dermal layer. The
high temperature of the water, the hydration of the skin and the
disrupting effects of CBPs on the skin barrier are all factors that in
combination decrease the water-holding capacity of the skin stratum
corneum\textsuperscript{34} and greatly facilitate the permeation of
CBPs across the skin, especially thin areas such as the scrotum.

\textbf{Work-related exposure}

Lifeguards, swim teachers and physiotherapists have the highest CBPs
cumulative exposure when compared to other swimming-pool
workers\textsuperscript{21}. In order to protect workers but also
swimmers, WHO has imposed a reference value for NCl\textsubscript{3} of
0.5 mg/m\textsuperscript{3}. However, airborne NCl\textsubscript{3} is
not regularly monitored in most European countries.

Dose-response relationships between NCl\textsubscript{3} levels and
different respiratory (runny nose, blocked nose, voice loss) and ocular
(red or itchy eyes) symptoms have been reported from a level of 0.5
mg/m\textsuperscript{3} onwards\textsuperscript{35}. Interestingly,
another study demonstrated increasing risk of respiratory symptoms up to
a level of 0.2-0.3 mg/m3 of NCl\textsubscript{3}, urging to revisit the
WHO occupational exposure limit\textsuperscript{21}. This is also in
line with other study, where very low levels of NCl\textsubscript{3} in
indoor swimming-pools (0.017-0.15 mg/m3) were detected with increased
risk for sore throat (OR: 11.28; 95\% CI: 1.44--88.33) and phlegm (OR:
4.22; 95\% CI: 1.16--15.4)\textsuperscript{36}.

Upper and lower respiratory symptoms while on duty were related to
duration of lifetime exposure. Lifeguards exposed \textgreater{} 500
hours in the previous 12 months experienced more cough, throat and eye
irritation than non- or less-exposed lifeguards, and those with prior
asthma had a significantly higher risk of suffering from asthma
attack(s) than non-exposed asthmatic subjects\textsuperscript{37}.
Physician-diagnosed asthma was high among lifeguards
(23\%)\textsuperscript{37}.

\textbf{Intensive sports}

\emph{Respiratory symptoms}

Competitive and synchronized swimming ranked second among sport
disciplines associated with increased prevalence of asthma
symptoms\textsuperscript{38}. The long-term exposure to CBPs in a sport
setting underlines some aspects: 1) the role in inducing and sustaining
airway inflammation; 2) the contribution to airway remodeling; and 3)
possible promotion of allergic sensitization in regularly exposed
competitive swimmers.

A significantly higher rate of BHR with increased inflammatory
parameters have been observed in elite swimmers. Long-term swimming-pool
exposure effects included increase in both eosinophilic and neutrophilic
inflammation, as reflected not only in sputum cell counts but also in
higher concentration of sputum eosinophil peroxidase and human
neutrophil lipocalin, respectively\textsuperscript{39}. Inflammatory and
remodeling changes reported in bronchial biopsies of competitive
swimmers were similar to non-exercising mild asthmatics and were present
also during off-training period. Discontinuation of a swimming career
decreases eosinophilic and neutrophilic inflammation and reduces BHR,
although these findings should be interpreted with caution given the
small sample sizes\textsuperscript{40,41}. These inflammatory changes
did not seem, however, to correlate with BHR. A study carried out in a
mixed population of competitive athletes including mostly non-asthmatic
swimmers and speed skaters indicated that the baseline pattern of
proinflammatory cytokine TNF-\selectlanguage{greek}α \selectlanguage{english}and anti-inflammatory IL-1ra
concentrations in the lower airways appear to be similar in top level
athletes and asthmatic patients, but different in healthy
controls\textsuperscript{42}.

Increased airway edema due to CBPs-induced vascular leakage has been
also hypothesized for airway inflammation in swimmers. A significant
association of vascular permeability index (quotient of albumin levels
in sputum and in serum) with increased sputum eosinophil and neutrophil
counts was found\textsuperscript{43}, although vascular leakage did not
correlate with lung function and BHR. In synchronized swimmers no
evidence was found for negative influence of~CBPs on the pulmonary
function\textsuperscript{44}.

A study assessing rhinitis in swimmers showed 44\% presented baseline
allergic rhinitis and 35\% had inflammation with neutrophilic
predominance\textsuperscript{45}. Neutrophilic influx is mainly
attributed to irritation through CBPs exposure and is possibly reversed
-- contrarily to eosinophil infiltration -- after nose clip
introduction\textsuperscript{45}. Mucociliary transport impairment and
reduced ciliary beats frequency have been described in swimmers and also
attributed to irritation by CBPs. Nasal lavage fluid (NLF) collected
immediately after competitive swimming contains more neutrophils with
decreased phagocytic activity. However, NLF changes tend to subside in
swimmers shortly after training cessation or introduction of protective
measures, such as nose clip\textsuperscript{46}. In the
study\textsuperscript{42} involving swimmers and speed skaters, TNF-\selectlanguage{greek}α
\selectlanguage{english}concentrations in nasal secretions were similar between athletes,
asthmatics and healthy controls. However, IL-1ra levels in upper airways
were higher in athletes and asthmatics than healthy subjects. Seemingly
paradoxical, this fact may reflect a local anti-inflammatory response of
the nasal mucosa.

\emph{Non-respiratory symptoms}

A wide spectrum of dermatoses of various etiologies (infectious,
traumatic, irritant, allergic, neoplastic etc.) are listed in the
context of regular swimming-pools use or aquatic sports
performance\textsuperscript{47}. Xerosis is one of the most frequent
condition experienced by swimmers\textsuperscript{48}, and especially
among those with sensitive and eczematous skin\textsuperscript{49}. The
dryness effect is particularly pronounced in atopic skin, since the
threshold residual chlorine concentration required for considerable drop
in water-holding properties is significantly lower than in healthy
subjects (0.5 mg/l vs. 2.0 mg/l, respectively)\textsuperscript{34},
possibly explaining why the higher probability of skin symptoms compared
to other disinfection methods (bromine, ozone, UV lamps and salt
electrolysis)\textsuperscript{49}. Also eye symptoms are more
significantly associated with chlorine-disinfected pools, comparing with
other disinfection methods\textsuperscript{49} and often listed as a
common problem in competitive swimmers. The risk of otitis externa in
swimmers and polo players was higher than in soccer
players\textsuperscript{50}.

\textbf{Recreational attendance}

\textbf{Table 2} summarizes studies that have investigated the
respiratory effects of NCl\textsubscript{3} and other inhalable CBPs
among recreational swimmers. The first study was conducted among
schoolchildren in Belgium\textsuperscript{51}. While assessing the
effects of ambient air pollution, the authors unexpectedly found that
indoor chlorinated-pools attendance correlated with lung epithelium
hyperpermeability and asthma prevalence. Further studies in Belgium
revealed that the asthma risk among adolescents and children using
chlorinated-pools stems from an interaction with atopic
status\textsuperscript{52,53}. Of interest, also the risk of allergic
asthma was most strongly linked to pool attendance during early
childhood\textsuperscript{52}. Two studies in Sweden confirmed these
observations while showing that the risk of allergic asthma correlated
with the cumulative inhalation exposure to
NCl\textsubscript{3}\textsuperscript{54,55}.

Associations between asthma and recreational swimming in
chlorinated-pools were also reported in Ireland\textsuperscript{56},
Italy\textsuperscript{57} and Portugal\textsuperscript{58}. Several
other studies, however, provided no evidence of an increased asthma risk
in recreational swimmers\textsuperscript{59-62}. Of these, one of the
most contradictory but also the most influential owing to its large size
is the UK prospective birth cohort study (ALSPAC
study)\textsuperscript{61}, which was suggestive, if anything, of a
protective effect of swimming towards asthma risk. There are several
possible explanations for these contrasting observations. A first
explanation is that children examined in these negative
studies\textsuperscript{59-62} were too young to detect associations
with allergic asthma. Another possible explanation is an underestimation
of the exposure with consequently a risk of miss-classifying some
categories of swimmers\textsuperscript{63,64}.

Associations have also been reported between indoor chlorinated-pool
attendance and the risks of allergic rhinitis\textsuperscript{53,65},
autonomic changes\textsuperscript{58} and airway inflammation assessed
by the exhaled NO test\textsuperscript{52}. Further complicating the
issue, some studies suggest that early swimming in chlorinated-pools may
increase the risks of allergic sensitization in particular to perennial
allergens\textsuperscript{62,66,67}.

Last, respiratory risks when swimming in chlorinated-pools are probably
not limited to the exposure to NCl\textsubscript{3}. Swimming in indoor
chlorinated-pools during infancy has also been associated with a higher
risk of bronchiolitis or recurrent respiratory infection mainly in
children with family history of atopic
diseases\textsuperscript{9,68,69}.

Biomarkers studies have revealed that the attendance of
chlorinated-pools correlates with a disruption of airway epithelial
barrier as reflected by altered serum levels of lung epithelium-specific
proteins (pneumoproteins). Several studies have shown that early
swimming in chlorinated-pools is associated with decreased serum levels
of CC16\textsuperscript{9,62,70,71}. Lower levels of circulating CC16 in
children are associated with subsequent decreased lung function and
increased risks of developing asthma and other respiratory
diseases\textsuperscript{71-74}.

\textbf{Other health effects}

Many \emph{in vitro} and \emph{in vivo} toxicological studies have
provided evidence about genotoxic and cytotoxic effects induced by CBPs
and the WHO International Agency for Research on Cancer acknowledges
sufficient evidence for the carcinogenicity of chloroform and other
widespread CBPs in animals\textsuperscript{75}.

In humans, however, the epidemiologic evidence overall has generally
been considered insufficient to declare CBPs to be carcinogenic, with
bladder cancer presenting the most consistent evidence by providing the
greatest likelihood of causality. It is worth noting that the majority
of the studies evaluate the risk of cancer related to drinking water and
not exposure in swimming-pools, so this lack of evidence should be
considered with concern and not extrapolated. In fact, a recent study
showed that for elite swimmers and their coaches, the levels of THMs in
a Portuguese swimming-pool exceeded the limits for cancer
risk\textsuperscript{76}.

Regarding bladder cancer, several epidemiological studies have evaluated
its risk in relation with CBPs, of which some are of sufficient quality
to provide meaningful evidence towards causal inference, including
meta-analysis\textsuperscript{77} and two pooled
analyses\textsuperscript{78,79}. While the majority were related to
drinking water, there are also studies finding increased risk of bladder
cancer related to showering, bathing, or swimming exposures to
THM\textsuperscript{80-82}.

Associations with other types of cancer have been suggested, namely
melanoma risk associated with a history of
swimming\textsuperscript{83}and colorectal cancer risk with CBPs
exposure in drinking water\textsuperscript{84}.

Regarding reproductive effects, there is no clear evidence linking CBPs
exposure to poor pregnancy outcomes, except for a slight association
with fetal growth-related outcomes and sporadic associations with some
categories of congenital anomalies\textsuperscript{85}.

Potential impact of CBPs on male fertility has been much less studied
and is of great concern given the remarkable permeability of the scrotal
skin.~Most studies have addressed mainly the risks related to drinking
water, while one study addressed the exposure through swimming-pool
water and found that adolescents having attended indoor
chlorinated-pools for \textgreater{} 250 h before the age of 10 years or
\textgreater{} 125 h before the age of 7 years were three times more
likely to have an abnormally low serum inhibin B and / or total
testosterone than their peers who never visited these pools and those
who attended outdoor chlorinated-pools or a copper--silver
pool\textsuperscript{86}.

\textbf{RISK FACTORS}

There is a complex interaction between the building environment,
infectious agents, allergens, occupational exposures, school environment
and recreational exposures, which contribute to shape the
exposome\textsuperscript{3}.

The amount and impact of CBPs exposure may be influenced by the dose of
disinfectant, the resultant concentration of CBPs in the water and the
air, the number of attending swimmers, temperature of water and air,
ventilation rates in the building, duration of swimming, and the water
turbulence\textsuperscript{2,87}. The three routes of exposure
(inhalation, ingestion and dermal absorption) vary for different age
groups and are affected by several factors (\textbf{Figure 2} ). Some
conditions related to competitive swimmers are highlighted
in\textbf{table 3} .

\emph{Inhalation} -- Swimming-pool attendants inhale from the atmosphere
just above the water's surface, and the volume of air inhaled is a
function of the effort intensity and time. In indoor swimming-pools,
individuals also breathe air in the wider area of the building housing
the pool. A correlation between physical activity and THM
concentrations\textsuperscript{88} has been identified.

\emph{Ingestion} -- Inadvertent water intake in the swimming-pool varies
according to age and sex, with adult women ingesting the least and male
children ingesting the most, especially babies.

\emph{Dermal/mucosal absorption} - Chlorination of bathing water showed
to change the dermal barrier function, especially of atopic
skin\textsuperscript{89}, the same being expected for chlorination of
the swimming-pool water. Infant swimming practice combined with atopy
has been shown to increase the prevalence of eczema\textsuperscript{90}.

Age seems to be the most relevant personal risk factor for respiratory
and reproductive health effects of CBPs exposure in swimming pools. The
first years of life may be seen as a ``window of sensitivity'' given the
progressive increase in maturation of respiratory tract and reproductive
system.

Age also directly impacts the other risk factors, including the surface
areas of both the head and the body, the breathing rate and body
weight\textsuperscript{2}. The contribution from each exposure route
changes dramatically for each age group, and the time spent swimming
must also be taken into consideration. Adjusted for body weight, the
uptake of CBPs by all routes is clearly higher in infants or children
and decreases with age. A schematic representation is presented
in\textbf{figure 3} .

As previously mentioned, the use of indoor chlorinated-pools especially
by young children interacts with atopic status to promote the
development of childhood asthma\textsuperscript{52}, and a synergistic
action of exposure to pets and environmental tobacco smoke in
chlorinated-pools attendants predisposes to the development of
asthma\textsuperscript{51}.

\textbf{RECOGNIZING CBPs EXPOSURE-ASSOCIATED HEALTH EFFECTS}

Depending on the exposed epithelium, the level of exposure, the past
medical history and/or certain individual characteristics, different
signs and symptoms associated with CBPs exposure will be observed. These
symptoms will be exacerbated in those patients with an underlying
chronic inflammatory disease (asthma, eczema, allergy, dermatosis,
etc.).

The diversity of tissues exposed to CBPs in swimming-pools attendants
offers a wide variety of clinical conditions (summarized in\textbf{Table
4} ), which require a differential diagnosis with other disorders that
present similar symptoms and signs, although their history is different.
More detailed information on this topic is provided as \emph{online
supplementary material} .

\textbf{MANAGEMENT}

Although evidence is lacking, there is consensus on the recommendation
to assure that water treatment processes prevent CBPs formation in order
to minimize the chance of an increased risk of cancer from its long-term
exposure. Current standards for the assessment of THM exposure are
mostly defined for the THM content in swimming-pool water, although THM
are quite volatile and likely to be present in appreciable
concentrations also in the air of indoor swimming-pool facilities.
Though it has been progressively acknowledged that airborne THM levels
have a central role in inducing CBP-related adverse health effects,
there are presently no standards or guidelines for controlling THM
levels in indoor air of swimming-pool amenities. There is currently no
international standard for the treatment of swimming-pools, with
different regulations often provided by state or local governing bodies.

Inhalation of airborne THM and other CBPs seems to be the predominant
route of exposure for competitive swimmers, who have an increased
breathing rate throughout their regular and prolonged sports and
training actions and for coaches and other pool workers and staff, who
experience an intense occupational exposure to the THM-rich environment
that surrounds the pool. In fact, data on the real long-term exposure to
CBPs and the risks that this exposure may represent for the health of
competitive swimmers and coaches over the course of their careers is
currently lacking. Nevertheless, a few easy and effective steps that all
can take to maintain water and air quality are presented as a checklist
in \textbf{table 5} .

\textbf{RECOMMENDATIONS AND UNMET NEEDS}

The expansion of indoor aquatic activities resulted in a major focus of
public authorities and local legislators on the prevention of
water-borne infectious diseases, through the implementation and
inspection of water disinfection practices. Comparatively, much less
attention has been dedicated from health authorities to the indoor air
quality (IAQ) of aquatic facilities, and there are still unmet needs to
guarantee a generally safe and healthy indoor sport environment for both
recreational and professional swimmers, and to those involved in their
instruction, training, safety vigilance and pool maintenance.

There is still very limited information regarding additional hazardous
pollutants, such as volatile organic compounds (VOCs) other than CBPs
and ultrafine particulate matter (UFPs), and their possible long-term
and cumulative health effects on swimming-pool
attendants\textsuperscript{103}. No guidelines are defined for UFP or
THM, except for occupational chloroform exposure.

Due to the presence of both indoor THM and non-THM VOC, effective
ventilation and acclimatization systems are a particular need for indoor
swimming facilities to prevent the accumulation and promote the
effective elimination of these harmful chlorine-derived volatile
compounds.

Among the available options for water disinfection, other than
chlorine-derived solutions should be considered in the planning and
development of new public indoor swimming-pools. For existing
facilities, avoiding any factors that promote the development,
introduction and retention of air pollutants, i.e. controlling pollutant
sources and ventilation levels, constitute the major action plans
proposed for IAQ improvements of swimming-pools\textsuperscript{103}.

Proper maintenance schedules and ventilation conditions are needed to
guarantee a stable indoor environment -- temperature and relative
humidity - in the areas of water activities. Water-related factors --
air/water temperature ratio and pH, the number of swimmers within the
pool -- also explain variations of the VOC levels found in the
water-surface air, the air zone that is regularly inhaled by swimmers.
Thus, maintaining water pH between 6.9 and 8.0 and air temperature 2 \selectlanguage{ngerman}°C
above the pool water are recommended to avoid level fluctuations and the
undesired volatilization of CBP, particularly during periods of high
attendance\textsuperscript{103}. Recommendations concerning prophylactic
procedures during occupational exposure are lacking but given the
fluctuations of indoor pollutants concentrations found throughout a
working day\textsuperscript{103}, it is advisable that pool maintenance
staff minimize occupational exposure by carrying in the early morning
activities that require a prolonged stay in the swimming-pool
surrounding area.

Checking declared indoor sources of VOC emissions, and the heating,
ventilation and air conditioning (HVAC) systems (particulate matter
filtration capacity and efficient removal of indoor pollutants), should
also be considered\textsuperscript{104}, as well as the HVAC system
design, in order to guarantee that fresh air supply and exhaust airflows
do not mix by proximity.

Findings suggest that early and chronic exposure to swimming-pool CBP
may have a promoting effect not only on airway inflammation and
hyperreactivity, but also on the process of allergic sensitization
itself. Other health outcomes, namely male fertility and bladder cancer,
are of particular concern, as the majority of published studies evaluate
these risks in relation to drinking water and not swimming-pools
exposure. Early age exposure (baby and pre-school swimming) may turn to
be a relevant personal risk factor for respiratory and reproductive
health effects of BP exposure in swimming pools, given the progressive
increase in maturation of respiratory tract and reproductive system.

There is still need of more environmental and epidemiological research
data, to ascertain the health risk associated with the exposure of
different swimming pool users, namely babies, infants and children,
lifeguards and swimming pool maintenance staff, coaches and elite
swimmers. Additional prospective and intervention studies are also
needed to confirm the relationship between exposure to pollutants in
swimming-pool environments and the risk of certain health effects.

\textbf{Contribution by each author}

MC, AB, LD; FD, MK, AM, RRA, MR, SS and MW each prepared and wrote one
section of the manuscript. MC and SQ were responsible for collecting and
integrating all sections and prepare the final versions. All authors
reviewed and approved the last version of the manuscript.

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Liu J, Zhang X, Mitch W, Gracia-Lavedan E, Arjona L, de Bont J, Tares L,
Vineis P, Kogevinas M, Villanueva CM. Exposure to disinfection
by-products in swimming pools and biomarkers of genotoxicity and
respiratory damage - The PISCINA2 Study. Environ Int 2019;131:104988

95. Nickmilder M, Bernard A. Ecological association between childhood
asthma and availability of indoor chlorinated swimming pools in Europe.
Occup Environ Med 2007;64:37-46

96. Bernard A, Nickmilder M, Voisin C. Outdoor swimming pools and the
risks of asthma and allergies during adolescence. Eur Respir J
2008;32:979-88

97. Nystad W, Haberg SE, London SJ, Nafstad P, Magnus P. Baby swimming
and respiratory health. Acta Paediatr 2008;97:657-62

98. Schoefer Y, Zutavern A, Brockow I, Schafer T, Kramer U, Schaaf B,
Herbarth O, von Berg A, Wichmann HE, Heinrich J. Health risks of early
swimming pool attendance. Int J Hyg Environ Health 2008;211:367-73

99. Schuez-Havupalo L, Karppinen S, Toivonen L, Kaljonen A, Jartti T,
Waris M, Peltola V. Association between infant swimming and
rhinovirus-induced wheezing. Acta Paediatr 2014;103:1153-8

100. Bernard A, Sardella A, Voisin C, Dumont X. Nasal epithelium injury
by chlorination products and other stressors predicts persistent
sensitization to aeroallergens in young schoolchildren. Environ Res
2017;158:145-52

101. Marco E, Lourencetti C, Grimalt JO, Gari M, Fernandez P,
Font-Ribera L, Villanueva CM, Kogevinas M. Influence of physical
activity in the intake of trihalomethanes in indoor swimming pools.
Environ Res 2015;140:292-9

102. Bozym M, Wzorek M, Klosok-Bazan I. Health risk as a consequence of
exposure to trihalomethanes in swimming pool water. Rocz Panstw Zakl Hig
2017;68:331-7

103. Felgueiras F, Mour\selectlanguage{ngerman}ão Z, Morais C, Santos H, Gabriel MF, de Oliveira
Fernandes E. Comprehensive assessment of the indoor air quality in a
chlorinated Olympic-size swimming pool. Environ Int 2020;136:105401.

104. Gabriel MF, Felgueiras F, Mourão Z, Fernandes EO. Assessment of the
air quality in 20 public indoor swimming pools located in the Northern
Region of Portugal. Environ Int 2019;133(Pt B):105274

\textbf{Table 1} : Studies describing short-term changes in respiratory
biomarkers.\selectlanguage{english}
\begin{longtable}[]{@{}llll@{}}
\toprule
\begin{minipage}[b]{0.22\columnwidth}\raggedright\strut
\textbf{Authors}\strut
\end{minipage} & \begin{minipage}[b]{0.22\columnwidth}\raggedright\strut
\textbf{Conditions}\strut
\end{minipage} & \begin{minipage}[b]{0.22\columnwidth}\raggedright\strut
\textbf{Biomarkers}\strut
\end{minipage} & \begin{minipage}[b]{0.22\columnwidth}\raggedright\strut
\textbf{Main findings}\strut
\end{minipage}\tabularnewline
\midrule
\endhead
\begin{minipage}[t]{0.24\columnwidth}\raggedright\strut
Carbonnelle et al. 2002 (30)\strut
\end{minipage} & \begin{minipage}[t]{0.24\columnwidth}\raggedright\strut
Chlorinated-pool (NCl\textsubscript{3} mean concentration: 490
\selectlanguage{greek}µ\selectlanguage{english}g/m\textsuperscript{3}) for recreational swimmers. Chlorinated-pool
(NCl\textsubscript{3} mean concentration: 355 \selectlanguage{greek}µ\selectlanguage{english}g/m\textsuperscript{3})
\emph{Vs} copper/silver pool for trained swimmers\strut
\end{minipage} & \begin{minipage}[t]{0.24\columnwidth}\raggedright\strut
Serum SP-A, SP-B and CC16\strut
\end{minipage} & \begin{minipage}[t]{0.24\columnwidth}\raggedright\strut
CC16 was not increased in recreational swimmers In trained swimmers CC16
peaked immediately after strenuous exercise, both in the copper/silver
and in the chlorinated pools SP-A and SP-B were unaffected by strenuous
exercise in the copper/silver pool SP-A and SP-B were significantly
increased in a time-dependent manner in recreational and trained
swimmers attending the chlorinated-pool\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.24\columnwidth}\raggedright\strut
Carbonnelle et al. 2008 (91)\strut
\end{minipage} & \begin{minipage}[t]{0.24\columnwidth}\raggedright\strut
Chlorinated-pool (NCl\textsubscript{3} concentration: 160-280
\selectlanguage{greek}µ\selectlanguage{english}g/m\textsuperscript{3} ) \emph{Vs} copper/silver-pool
(NCl\textsubscript{3} \textless{}20 \selectlanguage{greek}µ\selectlanguage{english}g/m\textsuperscript{3})\strut
\end{minipage} & \begin{minipage}[t]{0.24\columnwidth}\raggedright\strut
FeNO; serum SP-A, SP-B, CC16, KL-6\strut
\end{minipage} & \begin{minipage}[t]{0.24\columnwidth}\raggedright\strut
FeNO increased in the copper/silver pool, whereas it did not change in
the chlorinated-pool, suggesting that chlorination might inhibit
NO-induced vasodilation in exercise Serum pneumoproteins were unchanged
excepted SP-A which decreased after exercise in the chlorinated pool (P
\textless{} 0.05)\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.24\columnwidth}\raggedright\strut
Font-Ribera et al. 2010 (92)\strut
\end{minipage} & \begin{minipage}[t]{0.24\columnwidth}\raggedright\strut
Chlorinated indoor pool\strut
\end{minipage} & \begin{minipage}[t]{0.24\columnwidth}\raggedright\strut
FeNO; serum SP-D and CC16; 8-isoprostane, several cytokines* and VEGF in
EBC\strut
\end{minipage} & \begin{minipage}[t]{0.24\columnwidth}\raggedright\strut
CC16 slightly increased after a swimming session No significant changes
in lung function, SP-D, 8-isoprostane, cytokines, or VEGF.\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.24\columnwidth}\raggedright\strut
Fern\selectlanguage{ngerman}ández-Luna et al. 2013 (93)\strut
\end{minipage} & \begin{minipage}[t]{0.24\columnwidth}\raggedright\strut
Chlorinated-pool \emph{Vs} ozone-treated pool\strut
\end{minipage} & \begin{minipage}[t]{0.24\columnwidth}\raggedright\strut
Serum SP-D and CC16\strut
\end{minipage} & \begin{minipage}[t]{0.24\columnwidth}\raggedright\strut
No change was observed in lung function and SP-D in swimmers attending
both pools CC16 was significantly increased in subjects attending the
chlorinated-pool but not in those using the ozone-treated pool\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.24\columnwidth}\raggedright\strut
Font-Ribera et al. 2019 (94)\strut
\end{minipage} & \begin{minipage}[t]{0.24\columnwidth}\raggedright\strut
Chlorinated-pool (NCl\textsubscript{3} mean concentration: 473
\selectlanguage{greek}µ\selectlanguage{english}g/m\textsuperscript{3})\strut
\end{minipage} & \begin{minipage}[t]{0.24\columnwidth}\raggedright\strut
Serum CC16; exhaled breath THMs; urinary TCAA; genotoxicity
biomarkers\textsuperscript{\#}\strut
\end{minipage} & \begin{minipage}[t]{0.24\columnwidth}\raggedright\strut
Creatinine-adjusted urinary TCAA increased by 3.1 \selectlanguage{greek}μ\selectlanguage{english}mol/mol Urine
mutagenicity, MN-PBL, MN-Ret and serum CC16 levels remained unchanged
after swimming No correlation between CBP exposure and MN-PBL, urine
mutagenicity and CC16 Moderate associations observed for MN-Ret and CBP
exposure\strut
\end{minipage}\tabularnewline
\bottomrule
\end{longtable}

* RANTES, Ip10, TNF, IL-12p70, IL-10, IL-8, IFN-\selectlanguage{greek}γ, \selectlanguage{english}IL-4.

\textsuperscript{\#} Urine mutagenicity, micronuclei in peripheral blood
lymphocytes (MN-PBL) and micronuclei in reticulocytes (MN-Ret).

CC: Clara cell protein; CBP: chlorination by-products; EBC: exhaled
breath condensate; FeNO: fractional exhaled nitric oxide; KL-6: Krebs
von den Lungen-6 protein; TCAA: Trichloroacetic acid; THMs:
Trihalomethanes; SP: Surfactant-associated protein; VEGF: vascular
endothelial growth factor.

\textbf{Table 2:} Risks of respiratory diseases, aeroallergen
sensitization and airway epithelial defects associated with recreational
swimming in indoor and/or outdoor chlorinated-pools.\selectlanguage{english}
\begin{longtable}[]{@{}lllllll@{}}
\toprule
\begin{minipage}[b]{0.14\columnwidth}\raggedright\strut
\textbf{Authors}\strut
\end{minipage} & \begin{minipage}[b]{0.14\columnwidth}\raggedright\strut
\textbf{Country}\strut
\end{minipage} & \begin{minipage}[b]{0.14\columnwidth}\raggedright\strut
\textbf{Country}\strut
\end{minipage} & \begin{minipage}[b]{0.14\columnwidth}\raggedright\strut
\textbf{Type of study}\strut
\end{minipage} & \begin{minipage}[b]{0.14\columnwidth}\raggedright\strut
\textbf{N (age, yrs)}\strut
\end{minipage} & \begin{minipage}[b]{0.14\columnwidth}\raggedright\strut
\textbf{NCl\textsubscript{3}} \textbf{mg/m\textsuperscript{3}}\strut
\end{minipage} & \begin{minipage}[b]{0.14\columnwidth}\raggedright\strut
\textbf{Main findings}\strut
\end{minipage}\tabularnewline
\midrule
\endhead
\begin{minipage}[t]{0.14\columnwidth}\raggedright\strut
Bernard et al. 2003 (51)\strut
\end{minipage} & \begin{minipage}[t]{0.14\columnwidth}\raggedright\strut
Belgium\strut
\end{minipage} & \begin{minipage}[t]{0.14\columnwidth}\raggedright\strut
Belgium\strut
\end{minipage} & \begin{minipage}[t]{0.14\columnwidth}\raggedright\strut
Cross-sectional\strut
\end{minipage} & \begin{minipage}[t]{0.14\columnwidth}\raggedright\strut
226 (8-12) 1,881 (7-14)\strut
\end{minipage} & \begin{minipage}[t]{0.14\columnwidth}\raggedright\strut
-\strut
\end{minipage} & \begin{minipage}[t]{0.14\columnwidth}\raggedright\strut
Dose-effect relation between CCPA and serum SP-A and SP-B (n=226).
Correlations between the prevalence of asthma and the CCPA
(n=1881).\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.12\columnwidth}\raggedright\strut
Nystad et al. 2003 (68)\strut
\end{minipage} & \begin{minipage}[t]{0.12\columnwidth}\raggedright\strut
Norway\strut
\end{minipage} & \begin{minipage}[t]{0.12\columnwidth}\raggedright\strut
Norway\strut
\end{minipage} & \begin{minipage}[t]{0.12\columnwidth}\raggedright\strut
Cross-sectional\strut
\end{minipage} & \begin{minipage}[t]{0.12\columnwidth}\raggedright\strut
2,862 children\strut
\end{minipage} & \begin{minipage}[t]{0.12\columnwidth}\raggedright\strut
-\strut
\end{minipage} & \begin{minipage}[t]{0.12\columnwidth}\raggedright\strut
Increased risk of recurrent respiratory tract infections in baby
swimmers from atopic parents (aOR, 2.08, 95\% CI: 1.08-4.031).\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.12\columnwidth}\raggedright\strut
Lagerkvist et al. 2004 (70)\strut
\end{minipage} & \begin{minipage}[t]{0.12\columnwidth}\raggedright\strut
Sweden\strut
\end{minipage} & \begin{minipage}[t]{0.12\columnwidth}\raggedright\strut
Sweden\strut
\end{minipage} & \begin{minipage}[t]{0.12\columnwidth}\raggedright\strut
Cross-sectional\strut
\end{minipage} & \begin{minipage}[t]{0.12\columnwidth}\raggedright\strut
57 (10-11)\strut
\end{minipage} & \begin{minipage}[t]{0.12\columnwidth}\raggedright\strut
-\strut
\end{minipage} & \begin{minipage}[t]{0.12\columnwidth}\raggedright\strut
Significant decrease of serum CC16 in children (n=20) regularly visiting
indoor chlorinated-pools\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.14\columnwidth}\raggedright\strut
Kohlhammer et al. 2006 (65)\strut
\end{minipage} & \begin{minipage}[t]{0.14\columnwidth}\raggedright\strut
Germany\strut
\end{minipage} & \begin{minipage}[t]{0.14\columnwidth}\raggedright\strut
Cross-sectional\strut
\end{minipage} & \begin{minipage}[t]{0.14\columnwidth}\raggedright\strut
Cross-sectional\strut
\end{minipage} & \begin{minipage}[t]{0.14\columnwidth}\raggedright\strut
2,606 (35-74)\strut
\end{minipage} & \begin{minipage}[t]{0.14\columnwidth}\raggedright\strut
-\strut
\end{minipage} & \begin{minipage}[t]{0.14\columnwidth}\raggedright\strut
Dose-related associations between the risk of hay fever and the current
and school-age pool attendance.\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.12\columnwidth}\raggedright\strut
Bernard et al. 2006 (52)\strut
\end{minipage} & \begin{minipage}[t]{0.12\columnwidth}\raggedright\strut
Belgium\strut
\end{minipage} & \begin{minipage}[t]{0.12\columnwidth}\raggedright\strut
Belgium\strut
\end{minipage} & \begin{minipage}[t]{0.12\columnwidth}\raggedright\strut
Cross-sectional\strut
\end{minipage} & \begin{minipage}[t]{0.12\columnwidth}\raggedright\strut
341 (10-13)\strut
\end{minipage} & \begin{minipage}[t]{0.12\columnwidth}\raggedright\strut
0.25-0.54\strut
\end{minipage} & \begin{minipage}[t]{0.12\columnwidth}\raggedright\strut
Increased risk of asthma (doctor-diagnosed or EIB) with CCPA in children
with serum IgE \textgreater{} 100 kIU/L (aOR for each 100-hr increase in
CCPA = 1.79; 95\% CI, 1.07-2.72).\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.14\columnwidth}\raggedright\strut
Nickmilder and Bernard, 2007 (95)\strut
\end{minipage} & \begin{minipage}[t]{0.14\columnwidth}\raggedright\strut
Belgium\strut
\end{minipage} & \begin{minipage}[t]{0.14\columnwidth}\raggedright\strut
Belgium\strut
\end{minipage} & \begin{minipage}[t]{0.14\columnwidth}\raggedright\strut
Ecological\strut
\end{minipage} & \begin{minipage}[t]{0.14\columnwidth}\raggedright\strut
(13-14) (6-7)\strut
\end{minipage} & \begin{minipage}[t]{0.14\columnwidth}\raggedright\strut
\_\strut
\end{minipage} & \begin{minipage}[t]{0.14\columnwidth}\raggedright\strut
In both age groups, the prevalence of ever asthma across Europe
correlated with the availability of indoor chlorinated-pools.\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.12\columnwidth}\raggedright\strut
Bernard et al. 2007 (9)\strut
\end{minipage} & \begin{minipage}[t]{0.12\columnwidth}\raggedright\strut
Belgium\strut
\end{minipage} & \begin{minipage}[t]{0.12\columnwidth}\raggedright\strut
Belgium\strut
\end{minipage} & \begin{minipage}[t]{0.12\columnwidth}\raggedright\strut
Cross-sectional\strut
\end{minipage} & \begin{minipage}[t]{0.12\columnwidth}\raggedright\strut
341 (10-13)\strut
\end{minipage} & \begin{minipage}[t]{0.12\columnwidth}\raggedright\strut
-\strut
\end{minipage} & \begin{minipage}[t]{0.12\columnwidth}\raggedright\strut
Decrease of serum CC16 and higher risks of asthma and bronchitis in 43
children who swam in indoor chlorinated-pools during infancy\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.12\columnwidth}\raggedright\strut
Bernard et al. 2008 (96)\strut
\end{minipage} & \begin{minipage}[t]{0.12\columnwidth}\raggedright\strut
Belgium\strut
\end{minipage} & \begin{minipage}[t]{0.12\columnwidth}\raggedright\strut
Belgium\strut
\end{minipage} & \begin{minipage}[t]{0.12\columnwidth}\raggedright\strut
Cross-sectional\strut
\end{minipage} & \begin{minipage}[t]{0.12\columnwidth}\raggedright\strut
847 (13-18)\strut
\end{minipage} & \begin{minipage}[t]{0.12\columnwidth}\raggedright\strut
-\strut
\end{minipage} & \begin{minipage}[t]{0.12\columnwidth}\raggedright\strut
Use of outdoor pools was associated with higher risks of elevated FeNO,
cat or HDM sensitization and asthma in subjects with serum
IgE\textgreater{}25 kIU/L\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.14\columnwidth}\raggedright\strut
Nystad et al. 2008 (97)\strut
\end{minipage} & \begin{minipage}[t]{0.14\columnwidth}\raggedright\strut
Norway\strut
\end{minipage} & \begin{minipage}[t]{0.14\columnwidth}\raggedright\strut
Norway\strut
\end{minipage} & \begin{minipage}[t]{0.14\columnwidth}\raggedright\strut
Prospective\strut
\end{minipage} & \begin{minipage}[t]{0.14\columnwidth}\raggedright\strut
30,870 (0.5-1.5)\strut
\end{minipage} & \begin{minipage}[t]{0.14\columnwidth}\raggedright\strut
-\strut
\end{minipage} & \begin{minipage}[t]{0.14\columnwidth}\raggedright\strut
Increased risk of wheeze (aOR, 1.24, 95\% CI 1.11, 1.39) in baby
swimmers from atopic mothers.\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.12\columnwidth}\raggedright\strut
Schoefer et al. 2008 (98)\strut
\end{minipage} & \begin{minipage}[t]{0.12\columnwidth}\raggedright\strut
Germany\strut
\end{minipage} & \begin{minipage}[t]{0.12\columnwidth}\raggedright\strut
Germany\strut
\end{minipage} & \begin{minipage}[t]{0.12\columnwidth}\raggedright\strut
Prospective\strut
\end{minipage} & \begin{minipage}[t]{0.12\columnwidth}\raggedright\strut
2,196 (6)\strut
\end{minipage} & \begin{minipage}[t]{0.12\columnwidth}\raggedright\strut
-\strut
\end{minipage} & \begin{minipage}[t]{0.12\columnwidth}\raggedright\strut
Baby swimmers had higher risk of asthma (aOR 2.15 95\% CI 1.16-3.99) due
potentially to reverse causation and respiratory infections in the 1st
yr\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.12\columnwidth}\raggedright\strut
Cotter and Ryan 2009 (56)\strut
\end{minipage} & \begin{minipage}[t]{0.12\columnwidth}\raggedright\strut
Ireland\strut
\end{minipage} & \begin{minipage}[t]{0.12\columnwidth}\raggedright\strut
Ireland\strut
\end{minipage} & \begin{minipage}[t]{0.12\columnwidth}\raggedright\strut
Cross-sectional\strut
\end{minipage} & \begin{minipage}[t]{0.12\columnwidth}\raggedright\strut
97 (6-12)\strut
\end{minipage} & \begin{minipage}[t]{0.12\columnwidth}\raggedright\strut
-\strut
\end{minipage} & \begin{minipage}[t]{0.12\columnwidth}\raggedright\strut
Associations between CCPA and the risk of diagnosed asthma and wheezing
in the last 12 months\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.12\columnwidth}\raggedright\strut
Bernard et al. 2009 (53)\strut
\end{minipage} & \begin{minipage}[t]{0.12\columnwidth}\raggedright\strut
Belgium\strut
\end{minipage} & \begin{minipage}[t]{0.12\columnwidth}\raggedright\strut
Belgium\strut
\end{minipage} & \begin{minipage}[t]{0.12\columnwidth}\raggedright\strut
Cross-sectional\strut
\end{minipage} & \begin{minipage}[t]{0.12\columnwidth}\raggedright\strut
847 (13-18)\strut
\end{minipage} & \begin{minipage}[t]{0.12\columnwidth}\raggedright\strut
0.30-0.50\strut
\end{minipage} & \begin{minipage}[t]{0.12\columnwidth}\raggedright\strut
Among atopic adolescents, aOR for asthma, hay fever or allergic rhinitis
increased with CCPA but not with the Cu/Ag pool attendance.\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.12\columnwidth}\raggedright\strut
Voisin et al. 2010 (69)\strut
\end{minipage} & \begin{minipage}[t]{0.12\columnwidth}\raggedright\strut
Belgium\strut
\end{minipage} & \begin{minipage}[t]{0.12\columnwidth}\raggedright\strut
Belgium\strut
\end{minipage} & \begin{minipage}[t]{0.12\columnwidth}\raggedright\strut
Cross-sectional\strut
\end{minipage} & \begin{minipage}[t]{0.12\columnwidth}\raggedright\strut
430 (5-7)\strut
\end{minipage} & \begin{minipage}[t]{0.12\columnwidth}\raggedright\strut
-\strut
\end{minipage} & \begin{minipage}[t]{0.12\columnwidth}\raggedright\strut
Infant swimming in indoor or outdoor chlorinated-pools is associated
with increased risks of bronchiolitis and later of allergic
sensitization\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.14\columnwidth}\raggedright\strut
Font-Ribera et al. 2011 (61)\strut
\end{minipage} & \begin{minipage}[t]{0.14\columnwidth}\raggedright\strut
UK\strut
\end{minipage} & \begin{minipage}[t]{0.14\columnwidth}\raggedright\strut
UK\strut
\end{minipage} & \begin{minipage}[t]{0.14\columnwidth}\raggedright\strut
Prospective\strut
\end{minipage} & \begin{minipage}[t]{0.14\columnwidth}\raggedright\strut
5,738 (7 and 10)\strut
\end{minipage} & \begin{minipage}[t]{0.14\columnwidth}\raggedright\strut
-\strut
\end{minipage} & \begin{minipage}[t]{0.14\columnwidth}\raggedright\strut
Swimming was associated with increased lung function and lower risk of
asthma symptoms.\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.12\columnwidth}\raggedright\strut
Ferrari et al. 2011 (57)\strut
\end{minipage} & \begin{minipage}[t]{0.12\columnwidth}\raggedright\strut
Italy\strut
\end{minipage} & \begin{minipage}[t]{0.12\columnwidth}\raggedright\strut
Italy\strut
\end{minipage} & \begin{minipage}[t]{0.12\columnwidth}\raggedright\strut
Prospective\strut
\end{minipage} & \begin{minipage}[t]{0.12\columnwidth}\raggedright\strut
1,136 (18-55)\strut
\end{minipage} & \begin{minipage}[t]{0.12\columnwidth}\raggedright\strut
-\strut
\end{minipage} & \begin{minipage}[t]{0.12\columnwidth}\raggedright\strut
Higher risk of new-onset asthma associated with CCPA.\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.14\columnwidth}\raggedright\strut
Jacobs et al. 2012 (62)\strut
\end{minipage} & \begin{minipage}[t]{0.14\columnwidth}\raggedright\strut
Netherlands\strut
\end{minipage} & \begin{minipage}[t]{0.14\columnwidth}\raggedright\strut
Netherlands\strut
\end{minipage} & \begin{minipage}[t]{0.14\columnwidth}\raggedright\strut
Cross-sectional\strut
\end{minipage} & \begin{minipage}[t]{0.14\columnwidth}\raggedright\strut
2,359 (6-13)\strut
\end{minipage} & \begin{minipage}[t]{0.14\columnwidth}\raggedright\strut
0.21\strut
\end{minipage} & \begin{minipage}[t]{0.14\columnwidth}\raggedright\strut
Association of HDM sensitization with frequent baby swimming and lower
serum CC16 (n=419). No association with asthma.\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.14\columnwidth}\raggedright\strut
Font-Ribera et al.~2013 (60)\strut
\end{minipage} & \begin{minipage}[t]{0.14\columnwidth}\raggedright\strut
Spain\strut
\end{minipage} & \begin{minipage}[t]{0.14\columnwidth}\raggedright\strut
Spain\strut
\end{minipage} & \begin{minipage}[t]{0.14\columnwidth}\raggedright\strut
Prospective\strut
\end{minipage} & \begin{minipage}[t]{0.14\columnwidth}\raggedright\strut
2,205 (0-1.17)\strut
\end{minipage} & \begin{minipage}[t]{0.14\columnwidth}\raggedright\strut
-\strut
\end{minipage} & \begin{minipage}[t]{0.14\columnwidth}\raggedright\strut
No association between indoor or outdoor swimming pool attendance during
the 1st year of life and LRTI, wheezing, atopic eczema or otitis\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.14\columnwidth}\raggedright\strut
Voisin et al. 2013, 2014 (66, 67)\strut
\end{minipage} & \begin{minipage}[t]{0.14\columnwidth}\raggedright\strut
Belgium\strut
\end{minipage} & \begin{minipage}[t]{0.14\columnwidth}\raggedright\strut
Belgium\strut
\end{minipage} & \begin{minipage}[t]{0.14\columnwidth}\raggedright\strut
Prospective\strut
\end{minipage} & \begin{minipage}[t]{0.14\columnwidth}\raggedright\strut
196 (5.7 and 7.7)\strut
\end{minipage} & \begin{minipage}[t]{0.14\columnwidth}\raggedright\strut
-\strut
\end{minipage} & \begin{minipage}[t]{0.14\columnwidth}\raggedright\strut
Swimming at indoor or outdoor chlorinated-pools before the age of 3 yrs
was associated with higher risks of HDM sensitization and increased
FeNO\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.14\columnwidth}\raggedright\strut
Schuez-Havupalo et al. 2014 (99)\strut
\end{minipage} & \begin{minipage}[t]{0.14\columnwidth}\raggedright\strut
Finland\strut
\end{minipage} & \begin{minipage}[t]{0.14\columnwidth}\raggedright\strut
Finland\strut
\end{minipage} & \begin{minipage}[t]{0.14\columnwidth}\raggedright\strut
Prospective\strut
\end{minipage} & \begin{minipage}[t]{0.14\columnwidth}\raggedright\strut
1,827 (0-1.42)\strut
\end{minipage} & \begin{minipage}[t]{0.14\columnwidth}\raggedright\strut
-\strut
\end{minipage} & \begin{minipage}[t]{0.14\columnwidth}\raggedright\strut
Association between infant swimming and rhinovirus-associated wheezing
among children with atopic eczema (n=635, p = 0.006).\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.12\columnwidth}\raggedright\strut
Font-Ribera et al. 2014 (59)\strut
\end{minipage} & \begin{minipage}[t]{0.12\columnwidth}\raggedright\strut
Spain\strut
\end{minipage} & \begin{minipage}[t]{0.12\columnwidth}\raggedright\strut
Spain\strut
\end{minipage} & \begin{minipage}[t]{0.12\columnwidth}\raggedright\strut
Cross-sectional\strut
\end{minipage} & \begin{minipage}[t]{0.12\columnwidth}\raggedright\strut
2,758 (6-12)\strut
\end{minipage} & \begin{minipage}[t]{0.12\columnwidth}\raggedright\strut
-\strut
\end{minipage} & \begin{minipage}[t]{0.12\columnwidth}\raggedright\strut
No associations between regular indoor pool attendance before 2 yrs and
asthma, wheezing, eczema.\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.12\columnwidth}\raggedright\strut
Bernard et al. 2015 (81)\strut
\end{minipage} & \begin{minipage}[t]{0.12\columnwidth}\raggedright\strut
Belgium\strut
\end{minipage} & \begin{minipage}[t]{0.12\columnwidth}\raggedright\strut
Belgium\strut
\end{minipage} & \begin{minipage}[t]{0.12\columnwidth}\raggedright\strut
Cross-sectional\strut
\end{minipage} & \begin{minipage}[t]{0.12\columnwidth}\raggedright\strut
835 (13-18)\strut
\end{minipage} & \begin{minipage}[t]{0.12\columnwidth}\raggedright\strut
-\strut
\end{minipage} & \begin{minipage}[t]{0.12\columnwidth}\raggedright\strut
Associations of serum CC16/SP-D with CCPA, allergic sensitization
(especially to HDM) and allergic diseases among sensitized
adolescents\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.14\columnwidth}\raggedright\strut
Andersson et al. 2015 (55)\strut
\end{minipage} & \begin{minipage}[t]{0.14\columnwidth}\raggedright\strut
Sweden\strut
\end{minipage} & \begin{minipage}[t]{0.14\columnwidth}\raggedright\strut
Sweden\strut
\end{minipage} & \begin{minipage}[t]{0.14\columnwidth}\raggedright\strut
Cross-sectional\strut
\end{minipage} & \begin{minipage}[t]{0.14\columnwidth}\raggedright\strut
1,~866 (11-12)\strut
\end{minipage} & \begin{minipage}[t]{0.14\columnwidth}\raggedright\strut
-\strut
\end{minipage} & \begin{minipage}[t]{0.14\columnwidth}\raggedright\strut
Asthma associated with indoor pool attendance ([?]1 week) only among
sensitized subjects (n= 1,652, aOR1.9, 95\% CI 1.09-3.32).\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.14\columnwidth}\raggedright\strut
Bernard et al. 2017 (100)\strut
\end{minipage} & \begin{minipage}[t]{0.14\columnwidth}\raggedright\strut
Belgium\strut
\end{minipage} & \begin{minipage}[t]{0.14\columnwidth}\raggedright\strut
Belgium\strut
\end{minipage} & \begin{minipage}[t]{0.14\columnwidth}\raggedright\strut
Prospective\strut
\end{minipage} & \begin{minipage}[t]{0.14\columnwidth}\raggedright\strut
121 (5.8, 7.8)\strut
\end{minipage} & \begin{minipage}[t]{0.14\columnwidth}\raggedright\strut
-\strut
\end{minipage} & \begin{minipage}[t]{0.14\columnwidth}\raggedright\strut
Low CC16 in NALF associated with CCPA predicts persistent sensitization
to aeroallergens, especially to HDM\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.12\columnwidth}\raggedright\strut
Cavaleiro-Rufo et al. 2018 (58)\strut
\end{minipage} & \begin{minipage}[t]{0.12\columnwidth}\raggedright\strut
Portugal\strut
\end{minipage} & \begin{minipage}[t]{0.12\columnwidth}\raggedright\strut
Portugal\strut
\end{minipage} & \begin{minipage}[t]{0.12\columnwidth}\raggedright\strut
Cross-sectional\strut
\end{minipage} & \begin{minipage}[t]{0.12\columnwidth}\raggedright\strut
858 (7-12)\strut
\end{minipage} & \begin{minipage}[t]{0.12\columnwidth}\raggedright\strut
-\strut
\end{minipage} & \begin{minipage}[t]{0.12\columnwidth}\raggedright\strut
Indoor pool attendance associated with autonomic changes and baseline
bronchoconstriction and before 3 yrs with functional asthma\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.12\columnwidth}\raggedright\strut
Andersson et al. 2018 (54)\strut
\end{minipage} & \begin{minipage}[t]{0.12\columnwidth}\raggedright\strut
Sweden\strut
\end{minipage} & \begin{minipage}[t]{0.12\columnwidth}\raggedright\strut
Sweden\strut
\end{minipage} & \begin{minipage}[t]{0.12\columnwidth}\raggedright\strut
Prospective\strut
\end{minipage} & \begin{minipage}[t]{0.12\columnwidth}\raggedright\strut
970 (16-17)\strut
\end{minipage} & \begin{minipage}[t]{0.12\columnwidth}\raggedright\strut
0.15\strut
\end{minipage} & \begin{minipage}[t]{0.12\columnwidth}\raggedright\strut
Early indoor pool attendance (\textless{}~3 yrs) associated with asthma
onset. Risks are particularly high for atopics. Dose-response
relationships with NCl\textsubscript{3}.\strut
\end{minipage}\tabularnewline
\bottomrule
\end{longtable}

CCPA, cumulative chlorinated-pool attendance; CC16, club cell protein~;
FeNO: fractional exhaled nitric oxide; SP-A, surfactant associated
protein A~; SP-D, surfactant-associated protein D; HDM, house dust mite;
LRTI, lower respiratory tract infection; EIB, exercise-induced
bronchoconstriction~; NCl\textsubscript{3}, nitrogen trichloride or
trichloramine in pool air; Cu/Ag pool, swimming pool disinfected by
copper~/silver electrofiltration. Age and NCl\textsubscript{3} values
are reported as mean or range.

\textbf{Table 3} : Conditions inherent to the competitive swimmers and
the respective consequences on their exposure to disinfection
by-products.\selectlanguage{english}
\begin{longtable}[]{@{}ll@{}}
\toprule
\textbf{Condition} & \textbf{Consequence}\tabularnewline
\midrule
\endhead
High physical effort & The internal dose of THMs increases significantly
with intensity of physical activity (101). The content of THMs in
swimmers' blood is correlated with their content in the ambient air, and
not in the water, of swimming-pools (102)\tabularnewline
& Stronger impact of the inhalation route compared to ingestion or
dermal absorption\tabularnewline
Oral inhalation of water droplets & Increases the amount of exposure and
may also alter the lung microbiome\tabularnewline
Greater swimming skills & Lower rate of ingestion in a comparable time
than for less skilled users\tabularnewline
\bottomrule
\end{longtable}

\textbf{Table 4} : Differential diagnosis of the Chlorine
exposure-related clinical conditions in pool attendants.\selectlanguage{english}
\begin{longtable}[]{@{}llll@{}}
\toprule
\begin{minipage}[b]{0.24\columnwidth}\raggedright\strut
organ or system\strut
\end{minipage} & \begin{minipage}[b]{0.24\columnwidth}\raggedright\strut
Pathology (SIGNS \& symptoms)\strut
\end{minipage} & \begin{minipage}[b]{0.24\columnwidth}\raggedright\strut
Diagnosis\strut
\end{minipage} & \begin{minipage}[b]{0.24\columnwidth}\raggedright\strut
Differential diagnosis\strut
\end{minipage}\tabularnewline
\midrule
\endhead
\begin{minipage}[t]{0.24\columnwidth}\raggedright\strut
Hair\strut
\end{minipage} & \begin{minipage}[t]{0.24\columnwidth}\raggedright\strut
Hair coloration/ discoloration, fragile and/or dry\strut
\end{minipage} & \begin{minipage}[t]{0.24\columnwidth}\raggedright\strut
Clinical History Medical examination\strut
\end{minipage} & \begin{minipage}[t]{0.24\columnwidth}\raggedright\strut
Other abrasive agents\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.24\columnwidth}\raggedright\strut
Eyes\strut
\end{minipage} & \begin{minipage}[t]{0.24\columnwidth}\raggedright\strut
Corneal epithelial erosions or dysfunction\strut
\end{minipage} & \begin{minipage}[t]{0.24\columnwidth}\raggedright\strut
Clinical History Medical examination\strut
\end{minipage} & \begin{minipage}[t]{0.24\columnwidth}\raggedright\strut
Corneal abrasion Recurrent corneal erosion\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.24\columnwidth}\raggedright\strut
\strut
\end{minipage} & \begin{minipage}[t]{0.24\columnwidth}\raggedright\strut
Conjunctivitis\strut
\end{minipage} & \begin{minipage}[t]{0.24\columnwidth}\raggedright\strut
Clinical History Medical examination\strut
\end{minipage} & \begin{minipage}[t]{0.24\columnwidth}\raggedright\strut
Allergic conjunctivitis Irritative conjunctivitis\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.24\columnwidth}\raggedright\strut
Ear\strut
\end{minipage} & \begin{minipage}[t]{0.24\columnwidth}\raggedright\strut
External Otitis ``Swimmer's Ear''\strut
\end{minipage} & \begin{minipage}[t]{0.24\columnwidth}\raggedright\strut
Clinical History Medical examination\strut
\end{minipage} & \begin{minipage}[t]{0.24\columnwidth}\raggedright\strut
Skin injuries, foreign bodies, chronic inflammation\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.24\columnwidth}\raggedright\strut
Nails\strut
\end{minipage} & \begin{minipage}[t]{0.24\columnwidth}\raggedright\strut
Surface damage of the nail plates\strut
\end{minipage} & \begin{minipage}[t]{0.24\columnwidth}\raggedright\strut
Clinical History Medical examination\strut
\end{minipage} & \begin{minipage}[t]{0.24\columnwidth}\raggedright\strut
Fungal infection Nail polish effects\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.24\columnwidth}\raggedright\strut
Teeth\strut
\end{minipage} & \begin{minipage}[t]{0.24\columnwidth}\raggedright\strut
Enamel erosion\strut
\end{minipage} & \begin{minipage}[t]{0.24\columnwidth}\raggedright\strut
Clinical History Medical Examination\strut
\end{minipage} & \begin{minipage}[t]{0.24\columnwidth}\raggedright\strut
Attrition and abrasion of the enamel\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.24\columnwidth}\raggedright\strut
Skin\strut
\end{minipage} & \begin{minipage}[t]{0.24\columnwidth}\raggedright\strut
Dry, itching, fragile skin Eczema\strut
\end{minipage} & \begin{minipage}[t]{0.24\columnwidth}\raggedright\strut
Clinical History Medical Examination\strut
\end{minipage} & \begin{minipage}[t]{0.24\columnwidth}\raggedright\strut
``Primary'' eczema Dermatoses and systemic illnesses with dry skin\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.24\columnwidth}\raggedright\strut
Respiratory system\strut
\end{minipage} & \begin{minipage}[t]{0.24\columnwidth}\raggedright\strut
Nose itching\strut
\end{minipage} & \begin{minipage}[t]{0.24\columnwidth}\raggedright\strut
Clinical History Medical Examination Skin prick tests\strut
\end{minipage} & \begin{minipage}[t]{0.24\columnwidth}\raggedright\strut
Allergic rhinitis\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.24\columnwidth}\raggedright\strut
\strut
\end{minipage} & \begin{minipage}[t]{0.24\columnwidth}\raggedright\strut
Anosmia\strut
\end{minipage} & \begin{minipage}[t]{0.24\columnwidth}\raggedright\strut
Clinical History Medical Examination Olfactive tests Imaging\strut
\end{minipage} & \begin{minipage}[t]{0.24\columnwidth}\raggedright\strut
Allergic rhinitis Obstructive/traumatic nasal diseases Sensorineural
diseases of the olfactive tract\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.24\columnwidth}\raggedright\strut
\strut
\end{minipage} & \begin{minipage}[t]{0.24\columnwidth}\raggedright\strut
Dyspnea, respiratory fatigue, cough, wheezing, chest tightness, muscular
fatigue\strut
\end{minipage} & \begin{minipage}[t]{0.24\columnwidth}\raggedright\strut
Clinical History Medical Examination Complementary test: Spirometry
pre/post-exposure, Monitored exercise test, pre/post- exercise DLCO,
Skin prick tests\strut
\end{minipage} & \begin{minipage}[t]{0.24\columnwidth}\raggedright\strut
Dyspneic pathologies: Cardiovascular Respiratory Hematology Oncology
Rheumatology immunology Environmental stress \ldots{}\strut
\end{minipage}\tabularnewline
\bottomrule
\end{longtable}\selectlanguage{english}
\begin{longtable}[]{@{}ll@{}}
\toprule
\begin{minipage}[t]{0.47\columnwidth}\raggedright\strut
\textbf{Table 5.} Healthy swimming water and air quality checklist,
based on the recommendations of the Centers for Disease Control and
Prevention and the guidelines from the World Health Organization.\strut
\end{minipage} & \begin{minipage}[t]{0.47\columnwidth}\raggedright\strut
\textbf{Table 5.} Healthy swimming water and air quality checklist,
based on the recommendations of the Centers for Disease Control and
Prevention and the guidelines from the World Health Organization.\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.48\columnwidth}\raggedright\strut
\textbf{Swimmers checklist}\strut
\end{minipage} & \begin{minipage}[t]{0.48\columnwidth}\raggedright\strut
Stay out of the water if you have: - diarrhea (for patients with
cryptosporidiosis, don't swim for an additional 2 weeks after diarrhea
has resolved) - a gastrointestinal (stomach) upset or skin or
respiratory infection - an open wound (for example, from surgery or a
piercing) that is not covered with a waterproof bandage Keep ears as dry
as possible and dry ears thoroughly after swimming\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.47\columnwidth}\raggedright\strut
\strut
\end{minipage} & \begin{minipage}[t]{0.47\columnwidth}\raggedright\strut
Shower before you get into the water, rinsing off in the shower for just
1 min removes most of the dirt or anything else on your body Remove
make-up\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.47\columnwidth}\raggedright\strut
\strut
\end{minipage} & \begin{minipage}[t]{0.47\columnwidth}\raggedright\strut
Don't pee or poop in the water\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.47\columnwidth}\raggedright\strut
\strut
\end{minipage} & \begin{minipage}[t]{0.47\columnwidth}\raggedright\strut
Don't swallow the water\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.47\columnwidth}\raggedright\strut
\textbf{Swimming pool checklist}\strut
\end{minipage} & \begin{minipage}[t]{0.47\columnwidth}\raggedright\strut
Check the pool's latest inspection results\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.47\columnwidth}\raggedright\strut
\strut
\end{minipage} & \begin{minipage}[t]{0.47\columnwidth}\raggedright\strut
Check the free chlorine level and pH before getting into the water:
proper free chlorine level (1--3 mg/L or parts per million) and pH
(7.2--7.8) maximize germ-killing power.\strut
\end{minipage}\tabularnewline
\bottomrule
\end{longtable}

\textbf{Figures legends:}

\textbf{Figure 1} : Chlorination by-products presented at the water and
the air of chlorinated swimming-pools - adapted from Bernard A (20).

\textbf{Figure 2} : The routes of exposure to disinfection by-products
in swimming-pools and the factors affecting each route - adapted from
Dyck et al (2).

\textbf{Figure 3:} Schematic representation of the relation between
water ingestion and surface area/body mass and respiratory rates
throughout different ages (based on data from WHO Training package for
the Health sector -- Children's health and the environment).\selectlanguage{english}
\begin{figure}[H]
\begin{center}
\includegraphics[width=0.70\columnwidth]{figures/Figure-1/Figure-1}

\end{center}
\end{figure}\selectlanguage{english}
\begin{figure}[H]
\begin{center}
\includegraphics[width=0.70\columnwidth]{figures/Figure-2/Figure-2}

\end{center}
\end{figure}\selectlanguage{english}
\begin{figure}[H]
\begin{center}
\includegraphics[width=0.70\columnwidth]{figures/Figure-3/Figure-3}

\end{center}
\end{figure}

\selectlanguage{english}
\FloatBarrier
\end{document}

