Chlorinated pool attendance, airway epithelium defects and the risks of allergic diseases in adolescents: Interrelationships revealed by circulating biomarkers

Bernard, Alfred; Nickmilder, Marc; Dumont, Xavier

doi:10.1016/j.envres.2015.03.034

Cited by 28 publications

(30 citation statements)

References 33 publications

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“…Exposure to bleach alone in concentrations below currently defined acceptable limits may lead to decline in lung function in asthmatic subjects (Sastre et al, ). Perhaps of greater public health concern is the effect of attendance in early life at chlorinated swimming pools, on the development of allergy and asthma (Bernard et al, ). Our results suggest that preventive treatment with a leukotriene modifier may be a useful adjunct to the treatment of respiratory symptoms caused by chlorine exposure, but appropriate trials in human subjects are required to confirm these conclusions.…”

Section: Discussionmentioning

confidence: 99%

Montelukast reduces inhaled chlorine triggered airway hyperresponsiveness and airway inflammation in the mouse

Hamamoto

Ano

Allard

et al. 2017

British J Pharmacology

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BACKGROUND AND PURPOSECysteinyl leukotrienes (CysLTs) are pro-inflammatory lipid mediators that exacerbate disease state in several asthma phenotypes including asthma induced by allergen, virus and exercise. However, the role of CysLTs in irritant-induced airway disease is not well characterized. The purpose of the current study was to investigate the effect of montelukast, a CysLT 1 receptor antagonist, on parameters of irritant-induced asthma induced by inhalation of chlorine in the mouse. EXPERIMENTAL APPROACHBALB/c mice were exposed to chlorine in air (100 ppm, for 5 min). Montelukast (3 mg·kg À1 ) or the vehicle (1% methylcellulose) was administered 24 and 1 h prior to chlorine exposure and 1 h prior to outcome measurements. Twenty-four hours after exposure, responses to inhaled aerosolized methacholine, cell composition and an array of cytokines/chemokines in bronchoalveolar lavage (BAL) fluid were measured. Neutralizing antibodies against IL-6 and VEGF were administered prior to exposures. KEY RESULTSMontelukast reduced chlorine -induced airway hyperresponsiveness (AHR) to methacholine in the peripheral lung compartment as estimated from dynamic elastance, but not in large conducting airways. Montelukast treatment attenuated chlorine-induced macrophage influx, neutrophilia and eosinophilia in BAL fluid. Chlorine exposure increased VEGF, IL-6, the chemokines KC and CCL3 in BAL fluid. Montelukast treatment prevented chlorine-induced increases in VEGF and IL-6. Anti-IL-6 antibody inhibited chlorine-induced neutrophilia and reduced AHR. CONCLUSIONS AND IMPLICATIONSPre-treatment with montelukast attenuated chlorine-induced neutrophilia and AHR in mice. These effects are mediated, in part, via IL-6. IntroductionIrritant-induced asthma (IIA) is a subtype of asthma that occurs following inhalation of noxious substances, with a short latency and does not require prior sensitization (Brooks and Bernstein, 2011;Tarlo and Lemiere, 2014). One of the most commonly reported toxic exposures that results in the development of IIA is inhalation of chlorine gas and chlorine-related compounds (see White and Martin, 2010). Chlorine is a highly reactive substance that mediates its inhalational toxicity through oxidative stress (Martin et al., 2003), resulting in a predominantly neutrophilic airway inflammation and airway hyperresponsiveness (AHR) to inhaled aerosolized methacholine (MCh). Chlorine-induced neutrophilia is responsible for further oxidative damage and the consequent airway dysfunction and is sufficient to engage the Nrf2-mediated antioxidant response (McGovern et al., 2015). Cysteinyl-leukotrienes (CysLTs) are lipid mediators which have been extensively studied in the context of allergen-driven airway dysfunction but have received less attention in the context of responses to irritants. Montelukast (MK) is a highly selective antagonist of CysLT 1 receptors (Jones et al.,1995), the predominant CysLT receptor expressed in the bronchial tree (Lynch et al., 1999). While CysLTs have not been usually associated with o...

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Section: Discussionmentioning

confidence: 99%

Montelukast reduces inhaled chlorine triggered airway hyperresponsiveness and airway inflammation in the mouse

Hamamoto

Ano

Allard

et al. 2017

British J Pharmacology

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“…Toxic compounds that reduce BALF and serum CC16 levels include oxidant-rich air pollutants such as CS 69;70;71 , nitrogen dioxide 72 , ozone 73 , chlorination products 74;75 , and toxic particles such as silica 76 and wood smoke 77 which is an important risk factor for COPD in developing countries. Pollutants likely reduce Club cell CC16 expression via their toxic effects on the cells.…”

Section: Club Cell Protein-16 (Cc16)mentioning

confidence: 99%

Club Cell Protein 16 (CC16) Augmentation: A Potential Disease-modifying Approach for Chronic Obstructive Pulmonary Disease (COPD)

Laucho-Contreras

Polverino

Tesfaigzi

et al. 2016

Expert Opinion on Therapeutic Targets

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Introduction Club cell protein 16 (CC16) is the most abundant protein in bronchoalveolar lavage fluid. CC16 has anti-inflammatory properties in smoke-exposed lungs, and chronic obstructive pulmonary disease (COPD) is associated with CC16 deficiency. Herein, we explored whether CC16 is a therapeutic target for COPD. Areas Covered We reviewed the literature on the factors that regulate airway CC16 expression, its biologic functions and its protective activities in smoke-exposed lungs using PUBMED searches. We generated hypotheses on the mechanisms by which CC16 limits COPD development, and discuss its potential as a new therapeutic approach for COPD. Expert Opinion CC16 plasma and lung levels are reduced in smokers without airflow obstruction and COPD patients. In COPD patients, airway CC16 expression is inversely correlated with severity of airflow obstruction. CC16 deficiency increases smoke-induced lung pathologies in mice by its effects on epithelial cells, leukocytes, and fibroblasts. Experimental augmentation of CC16 levels using recombinant CC16 in cell culture systems, plasmid and adenoviral-mediated over-expression of CC16 in epithelial cells or smoke-exposed murine airways reduces inflammation and cellular injury. Additional studies are necessary to assess the efficacy of therapies aimed at restoring airway CC16 levels as a new disease-modifying therapy for COPD patients.

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“…Levels also tend to be higher in indoor pool environments than outside swimming pools (Uyan et al 2009). Trichloramine causes respiratory irritation similar to formaldehyde and chlorine and has been shown to cause epithelial damage in rodents and respiratory tract irritation in lifeguards and other pool attendees (Bernard et al 2006(Bernard et al , 2015.…”

Section: Effects Of Swimming Pool Exposure On Allergy and Asthmamentioning

confidence: 99%

Update on effects of cleaning agents on allergy and asthma

2018

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Background: Cleaning and disinfecting agents are widely used in modern life, in homes, schools, public places, and workplaces as well as in recreational facilities such as swimming pools. Use has been for sanitizing purposes and to assist in reduction of infection as well as for deodorizing purposes. However, adverse respiratory effects have been associated with use of cleaning products ranging from effects in infancy and early childhood up to adults at home and work. Methods: This review summarizes recent published literature on the effects of cleaning agents used pre-natally, in childhood and adult life, at home, work, and in swimming pools. Results: Several studies have indicated that there is an increased risk of developing asthma among adults with frequent exposure to cleaning products at work and in the home. Potential mechanisms include sensitization and respiratory irritant effects. Exposure to irritant chlorine by-products from swimming pools have also been associated with respiratory effects and increased risk of asthma. Potential effects from maternal exposures to cleaning products on infants, and effects on early childhood atopy are less clear. Conclusions: Exposure to cleaning agents increases relative risks of asthma among workers, and adults using these agents in the home. Risks are also increased with exposure to chlorinated by-products from swimming pools, both in adults and children. Further studies are needed to understand the mechanisms of these associations.

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Chlorinated pool attendance, airway epithelium defects and the risks of allergic diseases in adolescents: Interrelationships revealed by circulating biomarkers

Cited by 28 publications

References 33 publications

Montelukast reduces inhaled chlorine triggered airway hyperresponsiveness and airway inflammation in the mouse

Montelukast reduces inhaled chlorine triggered airway hyperresponsiveness and airway inflammation in the mouse

Club Cell Protein 16 (CC16) Augmentation: A Potential Disease-modifying Approach for Chronic Obstructive Pulmonary Disease (COPD)

Update on effects of cleaning agents on allergy and asthma

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