Occupational Asthma Reference

Seys SF, Hox V, Van Gerven L, Dilissen E, Marijsse G, Peeters E, Dekimpe E, Kasran A, Aertgeerts S, Troosters T, Vanbelle V, Peers K, Ceuppens JL, Hellings PW, Dupont LJ, Bullens DM, Damage-associated molecular pattern and innate cytokine release in the airways of competitive swimmers, Allergy, 2015;70:187-194,

Keywords: swimmer, asthma, nitrogen trichloride, Belgium

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Abstract

Background
Daily intensive exercise by elite athletes can result in exercise-induced asthma especially in elite swimmers and this may be linked to epithelial damage.

Objective
To study airway epithelial damage and release of damage-associated molecular patterns (DAMPs) after intensive exercise in elite athletes and controls.

Methods
We recruited competitive swimmers (n = 26), competitive indoor athletes (n = 13) and controls (n = 15) without any history of asthma. Lung function was measured before, immediately after and 24 h after a 90-min intensive exercise protocol. Sputum induction was performed at baseline and 24 h after exercise. Exercise-induced bronchoconstriction (EIB) was assessed by the eucapnic voluntary hyperventilation test.

Results
Baseline sputum uric acid, high mobility group box-1, CXCL8 mRNA, sputum neutrophils and serum Clara cell protein-16 (CC-16) were significantly higher in competitive swimmers compared with controls. Intensive swimming for 90 min resulted in an increase of sputum IL-1ß, IL-6 and TNF mRNA in competitive swimmers, and of sputum IL-6 mRNA and sputum neutrophils in controls. Although all participants were asymptomatic, seven competitive swimmers, one indoor athlete and one control met the criteria for EIB.

Conclusion
Our findings show that the intensive training combined with exposure to by-products of chlorination induces airway epithelial damage in competitive swimmers. This is associated with increased damage-associated molecular patterns, innate cytokine release and neutrophilic airway inflammation.

Plain text: Background Daily intensive exercise by elite athletes can result in exercise-induced asthma especially in elite swimmers and this may be linked to epithelial damage. Objective To study airway epithelial damage and release of damage-associated molecular patterns (DAMPs) after intensive exercise in elite athletes and controls. Methods We recruited competitive swimmers (n = 26), competitive indoor athletes (n = 13) and controls (n = 15) without any history of asthma. Lung function was measured before, immediately after and 24 h after a 90-min intensive exercise protocol. Sputum induction was performed at baseline and 24 h after exercise. Exercise-induced bronchoconstriction (EIB) was assessed by the eucapnic voluntary hyperventilation test. Results Baseline sputum uric acid, high mobility group box-1, CXCL8 mRNA, sputum neutrophils and serum Clara cell protein-16 (CC-16) were significantly higher in competitive swimmers compared with controls. Intensive swimming for 90 min resulted in an increase of sputum IL-1b, IL-6 and TNF mRNA in competitive swimmers, and of sputum IL-6 mRNA and sputum neutrophils in controls. Although all participants were asymptomatic, seven competitive swimmers, one indoor athlete and one control met the criteria for EIB. Conclusion Our findings show that the intensive training combined with exposure to by-products of chlorination induces airway epithelial damage in competitive swimmers. This is associated with increased damage-associated molecular patterns, innate cytokine release and neutrophilic airway inflammation.

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Comments

This study excluded known asthmatics from all 3 groups. Despite this 6/26 swimmers had a positive eucapnic hyperventilation test compared with 1/15 non-athlete controls and 0/13 basketball or volleyball players. IL-1 beta, IL6 and TNF were increased 24 hours after swimming but not in the other two groups (the swimmers and controls swam for 90 minutes, the basket and volleyball athletes exercised in the gym)). We are given no information about the pool used, but the supplementary table gives the median air trichloramines as 0.28mg/m3 implying that the pool used chlorine as the main method of water sterilisation. Nor are we told how much swimming each group did, presumably the elite swimmers swam further in the 90 minutes of swimming and are likely to have hyperventilated more than the control group. This paper provides some further evidence for the asthmagenic properties of trichloramines in the air above chlorinated swimming pools.
2/9/2015

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