Abstract
Background: Swimming in pools entails a considerable exposure to carcinogenic and irritant disinfection by-products (DBPs). Biomarkers of lung epithelium permeability (serum CC16), genotoxicity (micronuclei (MN) in lymphocytes) and urine mutagenicity were previously found to be related to brominated trihalomethanes (THM) exposure during swimming. We replicated the study with doubled sample size and improved exposure assessment. Methods: 116 non-smoking adults swam 40 min in an indoor chlorinated pool. Major DBPs in water (THM, haloacetic acids, haloacetonitriles, haloketones, nitrosamines, total organic halogen), trichloramine in air and swimming distance were measured. Changes in exhaled THM, urine trichloroacetic acid (TCAA), serum CC16, urine mutagenicity, MN in lymphocytes and in retyculocytes were measured before and immediately, 30 min, 1h, 2h, 1h and 4d after swimming, respectively. Results: After swimming, exhaled THM and creatinine adjusted TCAA in urine increased 14.5 µg/m3 and 5.2 µmols/mol, respectively. Changes in CC16 were associated with swimming distance (β coefficient of adjusted linear regression=0.56 (95%CI=0.01-1.11) for an interquartilic range (IQR) increase in exposure) but not with trichloramine in air or exhaled THM. MN in lymphocytes and urine mutagenicity were not associated with exhaled THM, urine TCAA, trichloramine in air or any DBP in water. MN in reticulocytes were measured in 19 subjects and an association with increased exhaled THM was detected (β coefficient=0.59 (95%CI=0.14-1.03) for an IQR increase). Conclusions: Lung epithelium permeability, urine mutagenicity and MN in lymphocytes after swimming were not associated with DBPs exposure. This is the largest study with the most complete exposure assessment on the topic, but the levels of brominated THMs, that are more mutagenic and genotoxic, were around 5 times lower than in the previous study. The positive association with MN in reticulocytes should be further explored.
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