Route-resolved priority risks of disinfection by-products in indoor pools: the underestimated role of buccal/sublingual exposure for the public and competitive swimmers.
Using annual monitoring data from two indoor pools, the study reports route-specific modeled risks from chloroform, dichloroacetic acid, and trichloroacetic acid, identifying inhalation and buccal/sublingual exposure as potentially important pathways, particularly for children and competitive swimmers.
Open original publication →What the AI sees
Using annual monitoring data from two indoor pools, the study reports route-specific modeled risks from chloroform, dichloroacetic acid, and trichloroacetic acid, identifying inhalation and buccal/sublingual exposure as potentially important pathways, particularly for children and competitive swimmers.
Research significance
The evidence supports an exposure-prevention hypothesis rather than a cancer-treatment hypothesis: improved ventilation and reduction of TCAA precursors may lower modeled disinfection-byproduct exposure, but whether these measures reduce cancer incidence or other clinical outcomes was not tested.
Source abstract
Disinfection of swimming pools is essential for preventing waterborne diseases; however, reactions between disinfectants and organic/inorganic precursors lead to the formation of disinfection byproducts (DBPs). Swimmers are exposed to these compounds through dermal contact, inhalation, accidental ingestion, and buccal/sublingual uptake. This study evaluated carcinogenic and chronic toxic risks associated with chloroform (CF), dichloroacetic acid (DCAA), and trichloroacetic acid (TCAA) using annual monitoring data from two indoor pools with contrasting operational characteristics (SP-A and SP-B). Results showed that inhalation of CF was the dominant carcinogenic pathway, consistently exceeding the de minimis level in all swimmer groups, particularly competitive swimmers. Oral pathways dominated HAA-related cancer risk, with TCAA producing the highest ingestion-route risks and exceeding the de minimis in competitive swimmers, reaching the low-priority risk range in SP-B. Dermal carcinogenic risks were considerable for CF, while DCAA and TCAA remained negligible owing to their low dermal permeability. Importantly, the buccal/sublingual route, often ignored in DBP assessments, yielded risks comparable to accidental ingestion, especially for children and high-intensity swimmers. Non-cancer risks associated with the estimated water-contact exposure routes were generally below the threshold. However, dermal exposure to CF in SP-B exceeded the threshold under some upper-bound and worst-case scenarios. Because non-cancer risks via the inhalation route could not be estimated due to the lack of an available reference concentration (RfC), non-cancer risks may be underestimated, as inhalation exposure was excluded from the assessment. In addition, both cancer and non-cancer risks may be further underestimated because only targeted DBPs were considered, whereas potential contributions from non-targeted and unidentified DBPs were not included in the risk assessment. Overall, DBP-related risks were higher in SP-B, emphasizing the influence of pool chemistry, bather load, and ventilation. These findings highlight the need for regular multi-route-specific risk assessment especially for competitive athletes and improved operational controls, particularly reducing TCAA precursors and enhancing ventilation for CF.