Pool party poopers: Swimmers and pool workers exposed to haloacetic acids

Safe swimming

Swimming is one popular form of activity which people undertake to keep healthy, while many young people take to the water just to have fun. Either way, the exercise is beneficial to all taking part. However, swimming in pools is not without its hazards.

The chlorinating agents that are used to disinfect the water produce several series of unwanted by-products which can be harmful to humans if their concentrations are allowed to rise. Trihalomethanes and nitrosomethanes are both classified as carcinogens, and a third group, the haloacetic acids (HAAs), are carcinogenic, neurotoxic and cytotoxic.

The World Health Organization has set guidelines for mono-, di- and trichloroacetic acid (MCAA,DCAA, TCAA) at 20, 50 and 200 µg/L in drinking water but they tend to be unregulated in swimming pools. This is despite the fact that they have been measured at up to 800 µg/L in pools compared with normal levels of up to 100 µg/L in drinking water.

In fact, there have been very few studies of human exposure to HAAs in households or in swimming pools, according to a duo of Spanish researchers at the University of Cordoba, Spain. So, Mercedes Gallego and Maria Jose Cardador set out to conduct a detailed study examining the exposure of swimmers and workers to HAAs in indoor and outdoor pools.

Probing pool people

The subjects were 24 pool workers, 19 swimmers and 6 researchers who agreed to drink mineral water only to avoid exposure to drinks containing chlorinated water. This was necessary because the sampling medium was urine, which would be influenced by any other sources of HAAs apart from the pool water.

To begin with, the team studied the kinetics of HAA elimination from urine, using MCAA, DCAA and TCAA as biomarkers of HAAs, since they are known to be detectable in swimmers' urine. Samples from 4 swimmers and 4 workers were collected before exposure and at intervals following the end of exposure for analysis by headspace GC/MS.

The urine was mixed with tetrabutylammonium hydrogen sulphate, which formed ion pairs with the haloacetate anions that were solvent-exchanged with pentane. The anions were converted to their methyl esters by reaction with dimethyl sulphate in the pentane phase for analysis.

The GC/MS detection limits were 0.01-0.1 µg/L, well below the current recommended levels of HAAs in drinking water, and the relative standard deviations of the method were good at 8%.

No HAAs were detected in the urine samples before exposure at the pools. The most abundant HAA in the urine of swimmers was TCAA whereas that for workers was DCAA.

The difference reflects the principal routes of exposure, ingestion for swimmers and inhalation for workers. TCAA is the most concentrated congener in the pool water but DCAA was calculated to be the most abundant in aerosol droplets.

The biological half-lives of the acids were similar for swimmers and workers, at 60-70 minutes. For normal exposure levels, the concentrations of HAAs in urine fell below the detection limits within 3 hours.

Ingestion, inhalation or dermal absorption

The different exposure routes were examined more closely, using three different experiments. In the first place, 6 researchers sat near the edge of the indoor pool reading or working on a pc, ensuring minimal physical activity. They were dressed in lab coats and trousers with only their faces uncovered, so that inhalation was the only HAA route.

In the second experiment, the six subjects walked around in the pool for one hour with their heads above water, using sufficient energy to simulate swimming and permit exposure by inhalation and dermal absorption.

In the third phase, the subjects swam for one hour to activate all three of the exposure routes: inhalation, dermal absorption and ingestion.

MCAA was detected following ingestion only. The urinary levels of TCAA, DCAA and MCAA were 4400, 2300 and 560 ng/L, respectively, after swimming, and the proportions were 94, 5 and 1% for ingestion, inhalation and dermal exposure, respectively. There were no significant differences between the HCAA levels of swimmers in indoor and outdoor pools.

The HAA levels in workers' urine were always far lower than swimmers, with DCAA and TCAA levels at 300 and 120 ng/L, respectively, by the indoor pool. The outdoor levels were much lower and only DCAA was found in the urine of some workers.

The levels for workers were far higher for the indoor pool than the outdoor pool. This was attributed to the dissipation of aerosol droplets in the air outdoors compared with their accumulation indoors and was supported by the fact that none of the workers was in direct contact with the water during their shift, rendering inhalation the only possible exposure route.

This is the first study comparing the exposure of swimmer and workers to HAAs in indoor and outdoor pools. They are regarded as the part of the population that is most exposed to HAAs generated by water chlorination and the results will be useful in estimating the health risks associated with attendance at swimming pools.

The views represented in this article are solely those of the author and do not necessarily represent those of John Wiley and Sons, Ltd.