Ultraviolet (UV) irradiation is commonly applied as a secondary disinfection process in chlorinated pools. UV-based systems have been reported to yield improvements in swimming pool water and air chemistry, but to date these observations have been largely anecdotal. The objectives of this investigation were to evaluate the effects of UV irradiation on chlorination of important organic-N precursors in swimming pools.Creatinine, L-arginine, L-histidine, glycine, and urea, which comprise the majority of the organic-N in human sweat and urine, were selected as precursors for use in conducting batch experiments to examine the time-course behavior of several DBPs and residual chlorine, with and without UV254 irradiation. In addition, water samples from two natatoria were subjected to monochromatic UV irradiation at wavelengths of 222 nm and 254 nm to evaluate changes of liquid-phase chemistry. UV254 irradiation promoted formation and/or decay of several chlorinated N-DBPs and also increased the rate of free chlorine consumption. UV exposure resulted in loss of inorganic chloramines (e.g., NCl3) from solution. Dichloromethylamine (CH3NCl2) formation from creatinine was promoted by UV exposure, when free chlorine was present in solution; however, when free chlorine was depleted, CH3NCl2 photodecay was observed. Dichoroacetonitrile (CNCHCl2) formation (from L-histidine and L-arginine) was promoted by UV254 irradiation, as long as free chlorine was present in solution. Likewise, UV exposure was observed to amplify cyanogen chloride (CNCl) formation from chlorination of L-histidine, L-arginine, and glycine, up to the point of free chlorine depletion. The results from experiments involving UV irradiation of chlorinated swimming pool water were qualitatively consistent with the results of model experiments involving UV/chlorination of precursors in terms of the behavior of residual chlorine and DBPs measured in this study.The results indicate that UV254 irradiation promotes several reactions that are involved in the formation and/or destruction of chlorinated N-DBPs in pool settings. Enhancement of DBP formation was consistent with a mechanism whereby a rate-limiting step in DBP formation was promoted by UV exposure. Promotion of these reactions also resulted in increases of free chlorine consumption rates.
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