The Drinking Water and Swimming Pool Disinfectant Trichloroisocyanuric Acid Causes Chlorination Stress Enhancing Solar UV-Induced Inflammatory Gene Expression in AP-1 Transgenic SKH-1 Luciferase Reporter Mouse Skin.

Abstract

Freshwater sanitation and disinfection using a variety of chemical entities as chlorination agents is an essential public health intervention ensuring water safety for populations at a global scale. Recently, we have published our observation that the small molecule oxidant, innate immune factor and chlorination agent HOCl antagonize inflammation and photocarcinogenesis in murine skin exposed topically to environmentally relevant concentrations of HOCl. Chlorinated isocyanuric acid derivatives (including the chloramines trichloroisocyanuric acid [TCIC] and dichloroisocyanuric acid [DCIC]) are used worldwide as alternate chlorination agents serving as HOCl precursor and stabilizer compounds ensuring sustained release in aqueous environments including public water systems, recreational pools and residential hot tubs. Here, for the first time, we have examined the cutaneous TCIC-induced transcriptional stress response (in both an organotypic epidermal model and in AP-1 luciferase reporter SKH-1 mouse skin), also examining molecular consequences of subsequent treatment with solar ultraviolet (UV) radiation. Taken together, our findings indicate that cutaneous delivery of TCIC significantly enhances UV-induced inflammation (as profiled at the gene expression level), suggesting a heretofore unrecognized potential to exacerbate UV-induced functional and structural cutaneous changes. These observations deserve further molecular investigations in the context of TCIC-based freshwater disinfection with health implications for populations worldwide.