Liu_2025_Environ.Toxicol.Chem__

Halogenated disinfection byproducts are contaminants in drinking water that pose a significant public health concern. The intestine is particularly susceptible to the effects of disinfection byproducts through oral ingestion; however, the intestinal toxicity of these compounds remains largely unexplored. This study aimed to assess the impact of ten haloacetic acids, a major class of drinking water disinfection byproducts, on intestinal barrier function using Caenorhabditis elegans as a model animal. Additionally, changes in the expression of five genes related to intestinal barrier function (mucin-like gene (mul-1), zonula occludens ortholog gene (zoo-1), gut esterase 1 gene (ges-1), cytochrome P450 gene (cyp13a7), and saposin-like protein family gene (spp-5)) were examined using quantitative real-time polymerase chain reaction. Among the investigated haloacetic acids (chloroacetic acid, bromoacetic acid, iodoacetic acid, dibromoacetic acid, dichloroacetic acid, bromochloroacetic acid, bromodichloroacetic acid, dibromochloroacetic acid, trichloroacetic acid, and tribromoacetic acid), exposure to five haloacetic acids (dichloroacetic acid, bromodichloroacetic acid, dibromochloroacetic acid, trichloroacetic acid, and tribromoacetic acid) could lead to significant disruption of the intestinal barrier, as evidenced by the induced increase in intestinal permeability in C. elegans. The order of enterotoxicity, based on assessments of intestinal permeability, is trichloroacetic acid > bromodichloroacetic acid = dibromochloroacetic acid = tribromoacetic acid > dichloroacetic acid. These five compounds suppressed the expression of both the tight junction (zoo-1) and xenobiotic-metabolising (ges-1) genes, suggesting that these two genes may be of vital importance in haloacetic acid-induced intestinal toxicity. This work contributes to improving the available knowledge on the toxicity of haloacetic acids and provides a basis for understanding their mechanism of intestinal toxicity.