The disinfection by-products dichloro-, dibromo-, and bromochloroacetic acid impact intestinal microflora and metabolism in Fischer 344 rats upon exposure in drinking water

Human consumption of chlorinated drinking water has been linked epidemiolog ically to bladder, kidney, and rectal cancers. The disinfection by-product (DBP) dichloroacetic acid is a hepatocarcinogen in Fischer 344 rats and B6C 3F1 mice. The objective of this study is to determine the effect of the DBP s dichlorobromochloro-, and dibromoacetic acids (DCA, BCA, DBA) on intestin al microbial populations and their metabolism, with emphasis on enzymes inv olved in the bioactivation of procarcinogens and promutagens. One-month-old male Fischer 344 rats were provided water ad libitum containing 1 gn DCA, BCA, or DBA for up to 5 weeks. At 1, 3, and 5 weeks of treatment, beta-gluc uronidase (GLR), beta-galactosidase (GAL), beta-glucosidase (GLU), nitrored uctase (NR), azoreductase (AR), and dechlorinase (DC) activities were deter mined in cecal and small and large intestinal homogenates. After 5 weeks of treatment, intestinal populations were enumerated on selective media. Ceca l GAL (DCA, BCA, DBA) and GLR (DCA, DBA) activities were reduced after 1 an d 3 weeks of treatment and GAL activity was elevated at 5 weeks (BCA). Larg e intestinal GAL (DCA, BCA) and GLU (DCA, BCA, DBA) activities were elevate d after 5 weeks of treatment. Week 5 cecal AR (DCA, BCA, DBA), NR (DCA), an d DC (DCA, DBA) activities were reduced. Even though some significant chang es in intestinal populations were observed, use of selective media was not sensitive enough to explain fluctuations in enzyme activity. Haloacetic aci ds in the drinking water alter intestinal metabolism, which could influence bioactivation of promutagens and procarcinogens in the drinking water.