The epidemiology and possible mechanisms of disinfection by-products in drinking water.Major limitations in exposure assessment, small sample sizes and potential biases may account for the inconclusive and inconsistent results in epidemiological studies.

Philos Trans A Math Phys Eng Sci. 2009 Oct 13;367(1904):4043-76. doi: 10.1098/rsta.2009.0116. The epidemiology and possible mechanisms of disinfection by-products in drinking water. Nieuwenhuijsen MJ, Grellier J, Smith R, Iszatt N, Bennett J, Best N, Toledano M. SourceCentre for Research in Environmental Epidemiology (CREAL), Parc de Recerca Biomèdica de Barcelona-PRBB (Office 183.05), , C. Doctor Aiguader, 88, 08003 Barcelona, Spain. mnieuwenhuijsen@creal.cat Abstract This paper summarizes the epidemiological evidence for adverse health effects associated with disinfection by-products (DBPs) in drinking water and describes the potential mechanism of action. There appears to be good epidemiological evidence for a relationship between exposure to DBPs, as measured by trihalomethanes (THMs), in drinking water and bladder cancer, but the evidence for other cancers including colorectal cancer is inconclusive and inconsistent. There appears to be some evidence for an association between exposure to DBPs, specifically THMs, and little for gestational age/intrauterine growth retardation and, to a lesser extent, pre-term delivery, but evidence for relationships with other outcomes such as low birth weight, stillbirth, congenital anomalies and semen quality is inconclusive and inconsistent. Major limitations in exposure assessment, small sample sizes and potential biases may account for the inconclusive and inconsistent results in epidemiological studies. Moreover, most studies have focused on total THMs as the exposure metric, whereas other DBPs appear to be more toxic than the THMs, albeit generally occurring at lower levels in the water. The mechanisms through which DBPs may cause adverse health effects including cancer and adverse reproductive effects have not been well investigated. Several mechanisms have been suggested, including genotoxicity, oxidative stress, disruption of folate metabolism, disruption of the synthesis and/or secretion of placental syncytiotrophoblast-derived chorionic gonadotropin and lowering of testosterone levels, but further work is required in this area.