A review on the 40th anniversary of the first regulation of drinking water disinfection by-products

Abstract

Water disinfection, primarily by chlorination, is one of the greatest achievements of public health. However, more than half a century after its introduction, studies in the 1970s reported that (a) chlorine interacted with organic matter in the water to form disinfection by-products (DBPs); (b) two DBPs, chloroform and bromoform, both trihalomethanes (THMs), were rodent carcinogens; (c) three brominated THMs were mutagenic; in six studies chlorinated drinking waters in the United States and Canada were mutagenic; and (d) in one epidemiological study there was an association between bladder cancer mortality and THM exposure. This led the U.S. Environmental Protection Agency to issue its first DBP regulation in 1979. Forty years later, >600 DBPs have been characterized, 20/22 have been shown to be rodent carcinogens, >100 have been shown to be genotoxic, and 1000s of water samples have been found to be mutagenic. Data support a hypothesis that long-term dermal/inhalation exposure to certain levels of the three brominated THMs, as well as oral exposure to the haloacetic acids, combined with a specific genotype may increase the risk for bladder cancer for a small but significant population group. Improved water-treatment methods and stricter regulations have likely reduced such risks over the years, and further reductions in potential risk are anticipated with the application of advanced water-treatment methods and wider application of drinking water regulations. This 40-year research effort is a remarkable example of sustained cooperation between academic and government scientists, along with public/private water companies, to find answers to a pressing public health question.

Keywords: carcinogenicity; drinking water; genotoxicity; mutagenicity; swimming.

Figure 1.

Data from DeMarini et al. (1995a, 1997) and Kundu et al. (2004). Mutation spectra were determined at the hisG46 base-substitution allele in Salmonella TA100, except for those DBPs evaluated in the presence of GSTT1–1, where strain RSJ100 was used. RSJ100 expresses the rat GSTT1–1 gene and is a derivative of strain TA1535, which is the parent strain of TA100. All data were generated in the absence of metabolic activation (S9 mix). OZ H₂O, ozonated water; MX, mutagen X [3-chloro-4-(dichloromethyl)-5-hydroxy-2(5H)-furanone]; Cl H₂O, chlorinated water; CHN H₂O, chloraminated water; DBM, dibromomethane; BCM, bromochloromethane; at BCNM, bromochloronitromethane; DCA, dichloroacetic acid; CNM, chloronitromethane; TBM, tribromomethane; BDCM, bromodichloromethane; and DBCM, dibromochloromethane.

Figure 2.

A hypothesis for the induction of bladder cancer from primarily the brominated THMs and haloacetic acids in drinking water (Cantor et al. 2010; Regli et al. 2015). No mutations would be induced via the oral route if the DBPs were inactivated by CYP2E1. GC to AT mutations are the predominant base-substitution mutation found in bladder tumors of non-smokers (Alexandrov et al. 2016).