Academic journal article Journal of Environmental Health

Mutagenicity and Genotoxicity of Water Treated for Human Consumption Induced by Chlorination By-Products

Academic journal article Journal of Environmental Health

Mutagenicity and Genotoxicity of Water Treated for Human Consumption Induced by Chlorination By-Products

Article excerpt

Introduction

Most of the routine analyses performed for drinking water quality are focused on physicochemical and microbiological tests. Based on these analyses, some criteria for water used for human consumption have been established. In this way, with the introduction of water disinfection, the population can be ensured that their drinking water is likely to be free of waterborne infectious diseases (Boorman et al., 1999). Alternatives methodologies exist, but none of them offers continuous protection against pathogens through the distribution network.

Since the 1970s, a new risk for human health appeared in drinking water, as findings showed that it can contain mutagenic and carcinogenic compounds known as disinfection by-products (DBPs) (Hemming, Holmbom, Reunanen, & Kronberg, 1986; Kusamran et al., 1994; Meier, Blazak, & Knohl, 1987). When chlorine reacts with humic and fulvic acids present naturally in the water, it can produce several compounds such as trihalomethanes, halofuranes, haloacetic acids, halophenols, halopropanones, and others that are well known for their mutagenic and carcinogenic properties (Langvik & Holmbom, 1994; Richardson, Although most of the information presented in the Journal refers to situations within the United States, environmental health and protection know no boundaries. The Journal periodically runs International Perspectives to ensure that issues relevant to our international membership, representing over 20 countries worldwide, are addressed. Our goal is to raise diverse issues of interest to all our readers, irrespective of origin. Plewa, Wagner, Schoeny, & DeMarini, 2007; Richardson, Simmons, & Rice, 2002; Shi et al., 2009). A large number of those compounds have been isolated from chlorinated waters (McDonald & Komulainen, 2005; Richardson et al., 2007). The trihalomethanes (THMs) include chloroform (CH[Cl.sub.3]), dibromochloromethane (CH[Br.sub.2]Cl), bromodichloromethane (CHBr[Cl.sub.2]), and bromoform (CH[Br.sub.3]); these compounds represent between 5% and 20% of the total DBPs (Fayad, 1993).

Other compounds with similar properties have been identified and quantified in chlorinated water, and it is believed that they are responsible for the rest of the mutagenic activity. Within the compounds detected are the haloacetic acids (HAAs) (Krasner et al., 2006) and chlorohydroxyfuranones (MXs) (Kronberg & Vartiainen, 1988; Smeds, Vartiainen, Maki-Paakkanen, & Kronberg, 1997). Hemming and co-authors (1986) identified and quantified 3-chloro-4-(dichloromethyl)5-hydroxy-2(5H)-furanone (MX), one of the most potent bacterial mutagens that is the product of the reaction of chlorine with the organic material present in water. Figure 1 shows the structure of MX and its open isomeric forms, Z-MX ([Z]-2-chloro-4-[dichloromethyl]-4-oxo-butenoic acid) and E-MX ([E]-2-chloro-3-[dichloromethyl]4-oxobutenoic acid) (Franzen & Kronberg, 1994; Richardson et al., 2007).

MX can be found at low levels (2-310 ng/L) in drinking water (Kronberg, Christman, Singh, & Ball, 1991; McDonald & Komulainen, 2005; Wright et al., 2002). It has been estimated, however, that this compound may contribute about 3% to 67% of the total mutagenicity of chlorinated waters, inducing a wide spectrum of mutations in bacterial and mammalian cells (Hyttinen, Myohanen, & Jansson, 1996; Jansson & Hyttinen, 1994; Maki-Paakkanen & Hakulinen, 2008; Wright et al., 2002). In Salmonella typhimurium strains TA100 and TA102, MX induces damage of the DNA by base-pair substitution (Hemming et al., 1986; Kronberg & Vartiainen, 1988) and in Salmonella typhimurium TA98, a bacterial strain sensitive to frameshift mutations, MX produces loss or gain of a pair of bases (DeMarini, AbuShakra, Felton, Patterson, & Shelton, 1995). TA98 and TA100 have been widely used to test a numerous series of chemical mutagens and carcinogens.

MX also induced a wide variety of DNA damage in mammalian cells in vitro (Jansson & Hyttinen, 1994; Maki-Paakkanen & Hakulinen, 2008) including human cells (Chang, Daniel, & Deangelo, 1991) such as sister chromatid exchange (SCE), chromosomal aberrations (Hyttinen et al. …

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