Academic journal article Environmental Health Perspectives

Bladder Cancer and Water Disinfection By-Product Exposures through Multiple Routes: A Population-Based Case-Control Study (New England, USA)

Academic journal article Environmental Health Perspectives

Bladder Cancer and Water Disinfection By-Product Exposures through Multiple Routes: A Population-Based Case-Control Study (New England, USA)

Article excerpt

Introduction

Disinfection by-products (DBPs) are formed when organic constituents in source water react with chlorine or other disinfecting agents. Trihalomethanes (THMs), the most common of the DBPs, were first discovered in the 1970s (Bellar and Lichtenberg 1974; Rook 1974), and hundreds of DBP species have been identified since. The by-products formed when water is treated depend on many factors, including the specific disinfection processes used (e.g., chlorination, ozonation, chloramination, use of chlorine dioxide), levels of naturally occurring organic material and anthropogenic compounds, and other characteristics of the raw water such as temperature, pH, and bromide concentration (Richardson et al. 2007). In the United States, three chemical classes of DBPs are regulated: total THMs (chloroform, bromoform, bromodichloromethane, and chlorodibromomethane), haloacetic acids (HAA), and oxyhalides (U.S. EPA 1998). Since the identification of THMs, several studies have reported that exposure to chlorinated water is positively associated with bladder cancer (Villanueva et al. 2004). In its 1991 review, the International Agency for Research on Cancer (IARC) determined that there was inadequate evidence to characterize the use of chlorinated drinking water as carcinogenic to humans (IARC 1991) and that some individual compounds are not classifiable with regard to their carcinogenicity (bromoform, chlorodibromomethane). In addition, IARC has not classified any individual DBPs as Group 1 human carcinogens, although several have been classified as possible [Group 2B; specifically, dichloroacetic acid, trichloroacetic acid, dibromoacetic acid, bromochloroacetic acid, and Mutagen X (MX; 3-chloro-4-(dichloromethyl)-5hydroxy-5H-furan-2-one)] or probable (Group 2A; specifically, chloral and chloral hydrate) human carcinogens (IARC 1999, 2004, 2013). Additional epidemiologic studies published in the last decade are supportive of an exposure-response relationship between THM exposure and bladder cancer risk, with associations apparently stronger in men than in women (Costet et al. 2011; Villanueva et al. 2004, 2007). In its 2001 toxicological review of chloroform, the most common THM, the U.S. EPA noted that the majority of mutagenicity assays were negative and concluded that positive assays may have been an indirect consequence of cytotoxicity and cell regeneration in response to high exposures rather than a direct genotoxic effect (U.S. EPA 2001). Brominated THMs have been shown to be mutagenic when activated by glutathione S-transferase theta 1 (GSTT1), in contrast to chloroform, which is not activated to a mutagen (Richardson et al. 2007). These brominated compounds are formed when the levels of bromide are high in the source water, and recent reports from water utilities have suggested increasing levels of brominated THMs in in the United States (Regli et al. 2015).

DBPs encompass a wide and expanding list of compounds to which humans might be exposed (Richardson et al. 2007). THM levels in water supplies have been regulated longer than other classes of DBPs; thus, data are more readily available to estimate past exposures to total THMs than other classes of DBPs, and total THMs are often used as a surrogate measure of overall DBP exposures in epidemiologic studies. However, total THMs may not represent the most etiologically relevant DBP exposures.

Beyond considering THM level, route of exposure has been of increasing interest in epidemiologic studies of DBPs. Until recently, ingestion was the major focus in most epidemiologic studies (Costet et al. 2011; Villanueva et al. 2004). Other routes of exposure such as inhalation or dermal absorption may be important for the volatile, nonpolar constituents (Richardson et al. 2007). Showering, bathing, and use of chlorinated or brominated swimming pools likely represent important sources of these exposures (Richardson et al. 2010). To our knowledge, only one study has examined the association between bladder cancer and DBP exposures resulting from showering, bathing, or swimming pool use. …

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