Disinfection Byproducts: The Next
Generation SUSAN D. RICHARDSON, JANE
ELLEN SIMMONS,
AND GLENN RICE
There are still compounds to identify, and new data indicate that already known DBPs may pose additional health risks.
D
PHOTO COURTESY OF SUSAN D. RICHARDSON
isinfection of drinking water is rightly hailed as a major public health triumph of the 20th century. Before its widespread use, millions of people died from typhoid, cholera, and other infectious waterborne diseases. Disinfection targeted the microbial pathogens causing these diseases, and deaths attributable to these waterborne pathogens virtually ceased in developed nations (1). Recent outbreaks of Escherichia coli-induced gastroenteritis (Walkerton, Ontario, 2000), cryptosporidiosis (Milwaukee, Wisc., 1993), and cholera (Peru beginning in 1991) serve as dramatic reminders of the need to properly disinfect drinking water and continually reevaluate and improve disinfection techniques. Although pathogenic organisms provide the primary human health risk from drinking water, chemical disinfection byproducts (DBPs) are another, albeit unintended, health hazard. Disinfectants are powerful oxidants that convert organic matter and naturally occurring bromide in source waters to DBPs. Chlorine, ozone, chlorine dioxide, and chloramine are the most common disinfectants in use today, and each produces its own suite of chemical DBPs in drinking water (2). Most developed nations regulate or control DBPs to minimize consumers’ exposure to © 2002 American Chemical Society
hazardous compounds, while maintaining adequate disinfection and control of targeted pathogens. As such, developed nations often have the opportunity to evaluate the nature and magnitude of human health risks posed by DBPs and implement changes in drinking water treatment when necessary. This has led to research on and use of alternative disinfection strategies. In this article, we review the current status of DBP research, describing new human epidemiological, animal toxicological, and occurrence data, as well as new research efforts to identify additional compounds. We also outline arenas for future work.
Isn’t this problem solved? In 1974, Rook identified the first DBPs—chloroform and the other trihalomethanes (THMs)—in chlorinated drinking water (3). Two years later, the U.S. EPA published a national survey that showed that chloroform and the other THMs were ubiquitous in chlorinated drinking water (4). That same year, the National Cancer Institute (NCI) published results linking chloroform to cancer in laboratory animals (5). An important public health and regulatory issue was born. Today, many drinking water utilities are switching from chlorine to alternative disinfectants such as ozone, chlorine dioxide, and chloramine to comply with regulations (6, 7) controlling THMs and haloacetic acids (HAAs) (see sidebar on the next page), but this has created new issues. Source water conditions, including bromide, iodide, and natural organic matter (NOM) concentrations, and pH, can affect the levels and types of DBP species formed. For example, ozone use can significantly reduce or eliminate THM and HAA formation; however, it can produce bromate—a potent carcinogen in laboratory animals (8)—in source waters with elevated bromide levels. Another concern is that although ~500 DBPs are known (2), few have been investigated for their quantitative occurrence and health effects. DBPs that have been quantified in drinking water are generally present at nanogram to microgram per liter (µg/L or parts-per-billion [ppb]) levels. Until recently, health effects studies were directed primarily toward linkMAY 1, 2002 / ENVIRONMENTAL SCIENCE & TECHNOLOGY
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ing chronic DBP exposure and cancer initiation or mutagenicity. Moreover, there are still unknown DBPs; only ~50% of total organic halide (TOX) formed during drinking water chlorination has been identified (9). Studies are under way to uncover the missing DBP fraction, such as unidentified TOX and assimilable organic carbon (AOC) compounds in ozonated drinking water. As a
Controlling DBP exposure Following the identification of DBPs in drinking water, EPA issued a regulation in 1979 to control THMs at 100 µg/L (ppb) in drinking water (6 ). Subsequently, in 1998, the Stage 1 Disinfectants/Disinfection By-products (D/DBP) Rule was promulgated, lowering permissible levels of THMs to 80 µg/L and regulating five of the HAAs, bromate, and chlorite for the first time (Table 1) (7). Stage 1 regulations are based on running annual averages—averages of all samples collected in a utility’s distribution system over a one-year period. The Rule took effect January 1, 2002. TA B L E 1
DBPs regulated under the Stage 1 D/DBP Rule DBP
MCL (mg/L)
Total THMsa HAAsb Bromate Chlorite
0.080 0.060 0.010 1.0
aTotal
THMs are the sum of the concentrations of chloroform, bromoform, bromodichloromethane, and dibromochloromethane. bThe HAAs are the sum of monochloro-, dichloro-, trichloro-, monobromo, and dibromoacetic acids. Source:Reference (7).
Stage 2 D/DBP Rule, to be proposed in 2002, will maintain the Stage 1 Rule maximum contaminant levels (MCLs) for THMs and HAAs, but will require that MCLs for THMs and HAAs be based on locational running annual averages—each location in the distribution system will need to comply on a running annual average basis. The change arises because the running annual averages used with the Stage 1 D/DBP Rule permitted some locations within a water distribution system to exceed MCLs, as long as the average of all sampling points did not exceed the MCLs. As a result, some consumers could receive water that regularly exceeded the MCLs. The Stage 2 D/DBP Rule targets those higher DBP levels and reduces the variability of exposure within a distribution system. Although the Stage 2 D/DBP Rule will maintain the MCLs for bromate and chlorite, EPA plans to re-examine the bromate MCL as part of its six-year review process.
result, new research is focusing on highly polar, highmolecular-weight compounds. In addition, epidemiological studies are raising new concerns about DBPs’ effects on reproduction and development, including low birth weight, intrauterine growth retardation, and spontaneous abortion. Generally, these studies only can show a correlation between exposure and health effects, not 200 A
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causality. Moreover, it is difficult to assess a consumer’s exposure to DBPs or mixtures of DBPs, which creates additional uncertainties in these epidemiological studies. Currently available single-chemical studies with animals cannot alone explain the adverse health effects observed in some epidemiological studies. Thus, toxicological investigations of DBP mixtures are needed. Other routes of exposure are now being recognized as significant. For example, recent work shows that a person showering or bathing can receive twice the exposure to THMs as ingesting 2 L of water (10). New human exposure work is also being conducted in which blood and urine are being monitored for DBP exposures (11−15). Numerous workshops and conferences have been organized to address the new concerns about DBPs. These include a Health Canada-sponsored conference on assessing exposure in epidemiological studies of DBPs in 2000; the International Society of Exposure Analysis symposium on new DBP exposure and epidemiological studies in 2000; an international conference entitiled “Disinfection By-products: The Way Forward” in 1998; an American Water Works Association symposium on microbial and DBP health effects in 2000; an International Life Sciences Institute workshop on the health effects of DBPs in 1995; “Balancing Chemical and Microbial Risks of DBPs” in 1993 and 1999; “Identification of New and Uncharacterized DBPs” in 1998; and an EPA-sponsored workshop called “Risk Assessment of DBPs and Considering Unidentified DBPs” in 2000.
Epidemiological and human exposure studies Of the recently conducted epidemiological studies, Swan and Waller’s 1998 study of spontaneous abortions for more than 5000 pregnant women in California probably attracted the most attention (16, 17). One test group consumed tap water high in THMs (≥75 µg/L) but within EPA’s regulatory limits; another consumed water lower in THMs (500 Da, ~30% had an apparent molecular weight of 500–3000 Da, and ~8% had an apparent molecular weight >10,000 Da. Although it is nearly impossible to precisely identify a compound with a molecular weight
>1000 Da using current analytical tools, toxicologists often assume that compounds above ~5000 Da are probably not absorbed in the body and may not be important from a toxicological standpoint. This remains to be determined experimentally. Moreover, it is unknown whether human enzymes or acid-catalyzed hydrolysis might break these large molecules into smaller ones that could be absorbed. Although analysis of the unidentified, high-molecular-weight (>1000 Da) fraction is daunting, University of Illinois and the Metropolitan Water District of Southern California researchers have designed studies to address the issue (59). To improve the detection of this high-molecular-weight TOX, labeling studies are being carried out using 36Cl-labeled chlorine with analysis of the DBPs using ultrafiltration/size exclusion chromatography, electrospray ionization MS, and MS/MS. FIGURE 1
Missing DBPs The two pie charts show (a) the relative amounts of halogenated DBPs as a proportion of total organic halides in chlorinated drinking water from a representative chlorination plant and (b) the relative amounts of ozone DBPs in drinking water from an ozone demonstration plant as a proportion of the total assimilable organic carbon, which clearly indicate that a large fraction of DBPs is not identified. Chlorine DBPs Trihalomethanes Cyanogen chloride 20.1% 1% Haloacetonitriles 2% Unknown Chloral hydrate organic 1.5% halogen Sum of five 62.4% haloacetic acids 10%
(a)
Bromochloroacetic acid 2.8% Ozone DBPs Aldehydes Aldoketoacids 4% 7% Carboxylic acids 26%
Unknown assimilable organic carbon 63%
(b) Source: Adapted from data collected by Stuart W. Krasner, Metropolitan Water District of Southern California, Los Angeles, Calif.
Reducing DBPs Mainly because of stricter DBP regulations, efforts have been made to minimize certain compounds before, during, or after disinfectant treatment. Enhanced coagulation, which is used at many utilities, removes precursor NOM before disinfection. Although all of the NOM is not removed, this practice reduces DBP levels. Advanced precursor removal technologies include granular activated carbon (GAC) and memMAY 1, 2002 / ENVIRONMENTAL SCIENCE & TECHNOLOGY
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branes—nanofiltration or reverse osmosis. Because enhanced coagulation and GAC do not remove bromide, the bromide/NOM ratio is higher in treated water and can shift DBP formation to more brominated compounds. Membranes such as reverse osmosis and, to varying extents, nanofiltration can remove bromide. During treatment, the type of disinfectant can be changed (e.g., from chlorine to chloramine or another alternative) to alter the levels of THMs and HAAs. Current researchas part of the Nationwide DBP Occurrence Studyis showing that alternative disinfectants are better at controlling THMs and trihalogenated HAAs than dihalogenated HAAs and other DBPs of health concern (38). In fact, the highest levels of iodinated THMs occurred at a plant using chloramination with no prechlorination, and the highest concentration of dichloroacetaldehyde occurred at a plant using chloramine and ozone (38). Additionally, concentrations of trihalonitromethanes—including brominated species—appear to be increased by preozonation. At the end of the treatment, biologically active filters can be used to remove AOC, which includes aldehydes, ketones, and carboxylic acids, and certain HAAs. Because the presence of AOC in the distribution system promotes bacterial regrowth, many ozone drinking water treatment plants use biological filtration to remove this material. Greater opportunities to make drinking water as safe as possible for all consumers will come with improved understanding of formation, exposure, and health risk issues associated with DBPs. It is hoped that the next generation of DBP research will answer new questions raised by recent epidemiological studies and resolve older questions regarding the possible carcinogenicity of DBPs. Ultimately, the aim is to improve capabilities for minimizing drinking water pathogen risks, while minimizing any chemical DBPs that may pose unintended human health risks.
Acknowledgments The authors thank StuartW. Krasner of the Metropolitan Water District of Southern California, Pat Fair of EPA’s Office of Water in Cincinnati, and Linda Teuschler of EPA’s National Center for Environmental Assessment in Cincinnati for valuable input on this paper. We also gratefully acknowledge Rex Pegram, Dave Thomas, and Glenn Suter for their manuscript review. This paper has been reviewed in accordance with the EPA’s peer and administrative review policies and approved for publication. Mention of trade names or commercial products does not constitute endorsement or recommendation for use by EPA.
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Susan D. Richardson is a research chemist at the U.S. EPA’s National Exposure Research Laboratory in Athens, GA, and the leader of the Nationwide DBP Occurrence Study. Her research focuses on the identification of new DBPs, with special emphasis on alternative disinfectants and polar byproducts. Jane Ellen Simmons is a toxicologist at the U.S. EPA’s National Health and Environmental Effects Research Laboratory in Research Triangle Park, NC, and project coordinator for the Integrated DBPs Research Project to evaluate complex mixtures of DBPs. Glenn Rice is an environmental health scientist at the U.S. EPA’s National Center for Environmental Assessment in Cincinnati, OH. His research interest is human health risk assessment.
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