Granular Activated Carbon Treatment May Result in Higher Predicted

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Granular Activated Carbon Treatment May Result in Higher Predicted Genotoxicity in the Presence of Bromide Stuart W. Krasner, Tiffany Chih Fen Lee, Paul Westerhoff, Natalia Fischer, David Hanigan, Tanju Karanfil, Wilson Beita-Sandi, Liz Taylor-Edmonds, and Robert C. Andrews Environ. Sci. Technol., Just Accepted Manuscript • DOI: 10.1021/acs.est.6b02508 • Publication Date (Web): 28 Jul 2016 Downloaded from http://pubs.acs.org on August 2, 2016

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Environmental Science & Technology

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Granular Activated Carbon Treatment May Result in Higher Predicted Genotoxicity in the

2

Presence of Bromide

3 4

Stuart W. Krasner*,†, Tiffany Chih Fen Lee†, Paul Westerhoff‡, Natalia Fischer‡, David

5

Hanigan‡‡, Tanju Karanfil§, Wilson Beita-Sandí§,**, Liz Taylor-Edmonds††, and Robert C.

6

Andrews††

7 8

†

Metropolitan Water District of Southern California, Water Quality, La Verne, CA, USA 91750,

9

‡

Arizona State University, School of Sustainable Engineering and the Built Environment,

10

Tempe, AZ, USA 85259-3005, ‡‡University of Nevada, Department of Civil and Environmental

11

Engineering, Reno, NV, USA 89557-0258, §Clemson University, Department of Environmental

12

Engineering and Earth Sciences, Anderson, SC, USA 29625,

13

Research Center of Environmental Pollution (CICA), San José, Costa Rica 2060, and

14

††

**

University of Costa Rica,

University of Toronto, Department of Civil Engineering, Toronto, ON, Canada, M5S 1A4

15 16

*

17

[email protected]

Corresponding author telephone:

(909) 392-5083; fax:

(909) 392-5246; and e-mail:

18 19 20

ABSTRACT: Certain unregulated disinfection byproducts (DBPs) are more of a health concern

21

than regulated DBPs. Brominated species are typically more cytotoxic and genotoxic than their

22

chlorinated analogs.

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formation of regulated and selected unregulated DBPs following chlorine disinfection was

The impact of granular activated carbon (GAC) on controlling the

ACS Paragon Plus Environment


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evaluated.

The predicted cyto- and genotoxicity of DBPs was calculated using published

25

potencies based on the comet assay for Chinese hamster ovary cells (assesses the level of DNA

26

strand breaks). Additionally, genotoxicity was measured using the SOS-ChromotestTM (detects

27

DNA-damaging agents). The class sum concentrations of trihalomethanes, haloacetic acids, and

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unregulated DBPs, and the SOS genotoxicity followed the breakthrough of dissolved organic

29

carbon (DOC), however the formation of brominated species did not. The bromide/DOC ratio

30

was higher than the influent through much of the breakthrough curve (GAC does not remove

31

bromide), which resulted in elevated brominated DBP concentrations in the effluent. Based on

32

the potency of the haloacetonitriles and halonitromethanes, these nitrogen-containing DBPs were

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the driving agents of the predicted genotoxicity. GAC treatment of drinking or reclaimed waters

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with appreciable levels of bromide and dissolved organic nitrogen may not control the formation

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of unregulated DBPs with higher genotoxicity potencies.

36 37

INTRODUCTION

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Epidemiology studies suggest an association between exposure to halogenated disinfection

39

byproducts (DBPs) and bladder cancer; in particular to brominated trihalomethanes (THMs).1-3

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However, recent toxicology studies have shown that the regulated THMs are not the drivers of

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toxicity but rather they may serve as a surrogate for the formation potential of other DBPs of

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higher health concern. Extensive toxicity testing indicate that certain unregulated DBPs (e.g.,

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haloacetonitriles

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substantially (orders of magnitude) more toxic than currently regulated DBPs.4-8 Among these

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DBPs, the bromine (Br)-containing species are more geno- and cytotoxic than their chlorinated

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analogs.

[HANs],

halonitromethanes

[HNMs],

haloacetaldehydes


[HAs])

are

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Jeong and colleagues integrated quantitative in vitro cyto- and genotoxicity data with

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determinations of regulated and unregulated DBPs at a number of epidemiology study sites.9

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Chronic mammalian cell cytotoxicity (72 h) using Chinese hamster ovary (CHO) cells correlated

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highly with the numbers of DBPs identified and the concentrations of the DBPs. However, the

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genotoxic responses based on the CHO comet assay did not correlate as well with the DBPs.

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This was attributed to possible synergistic effects, activity of unidentified DBPs or other toxic

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water contaminants.

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formation of chloro-, bromo-, and iodo-THMs during chlorination and chloramination, alongside

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a theoretical cytotoxicity evaluation.10 These researchers calculated the overall predicted

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cytotoxicity based on their occurrence and their potency in chronic CHO cytotoxicity and

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demonstrated that the presence of bromide increased dibromoiodomethane formation, which is

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more cytotoxic than dichloroiodomethane. In a recent study, the impact of coagulation and

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bromide on the cytotoxicity (mammalian cell testing using a human white blood cell based

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bioassay) of water was studied.11 Coagulation significantly reduced the cytotoxicity of water,

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indicating that the removal of total organic carbon (TOC) and DBP precursors is an important

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factor. However, increasing bromide concentration shifted the haloacetic acid (HAA) species

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distribution to greater bromine substitution and increased the cytotoxicity. Thus, the efficacy of

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DBP precursor removal technologies is impacted by the removal of TOC and the inability to

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remove bromide. Plewa and Wagner proposed an integrated DBP research pathway, which

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included identification of the forcing agents (DBPs or classes of DBPs) associated with the cyto-

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and genotoxity of drinking water.12

A similar approach was performed by Allard and colleagues on the

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Granular activated carbon (GAC) is an effective DBP precursor removal technology. A key

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benefit of GAC to water utilities is that it allows them to continue using free chlorine without



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exceeding regulatory THM and HAA limits. Although GAC removes dissolved organic carbon

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(DOC), it does not remove bromide.13-15 Chiu and colleagues found that GAC preferentially

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removed bulk DOC over dissolved organic nitrogen (DON).15 As a result, the ratio of bromide

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to DOC in the GAC effluent was higher than in the influent and the ratio of bromide to DON was

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often higher in the GAC effluent. Because the chlorine demand of GAC effluent is lower than

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the influent, the free available chlorine (FAC) to bromide ratio will be lower when the chlorine

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dose is dictated by the demand.13 An increase in bromide/DOC or a decrease in FAC:bromide

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will result in higher bromine incorporation.13-15 Also, some nitrogenous (N-) DBPs are of higher

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health concern than the regulated carbonaceous (C-) DBPs, and Br-DBPs are generally more

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cyto- and genotoxic than their chlorine-containing analogs.4-8 Taken together, GAC performance

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in terms of regulated THM control during post-chlorination may not reflect the control of these

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unregulated DBPs of higher health concern for waters with moderate or high levels of bromide.

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In the United States (U.S.) DBP Rule for drinking water, GAC is used for the removal of

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DBP precursors, specifically for the control of the regulatory DBP sums, including four THMs

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(THM4) and five HAAs (HAA5).16 The maximum contaminant level (MCL) for THM4 in the

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U.S. is 80 µg/L at each sample location on a running annual average basis (based on quarterly

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sampling).16 However, utilities aim to operate below this level by designing a process to provide

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a safety factor (e.g., 20% [i.e., goal is to achieve ≤80% of the MCL]). The implementation of

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GAC treatment on wastewater effluents for potable reuse schemes or to remove trace organic

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contaminants prior to discharge is increasing.17 The objective of this paper is to assess the use of

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GAC to control the formation (during post-chlorination) of regulated and unregulated DBPs of

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health concern (Br-DBPs, N-DBPs). The formation of 31 DBPs was measured along the GAC

92

breakthrough curves treating surface and wastewater. The analytical data were complemented


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by measuring SOS chromotest genotoxicity (a bacterial test for detecting DNA-damaging

94

agents), as well as calculating the predicted cyto- and genotoxicity using published potency data.

95 96 97

MATERIALS AND METHODS GAC Bench-Scale Tests. Rapid small-scale column tests (RSSCTs) were conducted.18 All

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columns were prepared using proportional diffusivity (PD) designs.19

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Information (SI) for details (Table S1). Four columns were packed with bituminous coal based

See the Supporting

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GAC (Calgon F400) and another with lignite coal based GAC (Norit HD3000).

The

101

characteristics of the GACs are provided elsewhere.20-21 The RSSCTs were designed to simulate

102

a 10-min empty bed contact time. DBP formation was determined in the GAC influents and

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effluents at up to nine distinct bed volumes (BVs) along the breakthrough curve.

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genotoxicity of the GAC influents and the effluents at three different BVs were measured at the

105

start, middle, and end of a given breakthrough curve. Together, these measurements accounted

106

for 100% of the effluent of the columns (i.e., the entire volume exiting the columns was collected

107

and aggregated into 3 samples [early, middle, end]).

The

108

Waters Tested. A surface water, a treated wastewater (wastewater), and a combination of

109

10% wastewater : 90% surface water (blend) were evaluated. Many drinking water supplies are

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wastewater-impacted (e.g., 10-30% for moderately impacted), where some are wastewater-

111

dominated (>50%).22 Wastewater is higher in DON than surface waters and is a source of

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precursors for certain emerging N-DBPs.23 Wastewater is also typically higher in bromide than

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surface waters.24 The treated wastewater tested had 5.7 mg C/L of DOC, 0.53 mg N/L of DON,

114

0.121 cm-1 of ultraviolet absorbance at 254 nm (UV254), and 0.10 mg/L of bromide. (See the SI

115

for the DON method.) The surface water tested had 3.0 mg C/L of DOC, 0.21 mg N/L of DON,



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0.045 cm-1 of UV254, and 0.08 mg/L of bromide. The blended water had 3.2 mg C/L of DOC,

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0.26 mg N/L of DON, 0.054 cm-1 of UV254, and 0.09 mg/L of bromide. Note, in this case, the

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surface water and treated wastewater bromide levels were relatively comparable.

119

normally applied at drinking water treatment plants to the settled water. That was not done in

120

this set of tests. However, the surface water evaluated was low in specific UV absorbance

121

(SUVA) (1.5 L/mg-m), where conventional coagulation will not remove that much DOC.

GAC is

122

DBPs Measured. Four regulated THMs (THM4), nine bromine/chlorine-containing HAAs

123

(HAA9), six HANs (two mono-, trichloro-, and the three dihaloacetonitriles [DHANs]), five

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HNMs (bromo-, trichloro-, three dihalonitromethanes [DHNMs]), and seven HAs (the three

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dihalo- and the four trihaloacetaldehydes [THAs]) were measured. All of the halogenated (X-)

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DBPs, except for the HAAs, were analyzed with solid-phase extraction (SPE) and gas

127

chromatography (GC)/mass spectrometry.25 The HAAs were determined with diazomethane

128

derivatization, liquid/liquid extraction, and GC/electron capture detection.26

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reporting level for each DBP was 1 µg/L, except for the dihalogenated acetaldehydes and

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bromonitromethane, which were 2.5 µg/L each. DBP formation was evaluated under uniform

131

formation conditions (UFC).27 Briefly, samples were chlorinated at room temperature or at 25°C

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at pH 8 and held for 24 h. The chlorine dose was selected to achieve a residual of ~1.0 mg/L as

133

Cl2 after 24 h. The values in the UFC test were based on typical conditions in U.S. distribution

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systems.14 Note, this test was originally developed for the evaluation of GAC effluents, to

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provide a standardized set of conditions to evaluate this technology rather than site-specific

136

ones.14 However, in some countries (e.g., in Europe), much lower chlorine residuals are used,

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which would mean a lower FAC/bromide ratio and, thus, more bromine incorporation13 than that

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evaluated in this paper.


The minimum

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The bromine incorporation factor (BIF) for THMs is defined as follows:13

140 141

where the THM concentrations are on a molar basis. For the THMs, BIF values range from 0

142

(all chloroform [CHCl3] to 3 (all bromoform [CHBr3]). A BIF of 1 corresponds to a water in

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which the “average” species is bromodichloromethane (CHCl2Br). A similar equation was used

144

to determine the BIF for other trihalogenated DBPs (i.e., trihalogenated HAAs [TXAAs or

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THAAs], THAs).

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For the dihalogenated HAAs (DXAAs or DHAAs) (or other dihalogenated DBPs), a similar

147

equation was used for those three species, where the BIF values range from 0 (all dichloroacetic

148

acid) to 2 (all dibromoacetic acid). The BIF for di- and trihalogenated species was normalized

149

by the number of halogens (BIF/X) in order to obtain a common range of values.

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Toxicity Determinations. Two liters of influent surface water, wastewater, and blended

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water were collected, as well as three GAC effluents at three bed volumes (average bed volume

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for each sample: 795; 3,170; 9,770) during the breakthrough study. All samples were subject to

153

bench-scale chlorination (UFC described above) and concentrated using SPE cartridges (HLB

154

Oasis columns, Waters Limited, Mississauga, Ont., Canada). A full description of the SPE

155

protocol is provided in the SI.28 Influent samples without exposure to bench-scale chlorination

156

were also processed and assayed to determine baseline toxicity. The SPE enrichment factor for

157

each sample is expressed as the relative enrichment factor (REF) upon dilution in the bioassay;

158

this REF was used as the sample concentration for subsequent calculations.29 Genotoxicity was

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determined using the SOS-Chromotest™ (EBPI, Mississauga, Ontario, Canada) as per

160

manufacturer’s instructions, which is a bacterial test for detecting DNA-damaging agents.28,30

161

The assay captures the induction of Escherichia coli SOS repair genes, which are activated in



162

response to either direct DNA damage or indirect damage to DNA, such as oxidative stress. The

163

colorimetric induction response of the cell after a 2-h incubation period with the SPE sample was

164

measured using β-galactosidase SOS reporter gene. Induction values of the treated cells was

165

divided by the control and expressed as the induction factor (IF), where values greater than 1.5

166

(or 50% induction compared to non-treated cells) were considered to have a positive genotoxic

167

response.31 Each sample was run in duplicate on a microplate on two separate days, and multiple

168

solvent, negative, and positive control wells were run in parallel for quality control. The effect

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concentration (EC) or REF needed to elicit a positive response (IF = 1.5) was derived from the

170

linear concentration-response curves, and expressed as REF1F1.5 for cells with 70% survival or

171

higher.32 Toxicity result plots are presented as 1/REFIF1.5; therefore higher numbers represent a

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higher genotoxic effect .33

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The predicted genotoxicity of the measured DBPs (i.e., THMs, HAAs, HANs, HNMs, and

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HAs), which is a unitless value, was calculated by dividing the measured concentration by the

175

published genotoxicity potencies in the CHO comet assay, which is the dose required to elicit a

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toxic response in 50% of the cells (EC50) (Table S2).4-8 CHO genotoxicity potency of HANs

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ranged widely; the most potent HAN was dibromoacetonitrile (DBAN), 4.71E-05 M (4.71 x

178

10-5 M), followed by bromochloroacetonitrile (BCAN), 3.24E-04 M, and dichloroacetonitrile

179

(DCAN), 2.75E-03 M.4 DBAN is an order of magnitude more genotoxic than BCAN and two

180

orders of magnitude more genotoxic than DCAN. For context, a EC50 potency of 4.71E-05 M

181

translates into a concentration of 9,363.5 µg/L of DBAN is required to elicit a toxic response.

182

Other toxicity studies have also shown brominated HANs to be more toxic than their chlorine-

183

containing analogs.4


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Similarly, predicted cytotoxicity was calculated based on published LC50 values (the

185

concentration at which induces 50% viability of the cells as compared to the concurrent negative

186

control) for CHO cells (72-h exposure vs. 4-h exposure for genotoxicity) and presented in Table

187

S3.4-8

188

(BCAN) > 5.73E-05 M (DCAN).4 In other research comparing chlorination to chloramination

189

and the formation of chlorine-, bromine-, and iodine-containing THMs, a similar predicted

190

cytotoxicity evaluation was conducted.10

When considering DHANs, LC50 values were 2.85E-06 M (DBAN) > 8.46E-06 M

191 192

RESULTS AND DISCUSSION

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Breakthrough Curves. Breakthrough curves for DOC, UV254, DON, and DBP precursors for

194

the surface water and the wastewater treated with F400 GAC are presented in Figures 1 and S1,

195

respectively.

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absorbing organic matter better than bulk DOC, whereas DON was not well removed. The

197

treated surface and wastewater at 3,647 BVs had similar removals of UV254 (76% in surface

198

water, 77% in wastewater) and DOC (59%, 57%) and low removals of DON (46%, 22%).

199

Because the GAC preferentially removed UV-absorbing organic matter, the SUVA of the GAC

200

effluent was less than that of the GAC influent (Table S4). Thus, the GAC effluent should have

201

lower yields for THM or HAA formation compared against influent water. The removals of

202

THM, HAA, and DHAN precursors were bracketed by the DOC and UV254 curves.

203

example, at 3,647 BVs similar removal efficiencies were observed for both surface and

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wastewater: UFC THM4 (60% in surface water vs. 72% in wastewater), UFC HAA9 (68% vs.

205

71%), and UFC DHANs (78% vs. 64%). Although the DHANs are an N-DBP, the removal of

206

their precursors followed the breakthrough curve for DOC or UV254, not that of DON. In

Similar to that of Chiu and colleagues15, GAC preferentially removed UV-


For


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previous research, there was rapid breakthrough of the DBAN formation, whereas the DCAN

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formation followed the same trend as the DHANs above.15 In this study, there was a similar

209

impact on the brominated vs. chlorinated DHANs (see below).

210

breakthrough curves were observed with the F400 GAC. However, when the HD3000 GAC was

211

used, DOC and UV254 were not as well removed (Figure S2).

For the blend, similar

212

The untreated UFC THM4 for the surface and wastewater was 81 and 140 µg/L, respectively,

213

representing the THM formation at a plant treating such water or wastewater before the

214

installation of GAC at that plant. Note, conventional treatment would not have reduced THM

215

formation that much, as the waters evaluated in this study were low in SUVA (1.5 and

216

2.1 L/mg-m for the surface and wastewater, respectively). The UFC THM4 values represent a

217

worse-case scenario where bench-scale chlorination was conducted at a temperature

218

representative of summertime (25°C), where THM formation is higher. While one set of UFC

219

tests does not reflect all of the variables associated with THM formation, the UFC test is a good

220

indicator of full-scale THM formation.

221

wastewater-dominated water might be operated up to 4,447 BVs, which achieved a UFC THM4

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of 57 µg/L (Figure S3) (51% DOC removal [Figure S1]). Alternatively, the GAC filter treating a

223

non-impacted surface water may be operated up to 5,147 BVs (achieved 53% DOC removal

224

[Figure 1] and a UFC THM4 of 46 µg/L [Figure 2]).

Thus, for this database, the GAC filter treating

225

The molar sum of UFC THM, as well as the individual species, for the surface and the

226

wastewater breakthrough curves (Figures 2 and S3) shows that UFC THM4, TCM, and

227

bromodichloromethane

228

dibromochloromethane (DBCM) and TBM were not. For example, for the surface water at

229

5,147 BVs, C/Co for UFC of THM4, TCM, and BDCM were 0.47, 0.16, and 0.47, respectively,

(BDCM)

were

well-controlled


with

GAC,

whereas

UFC

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whereas C/Co for UFC DBCM and TBM were 1.0 and 2.5, respectively. The same trend was

231

more pronounced in the wastewater where the bromide content was somewhat higher, resulting

232

(at 3,647 BVs) in C/Co for UFC DBCM and TBM of 1.7 and 2.9, respectively, indicating that the

233

GAC effluent formation was often higher than in the influent, especially at intermediate (e.g.,

234

~3,500) BVs. On a molar basis, the brominated THMs accounted for 84% of the THM class sum

235

for the surface water at 5,147 BVs and 65% for the wastewater at 3,647 BVs. The inability of

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GAC to control the formation of BDCM and TBM during post-chlorination has been previously

237

reported for THMs,13-15 however, in these other studies, emerging DBPs and/or predicted cyto-

238

and genotoxicity were not evaluated.

239

Impact of Bromide/DOC Ratio. A key finding of this research centers on the observed

240

increase in the bromide/DOC ratio for GAC effluents vs. the influent, especially at low BVs

241

(Table S5).

242

0.018 mg Br-/mg DOC and, while bromide in the effluent was the same concentration as the

243

influent, the bromide/DOC ratio increased to 0.135, 0.069, and 0.036 mg/mg after 167, 2,147,

244

and 4,447 BVs, respectively. The increase in the bromide/DOC ratio occurs in the earlier stages

245

of the breakthrough curve, when DOC is effectively removed by GAC treatment, but that

246

eventual failure to effectively remove DOC after >5,000 BVs leads to a concomitant decrease in

247

bromide/DOC. The impact of the bromide/DOC ratio on the normalized BIF for the DBP classes

248

is shown in Figure S4. Among these different DBP classes, the highest bromine incorporation

249

was observed for DHNMs and DHANs. As a result, the UFC formation of DBAN increased

250

from 0.006 µmol/L in the GAC influent to 0.011 µmol/L in the GAC effluent at 3,647 BVs,

251

whereas the UFC formation of DCAN decreased from 0.105 µmol/L in the GAC influent to

252

0.023 µmol/L in the GAC effluent at 3,647 BVs, The same phenomenon was reported for

Bromide is not removed by GAC.

In the wastewater, the influent ratio was



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DHANs in other studies34-36 and for DHNMs.35 THAs and TXAAs had relatively low BIF/X

254

values, which is also corroborated in the literature.35 Three potential reasons for less bromine

255

incorporation in the THAs or TXAAs are as follows. The first is based on steric hindrance of the

256

carboxylic acid group in the TXAAs, which impacted bromine incorporation.

257

brominated TXAA formation and degradation may have resulted in less of a net increase. The

258

second hypothesis is supported by the observation that brominated TXAAs decomposed to

259

varying degrees via a decarboxylation pathway.37 For the THAs, bromine incorporation may

260

have been impacted by THA instability, based on the findings by Xie and Reckhow, where

261

brominated THAs were reported to undergo base-catalyzed hydrolysis.38 A third possibility is

262

that GAC removed a fraction of natural organic matter that is more reactive with bromine.

Secondly,

263

The impact of the bromide/DOC ratio on the normalized BIF for the surface water had a

264

similar trend (Figure 3). Increasing FAC/Br- decreased BIF/X due to chlorine substitution

265

competition with bromine (Figure S5 shows an example for the wastewater). Note, for these

266

samples, the chlorine demand was 2.6-6.5 and 10.4 mg/L as Cl2 for the GAC effluent and

267

influent, respectively, for the wastewater, and 0.4-1.4 and 1.9 mg/L as Cl2 for the GAC effluent

268

and influent, respectively, for the surface water.

269

Toxicity Findings. Influent genotoxicity was assayed using the SOS-Chromotest™, where

270

toxicity is expressed as the concentration factor (number of REFs) needed to achieve an effect

271

(50% increase in the induction factor of the SOS repair genes) expressed as REFIF1.5. Toxicity

272

result plots are presented as 1/REFIF1.5; therefore higher numbers represent a higher genotoxic

273

effect and values of 1 indicate that the sample did not require a concentration factor to elicit a

274

genotoxic response. For each influent type, similar trends were observed between the pre- and

275

post-chlorinated samples, where the genotoxicity of the surface water was 0.0029 and increased


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to 0.0077; the wastewater sample was more genotoxic (0.0067), as expected, and increased to

277

0.0106 upon chlorination. Overall, GAC treatment reduced the SOS genotoxicity of the UFC

278

samples and all of the tested effluents had a lower genotoxicity than their respective influents

279

(Figures 1 and S1). For example, for the surface water, C/Co for the 1/REFIF1.5 was 0.12, 0.31,

280

and 0.51 for BVs of 795, of 3,170, and of 9,770, respectively, and for the wastewater was 0.19,

281

0.26, and 0.78, respectively (Figures 4 and S6). Along the breakthrough curves for each water

282

type, the increase in the SOS genotoxicity was similar to that of the DOC, UFC THM4 and

283

HAA9 (Figures 1 and S1). For example, the C/Co for surface water DOC was 0.2. 0.35, and 0.6,

284

respectively.

285

In addition to the measured genotoxicity, predicted genotoxicities were calculated based on

286

published potencies for all of the measured DBPs in this study. For example, chlorinated

287

wastewater (GAC influent) had 12 µg/L of DCAN, 3.9 µg/L of BCAN, and 1.2 µg/L of DBAN.

288

DBAN is two orders of magnitude more potent than DCAN (see methods section) and was the

289

main driver of the overall predicted genotoxicity. The predicted or calculated genotoxicity for

290

each DHAN species was 3.83E-05, 7.82E-05, and 1.33E-04, respectively, where the class sum

291

(sum of the predicted toxicity for each compound) was 2.49E-04.

292

genotoxicity (sum of all the measured DBPs or X-DBPs) was 3.45E-04. DHANs (and DBAN

293

alone) contributed to 72 (and 39)% of the overall (X-DBP) predicted genotoxicity (Figure S8),

294

even though it represented a small portion (6.1 and 0.4%, respectively) of the X-DBPs on a

295

weight basis.

296

slightly lower BCAN (3.3 µg/L), and slightly higher DBAN (1.9 µg/L) values when compared to

297

chlorinated wastewater. The predicted genotoxicity for each species was 9.72E-06, 6.61E-05,

298

and 2.08E-04, respectively, where the class sum for DHANs was 2.83E-04, and the overall X-

The overall predicted

In another example, chlorinated surface water had lower DCAN (2.9 µg/L),



299

DBPs was 3.89E-04; in this example, DHANs (and DBAN alone) accounted for 73 (and 53)% of

300

the overall predicted genotoxicity for the X-DBPs. Because DBAN was a forcing agent of the

301

predicted genotoxicity, it is represented in the toxicity breakthrough (C/Co) curves alongside the

302

sums for the X-DBPs (Figures 4 and S6). Note, although the level of each DHAN in the surface

303

water sample was close to the quantification limit of 1.0 µg/L, the results were reproducible. For

304

example, as part of this testing, the blend was evaluated in replicate GAC columns, each of

305

which was separately evaluated for UFC DHAN formation. At bed volume 10,147, the replicate

306

UFC DHANs were 1.0 and 0.7 µg/L of DCAN, 1.5 and 1.5 µg/L of BCAN, and 1.6 and 1.6 µg/L

307

of DBAN.

Page 14 of 31

308

Figures 5 and S7 depict the measured (expressed as 1/REFIF1.5) and predicted genotoxicity

309

(based on dividing the measured DBP concentrations by their published genotoxicity potencies)

310

on an absolute basis. For the measured genotoxicity, a value of 1 indicates that no concentration

311

factor (REF) was needed for the sample to achieve a response (IF=1.5); whereas for the predicted

312

genotoxicity, a value of 1 represents a sufficient dose to achieve an EC50. However, the predicted

313

and measured values cannot be compared directly due to differences in the determination of

314

genotoxicity with the SOS test and the CHO comet assay. In addition, the predicted genotoxicity

315

only represents the measured X-DBPs, which is a small portion of the overall DBPs formed.

316

Nonetheless, trends associated with the predicted genotoxicities are informative, as the presence

317

of DBAN, for example, can reflect the presence of unknown brominated and nitrogenous DBPs.

318

As discussed above, the UFC DBP class sums followed the DOC breakthrough curve;

319

however the formation of brominated species often did not. Although the absolute levels of the

320

bromine-containing DBPs were low, they are more genotoxic than their chlorine-containing

321

analogues, especially for N-DBPs (Table S2).

This resulted in an increase in the overall


Page 15 of 31


322

predicted genotoxicity for the UFC X-DBPs (Figure S8) in the wastewater. For a BV that

323

controlled UFC THM4 formation (below the regulatory 80 µg/L limit) in the wastewater (4,447),

324

DCAN was lowered from 12 µg/L (0.10 µmol/L) in the chlorinated GAC influent to 2.3 µg/L

325

(0.021 µmol/L) in the chlorinated GAC effluent, whereas DBAN increased slightly from 1.2

326

(0.006 µmol/L) to 2.1 µg/L (0.010 µmol/L). Note, although the change in DBAN was small, the

327

results were reproducible. For the blend sample evaluated on replicate GAC columns, for all of

328

the bed volumes evaluated, UFC DBAN for each column differed by 0 or 0.1 µg/L for seven of

329

the bed volumes (e.g., 1.4 vs. 1.5 µg/L) and differed by 0.3 µg/L for the lowest bed volume (i.e.,

330

0.6 vs. 0.9 µg/L). The molar ratio of DBAN to DCAN increased from 0.06 in the chlorinated

331

GAC influent to 0.48 in the chlorinated GAC effluent. Thus, by not controlling the formation of

332

the most toxic species in this class, the predicted genotoxicity of the sample was not reduced

333

(Figure S8), even though there was a substantial reduction in DOC, and UFC THM4 and HAA9.

334

Predicted genotoxicity breakthrough (C/Co) curves for the sum of UFC X-DBPs and DBAN,

335

and the measured (SOS) genotoxicity for the surface water (Figure 4) and the wastewater sample

336

(Figure S6) using F400 GAC are presented. At low BVs (167), there was a substantial decrease

337

in predicted genotoxicity for X-DBPs (76-83%) and DBAN, however at the next tested BV

338

(1,122), the predicted genotoxicity of the chlorinated GAC effluent was similar to that of the

339

chlorinated GAC influent for the wastewater sample (Figure S6), mainly driven by the increase

340

in DBAN concentration (from 1.2 to 2.1 µg/L). At higher BVs (e.g., 3,647), the chlorinated

341

GAC effluent predicted genotoxicity was 1.5 times that of the chlorinated GAC influent for the

342

wastewater sample. As breakthrough continued, the predicted genotoxicity of the chlorinated

343

effluent matched that of the chlorinated influent for the wastewater sample. Although the overall

344

predicted genotoxicity was driven in large part by DBAN, the regulated HAAs contributed little



345

to this sum.

346

concentrations at 3,647 BVs for the wastewater treated with F400 GAC (e.g,, THM4 reduced

347

from 140 to 49 µg/L of THM4, HAA9 reduced from 93 to 29 µg/L of HAA9, DHANs reduced

348

from 17 to 7 µg/L of DHANs).

349

treatment, where chlorinated effluent values never exceeded that of the chlorinated influent.

350

Note, the predicted genotoxicity breakthrough curve (C/Co) for the UFC X-DBPs for the surface

351

water sample was more consistent with the measured (SOS) genotoxicity, although the predicted

352

genotoxicity for DBAN broke through earlier (Figure 4).

Page 16 of 31

This is in sharp contrast to the actual reduction in UFC DBP class sum

The measured genotoxicity was also controlled by GAC

353

Predicted cytotoxicity was also calculated based on the CHO chronic cytotoxic potency data.

354

Absolute concentrations (Figures 6 and S9) and breakthrough (C/Co) curves for N- and C-DBPs

355

are presented for both the surface and wastewater samples treated with F400 GAC (Figures 4 and

356

S6) to highlight the differences in the overall predicted chronic cytotoxicity of these two distinct

357

groups of DBPs. N-DBPs dominated the predicted cytotoxicity; where, at a relatively low BV

358

(2,147), the chlorinated effluent value for the wastewater was only 14% lower than that of the

359

chlorinated influent. C-DBPs were better controlled by GAC treatment for both the surface and

360

wastewater samples. GAC was better suited for the treatment of the surface water sample for the

361

control of C- and N-DBP cytotoxicity. As expected, when the concentration of each species was

362

factored in, the DHANs contributed heavily to the overall cytotoxicity index for the X-DBPs

363

(Figure S8) (e.g., at 5147 BVs, DHANs [and DBAN] accounted for 83 [and 45]% of the overall

364

predicted chronic cytotoxicity of the chlorinated wastewater sample).

365

In summary, DBPs such as the DHANs and DHNMs contributed the most to the overall

366

predicted cyto- and/or genotoxicity (Figures S8 and S10) even though their absolute

367

concentrations were low, as these classes of DBPs are more genotoxic (Table S2) and have a


Page 17 of 31


368

higher percent of bromine incorporation (Figure 3). Conversely, DBPs such as the TXAAs

369

contributed less to the overall predicted genotoxicity because this class of DBPs had lower

370

bromine incorporation (Figure 3) and, thus, lower formation of the more toxic species. This

371

exercise shows the relative impact of GAC on controlling regulated and unregulated DBPs (C-

372

vs. N-DBPs, Cl- vs. Br-DBPs).

373

It is important to note that one compound cannot be the only driver of the risk or the main

374

parameter for evaluating GAC performance. DBAN is just one example of a brominated DBP

375

with higher toxicity than its chlorinated analogs, which preferentially formed during the early

376

phase of DOC breakthrough across the GAC contactors.

377

cytotoxic compounds that was measured, but there may be others or perhaps synergistic impacts

378

of mixtures. That said, the overall mixture effect was quantified using the SOS chromotest and

379

the GAC was able to control the measured genotoxicity, where effluents were consistently lower

380

in response when compared to their respective influents along the breakthrough curves. This

381

could be attributed to mixture effects, such as competitive inhibition between DBPs.

DBAN is one of the geno- and

382

It is important to understand the limitations of GAC treatment for waters with high

383

bromide levels and relatively high levels of DON. Waters with even moderate levels of bromide

384

(e.g., 0.08-0.10 mg/L) will have significantly higher levels of bromine incorporation for other

385

classes of DBPs, including those not measured in this study or ones yet to be identified.35 Also,

386

waters with relatively high DON (e.g., 0.53 mg/L as N) will contain precursors for other N-DBPs

387

of health concern (e.g., haloacetamides, which were not included in this study).39-41 In a recent

388

study of potable reuse waters, weighting DBP concentrations by their cytotoxicity (CHO)

389

potencies highlighted the potential significance of HANs, which were not effectively removed by

390

reverse osmosis and advanced oxidation, to the DBP-associated toxicity.42 In this paper, the



Page 18 of 31

391

cytotoxicity of the reuse water was a function of both their DBP concentrations and cytotoxic

392

potencies.

393 394

IMPLICATIONS

395

For plants that use GAC to treat water with precursors for N-DBPs and with moderate levels

396

of bromide, the control of bromine-containing DBPs of health concern (e.g., DBAN) will not be

397

the same as what is required to control THM4 or HAA9. Because GAC removes DOC but does

398

not remove bromide, a substantial portion of the breakthrough curve may have more formation

399

of these DBPs of concern.

400

FAC/bromide ratio) on bromine incorporation. Moreover, bromide is an important risk factor,

401

because bromide in drinking water is increasing.43 Although the formation of these emerging

402

DBPs may be small on an absolute basis, they are more geno- and cytotoxic than their chlorine-

403

containing analogues. Thus, they accounted for much of the predicted geno- and cytotoxicity of

404

the chlorinated GAC effluents. However, the measured genotoxicity showed that GAC was able

405

to control the formation of precursors of DBPs that either directly or indirectly damage DNA.

406

The SOS test measures the whole mixture and accounts for additive or competitive inhibition of

407

toxic actions and may better represent the synergy of the formed DBPs. In addition, perhaps the

408

forcing agent(s) was (were) not measured or the field has yet to discover the most significant

409

toxicity forcing agent(s), whose precursors are well removed by GAC, which would explain the

410

departure between predicted and measured toxicity.

This is due to the impact of the bromide/DOC ratio (and

411

This study demonstrated that the removal of DOC or the control of THM4 or HAA5 can be

412

used to evaluate the efficacy of GAC, but they may not represent the removal of the more geno-

413

and cytotoxic species. For example, the bromine-containing DHANs are substantially more


Page 19 of 31


414

geno- and cytotoxic, have sufficient concentration and bromine incorporation, and their

415

formation was not controlled by GAC treatment, which resulted in their accounting for much of

416

the predicted geno- and cytotoxicity of the sum of the measured X-DBPs. Thus, the control of

417

certain emerging DBPs (e.g., the DHANs) should be considered in GAC studies and monitoring

418

programs, as well as toxicity testing (e.g., the SOS Chromotest™). Another option is to include

419

total organic bromine (TOBr), which represents the sum of the known and unknown bromine-

420

containing portions of the total organic halogen (TOX).44

421

This study highlights the gap in knowledge regarding the occurrence and the impact of

422

treatment on emerging DBPs and to prioritize the control of DBPs of health concern. Additional

423

treatment strategies to control bromide and DON are needed and risk factors for high bromide

424

and/or DON waters should be explored (e.g., wastewater impacts).

425 426

ASSOCIATED CONTENT

427

Supporting Information

428

The Supporting Information is available free of charge on the ACS Publications website.

429 430

ACKNOWLEDGMENTS

431

We thank the water and wastewater plants for providing samples. We acknowledge Isabelle

432

Netto at the University of Toronto for her assistance on this study. Natalia Fischer was partially

433

supported by the Brazilian Ministério da Educação Program: Coordenação de Aperfeiçoamento

434

de Pessoal de Nível Superior – CAPES. Wilson Beita-Sandi was partially supported by the

435

University of Costa Rica.

436 437



438

Page 20 of 31

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580

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581


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582

FIGURES

583

Figure 1. Breakthrough curves for DOC, UV254, DON, DBP precursors (on a molar basis), and

584

SOS genotoxicity (1/REF) for the surface water sample treated with F400 GAC.

585

Figure 2. Breakthrough curves for UFC THMs for the surface water sample treated with F400

586

GAC.

587

Figure 3. Impact of bromide (Br-)/DOC ratio on the normalized BIF for the surface water

588

sample treated with F400 GAC.

589

Figure 4. Breakthrough curves for measured SOS genotoxicity (1/REFIF1.5), predicted chronic

590

cytotoxicity, and predicted genotoxicity of UFC DBPs for surface water sample treated with

591

F400 GAC.

592

Figure 5. Measured (SOS-Chromotest) and predicted genotoxicty of UFC DBPs for surface

593

water sample treated with F400 GAC. SOS is expressed as 1/REFIF1.5; predicted genotoxicity of

594

the sum of X-DBPs and of DBAN is presented on the secondary y-axis.

595

Figure 6. Breakthrough curves for predicted chronic cytotoxicity of UFC DBPs (N- and C-DBPs

596

and DBAN) for surface water sample treated with F400 GAC.

597 598



599 600

Figure 1. Breakthrough curves for DOC, UV254, DON, DBP precursors (on a molar basis), and SOS genotoxicity (1/REFIF1.5) for the surface water sample treated with F400 GAC.

601

602 603

Figure 2. Breakthrough curves for UFC THMs for the surface water sample treated with

604

F400 GAC.

605


Page 28 of 31

Page 29 of 31


606 607

Figure 3. Impact of bromide (Br-)/DOC ratio on the normalized BIF for the surface water

608

sample treated with F400 GAC.

609

610 611

Figure 4. Breakthrough curves for measured SOS genotoxicity (1/REFIF1.5), predicted

612

chronic cytotoxicity, and predicted genotoxicity of UFC DBPs for surface water sample

613

treated with F400 GAC.



614 615

Figure 5.

616

surface water sample treated with F400 GAC. SOS is expressed as 1/REFIF1.5; predicted

617

genotoxicity of the sum of X-DBPs and of DBAN is presented on the secondary y-axis.

Measured (SOS-Chromotest) and predicted genotoxicty of UFC DBPs for

618

619

Figure 6. Breakthrough curves for predicted chronic cytotoxicity of UFC DBPs (N- and C-

620

DBPs and DBAN) for surface water sample treated with F400 GAC.


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TOC/Abstract art

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Granular Activated Carbon Treatment May Result in Higher Predicted

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