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Remediation and Control Technologies

Oxidation of microcystin-LR via activation of peroxymonosulfate using ascorbic acid: Kinetic modeling and toxicity assessment Shiqing Zhou, Yanghai Yu, Weiqiu Zhang, Xiaoyang Meng, Jinming Luo, LIN DENG, Zhou Shi, and John C. Crittenden Environ. Sci. Technol., Just Accepted Manuscript • DOI: 10.1021/acs.est.7b06560 • Publication Date (Web): 07 Mar 2018 Downloaded from http://pubs.acs.org on March 8, 2018

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Environmental Science & Technology

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Oxidation of microcystin-LR via activation of peroxymonosulfate

2

using ascorbic acid: Kinetic modeling and toxicity assessment

3

Shiqing Zhou,†,‡ Yanghai Yu,† Weiqiu Zhang,‡ Xiaoyang Meng,‡ Jinming Luo,‡ Lin Deng,†,‡ Zhou

4

Shi† and John Crittenden *,‡

5

†

6

Changsha, Hunan, 410082, China

7

‡

8

Engineering, Georgia Institute of Technology, Atlanta, Georgia 30332, United States

Department of Water Engineering and Science, College of Civil Engineering, Hunan University,

Brook Byer Institute for Sustainable Systems and School of Civil and Environmental

9 10 11

Corresponding Author

12

John Crittenden

13

*E-mail: [email protected]. Tel.: +1 404 894 5676; fax: +1 404 894 7896

1

ACS Paragon Plus Environment


PMS

Intensity

SO4·-

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H2O H2A H+ HA-

PMS

HO·

SO4·-

H2O

Concentration of radicals (M)

Magnetic field

A.-

8.0x10

-13

6.0x10

-13

4.0x10

-13

2.0x10

-13

Sulfate radical Hydroxyl radical Ascorbyl radical

0.0

-7

8.0x10

-8

4.0x10

-8

0.0 0

14

1.2x10

5

10

15

20

Time (min)

2


25

30

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ABSTRACT

16

Advanced oxidation processes (AOPs) have been widely used for the destruction of

17

organic contaminants in the aqueous phase. In this study, we introduce an AOP on

18

activated peroxymonosulfate (PMS) by using ascorbic acid (H2A) to generate sulfate

19

radicals (SO4•-). Sulfate radicals, hydroxyl radicals (HO•) and ascorbyl radicals (A•-)

20

were found using electron spin resonance (ESR). But we found A•- is negligible in the

21

degradation of microcystin-LR (MCLR) due to its low reactivity. We developed a

22

first-principles kinetic model to simulate the MCLR degradation and predict the

23

radical concentrations. The MCLR degradation rate decreased with increasing pH.

24

The scavenging effect of natural organic matter (NOM) on SO4•- was relatively small

25

compared to that for HO•. Considering both energy consumption and MCLR removal,

26

the optimal H2A and PMS doses for H2A/PMS process were determined at 1.0×10-6 M

27

and 1.6×10-5 M, respectively. In addition, we determined the toxicity using the protein

28

phosphatase 2A (PP2A) test and the results showed that MCLR was readily detoxified

29

and its oxidation by-products were not hepatotoxic. Overall, our work provides a new

30

type of AOP and a promising, efficient and environmental-friendly method for

31

removing microcystins in algae-laden water.

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32

INTRODUCTION

33

In recent years, cyanobacterial blooms frequently occur worldwide and pose a

34

serious threat to drinking water.1 Microcystins (MCs), a class of hepatotoxic

35

monocyclic heptapeptides, are the most common toxins produced by cyanobacteria.2, 3

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MCs can cause both acute liver damage and chronic diseases, as they potentially

37

inhibit protein phosphatase 1 (PP1) and protein phosphatase 2A (PP2A).4 More than

38

80 variants of MCs have been identified based on their methylation pattern and two

39

variable amino acids.3 Microcystin-LR (MCLR) is the most toxic and abundant

40

variant and accounts for 46.0-99.8% of the total MC concentrations during a

41

cyanobacterial bloom.5 The World Health Organization (WHO) has set a provisional

42

concentration limit of 1.0 µg L-1 for MCLR in drinking water.6

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MCLR is a very stable toxin due to its cyclic peptide structure. Conventional water

44

treatment processes such as coagulation, flocculation, sedimentation and filtration can

45

effectively remove the intact cells and the majority of intracellular MCLR; however,

46

these processes do not detoxify the dissolved extracellular MCLR released from cell

47

lysis.7-10 Moreover, the conventional processes simply transfer the toxins from one

48

phase to another when algal cells are ruptured.11 Advanced treatment technologies are

49

required to remove or destroy MCLR from drinking water.

50

Advanced oxidation processes (AOPs) have been shown to possess outstanding

51

ability to oxidize and destroy a variety of toxic and refractory organic contaminants in

52

the aqueous phase. AOPs seldom generate toxic chlorinated organic compounds

53

(known as disinfection by-products, DBPs) that are formed by chlorination.12, 13 Due

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54

to the high standard redox potentials of hydroxyl radicals (HO•, 2.7 V) and sulfate

55

radicals (SO4•-, 3.1 V), AOPs have received much attention for destroying organic

56

pollutants; the underlying mechanism involves hydrogen abstraction, double bond

57

addition, electron transfer reactions and electrophilic substitution of aromatic

58

compounds.14,

59

peroxide (H2O2), peroxodisulfate (S2O82-, PDS), and peroxymonosulfate (HSO5-, PMS)

60

by transition metals and minerals activation, photolysis, thermolysis and sonolysis

61

methods.16-26 In addition to these catalytic methods, it has been reported that some

62

reducing organic species such as phenols, hydroxylamine, hydroquinone and

63

semiquinone moieties in reduced humic acid and biochar could also activate oxidants

64

to generate radicals through an electron transfer mechanism.27-31

15

These radicals can be generated through activation of hydrogen

65

As an eco-friendly reducing agent, ascorbic acid (C6H8O6, H2A) contains two

66

ionizable hydroxyl moieties and can undergo sequential electron transfer reactions.32,

67

33

68

oxidation by H2O2 to yield HO•, dehydroascorbic acid and an intermediate ascorbyl

69

radical (A•-). Curtin et al.34 reported that ascorbate reacted with PDS to initiate SO4•-

70

production, which significantly accelerated the reaction rate between PDS and

71

formate. PMS and PDS are similar in structure, and both have an O-O bond. PMS can

72

be generated by replacing one hydrogen atom in H2O2 with SO3, while PDS is

73

generated by replacing two hydrogen atoms in H2O2 with SO3.35 Considering the

74

similar PDS and PMS structures, it is hypothesized that PMS could also be activated

75

by H2A (HA-), although the mechanism involving PMS and H2A is still unknown.

For instance, Nappi and Vass32 found that ascorbic acid could undergo a two-step

5



76

In this study, we investigate the activation reactions between H2A and PMS and the

77

kinetics of MCLR oxidation. Electron spin resonance (ESR) was used to verify the

78

generation of HO• and SO4•-. Based on our experimental results and the kinetic

79

parameters obtained from the literature, we developed a first-principles kinetic model

80

to simulate the MCLR degradation and to predict the radical concentrations. PMS and

81

H2A dosages, solution pH values and natural organic matter (NOM) concentrations

82

were modeled to improve the understanding of MCLR degradation in the H2A/PMS

83

process. The hepatotoxicities of MCLR and its oxidation products were evaluated

84

using the PP2A assay.

85

MATERIALS AND METHODS

86

Chemicals. All chemicals were of analytical grade, and used as received without

87

further purification. All solutions were prepared with ultrapure water, unless

88

otherwise specified. The specific chemicals and reagents are provided in the

89

Supporting Information (SI) Text S1.

90

Experimental Procedures. Batch experiments were conducted in the open air and

91

in a series of borosilicate glass jars containing 100 mL of solutions at room

92

temperature (25± 2°C). The initial concentration of MCLR was fixed at 2.0×10-7 M.

93

The pH of the bulk solution containing MCLR and H2A was initially adjusted to pH 4,

94

5, 6 and 12 using H2SO4 or NaOH. At each given time interval, sample aliquots were

95

harvested and mixed immediately with appropriate amounts of Na2S2O3 to quench the

96

reaction. Then the samples were immediately analyzed.

97

Analytical Methods. The MCLR concentrations were determined by LC/MS/MS

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(Agilent 1290/6460 Triple Quad, USA) equipped with a Symmetry C18 column (50

99

mm × 2.1 mm × 5 mm, Agilent, USA). A mixture of ultrapure water (0.1% formic

100

acid) and acetonitrile (v: v = 65:35) was used as the mobile phase. The flow rate was

101

0.2 mL min-1 and the injection volume was 10 µL. The intermediates of MCLR were

102

also identified using LC/MS/MS (Agilent 1290/6460 Triple Quad, USA) according to

103

the method of our previous study.36

104

The electron spin resonance (ESR) experiment was conducted using a Bruker A300

105

spectrometer

(Bruker

Instrument,

Germany)

with

or

without

5,

106

5-dimethyl-1-pyrroline-N-oxide (DMPO) as a spin-trapping agent. The detailed ESR

107

procedure is available in SI Text S2-S3. The hepatotoxicities of MCLR and its

108

oxidation products were evaluated by the PP2A activity assay using a MicroCystest

109

kit (ZEU Inmunotec, Spain) according to the method of James et al.,37 and the

110

detailed information is presented in SI Text S4.

111

Kinetic Model. Table 1 summarizes the reactions in the H2A/PMS system. The

112

associated rate constants are generally obtained either from the literature or by fitting

113

experimental data. The genetic algorithm (GA) was used to minimize the objective

114

function (OF) and to determine the rate constants as described in our former work.38

115

The backward differentiation formula (BDF) method [i.e., Gear’s method]39 was used

116

to solve the ordinary differential equations (ODEs) by using MATLAB. Our model

117

had 30 rate constants, 19 from the literature and 11 determined by fitting the model to

118

the data. The detailed modeling approaches and kinetic equations are provided in SI

119

Text S5 and S6, respectively.

7



120

OF = ∑[(C − C )/C ]

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(1)

121

Here, n is the number of data points, and C and C are the experimental and

122

calculated concentrations of MCLR, respectively. Table 1

123 124

RESULTS AND DISCUSSION

125

MCLR Degradation and Reactive Radicals Identification. Figure 1 compares

126

the degradation of MCLR by H2A alone, PMS alone and the H2A/PMS process. No

127

significant degradation of MCLR was observed in 30 min when the MCLR solution

128

was treated by H2A alone, suggesting that H2A does not oxidize MCLR. On the other

129

hand, although PMS itself is an oxidant (E0 = +1.82 V/SHE), the loss of MCLR was

130

also negligible for a molar ratio of [PMS]/[MCLR] up to 25. However, approximately

131

91% of MCLR was destroyed after 30 min using the H2A/PMS process (for the same

132

molar ratio of [PMS]/[MCLR] of 25), and the degradation followed pseudo-first-order

133

kinetics with a rate constant of 1.2×103 s-1. Based on this phenomenon, H2A reacted

134

with PMS and produced other reactive radicals in the H2A/PMS process.

135

Figure 1

136

To identify the reactive radicals involved in the H2A/PMS process, ESR tests

137

with/without DMPO were conducted (Figure 2). DMPO was employed as a

138

spin-trapping agent to identify hydroxyl radicals or sulfate radicals, in which HO• and

139

SO4•- could be discerned by determining the signals of DMPO-OH adducts and

140

DMPO-SO4 adducts, respectively.50 As shown in Figure 2a, both DMPO-OH adducts

141

(with α(N) = α(H) = 14.9 G) and DMPO-SO4 adducts (with α(N) = 13.2 G, α(H) = 9.6

8


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G, α(H) = 1.48 G, α(H) = 0.78 G) were detected during the whole reaction process.

143

This result suggests that H2A successfully activated PMS to generate SO4•- and HO• in

144

the H2A/PMS process.28, 50

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Figure 2b shows the typical ESR signal of A•- (with α(H) = 1.76 G) during the

146

reaction of H2A and PMS.51 The ascorbyl radical is stable and nonreactive, therefore

147

directly observable by ESR. Moreover, the ascorbyl radical reacts preferentially with

148

itself thus terminating the propagation of free radical reactions. Despite the short

149

lifetime of the free radicals, the ESR signals in Figure 2b verified the generation of

150

ascorbyl radicals during the H2A/PMS process. Based on the results of HO•, SO4•- and

151

A•- verified by ESR tests, the detailed activation mechanism of PMS by ascorbic acid

152

is proposed (SI Figure S2) and the elementary reactions are listed in Table 1.

153

Figure 2

154

Kinetic Modeling and Radical Concentrations. Due to the low reactivity of A•-,

155

the contribution of A•- to the degradation of MCLR is negligible in this work. Our

156

model was built based on the hypothesis that the degradation of MCLR is primarily

157

caused by SO4•- and HO•. The contribution of other reactive species can also be

158

neglected due to their low concentration in the H2A/PMS process. For example, the

159

concentration of SO5•- is predicted to be 1.4×10-15 M (SI Figure S3), which is lower

160

than one-percent of the model-predicted SO4•- concentration. By fitting the

161

experimental data to our kinetic model, we determined the rate constants of SO4•- and

162

HO• with the targeted compounds and other unknown rate constants using the genetic

163

algorithm (an algorithm that can better locate the global minimum with respect to a

9



164

large number of dimensions and computational efficiency). Table 1 provides the fitted

165

rate constants for these elementary reactions which have not been previously reported.

166

The model was able to simulate the MCLR degradation (as discussed in the following

167

sections) and predict the radical concentrations, especially the concentrations of A•-.

168

The model-predicted concentration profiles of HO•, SO4•- and A•- are shown in

169

Figure 3. The concentration of SO4•- gradually decreased while the concentration of

170

HO• increased and then decreased as the reaction time increased. The predicted results

171

are highly consistent with the ESR test results (Figure 2). As the intensity of DMPO

172

radical adduct signals are proportional to the concentrations of reactive radicals, it

173

was determined that the concentration of SO4•- gradually decreased from 0 min to 30

174

min, while the concentration of HO• increased linearly from 0 min to 20 min and then

175

decreased from 20 min to 30 min (SI Figure S4). The intensity of the DMPO-OH

176

adduct signals was much stronger than that of the DMPO-SO4 adducts, and the

177

transformation of DMPO-SO4 adducts to DMPO-OH adducts could occur via

178

nucleophilic substitution (by H2O/OH-).52, 53

179

The model-predicted concentrations of A•- initially increased to its maximum

180

(1.0×10-7 M) and then sharply decreased with the reaction time. Similar to the ESR

181

tests, the intensity of A•- signals gradually decreased and disappeared within 30 min

182

(SI Figure S4). In the H2A/PMS process, A•- is an important radical formed by a

183

reaction between H2A and PMS. Bielski reported that A•- reacts preferentially with

184

itself and exhibits a strictly second-order decay that depends on pH.54 Due to the high

185

concentration of A•- found in the system, the reaction between A•- and A•- was

10


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186

considered in our model (reaction 11 in Table 1). In addition, we also considered the

187

A•- reaction with HO• and SO4•- (reactions 12 and 13 in Table 1), which forms

188

dehydroascorbic acid. The above proposed reactions have a significant influence on

189

the decay of A•-; without considering these reactions, the concentration of A•- would

190

be overestimated. To the best of our knowledge, no similar studies have predicted the

191

concentration of A•- as a function of time.

192

Figure 3

193

To further evaluate the kinetic model, we investigate the impact of H2A dosage,

194

PMS dosage, solution pH and NOM on MCLR degradation during the H2A/PMS

195

process.

196

Effect of H2A and PMS Dosage. Figure 4a shows the experimental profiles of

197

MCLR degradation and the model fitting under different H2A dosages. The objective

198

function (OFH2A) values are listed in SI Table S1. At a given PMS dosage (5.0×10-6

199

M), the MCLR degradation increased with an increasing H2A dosage from 1.0 to 5.0

200

×10-6 M but then decreased at higher H2A concentrations (i.e., 1.0×10-5 M). This

201

phenomenon can be explained by the fact that excess H2A in a high-concentration

202

would act as a scavenger of reactive radicals and decrease the destruction of MCLR if

203

the dosage is too high, as shown in Table 1, reactions 3 and 4.34

204

Figure 4b shows the experimental profiles of MCLR degradation and the model

205

fitting under different PMS dosages. The objective function (OFPMS) values are listed

206

in SI Table S1. At a given H2A dosage (2.0×10-6 M), the MCLR degradation gradually

207

increased as the PMS dosage increased from 1.0×10-6 to 1.0×10-5 M. As shown in

11



208

Table 1, excess PMS could enhance the MCLR degradation due to the generation of

209

more SO4•- and HO• in the H2A/PMS system. Moreover, Antoniou et al.24 reported

210

that the direct oxidation of MCLR by PMS could occur at a high ratio (50 or 100) of

211

[PMS]/[MCLR]. Therefore, the contribution of SO4•- and HO• is significantly affected

212

by excess PMS.

213

Figure 4

214

Effect of pH. Figure 5a shows the experimental profiles of MCLR degradation and

215

the model predictions under different initial solution pH values from 4 to 12 which

216

cover the pKa range. The objective function (OFpH) values listed in SI Table S1 were

217

below or equal to 0.11. The oxidation of MCLR in the H2A/PMS process was strongly

218

pH-dependent, and the maximum rate of MCLR degradation was achieved at pH 4.

219

Figure 5b presents the experimental and predicted pseudo-first-order rate constants of

220

MCLR degradation under different pH values. The overall degradation rate constant

221

decreased from 1.2×10-3 s-1 to 6.3×10-4 s-1 as the pH increased from 3 to 6. As the

222

dissociation constants of H2A are 4.2 and 11.6 (SI Figure S5), H2A can dissociate to

223

different species under different pH values.55 As the pH increased from 4 to 6, the

224

percentage of HA- increased, while the percentage of H2A decreased dramatically. In

225

addition, HA- could react with PMS to generate SO4•- but more slowly than H2A

226

(reactions 1 and 2 in Table 1). Therefore, the degradation of MCLR decreased with

227

increasing pH. Furthermore, at pH 12, HA- almost transformed into dianionic ascorbic

228

acid (C6H6O62-, A2-), and A2- became the dominant form of H2A. As A2- could not

229

activate PMS to produce SO4•- or HO•, the degradation of MCLR was negligible at pH

12


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230

12 (Figure 5a).

231

Figure 5

232

Effect of NOM. Figure 6a shows the experimental profiles of MCLR degradation

233

and the model predictions under different NOM concentrations. The objective

234

function (OFNOM) values listed in SI Table S1 were below or equal to 0.11. MCLR

235

degradation decreased as the NOM concentration increased. Figure 6b presents the

236

experimental and predicted pseudo-first-order rate constants of MCLR degradation in

237

the presence of different NOM concentrations. The overall degradation rate constant

238

decreased from 1.2×10-3 s-1 to 3.2×10-4 s-1 as the NOM concentration increased from 0

239

mg L-1 to 5.0 mg L-1, because NOM could compete with MCLR to scavenge SO4•- and

240

reduce the SO4•- concentration in the H2A/PMS system. The second-order rate

241

constants of NOM reacting with HO• and SO4•- were 3.0×108 Mc-1 s-1 and 2.35×107

242

Mc-1 s-1, respectively (reaction 28 and 29 in Table 1).49

243

To further clarify the scavenging effect of NOM on MCLR degradation, we also

244

modeled and presented the HO• and SO4•- concentrations (SI Figure S6). As the NOM

245

concentration increased, the concentrations of HO• and SO4•- were gradually reduced.

246

Compared with the SO4•- concentration reduction, the reduction of HO• was much

247

higher. Indeed, according to our model predictions, the concentration of HO• was

248

reduced by more than 90%, while the concentration of SO4•- decreased by

249

approximately 50% in the presence of 5.0 mg L-1 of NOM. The smaller decrease in

250

the concentration of SO4•- could be attributed to the difference in the second-order rate

251

constants of NOM reacting with HO• and SO4•-.

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252

Figure 6

253

Optimization of MCLR removal in the H2A/PMS process. As discussed above,

254

our kinetic model has a good agreement with experimental data. In order to optimize

255

MCLR removal, electrical energy per order (EE/O) was applied to evaluate the energy

256

and cost in the H2A/PMS process.38, 56 The consumption of H2A and PMS which

257

would be required for an order of MCLR removal (i.e., 90% destruction of MCLR)

258

was calculated using Eqs. 2 and 3, respectively.

259

H A/O =

[ ] [ ]

260

PMS/O =

[&'(] [&'(]

! ( " ) !

(mg H2A L-1)

(2)

(mg PMS L-1)

(3)

!

(!" )

261

Here, Ci and Cf are the MCLR concentration (mol L-1) at reaction time of 0 and t,

262

respectively; [H2A]0 and [H2A]f are the concentration of H2A at reaction time of 0 and

263

t, respectively; [PMS]0 and [PMS]f are the concentration of PMS (mg L-1) at reaction

264

time of 0 and t, respectively. According to the method of Rosenfeldt et al.,57 the

265

electrical energy use to produce H2A and PMS were calculated to be 17.44 and 20.93

266

kWh lb-1, respectively (SI Text S7). Thus, H2A/O and PMS/O were converted to

267

EE/OH2A and EE/OPMS in the energy unit of kWh L-1, and the total energy

268

consumption can be calculated by Eqs. 4.

269

EE/O** = EE/O + EE/O&'(

(4)

270

The operational parameters, H2A and PMS doses, were varied to determine the

271

most energy efficient condition. Figure 7 presents the EE/Ototal of H2A/PMS process

272

vary with H2A and PMS doses. For the same H2A dose, EE/Ototal first decreased and

273

then increased as the PMS dose increased from 1.0×10-6 to 5.0×10-5 M (SI Figure

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274

S7a). Similarly, for the same PMS dose, EE/Ototal first decreased and then increased as

275

the H2A dose increased from 1.0×10-7 to 1.0×10-5 M (SI Figure S7b). On the basis of

276

calculated EE/Ototal values, the optimal H2A and PMS doses for the H2A/PMS process

277

were determined at 1.0×10-6 M and 1.6×10-5 M, respectively. Of note, the economic

278

analysis based on EE/O only provides some theoretical instructions rather than full

279

economic analysis of the process. Further economic analysis would be conducted in

280

field water and at some scale-up processes in our future studies.

281

Figure 7

282

Oxidation Products and Toxicity Assessment. To gain insight into the mechanism

283

of MCLR oxidation by the H2A/PMS process, the oxidation products generated

284

during MCLR degradation were analyzed using LC/MS/MS analysis. Table S2 (SI)

285

summarizes the 11 identified major oxidation byproducts, and the primary oxidation

286

pathways are presented in SI Figures S8 and S9. While the H2A/PMS process is

287

effective for the oxidation of MCLR, the hepatotoxicities of MCLR and its oxidation

288

products should not be neglected. As MCLR is a powerful inhibitor of PP2A, the

289

PP2A activity is usually used as an indicator of hepatotoxicity.58 As shown in Figure 8,

290

the decrease in the hepatotoxicities of the oxidation by-products showed a similar

291

trend with the decrease in the MCLR concentration measured by LC/MS/MS. The

292

results suggest that MCLR was readily detoxified by the H2A/PMS process and the

293

oxidation by-products of MCLR were not hepatotoxic.

294 295

Figure 8 Environmental Implications. Ascorbic acid (vitamin C) is a non-toxic and

15



296

eco-friendly organic acid that is commercially available worldwide. Using ascorbic

297

acid to activate PMS for water treatment offers a promising capability of eliminating

298

organic contaminants in the aqueous phase. In this work, MCLR was used as a model

299

compound, and we develop a first-principles kinetic model to simulate the MCLR

300

degradation and to predict the radical concentrations. The predicted concentrations of

301

HO• and SO4•- ranged from 10-14 M to 10-12 M, which were similar to the

302

concentrations of radicals in other AOPs in practical water treatments.59 Therefore, the

303

H2A/PMS process showed potential application for other selective contaminant

304

destruction. Our model can be used to predict and simulate the degradation of other

305

organic compounds by using this technique. Moreover, our model can determine the

306

optimization of the operational parameters, such as H2A and PMS doses. Our work

307

provides a promising alternative method to other AOPs for water treatment.

308

ASSOCIATED CONTENT

309

Supporting Information

310

The supporting information is available free of charge via the Internet at

311

http://pubs.acs.org.

312

Supplemental text describing chemicals, ESR procedures for detection of sulfate,

313

hydroxyl and ascorbyl radicals, toxicity assessment of MCLR, modeling

314

approach and rate constants determination, kinetic equations, and energy costs.

315

Tables showing objective function values for kinetic model, and oxidation

316

products of MCLR. Figures showing calibration curve for toxicity assessments,

317

and proposed activated mechanism of PMS by ascorbic acid; model-predicted

318

peroxymonosulfate radical concentrations; intensity profiles of hydroxyl radical,

16


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319

sulfate radical and ascorbyl radical; fractions of H2A, HA- and A2- species under

320

different pH values; model-predicted sulfate radical and hydroxyl radical

321

distributions under different NOM concentrations; EE/Ototal (in kWh L-1) of

322

H2A/PMS process vary with H2A and PMS doses; proposed pathways of MC-LR

323

degradation in the H2A/PMS process.

324

AUTHOR INFORMATION

325

Corresponding Authors

326

* Phone: 404-894-5676; fax: 404-894-7896; e-mail: [email protected]

327

Notes

328

The authors declare no competing financial interest.

329

ACKNOWLEDGEMENT

330

This work was financially supported by the National Natural Science Foundation

331

(51508174). Financial support from the China Scholarship Council for Zhou’s visiting

332

research in Georgia Institute of Technology is especially acknowledged. This research

333

was also supported by the Brook Byers Institute for Sustainable Systems, Hightower

334

Chair, and the Georgia Research Alliance at the Georgia Institute of Technology. W.

335

Zhang also acknowledges financial support from the China Scholarship Council. The

336

views and ideas expressed herein are solely of the authors and do not represent the

337

ideas of the funding agencies in any form.

338

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25



515

Page 26 of 35

Table 1 Elementary reactions in the H2A/PMS system. No.

Elementary reactions

k (M-1 s-1)

Reference

1

. H A + HSO- → H / + H O + SO. 0 + A

3.1×103

fitted

2

HA + HSO- → H O + SO0. + A.

2.9×103

fitted

3

SO. 0 + H O → HO ∙ +HSO0

k8[H2O]=1.8×103 s-1

4

SO. - + H O → HO ∙ +HSO-

k8[H2O]=1.0×103 s-1

38

5

/ . SO. 0 + H A → 2H + SO0 + A

1.9×109

fitted

6

/ . SO. 0 + HA → H + SO0 + A

8.0×109

fitted

7

HO ∙ +H A → H / + H O + A.

4.3×109

fitted

8

HO ∙ +HA → H O + A.

9.9×109

fitted

9

. SO. 0 + HSO- → SO- + HSO0

1.0×106

41

10

HO ∙ +HSO- → SO. 0 + H O + 0.5O

1.7×107

42

11

A. + A. → A

2.2×105

fitted

12

A. + SO0. → SO 0 +A

1.0×109

fitted

13

A. + HO ∙→ OH + A

6.9×109

fitted

14

SO0. + SO. 0 → S O6

1.6×108

15

. SO. 0 + SO- → S O6 + 0.5O

8.96×109

16

HO ∙ +HO ∙→ H O

5.0×109

17

HO ∙ +H O → H O + HO ∙

2.7×107

18

HO ∙ +HO ∙→ H O + O

6.6×109

19

HO ∙ +HO ∙→ H O + O

8.3×105

20

HO ∙ +H O → HO ∙ +O + OH

3.0

21

SO0. + H O → HSO0 + HO ∙

1.2×107

22

SO. 0 + HO ∙→ HSO0 + O

3.5×109

23

SO. 0 + HO ∙→ HSO-

1.0×1010

24

SO-. + SO-. → S O 6 + O

2.2×108

25

SO-. + SO-. → SO0. + SO 0 + O

2.1×108

26

. S O 6 + HO ∙→ SO0 + HSO0 + 0.5O

1.2×107

In the presence of MCLR

26


40

43

38

44

44

45

46

44

47

47

41

41

41

48

Page 27 of 35


27

SO0. + MCLR → Products + SO 0

7.5×109

fitted

28

HO ∙ +MCLR → Products

2.6×109

fitted

In the presence of NOM 29

SO0. + NOM →

2.35×107 Mc-1 s-1

49

30

HO ∙ +NOM →

3.0×108 Mc-1 s-1

49

516

27


MCLR concentration (M)


2.0x10

-7

1.5x10

-7

1.0x10

-7

5.0x10

-8

Page 28 of 35

H2A in dark PMS in dark H2A/PMS process in dark

0.0 0

5

10

15

20

25

30

Time (min)

517 518 519 520

Figure 1 Concentration profiles of MCLR with H2A alone, PMS alone, and the H2A/PMS process. Experimental conditions: [MCLR]0 = 2.0×10-7 M, H2A = 2.0×10-6 M, PMS = 5.0×10-6 M, and pH0 = 4.0.

28


Page 29 of 35


(a)

t=2.0 min t=4.0 min

Intensity

t=10.0 min

t=20.0 min

t=30.0 min

3320

3340

3360 3380 Magnetic field (G)

3400

521

(b) t=2.0 min

Intensity

t=4.0 min

t=10.0 min

t=20.0 min

t=30.0 min

3480

522 523 524

3500 3520 Magnetic field (G)

3540

Figure 2 ESR spectra of DMPO-OH and DMPO-SO4 (a) and the ascorbyl radical (b) during the H2A/PMS process. DMPO-OH adducts; DMPO-SO4 adducts; ascorbate radicals.

29



Page 30 of 35

-13

-7

Concentration of radicals (M)

8.0x10

1.2x10 Sulfate radical Hydroxyl radical Ascorbyl radical

-13

6.0x10

-8

8.0x10 -13

4.0x10

-8

4.0x10 -13

2.0x10

0.0

0.0 0

5

10

15

20

25

30

Time (min)

525 526 527

Figure 3 Model-predicted sulfate radical, hydroxyl radical and ascorbyl radical concentrations during the H2A/PMS process. Conditions: H2A = 2.0×10-6 M, PMS = 5.0×10-6 M, and pH0 = 4.0.

30


Page 31 of 35


Concentration of MCLR (M)

(a) -7

1.0E-6 M H2A

2.0x10

2.0E-6 M H2A 5.0E-6 M H2A

-7

1.5x10

1.0E-5 M H2A -7

1.0x10

-8

5.0x10

0.0 0

5

10

15

20

25

30

Time (min)

528


(b) 1.0E-6 M PMS 2.0E-6 M PMS 5.0E-6 M PMS 1.0E-5 M PMS

-7

2.0x10

-7

1.5x10

-7

1.0x10

-8

5.0x10

0.0 0

5

10

529 530 531 532 533

15

20

25

30

Time (min)

Figure 4 (a) Concentration profiles of MCLR under different H2A concentrations. (b) Concentration profiles of MCLR under different PMS concentrations. The dots show the experimental results, and the solid lines are model fits. Conditions: [MCLR]0 = 2.0×10-7 M, H2A = 1.0×10-6-1.0×10-5 M, PMS = 1.0×10-6-1.0 ×10-5 M, and pH0 = 4.0.

31



Page 32 of 35


(a) -7

2.0x10

pH 4 pH 5 pH 6 pH 12

-7

1.5x10

-7

1.0x10

-8

5.0x10

0.0 0

5

10

15

20

25

30

Time (min)

534 (b)

Experimental result Model prediction

2.4

-3

-1

Rate constants (10 s )

2.8

2.0 1.6 1.2 0.8 0.4 0.0 3

4

5

6

7

pH

535 536 537 538

Figure 5 (a) Concentration profiles of MCLR under different initial solution pH values. (b) Effect of pH on the pseudo-first-order rate constant for the oxidation of MCLR. The dots show the experimental results, and the solid lines represent the model predictions. Note that the

539 540

concentration profile of MCLR at pH 12 was not modeled because of the non-reactivity of A . Conditions: [MCLR]0 = 2.0×10-7 M, H2A = 2.0×10-6 M, and PMS = 5.0×10-6 M.

2-

32


Page 33 of 35


(a) Concentration of MCLR (M)

-1

0 mg L NOM -1 1.0 mg L NOM -1 3.0 mg L NOM -1 5.0 mg L NOM

-7

2.0x10

-7

1.5x10

-7

1.0x10

-8

5.0x10

0.0 0

5

10

15

20

25

30

Time (min)

541

1.6

Experimental result Model prediction

-3

-1

Rate constants (10 s )

(b) 2.0

1.2

0.8

0.4

0.0 0

1

2

3

4

5

-1

542 543 544 545 546

NOM (mg L )

Figure 6 (a) Concentration profiles of MCLR under different NOM concentrations. (b) Effect of NOM concentrations on the pseudo-first-order rate constant for the oxidation of MCLR. The dots show the experimental results, and the solid lines represent the model predictions. Conditions: [MCLR]0 = 2.0 ×10-7 M, H2A = 2.0×10-6 M, PMS = 5.0×10-6 M, and pH0 = 4.0.

33



-5

Page 34 of 35

-4

x 10

x 10

5 10 4

PMS Dose (M)

8 3 6 2 4 1 2 2

4

6

H2A Dosage (M)

8

10 -6

x 10

547 548 549

Figure 7 EE/Ototal (in kWh L-1) of H2A/PMS process vary with H2A and PMS doses. Conditions: [MCLR]0 = 2.0 ×10-7 M, H2A = 1.0×10-7-1.0×10-5 M, PMS = 1.0×10-6-5 ×10-5 M, and pH0 = 4.0.

34


Page 35 of 35


-7

MCLR concentration (M)

2.0x10

LC/MS/MS analysis PP2A assessment

-7

1.5x10

-7

1.0x10

-8

5.0x10

0.0 0

2

5

10

20

30

Time (min)

550 551 552

Figure 8 Variations of MCLR concentrations and hepatotoxicity by the H2A/PMS process. Conditions: [MCLR]0 = 2.0 ×10-7 M, H2A = 2.0×10-6 M, and PMS = 5.0×10-6 M.

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Kinetic modeling and toxicity assessment - ACS Publications

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