Chapter 13: Cyanobacterial toxin removal 

recreational waters 

Judy A Westrick 

Abstract 

Although federal drinking water regulations determine the quality of potable water, many specifics influence how each utility chooses to treatment 

water. Some of the specifics include source water quality, storage capacity, existing unit process, and space. An overview of the US recreational 

and drinking water regulations were discussed in context of cyanobacterial 

toxin removal and inactivation by ancillary as well as auxiliary treatment 

practices. Ancillary practice refers to the removal or inactivation of algal 

toxins by standard daily operational procedures where auxiliary treatment 

practice refers to intentional treatment. An example of auxiliary treatment 

would be the addition of powder activated carbon to remove taste and odor 

compounds. The implementation of new technologies as such ultraviolet 

disinfection and membrane filtration, to meet current and purposed regulations, can greatly affect the algal toxin removal and inactivation efficiencies. A discussion on meeting the current regulations by altering chemical 

disinfection, ozone, chlorine, chloramines and chlorine dioxide included 

their ancillary effects on the protection against algal toxins. Although 

much of the research has been on the efficiency of the removal and inactivation of microcystin LR and several microcystin variants, the discussion 

included other algal toxins: anatoxin–a, saxitoxins, and cyclindrospermopsin. 

in drinking water treatment processes and 
276 J.A. Westrick 

Introduction 

Before the United States Environmental Protection Agency (USEPA) can 

develop guidelines or regulations concerning the permissible concentrations of algal toxins for drinking water, they must first determine if 

cyanoalgal toxins can be removed or inactivated through common drinking 

water treatment practices. In 2000, a group of experts, through a USEPA 

initiative, created a cyanoalgal toxin priority list that contained the microcystins, anatoxin–a, and cylindrospermopsin. Microcystins are cyclic peptide hepatotoxins with a conserved (2S, 3S, 8S, 9S)–3–amino–9–methoxy–

2,6,8–trimethyl–10–phenyl–deca–4,6–dioc acid, frequently abbreviated as 

Adda, and variable amino acids. Since there are over 70 variants of microcystins, a short list of four variants, LR, YR, LA and RR, referring to the 

changes in the amino acids, was recommended based on prevalence and 

toxicity. Cyanoalgal toxins can be either found inside of the cell, “intracellular”, or outside the cell, “extracellular”. The efficiency of a drinking 

water unit process with respect to the removal of cyanoalgal toxins depends on the total concentration of the algal toxins, the form of the toxin, 

and whether it is intracellular or extracellular. Commonly, dissolved contaminants such as extracellular cyanoalgal toxins are most costly to remove because conventional treatment (flocculation, coagulation, sedimentation and filtration) is usually not effective and advanced treatment 

processes must be implemented unless the contaminant is oxidized through 

disinfection. This paper reviews the literature on cyanotoxin removal during drinking water treatment with the initial focus on the removal of extracellular toxins followed by the removal of intracellular toxins. Published treatment reviews include Yoo (1995), Chorus (1999), Westrick 

(2003), Svrcek (2004), and Newcombe (2004). 

With more stringent drinking water regulations and decreases in surface 

water quality, drinking water treatment trains have become more complex 

with fewer utilities using conventional treatment (coagulation/sediment/filtration/chlorination) alone. New additions have included more traditional 

unit processes like powered activated carbon (PAC), pretreatment with 

oxidants other than chlorine, ballasted flocculation, as well as advanced 

treatment processes such as membrane filtration, ultraviolet photolysis, 

granular activated carbon (GAC) absorbers and ozone. The traditional oxidant/disinfectant, chlorine, has been replaced with, or supplemented by, 

ozone, potassium permanganate, chlorine dioxide, or chloramines to eliminate nuisance organisms (e.g., zebra mussels) from the intake, compounds 

that cause taste and odor problems, and more recently compounds that react with chlorine disinfectant to produce toxic chlorinated by products. 
Chapter 13: Cyanobacterial Toxin Removal 277 

Extracellular Cyanotoxin Inactivation by Chemical 

Disinfection Processes 

Usually the primary focus of the disinfection process is to inactivate 

pathogenic organisms. The disinfection process can also be used to degrade several nuisance compounds such as those that cause taste and odor 

problems and a few regulated organic contaminants such as, some pesticides and fungicides, and industrial waste products. However, the disinfectant may also react with organic compounds in the water to produce 

toxic or carcinogenic byproducts. With health risk concerns about the exposure to chlorinated disinfection byproducts; the traditional chlorination 

process is being replaced by or supplemented with chloramination, chlorine oxide, ozone, and UV disinfection. This section focuses on the effectiveness of disinfection oxidants at inactivating important cyanotoxins. 

Commonly, disinfectant effectiveness is expressed in terms of the product of the disinfectant concentration (C) in mgL-1 and the contact time (T) 

in minutes; hence CT values are in units of mgL-1min. The effectiveness of 

a disinfectant depends primarily on the water pH, the water temperature, 

the concentration of compounds in the water that can react with the disinfectant, and the target organism itself. Thus, CT values for a particular 

disinfectant will also vary according to these factors. Several federal regulations incorporate CT values to guide the inactivation of both microorganisms and chemical contaminants. An example is Table 1, which shows the 

CT values needed with chorine at different water temperatures and pH values to reduce the level of the protozoan pathogen Giardia lamblia by 

99.9%. As the temperature increases, the CT values for 99.9% inactivation 

of G. lamblia decrease. On the other hand, as pH increases, the CT values 

also increase. Since many utilities use these tables to determine which disinfectant dose to use, it is relevant to compare CT values needed to control 

G. lamblia with those needed to control the most common cyanotoxin, microcystin. 

The CT values for the inactivation of 10 ug/L and 50 ug/L microcystin 

LR (MCYLR) for a batch reactor are presented in Table 2 (Acero 2005). 

When comparing Tables 1 and 2, at pH values of 6 and 7, the chlorine CT 

values needed for 99.9% inactivation of G. lamblia would also decrease 50 

ug/L and 10 ug/L microcystin below the World Health Organization’s 

drinking water guideline of 1 ug/L MCYLR , except perhaps at warm water temperatures. However, at a pH above 8, several of the CT values associated with the initial doses of 50 ug/L and 10 ug/L are much larger than 

those for 99.9% inactivation of G. lamblia. The larger CT values for both 

G. lamblia and microcystin inactivation at pH 8 and 9 reflect the change of 
27

the equilibrium from a strong oxidant, hypochlorous acid, to a weak oxidant, hypochlorite ion. Determining chlorine CT values for the inactivation of MCYLR gives the utilities a familiar tool which can easily be incorporated into treatment practices. 

Two recent publications (Acero 2005 and Ho 2005) proposed chlorine 

inactivation mechanisms for several microcystins. Acero reported that 

MCYLR, microcystin RR (MCYRR) and microcystin YR (MCYYR) react 

with chlorine at a similar rate, suggesting that hydroxylation of the conversed Adda moiety is the likely site of deactivation. In contrast, Ho and 

coworkers reported that the reaction rates with chlorine for the four MCYs 

they studied differed, where MCYYR>MCYRR>MCYLR>MCYLA, suggesting the oxidation of various amino acids was the most important 

mechanism of deactivation. Regardless of the mechanism, both reports 

suggested that chlorination is an effective treatment for destroying the 

studied microcystins. 

Table 1. Chlorine CT values for 99.9% (3-log) inactivation of G. lamblia cysts. 

Modified version (EPA Guidance Manual, 2003) 

pH CT values (mgL-1min) 

 10oC 15oC 20oC 25oC 

6 87 58 44 29 

7 124 93 62 41 

8 182 122 91 61 

9 265 177 132 88 

 

Table 2. Chlorine CT values for reducing microcystin concentration to 1 ugL-1 

for a batch reactor. 

pH MCYLR CT values (mgL-1min) 

 (ug/L) 10oC 15oC 20oC 25oC 

6 50 46.6 40.2 34.8 30.8 

 10 27.4 23.6 20.5 17.8 

7 50 67.7 58.4 50.6 44.0 

 10 39.8 34.4 29.8 25.9 

8 50 187.1 161.3 139.8 121.8 

 10 110.3 94.9 82.8 71.7 

9 50 617.2 526.0 458.6 399.1 

 10 363.3 309.6 269.8 234.9 

The inactivation of saxitoxins, cylindrospermopsin and anatoxin–a by 

chlorination has not been studied as thoroughly as the degradation of the 

microcystins by chlorination. Recent work suggests that the degradation 

of saxitoxins by chlorine is also pH dependent; however, in contrast with 

8 J.A. Westrick 
 279 

the microcystins, higher pH values increase the inactivation rate of saxitoxin and thus decrease the CT values needed for inactivation. At pH 9, a 

CT value of 15 mgL-1min (chlorine residual of 0.5 mgL-1 for 30 minutes) 

degraded the five studied saxitoxins by 90% (Nicholson, 2003). The saxitoxins order of reactivity towards chlorine was as follows, with the most 

toxic saxitoxin being the most susceptible: 

GTX5=dcSTX>STX>GTX3=C2>GTX2 

Cylindrospermopsin is very susceptible to oxidation by chlorine when the 

free chlorine residual is above 0.5 mgL-1 with a 30 minute contact time, 

CT values 15 mg min/L and at a pH above 6 (Senogles 2000), implying 

that cylindrospermopsin is more susceptible to chlorination than microcystins. These researchers suggested that the more effective degradation 

of both saxitoxins and cylindrospermopsin at higher pH values is probably 

due to both the saxitoxins and cyclindrospermopsin being in the unprotonated form. Anatoxin–a is not degraded by chlorination (Carlile 1994). 

Thus, different cyanotoxins react differently to chlorine. When a cocktail 

of cyanotoxins is present in a drinking water source, it is important to note 

that cylindrospermopsin and microcystin are more effectively inactivated 

at lower pH values, while saxitoxins are more effectively inactivated at 

higher pH values and anatoxin–a may not be degraded appreciably. 

The toxicities of chlorination byproducts of microcystins, nodularin, 

saxitoxin and cylindrospermopsin have been examined. Microcystin and 

nodularin byproducts are not toxic by acute toxicity tests such as the 

mouse bioassay (Nicholson 1994), protein phosphatase inhibition assay, 

and mutagenicity (Tsuji 1997). Similarly, the byproducts from the chlorination of saxitoxins have been tested by mouse bioassay and have found 

not to be acutely toxic (Newcombe 2002a and Nicholson 2003). In contrast, the chlorination byproducts of cylindrospermopsin produce a low 

level of liver damage and genotoxicity (Shaw 2001). An oral 90 and 170 

day toxicity study of chlorinated solutions with microcystin, saxitoxin and 

cylindrospermopsin showed that only cylindrospermopsin byproducts produced ill effects, i.e. fatty vacuolations of the liver in mouse (Senogles–

Derham 2003). Chronic testing has not been performed for any of the algal 

toxins. 

Other chlorine disinfection processes such as chloramines and chlorine 

dioxide have shown little promise towards degrading cyanotoxins. 

Chloramine doses, as high as 20 mgL-1 with 2 day exposures, did not degrade microcystins (Nicholson 1994). Although chlorine dioxide is used 

in several plants to remove taste and odor compounds, it is not recommended for treatment of microcystins since the dosage would not be cost 

Chapter 13: Cyanobacterial Toxin Removal
280

effective (Kull 2004). Although one might speculate that cylindrospermopsin, anatoxin–a, and saxitoxins are not susceptible to chloramine and 

chlorine dioxide treatment, studies are needed to validate this statement. 

Ozone is an effective disinfectant that oxidizes organic compounds either directly as molecular ozone or indirectly through a hydroxyl radical. 

Microcystin and anatoxin–a are inactivated at ozone doses where a residual is maintained for several minutes, CT values of 0.1 ugL-1min and 0.3 

ugL-1min, respectively. (Keijola 1988, Himberg 1989, Bruchet 1998, Hart 

1998, Rositano 1998, 2001, Newcombe 2002b). An acute toxicity screen 

was negative for microcystin ozone byproducts. The saxitoxin family appears to have low to moderate susceptibility to ozone oxidation, with a CT 

value of 6.9 mg/L min not being effective (Rositano 2001, Newcombe 

2002b). The author of this review speculates that ozone would be an effective treatment to inactivate cylindrospermopsin because ozone is highly 

reactive toward unsaturated bonds. The confounding factors of ozone 

treatment for cyanoalgal toxins are 1) oxidation of the dissolved carbon 

competes with the destruction of algal toxins and 2) sensitive to alkalinity 

and temperature. 

Extracelluar Cyanotoxin Removal by Activated Carbon 

Adsorption 

Two types of activated carbon are used in the drinking water industry: 

powdered activated carbon (PAC) and granular activated carbon (GAC). 

Common sources of activated carbon are coal, coconut, and wood. Several 

studies suggest that mesoporous (i.e., pore diameters between 2–50 nm),

wood–based activated carbon is more effective at removing cyanotoxins 

than other types of activated carbon. PAC is usually used seasonally to remove taste and odor compounds and agricultural chemicals, or as an emergency barrier during industrial/commercial spills. Drinking water utilities 

can test the relative effectiveness of various PAC types for removing a 

contaminant(s) of concern by performing jar tests, and then purchase the 

carbon with the most capacity for their target contaminants. A series of jar 

tests suggest different microcystins have different adsorption efficiencies: 

RR>YR>LR>LA (Cook 2002) 

The efficiency of saxitoxins removal by PAC mirrors the order of toxicity, 

with saxitoxin STX being the most toxic: 

STX>GTX>C (Newcombe 2004) 

 J.A. Westrick 
 281

Very little work has been performed on the adsorption of anatoxin–a and 

cylindrospermopsin to PAC. More systematic studies are needed to determine which PAC type, dosage, and contact time are most appropriate. 

Although more research is needed to guide drinking water utilities on the 

effectiveness of PAC for anatoxin–a, cylindrospermopsin and mixtures of 

cyanotoxins, the author of this review still stresses the importance of site 

specificity and in–house jar testing to select the most effective activated 

carbon. 

GAC can be used in filter beds along with other filter media or can be 

used as a stand–alone fixed bed adsorber. GAC filters are used primarily 

to remove toxic chemicals and occasionally to remove substances in the 

water that cause taste and odor problems. They lose their organic compound adsorption capabilities usually within a couple of months of use and 

any organic removal after that comes from biological activity on the filter. 

Commonly, the effectiveness and degradation of a GAC filter is measured 

by total organic carbon (TOC) in the filter effluent. When 70–80% of the 

TOC entering the filter is measured in the filter effluent, usually after at 

least three months of service, the GAC media is replaced or reactivated. 

Newcombe and co–workers (2002b) reported microcystin in the GAC effluent at 80% TOC breakthrough suggesting that GAC filters would not be 

an effective barrier for controlling microcystin, since GAC media is not 

replaced monthly. However, frequently GAC absorbers are designed to 

last several months before 80% TOC breakthrough occurs, and since the 

adsorber media is replace upon 80% TOC breakthrough, GAC adsorbers 

may be an effective microcystin and other algal toxin barrier. Newcombe 

and coworkers (2002b) also studied the effect on cyanotoxins of ozonating 

the water before GAC adsorber entry, using two unit processes as one barrier. This barrier will oxidize microcystin, cylindrospermopsin and anatoxin–a, and the GAC absorber would provide an additional barrier to saxitoxins not oxidized by this treatment. To the best of the author’s knowledge, the removal of cylindrospermopsin and anatoxin–a by GAC 

adsorption has not been investigated. 

Extracellular Cyanotoxin Inactivation by Advanced 

Drinking Water Treatment Processes 

The absorbance of ultraviolet (UV) energy can break molecular bonds 

without chemical addition and is used to inactivate many pathogens in 

drinking water. Normally, the UV treatment process uses a low to medium 

pressure lamp with wavelengths between 200 and 300 nm. Commonly, in 

Chapter 13: Cyanobacterial Toxin Removal
28

the water treatment industry, the UV dose is expressed in milli–joules/cm2

(mJ/cm2

). A dose of 40 mJ/cm2 for the inactivation of Crytosporidium 

parvum oocysts is considered economically feasible. Much work has been 

done on the photolytic destruction of microcystins, cylindrospermopsin, 

and anatoxin–a, but the UV doses that effectively degrade microcystin, 

cylindrospermopsin, and anatoxin–a range from 1530 to 20,000 mJ/cm2 

(Tsuji 1995, Chorus 1999, Senogles 2000), or several orders of magnitude 

higher than that needed for Cryptosporidium oocyst. Thus, UV irradiation 

is not considered economically feasible for cyanotoxin degradation. 

The use of titanium dioxide and UV photolysis together successfully 

degrades MCYLR and cylindrospermopsin (Lawton 1999, Feitz 1999, 

Cornish 2000, Senogles 2001, Sherpard 2002). Although this is not a cost 

efficient treatment process for utilities, it may be viable in point–of–use 

treatment (e.g., devices used in the home). The combination of hydrogen 

peroxide with either ozone or UV irradiation enhances the efficiency of 

microcystin destruction (Rositano 1998, Qiao 2005, respectively). With 

hydrogen peroxide at 0.1 mgL-1 and ozone at 0.2 mgL-1, 1 mgL-1 of 

MCYLR was completely removed in 30 minutes (CT value of 6 mgL1

min). However, more research on these combinations for the degradation 

of cyanotoxins is needed to assess their feasibility. 

Extracelluar and Intracellular Cyanotoxin Removal by 

Filtration (other than GAC) 

Semi–permeable membranes such as those used in reverse osmosis filters 

remove many contaminants from water, especially those whose size is larger than the membrane pores. Advances in membrane technology have 

made this process more versatile, dependable and economically feasible as 

a drinking water treatment process. Reverse osmosis and nanofiltration 

membranes remove all pathogens and also large molecules above the 

membrane pore size (100 Daltons for reverse osmosis, 200 Daltons for 

nanofilters). However, the membranes are not necessarily foolproof. 

When concentrations of the removed substance become sufficiently high 

traces of inorganic and organic compounds may pass through the membrane barrier. A reverse osmosis membrane study using between 10 ugL-1

and 130 ugL-1 of MCY LR, RR and nodularin removed greater than 95% 

of the toxin from waters with a range of salinities (Neumann 1998, Vouri 

1997). A water with high conductivity such as brackish water may allow 

slightly greater breakthrough of cyanotoxins than otherwise (Vuori 1997). 

2 J.A. Westrick 
 283

Several nanofiltration studies report from 82% to complete microcystin 

removal (Fawell 1993, Muntisov 1996, Simpson 2002, Smith 2002). 

Microfiltration and ultrafiltration use membranes with greater pore sizes 

than the membranes used in reverse osmosis and nanofiltration. Ultrafiltration is capable of removing intact bacteria (including the cyanobacteria), 

but not all dissolved organic compounds (Fig. 1). Microfiltration, with its 

larger pore size, may not remove all intact bacteria and is not effective in 

removing dissolved organic compounds. Since 50% to 95% of the 

cyanotoxin is intracellular, ultrafiltration and (to a degree) microfiltration 

are effective in removing intracellular cyanotoxins in drinking water supplies. Studies (Chow 1997, and Zhou 2001) suggest that both microfiltration and ultrafiltration either as a stand–alone treatment process or as a replacement to conventional filtration are excellent at removing intact 

cyanobacteria and their intracellular toxins. With regard to conventional 

water filtration (coagulation, sedimentation, and then filtration), a bench –

top jar test apparatus and a full –scale pilot plant resulted in 70% and 

99.9% removal, respectively, of Microcystis cells (Drikas 2001). This 

study suggests that conventional treatment is effective in removing intracellular cyanotoxins. These studies reported very little cell breakage during 

the cell removal process, implying that the process did not cause significant intracellular cyanotoxin release. 

0.01 0.1

100

0.001 1.0 10

Micron 

Scale

MW

100

103

104 105 5*105

Select

Water 

Constituents

Salts Colloids

BACTERIA

Gairdia

Cryptosporidium

Viruses

Dissolved Organics

Membrane

Process

Reverse Osmosis

Nanofiltration

Ultrafiltration

Microfiltration

Particle Filtration

Fig. 1. A summary of membrane processes and their filtration characteristics. 

Modified version (Tech Brief 1999) 

Chapter 13: Cyanobacterial Toxin Removal
28

Through Plant Removal and Inactivation of Cyanotoxins: 

A Multi–barrier Approach 

Toxin–producing cyanobacteria are abundant in surface waters and so they 

impose a degree of risk to drinking water utilities. The toxicity of microcystin LR has prompted the World Health Organization to publish a guideline value of 1.0 ug MCYLR/L for drinking water. Several studies have 

investigated the concentration of cyanotoxins in drinking water treatment 

plants. The most recent studies have been done by Carmichael (2001), 

Karner (2001), Hoeger (2005), and Wood (2005). 

During two year study, 1996 to 1997, Carmichael (2001) measured toxins in source and finished (i.e., filtered) waters in 10 utilities in North 

America. Of the 677 samples tested, 539 (80%) were positive for microcystins when tested using the enzyme linked immunosorbent assay 

(ELISA). Of the positive samples, 4.3% were higher than the 1 ug/L 

WHO guideline. Only two finished water samples were above 1 ugL-1, 

suggesting that during the study many of the utilities were adequately removing or inactivating microcystins. 

Karner’s (2001) study evaluated source and treated water from five 

Wisconsin drinking water plants with four plants located on one lake. The 

reported total concentration of microcystin (intracellular and extracellular 

toxin) was determined by ELISA. The source waters ranged from tenths 

of ugL-1 to 7 ugL-1. The five plants demonstrated 1-3 log removal of microcystin. This study suggested that pretreatment alone (i.e., before filtration) with potassium permanganate, copper sulfate, and PAC reduced algal 

toxins as much as 61%. Karner reported the percent of removal, but did not 

mention the initial microcystin concentrations. There may be several site 

specific reasons that pretreatment worked for these plants; two of the utilities have at least 5.5 day water detention times before being distributed to 

the public and another plant used a lower dose of KMnO4. These conditions could have played an important role in achieving the 61% decrease of 

microcystin. This study stresses the uniqueness of individual treatment 

trains. 

Hoeger’s study investigated microcystin removal through two drinking 

water plants. One plant had pre–ozonation (1.0 mgL-1), rapid sand filtration, intermediate ozonation (0.5 mgL-1), GAC filtration follow by slow 

sand filtration and the other had conventional treatment followed by 

chlorination. The first plant was challenged with a microcystin concentration of approximately 8.0 MCY ugL-1 where as the conventional plant was 

challenged with a concentration of 0.2 MCY ugL-1. Both treatment plants 

removed microcystin below the WHO guideline. 

4 J.A. Westrick 
 285 

During the summer of 2005, Wood and coworkers (2005) studied 

cyanobacteria and algal distribution as well as microcystin concentrations 

in source and finished waters from five utilities in Oklahoma, Vermont, 

Texas, California and Florida. They found that several of the source waters 

had low levels of microcystin from 0.2 ugL-1 MCY to 0.5 ugL-1 MCY and 

none of the finished waters were above 0.05 ugL-1 MCY, as determined by 

ELISA. This study also showed that typical conventional treatment removed from 2 to 5 log of algal units mL-1 (Fig. 2) and finished water 

commonly contained less than 2 algal units mL-1. 

New Technologies 

Electrochemical degradation was investigated as a new drinking water 

technology to degrade extracellular microcystin LR through a hydroxyl 

radical mechanism similar to other advanced oxidation processes (Feng 

2005). At an applied current of 100mA, the degradation rate was 0.219 

min-1 and the half–life was 2.5 min. This experiment suggested that the 

electrochemical oxidation may be a promising approach for microcystin 

degradation.

Chapter 13: Cyanobacterial Toxin Removal
1

0

10

100

1,000

10,000

100,000

1,000,000

05/04/05

05/14/05

05/24/05

06/03/05

06/13/05

06/23/05

07/03/05

07/13/05

07/23/05

08/02/05Date

Log of Algal Counts (units/mL)

1.201.000.800.600.400.200.00

Microcystin Concentrations from 

ELISA (ppb)

Source Total Algal Units Source Toxin ProducersDistribution Total Algal UnitsDistribution Toxin ProducersSource MCY (secondary axis)Distribution MCY (secondary axis)

Fig. 2. This graph depicts the removal of intact algal cells and microcystin by conventional 

treatment.

286 J.A. Westrick 
 287 

Conclusion 

Drinking water utility managers have several source water and treatment 

options for removing and inactivating both intracellular and extracellular 

cyanotoxins. The first consideration should be to optimize the effectiveness of existing processes. Intracellular cyanotoxins can be removed effectively by conventional treatment and membrane filtration. Chloramination 

and UV treatment are not effective for inactivating extracellular algal toxins. Although several oxidants inactivate some cyanotoxins, it is important 

to remember that not one oxidant inactivates all cyanotoxins. Chlorine effectively degrades extracellular cyanotoxins both microcystins and cylindrospermopsin between pH 6.0 and 8.0, and saxitoxins at pH values at 9 

and higher. Utilities that want to determine the risk of cyanotoxins to their 

system may use a simple and rapid procedure published by the World 

Health Organization (Chorus 1999). 

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