**4. Cyanobacteria/cyanotoxins risk assessment**

Risk assessment consists in the identification and determination of quantitative or qualitative value of risk related to the exposure to a given hazard, taking into account possible harmful effects on individuals or populations exposed to that hazard and all the possible routes of exposure. The risk assessment process includes four steps: the hazard identification, hazard characterization, exposure assessment, establishment of dose–effect and dose–response relationships in likely target individuals and populations (Duffus et al., 2007). A schematic representation of the steps involved in risk assessment of cyanotoxins is depicted in Fig. 3.

The scientific knowledge on cyanotoxins still does not enable to correctly assess the risk of human exposure to toxic cyanobacteria. Many toxicological aspects remain to clarify, epidemiological data are insufficient and the exposure assessment is a very complex task.

The human exposure to cyanobacterial cells and/or its toxins may occur through water swallowing or inhalation during recreational activities such as swimming, canoeing, sailboarding and paddling, through the intake of contaminated drinking water and through hemodialysis treatment.

Most episodes of human illness related with cyanobacteria/cyanotoxins resulted from an acute intoxication through the exposure routes mentioned above (for review see Chorus et al., 2000; Duy et al., 2000; van Apeldoom et al., 2007), such as the following examples:

Example 1 – Symptoms after exposure through recreational activity: nausea, abdominal pain, fever, dyspnea, respiratory distress, atypical pneumonia and hepatotoxicosis with a significant increase of hepatic damage biomarkers (Giannuzzi et al., 2011);

the summer a great variety of microalgae and cyanobacteria usually co-exist in the same water body, towards the end of summer this diversity may drop drastically as the result of the mass development of the cyanobacterial communities (blooms) (Sze, 1986). These blooms may be formed by a consortium of cyanobacteria producing different amounts of toxins at different rates, with the same bloom-forming species having both toxigenic and non-toxigenic strains, indistinguishable by morphological examination. Cyanobacterial

Cyanobacteria are able to produce secondary metabolites that present a vast diversity of structures and variants. Most of cyanobacterial secondary metabolites are alkaloids, or possess peptidic substructures synthesised by NRPS (non-ribosomal peptide synthesis, involving peptide synthetases) or NRPS/PKS (involving peptide synthetases and polyketide

Cyanotoxins are usually classified according to their target in mammals, being divided in hepatotoxins (liver damaging), neurotoxins (nerve damaging), cytotoxins (cell damaging) and toxins responsible for allergenic reactions (dermatotoxins), presenting several kinds of mechanisms of action. A considerable number of these different types of toxins have been

Risk assessment consists in the identification and determination of quantitative or qualitative value of risk related to the exposure to a given hazard, taking into account possible harmful effects on individuals or populations exposed to that hazard and all the possible routes of exposure. The risk assessment process includes four steps: the hazard identification, hazard characterization, exposure assessment, establishment of dose–effect and dose–response relationships in likely target individuals and populations (Duffus et al., 2007). A schematic representation of the steps involved in risk assessment of cyanotoxins is

The scientific knowledge on cyanotoxins still does not enable to correctly assess the risk of human exposure to toxic cyanobacteria. Many toxicological aspects remain to clarify, epidemiological data are insufficient and the exposure assessment is a very complex task.

The human exposure to cyanobacterial cells and/or its toxins may occur through water swallowing or inhalation during recreational activities such as swimming, canoeing, sailboarding and paddling, through the intake of contaminated drinking water and through

Most episodes of human illness related with cyanobacteria/cyanotoxins resulted from an acute intoxication through the exposure routes mentioned above (for review see Chorus et al., 2000; Duy et al., 2000; van Apeldoom et al., 2007), such as the following examples:

Example 1 – Symptoms after exposure through recreational activity: nausea, abdominal pain, fever, dyspnea, respiratory distress, atypical pneumonia and hepatotoxicosis with a

significant increase of hepatic damage biomarkers (Giannuzzi et al., 2011);

isolated from cyanobacteria, belonging to different taxa, as summarized in Table 1.

blooms are complex and can develop in a rather sudden and unpredictable way.

**3. Cyanotoxins** 

depicted in Fig. 3.

hemodialysis treatment.

synthases) hybrid pathways (Valério et al., 2010).

**4. Cyanobacteria/cyanotoxins risk assessment** 

Example 2 – Symptoms after exposure during heamodialysis treatment: weakness, muscular pain, nauseas, vomiting, neurologic symptoms (head pain, vertigo, deafness, blindness and seizures), increase of hepatic damage biomarkers, hepatomegaly, hepatic failure and death (reviewed in Pouria et al, 1998).

Fig. 3. Organizational chart of the steps involved in risk assessment (adapted from Dolah et al. 2001).

Besides the acute effects mentioned above, few papers reports the association between the ingestion of water contaminated with microcystins and the increase of hepatocarcinoma (Yu, 1995; Ueno et al., 1996) and colorectal cancer (Zhou et al, 2002) in human populations supplied with untreated- or ineffective-treated water.

Laboratorial studies have demonstrated that, in fact, microcystins, nodularins and cylindrospermopsin are genotoxic (reviewed in Zĕgura et al., 2011) and the carcinogenic

Risk Assessment of Cyanobacteria and Cyanotoxins,

**Cyanobacterial cells** 

< 20,000 of total cyanobacterial

< 10 μg L-1 chlorophyll-*a* with dominance of cyanobacteria

< 2.5 mm3 L-1 cyanobacterial

10 - 50 μg L-1 chlorophyll-*a* with dominance of cyanobacteria

2.5 - 12.5 mm3 L-1 cyanobacterial

Cyanobacterial scum formation in contact recreation areas

> 100,000 of total cyanobacterial

> 50 μg L-1 chlorophyll-*a* with dominance of cyanobacteria

> 12.5 mm3 L-1 cyanobacterial

20,000 - 100,000 of total cyanobacterial cells mL-1

cells mL-1 OR

OR

OR

OR

OR

OR

biomass

**4.1 Derivation of guideline values** 

biomass

cells mL-1 OR

biomass

**WHO guideline levels** 

Low

Moderate

High

(WHO, 2003).

effect-level (**LOAEL**).

the Particularities and Challenges of *Planktothrix* spp. Monitoring 67

**and chlorophyll levels Health risks Recommended action** 

Short term adverse health

Short term adverse health outcomes, e.g. skin irritations, gastrointestinal illness, probably at low frequency

Short term adverse health outcomes such as skin irritations or gastrointestinal illness following contact or accidental ingestion Severe acute poisoning is possible in worst ingestion

cases

Characterization of human hazards usually relies mainly on animal studies, or incidents

Few studies in rodents and pigs enabled to estimate the tolerable daily intake (**TDI**) of some cyanobacterial toxins (Duy et al., 2000; Falconer et al., 1999; Humpage and Falconer, 2003). Usually, studies with different quantitative animal dosing data, with follow-up over extended periods (preferably over the lifetime of the animal being tested) are necessary to estimate a no-observed-adverse-effect level (**NOAEL**), or at least a lowest-observed-adverse-

NOAEL orLOAEL

Table 2. WHO guideline values for safe practice in managing bathing waters that may contain cyanobacterial cells, according to the level of probability of adverse health effects

from which quantitative estimates of the hazards to humans can be extrapolated.

For drinking water, the TDI for cyanotoxins can be estimated as:

�����

outcomes unlikely Continue monitoring

Add signs to indicate MODERATE alert level - increased health risk for swimming and other water contact activities

Immediate action to prevent contact with

Add signs to indicate HIGH alert level warning of danger for swimming and other water contact activities

scums

UF (1)

potential of these toxins have been postulated (Gehringer, 2004; Kinnear, 2010). However, there are still many uncertainties that difficult an unequivocal conclusion about this issue.

The problem of chronic effects are particularly relevant in the case of continuous exposure to low levels of cyanotoxins, even at residual levels, that are not detected by the conventional methods employed in the monitoring procedures. Moreover, the scientific and analytical limitations hinder the complete determination of the toxicological properties of cyanotoxins, and the correct assessment of human exposure to cyanotoxins, as well as lack to provide epidemiological evidence that could confirm the chronic effects of cyanotoxins on human health. Therefore, although the surveillance programs can somehow protect against the cyanotoxins acute effects, risk assessment procedures should be developed and implemented, particularly in what concerns to chronic exposure to cyanotoxins.

During the last decade, the WHO has been regularly reviewing the public health significance of cyanobacteria occurrence in freshwater and developed guidelines for drinking and recreational water environments (WHO, 1998, 2003). This organization recommends that the approach to developing guidelines for cyanobacteria in freshwater should consider:


WHO (2003) has divided the health effects into two categories:


Given the two types of severity of the symptoms, the WHO considered that the establishment of a single guideline value was not appropriate and, therefore, it has defined several guideline values associated with increasing severity and probability of impact of cyanobacteria/cyanotoxins in health at three levels for bathing waters (Table 2) and guideline values for cyanotoxins in drinking water (see 4.1).

Cyanotoxin analysis will generally be required in one of the following circumstances (WHO, 1999):


A brief summary of the steps that must be taken into account, when performing cyanobacteria monitoring, are presented in Fig. 4.

potential of these toxins have been postulated (Gehringer, 2004; Kinnear, 2010). However, there are still many uncertainties that difficult an unequivocal conclusion about this issue. The problem of chronic effects are particularly relevant in the case of continuous exposure to low levels of cyanotoxins, even at residual levels, that are not detected by the conventional methods employed in the monitoring procedures. Moreover, the scientific and analytical limitations hinder the complete determination of the toxicological properties of cyanotoxins, and the correct assessment of human exposure to cyanotoxins, as well as lack to provide epidemiological evidence that could confirm the chronic effects of cyanotoxins on human health. Therefore, although the surveillance programs can somehow protect against the cyanotoxins acute effects, risk assessment procedures should be developed and

During the last decade, the WHO has been regularly reviewing the public health significance of cyanobacteria occurrence in freshwater and developed guidelines for drinking and recreational water environments (WHO, 1998, 2003). This organization recommends that the approach to developing guidelines for cyanobacteria in freshwater

 the occurrence of cyanobacteria in general (in addition to their toxins) as part of the hazard, because it is not clear that all known toxic components have been identified and

the hazard associated with the potential of scums formation, which increase the local

Symptoms associated with skin irritation and allergic reactions resultants from dermal

 Potentially more severe effects due to the exposure to high concentrations of already known cyanotoxins, particularly microcystins (the most commonly found and more

Given the two types of severity of the symptoms, the WHO considered that the establishment of a single guideline value was not appropriate and, therefore, it has defined several guideline values associated with increasing severity and probability of impact of cyanobacteria/cyanotoxins in health at three levels for bathing waters (Table 2) and

Cyanotoxin analysis will generally be required in one of the following circumstances (WHO,

1. Action Level 1 status (i.e. > 2000 cells mL-1) predominated by *Microcystis aeruginosa*, or when concentrations of other potentially toxic taxa (see Table 1) exceed 15 000 cells mL-1. 2. Action Level 2 status where numbers of a cyanobacterial taxa not previously recorded as toxic exceed 100,000 cells mL-1 (recommended toxicity analysis by mouse bioassay or

A brief summary of the steps that must be taken into account, when performing

irritation symptoms reported may be caused by these unknown substances;

the particular hazard caused by the well-known cyanotoxins; and

WHO (2003) has divided the health effects into two categories:

exposure to unknown cyanobacterial substances, and

guideline values for cyanotoxins in drinking water (see 4.1).

implemented, particularly in what concerns to chronic exposure to cyanotoxins.

should consider:

hazard concentration.

studied cyanotoxins).

comparative method).

cyanobacteria monitoring, are presented in Fig. 4.

1999):


Table 2. WHO guideline values for safe practice in managing bathing waters that may contain cyanobacterial cells, according to the level of probability of adverse health effects (WHO, 2003).

#### **4.1 Derivation of guideline values**

Characterization of human hazards usually relies mainly on animal studies, or incidents from which quantitative estimates of the hazards to humans can be extrapolated.

Few studies in rodents and pigs enabled to estimate the tolerable daily intake (**TDI**) of some cyanobacterial toxins (Duy et al., 2000; Falconer et al., 1999; Humpage and Falconer, 2003).

Usually, studies with different quantitative animal dosing data, with follow-up over extended periods (preferably over the lifetime of the animal being tested) are necessary to estimate a no-observed-adverse-effect level (**NOAEL**), or at least a lowest-observed-adverseeffect-level (**LOAEL**).

For drinking water, the TDI for cyanotoxins can be estimated as:

$$\text{TDI} = \frac{\text{NOAEL or LOAEL}}{\text{UF}} \tag{1}$$

Risk Assessment of Cyanobacteria and Cyanotoxins,

et al., 2005; van Apeldoorn et al., 2007).

**4.2 Guidelines for microcystins** 

in drinking water.

(Codd et al., 2005).

**4.3 Guidelines for nodularin** 

**4.4 Guidelines for anatoxin-a** 

if tumor promotion is considered (Codd et al., 2005).

The guideline value (**GV**; µg/L water) can be calculated as:

the Particularities and Challenges of *Planktothrix* spp. Monitoring 69

Additionally, it may be also necessary consider a UF of 5 if the LOAEL is used and a UF of 3,

GV� �TDI �×body wt ×AF

Where body weight is usually assumed to be 60 kg for a human adult and AF is the allocation factor, which is the proportion of daily exposure arising from drinking water ingestion. Because some oral exposure may occur via food or dietary supplements or other route, therefore, an AF of 0.8 (80% of total intake) is assumed for drinking water. Finally, C is the volume of drinking water consumption per day, assumed to be 2 L for an adult (Codd

The drinking water guideline for microcystins was determined from a sub-cronic study (Fawell et al., 1993) with mice orally administered with microcystin-LR (since it is one of the most toxic and frequent microcystin variant and for which more information is available). In this study a NOAEL of 40 µg/kg bw was derived and a TDI of 0.040 was calculated using an uncertainly factor of 1000 (10 for intra-specific variations, 10 for inter-specific variations and 10 for limitations in the database). The resulting guideline value, using an allocation factor of 0.80 for total microcystin-LR (free plus cell bound), was aprox. 1 µg/L

A similar TDI for microcystins was obtained (0.067 *vs.* 0.040) from a study with pigs using freeze-thawed *Microcystis* cells containing quantified microcystins (Falconer et al., 1994).

For safety reasons, the World Health Organization (WHO) has adopted the lowest value (1

However, if tumour-promoting actions of microcystins are also considered, then an additional UF of 3 for this hazard must be used, thus originating a GV of about 0.3 µg/L

The Australian guideline is 1.3 μg/L for total microcystin. This slightly differs from the WHO provisional guideline of 1 μg/L microcystin-LR due to the use of a different average

No NOAEL can be derived for nodularin(s) due to the absence of suitable toxicological data. However, since nodularin(s) and microcystin-LR have identical mechanisms of action, the

A NOAEL of 98 µg/kg has been derived from a 28-day gavage study using mice (Fawell et al., 1999). If a uncertainly factor (UF) of 1000 (10 for intra-specific variations, 10 for inter-

body weight for an adult (70 kg *vs.* 60 kg) and different Alocation Factor (0.9 *vs.* 0.8).

guideline value determined for MC-LR (1 µg/L) can also be used for nodularin(s).

These resulted in similar GVs : 1 µg/L for mice *vs.* 1.61 µg/L for pigs.

µg/L) as the GV for microcystin in drinking water for adults (WHO, 1998).

C (3)

Where, TDI units are mg/kg body wt/day, or µg/kg body wt/day, and UF is the product of uncertainty factors, e.g

Fig. 4. Organizational chart of the steps involved in cyanobacteria risk management (adapted from Bartram et al. 1999).

Additionally, it may be also necessary consider a UF of 5 if the LOAEL is used and a UF of 3, if tumor promotion is considered (Codd et al., 2005).

The guideline value (**GV**; µg/L water) can be calculated as:

$$\text{AGV} = \frac{\text{(TDI \text{ }\text{\textdegreebody wt} \times \text{AF})}}{\text{C}} \tag{3}$$

Where body weight is usually assumed to be 60 kg for a human adult and AF is the allocation factor, which is the proportion of daily exposure arising from drinking water ingestion. Because some oral exposure may occur via food or dietary supplements or other route, therefore, an AF of 0.8 (80% of total intake) is assumed for drinking water. Finally, C is the volume of drinking water consumption per day, assumed to be 2 L for an adult (Codd et al., 2005; van Apeldoorn et al., 2007).

### **4.2 Guidelines for microcystins**

68 Novel Approaches and Their Applications in Risk Assessment

Where, TDI units are mg/kg body wt/day, or µg/kg body wt/day, and UF is the product of

Fig. 4. Organizational chart of the steps involved in cyanobacteria risk management

(adapted from Bartram et al. 1999).

10 (intra-specific variations) 10ሺinter-specific variationsሻ 10 ൫less-than-lifetime study൯

ቑ (2)

UF=ͳͲͲͲ ቐ

uncertainty factors, e.g

The drinking water guideline for microcystins was determined from a sub-cronic study (Fawell et al., 1993) with mice orally administered with microcystin-LR (since it is one of the most toxic and frequent microcystin variant and for which more information is available). In this study a NOAEL of 40 µg/kg bw was derived and a TDI of 0.040 was calculated using an uncertainly factor of 1000 (10 for intra-specific variations, 10 for inter-specific variations and 10 for limitations in the database). The resulting guideline value, using an allocation factor of 0.80 for total microcystin-LR (free plus cell bound), was aprox. 1 µg/L in drinking water.

A similar TDI for microcystins was obtained (0.067 *vs.* 0.040) from a study with pigs using freeze-thawed *Microcystis* cells containing quantified microcystins (Falconer et al., 1994). These resulted in similar GVs : 1 µg/L for mice *vs.* 1.61 µg/L for pigs.

For safety reasons, the World Health Organization (WHO) has adopted the lowest value (1 µg/L) as the GV for microcystin in drinking water for adults (WHO, 1998).

However, if tumour-promoting actions of microcystins are also considered, then an additional UF of 3 for this hazard must be used, thus originating a GV of about 0.3 µg/L (Codd et al., 2005).

The Australian guideline is 1.3 μg/L for total microcystin. This slightly differs from the WHO provisional guideline of 1 μg/L microcystin-LR due to the use of a different average body weight for an adult (70 kg *vs.* 60 kg) and different Alocation Factor (0.9 *vs.* 0.8).

#### **4.3 Guidelines for nodularin**

No NOAEL can be derived for nodularin(s) due to the absence of suitable toxicological data. However, since nodularin(s) and microcystin-LR have identical mechanisms of action, the guideline value determined for MC-LR (1 µg/L) can also be used for nodularin(s).

#### **4.4 Guidelines for anatoxin-a**

A NOAEL of 98 µg/kg has been derived from a 28-day gavage study using mice (Fawell et al., 1999). If a uncertainly factor (UF) of 1000 (10 for intra-specific variations, 10 for inter-

Risk Assessment of Cyanobacteria and Cyanotoxins,

**Toxin Drinking water** 

MC-LR

Nodularin

Anatoxin-a

Anatoxin-a(S)

Cylindrospermo psin

not determined.

**guideline values**

1.0 µg/L (most generally accepted)

No guideline, however, hazard assessment can be guided by that for microcystins

> 3.0 µg/L (no official guideline)

> > Nd

1.0 µg/L (suggested)

STX 3.0 µg STX eq/L

Aplysiatoxins nd Lyngbyatoxins nd

the Particularities and Challenges of *Planktothrix* spp. Monitoring 71

MC-LR 1.3 µg/L Australia Canada Chorus, 2005;

1.0 µg/L New Zealand

6.0 µg/L New Zealand Homoanatoxin-a 2.0 µg/L New Zealand Chorus, 2005

1.0 µg/L New Zealand

Table 3. Guideline values (GV) estimated for cyanobacterial toxins in drinking water. Nd –

Canada, New Zealand

Australia Brazil New Zealand

15.0 μg/L Brazil Chorus, 2005

**Countries using** 

Brazil Czech Republic Denmark France Great Britain Greece Italy New Zealand Poland Portugal South Africa Spain U.S.A.

**the GV References** 

Chorus, 2005; Codd et al., 2005; van Apeldoorn et al., 2007

van Apeldoorn et al., 2007

Fitzgerald et al., 1999; Chorus, 2005; van Apeldoorn et al., 2007

Codd et al., 2005; Svrcek & Smith, 2004; Chorus, 2005

Chorus, 2005

Humpage &Falconer, 2003; Svrcek & Smith, 2004;

Svrcek & Smith, 2004; Chorus, 2005; Codd et al., 2005

specific variations and 10 for limitations in the database) is used, a TDI of 0.1 µg/kg bw can be reached. Svrcek & Smith (2004) have suggested a guideline limit of 3.0 µg/L.

### **4.5 Guidelines for anatoxin-a(S)**

There are no sufficient data to derive an NOAEL or LOAEL and, consequently, insufficient data to determine a TDI for anatoxin-a(S). However, in the Guidelines for Drinking-Water Quality Management for New Zealand 2005, a Maximum Acceptable Values (MAVs) for anatoxin-a(S) of 1.0 µg/L is suggested (Chorus, 2005).

#### **4.6 Guidelines for cylindrospermopsin**

According to the 90-day study of Shaw et al. (2000) using drinking water in mice a NOAEL of 150 µg/kg bw was obtained. A second study with mice administered by gavage with cylindrospermopsin for 11-weeks from Humpage and Falconer (2003) resulted on a NOAEL of 30 µg/kg bw. If a uncertainly factor (UF) of 1000 (10 for intra-specific variations, 10 for inter-specific variations and 10 for limitations in the database) is used, a TDI of 0.03 µg/kg bw can be calculated. Considering the ''standard'' adult body wt of 60 kg and a 0.9 AF, a GV of 0.81 is obtained, leading the authors to propose a Guideline Value of 1 μg/L (Humpage and Falconer, 2003).

#### **4.7 Guidelines for saxitoxin**

There are no attempts to determine a NOAEL or LOAEL and thus calculate a TDI for saxitoxin, because the range of lowest concentration where adverse effects were observed varies greatly. Given the different susceptibilities of person, it has been difficult to decide which uncertainty factor should be also used (van Appeldoorn et al., 2007).

Although there are no official guidelines, Australia considers a GV of 3 µg STX eq/L of drinking water, which was based on the data from marine shellfish toxicity (van Appeldoorn et al., 2007).

#### **4.8 Guidelines for aplysiatoxin and lyngbyatoxins**

There are no sufficient data to derive an NOAEL or LOAEL and thus calculate a TDI for these toxins.

The members of the population presenting greatest risk when exposed to cyanotoxins are children because of their water intake: body weight ratio, which is higher than that of adults (Falconer, 1999). Also the people having already certain pathologies may be more susceptible to the intake of the toxins (Falconer, 1999).

Ideally, the guidelines values established should protect against acute and chronic effects derived from the contact with cyanobacteria and their toxins, although, such it was stated above, the knowledge on the chronic effects of cyanotoxins still presents many gaps. The guideline values determined/suggested for each known cyanotoxin are summarized in Table 3.

specific variations and 10 for limitations in the database) is used, a TDI of 0.1 µg/kg bw can

There are no sufficient data to derive an NOAEL or LOAEL and, consequently, insufficient data to determine a TDI for anatoxin-a(S). However, in the Guidelines for Drinking-Water Quality Management for New Zealand 2005, a Maximum Acceptable Values (MAVs) for

According to the 90-day study of Shaw et al. (2000) using drinking water in mice a NOAEL of 150 µg/kg bw was obtained. A second study with mice administered by gavage with cylindrospermopsin for 11-weeks from Humpage and Falconer (2003) resulted on a NOAEL of 30 µg/kg bw. If a uncertainly factor (UF) of 1000 (10 for intra-specific variations, 10 for inter-specific variations and 10 for limitations in the database) is used, a TDI of 0.03 µg/kg bw can be calculated. Considering the ''standard'' adult body wt of 60 kg and a 0.9 AF, a GV of 0.81 is obtained, leading the authors to propose a Guideline Value of 1 μg/L (Humpage

There are no attempts to determine a NOAEL or LOAEL and thus calculate a TDI for saxitoxin, because the range of lowest concentration where adverse effects were observed varies greatly. Given the different susceptibilities of person, it has been difficult to decide which uncertainty factor should be also used (van Appeldoorn et al.,

Although there are no official guidelines, Australia considers a GV of 3 µg STX eq/L of drinking water, which was based on the data from marine shellfish toxicity (van

There are no sufficient data to derive an NOAEL or LOAEL and thus calculate a TDI for

The members of the population presenting greatest risk when exposed to cyanotoxins are children because of their water intake: body weight ratio, which is higher than that of adults (Falconer, 1999). Also the people having already certain pathologies may be more

Ideally, the guidelines values established should protect against acute and chronic effects derived from the contact with cyanobacteria and their toxins, although, such it was stated above, the knowledge on the chronic effects of cyanotoxins still presents many gaps. The guideline values determined/suggested for each known cyanotoxin are summarized in

be reached. Svrcek & Smith (2004) have suggested a guideline limit of 3.0 µg/L.

**4.5 Guidelines for anatoxin-a(S)** 

anatoxin-a(S) of 1.0 µg/L is suggested (Chorus, 2005).

**4.8 Guidelines for aplysiatoxin and lyngbyatoxins** 

susceptible to the intake of the toxins (Falconer, 1999).

**4.6 Guidelines for cylindrospermopsin** 

and Falconer, 2003).

2007).

these toxins.

Table 3.

**4.7 Guidelines for saxitoxin** 

Appeldoorn et al., 2007).


Table 3. Guideline values (GV) estimated for cyanobacterial toxins in drinking water. Nd – not determined.

Risk Assessment of Cyanobacteria and Cyanotoxins,

the Particularities and Challenges of *Planktothrix* spp. Monitoring 73
