Classification of the Cyanobacterial toxins Cyanobacteria toxins and the current state of knowledge on water treatment options: a review by Clark Svrcek; Smith, D W. Journal of Environmental Engineering and Science3.3 (May 2004): 155-185. Secondary metabolites refer to those compounds that are not used by an organism for its primary metabolism (cell division or energy production). Secondary metabolites include compounds that act as hormones, antibiotics, and toxins. Toxins are secondary compounds that have a harmful effect on other tissues, cells, or organisms. While it is not known for certain why cyanobacteria produce toxins, it has been surmised that they are evolutionary carry-overs and may function as protective secretions, since researchers have shown some cyanobacteria toxins to be potent inhibitors of aquatic invertebrate grazers (Carmichael 1992b). Toxins are formed at all stages of cyanobacteria growth. They generally remain in the cell (termed intracellular toxin) until age or stress causes their release into the surrounding water (extracellular toxin) during cell lysis (Sivonen and Jones 1999). Intracellular toxin content is typically highest in the late logarithmic growth phase, and the toxin content apparently shows a positive correlation with cyanobacteria biomass (Carmichael 2001). There is a transition from intracellular to extracellular toxin pools, due mainly to the release of the toxins during cell lysis in the decline of blooms and breakdown of the cyanobacterial biomass. Some active release of toxins can also occur from young growing cells (Ressom et al. 1994), though it should be noted that cylindrospermopsin, a relatively newly-characterized toxin, can be found in comparatively high concentrations as extracellular toxin at all stages of the life cycle, the cause of which is unknown (Chiswell et al. 1999; Carmichael 2001). Cyanobacteria toxins (more succinctly termed the cyanotoxins) fall into three main groups based on their chemical structure: cyclic peptides, alkaloids, and lipopolysaccharides (Sivonen and Jones 1999). The specific species of cyanobacteria that generate each toxin were previously listed in Table 2. It should be noted that several species of cyanobacteria are capable of producing a variety of toxins, thus making the source tracking of any one particular toxin somewhat difficult in multiple-species water blooms. The hepatotoxic cyclic peptides, the neurotoxic alkaloids, and the cytotoxic alkaloid cylindrospermopsin are produced by cyanobacteria commonly found in surface water supplies and therefore appear to be of the most relevance to water supplies at present (Carmichael 1992b; Fawell et al. 1993). Table 3 presents some of the confirmed and suspected cyanobacteria poisoning episodes on record. Cyclic peptide hepatotoxins The most frequently found cyanotoxins in harmful algal blooms from fresh and brackish waters are the cyclic peptide toxins of the microcystin and nodularin families (Sivonen and Jones 1999). These structurally-similar hepatotoxins (liver toxins) are large natural products with molecular weights (MW) in the range of 800 to 1100, though they are relatively small compounds when compared to cell proteins, for example (MW > 10000). The most ubiquitous cyanotoxins are the microcystins, a group of more than 75 cyclic heptapeptides (a seven amino acid ring) that share a common structure. These toxins are named for the genera of cyanobacteria from which they were first extracted, Microcystis aemginosa (Codd 2000). It is now known that several microcystin congeners may be produced during a given bloom, more than 20 in some cases, and other cyanobacteria species and genera are capable of producing microcystins (Sivonen and Jones 1999; Nicholson and Burch 2001). They range in molecular weights from 900 to 1100, and with the assistance of molecular models, the diameter of microcystin-LR has been estimated to be between 1.2 and 2.6 nm (Donati et al. 1994). Structurally, the microcystins are monocyclic heptapeptides that contain seven variable amino acids. The amino acid of prominent note is the nonpolar-linked C2o amino acid, (2S,3S,8S,9S)-3-amino-9-methoxy-2,6,8-trimethyl-10-phenyldeca-4,6- dienoic acid, abbreviated as Adda (Sivonen and Jones 1999). Cleavage of the Adda side chain from the cyclic peptide renders both components non-toxic, as does major alteration of the Adda chain (Carmichael 1992b; Ressom et al. 1994). The general structure of the microcystins is cyclo(-D-Ala^sup 1^X^sup 2^-D-MeAsp^sup 3^-Z^sup 4^-Adda^sup 5^-D-Glu^sup 6^-Mdha^sup 7^-) in which X and Z are variable L-amino acids (Fig. 1a). The variation of microcystin names is due to the variable L-amino acids; the X is commonly leucine (L), arginine (R), or tyrosine (Y), and the Z is usually arginine (R), alaninc (A), or methionine (M) (Nicholson and Burch 2001). For example, microcystin-LR contains leucine and arginine, whereas microcystin-YA contains tyrosine and alanine (Carmichael 1992b). Other amino acid variations include differing degrees of methylation of the Mdha and (or) MeAsp, and configuration of the Adda chain (Rinehart et al. 1994; Nicholson and Burch 2001). Demethylation of the MeAsp amino acid, for example, is written as [D-Asp^sup 3^] microcystin-LR. There are also many optical isomers of the microcystins. Although several microcystins may be produced during a given bloom, microcystin-LR (Fig. 1b) is the most commonly occurring and one of the most toxic variants of the microcystin family, and as such it is the best characterized of all the cyanotoxins (Carmichael 19926; Fawell et al. 1993). Most of the analytical and treatment work has been conducted using this variant for this very reason. Microcystins are known to be relatively stable compounds over a range of pH and temperatures, possibly because of their cyclic structure (Lawton and Robertson 1999). They can withstand many hours of boiling and may persist for many years when stored dry at room temperature. The toxins are resistant to enzymatic hydrolysis by some common enzymes, such as pepsin, trypsin, and chymotrypsin (Cousins et al. 1996; Harada and Tsuji 1998). Due to their high molecular weight and high solubility in water, they have a low volatility and are unable to easily penetrate biological membranes and bioconcentrate (Health Canada 2002). Microcystin-LR does, however, become more hydrophobic in water with decreasing pH (De Maagd et al. 1999). Several microcystin congeners (microcystin-LL, -LF, -LV, and -LM) have been identified as having greater hydrophobicity than microcystin-LR (Craig et al. 1993). This is based on analytical retention times, therefore the solubility of these toxins is rarely, if ever, reported as a quantified number. Hydrophobic variants occur in very small quantities (ng loxin/g cell mass) relative to hydrophilic ones, like microcystin-LR (μg toxin/g cell mass) (Carmichael 1997). The nodularins (MW approximately 800) are structurally similar to the microcystins in that they are a carbon ring with the Adda molecule attached that causes toxicity; however, the nodularins are a cyclic pentapeptide, containing only five variable amino acids instead of seven. The chemical structure of the nodularin molecule iscyclo-(D-MeAsp^sup 1^-L-Arg^sup 2^-Adda^sup 3^-DGlu^sup 4^-Mdhb^sup 5^), in which the Mdhb is 2-(methylamino)-2-dehydrobutyric acid. Nodularin is shown in Fig. 1c. The nodularins contain fewer variants than the microcystins; for example, in motuporin, the L-arginine is replaced by L-valine and in [LHar^sup 2^]-nodularin, arginine is replaced by homoarginine (Sivonen and Jones 1999). Two demethylated variants have been found, one with D-Asp^sup 1^ and the other with DMAdda^sup 3^, as well as a nontoxic nodularin having the 6Z-stereoisomer of Adda^sup 3^. As well, it should be pointed out that the nodularins (from the genus Nodularia) are primarily of brackish water origin, though a unique case of N. spumigena growth in freshwater exists in Lake Alexandrina in South Australia (Fitzgerald et al. 1999). This recurring case of nodularin occurrence in freshwater is particularly important as Lake Alexandrina is used as a source of potable water. Nodularins have many of the same qualititative properties as microcystin-LR in that they are very soluble, are very stable in dissolved form, and are not very volatile. The Alkaloid Toxins The alkaloid toxins are a diverse group of cyanotoxins, both in chemical structure and mammalian toxicity (Sivonen and Jones 1999). Alkaloids are, for the most part, heterocyclic nitrogenous compounds with at least one nitrogen-carbon bond. Three families of cyanobacterial alkaloid neurotoxins (toxins that affect the nervous system) are shown in Table 2: anatoxin-a (and homoanatoxin-a), anatoxin-a(S), and the saxitoxins (also called paralytic shellfish poisons, or PSPs). The non-sulphated alkaloid toxins of freshwater cyanobacteria (anatoxin and saxitoxin) are both neurotoxins. The sulphated PSPs, C-toxins, and gonyautoxins (the sulphated derivatives of saxitoxin) are also neurotoxins, but the sulphated alkaloid cylindrospermopsin is mainly hepatotoxic, though it also affects other organs and appears to be genotoxic as well (Sivonen and Jones 1999; Humpage et al. 2000). There are also some marine cyanobacteria that produce alkaloids (lyngbyatoxins and aplysiatoxins) that are skin irritants. Neurotoxic alkaloids Neurotoxic cyanobacteria have been recorded in North America, Europe, and Australia where they have caused animal poisonings, however they are not considered to be as widespread as the cyclic peptide hepatotoxins in water supplies (Fawell et al. 1993; Sivonen and Jones 1999). While they do not appear to pose the same degree of risk from chronic toxicity as the cyclic peptide hepatotoxins (Fawell et al. 1993), both anatoxin-a(S) and saxitoxin have very low lethal doses (see Table 4). Anatoxin-a (and its natural analog, homoanatoxin-a) was the first toxin from a freshwater cyanobacterium that was chemically and functionally defined. Anatoxin-a is an alkaloid neurotoxin with a molecular weight of about 165. It is shown in Fig. 2a, while homoanatoxin-a is depicted in Fig. 2b. Homoanatoxin-a differs in structure by the substitution of a propionyl group for an acetyl group. Anatoxin-a undergoes rapid photochemical degradation in sunlight, with a half-life of 1 to 2 h (Sivonen and Jones 1999). Anatoxin-a(S) is structurally quite different from anatoxin-a. Anatoxin-a(S) (designated with an S because the major symptom associated with this toxin is excessive salivation) is a naturally-occurring organophosphate (see Fig. 2c). Rare occurrence and inherent chemical instability has limited new research of its structure-function properties and its role in water-based diseases (Carmichael 1997). Structural variants of ana-toxina(S) have not yet been detected (Sivonen and Jones 1999). Anatoxin-a(S) decomposes rapidly in basic solutions but is relatively stable under neutral and acidic conditions (Matsunaga etal. 1989). The final category of alkaloid neurotoxins are the saxitoxins and neosaxitons, also known as the paralytic shellfish poisons (PSPs) (Carmichael 2001). These particular toxins are not unique to cyanobacteria; they have long been known as the PSPs that are produced by marine dinoflagellate blooms, or red tide. Saxitoxins are a complex family of more than 20 compounds that can be divided into three groups based on the R^sub 4^ functional group or the compound charge (Nicholson and Burch 2001). These alkaloid toxins can also be either non-sulphated (saxitoxins), singly sulphated (gonyautoxins), or doubly sulphated (C-toxins). The general chemical structure of the saxitoxin family depicting possible variants is shown in Fig. 2d, while the chemical structure of saxitoxin and neosaxitoxin are provided in Figs. 2e and 2f, respectively. The molecular weight of these toxins varies but is around 388. Saxitoxins have varying chemical stabilities and often undergo spontaneous transformations to by-products that may have higher or lower toxicity (Sivonen and Jones 1999). For instance, boiling of water with Anabaena extract containing primarily C-toxins can substantially increase the toxicity of the solution. Cytotoxic alkaloids The most recent cyanobacterial taxa to have its toxin chemically characterized is the filamentous Cylindrospermopsis raciborkii; hence, the name of the new cyanotoxin is cylindrospermopsis. Cylindrospermopsin is a cytotoxic guadinine alkaloid with a molecular weight of 415 (Falconer 1999). Figure 3 is the chemical structure of Cylindrospermopsin. While predominantly hepatotoxic in its pure form, Cylindrospermopsin has also shown to induce pathological symptoms in the kidneys, spleen, intestine, thymus, heart, and eye (Sivonen and Jones 1999). There is also mounting evidence that this alkaloid toxin is genotoxic (Humpage et al. 2000) and neurotoxic (Kiss et al. 2002). While Cylindrospermopsin was originally found in tropical Australian waters (Hawkins et al. 1985) it has since shown up in Hungary, Japan, and Israel, and the cylindrospermopsinproducing genera has been found in other parts of Europe and the USA (Sivonen and Jones 1999). This trend of spreading toxic cyanobacteria populations is mostly the result of expanding research programs and refined isolation, culturing, and analytical methods. Compared with other cyanotoxins, Cylindrospermopsin can be found free in water in large concentrations even when cells are healthy (Chiswell et al. 1999; Carmichael 2001). Recently, other toxic metabolites identified as 7-epicylindrospermopsin and deoxycylindrospermopsin have been isolated from other genera of cyanobacteria, suggesting that variants of this new toxin will need to be considered (Li et al. 2001 ; Nicholson and Burch 2001). Pure Cylindrospermopsin is relatively stable in sunlight, and decomposes slowly in temperatures ranging from 4 to 50 °C at a pH of 7 (Chiswell et al. 1999). It is also very soluble, and boiling does not cause significant degradation. Benthic marine cyanobacteria such as Lyngbya, Oscillatoria, and Schizothrix may produce toxins causing severe dermatitis (skin inflammation) among swimmers in coastal waters (Sivonen and Jones 1999). The aplysiatoxins and debromoaplysiatoxin are inflammatory agents, and lyngbyatoxin-a has caused dermatitis and severe oral and gastrointestinal inflammation. These marine cyanobacterial-based contact irritants continue to cause problems, especially in tropical areas such as Hawaii (Carmichael 1997). Lipopolysaccharide (LPS) endotoxins Other cyanobacterial toxins include the LPS endotoxins, although few have been characterized, partly because of their infrequent occurrence as well as their short persistence because of mixing and dilution effects. These toxins comprise part of the outer wall of both cyanobacteria and Gram-negative bacteria, though the toxins are generally found in higher concentrations when associated with the regular Gram-negative bacteria (Nicholson and Shaw 2001 ; Rapala et al. 2002b). The LPS endotoxins produced by cyanobacteria are less toxic than those produced by bacteria (Nicholson and Shaw 2001). Endotoxins are highly inflammatory agents that can irritate humans through direct skin contact or ingestion of water, or inhalation of water aerosols (Rapala et al. 2002b). It has recently been suggested that endotoxins of cyanobacterial origin may reinforce the adverse effects of microcystins by inhibiting key enzymes required for the detoxification of these hepatotoxins (Best et al. 2002). More work is required to evaluate the chemical structures and health risks of cyanobacterial lipopolysaccharides (Sivonen and Jones 1999). Toxicity and health effects Most of the knowledge about the toxicity and dose-response relationships of the various cyanotoxins comes from laboratory tests on mice (Carmichael 1997). Table 4 summarizes the lethal dosages for each of the major cyanotoxins. The primary types of toxicosis when exposure to cyanobacteria toxins occurs includes acute hepatotoxicosis, peracute neurotoxicosis, gastrointestinal disturbances, and respiratory and allergic reactions (Carmichael 1997). Recent work has assessed the toxicity of cyanobacterial toxin mixtures (Wolf and Frank 2002). Acute hepatotoxicosis involving hepatotoxins is the most commonly encountered toxicosis involving cyanobacteria (Carmichael 1997). Infrequent, but repeated, cases of wild and domestic animal poisonings, especially among cattle, sheep, horses, pigs, and ducks still comprises the main problem involving hepatotoxic cyanotoxins. The symptoms of hepatotoxic poisoning include weakness, anorexia, pallor, cold extremities, laboured breathing, vomiting and diarrhoea (Carmichael 1992b). Death occurs within a few hours to a few days after initial exposure and may be preceded by coma, muscle tremors, and forced expiration of air. The acute mode of action for hepatotoxins is to cause cellcell separations of the liver cells (hepatocytes), allowing for accumulation of blood in the liver and eventual death of the animal by haemorrhagic (internal bleeding) shock or liver failure (Carmichael 1997). There is also mounting epidemiological evidence from China linking the cyclic peptide hepatotoxins and cancer (Carmichael 1992b, 1997; Ueno et al. 1996). The cyclic peptides have been shown to produce liver tumours in laboratory rodents, and there is also indirect evidence that microcystins may promote tumours in humans from drinking water. View Image - Fig. 2. Chemical structure of the neurotoxic alkaloids, (a) Anatoxin-a; (b) Homoanatoxin-a; (c) Anatoxin-a(S); (d) Generic saxitoxin with various groupings; (e) Saxitoxin; and (f) Neosaxitoxin. The toxicities of the hepatotoxins vary markedly, even within the family of microcystin variants (see Table 4). The microcystin toxicity variation depends on the degree of methylation of the MeAsp and Mdha amino acids, and on the stereoisomers of the Adda chain. Most neurotoxins are acute acting - that is, they act immediately with a very little dose; thus, chronic exposure does not generally occur. Symptoms of exposure to anatoxin-a include staggering, muscle twitching and gasping in animals, opisthotonus in birds (head and neck stretched backwards along the back), and rapid death by respiratory arrest (Codd et al. 1999). Death due to respiratory arrest occurs within minutes or a few hours, depending on species, dosage, and prior food consumption (Carmichael 1992b). Anatoxin-a and anatoxina(S) both interfere with the acetylcholine-acetylcholinesterase coordination of the nervous system, disrupting communication between neurons and muscle cells, albeit somewhat differently (Carmichael 1994). Whereas anatoxin-a attaches to receptor molecules and cannot be degraded by acetylcholinesterase, anatoxin-a(S) inhibits acetylcholinesterase from degrading acetylcholine; both cause muscle overstimulation, inducing twitching and cramping, followed by fatigue and paralysis. If respiratory muscles are affected, the animal may suffer convulsions (from lack of oxygen to the brain) and die of suffocation. Anatoxin-a(S) has the additional symptom of excessive salivation. It is interesting to note that as it is a naturally occurring organic phosphate, anatoxin-a(S) actually functions much like synthetic organophosphate insecticides (Carmichael 1994). The fast-acting neurotoxins saxitoxin and neosaxitoxin again disrupt the nervous system, but do so by preventing acetylcholine from ever being released by neurons. Exposure limits for cyanotoxins At least eight countries have started national programs on water quality and cyanobacteria-based issues (Australia, Brazil, Canada, Finland, Great Britain, Japan, Portugal, and the US) (Carmichael 1997). Using data from animal studies and epidemiological studies, several of these countries (namely Australia, Canada, Great Britain, and the US) are moving to establish maximum acceptable concentrations (MAC) for microcystins in drinking water based on no adverse effects levels (Table 5). View Image - Table 5. Summary of cyanotoxin health-based exposure guidelines (see U.S. EPA 1998; WHO 1998; Gilroy et al. 2000; Carmichael 2001; NHMRC and ARMCANZ 2001; Health Canada 2002; Humpage and Falconer 2003). View Image - Fig. 3. Chemical structure of cylindrospermopsin, a cytotoxic alkaloid. The recent update to the Guidelines for Canadian Drinking Water Quality included a MAC of 1.5 Mg/L for microcystin-LR, which represents an estimate of the concentration of microcystinLR that does not present a significant risk to the health of the consumer over a lifetime of exposure (Health Canada 2002). The guideline value applies to the sum of the intra- and extracellular microcystin toxins in the event of cyanobacterial cells being present in the water. The World Health Organization (WHO) has set a similar microcystin-LR guideline at 1.0 μg/L (WHO 1998), whereas Australia has set a guideline value of 1.3 μg/L for total microcystin-LR toxicity equivalents, where the microcystin variants of lower toxicity are accorded a lower concentration than their actual value in the sum of the concentrations (NHMRC and ARMCANZ 2001). These MACs do not currently include consideration for the tumour-promoting action of microcystins. Future considerations of microcystins as cancer initiating and promotion agents may decrease the guideline numbers in Table 5 (Carmichael 1997). New Zealand, interestingly, has adopted a factor of 10 to account for possible carcinogenicity of the microcystins. The guideline value for microcystins should not be used as a baseline down to which water quality could be degraded; rather, it indicates the need for exceedences to be investigated, including public health consultation and the possible need for intervention and remedial action. Some of the other cyanobacteria toxins of potential concern in drinking water, such as anatoxin-a and cylindrospermopsin, require more data on mammalian oral toxicity and estimates of tolerable daily intakes before drinking water guidelines can be derived (Codd 1995; WHO 1998; Chorus and Bartram 1999; Health Canada 2002). It has been suggested that in situations where M. aeruginosa occurs in drinking water supplies, and toxin monitoring data are unavailable, cyanobacteria cell numbers could be used to provide a preliminary orientation to the potential hazard to public health (NHMRC and ARMCANZ 2001). For example, for a highly toxic population of M. aeruginosa (toxic cell quota = 0.2 pg total microcystin/cell), a cell density of approximately 6500 cells/mL is equivalent to the Australian guideline of 1.3 μg/L microcystin-LR total equivalents, if the toxin was fully released into the water. This number is an estimate only, and for health risk assessment quantification of microcystin-LR total equivalents would need to be determined. Detection methods for cyanobacteria and cyanotoxins The successful treatment of cyanotoxins by a water utility, like most other contaminants of concern, is dependent upon their timely identification and quantification in the source water. The reader is referred to several excellent reviews of analytical detection techniques for cyanotoxins (An and Carmichael 1994;Coddetal. 1994;Harada 1996;Carmichael 1997;Nicholson and Burch 2001 ; Nicholson and Shaw 2001), and to some other papers for a review of purification and preservation techniques (Lawton and Edwards 2001 ; Nicholson and Burch 2001; Nicholson and Shaw 2001). As well, a visit to an academic database search engine will yield numerous results on the latest advancements in this blossoming topic. A succinct summary will suffice for this review. An important consideration in analyzing water samples for cyanotoxins is differentiating between intra- and extracellular toxins. To determine total levels of toxins, any cyanobacteria cells in the sample must first be lysed to liberate intracellular toxins, usually by freeze-thawing, as current analytical procedures can only determine toxins in the free or dissolved state (Nicholson and Burch 2001). A recent study suggested that sonication with a probe sonicator was more effective at cyanobacterial cell lysis than freeze-thawing and ultrasonication bath, suggesting that studies using the freeze-thaw method to liberate toxins from intact cells may underestimate toxin concentrations (Rapala et al. 2002a). In environmental raw water samples, this toxin liberation is a necessity; in a filtered water sample, such as post-water treatment plant, all toxins will likely be in solution and total toxin will be measured by analyzing for total dissolved toxins. The analytical techniques available for microcystin determination range from immunological or biochemical screening techniques based on the ELISA (enzyme linked immunosorbent assay) or protein phosphatase inhibition assays, to quantitative Chromatographie techniques based on high performance liquid chromatography (HPLC). More expensive and sophisticated liquid chromatography-mass spectrometry (LC-MS) is available for microcystin quantification as well as saxitoxin and cylindrospermopsin determination. Mouse bioassays are also available for screening the entire range of toxins, but do not have sufficient sensitivity for application to water samples without impractical levels of preconcentration (Nicholson and Burch 2001) and, coupled with the decisions of some researchers to move away from animal bioassays, do not provide a practical means of analysing for toxins. Table 6 compares some of the most common methods of measuring cyanotoxins in recreational and drinking waters. The best method for cyanotoxin analysis depends on the goal of the sampling program. There are several commercial ELISA kits that have a high sensitivity for microcystins that are quick and easy to use. Enzyme linked immunosorbent assay can yield total microcystin concentration results, repeatability, reproducibility, and variability comparable to HPLCPDA (photo-diode array) or HPLC-UV (ultraviolet) and LCMS (Lawrence et al. 2001; Fastner et al. 2002; Rapala et al. 2002a). The drawback in the assay cornes from the high structural variation of microcystins and the subsequent crossreactivity of the antibodies with different microcystin variants, which can make it difficult to correlate the overall concentration of a microcystin mixture to its toxicity. Both HPLC-PDA/UV and LC-MS are capable of identifying and quantifying microcystin variants in a sample if suitable standards are present (Nicholson and Burch 2001), though complete identification of microcystin variants requires mass spectrometry and amino acid analyses with nuclear magnetic resonance studies (Rapala et al. 2002a). These Chromatographie techniques require expensive equipment and more time to perform the analyses, and are further hampered by the large number of microcystin variants and the lack of certified commercial standards. Enzyme linked immunosorbent assay therefore shows great promise in acting as a quick screening tool for water utilities to test their raw and treated waters (and indeed it is already used quite commonly by utilities to test for total microcystins), whereas HPLCPDA/UV or LC-MS is the method of choice for confirming and identifying the toxin variants in an unknown sample, thus providing enough information to determine toxicity equivalents for mixtures of microcystin variants. Several researchers have also identified the international requirement for the production and availability of certified reference materials of purified and quantified microcystins to ensure that routine analysis of microcystins in laboratories is standardized (Fastner et al. 2002; Rapala et al. 2002a). A range of molecular characterization techniques have been developed to identify toxic strains of cyanobacteria from nontoxic strains (Baker et al. 2001?, 2001b). These techniques utilize polymerase chain reaction (PCR) to identify cyanobacteria genera, and genetic oligonucleotide probes to determine cyanobacteria toxigenicity. These genetic probes are effective on environmental samples, eliminating the labour-intensive need for isolation and culturing of the microorganisms. Refinement of these new tests will allow water utilities and operators to determine the presence and type of cyanobacteria in the raw water source both quickly and easily. Management options for cyanobacteria and cyanotoxins The management of cyanobacteria in raw water supplies, and consequently of cyanotoxins in the drinking water system, can be tended to at several different points from source to tap. Prevention of cyanobacteria blooms through prevention of natural water eutrophication is the most important long-term management goal of controlling cyanobacteria. The next point in watershed management involves water body management whereby the hydrophysical conditions of the water body are altered in an attempt to allow the environment to favour other phytoplankton over the cyanobacteria (Hrudey et al. 1999). This can be done by several means, usually artificial destratification by bubble aeration or surface mechanical mixers (Brookes et al. 2002) or by destruction of cyanobacteria gas vacuoles by ultrasonic irradiation (Nakano et al. 2001 ; Lee et al. 2002). More immediate, short-term control techniques involve selective abstraction of raw water to avoid cyanobacteria and cyanotoxin contamination by strategic positioning of offtakes, selection of intake depth, offtake by bank filtration, and the use of barriers to restrict scum movement (Hrudey et al. 1999). These methods of abstraction can be utilized to reduce the amount of cyanobacteria in raw water, consequently reducing the amount of intracellular toxin coming in to a water treatment plant (WTP). Chemical treatment with algicides has been used to control cyanobacteria in water bodies, though various environmental toxicity considerations are beginning to curb the frequency of their usage. An excellent review of algicides for control of cyanobacteria can be found in Burch et al. (2001). Algicides should be used only in the early stages of bloom development when cell numbers are low to minimize the release of intracellular toxins, as toxins have been shown to persist in lakes for weeks or months (Jones et al. 1994, 1995; Jones and Orr 1994; Lahti et al. 1997). This suggests that toxins may be present in water bodies at low concentrations for weeks after the visible mass of a cyanobacteria bloom has disappeared. The final point to control cyanobacteria and cyanotoxins in the water supply is within the water treatment system. Depending on whether cell lysis has occurred in the source water, cyanotoxins could enter a WTP as intra-or extracellular toxins. Intracellular toxins can be removed by removing the cyanobacterial cells themselves, and an operational strategy must be identified as to whether the treatment process should be optimized to remove the intracellular toxins or to lyse the cells and deal with dissolved extracellular toxins (Hart et al. 1998). Once dissolved cyanotoxins are in the treatment plant, methods of removal involve combinations of physical removal and (or) chemical or biological transformation. Chemical and biological processes may transform the toxins, thus reducing the original water quality problem and lending the appearance of toxin destruction. However, it must be ensured that the transformation has not yielded toxic intermediates or end-products. A wealth of information has been published on cyanotoxin removal during drinking water treatment. Many of the studies focus on single unit processes and operations, though a few studies have investigated common treatment train combinations. The remainder of this paper is divided into conventional and advanced water treatment processes for the removal or transformation of the cyanotoxins.
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