New Zealand: Chapter 9: Cyanobacterial compliance

This article or the pdf file dated June, 2017, accessed September, 2017, titled Guidelines for Drinking water Quality Management for New Zealand 2017 provides some good information on cyanobacteria. Some of it, I feel, isn`t completely up to date but for the most part its accuracy will depend on the bacteria species in the water. I recommend reading the whole article even if you are an expert on cyanobacteria because its like a procedural manual or how to manual. The article does state “Do not use water source for drinking again until four weeks after cell counts have returned to less than 500 cells per mL, less than 0.4 mm3/L where the known toxin producer is dominant, or until testing shows that the toxin levels are less than 50 percent of their MAV.” I hope this advise is wrong because that will mean the folks in Toledo may have to use an alternate water source for a long time.

9.1 Introduction
This chapter provides a large amount of information on cyanobacteria and cyanotoxins because of the increasing number of supplies that encounter difficulties with these micro-organisms, and because many water suppliers may have little understanding of how to manage them. Although prepared primarily for use in relation to drinking-water supplies, the information should also be of use to those managing recreational waters.

Over recent years, water supplies in some parts of New Zealand have experienced an increase in the number of cyanobacterial blooms affecting their water sources. These events have the potential to introduce into the water toxins that can have acute and, if their concentrations are high enough, fatal consequences for consumers. Experience of such events in New Zealand is still relatively limited, and consequently this section provides substantial detail to assist water suppliers in dealing with cyanobacteria. In preparing this section, extensive use has been made of Toxic Cyanobacteria in Water: A guide to their public health consequences, monitoring and management Chorus and Bartram (editors), published on behalf of the World Health Organization 1999. Cyanobacteria may also be referred to as blue-green algae, or harmful algal blooms (HAB) and a publication in 2008 provides holistic coverage of cyanobacteria (Hudnell 2008), with a chapter on cyanotoxin removal during drinking-water treatment (Westrick 2008).

9.1.1 Algal bloom development
Cyanobacteria are members of the community of phytoplankton (which means small free floating plants; however cyanobacteria are actually bacteria, have no defined nucleus, rather than plants, which do have a defined nucleus) and the bottom-dwelling organisms living on the surface of the sediments and stones in most water-bodies. The right combination of environmental conditions, particularly high nutrient levels, may cause their excessive growth (bloom formation), leading to blue, brown or greenish discolouration of water through the high population density of suspended cells, and to the formation of surface scums. Such accumulations of cells may lead to high toxin concentrations.

Cyanobacteria have few natural enemies, which in combination with their ability to avoid sedimentation through buoyancy control, results in a low loss rate in their population. This compensates for their slow growth rates, once they have become established.

Blooms of benthic (attached or mat-forming) cyanobacteria can occur in rivers and at the edges of lakes. In rivers, benthic cyanobacterial mats are usually observed during periods of stable (but not necessarily) low flow. Benthic cyanobacteria are widespread throughout New Zealand rivers and are found in a wide range of water quality conditions, including oligotrophic waters (waters with low nutrients). The potential for these cyanobacteria to develop in waters with low nutrients requires vigilance from drinking-water operators using river water. The most common mat-forming benthic cyanobacterial genus in New Zealand is Phormidium. During stable flow conditions Phormidium mats can proliferate, at times forming expansive black/brown leathery mats across large expanses of river substrate. Flow conditions, substrate, water chemistry and species composition can influence the macroscopic appearance of benthic cyanobacterial mats and at times they may be confused easily with other algal groups, eg, diatoms, green algae. Microscopic confirmation should be undertaken to confirm whether cyanobacteria are the dominant component of attached communities. These mats also commonly detach from river/lake substrates and float on the water surface, forming floating rafts in rivers, lakes and
reservoirs. This is because under certain environmental conditions, or as mats become thicker (and bubbles of oxygen gas become entrapped within them), they will detach from the substrate and may accumulate along river edges. During these events the risk to human and animal health is higher due to accessibility of toxins to river users and bankside abstractions. Additionally, during these periods the cells are likely to be lysing and releasing toxins.

9.1.2 Health significance of cyanotoxins
Cyanobacteria do not multiply within the human body and are therefore not infectious. Many cyanobacteria, however, produce potent toxins. Exposure to these toxins, either in the cells or the water, through ingestion, inhalation or through contact with the skin, is therefore the primary health concern associated with cyanobacteria.

Generally, toxicity is not a trait specific for certain species; rather, most species comprise toxic and nontoxic strains. For microcystins, it has been shown that toxicity of a strain depends on whether or not it contains the gene for microcystin production (Rouhiainen et al 1995; Dittmann et al 1996) and that field populations are a mixture of both genotypes with and without this gene (Kurmayer et al 2002). Experience with cyanobacterial cultures also shows that microcystin production is a fairly constant trait of a given strain or genotype, only somewhat modified by environmental conditions (see various contributions in Chorus 2001). While conditions leading to cyanobacterial proliferation are well understood (the physiological or biochemical function of toxins for the cyanobacteria is the subject of many hypotheses: Chorus and Bartram 1999), the factors leading to the dominance of toxic strains over non-toxic ones are not. See WHO (2003) for reference details.

9.1.2 Health significance of cyanotoxins
Cyanobacteria do not multiply within the human body and are therefore not infectious. Many cyanobacteria, however, produce potent toxins. Exposure to these toxins, either in the cells or the water, through ingestion, inhalation or through contact with the skin, is therefore the primary health concern associated with cyanobacteria.

Generally, toxicity is not a trait specific for certain species; rather, most species comprise toxic and nontoxic strains. For microcystins, it has been shown that toxicity of a strain depends on whether or not it contains the gene for microcystin production (Rouhiainen et al 1995; Dittmann et al 1996) and that field populations are a mixture of both genotypes with and without this gene (Kurmayer et al 2002). Experience with cyanobacterial cultures also shows that microcystin production is a fairly constant trait of a given strain or genotype, only somewhat modified by environmental conditions (see various contributions in Chorus 2001). While conditions leading to cyanobacterial proliferation are well understood (the physiological or biochemical function of toxins for the cyanobacteria is the subject of many hypotheses: Chorus and Bartram 1999), the factors leading to the dominance of toxic strains over non-toxic ones are not. See WHO (2003) for reference details.

Cyanotoxins belong to a diverse group of chemical substances, each of which shows specific toxic mechanisms in vertebrates. Some cyanotoxins are strong neurotoxins (anatoxin-a, anatoxin-a(S), saxitoxins), others are primarily toxic to the liver (microcystins, nodularin and cylindrospermopsin) and yet others (such as the endotoxins) appear to cause health impairments (such as gastroenteritis), which are poorly understood. Assignment of health effects to specific species or toxins is often difficult because several cyanobacterial species may co exist in a water body. Global data show that hepatoxins (those causing liver damage) occur most frequently, although there have been blooms producing neutrotoxins that have lead to animal deaths.

The effects of cyanotoxins can be both acute and chronic, and protection against both long-term exposure, and short-term exposure, is required. While some short-term exposure can lead to health effects from which recovery is complete, it can also result in long-term damage to target organs:

Acute effects:
• dermal exposure, particularly if cells are accumulated under swimsuits and wet suits, may lead to skin irritations and allergic reactions (Pilotto et al 1997)
• symptoms involving irritation of internal and external mucous membranes, ie, gastro-intestinal or respiratory organs, eyes, ears, mouth and throat are also reported
• exposure to cell material of any cyanobacteria can cause illness such as fever, probably evoked by lipopolysaccharides contained in the cell wall of cyanobacteria (Keleti et al 1979; Lippy and Erb 1976)
• neurotoxins administered in mouse studies led to rapid respiratory arrest

• extensive kidney and liver damage following exposure to cyanotoxins has been reported (eg, Hawkins et al 1985)
• severe acute effects on human health appear to be rare, the only fatalities associated with cyanobacteria or their toxins having been reported in Brazil. In 1988 a new impoundment in Brazil developed an immense cyanobacterial bloom and there followed approximately 2000 gastroenteritis cases, 88 of which resulted in death. Cyanobacterial toxins were the likely cause (Teixera et al 1993), with contamination by heavy metals and pathogens ruled out. In 1996 (Jochimsen et al 1998; Carmichael et al 2001; Azavedo et al 2002), over 100 kidney patients developed liver disease and over 50 deaths were attributed to dialysis with water containing cyanobacterial toxins (Jochimsen et al).

Chronic effects:
• the key concerns of chronic effects associated with cyanotoxins are liver and kidney damage as well as tumour promotion, but there is a lack of clinical studies relating to chronic exposure (such as tumour promotion, eg, Ueno et al 1996, and liver damage), and this hinders the determination of safe levels for long-term exposure
• animal experiments have shown chronic liver injury from continuing oral exposure to cyanotoxins.

Members of the population at greatest risk when exposed to cyanotoxins are children (because their water intake:bodyweight ratio is higher than that of adults), and those who already have damaged organs that may be the target of the toxins.

The health risks associated with cyanotoxins are greatest when cyanobacterial cell concentrations are high due to excessive growth (ie, bloom events). The highest cyanotoxin levels are usually contained within the cells (intracellular), and toxin concentrations dissolved in the water (extracellular toxins) are rarely reported above a few g/L (Chorus and Bartram 1999). While the risks associated with cyanobacteria may rise and fall with the development and decay of bloom events, in some countries cyanobacteria may be present in water bodies over extended periods of time which results in continued exposure to subacute concentrations (Ressom et al 1994; Hitzfeld et al 2000), and the possibility of chronic health effects.

When a cyanobacterial bloom develops in a water body, exposure of those using the water for recreational purposes to hazardously high cyanotoxin concentrations will be most likely where cell densities are high, particularly in surface scums. Wind-driven accumulations of surface scums can result in toxin concentrations increasing by a factor of 1000 or more. Such situations can change within very short time periods, ie, hours. Children playing in shallow zones along the shore where scums accumulate are particularly at a risk.

The death of cyanobacterial cells, through the organism reaching the end of its lifecycle or through measures taken to control blooms, can result in higher than normal concentrations of extracellular toxin. Episodes of acute sickness have been reported after treatment of cyanobacterial blooms with copper sulphate to control the bloom, which then resulted in release of cyanotoxins into the water and breakthrough of dissolved toxins into drinking-water supplies.

It is preferable to control the health hazards associated with cyanotoxins by reducing the likelihood of bloom formation, rather than having to remove the cyanobacteria and any extracellular toxin present from the water. Monitoring of source water for evidence of the start of bloom development, or the potential for bloom formation, overcomes difficulties such as inadequate analytical methods associated with the measurement of cyanotoxins themselves.

9.1.3 Taste and odour caused by cyanobacteria
Cyanobacteria have, for a long time, been recognised as a nuisance in the drinking-water industry because of the ability of several taxa to produce earthy and musty smelling compounds, notably geosmin and 2-methyl isoborneol (2-MIB), for which the odour detection thresholds of less than 10 ng/L are remarkably low amongst sensitive individuals.

The cyanobacterial genera that are known to produce geosmin are Anabaena, Aphanizomenon, Lyngbya, Microcystis, Oscillatoria, Phormidium, Schizothrix and Symploca (Perrson 1983, cited in Chorus and Bartram 1999). All of these (except Symploca) are also known to include toxin-forming species and strains. Because of this, the possibility of using odour compounds as an early warning for the development of toxin-producing cyanobacterial blooms has been considered. However, there is no evidence of a correlation between toxin production and the production of taste- and odour- producing compounds that would provide a warning of toxicity. It is very unlikely that the production of taste and odour compounds is biochemically connected to the production of cyanotoxins (Chorus and Bartram 1999).

9.1.4 Occurrence of toxic cyanobacteria internationally and in New Zealand
Not all cyanobacteria that have been found to produce toxins have been identified in New Zealand. Table 9.1 lists, in alphabetical order some of the species found internationally to produce toxins, the nature of the toxin produced and where the species was found. This list is continually increasing, and should not be regarded as definitive. It is provided as a guide to those trying to determine whether a cyanobacterial species found in a water may be a toxin producer.

Table 9.1: Toxic cyanobacteria species and their geographical distribution
Refer to the above link to view the tables.

Table 9.2: Cyanobacteria genera known to occur in New Zealand fresh waters and the toxins they are known to produce
Refer to the above link to view the tables.

There have been two reports of cyanobacterial data collected from waters throughout New Zealand, Podivinsky and Williamson (2009); Nokes (2010). A key finding (Nokes 2010) was:
Where substantial blooms develop, toxin concentrations readily exceed provisional maximum acceptable values (PMAV) by a factor of 10, and in some instances by four-to-five orders of magnitude. Cyanobacteria are an extremely dangerous hazard in drinking and recreational waters because of the speed at which cyanobacterial toxin producers multiply, the concentrations toxins can reach, the difficulty in removing toxins from the water, and the severity of the health effects that can be associated with them. The most effective strategy for defence against them is to take measures to stop blooms developing.

9.2 Risk management
9.2.1 Assessment of risk
Assessing the risk posed by cyanobacterial toxins, or the potential for development of cyanobacterial blooms, and linking this to effective measures for the protection of public health within available resources, is complex. Situation assessment may be proactive (ie, carried out with the intention of preventing the bloom from developing), to determine whether contingency planning is required or to initiate long-term action, such as pollution control to minimise bloom formation, for example; or it may be reactive (ie, carried out as a response to the development of the bloom), such as assisting in interpretation of specific local events or conditions to provide information on which to base emergency or incident responses.

The type of information that could be used to assess the risk due to cyanobacteria is summarised in Table 9.3.

Table 9.3: Information that may help in situation assessment and management
Refer to the above link to view the tables.

9.5.1 Sample testing

Whichever laboratory is used for testing, advice should be obtained from the laboratory about sampling containers for the particular determinand in question, before collecting the samples, because there is some evidence that common additives in plastics could contaminate water samples and co-elute with microcystins to give erroneously high readings (van Apeldoorn et al 2007).

• Aluminium sulphate and ferric chloride are able to remove some cyanobacterial cells without physical damage and the release of toxins, eg, Microcystis aeruginosa and Anabaena circinalis cells (Drikas et al 2001). However, under normal bloom conditions it is highly likely that the cells are in various stages of their growth cycle, with some already dying and releasing toxins. A further treatment step may therefore be required to remove extracellular toxins.

Boiling water typically does not destroy toxins, and cell destruction can lead to the release of greater amounts of toxin into the water. If boiling of water is used as a means of destroying other micro-organisms, further water treatment must be undertaken to deal with the cyanotoxins.

9.7.2.4 Drinking-water treatment for households and small communities
Domestic treatment of drinking-water has been a recent issue of concern in New Zealand. Many reticulated supplies provide excellent quality drinking-water and additional household treatment may actually cause deterioration rather than improvement. However, domestic treatment may have a role in regions supplied with poor quality drinking-water. Such treatment, using filtration, activated carbon and oxidation has shown a good removal of health hazards associated with cyanobacteria.

New (unused) point-of-use filter cartridges can achieve a removal of microcystin variants in the range 30–60 percent, and this degree of removal could be increased to about 90 percent by the passage of the water through three such filters. The removal may drop to 15 percent, however, by the time the filter is halfway through its expected life. The form of the cyanobacteria also has an influence on the efficiency of removal. A filter consisting of activated carbon and ion exchange resins may remove about 60 percent of the filamentous cyanobacteria, while up to 90 percent of the single cells pass through (eg, Microcystis). As with other filter systems, the death and lysis of cells retained on the filter creates a potential concern.

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