Page 11: Guidelines for Canadian Recreational Water Quality – Third Edition
Part II: Guideline Technical Documentation
The recommended guideline values for cyanobacteria and their toxins in recreational waters are:
- Total cyanobacteria: 100 000 cells/mL
- Total microcystins: 20 µg/L (expressed as microcystin-LR)
Exceedance of these values, or the development of a bloom indicates the potential for exposure to cyanobacterial cells and/or their toxins in amounts which may, in some cases, be sufficient to be harmful to human health. In general, contact with waters where a bloom exists or has very recently collapsed should be avoided.
An appropriate monitoring program is advantageous to reduce the potential risk of user exposure to cyanobacterial blooms and their toxins. It is advised that managed recreational water areas that are suspected or are known to be susceptible to blooms be routinely monitored during the bathing season. Authorities should visually monitor such supplies for cyanobacterial growth. A swimming advisory may be issued at the discretion of the responsible authority.
In the event of bloom development, in order to fully characterize the extent of the risk posed by the cyanobacterial population, it is further advised that authorities conduct sampling during, and after the collapse of, the bloom. Should either of the guideline values be exceeded, a swimming advisory may be issued by the responsible authority. When measuring the toxins it is important that one measures total microcystins. "Total microcystins" includes both the microcystin that is occurring free in the water and the microcystin that is bound to or inside the cyanobacterial cells.
Contact with waters where an advisory has been issued should be avoided until the advisory has been rescinded. Published texts are available that can provide further information with respect to the design and implementation of recreational water monitoring programs (e.g., Chorus and Bartram, 1999)
Cyanobacteria are bacteria that share features of both bacteria and algae. They are similar to algae in size, possess blue-green pigmentation and are capable of photosynthesis; thus, they are often termed blue-green algae (WHO, 2003a). Most planktonic cyanobacteria, including the species found in Canadian lakes, form colonies, which can appear as irregular groupings of cells or as filamentous chains that can be straight, coiled or branched (Chorus and Bartram, 1999; Falconer, 2005). In a typical summer, a lake water sample can contain several species of cyanobacteria, along with numerous other species of algae. Cyanobacterial cells contain small gas bubbles called vacuoles, which allow them to control their buoyancy. The cells use this buoyancy control to move up in the water column to where light is the greatest and down in the water column to where nutrients are more abundant (Falconer, 2005). In still, stratified surface waters, cyanobacteria effectively use the light and nutrients to proliferate intensively, creating a visible discoloration known as cyanobacterial blooms (Chorus and Bartram, 1999; Falconer, 2005). These blooms can be very dense and can have the appearance of being gelatinous or resemble a collection of fine grass clippings or appear as a homogeneous, soupy mass, as if green paint has been spilled into the water (WHO, 2003a; Falconer, 2005). Surface blooms or scums can occur when the cells develop excess buoyancy and the water is calm enough to let them float to the surface. This excess buoyancy develops when turbulence (e.g., during storms) sends the cellsa too deep, during the hours of darkness, under carbon dioxide-limiting conditions, when the population is at the end of the growth cycle or any combination of these factors. Offshore winds may then drive these scums towards the shore where they can accumulate (Chorus and Bartram, 1999; Falconer, 2005). In this manner, cyanobacterial blooms may increase their density by a factor of 1000 or more in a very short period of time (Chorus et al., 2000).
Cyanobacteria possess a number of special properties that determine their relative importance in phytoplankton communities. Cyanobacteria have lower light intensity requirements and demonstrate a greater affinity for nitrogen and phosphorus than do other algae and phytoplankton and, thus, can outcompete these organisms under conditions where these factors might be limiting (e.g., in turbid waters). The maximum growth rate for cyanobacteria has been reported to occur at temperatures above 25°C (Chorus and Bartram, 1999). The combination of these factors may help explain why blooms typically occur in the late summer months when waters are warmer and the hours of daylight are beginning to grow shorter (Chorus and Bartram, 1999, Falconer, 2005). As well, toxic cyanobacteria may not be grazed by zooplankton to the same extent as other species of algae (Chorus and Bartram, 1999). More recently, it has been suggested that certain mussel species (zebra mussels Dreissena polymorpha, quagga mussels D. bugensis) selectively reject certain strains of Microcystis, possibly leaving toxic species to proliferate under conditions of reduced competition (Brittain et al., 2000; Vanderploeg et al., 2001).
The nutrient enrichment (eutrophication) of surface waters can also have a significant impact on the frequency and severity of cyanobacterial blooms (Chorus and Bartram, 1999, Falconer, 2005). Nitrogen and phosphorus enter the environment as a result of both natural processes and human activities (Chambers et al., 2001). Sources include runoff or erosion from naturally or artificially fertilized soils, storm sewer discharges and discharges of agricultural, industrial or sewage wastes (Jones and Armstrong, 2001). On-site wastewater disposal systems from isolated dwellings (both urban and rural) can also be a significant source of nutrients.
Cyanobacterial blooms are considered a public health concern because direct contact with a bloom can cause allergenic-like reactions; and some cyanobacterial species can produce toxins that may have harmful effects on humans (Chorus and Bartram, 1999). Over 46 species of cyanobacteria are capable of producing toxins (Sivonen and Jones, 1999). The most common toxin-producing genera in fresh water are Anabaena, Aphanizomenon, Cylindrospermopsis, Microcystis, Nodularia and Planktothrix (syn. Oscillatoria) (Falconer, 2005). Although the conditions leading to the development of a bloom are relatively well known, the factors responsible for the dominance of toxin-producing strains are not completely understood (Chorus and Bartram, 1999; Falconer, 2005). Consequently, toxin formation from cyanobacteria is even less predictable than the cyanobacterial blooms themselves. Lakes that have never had a problem can suddenly develop blooms that may contain toxins. Conversely, lakes that have shown toxic blooms in the past may never show it again. It has been suggested that worldwide, an average of 60% of the cyanobacterial bloom samples investigated have been positive for cyanobacterial toxins (range, 10-90%) (Chorus et al., 2000; WHO, 2003a). As a result, any bloom encountered should be treated as potentially toxic. Cyanobacterial toxins for the most part are associated with the cyanobacterial cells--either bound within membranes or occurring freely within the cells. Toxin release to the surrounding waters can occur as the cells die or are damaged and leak their contents (Chorus and Bartram, 1999). The bulk of the toxicity, if present, generally lasts as long as the bloom; however, some toxin may still persist for a short period after the bloom is gone (Chorus and Bartram, 1999; Falconer, 2005). Subsequently, contact with waters in which a bloom has developed should be avoided until it can be unequivocally determined that there is not a risk of contact with cyanobacterial toxins. The time of toxin persistence can depend on factors such as the concentration before the bloom's disappearance, and the efficiency of degradation by natural microbial populations in the water (Falconer, 2005).
Some toxic benthic species (e.g., Lyngbya spp.) can grow to form dense, bottom-covering mats of cyanobacterial material (Chorus and Bartram, 1999; WHO 2003a). These mats typically occur in clear, shallow waters where sunlight can penetrate to the bottom. The mats can occasionally be dislodged and washed ashore, where they may be scavenged by animals. Human health risks from these mats are considerably less than those from scums produced by other cyanobacterial species; however, they can still present a risk for domestic pets and livestock (WHO 2003a).
There are other known toxic marine algal species that are capable of forming blooms (e.g., Alexandrium spp. and the phenomenon known as "red tide") and producing toxins (i.e., those toxins responsible for shellfish poisonings) (Chorus and Bartram, 1999). However, as the focus of this section is the human health risks from exposure to toxic cyanobacteria through recreational water activities, they will not be discussed here.
Confirmation of toxins within a bloom cannot be accomplished by visual inspection; samples must be sent to a laboratory for analysis. Warning signs may be observed, such as the presence of dead waterfowl or other wildlife along the shoreline or reports of domestic animal poisonings (specifically cattle and dogs) (Chorus and Bartram, 1999). Still, toxic blooms can occur without any noticeable effect on the local animal populations.
Increased awareness of cyanobacterial blooms, coupled with occasional escalations in bloom detection, has prompted a growing concern over the possible development of blooms in recreational waters and the resulting health implications for recreational water users. Both drinking water and recreational water are potential sources of exposure. In general, because of circumstances such as the seasonality and localized nature of blooms, their unappealing aesthetic properties and the way drinking water supplies and monitored recreational water areas are managed, the likelihood of exposure to cyanobacterial toxins in sufficient amounts to constitute a chronic or acute health risk is considered to be relatively low. Under circumstances where a recreational area is experiencing prolonged and persistent blooms and where intensive recreational activities are continuing, the risks of acute exposure may be greater (Funari and Testai, 2008).
Direct epidemiological evidence of adverse health effects associated with recreational exposure to cyanobacteria is limited. Information on human symptoms of illness have come largely from anecdotal and case reports, many of which have gaps in the information on cyanobacterial conditions at the time of exposure (e.g., species present, cell and/or toxin concentrations). The symptoms most frequently described in these reports have been hay fever-like symptoms, gastrointestinal symptoms and skin irritations (Stewart et al., 2006a). Additional information has been provided from toxicological studies that used animal models, as well as from occasional accounts of animal poisonings.
There are three main routes for human exposure to cyanobacteria and their toxins in recreational waters: ingestion, inhalation and direct body contact (Chorus and Bartram, 1999). Cases of illness have been reported that have provided anecdotal evidence of toxicity to recreational water users in bloom-impaired waters through the accidental swallowing of water (Chorus and Bartram, 1999; Stewart et al., 2006a). There has also been experimental evidence to suggest that inhalation of contaminated aerosols may be equally important as a potential route of exposure (Fitzgeorge et al., 1994; Chorus and Bartram, 1999). This route would be relevant for activities in areas where aerosols are generated, such as waterskiing. Activities involving sudden or repeated immersion of the head (such as diving, windsurfing or kayaking) may also lead to ingestion or inhalation exposure via water forced into the mouth and/or nasal passages. Direct contact with cyanobacterial populations has also been known to cause irritative effects of varying severity, although the exact mechanisms for this are not fully understood. Some allergic reactions have been reported in sensitive individuals. It has been suggested that the irritations are due to unknown cyanobacterial components, separate from the toxins (Chorus and Bartram, 1999). Bathing suits and wet suits may also function to exacerbate the potential for skin irritations by trapping the cells and then disrupting their contents as a result of the friction created between the suit material and the user's skin (Chorus and Bartram, 1999).
There are several known cyanobacterial toxins that can pose concerns for recreational water users. These include microcystins, nodularins, anatoxins, cylindrospermopsin, dermatotoxins and irritant toxins (Chorus and Bartram, 1999). Microcystins and nodularins are cyclic peptides that affect the liver (hepatotoxins), anatoxins are alkaloids that target the nervous system (neurotoxins) and cylindrospermopsin is an alkaloid that affects a wide range of organs (general cytotoxin) (Chorus and Bartram, 1999). The dermatotoxins (alkaloids) and irritant toxins (lipopolysaccharides) are toxins that cause irritations of exposed tissues (Chorus and Bartram, 1999).
Microcystins are hepatotoxins that disrupt the functioning of enzymes called protein phosphatases, which are important metabolic switches in human and animal cells (WHO, 2003a). Their primary target is the liver, with the main route of entry into cells occurring through a membrane transport mechanism known as the bile acid carrier (Chorus and Bartram, 1999).
Microcystins are produced by most species of Microcystis and some species of Anabaena--two notable scum producers (WHO, 2003a). Other cyanobacteria capable of producing the toxin are Oscillatoria (syn. Planktothrix), Nostoc and Anabaenopsis. Over 70 microcystin variants have been isolated from bloom samples (Sivonen et al., 1992). Variants are named according to the variable amino acid position encountered in their structure. Microcystin-LR, the most commonly encountered variant, is named for possessing the amino acids leucine (L) and arginine (R) in the variable position (Chorus and Bartram, 1999). Microcystins and, more specifically, microcystin-LR represent the most frequently encountered cyanotoxins in cyanobacterial blooms in temperate surface waters in North America, based on available monitoring data. Therefore, they are the cyanotoxins of most relevance for recreational waters in Canada.
Symptoms reported from incidences of human recreational water exposures to waters contaminated by blooms of Microcystis and Anabaena have included headaches, nausea, vomiting, diarrhoea, abdominal pain, muscle aches, fever, mouth ulcers, blistering of the lips, sore throat, skin rashes and ear and eye irritations (Chorus and Bartram, 1999). Cases of animal poisonings (cattle, sheep and canines) resulting from contact with Microcystis blooms have provided evidence of liver toxicity and have included fatalities, substantiating the concern for human health effects from exposure. To date, no human fatalities have been reported as a result of exposure to microcystins through recreational water activities.
Toxicological studies using animal models have been used to provide further evidence of possible human health effects (Chorus et al., 2000). Microcystin-LR has been shown to be toxic following acute exposures in rodents. The oral (by gavage) LD50 is 5000 µg/kg body weight (bw) in mice and higher in rats (Fawell et al., 1999). Studies of acute and short-term exposures have demonstrated evidence of liver enzyme changes and tissue damage (inflammation, haemorrhaging, lesions) in mice as a result of exposure to microcystin-LR through oral administration (Fawell et al., 1999). Chronic exposures to low levels of microcystins have been shown to lead to progressive liver injury in experimental studies in pigs and mice (Chorus and Bartram, 1999). Microcystins are thought to be capable of promoting tumour development by interfering with the normal mechanisms of cell division. Evidence has been provided on the ability of microcystin-LR to promote the growth of certain types of tumours in mice subjected to prolonged exposure to the toxin through oral administration (Falconer, 2005). Presently there is insufficient evidence for the carcinogenicity or genotoxicity of microcystin-LR (Funari and Testai, 2008; Gaudin et al., 2009). However, the toxin has been listed as "possibly carcinogenic to humans" by the International Agency for Research on Cancer as a result of its tumour-promoting potential (IARC, 2010).
Both toxic and non-toxic species exist for all of the predominant microcystin-producing genera, and it is thought that different species or strains can vary in their toxic potential (Chorus and Bartram, 1999; Carillo et al., 2003; Dittmann and Börner, 2005). As a result a single bloom may consist of a mixture of non-toxic and variably toxic strains. It is generally felt that variations in toxicity within a bloom are due to the rise and fall of subpopulations of strains having different toxic potential. Environmental factors (e.g., conditions of winds, sunlight and temperature) are also thought to contribute to this phenomenon, but less significantly (Chorus and Bartram, 2003). Recently, the genes responsible for microcystin production (mcy genes) have been identified and sequenced (Falconer, 2005). Numerous studies have subsequently confirmed the detection of the mcy gene cluster as a tool to discriminate between toxic and non-toxic strains of Microcystis, Anabaena and Planktothrix in both laboratory samples and field isolates (Dittmann and Börner, 2005).
Nodularins are hepatotoxins found in blooms caused by strains of the brackish-water species Nodularia spumigenia. The toxins are closely related to microcystins in both structure and function and thus act similarly by inhibiting protein phosphatase activity in liver cells (Chorus and Bartram, 1999).
Data derived from experimental studies, although limited, have suggested that nodularin exhibits toxicity similar to that of microcystin-LR. Results obtained from chronic toxicity studies using animal models have suggested that nodularins may be a more potent tumour promoter than the microcystins (Chorus and Bartram, 1999).
Nodularia blooms have been encountered in brackish lakes in Australia and New Zealand, as well as in the Baltic Sea. In general, blooms in fresh water are considered extremely rare (Chorus and Bartram, 1999). To date, there have been no recorded occurrences of Nodularia blooms in North American waters. As a result, they are not considered to be a significant public health threat in Canadian recreational waters.
The anatoxins (anatoxin-a, anatoxin-a(S), homoanatoxin-a) are neurotoxins that can be found in blooms produced by Anabaena (anatoxin-a, anatoxin-a(S)), Oscillatoria (anatoxin-a, homoanatoxin-a) and Aphanizomenon (anatoxin-a). Anatoxins interfere with the activity of the nerve transmitter acetylcholine, which affects the functioning of the nervous system by disrupting communication between neurons and muscle cells (Chorus and Bartram, 1999). Acute toxicity is characterized by paralysis of both the skeletal and respiratory muscles, resulting in tremors, convulsions and, ultimately, death due to respiratory failure (Rogers et al., 2005).
Information on health effects associated with anatoxins has been gleaned from occasional accounts of animal poisonings and toxicological investigations. Anatoxin-a has been the most widely studied member of this group. Limited data are available for homoanatoxin-a and anatoxin-a(S) (Chorus and Bartram, 1999). However, it is generally regarded that although the toxins have somewhat different mechanisms of action, each is capable of causing fatalities at elevated doses. The oral LD50 of anatoxin-a is reported to be greater than 5000 µg/kg bw (Fitzgeorge et al., 1994). Anatoxin-a was shown to be toxic in experimental mice upon acute exposure to high levels of the toxin (15 000 µg/kg bw). Death was reported to occur within minutes (Chorus and Bartram, 1999). Conversely, in a number of experimental studies, recovery after exposure to sublethal doses of anatoxin-a was complete, with no signs of clinical toxicity. To date, there has been only one reported fatality resulting from exposure to cyanobacterial neurotoxins in natural waters. Exposure occurred through ingestion of contaminated water during accidental immersion at a location where swimming was not permitted (Falconer, 2005).
Blooms of anatoxin-producing species are not routinely reported in North American waters and are considered to occur far less frequently than those of the microcystin-producing cyanobacteria. In addition, the anatoxins are relatively unstable and, as such, are not considered to be as widespread as microcystins in water supplies (Chorus and Bartram, 1999). As a result, anatoxins are currently considered to be of lesser concern than microcystins for Canadian recreational waters.
Cylindrospermopsin is a relatively new cyanobacterial toxin named after the species from which it was first isolated: Cylindrospermopsis raciborskii. It is a member of the alkaloid family of toxins; however, the mode of action is considerably different from that of the anatoxins. Similarly, cylindrospermopsin does exhibit hepatotoxic activity, but operates by a mechanism much different from that of the other microcystins (Chorus and Bartram, 1999). The toxin has been isolated from certain species of a few other genera of cyanobacteria, including Anabaena and Aphanizomenon (Falconer and Humpage, 2006).
Cylindrospermopsin is considered to be a general cytotoxin, which acts by inhibiting protein synthesis. Cellular damage is caused by blocking the functioning of key proteins and enzymes. The liver and kidneys are considered the main targets for the toxin; however, crude extracts of Cylindrospermopsis given to mice have also demonstrated evidence of injury to other organs, such as the lung, spleen, thymus and heart (Chorus and Bartram, 1999). Data, derived from a study in which mice orally dosed with cylindrospermopsin demonstrated a positive but not statistically significant increase in the number of tumours, have provided evidence that the toxin may also possess carcinogenic properties (Falconer and Humpage, 2001).
The first recorded incident of human cylindrospermopsin poisoning occurred in 1979. Initially termed "Palm Island Mystery Disease," this outbreak of hepatoenteritis among residents of a tropical island off the coast of Queensland, Australia, was later attributed to a bloom of C. raciborskii in the drinking water reservoir. Patients had reported symptoms that included vomiting, malaise, headache and constipation, later followed by bloody diarrhoea. Blood and urine analysis revealed evidence of liver and kidney damage; however, all patients were reported to have recovered following treatment. Follow-up research led to the identification of the toxin cylindrospermopsin produced by this cyanobacterial species. At present, there have been no human fatalities associated with cylindrospermopsin, and there have been no other recorded poisonings since the Palm Island outbreak (Chorus and Bartram, 1999).
Cylindrospermopsis is more frequently encountered in the warmer waters found in tropical and subtropical locations of the world. Blooms have been routinely encountered in freshwater lakes and drinking water reservoirs in Australia, South and Central America, and the state of Florida. To date, the organism has been only occasionally encountered in temperate fresh waters. In North America, populations have been detected in several northern U.S. states (Michigan, Ohio, Minnesota, Illinois and Indiana), as well as in the province of Manitoba.
There are several notable differences between populations of Cylindrospermopsis and those of cyanobacteria having microcystin-producing potential such as Microcystis or Anabaena. Cylindrospermopsis does not form slicks or scums of the type produced by these organisms. In Cylindrospermopsis blooms, the regions of highest cell concentrations are located beneath the surface (Falconer, 2005). As well, in these blooms, a significant portion of the toxin is released into the surrounding water, in contrast to the situation in microcystin-producing species in which the toxin is predominantly retained within the cells and released only upon cell rupture or death (Falconer, 2005). Blooms of Cylindrospermopsis are considered infrequent in Canadian waters. Those caused by microcystin-producing species are far more prevalent. Nonetheless, the increasing frequency at which this organism is being detected in temperate fresh waters has resulted in the identification of Cylindrospermopsis blooms as a potentially emerging concern for recreational waters in Canada and the United States.
Saxitoxins are neurotoxins that belong to a larger family of toxins referred to as Paralytic Shellfish Poisoning (PSP) toxins. These toxins, originally isolated from shellfish having fed on toxic species of marine dinoflagellates, have also been isolated from several genera of freshwater cyanobacteria, including Aphanizomenon, Anabaena, Cylindrospermopsis, Lyngbya and Planktothrix (Oscillatoria) (Chorus and Bartram, 1999; Aráoz et al., 2010). Saxitoxins act by blocking ion channels in nerve and muscle cells, which prevents the transmission of electrical impulses. This can lead to neuromuscular paralysis, which can ultimately be fatal owing to the resulting respiratory failure.
Most of the toxicological information on saxitoxins has been obtained from studies using toxins produced by the marine dinoflagellates (e.g., Alexandrium spp.). Nevertheless, saxitoxin types derived from different sources remain identical in structure and toxicological profile (Funari and Testai, 2008). Saxitoxin is considered one of the most toxic of the PSP toxins (Chorus and Bartram, 1999). The oral LD50 reported for saxitoxin is 263 µg/kg bw (Mons et al., 1998; Funari and Testai, 2008). Animal deaths have been linked to contact with cyanobacterial blooms containing saxitoxin (Negri et al., 1995). There have been no saxiotoxin-related illnesses reported for humans through drinking water or recreational water exposure (Chorus and Bartram, 1999; Aráoz et al., 2009).
Saxitoxin-containing blooms are considered widespread in Australia, and toxic blooms have also been detected in waters in Brazil and in the southern and northern United States (Chorus and Bartram, 1999; dos Anjos et al., 2006). Presently, saxitoxins are not considered to be as significant a concern as microcystins in Canadian recreational waters. However, the detection of saxitoxins in blooms in temperate fresh waters suggests that this issue should continue to be monitored.
Dermatotoxins and other irritant toxins
Certain marine cyanobacteria such as Lyngbya, Oscillatoria and Schizothrix can produce toxins called aplysiatoxins and lyngbyatoxins, which have been reported to cause severe dermatitis among swimmers who come in contact with the cyanobacterial filaments. Aplysiatoxins are considered potent tumour promoters and are also thought to demonstrate other properties that may be linked to carcinogenesis (Chorus and Bartram, 1999). As these are primarily marine species, they are not thought to be of concern for freshwater lakes and rivers.
Although not well understood, it is also thought that the lipopolysaccharide component of the cyanobacterial cell wall can elicit an irritant or allergenic response in humans. Lipopolysaccharides have been known to exhibit pyrogenic (fever-inducing) and toxic properties. It is generally regarded, though, that lipopolysaccharides from cyanobacteria are considerably less toxic than those of other Gram-negative bacteria, such as Salmonella (Chorus and Bartram, 1999). Nonetheless, it is thought that they may be at least partially responsible for some of the non-specific irritative effects associated with human exposure to cyanobacterial blooms.
Compound of interest: B-methylamino-L-alanine (BMAA)
An emerging topic of interest involves the unusual amino acid B-methylamino-L-alanine (BMAA), its links to cyanobacteria and the research findings concerning its potential neurotoxic capabilities. The present evidence does not suggest that BMAA is a recreational water quality hazard of human health concern. Information is provided on the current state of evidence on this issue.
BMAA was first identified during exploratory studies into the high rate of amyotrophic lateral sclerosis/parkinsonism-dementia complex (ALS-PDC, a neurodegenerative disease with symptoms similar to Parkinson's disease and Alzheimer's disease) observed among the Chamorro people of Guam. Findings reported by the researchers during investigations into this issue included that BMAA could be detected in brain tissues of ALS-PDC patients in Guam and Canada (Cox et al., 2003), and that BMAA could be found in virtually all groups of cyanobacteria including the notable freshwater genera: Anabaena, Aphanizomenon, Microcystis, Nodularia and Oscillatoria (Cox et al., 2005; Metcalf et al., 2008). The further observation that BMAA could be detected in flying foxes (i.e., bats, which constitute a portion of the Chamorro diet) led the researchers to hypothesize that BMAA could be subject to magnification up the food chain.
These findings and the proposed implications are currently the subject of debate (CRC 2005). Some researchers have provided conflicting evidence regarding BMAA detection in brain tissue of ALS-PDC patients (Montine et al., 2005), while others have questioned the data relating to neurotoxicity and food chain magnification (Duncan and Marini, 2006).
Research into this issue is considered preliminary, requiring further investigation. It is proposed that much more work is needed before a cause and effect relationship between BMAA and neurological disease can be established or discounted (CRC, 2005). Similarly, there is insufficient evidence at this time to suggest that water supplies or dietary sources could constitute a significant source of BMAA exposure. Developments on this topic will continue to be monitored.
The recommended guideline values for total cyanobacteria and total microcystins in Canadian recreational waters are based upon the approach used in the derivation of the maximum acceptable concentration (MAC) for microcystin-LR in the Guidelines for Canadian Drinking Water Quality (Health Canada, 2002). The use of single guideline values for total cyanobacterial cell density and total microcystin concentration is the preferred approach to setting guidelines for Canadian recreational waters at this time. They are intended to protect against both the risk of exposure to microcystins through inadvertent ingestion of water as well as from other harmful effects that may be possible after exposure to high densities of cyanobacterial material. In this situation, values were derived based on children as they may be more intensely affected because they spend more time in water than adults and are more likely to accidentally swallow contaminated water. The guideline value for total microcystins (expressed as microcystin-LR) is intended to be protective against exposure to other microcystin variants that may be present.
For microcystin-LR, the tolerable daily intake (TDI) for recreational water exposures is derived as follows:
The equation used to calculate the tolerable daily intake (TDI) for microcystin-LR
Description of the equation used to calculate the tolerable daily intake (TDI) for microcystin-LR - Text Equivalent
- 40 µg/kg bw per day is the NOAEL for liver changes derived from the 13-week mouse study conducted by Fawell et al. (1999); and
- 100 is the uncertainty factor (×10 for intraspecies variation, ×10 for interspecies variation).
An additional uncertainty factor for less-than-lifetime study was not considered necessary, as the types of exposures being considered are short term and episodic in nature.
The guideline value for total microcystins is calculated from the TDI for microcystin-LR as follows:
The equation used to calculate the Maximum Limit for total microcystins
Description of the equation used to calculate the Maximum Limit for total microcystins - Text Equivalent
- 0.4 µg/kg bw per day is the TDI, as derived above;
- 13 kg bw is the average weight of a child aged 7 months to 4 years (Health Canada, 1994); and
- 0.25 L/day (250 mL/day) is the estimated amount of water accidentally ingested per day during recreational water activities by a child.
The value used for the amount of water accidentally ingested per day is probably a conservative estimate. Risk assessment models developed for enteric pathogens in recreational waters have typically assumed a value of 100 mL for the amount of water likely to be swallowed through recreational water activities (Haas, 1983; Gerba et al., 1996; Mena et al., 2003). Yet the basis for this appears to be more historical than empirical. WHO (2003a) suggests that a child may be capable of consuming 250 mL of water during extensive playing. During an empirical investigation of the volume of water swallowed during swimming activities, Evans et al. (2006) reported average values of 24 mL for adults (95% range, 2-84 mL) and 47 mL for children (95% range, 3-142 mL). The authors further observed that some swimmers swallowed up to 280 mL/hour.
In addition to being capable of initiating toxic effects through ingestion, microcystins have been suspected to be associated with other irritative effects that can occur through recreational water contact, such as injuries to the tissues of the mouth and lips. As a result, it is possible that a more conservative estimate is appropriate as a worst-case scenario to account for the total amount of water ingested, and not just the portion accidentally swallowed. The value of 250 mL represents a risk management decision, derived based on the assessment of the available information regarding the likely risk of ingestion and of the potential risks for the recreational water user.
The guideline value for cyanobacterial cell density (expressed as total cyanobacteria) represents a general indication of the potential for bloom development and is intended to be protective against exposure to high densities of cyanobacterial material. It similarly may be used to provide protection against exposure to blooms of other cyanobacteria with toxic potential, and not just the microcystin-producing species. It is calculated based on the microcystin guideline value using the recognized reference value for the average toxin quota for Microcystis cells and reflects the highest likely water quality hazard scenario of a toxic bloom containing high levels of microcystin (WHO, 2003a; NHMRC, 2008):
The equation used for calculating the Maximum Limit for total cyanobacteria
Description of the equation used for calculating the Maximum Limit for total cyanobacteria - Text Equivalent
- 20 µg/L is the guideline value for total microcystins in recreational waters, as derived in the previous section;
- 2 × 10−7 µg/cell is the toxin cell quota for total microcystins per cell (WHO, 2003a; NHMRC, 2008); and
- 10−3 L/mL is the factor converting litres to millilitres.
Currently, there is insufficient evidence to derive recreational water guidelines for other cyanobacterial toxins, such as the anatoxins or cylindrospermopsin. Based on the assessment, it was similarly determined that there is not sufficient data upon which to base a guideline whose intent is to provide protection from the risk of allergenic or other irritative effects caused by unknown cyanobacterial substances. Studies conducted by Pilotto et al. (1997, 2004) on the effects of human skin contact with cyanobacteria were reviewed. Both studies reported that skin contact with cyanobacteria across a wide range of cell densities resulted in reactions of only mild severity in only a very small proportion of subjects. No dose-response relationships or thresholds for irritation could be observed. It was judged that these findings did not provide sufficient argument for the need for a separate guideline.
This approach and guideline value for microcystin are consistent with criteria derived by the province of Québec for microcystin-LR toxic equivalents in recreational waters: 16 µg/L (INSPQ, 2004). Further, the guideline value for total cyanobacteria is consistent with the WHO guideline of 100 000 cyanobacterial cells/mL for the moderate probability of adverse health effects. In its supporting documentation, WHO (2003a) further proposes that at this cyanobacterial density, a concentration of 20 µg microcystin/L is likely if the bloom consists of Microcystis with an average toxin content of 2 × 10-7 µg/cell.
The Canadian approach is also similar in principle to the Australian Level 1 Guidelines (NHMRC, 2008); however, a different animal model and derivation process have been used in the Canadian calculations. The Australian approach was based on data considered to be the most suitable for deriving guidelines for toxic cyanobacteria in Australian recreational waters.
Occurrence in the environment
In a 1995 survey of 16 recreational water bodies in southern Manitoba, Jones et al. (1998) reported that microcystin-LR could be found at 44% of the sites, with concentrations occurring in the 0.1-0.6-µg/L range. The authors further reported that cyanobacterial cell density was not a good predictor of microcystin-LR and that there was no correlation between toxin concentration and the other environmental variables monitored in the study.
Kotak et al. (1996) reported on a 3-year investigation that measured microcystin concentrations encountered in phytoplankton and surface water samples collected from four freshwater lakes in central Alberta. Phytoplankton concentrations of microcystin were found to be highest in the two most hypertrophic lakes (Driedmeat and Little Beaver lakes). The highest microcystin concentrations were observed in August and September, and were reported to correspond to periods where Microcystis cell counts were at their highest (>200 000 cells/mL). Levels reported during these months at one of the lakes (Driedmeat) ranged from 1.2 to 6.1 µg/L. The highest microcystin concentration observed during the course of the study was 11 µg/L in a sample collected from Little Beaver Lake in mid-August.
Giani et al. (2005) reported total microcystin concentrations of 0.008-1.91 µg/L (mean, 0.140 µg/L) in water samples collected during a survey of 22 freshwater lakes in southern Québec. None of the lakes were reported to be affected by cyanobacterial blooms at the time of sampling. The authors reported that all lakes contained detectable levels of cyanobacterial genera having toxic potential (including Microcystis, Anabaena and Oscillatoria), although these were typically encountered at concentrations considered far below levels of concern.
Rinta-Kanto et al. (2005) reported on the characterization of two separate bloom events that had developed in the western basin of Lake Erie: the first in August 2003 and the second in August 2004. Satellite imaging was used by the researchers to detect the presence of the blooms and was similarly applied to identify potential sites for analysis. Bloom samples were collected and analysed for total microcystin concentrations (cell-bound fraction). At the same time, estimates of the presence of total and toxic Microcystis concentrations were determined by QPCR analysis, with targets specific for a Microcystis 16S rDNA gene fragment and the microcystin synthase gene mcyD. Microcystin concentrations encountered in the 2003 bloom ranged from <0.3 to 15.4 µg/L, and estimates of the corresponding Microcystis concentration ranged from below the quantifiable limits of detection to a peak value of 3.9 × 108 Microcystis equivalents/L. In the bloom encountered the following year, microcystin concentrations ranged from 0.1 to 2.6 µg/L, and estimates of the total Microcystis concentration spanned from approximately 5 × 103 to 3 × 106 Microcystis equivalents/L.
No human cyanotoxin-related deaths have been associated with exposure via recreational water. To date, there have been only two reported instances of human fatalities as a result of exposure to cyanobacterial toxins. The most notable are those associated with the human dialysis tragedy that occurred in Caruaru, Brazil, in 1996 (Jochimsen et al., 1998). In total, 56 patients at a haemodialysis clinic died as a result of liver failure from exposure to microcystins in the water used for dialysis. The presence of toxic cyanobacteria in the city's drinking water reservoir and insufficient water treatment were cited as major factors contributing to the deaths. More recently, in 2002, a Wisconsin teenager died following exposure to a toxic scum in a pond on a public golf course where swimming was not permitted (Falconer, 2005). Blood and stool samples collected revealed the presence of both the cyanobacterial species Anabaena flos-aquae and the neurotoxin anatoxin-a.
There have been few reported accounts of human illness as a result of contact with toxic cyanobacterial populations in recreational waters worldwide. The predominant health effects encountered from such exposures may be gastrointestinal or flu-like in nature and thus may often go unreported or are attributed to other causes (Falconer, 2005). As well, most of the cases of illness are investigated retrospectively; thus, information regarding the exact conditions of exposure (number and type of organisms, identification and/or concentration of toxins) is rarely available.
In Saskatchewan in 1959, despite warnings and reports of livestock deaths, people swam in a lake infested with cyanobacteria. Thirteen individuals in total became ill, reporting symptoms of nausea, muscular pain, headache and diarrhoea (Dillenberg and Dehnel, 1960). In England in 1989, 10 of 20 soldiers became ill after canoe training and swimming in water affected by a Microcystis bloom. Swimming skills and the amount of water ingested were reported to have been related to the degree of illness (Turner et al., 1990). In 1991, in Australia, two teenage girls developed gastroenteritis and muscle pains after swimming in the Darling River near Wilcannia during a cyanobacterial bloom containing Anabaena (NHMRC, 2008). In the same year, two cases of conjunctivitis and one of dermal irritation were attributed to swimming during an Anabaena circinalis bloom in Lake Cargelligo, Australia (NHMRC, 2008).
Pilotto et al. (1997) reported on the results of a prospective epidemiological study designed to investigate the health effects encountered in swimmers after contact with cyanobacteria in recreational water. Symptoms were shown to increase significantly with the duration of water contact and increasing cyanobacterial cell density, but did not correlate with cyanotoxin concentrations. Participants in this study who were exposed to 5000 cells/mL for more than 1 hour had a higher rate of symptom occurrence than did unexposed participants. However, after controlling for previous exposure and prior illnesses, the data suggested that only a small number of people were affected, and only with mild irritation. Stewart et al. (2006b) conducted a prospective epidemiological study to examine the incidence of acute symptoms in recreational water users exposed to different amounts of cyanobacteria based on measurements of surface area per volume (SA/V). The authors observed that symptoms were more likely to be reported among persons exposed to high (>12 mm²/mL) versus low (<2.4 mm²/mL) SA/V levels, and that respiratory symptoms were recorded with the greatest frequency. Cyanotoxins were detected only occasionally and at low SA/V levels during the study.
Managing health risks
A multi-barrier approach is considered the best strategy to reduce the risk of exposure to cyanobacteria or their toxins in recreational waters. This approach combines the use of the recommended indicators of water quality alongside actions both to reduce the extent of the water quality hazard and to restrict swimmer exposures during periods or in areas perceived to be of increased risk.
The occurrence of cyanobacterial blooms in recreational waters is extremely difficult to predict. Bloom development is influenced by a variety of physical, chemical and biological factors. As a result of the interplay of these factors, there may be large year-to-year fluctuations in the levels of cyanobacteria and their toxins (Health Canada, 2002). Managed recreational water areas that are suspected or are known to be susceptible to blooms should be routinely monitored during the bathing season. Authorities should visually monitor such supplies for cyanobacterial growth. Toxicity within a bloom can vary considerably, particularly within large blooms. Further, a water body in which a bloom has developed may still contain toxins for a short period after the bloom has dissipated. In order to fully characterize the extent of the risk posed by the cyanobacterial population, authorities should conduct sampling during, and after the collapse of, the bloom. Collection of multiple samples may be required to identify any regional or localized differences in cyanobacterial cell density and toxin concentration. It is advised that both total cyanobacterial cell densities and total microcystin concentrations be monitored as part of a risk management strategy for cyanobacteria and their toxins in Canadian recreational waters. As discussed, monitoring of microcystin levels is necessary to determine the potential health risk posed by a cyanobacterial population, while cell count determinations are useful for providing a general indication of the potential for bloom development and, thus, the possible presence of cyanobacterial toxins.
Waters shown to exceed the established guideline values or those in which a bloom has developed may result in human exposure to cyanobacterial material or cyanotoxins in amounts sufficient to be harmful to human health. A swimming advisory may be issued at the discretion of the responsible authority. Contact with waters where an advisory has been issued should be avoided until the advisory has been rescinded. Further information on the posting of recreational waters can be found in Part I (Management of Recreational Waters).
Other barriers for risk reduction can include the provision of educational materials outlining steps the public may take to reduce their personal risk in the event of a bloom. Guidance provided in materials for public communication may include the following recommendations:
- Recreational water users should avoid areas with visible cyanobacterial blooms and/or scums, as all blooms have the potential to be toxic. Direct contact with bloom material or accidental ingestion of contaminated waters can be harmful to recreational water users. Inhalation may also be an important route of exposure to cyanobacterial toxins during activities in bloom-affected areas where aerosols might be generated.
- Users should shower or wash themselves as well as any item that may have accidentally come into contact with cyanobacterial material as soon as is practical upon exiting the water.
- Any user experiencing adverse health effects from recreational water activity should consult a medical professional and, if necessary, alert the appropriate authorities.
- Users should not let pets swim in or drink from areas where the water has taken on an abnormal discolouration consistent with that of a bloom, or where accumulations of cyanobacterial material are visible. Should pets come in contact with bloom-affected waters, they should be rinsed off immediately to remove all traces of cyanobacterial material that may accidentally be ingested.
The use of algicides is not recommended as a measure to control cyanobacterial populations. The addition of copper sulphate or other algicides to mature toxic blooms may have the effect of destroying the cyanobacterial cells; however, this action may also cause the release of significant amounts of cyanotoxin into the surrounding waters if present within the cells. Jones and Orr (1994) reported that microcystin-LR could be detected up to 21 days after algicide treatment of a toxic Microcystis aeruginosa bloom that had developed in a recreational lake. Environmental concerns have also been cited as additional reasons for not pursuing this approach, as the algicides can be detrimental to the healthy functioning of the aquatic ecosystem.
Longer-term risk management actions that may also be considered as barriers to reduce the impact of toxic cyanobacteria in surface waters may involve the identification of the major nutrient inputs, as well as the development of strategies to reduce nitrogen and phosphorus loading through effective control of agricultural, municipal sewage and residential waste disposal practices. Tracking total phosphorus levels in surface waters has been suggested as a proactive step for recognizing water bodies that have the potential for bloom development (Chorus and Bartram, 1999).
- The development of cyanobacterial blooms in waters that are used for recreational purposes is dependent on many factors that can be difficult to predict. Blooms can develop very rapidly under the appropriate conditions, and lakes that have never had a problem can suddenly become toxic.
- Serious swimmer illnesses have been reported following exposure to toxic cyanobacterial blooms in recreational waters. A water body containing a cyanobacterial bloom may still contain toxins after visible signs of the bloom have disappeared. In general, contact with waters where a bloom exists or has very recently collapsed should be avoided. Contact with waters where an advisory has been issued should be avoided until the advisory has been rescinded.
- To date, there have been very few reported cases of cyanobacterial toxin-related illness due to recreational water activity in Canadian or international waters. The combination of visual inspection, water quality monitoring and public notification and education alongside actions and procedures for reducing nutrient inputs represents the most effective approach to protecting the health of recreational water users.
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