11/00 
 Blue Green Algae, their Toxins and Public Health Issues 
 Lora E Fleming MD PhD MPH MSc 
NIEHS Marine and Freshwater Biomedical Sciences Center 
University of Miami 
Miami, FL 
  Background 
 The Cyanobacteria or blue green algae are an ancient and ubiquitous family of photosynthetic organisms 
(Chorus 1999, Carmichael 1994, Falconer 1989, NHMRC 1994). These organisms are able to fix 
nitrogen, and are therefore an important part of the food chain.  The cyanobacteria frequently are found 
growing on marine, brackish and fresh waters, including freshwater surface drinking sources, such as 
lakes and drinking water reservoirs.  Similar to the marine algal blooms, cyanobacteria periodically will 
grow exuberantly, known as "blooms."  The reasons for these blooms are not completely understood, but 
in some cases they may be related to nutrients added naturally and through man-made sources (such as 
fertilizer runoff) (Philipp 1991, Carmichael 1993, Rapala 1997).  These blooms can cause significant 
environmental impact due to the decrease in oxygen in the water, resulting in the die-off of fish and other 
organisms.  Furthermore, again similar to marine algal blooms or red tides, these blue green algal blooms 
can produce significant quantities of natural toxins, for reasons as yet unknown.  When they produce 
these highly active natural biotoxins, these blue green algal blooms are known as a "harmful algal bloom 
(HAB)."  To date at least 12 different species of Cyanobacteria have been shown to produce toxins, often 
several different toxins per species (Carmichael 1994).  The main toxic cyanobacterial genera include 
Anabaena, Aphanizomenon, Nodularia, Oscillatoria, and Microcystis (Carmichael 1993, NHMRC 1994, 
Chorus 1999).   
 Toxins 
These toxins, along with those produced by the marine organisms such as dinoflagellates and diatoms, are 
extremely toxic to many species.  There is a wide spectrum of blue green algal toxins, predominantly 
affecting the nervous, hepatic and dermatologic systems (ie. neurotoxic hepatotoxic and dermatotoxic). 
 The dermatotoxins include aplysiatoxins and lyngbyatoxin, and are often reported from marine 
cyanobacteria blooms.  These are potent tumor promoters and protein kinase C activators.  These toxins 
can cause severe dermatitis with only skin contact, as well as gastrointestinal inflammation with oral 
exposure (Chorus 1999). 
 The neurotoxins include: anatoxin a and anatoxin a (S) (both unique to the cyanobacteria), as well as 
saxitoxin and neosaxitoxin (also elaborated by marine dinoflagellates and associated with the human 
disease paralytic shellfish poisoning or PSP).  Anatoxin a acts like the neurotransmitter acetylcholine 
except that it cannot be degraded by acetylcholinesterase; anatoxin a (S) is a natural organophosphate, 
binding to the acetylcholinesterase enzymes; the saxitoxins are sodium channel blockers.   Singly or in 
mixtures, these cyanobacterial neurotoxins can cause death within minutes secondary to respiratory 
paralysis (Codd 1997, Carmichael 1994, Carmichael 1993).   
 The hepatotoxins are cyclic peptides, predominantly microcystins, nodularins, and cylindrospermopsin.  
Of note, these toxins are particularly toxic to the liver in part due to selective transport mechanisms that 
concentrate these toxins from the gut and blood into the liver cells; they damage the liver by deranging 
the cytoskeletal architecture of the hepatocytes.  Cylindrospermopsin is a protein synthesis inhibitor, 



 



 


resulting in wide spread necrosis of the tissues of many organs.  The microcystins and the nodularins are 
protein phosphatase inhibitors, as well as being potent tumor promoters in animals (similar to the 
carcinogen, okadeic acid, elaborated by marine dinoflagellates and associated with the human disease 
diarrheic shellfish poisoning or DSP).  The microcystins cause liver necrosis leading to death within 
hours to days (Elder 1993, Carmichael 1994, Humpage 1999, Yu 1995, Ohtani 1992, MacKintosh 1990, 
Repavich 1990, NHMRC 1994, Chorus 1999).  At lower doses, enteritis and hepatitis are seen shortly 
after ingestion of these toxins. 
 The same cyanobacteria species can produce both neurotoxins and hepatotoxins, even during the same 
bloom; often the presence of the hepatotoxin is masked by the premature death of the animal due to the 
neurotoxin.   In addition, there exist other toxins (including lipopolysaccharides, endotoxins and 
additional neurotoxins), as well as yet undescribed cyanobacterial toxins including additional tumor 
promoters (Falconer 1989, Codd 1997, Falconer 1994, Falconer 1996).   
 Animals 
There have been frequent reports of thirsty domestic animals and wildlife consuming freshwater 
contaminated with toxic blue green algal blooms, and dying within minutes to days from acute 
neurotoxicity and/or hepatotoxicity (Jochimsen 1998, Elder 1993, Carmichael 1994, Codd 1997, 
Mahmood 1988, Carbis 1995, Negri 1995, Repavich 1990).  Toxic blooms of cyanobacteria with 
associated animal poisonings have been reported in all continents except Antartica (NHMRC 1994).  
Mammals and birds appear to be more susceptible to the blue green algal toxins than aquatic invertebrates 
and fish, with some species variability.  Prolonged morbidity and mortality have also been reported in 
animals exposed to blue green algae in the wild.  For example, Carbis et al (1995) followed sheep 
exposed to Microcystis aeruginosa in a lake in Australia for 6 months; there was a 34% mortality over 
this period among the exposed sheep without clear etiology even after resolution of the initial liver 
toxicity observed during the first 3 weeks.  
 Experimentally, acute high dose administration of microcystin can lead to death from 
hepatoencepholopathy with in hours, and chronic administration to mice of sublethal amounts of 
Microcystis extracts in drinking water results in increased mortality with chronic active liver disease even 
at fairly low doses and in relatively short time periods (Heinze 1999).  Falconer et al (1992) gave intra 
peritoneal (ip) injections to mice of the gut and gut contents of boiled edible mussels from a water bloom 
of Nodularia in Western Australia.  The cell density of the bloom in the water had been up to 100,000 
cells/mL.  The ip injections were lethal secondary to acute (within 24 hours) hepatotoxicity to 1 kg mice 
at 89 mg dry weight/kg, the Nodularia bloom LD50 was 24.4 mg dry weight/kg.  Falconer et al (1992) 
conclude that edible mussels should not be collected for human consumption during a toxic blue green 
algal bloom.  
 Teratogenic activity has been demostrated in mice with oral administration of Microcystis extracts; 
approximately 10% of otherwise normal neonatal mice had small brains with extensive hippocampal 
neuronal damage (Carmichael 1993, Astrachan 1980).  Studies in cultured cells have also shown tumor 
promotion, and microcystins are preferentially taken up by hepatic cells, so that hepatic tumor promotion 
is likely (Falconer 1996, Carmichael 1994, Carmichael 1993, Sugimura 1986, Humpage 1999, Ito 1997). 
As noted above, the microcystins can cause tumor promotion in animals exposed to chronic low level 
non-lethal doses.  Nishikawa et al (1992) showed that microcystins are powerful tumor promoters of 
hepatic liver tumors in rats mediated through the inhibition of protein phosphatase type 1 and type 2A 
activity (Hong-Bing 1996).  Lyngbyatoxin A has been shown to be a potent tumor promoter in a two 
stage mouse skin carcinogenesis study by Fujiki et al (1984). 
 Humans 


 



 


There are relatively few case reports and even fewer epidemiologic studies of the human health effects of 
the blue green algal toxins (Carmichael 1993, Jalaludin 1992, Falconer 1999, Chorus 1999, Ressom 
1994). Humans can be exposed to the cyanobacteria and their toxins through direct skin contact or by 
drinking contaminated waters; other possible routes of exposure include inhalation of aerosol, 
consumption of contaminated food, and even through dialysis (Codd 1997, Chorus 1999).  Occupational 
exposures for fishermen, watermen, and scientists, as well as recreational exposures, are both possible 
(Codd 1997, Baxter 1991, Philipp 1991). 
 Recently, there have been a host of articles concerning cyanobacteria as a source of chronic relapsing 
diarrhea, especially in travelers (both immunocompromised and not) to developing nations; the illness 
seems to be associated with the organisms rather than the toxins, and furthermore may actually be a 
separate group of organisms that are cyanobacterium-like  (Soave 1986, Anon 1991,Hale 1994).  Some 
researchers have even postulated a role for the blue green algae as a carrier or reservoir of the bacteria 
Vibrio cholera, the latter responsible for the human bacterial disease cholera (Islam 1994, Chorus 1999).  
 There are individual case reports of persons exposed through swimming to blue green algal blooms with 
skin irritation and allergic reactions (both dermatologic and respiratory) with continued positive reaction 
on skin testing (Falconer 1989, Carmichael 1993, Falconer 1999, Hashimoto 1974, NHMRC 1994, 
Chorus 1999).  In particular, urticaria, blistering and even deep desquamation of skin in sensitive areas 
like the lips and under swimsuits has been reported, especially with Lyngbya majuscula in tropical areas.  
Consumption of or swimming in cyanobacterial toxin-contaminated waters has also yielded increased 
case reports of gastointestinal symptoms, especially diarrhea (Billings 1981, Probert 1995). Turner et al 
(1990) reported 2 cases of pneumonia in healthy army recruits following probable inhalation from a canoe 
on waters with a blue green algal bloom of Microcystis aeruginosa; 16 other exposed recruits reported of 
a variety of gastrointestinal (hepatoenteritis), dermatologic and respiratory complaints (Turner 1990).   In 
addition to gastrointestinal and dermatologic symptoms, eye irritation, asthma, and "hay fever symptoms" 
have been reported repeatedly with contaminated recreational water exposure in the US, Canada, UK, and 
Australia (NHMRC 1994). 
 In general, the few epidemiologic studies available have been performed after a significant community 
exposure event.  With a long history of episodes of possible adverse health effects in animals and humans 
in Australia, Pilotto et al (1997) studied the effects in South Australia of exposure to blue green algae as a 
result of recreational water activities.  They used a serial symptom questionnaire on a large sample (777 
"exposed" and 75 "unexposed"), as well as water sampling for cyanobacteria and toxin.  Although there 
was no difference in the type and quantity of symptoms reported acutely, the Investigators found a 
significant trend to increasing symptom occurrence with duration of exposure, and a symptom dose 
response that correlated with exposure to 5000 cells per ml for more than one hour; however, symptoms 
did not correlate with the presence of hepatotoxins in the water.  The Investigators suggested that the 
current safety threshold for exposure of 20,000 cells per mL may be too high.  El Saadi et al (1995) 
performed a case control study in 11 South Australian towns along the Murray River, a cyanobacterial 
historic epicenter, using gastrointestinal and dermatologic cases and controls with similar town 
distributions.  Persons who drank the river water, even after chlorination, were significantly more likely to 
have gastrointestinal symptoms, while those using river water for domestic purposes were significantly 
more likely to have both gastrointestinal and dermatologic symptoms, compared with persons using 
rainwater.  Furthermore, there was a correlation with report of symptoms and mean log cyanobacterial 
cell counts. 
 Seasonal gastroenteritis has been reported worldwide and may be related to the consumption of 
contaminated drinking water (Carmichael 1993, Volterra 1993, Codd 1984, Falconer 1999).  Some of the 
first reports of adverse health effects from exposure to the blue green algae were by Veldee (1931) when 
an estimated 9000 persons out of a population of 60,000 in Charleston (West Virginia) reported acute 



 



 


gastroenteritis after a period of low rain fall and reportedly contaminated drinking water; other outbreaks 
were seen along the Ohio River in the same year (Tisdale 1931).  Lipp and Erb (1976) reported that 62% 
of the population of 8000 of Sewickley (Pennsylvannia) suffered from acute gastroenteritis; the reservoir 
was found to be contaminated by Schizothrix calcicola.    In 1988, severe gastroenteritis was reported in 
Brazil after the flooding of a newly constructed dam and reservoir with 2000 cases and 88 deaths 
(particularly children) over a 42 day period; cases were restricted to the areas supplied by drinking water 
from the reservoir and had only consumed boiled water with negative bacterial and viral cultures, and 
Anabaena and Microcystis blooms were present (Chorus 1999, Teixera 1993). 
 Liver enzymes, especially GGT, have also been found to be increased after consumption of drinking 
water contaminated with Microcytis toxins in Australia.  Other Australian episodes have included a 
severe outbreak of hepatoenteritis after drinking water with a novel cyanobacterial toxin contamination on 
Palm Island in Queensland (Australia) (Falconer 1983, Carmichael 1993, Bourke 1983, Probert 1995, El 
Saadi 1995, Chorus 1999).  In this particular episode, the drinking water reservoir had been dosed with 
copper sulphate to remove a persistent cyanobacteria bloom of Cylindrospermopsis raciborskii, leading to 
lysis of the algal cells and substantial release of toxins into the drinking water.  Reportedly some of the 
children were critically ill with severe hepatoenteritis and kidney failure, and 150 persons (140 children) 
were ultimately hospitalized. Subsequent research identified the cytotoxic cylindrospermopsin as well as 
other toxins as the probable cause of the outbreak. In another study by Falconer (1994) in different area of 
Australia with a similar situation of cyanobacterial toxin contamination of a drinking water supply after 
the use of copper sulfate, clinical liver function data were examined.  There was a statistically significant 
increase in the liver enzyme GGT in persons drinking from the contaminated reservoir only during the 
period of bloom and cell lysis compared to all others in the same area with different water supplies.  GGT 
has also been used as an effective marker for liver injury in experimental animal studies with microcystin 
exposure (Falconer 1994a, Chorus 1999). 
 A recent and infamous outbreak occurred in Brazil when over 100 patients on kidney dialysis developed 
visual disturbances, nausea and vomiting, followed by 50 deaths from acute liver failure.  Apparently the 
dialysis water was contaminated with blue green algal toxins; microcystins produced by cyanobacteria 
were subsequently identified in the water and in the human tissues, as well as inadequate water treatment 
procedures leading to the contamination (Jochimsen 1998). 
 Pilotto et al (1999) attempted to look at perinatal outcome and the possible relationship with 
cyanobacterial contamination of drinking water in an ecological study.  The investigators examined the 
perinatal outcome (prematurity, low birth weight and very low birth weight, and congenital defects 
detected at birth) for 32,700 singleton live newborns of non-Aboriginal mothers from 1992-94 in South 
Eastern Australia; exposure data was based on weekly cell counts from 29 drinking water storage sites for 
the 156 towns in the same area (percentage of time occurrence and average cell counts), and the mother's 
address at the time of the newborn's birth.  This work was based on the concern raised by laboratory 
animal studies showing impaired fetal development (especially neurologic) and low birth weight after 
exposure to untreated reservoir water sampled during a bloom, as well as fetal mortality, small fetuses, 
and congenital malformation with injection of microcystins into pregnant rats.  Although there were 
statistically significant associations with particular exposure levels and particular birth outcomes 
(especially the very low birth weight category and exposure during the first trimester with percentage of 
time occurrence, and congenital malformations with average cell counts), there was an overall lack of 
dose response; similar results were seen for the whole gestation and the last 12 weeks of gestation.  The 
authors concluded that their ecological study did not provide clear evidence for an association.  However, 
as they pointed out, there were no individual drinking water exposure data and in areas with frequent 
known cyanobacterial contamination, systematic avoidance of drinking water can be common. 
 Cancer 


 



 


Yu et al and others (1989a, 1989b, 1995, Junshi 1990, Chorus 1999) have studied the possible 
relationship between the consumption of surface drinking water (pond, ditch, river vs well water or deep 
well) and an increased risk for primary hepatic cancer (as well as chronic gastrointestinal diseases) in 
China.  China has an extremely high rate of primary liver cancer, previously associated with hepatitis B 
and aflatoxin exposures (Yu 1995).  However, reportedly large epidemiologic studies in 1973 and in 1983 
were performed in Haimen, Quidong and Nanhui Counties (Guangxi province, China) to evaluate 
drinking water source, exposure and risk of primary hepatic cancer.  These studies found not only a 
significantly increased risk of primary liver cancer in areas of high surface drinking water consumption 
(SIR=2.6) compared with areas of non-surface drinking water consumption (SIR=0.34), but also a strong 
dose response relationship.  Reportedly, changing from pond/ditch to deep well (at least 200 m) water in 
Quidong lead to a stabilization with subsequent decrease of the mortality rate from primary hepatic 
cancer, while in Haimen where there was no change, the liver cancer mortality rates continued to increase 
during the same time period; in an area where there was a mixture of well and river water, there was no 
significant change in the mortality rate during this time period.  Monitoring studies using a sensitive 
ELISA test from microcystins revealed high levels of microcystins, as well as the presence of blue green 
algae, in the surface as opposed to other drinking water sources (Ueno 1996).  On average the surface 
water sources contained 130 pg/ml of microcystins compared to the well samples (the vast majority less 
than 49 pg/ml) (Falconer 1996).   
 Ito et al (1997) was able to induce neoplastic nodular formation in mouse liver by repeated ip injections of 
sublethal dose (20 ug/kg) microcystin LR without the use of an initiator; however, repeated oral 
administration of a sublethal dose (80 ug/kg) did not result in nodular formation.  Ueno et al (1996) 
postulated that the combined effects of a potent hepatocarcinogen such as aflatoxin from the diet with 
intermittent microcystin intake through drinking water could explain the high rates of primary liver cancer 
associated with surface drinking water source in this area.  Yu  (1995) reported on the results of 
experiments with male F-344 rat exposed to different mixtures of alflatoxin, deep well water, and 
pond/ditch water after partial hepatectomy.  The results showed significant increase in the gamma-
glutamyl transferase (GGT) liver enzyme in rats exposed to alfatoxins and pond/ditch water compared to 
the other groups including control.  Yu  (1995) postulated that mycrocystins are promoters with a 
synergistic effect between microcystins and alflatoxins for primary hepatocellular carcinoma.  As a result 
of this work, the Chinese government has reportedly urged their people to use deep water wells or 
minimally granular activated carbon filtration for their drinking water, as well as other interventions (ie. 
hepatitis B vaccine and shifting to rice instead of corn to avoid aflatoxins), to prevent primary liver cancer 
in China. 
 Treatment 
 In general, the only treatment available for exposure to the blue green algal toxins is supportive medical 
treatment after complete removal from exposure (Chorus 1999).  If the exposure was oral, administration 
of activated carbon to decrease gut absorption may be efficacious if given within hours of exposure.  
Artificial respiration with exposure to the neurotoxins (such as saxitoxin) should also be considered 
(NHMRC 1994).  Based on past outbreaks, monitoring of volume, electrolytes, liver and kidney function 
should all be considered in the case of acute gastroenteritis associated with some of the blue green algal 
toxins. 
 Although no specific treatments exist for the cyanobacterial toxins, Nagata et al (1995) have created at 
least 6 monoclonal antibodies (Mabs) to microcystin LR isolated from Microcystis aeruginoas.  These 
MABs showed a protective effect on the hepatotoxicity and inhibition of protein phosphatase of 
microcystin LR in vitro and in vivo in a dose dependent manner.   
 




 



 


Of note, activated carbon given to experimental animals pre-treatment was not an effective antidote for 
preventing effects from subsequent microcystin administration  (Mereish 1989, Beasley 1989).  
Hermansky et al (1991) used a variety of chemoprotectants in pre treatment prior to exposure of 
experimental mice to a lethal dose of microcystin LR (100 ug/kg); phenobarbital (but not the calcium 
channel blockers or water soluble anti-oxidants) provided partial protection, while the hydrophobic anti-
oxidants (such as Vitamin E and silymarin), glutathione active compounds (such as glutathione), and 
immunosuppressive agents (such as rifampin and cyclosporin A) provided significant protection if given 
48 hours prior to exposure to microcystin in laboratory animals. 
 Prevention 
 Due to their significant potential toxicity and the lack of specific treatment modalities available, the best 
treatment for the health effects of the blue green algae is the prevention of exposure to the blue green 
algal toxins.  Therefore, monitoring for these toxins in surface drinking and recreational waters, as well as 
other exposure venues, is crucial in the prevention of human health effects from the blue green algal 
toxins (NHMRC 1994, Chorus 1999). For example, recent monitoring studies in Florida (SJRWMD 
2000) of recreational and surface drinking water supplies with algal blooms, have found 87/167 samples 
(75 individual water bodies) with significant levels of toxin producing blue green algae.  All of these 
samples had positive identification of blue green algal toxins with 80% lethal in mice.  Monitoring should 
include visual monitoring for blooms, cell counts and identification, and toxin identification and toxicity 
testing; other monitoring indices have also been used, including phosphorus levels in the water , as well 
as surveillance of health effects in human and animal populations (Chorus 1999). 
 Falconer (1994a) recommended 20,000 cells/ml sampled in the top meter of open water as the maximum 
safe level of cyanobacteria in recreational waters.  Nevertheless, Falconer warned that if the bloom is 
toxic, swallowing or bathing in these waters should be considered hazardous.  Chorus et al (1999) used 
data from Pilotto et al (1997) to derive a guideline for acute non cumulative health effects resulting in 
discomfort, not serious health outcomes.  Significantly increased odds ratios for eye irritation, rash and 
gastrointestinal symptoms were associated with water contact for more than 1 hour above 5000 
cyanobacterial cells/mL and for persons bathing in water with 5000-20,000 cells/mL.  Pilotto et al (1997) 
suggested that the current safety threshold for exposure of 20,000 cells per mL might be too high based 
on their results. 
 With monitoring programs, response programs must be established based on the results of regular 
monitoring.  Australia and the UK have attempted to develop such monitoring and response programs for 
surface drinking water sources (NHMRC 1994, Jones 1993, Burch 1993) with alert levels and 
corresponding responses based on the number of cyanobacterial cells per ml in routine sampling.  For 
example, Burch et al (1993) and Chorus et al (1999)  propose Alert Levels 1 (cells 500-2000 cells/mL or 
offensive odor or taste), Level 2 (potentially toxic cells 2000-15,000 cells/mL for 2-3 consecutive samples 
or confirmed toxic bloom, persistent odor/taste, and obvious bloom), and Level 3 (persistent high 
numbers widespread, toxic, cells >15,000 cell/mL for toxic species, persistent bloom, and only partial 
success of control measures).  Level 1 is associated with increased monitoring; Level 2 results in media 
information release and consultation with health authorities as well as control measures (such as booms, 
activated carbon); and Level 3 results in the same actions as Level 2 as well as possible declaration of 
water as unsafe for consumption and provision of safe drinking water alternatives after consultation with 
health authorities.  Subsequent health surveillance and evaluation may be necessary, especially if 
exposure is suspected.  Separate guidelines should be developed for recreational and occupational use of 
potentially contaminated surface waters based on the probability and severity of potential health effect 
development from exposure to cyanobacterial toxins (Bartram and Rees 1999, Chorus 1999).  In areas of 
endemic toxic blue algal blooms, public education and awareness plans should be considered (Chorus 




 



 


1999), including issues such as avoidance of occupational and recreational exposure, description of 
possible health effects, and warnings that boiling water will not destroy the cyanobacterial toxins. 
 In general, the information available is considered inadequate for the calculation of a tolerable daily 
intake (TDI) for the majority of the cyanobacterial toxins (Chorus 1999).   In particular, data are not 
available on metabolic disposition, acute and subacute toxicity, repeated administration, developmental 
effects, and carcinogenicity and genotoxicity.  In such cases, a TDI can be derived using the LOAEL or 
NOAEL divided by appropriate safety and uncertainty factors, as described in the Addendum to the 
World Health Organization Guidelines for Drinking Water Quality (WHO 1998).  A study by Fawell et al 
(1994, Chorus 1999) derived a NOAEL of 40 ug/kg body weight per day in a mice gavage study with a 
1000 fold uncertainty factor (intra-species, inter-species, limitations of database) resulting in a provisional 
TDI of 0.04 ug/kg body weight per day of microcystin LR.  Falconer (1994a, 1994b) used the following 
10 fold safety factors: use of subchronic data applied to lifetime risk, use of pig data applied to humans, 
use of intra-human variation, and tumor promotion risk; therefore he applied a 10,000 overall safety 
factor.  He used subchronic exposure data in pigs that showed a lowest observed effect level of 280 
ug/kg/day, and an assumption of 2 liters water intake per day by a 60 kg adult.  This led him to a 
provisional TDI of 0.067ug/kg body weight per day.  The WHO (1998) adopted a provisional guideline 
(TDI x body weight x proportion of total daily intake of the contaminant ingested from drinking water 
divided by the daily water intake in liters) for microcystin LR of 1.0 ug/L.   
 Special exposure circumstances (such as dialysis water) may necessitate even stricter control levels 
(Chorus 1999).  Use of potentially contaminated water for irrigation is controversial since not only can 
the irrigation aerosol cause potential harm through skin and respiratory contact, but there is limited 
evidence that terrestrial plants, including food crops, can take up microcystins (MacKintosh 1990, Chorus 
1999). 
 Barriers that reduce exposure to cyanobacterial blooms at "critical control points" are the first step in 
prevention, especially for surface drinking water sources (Chorus 1999).  Of note, algacides, especially 
copper sulfate, can be added to water supplies to control toxic blooms, but acutely this leads to cell lysis 
and substantial release of the toxins into the water, as well as the possibility of copper toxicity, thus 
exacerbating the potential for health effects (Chorus 1999, Carmichael 1993, Falconer 1999, NHMRC 
1994).  Therefore, removal of intact cells is recommended (Chorus 1999).  Activated carbon, chlorination 
and ozonation in conjunction with other water treatment practices have all been used in the treatment of 
drinking water supplies with potential blue green algal contamination (NHMRC 1994, Jones 1993, 
Chorus 1999).  The use of activated carbon treatment during active blooms will decrease but not 
necessarily eliminate levels of cyanobacterial toxins in drinking water (Chorus 1999; J Burns SJRWMD, 
FL, verbal communication).  This is of particular concern when the toxin is a potential carcinogen, since 
low level chronic exposure may predispose to the development of cancer (Chorus 1999, Carmichael 1993, 
NHMRC 1994).  Changing drinking water sources and technology to groundwater should be explored 
(Chorus 1999). 
 Finally, there is a possibility of exposure to these toxins through the consumption of contaminated food 
(Prepas 1997, Falconer 1992).  For example, based on examination and experimentation of the gut 
contents of mussels during a bloom of Microcystis in Australia, Falconer et al (1992) concluded that 
edible mussels should not be collected for human consumption during a toxic blue green algal bloom.   
 Cyanobacteria (particularly Spirulina) have been used as food and possible therapeutic agent in the US, 
Canada, Mexico, and India (NHMRC 1994, Chorus 1999).  Although most cyanobacteria species are non 
toxic, the etiology and conditions for toxicity are not well understood, nor have the health risks and 
benefits of long term consumption of cyanobacteria been studied.  Therefore, monitoring for toxicity in 
cyanobacteria used purposely for human consumption is recommended. 



 



 


 Summary 
 In summary, blue green algal are ubiquitous in surface waters throughout the year in subtropical climates 
such as Florida, and they are associated with frequent toxic blooms.  Both occupationally and 
recreationally humans can be exposed via dermal and aerosol routes, as well as through consumption of 
drinking water and possibly contaminated foods.  The human health effects associated with the blue green 
algal toxins are predominantly by inference from their known health effects in a wide variety of 
organisms, especially neurotoxicity, hepatotoxicity and tumor promotion.   
 Short term and long term health effects have not been thoroughly evaluated in persons with occupational, 
recreational and consumption exposure to blue green algae and their toxins (NHMRC 1994). Current 
drinking water treatment practices in the US do not regularly monitor, or necessarily remove these toxins 
from the drinking water since this would involve extremely expensive measures (J Burns, SFWMD, 
verbal communication, Falconer 1989, Volterra 1993, Falconer 1999, Heinze 1999).  Even with 
treatment, low level chronic exposure to the carcinogenic hepatotoxins are possible in persons consuming 
drinking water derived from surface water drinking plants in Florida and other parts of the US. 
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