Harmful Algal Blooms (HABs) are on the increase globally. HABs occur when large masses of potentially toxic algae develop in freshwater or marine environments. Typically these blooms are fuelled by increasing human pollution of our water resources, most commonly inadequately-treated wastewater, leading to high concentrations of plant nutrients in our dams and rivers. A large percentage of South Africa’s water resources are already impaired by the sustained presence of blue-green algae.
Blue-green algae produce a large variety of toxins, singularly or in combination. Recently it has become apparent that all types of blue-green algae produce an unusual neurotoxin, called beta-methyl-amino-alanine, BMAA. BMAA in nature is only produced by blue-green algae (cyanobacteria). BMAA is neurotoxic and destroys nerve neurons (e.g. Vyas and Weiss 2009).
Research during the past 40 years has sought to link BMAA with motor neuron disease (Amyotrophic Lateral Sclerosis, ALS, Lou Gehrig’s Disease) and Parkinsons Disease (the so-called ALS-PDC, ALS/Parkinson’s Disease Dementia Complex). This research has focussed on three locations in the western Pacific where considerably higher than normal incidences of these diseases occur (e.g. Bradley and Cox 2009). BMAA has been measured in the brains of ALS-PDC cases, but not in control brain tissue, in the aforementioned clusters, as well as in Canada and elsewhere (e.g. Banack et al. 2009). The effect of BMAA in Parkinson’s symptoms has been confirmed by dosing rats with the toxin (Bradley and Mash 2009).
The disease is progressive, debilitating and fatal within 1-5 years, typically 3, following diagnosis. The findings to-date support the hypothesis that BMAA may contribute to selective MN loss in ALS/PDC (e.g. Rao et al. 2006). Various factors have been implicated as a cause for Alzheimers, e.g. bone fractures, exercise, agricultural work and exposure to animal skins) and BMAA is one more in this list. For my money it has more credibility than the others do.
In addition to the cluster areas, an increased incidence of ALS-PDC has been reported in a lakeside community in Enfield (USA) and a similar high reporting level of the disease amongst soldiers from the Gulf War may have been linked to inhaling dust containing cyanobacterial material (Cox et al. 2009). An as-yet unexplained six-fold increase in ALS in Italian soccer players has also been reported (Chio et al. 2008).
When I returned from a CYANONET meeting held in Scotland at the end of 2004, I brought back the early news of the likely ubiquitous production of BMAA by many species of cyanobacteria. I was able to source funds for researchers at NMMU (Port Elizabeth) to immediately screen for BMAA – and in due course they confirmed it present across the country and in all types of cyanobacteria tested. Similar findings have been reported from several countries (e.g. Metcalf et al, 2008).
Confirmation of a cause and effect pathway between exposure to BMAA is still lacking. However, the evidence to hand is of such an overwhelming nature that it would be irresponsible to ignore it. The implications are that exposure to BMAA through recreation in dams where cyanobacteria are present, via the contamination of leaf crops or possibly via milk and meat products, could result in susceptible individuals contracting ALS-PDC. BMAA and other toxins have also been reported in algal supplements (Dietrich et al. 2008). Both freshwater and marine cyanobacteria produce BMAA (e.g. Banack et al. 2007).
Blue-green algal blooms are common in South Africa. They occur in many of our drinking water supplies and in thousands of farm dams. Readers of this blog will have identified that a near-total lack of management to reduce eutrophication and offset noxious algal blooms exists in our water supplies. Calls for reduction in the wastewater-derived loads of nutrients, fuelling the algal blooms, go unheeded. Although seven years have passed since I announced the alert, no specific action on BMAA has been taken other than the screening study.
BMAA has been shown to occur in combination with other cyanobacterial toxins and is toxic to aquatic organisms (zebra fish, brine shrimp and protozoans) at environmentally-relevant levels (i.e. the levels naturally occurring in cyanobacterial blooms). Fruitflies fed with BMAA demonstrated a reduced lifespan and impaired neurological function (Zhou et al. 2009). The toxin has been implicated in Avian Vacuolar Myelinopathy (AVM) – affecting a wide range of waterfowl and other bird species (Bidigare et al. 2009). So, while the link to humans remains to be proven, there is clearly ecotoxicological significance (Metcalf and Codd 2009). The relevance in arid areas or where water supplies are scarce, is particularly relevant (think about all those algal-dominated waterholes in the national parks!). BMAA exposure has been linked to a Chinese soup made from cyanobacteria (Roney et al. 2009).
In summary, we know the following about BMAA:
- all cyanobacterial species produce it (both freshwater and marine types);
- exposure is likely to be ubiquitous;
- BMAA can be inserted into proteins – resulting in malformed proteins and RNA transcription;
- it is magnified in foodwebs;
- it is neurotoxic to motor neurons (at much lower concentrations than previously measured);
- individuals vary in their vulnerability to exposure (exposure is likely to be of a chronic nature);
- BMAA has been found in the brain tissue of affected persons, but not in control tissue.
We don’t know how well various water treatment processes remove BMAA, what the risks are via crops or whether BMAA can cross the blood/milk barrier in cows. No epidemiological studies have been done, e.g. at Brits or Schoemansville (Hartbeespoort Dam).
The possible risk is too serious to ignore!