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THE FACTS

Algae: Motor Neuron Disease

Like many aquatic systems, Tasmanian rivers and lakes have been impacted by a type of single-celled microalgae called blue-green algae (also known as Cyanobacteria, or more colloquially, pond scum). These algae have long been known to cause numerous health problems and have been correlated elsewhere with Motor Neurone Disease (MND; also called ALS or amyotrophic lateral sclerosis). Motor neurone disease is a progressive, terminal neurological disease that causes the muscles to weaken and waste away. Life expectancy from diagnosis to death is about 2 ½ years. This disease affects more than 2000 Australians and is increasing.

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In recent years, dense blooms of blue-green algae have been recorded downstream of inland salmon hatcheries, raising questions about potential health implications. Salmon hatcheries are placed throughout Tasmania's inland rivers, upstream of drinking water intakes. Any toxic substances in the water upstream of these intakes has the potential to be found in people's drinking water. There is growing concern that neurotoxins correlated with MND may be already present in our drinking water, or could be present in the future. Straight answers have been hard to come by. Here, we try to unpack this. 

One of the most pressing questions relating to blue-green algae -- and thus to salmon farming -- is about the relationship with Motor Neurone Disease. Motor Neurone Disease takes time to develop. Therefore, by the time a hotspot becomes known naturally, many people's fate is already sealed. This is just such an instance where it would be prudent to employ the Precautionary Principle. In years gone by, a potential health and safety hazard was basically considered safe until proven dangerous. Today, when uncertainty arises and there is a reasonable prospect of harm, the Precautionary Principle reverses the burden of proof to the individual or entity conducting the activity to prove that will not cause harm. In the present case, there is enough evidence to suggest that a serious problem could arise. 

 

To our knowledge, no cases of Motor Neurone Disease (MND) have yet been linked to salmon farming. However, also to our knowledge, this is not being tested nor monitored anywhere in the state, and it appears to be still entirely off the radar of the Tasmanian Government and TasWater at this point. To our knowledge, we are the first to raise this issue. 

What we know so far

LINK TO HATCHERY EFFLUENTS: Outside Tasmania, clusters of MND have been strongly correlated with consumption of or proximity to toxic blue-green algae. Blue-green algae occur naturally in most habitats, but bloom prolifically in areas with excess nutrients. Nutrients might sound like a good thing, but in this case they are not: it means raw sewage. Salmon hatcheries release *HUGE* amounts of untreated effluents from the fish. Research on water quality upstream and downstream of hatcheries has shown an alarming trend: water samples from downstream of hatcheries were very high in blue-green algae, while those from upstream were clean. Therefore, there is concern that nutrient-rich effluents from hatcheries may be stimulating blooms of blue-green algae. More research needs to be performed to better understand this relationship and its prevalence. 

 

Outside Tasmania, a strong correlation between blue-green algae and motor neurone disease has been known for decades. In Griffith (NSW), for example, the risk of motor neurone disease is seven times higher than our national average [1, 2], while near a lake in New Hampshire, the incidence of motor neurone disease is 10-25 times higher than the American average [3]. Many more cases have been published around the world, linking not only motor neurone disease, but also Parkinson’s, to:

  • consumption of seeds containing blue-green algae [4, 5],

  • consumption of seafood exposed to blue-green algae [6, 7],

  • inhalation by proximity to lakes and rivers with algal blooms [8],

  • watersports on contaminated water bodies [9], 

  • seaside communities with algal blooms [6]

  • people have become unwell from drinking water contaminated with blue-green algae [10, 11],

  • the neurotoxin has been found in crops irrigated with contaminated water [12],

  • even livestock are affected, suffering an agonizing death by poisoning from drinking water contaminated by blue-green algae [13], and blue-green algae cause mass fish deaths by suffocation, such as occurred in 2019 in the Murray-Darling [14]

 

NEUROTOXIN: Cyanobacteria give off a neurotoxin called β-methylamino-l-alanine (more conveniently shortened to BMAA)[15-17]. BMAA has been experimentally used in laboratory animals to induce symptoms such as neuro-plaques and tangles in the brain[18], which are consistent with MND; however, for obvious ethical reasons, these experiments cannot be replicated on humans. 

 

DRINKING WATER SOURCE: Hobart's water supply comes from the Derwent River. At least nine salmon hatcheries are located in rivers and lakes that feed into the Derwent. All the raw sewage, all the blue-green algae, all the antibiotics, all the pesticides, all of everything discharged from the hatcheries or stimulated by the discharge is upstream of our drinking water supply. Blue-green algae are already causing taste and odour problems upstream of the Bryn Estyn water supply for Hobart [19], requiring filtration in the summer. These places supply drinking water, people fish and play there, and they’re used for crop irrigation.

 

CLIMATE CHANGE EFFECT: Blue-green algae require two things for dense blooms to develop and persist: warm weather and a rich nutrient supply. All indications are that blue-green algae will only become worse as our climate warms [20, 21]. Given that the salmon farming industry is projected to double by 2030, an increase in nutrient load can be anticipated to exacerbate this effect. 

 

What we don't know yet

NEUROTOXINS IN TASMANIA:  There is no information available on whether blue-green algae in Tasmania are releasing BMAA into the water and air. To our knowledge, this has not yet been tested. However, 95% of blue-green algae genera tested produce BMAA [22], and Tasmania's commonest species fall within these groups, so the potential threat cannot be denied. 

 

NEUROTOXINS IN DRINKING WATER: We also do not yet know whether BMAA is actually in our drinking water. BMAA can be difficult to filter out, and at this point we have been unable to get straight answers on whether the water is being tested for BMAA or whether the types of filtration are effective against BMAA. Of course, not all users of water are downstream of the Bryn Estyn Water Treatment Plant, so not all users would have access to equal filtration. Smaller towns may draw water from upstream, and of course other regions draw from other rivers, some of which also have salmon hatcheries. 

 

CAUSE: Not everybody exposed to blue-green algae develops MND, and nobody knows why. Part of the difficulty of studying it is that it is slow to develop, and then quick to kill. A smoking-gun causal link between blue-green algae and MND has yet to be found. 

What we should be asking

​​

It is astonishing that this day and age, there isn't more publicly available information on blue-green algal blooms in Tasmania. Your motor neurones may one day thank you if you ask questions such as:
 

  • What routine monitoring is done on Tasmanian drinking water supplies for cyanobacteria? Does this include BMAA? What were the results?

  • What risk assessment, monitoring and preventative actions have been taken to manage this issue at a catchment scale?

  • How effective are Tasmania's water treatment plants at detecting and removing cyanobacterial compounds (e.g. taste and odour, BMAA and other toxins), and how will recently upgraded plants perform?

What we should be asking

Taste and odour problems due to blue-green algae occurred in Hobart's drinking water in 2015, requiring expensive upgrading of the water filtration system [23]. The compounds causing taste and odour problems are not generally harmful to humans, but they signal overproduction of blue-green algae, and thus the potential for other more harmful compounds to be released. In addition to BMAA, numerous other toxins (called cyanotoxins) are produced by blue-green algae, ranging in effect from neurotoxicity to liver toxicity to interfering with protein synthesis [24]. Blue-green algal blooms are a visible indicator that something is out of balance in the ecosystem, and they are a screaming loud indicator that a risk to human health may be present. We ignore it at our peril. 

References

[1] Main, B. Toxin linked to motor neuron disease found in Australian algal blooms, <http://theconversation.com/toxin-linked-to-motor-neuron-disease-found-in-australianalgal-blooms-95646> (2018). 

[2] Main, B. J., Bowling, L. C. et al. Detection of the suspected neurotoxin β-methylamino-lalanine (BMAA) in cyanobacterial blooms from multiple water bodies in Eastern Australia. Harmful Algae 74, 10-18, doi:10.1016/j.hal.2018.03.004 (2018).

[3] Caller, T. A., Doolin, J. W. et al. A cluster of amyotrophic lateral sclerosis in New Hampshire: A possible role for toxic cyanobacteria blooms. Amyotrophic Lateral Sclerosis 10, 101-108, doi:10.3109/17482960903278485 (2009).

[4] Cox, P. A. & Sacks, O. W. Cycad neurotoxins, consumption of flying foxes, and ALS-PDC disease in Guam. Neurology 58, 956–959 (2002).

[5] Dunlop, R. Toxic load: blue-green algae’s role in motor neuron disease, <https://theconversation.com/toxic-load-blue-green-algaes-role-in-motor-neuron-disease-16041> (2013).

[6] Masseret, E., Banack, S. et al. Dietary BMAA Exposure in an Amyotrophic Lateral Sclerosis Cluster from Southern France. PLoS ONE 8, e83406, doi:10.1371/journal.pone.0083406 (2013).

[7] Banack, S. A., Metcalf, J. S. et al. Detection of cyanobacterial neurotoxin β-N-methylamino-lalanine within shellfish in the diet of an ALS patient in Florida. Toxicon 90, 167-173, doi:10.1016/j.toxicon.2014.07.018 (2014).

[8] Torbick, N., Hession, S. et al. Mapping amyotrophic lateral sclerosis lake risk factors across northern New England. International Journal of Health Geographics 13, 1-14, doi:10.1186/1476-072X-13-1 (2014).

[9] Andrew, A. S., Caller, T. A. et al. Environmental and occupational exposures and amyotrophic lateral sclerosis (ALS) in New England. Neurodegenerative Diseases 17, 110–116, doi:10.1159/000453359 (2017).

[10] Byth, S. Palm Island mystery disease. Medical Journal of Australia 2, 40-42 (1980).

[11] Griffiths, D. J. & Saker, M. L. The Palm Island mystery disease 20 years on: A review of research on the cyanotoxin cylindrospermopsin. Environmental Toxicology 18, 78-93, doi:10.1002/tox.10103 (2003).

[12] Contardo-Jara, V., Schwanemann, T. et al. Uptake of a cyanotoxin, β-N-methylamino-Lalanine, by wheat (Triticum aestivum). Ecotoxicology and Environmental Safety 104, 127-131, doi:10.1016/j.ecoenv.2014.01.039 (2014).

[13] Anonymous. Blue-green algal poisoning of stock, <http://agriculture.vic.gov.au/agriculture/pests-diseases-and-weeds/animal-diseases/beefand-dairy-cows/blue-green-algal-poisoning-of-stock> (2017).

[14] Ogilvie, F. Scientists are on the hunt to discover the culprit behind the Murray-Darling fish deaths, <https://mobile.abc.net.au/news/science/2019-01-16/what-caused-menindee-fishkill-drought-water-mismanagement/10716080> (2019).

[15] Brand, L. E., Pablo, J. et al. Cyanobacterial blooms and the occurrence of the neurotoxin, beta-N-methylamino-L-alanine (BMAA), in South Florida aquatic food webs. Harmful Algae 9, 620–635, doi:10.1016/j.hal.2010.05.002 (2010).

[16] Jonasson, S., Eriksson, J. et al. Transfer of a cyanobacterial neurotoxin within a temperate aquatic ecosystem suggests pathways for human exposure. Proceedings of the National Academy of Sciences USA 107, 9252-9257 (2010).

[17] Chiu, A. S., Gehringer, M. M. et al. Review Does α-Amino-β-methylaminopropionic Acid (BMAA) Play a Role in Neurodegeneration? International Journal of Environmental Research and Public Health 8, 3728-3746, doi:10.3390/ijerph8093728 (2011).

[18] Cox, P. A., Davis, D. A. et al. Dietary exposure to an environmental toxin triggers neurofibrillary tangles and amyloid deposits in the brain. Proceedings of the Royal Society B 283, 20152397, doi:10.1098/rspb.2015.2397 (2016).

[19] Proemse, B., Whitehead, J. et al. River Derwent & Catchment Tributary Water Quality Report. 57 pp (Derwent Estuary Program, Hobart, 2018).

[20] Hofer, U. Climate change boosts cyanobacteria. Nature Reviews Microbiology 16, 122, doi:10.1038/nrmicro.2018.15 (2018).

[21] Ullah, H., Nagelkerken, I. et al. Climate change could drive marine food web collapse through altered trophic flows and cyanobacterial proliferation. PLOS Biology 16, art. e2003446, doi:10.1371/journal.pbio.2003446 (2018). 

[22] Cox, P. A., Banack, S. A. et al. Diverse taxa of cyanobacteria produce β-N-methylamino-lalanine, a neurotoxic amino acid. Proceedings of the National Academy of Sciences USA 102, 5074–5078, doi:10.1073/pnas.0501526102 (2005).

[23] TasWater. 2015. Greater Hobart - Feb 2015. TasWater, https://www.taswater.com.au/Community---Environment/Current-Alerts/Taste/odour-updates/Greater-Hobart---Feb-2015.
 

[24] Corbel S, Mougin C, Bouaïcha N. 2014. Cyanobacterial toxins: Modes of actions, fate in aquatic and soil ecosystems, phytotoxicity and bioaccumulation in agricultural crops. Chemosphere 96:1-15.

Related Article

 

They All Got Mysterious Brain Diseases. They’re Fighting to Learn Why. New York Times, August 2024.

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