The Monster We Help Create: The Algal Neurotoxin Getting a Helping Hand From Pollution

In 1998, 81 sea lions would find themselves stranded along the California coastline, exhibiting neurological symptoms. (Gulland et al., 2002; Ramsdell & Zabka, 2008). Confused and unable to continue their journey, they would receive treatment, but 55 of those sea lions would ultimately not survive. Over on land, just over a decade earlier, more than 100 people had fallen ill after ingesting contaminated mussels, and three of those individuals subsequently died of acute poisoning. (Mos, 2000). The microscopic thread tying these events together can be found riding the ocean’s currents, just under the water’s surface. The phytoplankton Pseudo-nitzschia, a unicellular form of algae, is capable of producing the neurotoxin domoic acid, an amino acid with the potential to generate an array of gastrological and neurological symptoms, ranging from vomiting and confusion, to seizures and memory loss, and in extreme cases, even permanent brain damage and death. (McKibben et al., 2016; Mos, 2000).

In this ecological chain reaction, a mere by-product of a microscopic phytoplankton spells trouble for marine mammals many orders of magnitude larger than itself. This by-product, domoic acid, even makes the jump out of water to affect humans. (Mos, 2000). Domoic acid finds itself incorporated into the food chain, when, along with its algal-progenitor, it is swept up by the shellfish who consume these plankton. (Mos, 2000). While many of these shellfish possess bacteria capable of metabolizing domoic acid, the marine mammals who feast upon shellfish do not, making them susceptible to the accumulation of domoic acid residing in the tissues of shellfish. (Mos, 2000). Both the 1987 outbreak in seafood consumers from Prince Edward Island and the 1998 mass mortality event in sea lions – as described above – are the result of acute domoic acid poisoning, which resulted from the consumption of shellfish by those higher on the food chain. (Gulland et al., 2002; Mos, 2000).

This neuroexcitatory toxin, once ingested by a susceptible host, travels to the brain, where it binds to the NMDA channel receptor protein, releasing the neurotransmitter glutamate. (Ramsdell & Zabka, 2008). The toxin passes with ease through the placental wall and accumulates in the amniotic fluid, where it is readily able to reach both the fetus’ and mother’s brains, positioning itself as a distinct threat to both. (Ramsdell & Zabka, 2008). While domoic acid traditionally doesn’t pose a significant threat to adult sea lions and other marine mammals, studies have indicated that prenatal and juvenile exposure can lead to hippocampal abnormalities and increased susceptibility to seizure activity, also leading those mammals exposed early in life to find themselves in heightened danger from the toxin at all stages of life. (Ramsdell & Zabka, 2008; Mos, 2000).

Over the last few years, domoic acid poisoning has become a more common threat to the marine mammals who ingest these shellfish, with large scale events like clusters of stranded marine mammals as a result of neurological symptoms, as well as mass mortalities both becoming more common. This increased prevalence and severity thus suggests external factors increasing prevalence. (Ramsdell & Zabka, 2008; Mos, 2000; Gulland et al., 2002). As it turns out, the increased prevalence of domoic acid poisoning may very well be another lasting legacy of human actions leaving scars on the earth and our ecosystem.

Our warming earth means warming waters, and the lasting impact of our carbon emissions appear to be at least partially responsible for the proliferation of harmful algal blooms, which have the ability to produce neurotoxins like domoic acid. (McKibben et al., 2016). Researchers have shown that with warmer temperatures, blooms of Pseudo-nitzschia have not only thrived, but seemingly demonstrated more toxic effects, meaning that these algal blooms in the ocean are an outgrowth of human activity back on land. (McKibben et al., 2016).

Yet, another cruel remnant of human activity would also find its way into the ocean to exacerbate the situation. The chemical catastrophe of organochlorines, more popularly known as “persistent organic pollutants” (Jones & de Voogt, 1999) or colloquially as “forever chemicals,” represent a hallmark of material comfort – except that now marine life are paying the price for our capitalist creature comforts.

I grew up during the Scotchgard craze, a time where you could go into just about any affluent suburban home and marvel at the carpets and fabrics that stayed clean almost by magic. Staring in wonderment at how liquids would simply bead atop the chemically-protected surfaces, not daring to bore through the mystical barrier was almost a rite of passage, but we did not realize then that this magic trick was the result of a chemical compound almost impossible to break down. (Jones & de Voogt, 1999). Nowadays, the specter of Scotchgard, just like the Teflon that coats our non-stick pans, or the pesticides we spray into the air, lurk through our oceans. The harmful effects of these organochlorines seem to be playing a significant role in the increased prevalence of domoic acid poisoning. (Tiedeken & Ramsdell, 2009; Ramsdell & Zabka, 2008; Ramsdell, 2010; Tanabe, 2002).

In recent years, the discovery of a chronic domoic acid poisoning syndrome, particularly in young California sea lions, has provoked curiosity into the concurrent factors creating enhanced susceptibility in these mammals. (Tiedeken & Ramsdell, 2009). Characterized by enhanced seizure susceptibility and behavioral abnormalities, researchers noted that in addition to this perplexing syndrome, California sea lions were carrying with them an exceptional burden of organochlorines. (Tiedeken & Ramsdell, 2009; Ramsdell & Zabka, 2008; Tanabe, 2002). This discovery led to experiments in zebrafish, which found that embryonic exposure to the pesticidal organochlorines DDT and DDE resulted in increased susceptibility to seizure-inducing toxins, like domoic acid, later in life. (Tiedeken & Ramsdell, 2009). The exact mechanism by which organochlorine-exposed animals find themselves at heightened risk from domoic acid is not completely certain, however there are some strong theories on the matter. This increased risk may be a result of environmental factors like chemical pollution and climate change being stressors that disrupt homeostasis, or due to the fact that organochlorines are known to be endocrine-blockers – and in some cases even present neurological disturbances of their own. (Tiedeken & Ramsdell, 2009; Tanabe, 2002; Jenssen, 2006; Jones & de Voogt, 1999). While these organochlorines, earning themselves the nickname “forever chemicals” for good reason, may be declining in production and usage recently, the damage they cause is far from being mitigated due to their chemical structure, which is characterized by uniquely strong chemical bonds paired with a stable molecule, which makes them nearly impossible to break down, and a ubiquitous threat across the planet. (Jones & de Voogt, 1999).

Much like the legal framework that largely protects these “forever chemicals” from facing restrictive legislation in the US, there is reason to believe that the fishing of domoic acid-contaminated shellfish might not be sufficiently regulated. A study found that chronic low-level exposure to domoic acid, significantly below the legal limits which had been based solely off of acute poisoning, caused cognitive deficits in rats. (Lefebvre et al., 2017). Legal frameworks in the US more often than not place an expectation that a substance be proven unequivocally hazardous before facing restrictive legislation, allowing “persistent organic pollutants” to fester freely in our ecosystem. The increased severity and prevalence of domoic acid poisoning, along with the chemical pollutants and climate change effects thought to drive it, are the ghosts of human negligence and consumption – but marine life, just like us, are forced to face the haunting.

References

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[2] Jenssen, Bjorn Munro. (2006) Endocrine-Disrupting Chemicals and Climate Change: A Worst-Case Combination for Arctic Marine Mammals and Seabirds? Environmental Health Perspectives, Vol. 114, No. 1. https://doi.org/10.1289/ehp.8057

[3] Jones, K. C. and P. de Voogt. (1999) Persistent organic pollutants (POPs): state of the science. Environmental Pollution, Vol. 100, Iss. 1-3. https://doi.org/10.1016/S0269-7491(99)00098-6

[4] Lefebvre, Kathi A., et al. (2017) Chronic low-level exposure to the common seafood toxin domoic acid causes cognitive deficits in mice. Harmful Algae, Vol. 64, pp. 20-29. https://doi.org/10.1016/j.hal.2017.03.003

[5] McKibben, S. Morgaine, et al. (2017) Climatic Regulation of the Neurotoxin Domoic Acid. PNAS, Vol. 114, Iss. 2. https://doi.org/10.1073/pnas.1606798114

[6] Mos, Lizzy. (2001) Domoic acid: a fascinating marine toxin. Environmental Toxicology and Pharmacology, Vol. 9, Iss. 3. https://doi.org/10.1016/S1382-6689(00)00065-X

[7] Ramsdell, John S. (2010) Neurological disease rises from ocean to bring model for human epilepsy to life. Toxins, Vol. 2, Iss. 7. https://doi.org/10.3390/toxins2071646

[8] Ramsdell, John S. and Tanja S. Zabka. (2008) In Utero Domoic Acid Toxicity: A Fetal Basis to Adult Disease in the California Sea Lion (Zalophus californianus). Marine Drugs, Vol. 6, No. 2. https://doi.org/10.3390/md6020262

[9] Tanabe, Shinsuke. (2002) Contamination and toxic effects of persistent endocrine disrupters in marine mammals and birds. Marine Pollution Bulletin, Vol. 45. https://doi.org/10.1016/S0025-326X(02)00175-3

[10] Tiedeken, Jessica A. and John S. Ramsdell. (2009) DDT Exposure of Zebrafish Embryos Enhances Seizure Susceptibility: Relationship to Fetal p,p′-DDE Burden and Domoic Acid Exposure of California Sea Lions. Environmental Health Perspectives, Vol. 117, No. 1. https://doi.org/10.1289/ehp.11685