Coastal Harmful Algal Blooms and Climate Change – Toxic Challenges for Emergency Medicine

I had never heard of red tides until moving to California for residency training.

The first encounter I had with red tides evoked a moment of complete awe. I was certain I was witnessing a once-in-a-lifetime show of nature. With each crashing wave, a shock of light would travel through the water, brightening the night like a lightning bolt. It was magical, to say the least, but little did I know the evil nature hiding beneath these infamous coastal red tides. Allow me to explain.

Red tides are created by a rapid growth and accumulation of marine plankton. These organisms are photosynthetic, and some possess the remarkable ability of producing bioluminescence, which explains the amazing phenomenon I witnessed that summer night in San Diego. These marine planktons are incredibly important for atmospheric carbon dioxide absorption and are the foundation of marine food chains. However, some species can also produce toxins that can cause significant harm to the health of coastal communities. These are called Harmful Algal Blooms (HABs).¹ HABs also occur in freshwater sources, such as the Great Lakes, with cyanobacteria that produce a liver toxin. The focus of this piece will be coastal marine HABs.

Climate change is altering aquatic ecosystems. As surface temperatures increase and oceans acidify, HABs become more prevalent. The 2021 Intergovernmental Panel on Climate Change's (IPCC) report, which is an aggregation of the leading climate science,  concluded that HABs and their harmful health effects to coastal communities are directly linked to climate change.

According to the IPCC, “Since the early 1980s, the occurrence of harmful algal blooms (HABs) and pathogenic organisms (eg, Vibrio) has increased in coastal areas in response to warming, deoxygenation and eutrophication, with negative impacts on food provisioning, tourism, the economy and human health (high confidence).”²

For clinicians, the science translates to bedside care and diagnoses. Given the unavailability of rapid assays, the diagnosis and management of poisoning from HABs is largely based on the emergency medicine clinician’s ability to interpret symptoms and exposure history. Failure to consider HABs poisoning in the right clinical context can have a significant impact on outcomes, given their association with adverse chronic health effects and potential lethality.³ As we continue to adapt to the detrimental health effect of climate change, it is our responsibility to continue to educate ourselves on the environmental health threats to the communities we serve. In this context, we will summarize the marine toxins presenting more frequently (as outlined in Goldfrank’s Toxicologic Emergencies).⁴

Saxitoxin (Paralytic Shellfish Poisoning)
Saxitoxin is a neurotoxin that acts by blocking voltage-sensitive sodium channels and can cause rapid development of symptoms within 30 minutes of ingestion. Severity of symptoms typically correlates with higher numbers of contaminated shellfish consumed. Symptoms are mostly neurologic and include perioral paresthesia, headaches, numbness, cerebellar dysfunction, cranial nerve dysfunction, muscle weakness, and ultimately respiratory failure may occur. Various assays for saxitoxin exist, but are generally not readily available; thus, diagnosis is largely based on history and clinical presentation. Mortality due to respiratory failure has recently been reported to be as high as 15% depending on availability of emergency care⁵ and typically occurs within the first 12 hours; however, with the appropriate supportive management, symptoms tend to resolve within a few days.

Brevetoxin (Neurotoxic Shellfish Poisoning)
Brevetoxin is a heat-stable toxin that induces symptoms by stimulating sodium channels of nerves and muscles. Symptoms typically develop within 3 hours of ingestion. Classically, patients present with gastrointestinal symptoms and neurologic symptoms such as headaches, myalgias, tremors, ataxia, dizziness, and dysphagia. Patients have also reported temperature-related dysesthesias, which is the reversal of hot and cold perception. Unlike saxitoxin, brevetoxin does not cause paralysis. Interestingly, if present at high concentrations during red tides, brevetoxin can be inhaled and cause respiratory irritation and bronchospasm. As with saxitoxin, various assays that identify brevetoxin exist; however, given their unavailability, diagnosis is based on history and treatment is supportive. In patients with respiratory symptoms, bronchodilators can be used. No deaths have been reported and most patients recover within 72 hours.

Domoic Acid (Amnesic Shellfish Poisoning)
Domoic acid is structurally similar to glutamate. It causes neuronal excitation which can lead to cellular death in the amygdala and hippocampus (hence the name amnestic). Symptoms typically develop at 5 hours after ingestion, but have been reported up to 38 hours after ingestion. GI symptoms such as nausea, vomiting, diarrhea, and abdominal cramps can occur. Neurologic symptoms include headaches, disorientation, chewing, grimacing, ophthalmoplegia, and in severe cases, anterograde memory loss, seizures, coma, and death. Cardiac and hemodynamic instability may occur. Treatment is largely supportive. While some deaths have been reported, mortality is less than 2% and typically occurs in older adults. Long-term memory deficits and neuropathies have been reported in up to 10% of patients.

Okadaic Acid (Diarrhetic Shellfish Poisoning)
There are several types of toxins that cause diarrhetic shellfish poisoning; however, okadaic acid is the most well-known. It acts by inhibiting phosphatase 1A and 2A, which causes localized gastrointestinal symptoms such as vomiting, diarrhea, and abdominal cramps. Treatment is supportive and symptoms resolve within 3 days. Interestingly, these toxins have been shown to be tumor-promoting and may have an association with some gastrointestinal malignancies.⁶

Ciguatera Toxin (Ciguatera Fish Poisoning)
Ciguatera toxin is a heat-stable, acid-stable, odorless, and tasteless toxin that acts by depolarizing voltage-dependent sodium channels and causing membrane depolarization. Illness typically develops after ingestions of a contaminated tropical reef fish, such as red snapper, barracuda, parrotfish, among others. Symptoms usually develop within 2-6 hours of ingestion of toxin, but can occur up to 72 hours after exposure.

Patients with ciguatera fish poisoning can present with a constellation of symptoms which typically involve the gastrointestinal, neurologic, and cardiovascular systems. Myalgias and arthralgias are commonly reported. GI symptoms usually include nausea, vomiting, diarrhea, and abdominal cramps. Neurologic symptoms can be substantial. These have been described as perioral paresthesia, metallic taste, blurry vision, sensation of loose or painful teeth, pruritus, temperature-related dysesthesias, peripheral paresthesias, and ataxia or other cerebellar dysfunction. Cardiovascular involvement may include bradycardia, heart-blocks, and hypotension. Life-threatening symptoms such as coma and respiratory distress are rare but have been reported. GI symptoms typically resolve in 1-2 days, but cardiovascular and neurological symptoms can persist for days to weeks.

The FDA is capable of testing fish for ciguatera toxin, but this is not readily available to clinicians. Given the difficulty accessing laboratory testing, diagnosis is largely based on history and clinical features. Vomiting and diarrhea tend to accelerate the elimination of toxins, therefore activated charcoal can be considered in patients that do not have vomiting. Mannitol has been reported to improve neurologic symptoms yet a clear benefit has not been proven and caution should be used in patients with hypotension. Associations have been documented between ciguatera fish poisoning and climate variability.⁷

Conclusion
In summary, climate change is altering the distribution and seasonality of coastal HABs via complex processes.⁸ These single-celled organisms produce toxins, which are ingested by other marine organisms and can subsequently be ingested by humans. At high enough concentrations, even walking or swimming in contaminated waters can cause illness. Most toxins produce a combination of gastrointestinal and neurologic symptoms. Since the diagnosis is primarily based on exposure history, a high index of suspicion is needed. Given the unavailability of antidotes, treatment is largely supportive. Preventing and minimizing exposure is therefore one of our most important tools.

We depend on better research and public health interventions to reduce morbidity and mortality, which in turn depends on our diligence in reporting suspected cases to the Centers for Disease Control and Prevention.⁹ Additionally, recognizing and addressing climate change as a public health issue will reduce future warming and health harms in our communities.

More on Climate Health
Tune in to our EMRA*Cast episode with Dr. Rublee to hear more about climate health, emergency medicine, and health policy. Listen online or on your favorite podcast platform.

References

1. Algal Blooms, National Institute of Environmental Health Sciences, Sept. 2021, www.niehs.nih.gov/health/topics/agents/algal-blooms/index.cfm.
2. IPCC, 2021: Climate Change 2021: The Physical Science Basis. Contribution of Working Group I to the Sixth Assessment Report of the Intergovernmental Panel on Climate Change [Masson-Delmotte, V., P. Zhai, A. Pirani, S.L. Connors, C. Péan, S. Berger, N. Caud, Y. Chen, L. Goldfarb, M.I. Gomis, M. Huang, K. Leitzell, E. Lonnoy, J.B.R. Matthews, T.K. Maycock, T. Waterfield, O. Yelekçi, R. Yu, and B. Zhou (eds.)]. Cambridge University Press. In Press.
3. Young N, Sharpe RA, Barciela R, Nichols G, Davidson K, Berdalet E, Fleming LE. Marine harmful algal blooms and human health: A systematic scoping review. Harmful Algae. 2020; Volume 98:101901. doi: 10.1016/j.hal.2020.101901
4. Fil LJ, Tunik MG. "Food Poisoning." Goldfrank’s Toxicologic Emergencies, Nelson SL et al., McGraw Hill, 2018, Chapter 39.
5. Faber S. Saxitoxin and the Induction of Paralytic Shellfish Poisoning. J Young Investig. 2012;23(1):1-7.
6. Hambright K., Zamor R., Easton J., Allison B. Algae. In: Encyclopedia of Toxicology. Third Edition. Elsevier Inc; 2014:130-141. doi:10.1016/B978-0-12-386454-3.00983
7. Gingold DB, Strickland MJ, Hess JJ. Ciguatera fish poisoning and climate change: Analysis of national poison center data in the United States, 2001-2011. Environmental health perspectives. 2014;122(6):580-586. doi:10.1289/ehp.1307196
8. Hinder SL, Hays GC, Edwards M, Roberts EC, Walne AW, Gravenor MB. Changes in marine dinoflagellate and diatom abundance under climate change. Nature climate change. 2012;2(4):271-275. doi:10.1038/nclimate1388
9. One Health Harmful Algal Bloom System, Centers for Disease Control and Prevention, www.cdc.gov/habs/using-ohhabs.html