Some of the first signs of the 2025 harmful algal bloom were reports of surfers complaining of sore or irritated eyes, nose and throat after surfing in water that had or was near areas of thick discoloured foam around the southern beaches of the Fleurieu Peninsula. Indeed, I experienced those symptoms after a windsurfing session in large waves in Encounter Bay, Victor Harbor, in mid-March. Since then, surfers, swimmers and divers have reported comparable symptoms to varying degrees after being in the water at most places where the bloom is present. In addition, many people have reported similar symptoms, simply by being on or near a beach affected by the bloom.
These observations indicate that are two main ways that people can come into contact with harmful components of the bloom: direct contact with bloom-affected water, such as during swimming or surfing; or contact with air-borne agents carried in aerosols from bloom-affected water, typically while walking along or near an affected beach..
All of the surfaces of the body are lined with epithelium. The epithelium of the skin (epidermis) is toughened and made water-resistant by a complex suite of proteins, most notably keratin. However, the epithelium layers lining the eyelids, nasal cavity, mouth and airways are much more delicate. They lack the keratin, and contain a variety of different cell types with specific functions, including cells that produce mucus, comparable to those in the gills of fish. These epithelial surfaces are the first points of contact with any of the various components of the algal bloom.
Contact with water – cytotoxicity
The epithelial cells of the eyelids, nose and throat would be expected to be susceptible to the cytotoxic actions of Karenia species in a similar way to those in fish gills. Following exposure to intact Karenia organisms, damage to these epithelial cells leads to increased mucus production and a mostly localised inflammatory response.
The inflammatory response consists of a complex set of interacting mechanisms which include increased local blood flow which causes redness and swelling. Cells of the immune system aggregate in the area of damage to fight potential infection and to promote tissue healing. As part of this process, these cells together with damaged epithelial cells release biochemical agents that activate specialised nerve fibres (nociceptors) lying in the connective tissues beneath the epithelium. This neural activation is perceived as itch, stinging or burning pain, depending on the level and type of inflammation. Some of these nerves feed back into the inflammatory process, helping to maintain it until the damage is repaired. It is important to realise that these inflammatory effects are not due to a neurotoxin. Understanding how these nerves work was a major research topic for my colleagues and me for 30 years.
The main results of these inflammatory processes include bloodshot eyes, runny nose and a scratchy throat, perhaps associated with a cough. These effects last significantly longer than the duration of contact with the algal bloom, typically from an hour or so up to a day or two. The inflammatory reaction itself can lead to headaches, feelings of malaise and nausea. These are not direct effects of algal toxins but the result of the body responding to the inflammation as the tissue damage is repaired. These responses nearly always resolve of their own accord.
As is the case for fish gills, irritation to the eyes, nose and throat probably requires direct contact with intact Karenia organisms. Nevertheless, sea water and sea foams containing high levels of Karenia fragments are still could generate an irritant effect.
Brevetoxin
The major source of brevetoxins in the current bloom is Karenia cristata. Most of the information about brevetoxins and how they impact on human health comes from studies of a close relative, Karenia brevis, also a significant producer of brevetoxin. As explained in detail elsewhere here, exposure to brevetoxin leads to tingling and numbness rather than stinging sensations. Furthermore, as far as is known, brevetoxin does not directly cause inflammation, so it is unlikely to be the cause of eye and throat irritation. Although brevetoxin acts to stimulate many types of nerves, at comparable concentrations, it is unlikely to directly stimulate nerves mediating stinging inflammatory pain, since they mostly lack the ion channels that are targeted by the toxin. (Click here to see more about the neurotoxic actions of brevetoxin). In other words, if brevetoxin does activate pain-sensing nerves, it would only occur after tingling, numbness and paralysis have already set in.
Brevetoxin is responsible for so-called Neurotoxic Shellfish Poisoning (NSP). This occurs when people eat shellfish that have accumulated high levels of brevetoxin. Symptoms can include nausea, vomiting, headache, tingling, and disturbances to balance, coordination and vision. These symptoms usually resolve relatively quickly, even if they are severe initially. It is important to note that such symptoms are rarely seen in people exposed to brevetoxin in other ways, eg, exposure to water or air containing brevetoxin. Despite many years of monitoring, there have been no recorded fatalities due to brevetoxin poisoning from recurrent Karenia brevis blooms in Florida1.
In addition to its neurotoxic effects, brevetoxin has been reported to have other actions2. Most notable are those causing asthma-like symptoms in the lower airways, which are discussed in detail below. However, these other reported actions occur at concentrations or doses 10-100x higher than those necessary to cause neurotoxic effects.3 Consequently, it is most unlikely that any of these possible actions of brevetoxin could occur in the absence of severe, potentially fatal, neurological effects. While severe inflammatory reactions have been reported in animals, such as manatees and dolphins, exposed to brevetoxin in Karenia brevis blooms, none of those studies has considered the possibility that the inflammation could be due to a cytotoxic action of Karenia brevis or other organisms in the bloom4.
Breathing the air – aerosols
Many people have reported symptoms of sore eyes and sore throat accompanied by coughing while at beaches where the bloom is present. The symptoms may subside quickly after leaving the area or they may persist, sometimes accompanied by headache and nausea. More rarely, people have reported asthma-like symptoms of wheezing and shortness of breath. Such observations have been associated with the red tides due to Karenia brevis in Florida for many years5. The critical observation here is that affected people have not had any direct contact with the water. Rather, there must be something in the air that is causing these responses.
Wave action and wind can combine to generate a fine seaspray or aerosol that can drift a considerable distance from the sea surface. This aerosol can contain, and therefore transport, substances that are dissolved or suspended in the seawater. Karenia organisms are very fragile and are likely to be broken up by the wave action required to generate aerosols. Furthermore, intact Karenia cells are too big to enter and be transported intact by aerosols6. Therefore, it is most unlikely that the cytotoxin actions of Karenia observed in water, which requires the Karenia to be intact, could occur in aerosols. In contrast, brevetoxin released from damaged Karenia can be transmitted by aerosols at levels that lead to its accumulation in human tissues7.
Brevetoxin in aerosols and asthma-like symptoms
Brevetoxin is primarily a neurotoxin. However, a variant form of brevetoxin that can be dispersed for large distances by aerosols has been demonstrated to cause asthma-like respiratory effects that are unrelated to its neurotoxicity. These effects are likely to be more pronounced in people with a pre-exisiting respiratory condition such as asthma or influenza8.
This brevetoxin variant interacts with immune system cells in the lower airways, ultimately leading to histamine release, which causes bronchoconstriction (narrowing of the airways) with concomitant wheezing or shortness of breath. These asthma-like symptoms of exposure to the variant brevetoxin can be reduced by antihistamines. Any neurotoxic forms of brevetoxin in the aerosol exacerbate the situation by over-stimulating bronchoconstrictor nerves in the airways.
It is important to note that this asthma-like effect of brevetoxin is not accompanied by irritant actions on the eyes or upper airways, such as the nose and throat. There is no evidence that it directly causes inflammation in these tissues and, at concentrations likely to occur in bloom-affected water or aerosols, it is not likely to significantly activate nerve endings responsible for painful sensations. Nevertheless, the possibility remains that a variant form of brevetoxin, or brevetoxin acting in conjunction with another toxic agent, could potentiate symptoms of irritation and inflammation in tissues outside the lower airways9.
Brevetoxin has been detected in at least some water samples taken during the current bloom. The most likely source is the recently identified Karenia cristata10. Karenia papilionacea which also can generate brevetoxin has been detected in the bloom, albeit at much lower levels than Karenia cristata. Karenia mikimotoi does not produce brevetoxin in any form.
Eye and throat irritation from aerosols – other possibilities
The effects on people of exposure to aerosols are generally similar to those of exposure to bloom-affected water: sore eyes, nose and throat. This strongly suggests that a cytotoxin is involved.
As mentioned previously, based on its well-established molecular actions, brevetoxin does not (and cannot) directly generate painful or stinging sensations and is not by itself likely to cause inflammation of tissues outside the lower airways. So brevetoxin is most unlikely be primarily responsible for the eye and throat irritation following exposure to bloom aerosols.
One strong possibility is that the aerosols contain breakdown products of components of the bloom that themselves are cytotoxic11. However, no such agents have been positively identified to date. Brevetoxins exist in multiple molecular forms and, in theory, one of them or its metabolite could have cytotoxic actions. However, again, no such products have yet been identified.
Another possibility is that the aerosols associated with the bloom contain an agent produced by an as yet unidentified microorganism, that can be taken up in aerosols and contribute to the symptoms experienced by people walking along affected beaches. Dinoflagellates and other phytoplankton have incredibly complex interrelationships with microbes (mostly bacteria, but also viruses) in their environment and even on their own surfaces12. There is good evidence that aerosols can contain and transmit marine bacteria and cyanobacteria or their breakdown products, some of which could cause an acute inflammatory response, largely independent of any direct effect of phytoplankton toxins 13. Once again, no such agents have been identified in the current bloom. Nevertheless, discoloured foam on bloom-affected beach contains high levels of potentially pathogenic bacteria associated with the decay of organic matter in the water, including the dinoflagellates themselves, dead fish and seagrasses14.
In each of these possibilities, it is highly likely that the coughing experienced by many people after exposure to bloom aerosols is secondary to the inflammation of the throat and upper airways and is unrelated to a brevetoxin action on the lower airways.
Nausea and headache
The nausea that some people experience after exposure to the bloom by contact with the water or foam, or when on an affected beach, could be due to more than one factor. Brevetoxin itself can cause nausea if ingested via affected shellfish15, and it is highly likely that ingestion of water with high levels of bloom micro-organisms would also generate a feeling of nausea. However, the levels of any brevetoxins in aerosols are probably not at sufficient to directly cause nausea16.
Any form of severe irritation that results in significant inflammation, such as that experienced in the eyes or nose following exposure to the algae, or the asthma-like symptoms of aerosoled brevetoxin, can lead to feelings of malaise, tiredness, headache, and, in some cases, nausea. An increase in reports of headaches following exposure to Karenia brevis red tides has been documented in Florida, but the direct cause of this (ie, brevetoxin, air-borne cytotoxin, or something else) has not been identified17.
Long term effects of exposure
While the short-term effects of human exposure to toxic algal bloom have been reasonably well studied, there are few if any studies on potential long-term effects on human health arising from exposure to algal toxins, especially those associated with Karenia species18.
The acute effects of brevetoxin wear off reasonably quickly, much like those of a local anaesthetic, for example. However, inhaled brevetoxin can be detected in the blood at very low levels for some time after exposure.19 Asthmatics repeatedly exposed to intermittent brevetoxin aerosols do not develop further chronic respiratory effects.20
The active agent in the bloom that causes eye and throat irritation via contact with water containing the bloom has a relatively short lifetime and apparently does not remain in our body systems. The agent in the aerosols is probably something similar, albeit with a somewhat longer lifetime, but this is still not certain with our current state of knowledge.
An important thing to keep in mind is that an inflammatory response to some noxious agents can (and usually does!) last much longer than contact with the agent itself, eg, a mosquito bite itches long after the insect has gone. Similarly, a burn or cut hurts for days after the initial damage is done (how this works was one of the things I used to research in my former life). So the fact that your throat hurts or eyes sting or you feel a bit brain fogged for a day or so after being exposed to the noxious agents in the bloom is not surprising, and it is not an indicator that some long-term effect is brewing.
Although there is little if any evidence for long term effects of algal toxins themselves, repeated or chronic exposure to aerosols containing algal and/or bacterial toxins may well lead to on-going inflammation, especially in the upper airways. To date there have been no systematic studies of such conditions.
Reactive oxygen species
It has been suggested that reactive oxygen species (ROS), such as hydrogen peroxide (H2O2) generated by Karenia species contribute to eye and airway irritation in people walking at or in the neighbourhood of beaches affected by the bloom. However, almost by definition, ROS are very short lived in the environment and are unlikely to be significant components of sea-side aerosols. Indeed, as explained elsewhere here, ROS generated by the interactions between Karenia species and affected cells exert their cytotoxin actions at molecular levels in the cell membranes through a mechanism that is secondary to the initial cell contact, and may contribute relatively little to the overall effect of that contact21. Although hydrogen peroxide is relatively stable compared with other ROS, it is only an irritant at very high concentrations which are most unlikely to be achieved in bloom-derived aerosols.
A metallic taste in the mouth?
One of the symptoms people have reported after exposure to the bloom, either from being in the water or walking along the beach is a metallic taste in the mouth. Getting to the bottom of why things taste the way they do is fiendishly complicated, involving complex biochemistry, cell biology and neuroscience. To make matters worse, although there is a large literature on factors leading to bad tastes in fresh water affected by cyanobacterial blooms22, they are not relevant here, and I can find no good quality research on the source of unusual tastes following exposure to marine dinoflagellate blooms. So what follows is pulled together from a range of diverse references.
We can taste many metals or their ions more or less directly, including sodium, potassium, iron, copper and magnesium (eg Na+, Fe++). The cell physiology of these taste mechanisms is really complicated and involvesa range of receptor molecules on different types of tastebuds. Almost certainly, we generate the taste sensation in the brain by assessing the combinatorial mix of inputs from these different receptors, as well as inputs from olfactory receptors in the nose. Some taste “salty” like sodium or potassium; others taste “metallic” like iron or magnesium23.
But there are two other families of compounds that can generate a metallic taste that are relevant to the bloom24. First, a range of fatty acids can taste metallic, and these are almost certainly components of the foams and aerosols, as a result of the breakdown of bloom organisms and marine organisms affected by the bloom. The fatty acids would come from the membranes of the damaged cells and they probably also contribute to the formation of the foams.
The other potential source of a metallic taste is hydrogen sulphide (H2S, rotten egg gas) which, together with other sulphur-containing compounds, is generated by the anaerobic decay of organic matter by bacteria. When dissolved in water at low levels, it can contribute to a metallic taste. Again this could easily be transported in aerosols. However, any H2S in aerosols almost certainly would come from shallow water, ie wave / wind action close to shore, since H2S from organic matter on the sea floor in deeper water would rapidly disperse and be diluted out. Another source of H2S could be decaying organic matter (seaweed, dead animals) floating in the sea surface, but it’s unlikely that this environment would have the anaerobic conditions favouring H2S production.
So my best guess is that this last combined explanation, lipids + H2S, is most likely. Taste is affected by other factors such as sea salt, so it gets complicated quickly. But these properties are consistent with what else is known about the nature of the foams and aerosols, ie, they contain the remains of broken down cells and algae, etc. Rather than being a direct effect of the bloom organisms themselves, the metallic taste is a consequence of their effect on other marine organisms.
How the same compounds or mixtures of compounds taste can vary immensely between different individuals, and can be influenced by genetic background, cultural context, previous experiences, and current health status. So two people at the same beach at the same time may have quite different sensations: one may have a metallic taste in the mouth, the other may not.
Health Symptoms Reporting portal
If you experience health symptoms following exposure to the bloom, you can report them via the Bloomin’ Algae citizen science reporting portal. The information you provide is anonymous and will be used to help create a database that can be analysed at a later date.
Click here to go to the portal.
Selected references
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Pradhan B et al (2022) Toxic effects and tumor promotion activity of marine phytoplankton toxins: a review. Toxins 14: 397, https://doi.org/10.3390/toxins14060397 ;
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Watkins SM et al (2008) Neurotoxic shellfish poisoning. Marine Drugs 6: 431-455, https://doi.org/10.3390/md6030431
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↩︎ - For example, the following paper, which has been widely quoted, only reports significant effects of brevetoxin at concentrations more than 1000x higher than those needed to affect ion channels on nerves: Hilderbrand SC et al (2011) Marine brevetoxin induces IgE-independent mast cell activation. Archives of Toxicology: Molecular Toxicology 85: 135-141, https://link.springer.com/article/10.1007/s00204-010-0564-2
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Lazensky R et al (2020) Investigating the gene expression profiles of rehabilitated Florida manatees (Trichechus
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Twiner MJ et al (2011) Concurrent exposure of bottlenose dolphins (Tursiops truncatus) to multiple algal toxins in Sarasota Bay,
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↩︎ - Fleming LE et al (2010) Review of Florida red tide and human health effects. Harmful Algae 10: 224-233, http://dx.doi.org/10.1016/j.hal.2010.08.006 ;
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↩︎ - Cunningham BR et al (2021) Detection of brevetoxin in human plasma by ELISA. Journal of Analytical Toxicology 46: 322-327, https://doi.org/10.1093/jat/bkab010 ;
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