Eutrophication – colored waters as a result of human activity

10 min read
Eutrophication – colored waters as a result of human activity
Picture: T.w. Van Urk | Dreamstime

The problem of eutrophication (water bloom) is widespread and serious, because according to UNEP (United Nations Environment Program) about 30-40% of lakes and reservoirs around the world have suffered from this phenomenon. In addition, eutrophication can occur both in fresh water and in sea water.

“What’s so bad about eutrophication?” – you ask. Unfortunately, the layer of algae that covers such reservoirs is just the tip of the iceberg that hides a real toxic cauldron.

You don’t even have to ask who is to blame for this, because the answer is painfully obvious – economic activity. Sources of pollution include municipal wastewater with a high phosphorus content (hello to detergent manufacturers that still use phosphates) and agricultural waste: phosphate and nitrogen fertilizer washes, silage.

How to solve the problem of eutrophication?

And, it seems, the problem is easily solved – you can ban phosphate-containing detergents and limit the use of nitrogen and phosphate fertilizers. But let’s first figure out what happens after a large amount of phosphorus and nitrogen is dumped into a conditional reservoir.

Action 1 – Occupation

It all starts with an imbalance between elements such as phosphorus (P), nitrogen (N) and silicon (Si). But a sharp increase in the proportion of N/Si and P/Si (an increase in phosphorus especially adds fuel to the fire) is not the only component that becomes a trigger for the active reproduction of phytoplankton. This also requires an optimal temperature of 23-28C. It is this killer combination that creates all the conditions for the maximum growth rate of algae.

Picture: Edita Meskoniene | Dreamstime

What do microscopic organisms that reproduce very actively do? They immediately form a rather dense layer on the surface of the water, gradually occupying the entire possible area.

The first victims of the occupation are green algae, for which sunlight is vital. Dead plants are decomposed by bacteria that consume oxygen. Thus, a little later, the consequences are already catching up with fish and other aerobic organisms, when “dead zones” with an ultra-low concentration of dissolved oxygen begin to form in the reservoir. Add also the outgoing biomass of the algae themselves, and, as a result, our reservoir is slowly and surely turning into a “stuffy burial ground”.

Action 2 – Upside down

Thus, in an ecosystem, in addition to an unjustified increase in primary productivity (biomass, which is created by microalgae), the relative abundance of species, taxonomic composition, and spatial distribution of primary producers in the aquatic ecosystem change.

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Changes in the composition and location of resources change the distribution and flow of energy in the food web. How exactly? In a normal aquatic ecosystem, phytoplankton (microscopic algae and other photosynthetic organisms) are used by zooplankton (fish larvae, daphnia, molluscs). Zooplankton is food for larger predators (for example, fish), and the waste products of all organisms are used by decomposers (bacteria). In the eutrification system, the main consumers are bacteria that decompose dead plants, part of algae and fish. As a consequence, organisms lose their ecological specialization.

But what we are more interested in is the impact of eutrophication on human health, so let’s move on.

Action 3 – Toxic Environment

In fact, only phytoplankton and anaerobic microorganisms remain alive in the reservoir. Typical representatives of phytoplankton are blue-green algae and representatives of other taxonomic groups that do not harm others. But in such an environment there is also a place for toxin-producing organisms, which, upon contact with a person, can cause harm. By the way, the word “contact” implies not only bathing in such water, but also its use.

Toxins that can be found in the open spaces of eutrophicated reservoirs are divided into several groups:

  • Hepatotoxins or cyclic peptides (microcystins and nodularins);
  • Alkaloids (cylindrospermopsin, toxoid-a and toxoid-a(s), saxitoxin);
  • Polyketides (aplysiatoxins);
  • Amino acids (-methylamino-L-alanine or VMAA).
Picture: Jon Benito Iza | Dreamstime

Algae toxins such as azaspiracid, brevetoxin, ciguatoxin, domoic acid, dinophysistoxin, hemolytic toxin, homoanatoxin, calotoxin, lingbiatoxin, maitotoxin, pectenotoxin, primnesin, and the like are not usually included in this classification.

Now is the time to find out exactly how eutrophicated water bodies can harm a person or even kill.

The harm of eutrophication

Microcystins and nodularins

The synthesis of microcystins is observed in some species of the genus Anabaena (A. circinalis, A. flosa-quae, A. lemmermannii, A. millerii), Arthrospira (A. fusiformis), Microcystis (M. aeruginosa, M. botrys, M. ichthyoblabe, M. viridis, M. wesenbergii), Nostoc (N. inckia, N. rivulare, N. zetterstedtii), Oscillatoria, Planktothrix and in some species (Spirulina subsalsa, Synechococcus bigranulatus). Nodularins are synthesized by Nodularia spumigena, which is common in sea water.

Microcystins and nodularins are sometimes called hepatotoxins because the liver is the main target for this group of compounds. But there are cases of accumulation of microcystin in the kidneys, large intestine, brain and other organs, the cells of which have the organic anion transporter OATP (Organic Anion Transporter).

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Why are they not neutralized in the stomach or in the liver? The fact is that these protein compounds consist of D-forms of amino acids (and L-forms of amino acids act as ligands for enzymes), so they are resistant to digestion.

Microcystins inhibit protein phosphatase, as a result of which cell proteins become phosphorylating – this creates conditions for the formation of tumors. The situation is worsened by the fact that the toxin increases the expression of proto-oncogenes (cfos, c-jun, c-mys, p53).

In addition, microcystins and nodularins activate c-Jun N-terminal kinase and other enzymes that are involved in oxidative stress of the cell. This is fraught with the occurrence of internal bleeding, and in the case of acute poisoning, the occurrence of hemorrhagic shock against this background.

Since microcystins cross the blood-brain barrier, a number of diseases associated with the nervous system are added to the list of pathologies. These include inflammation of the nervous tissue, as well as a number of neurodegenerative diseases.

Picture: Joaquin Corbalan | Dreamstime

The significance of the lethal dose for humans has not yet been determined, since different microcystins have different lipophilicity and polarity values. However, the average dose is considered to be 5-10 mcg/kg body weight.
But, fortunately, microcystins and nodularins can be neutralized. First, these compounds are intracellular and only enter the environment if the cell is damaged. Despite the fact that they are quite stable in the extracellular environment and are completely destroyed after 20 weeks, high temperature (40C) and critical pH values ​​can accelerate this process. Thus, the possible ways of poisoning with microcystins and nodularins is the use of thermally untreated water and products.


The most common and at the same time dangerous toxin produced by algae in fresh water is anatoxin-a. It is synthesized by representatives of the genera Anabaena (A. flosa-quae, Anabaena lemmermannii), Aphanizomenon, Phormidium (G. willei, G. terebriforme), Planktothrix, as well as some individual species (Arthrospira fusiformis, Spirulina subsalsa, Synechococcus bigranulatus).

Anatoxin is an agonist of peripheral and central acetylcholine receptors. When pre/postsynaptic binding to receptors, it opens sodium/potassium channels, which causes depolarization blockade. Thus, after entering the bloodstream, the toxin causes loss of muscle coordination, tremors and convulsions, and death occurs after peripheral respiratory paralysis (the muscles involved in breathing stop working).

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You can get poisoned by toxoid when bathing, drinking contaminated water and food additives. The lethal dose is from 20 mcg / g, the receipt of which causes death from respiratory paralysis in 1-2 minutes. That is why toxoid is often called the Very Fast Death Factor (VFDF).

What about toxoid-a(s)? The fact is that this compound, unlike toxoid-a, is unstable in the environment, therefore, as a rule, it does not pose a threat to humans.


Saxitoxins form some species from the genus Anabaena (A. circinalis), Aphanizomenon (A. flos-aquae), Cylindrospermopsis (C. philippinensis, C. raciborskii), Oscillatoria and the species Plectonema wollei. Saxitoxins are also synthesized by dinoflagellates (genus Alexandrium, Gymnodinium, Pyrodinium) and accumulate in mollusks living in sea and fresh water.

Saxitoxins, unlike microcystins and nodularins, are thermostable, but can be separated from water by sorption on activated carbon or by ozonization of water.

This alkaloid blocks sodium conduction in axons by binding to the pores of sodium channels, preventing the transmission of nerve impulses. In other words, it causes paralysis. Because of this, saxitoxin poisoning is called “paralytic shellfish poisoning.”

A person can easily consume about 100 micrograms of saxitoxin (this is about 50 micrograms / l with a daily intake of water in a volume of 2 liters). Does not tend to accumulate in the body.


Cylindrospermopsin is synthesized by species such as Cylindrospermopsis raciborskii, Aphanizomenon ovalisporum and Umezakia natans. Since the listed organisms are characteristic of freshwater reservoirs, the location of the toxin will not be difficult to guess.

Picture: T.w. Van Urk | Dreamstime

This toxin, similar to microcystins and nodularins, has a wide spectrum of action on the body. The main target of cylindrospermopsin is the liver, but it also negatively affects the eyes, spleen, lungs, thymus, heart, kidneys, and the like. In addition, cylindrospermopsin inhibits protein synthesis in cells, causes DNA fragmentation in vitro, and the formation of oxidative stress in cells against the background of inhibition of the synthesis of glutathione (a powerful endogenous antioxidant).

The lethal dose of cylindrospermopsin is 6 mg/kg. It dissolves in water and is stable at low pH levels. When water is heated to 100C, it remains active for 15 minutes, so the main method of neutralizing this toxin is long-term thermal treatment of water and products that can potentially be infected with cylindrospermopsin.


This is a toxin of non-protein nature, and it is produced by some species of algae of the genera Lyngbya, Schizothrix (S. calcicola), Oscillatoria, Phormidium nigro-viride species, which are characteristic inhabitants of marine waters.

Aplysiatoxin is able to activate protein kinase C, which contributes to increased protein phosphorylation. This, in turn, contributes to the further occurrence of tumors. In addition, upon contact with the skin, it can provoke the appearance of acute dermatitis, as well as inflammation of the mucous membranes if the toxin is ingested with food or by inhalation.

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The lethal dose of aplysiatoxin is 0.3 mg/kg. When boiling, it is unstable and collapses. But getting rid of aplysiatoxin in water is not the best option, because this way you risk poisoning with bromine fumes.

VMAA-methylamino-L-alanine is a non-protein amino acid that is synthesized by the genera Nostoc, Synechococcus and Synechocystis, as well as some individual species (Planktothrix aghardii, Anabaena variabilis, Cylindrospermopsis raciborskii) living in sea or fresh water. This amino acid accumulates in shellfish, some types of fish, as well as in the water itself.

VMAA is capable of provoking the development of amyotrophic lateral sclerosis (Lou Gehrig’s disease), Parkinson’s and Alzheimer’s, and other neurodegenerative disorders. It is also hypothesized that the amino acid increases protein ubiquitination, a major process in protein degradation.

Neurotoxic effects are manifested when a person consumes VMAA in an amount of about 4000 mg/kg of body weight. But in the case of this toxin, it is chronic intoxication that poses a great danger.
Thermal treatment of water or food, unfortunately, does not guarantee the neutralization of α-methylamino-L-alanine, because this compound is highly stable at high temperatures and low pH values.

Survive in the wild

One can endlessly describe the mechanisms of action of various toxins that can be formed in eutrophicated water bodies. But what is the most important thing here? Accept the fact that neglected eutrophication can lead to sad and sometimes tragic consequences. Therefore, it is in our interests to do everything to minimize the negative impact of this environmental problem in order to preserve health and life.

In order to protect yourself and your loved ones, you must follow three simple but very important rules.

  • First of all, be careful when choosing places to stay. It is not necessary to swim in eutrophicated waters – you can get poisoned even just by inhaling the toxin in the form of an aerosol.
  • Secondly, be careful when choosing seafood (especially if you are a fan of shellfish) – it is these organisms that most often accumulate toxins in themselves, which are sometimes simply impossible to get rid of at home.
  • And thirdly, try not to drink water from rivers, lakes, ponds and other bodies of water. Especially if you notice the first signs of eutrophication (turbidity of the water, a layer of algae on the surface). It is better to use bottled drinking water, because even long-term boiling of water is not effective for some toxins.
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