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This chapter is an introduction to the cyanobacterial (blue-green algae) ecology, with the main aim of better understanding the design of cyanobacterial blooms and cyanotoxins in the natural environments. Cyanobacteria are a diverse group of photoautotrophic organisms where their dominance represents a significant indicator of water quality. Several genera have the potential to produce toxins—hepatotoxins (microcystins, nodularins), cytotoxins (cylindrospermopsin), neurotoxins (saxitoxins, anatoxins, BMAA), dermatotoxins (lyngbyatoxin), and irritant toxins (lipopolysaccharide endotoxins). This chapter provides a concise and achievable summary of their negative impact on health and the environment, supplemented with tables and schemes that illustrate the ecology of cyanobacteria, the different types of cyanotoxins, and their health issues. The exposure routes are also discussed, which is particularly important due to the increasing eutrophication of water. It is emphasized that climate change, global warming, and increased eutrophication are responsible for cyanobacterial blooms. As a consequence, the risk they pose is likely to grow; accompanied by their ability to produce toxins, cyanobacteria represent an imminent danger to human and animal health. One of the primary goals of future research should be to share knowledge about cyanobacteria and cyanotoxins and to develop solutions for early detection and prevention of cyanobacterial bloom occurrence.
Faculty of Sciences, Department of Biology and Ecology, University of Novi Sad, Novi Sad, Serbia
*Address all correspondence to: dijana.pantelic@dbe.uns.ac.rs
1. Introduction
Have you heard about cyanobacteria? How about blue-green algae? Both terms refer to prokaryotic organisms found in many water and terrestrial environments throughout the world. Cyanobacteria are especially abundant in shallow, warm, nutrient-rich, or polluted water low in oxygen, where under favorable environmental conditions their increased growth may form visible scums on water surfaces referred to as cyanobacterial blooms [1, 2], which is concerning in aquatic environments as the rapid increase of algae alters the quality of the water (Figure 1).
Figure 1.
Cyanobacterial blooms and their relation to the environment.
This group of prokaryotes has a remarkable ability to tolerate extreme environmental changes by producing a diverse range of secondary metabolites (e.g., toxins—cyanotoxins and UV protective pigments—scytonemin and mycosporine-like amino acids), which gives them a competitive advantage [3]. We have all witnessed climate change and global warming over the past few decades (elevated temperature, increased atmospheric concentrations of carbon dioxide, elevated UV fluxes). The effects of global climate change and the associated accumulation of nutrients in water bodies by runoff from agricultural fertilizer, intensive farming practices, sewage discharge, and detergent usage are contributing to the accelerated decline in the quality of freshwater—eutrophication [1, 4]. Anthropogenic eutrophication of surface waters (Figure 2) implies rising nutrient levels (especially phosphorous but also nitrogen), low turbulence, stagnant water conditions, higher pH values, and higher temperature [4]. Drought can decrease water quality by concentrating pollutants (such as nutrients), and intense rain can wash fertilizers from crops, which are then discharged into water bodies. Resulting, cumulative conditions consequently stimulate the growth of cyanobacterial blooms in various geographic regions [5]. This accelerated growth of cyanobacteria in water bodies has severe impacts on ecosystem functioning—changes in biodiversity, light conditions or oxygen concentrations, and disturbances of relationships among organisms, which become a worldwide environmental problem. Approximately 50% of cyanobacterial secondary metabolites are known to produce extremely toxic metabolites known as cyanotoxins. Under these circumstances, cyanotoxins can reach high concentrations in waters and cause poisoning of animals and humans globally. Cyanotoxins can be intracellular, retained in cyanobacteria cells, and extracellular, released into the water during the life cycle and lysis [6]. Linked with negative environmental impacts large-scale cyanobacterial bloom events are classified as “harmful algal blooms” [7].
Figure 2.
Eutrophication and cyanobacterial blooms (created by Author using Canva).
The current and expected future rise in cyanobacterial populations due to increasing anthropogenic eutrophication and global climate change [8, 9] suggests that further reports of poisoning events will occur. Mass occurrences of toxic cyanobacteria and their toxins in reservoirs represent a great challenge to produce safe drinking water and the development of advanced monitoring techniques [10]. The first step for cyanotoxin control is the prevention of the eutrophication process and reducing cyanobacterial blooms in water bodies. There is a necessity for improvements in the knowledge of cyanobacterial occurrence and ecology, and further, consequences of exposure to cyanotoxins. This chapter emphasizes emerging factors that contribute to the future expansion of cyanobacterial toxic blooms from aquatic ecosystems, and according to the newest data, from terrestrial environments, especially due to climate change, global warming, and anthropogenic eutrophication. Such information is crucial as the lack of knowledge about the toxic properties of cyanobacterial blooms has resulted in intoxication episodes worldwide, posing a problem that requires constant vigilance.
This comprehensive chapter presented the scenario of global warming and eutrophication, which will increase the risk of cyanobacterial bloom occurrence. Controlling the spread of cyanobacteria has become a significant global challenge. From a huge database of cyanobacterial occurrence and cyanotoxin poisonings [11], the number of research papers dealing with cyanotoxins seems to have increased exponentially over recent decades (from <2% before 1949 to over 72% after 2000). However, there are still unevenly distributed scientific researches and studies, with dominance in wealthier countries of the world. Also, despite improvements in analytical techniques, access to expensive equipment and standards, technical staff, and necessary handling skills will continue to limit cyanotoxin monitoring activity in wealthier countries. Without proper management, cyanobacteria can begin producing toxins. Cyanobacterial blooms that happened in the past and that are currently happening suggest that more research oriented toward cyanotoxin detection and purification system is needed. Standard procedures dealing with cyanotoxin detection should be standardized and implemented in the regulation system worldwide, and those procedures should be achievable for every country. Scientists should work on developing test kits for the detection of all types of cyanotoxins, not just for microcystin, as the most common cyanotoxin. Monitoring frequency (parameters such as chlorophyll-a, phycocyanin, temperature, pH, and turbidity) should be increased due to the widespread presence of cyanobacteria and their cyanotoxins [11]. There is an urgent requiring of sharing knowledge about cyanobacteria and their toxins to overcome the limitations highlighted in this study and encourage new behaviors.
Cyanobacterial blooms with their production of potentially toxic secondary metabolites, cyanotoxins, present a worldwide threat to environmental and public health. Cyanotoxins are increasingly being viewed as contaminants of emerging concern (Figure 3). They are classified based on their target organs or cells. Cyanotoxins can affect the liver—hepatotoxins (microcystins, nodularin), nervous system—neurotoxins (anatoxin-a, homoanatoxin-a, anatoxin-a (S), saxitoxins and BMAA), cells—cytotoxins (cylindrospermopsin), or cause skin irritation—dermatotoxins (aplysiatoxin, debromoaplysiatoxin, lyngbyatoxin) and act like endotoxins (lipopolysaccharides) and other toxins [12, 13]. Cyanotoxins are recognized as one of the most lethal groups of biotoxins known [1], which could cause illness in humans [14, 15], animals [16], and even death [17, 18]. Not all cyanobacterial blooms are toxic, and early surveys (determined by mouse intraperitoneal (i.p.) bioassay) indicated an incidence of 25–75% [6, 7]. The natural functions of their toxins remain to be fully understood; it may be an adaptation in resource-limiting environments as conferring competitive advantage and as cyanobacterial physiological aides [11].
Figure 3.
Cyanobacteria and cyanotoxins in drinking/recreational water environments.
Lately, many countries have been faced with cyanobacterial blooms affecting large areas with an increase in bloom incidence, followed by higher economic losses to aquaculture and tourism. Various cyanobacterial genera are known to produce toxins responsible for human and animal poisonings [11]. Microcystins, recognized as the most ubiquitous cyanotoxins [19], anatoxins, cylindrospermopsis, and other toxins, cause illness in humans and animals. The highest cyanotoxin levels are usually contained within the cells (intracellular toxins), in the cytoplasm, and toxin concentrations dissolved in the water (extracellular toxins) are rarely reported above a few μg/L [1]. The concentration of cyanotoxins significantly increases as a defense mechanism in stressful conditions (lack of nutrients/light) [20]. Dead cyanobacterial cells, whether at the end of their lifecycle or due to bloom control measures, can cause an increase in the concentration of extracellular toxins. Cyanotoxins are a concern when they are released into the water as they can be ingested by aquatic invertebrates, aquatic vertebrates [21, 22, 23], and even plants [24]. This can pose a potential health risk to humans and animals who consume contaminated food [25, 26]. Furthermore, children are particularly vulnerable to cyanobacterial toxins due to their lower body weight, behavior, and the toxic effects they can have on development [27].
When cyanobacterial cell concentrations are high due to bloom events, cyanotoxins can cause a noxious taste and odor in drinking and recreational water. They decay and resulting high biomass of cyanobacteria cause low oxygen events that kill fish, blocks sunlight preventing the growth of other algae and disrupting food webs [28]. During cyanobacterial blooming events, it is necessary to take caution of water-related activity (Figure 3). The presence of high levels of cyanotoxins in recreational and drinking water may cause a wide range of symptoms in humans (Figure 4), including fever, headaches, muscle and joint pain, blisters, severe oral and gastrointestinal inflammation, vomiting, mouth ulcers, and irritation of the skin and mucous membrane of the eyes, nose and throat, cyanosis, paralysis, and respiratory or cardiac arrest, potentially resulting in death. The health issues caused by cyanotoxins can occur within minutes to days after exposure in accordance with exposure route(s), the types and concentration of cyanotoxins, age and body weight, and health conditions of the affected person (e.g., associated diseases). In severe cases, seizures, cyanosis, paralysis, liver failure, respiratory arrest, and (rarely) death may occur [1, 11, 29]. Cyanobacteria can persist in water bodies for a long time, leading to prolonged exposure to subacute concentrations of cyanotoxins and the possibility of chronic health effects, including possible carcinogenic changes [30, 31], neurodegenerative diseases in humans [32], and harm to other living organisms, including invertebrates [33] and plants [34, 35, 36]. It can cause leaf necrosis, inhibition of photosynthesis and growth, and oxidative stress [34, 35, 36].
Figure 4.
Target organ of toxicity and health issues (created by Author using Canva).
Based on the research [11], there were 183 recorded cyanotoxin poisonings of humans and animals reported worldwide, with most cases reported in North and Central America, followed by Europe and Australia/New Zealand. Microcystins were the most often recorded cyanotoxins worldwide (63%) followed by cylindrospermopsin (10%), anatoxins (9%), and saxitoxins (8%). Further, microcystins have been most commonly reported in cyanobacterial poisoning cases (42%), and nodularin has been least often (2%). A total of 15% of all the poisoning cases were assigned due to unknown reasons and 17% due to not analyzing cyanotoxins. Poisoning events caused by cyanotoxins affected in 63% of cases only animals, whereas 32% of the investigated poisonings involved only humans. The presented data [11] suggest that future research should be orientated toward the creation of new, inexpensive, and more widely available analytical techniques for cyanotoxin detection.
2.1 Structure and characteristics of cyanotoxins
Cyanotoxins are very diverse regarding their chemical structure and toxicity (Table 1 and Figure 5) [12, 37, 38, 39, 40]. A structurally similar group of cyclic hepta- and pentapeptides is known as microcystins and nodularins, respectively [41, 42]. Microcystins (MCs) are the most ubiquitous toxins detected in cyanobacterial blooms and produced by various cyanobacterial genera Aphanizomenon, Dolichospermum (Anabaena), Fischerella, Microcystis, Oscillatoria, Nostoc, Planktothrix, Synechococcus, and Trichodesmium [19, 43, 44]. Microcystins act primarily through the inhibition of protein phosphatases 1 and 2A. The primary target cell for MCs is the liver [45]; however, these toxins can affect other tissues (kidney, reproductive tissue, colon, brain) [46]. Microcystin-LR (MC-LR) causes potent hepatotoxicity and it acts as a tumor promoter [47, 48, 49, 50]. So far, about 250 variants of microcystin have been identified [51], but the most toxicological information is available for the MC-LR [52].
Toxins/structure (number of analogs)
Target organ and mechanism of action
Health effects
LD50 (i.p. mouse, μg/kg b.w.)
LD50 (oral, μg/kg b.w.)
Toxigenic genera
Reference
Hepatotoxins
Microcystins/cyclic heptapeptides (~250)
Irreversible inhibition of protein phosphatases (PP1 and PP2A), membrane integrity and conductance disruption; primary site of action: liver (also affect other tissues-kidney, reproductive tissue, colon, brain)
Nausea; vomiting; diarrhea; renal damage; hepatotoxic; tumor promoters; death (in some cases)/Immediate up to 24 hours
Irreversibly inhibits acetylcholinesterase, nerve hyper-excitability; Primary site of action: peripheral nervous system
Hyper salivation; diarrhea; paralysis; asphyxiation; decreased movement; exaggerated abdominal breathing; cyanosis; convul-sion; and ultimately death/Survival time of 10–30 min
Abbreviations: i.p. = intraperitoneal exposure; LD50-lethal dose, which causes the death of 50% of tested animals (μg/kg body weight); ND = not determined.
Figure 5.
Molecular structures of cyanobacterial toxins (created by Author using ChemSketch).
Nodularins (NODs) are highly toxic pentapeptides with a similar mechanism of toxicity to MCs (Table 1) [91, 92]. NODs are predominantly produced by Nodularia spumigena [93, 94]. Nodularin expresses toxicity through the inhibition of serine-threonine phosphatases, thus impairing signal transduction [49]. These potent toxins are able to cause oxidative stress in cells, which may promote hepatotoxicity and carcinogenicity [95]. Their production is generally limited to saline/brackish environments and terrestrial symbiotic associations [96]. More data from the cumulative or synergistic effects of NODs are urgently needed.
Cylindrospermopsin (CYN) is a highly toxic guanidine alkaloid that may act through disruption of the synthesis of glutathione and protein and cytochrome P450. This toxic compound is known to cause a range of harmful effects in mammals, including hepatotoxicity, neurotoxicity, genotoxicity, cytotoxicity, and carcinogenicity [97, 98]. Cylindrospermopsin was chemically characterized from the species Raphidiopsis raciborskii (formerly Cylindrospermopsis raciborskii) [61, 64], and two congeners, 7-epi-cylindrospermopsin and deoxycylindrospermopsin, have been identified [62, 99]. Besides genera Raphidiopsis (also known as Cylindrospermopsis) [62], a number of cyanobacterial genera (Table 1) e.g., Umezakia [100], Aphanizomenon [101], Lyngbya [66], Anabaena [65], Chrysosporum [63], Dolichospermum (Anabaena), Oscillatoria, Phormidium, and Planktothrix [98] have been found to produce CYN. These cyanobacterial species occur mostly in tropical or subtropical regions [99, 102, 103], usually concentrated several meters below the water surface increasing the risk in drinking water supplies since water is usually drawn into treatment plants from that depth [68].
Saxitoxins (STX) are a group of tricyclic neurotoxic alkaloids [104] that have gained notoriety as paralytic shellfish poisons. These toxins are known to accumulate in shellfish Saxidomus giganteus, from which the first identification of saxitoxins was made [104]. STX is considered among the most toxic compounds of biological origin described to date [84], with an LD50 of 5 μ kg−1 in mice (i.p.) [37]. They cause symptoms like respiratory muscle paralysis. In freshwaters, STXs are mainly produced by filamentous cyanobacterial species belonging to the orders Nostocales (Dolichospermum circinale (formerly Anabaena circinalis), Aphanizomenon gracile, Cuspidothrix issatschenkoi, Raphidiopsis raciborskii, Raphidiopsis brookii, Scytonema sp.), and Oscillatoriales (Lyngbya wollei, Geitlerinema spp., Phormidium uncinatum) [82, 84, 105, 106]. STX analogs have been identified from the freshwater mat-forming cyanobacteria Lyngbya wollei [107, 108, 109]. Neosaxitoxin (NSTX) is a variant of saxitoxin with an additional hydroxyl group at the N1 position of the 1,2,3 guanidinium (N1-OH). Both toxin variants block the inward flow of sodium ions across the membrane channels [110].
Anatoxin-a (ATX-a) is a type of secondary bicyclic amine alkaloid [70] that is produced by several different genera of cyanobacteria—Dolichospermum (Anabaena) [67, 111], Anabaena [59, 112, 113], Aphanizomenon [59, 114, 115], Oscillatoria [59, 116, 117], Planktothrix [118], Cylindrospermum [59, 79], Microcystis [119], Raphidiopsis [74], Nostoc [120], Phormidium [121], Arthrospira [122], Hydrocoleum [123], and Cuspidothrix [124, 125, 126]. ATX-a is a potent postsynaptic depolarizing neuromuscular blocking agent and causes neurotoxic effects in vertebrates, including muscle fasciculation, gasping, decreased movement, abdominal breathing, cyanosis, convulsions, and death within minutes to hours by respiratory arrest [37, 79]. ATX-a degrades rapidly, with a half-life of 1–2 hours [38]. A methylene analog with a propyl group replacing the acetyl group, homoanatoxin-a, was isolated from Phormidium (Oscillatoria) formosa. Homoanatoxin-a mimics acetylcholine and binds to the nicotinic-acetylcholine receptors with higher affinity than acetylcholine [67].
Anatoxin-a(S) (ATX-a(S)) is a unique phosphate ester of a cyclic Nhydroxyguanine, which is produced only in species of Dolichospermum genus (D. lammermannii, D. flos-aquae, D. spiroides) [75, 76, 79, 108]. Anatoxin-a(S) is different in structure and toxicity mechanism from ATX-a [39] and was named due to salivation by intoxicated animals [64]. The clinical signs of toxicosis are similar to anatoxin-a, characterized by excessive salivation, watery eyes, nasal discharge, tremors, loss of balance, cyanosis, convulsion, muscle twitching and cramping, diarrhea, and seizures leading to death [75, 105, 110, 127]. ATX -a(S) toxicosis has been reported in dogs, pigs, and geese, with survival times ranging from 5 to 30 minutes. So far, there have not been detected structural variants. It is rare detection can be due to chemical instability [76].
In Ref. [128], for the first time, lipopolysaccharides (LPS) from the cyanobacterial species Anacystis nidulans were isolated. Lipopolysaccharides form a crucial component of the cell wall in Gram-negative bacteria, which includes cyanobacteria [129]. These complex molecules play a vital role in regulating the immune response. Lipopolysaccharides are pyrogenic, dermatoxic compounds that cause allergenic reactions in humans and animals [130]. This is also a tumor promoter due to the potent activation of protein kinase C. The largest producer of these toxins is Lyngbya sp. (Lyngbya majuscula and L. wollei), which also produce a large array of these toxins [131]. Three congeners of lyngbyatoxin have been isolated—lyngbyatoxin A, B, and C [132]. Aplysiatoxin and analogs thereof have been isolated from Lyngbya majuscula [133], Schizothrix calcicola [89], Oscillatoria nigro-viridis [89], and Trichodesmium erythraeum [134]. Naturally occurring aplysiatoxin analogs have also been identified [89, 134]. Similar to lyngbyatoxin, aplysiatoxins induce contact dermatitis through the activation of protein kinase C. Cyanobacterial LPS has a smaller toxic effect than LPS of other bacteria [135].
Beta-N-methylamino-L-alanine (BMAA) is a non-proteinogenic amino acid produced by diverse aquatic and terrestrial cyanobacteria [136]. BMAA has been shown to be neurotoxic in a variety of animal models [32]. Also, there is a possible connection with the induction of several neurodegenerative diseases, including amyotrophic lateral sclerosis, Parkinsons’ disease, and dementia [32]. The only study about known exposure of humans to BMAA involves a terrestrial food web [137]. A recent case study [138] detected BMAA in postmortem olfactory tissues of individuals with varying stages of Alzheimer’s disease.
Aquatic cyanobacterial strains produce a wide array of potent cyanotoxins able to cause environmental problems and health issues. Exposure routes to toxic cyanobacterial blooms (Figure 6) are mostly introduced through ingestion of contaminated drinking water [30, 139, 140], contaminated fish or shellfish [141, 142] and food and dietary supplements [143], recreational use of lakes and rivers [144], inhalation of aerosols [145, 146], receiving dialysis with contaminated water (e.g., which was documented in Brazil) [147, 148], or irrigation of agricultural products with contaminated water [35, 147, 149, 150]. Potential consequences of cyanotoxin exposure range from mere nuisances to serious health threats in humans and animals, even with fatal outcomes [11, 17, 18].
Incidents of human and animal intoxications, after exposure to toxic blooms through drinking and recreational waters, have been documented worldwide [11]. Animals have been affected mostly through ingestion and direct exposure to cyanotoxins in Australia, Switzerland, Sweden, Scotland, the USA, Kenya, South Africa, and Russia [11]. From the extensive database, which is provided by Svirčev et al. [11], Australia has experienced the highest incidence and severity of cyanotoxin poisonings where the Darling River experienced a massive proliferation of D. circinalis (formerly Anabaena circinalis), which led to the death of 10,000 livestock [151]. Death cases of humans have been documented through hemodialysis reported in Portugal [152, 153], USA [154], as well as in Australia, where 149 people were hospitalized after ingestion of water from reservoir tank contaminated with cyanobacterial bloom (formerly) C. raciborskii [155]. Furthermore, 2000 persons, of which 88 died, manifested gastrointestinal symptoms after drinking water from the newly built dam reservoir in Brazil contaminated with cyanobacterial toxins [155, 156]. In addition, cases of cyanobacterial intoxication through the food chain have been documented in the literature. Cyanotoxin presence in water used for irrigation may have considerable impact on the growth and development of plants [34, 35], and through the food chain, it can potentially affect human health [11, 157]. The toxic effects of BMAA have mainly been reported through ingestion. According to the most recent study [149], BMAA has been found in the irrigation water and grains of certain cereal plants from farmlands that are irrigated with Nile River water (Egypt). BMAA was also accumulated in most vegetable plants in the concentrations correlated with BMAA concentrations detected in relevant irrigation water sites [149, 150]. The highest levels were obtained in zucchini fruits, followed by watercress, tomato fruits, green pepper fruits, radish leaves, and pea fruits [149]. It has been found that long-term intake of BMAA through diet is linked to the development of neurodegenerative disorders in humans [158]. However, recent studies suggest that exposure to BMAA through inhalation may also provide risks for neurodegenerative issues [137]. Furthermore, cyanotoxins can be accumulated in the fishes and mussels exposed to cyanobacterial blooms. Annually, around 2000 cases of human poisoning are reported globally, with a 15% mortality rate caused by the consumption of fish or shellfish that have fed on marine dinoflagellates, which are producers of saxitoxins [159]. Hepatotoxicosis and neurotoxicosis are the most common syndromes caused by toxic cyanobacterial blooms. After acute contact with cyanobacterial bloom, possible health problems are weakness, diarrhea, vomiting, abdominal pain, skin irritation, irritation in the eyes, nose, and throat, asthmatic attacks, muscle tremors, nausea, tingling in fingertips and toes, dizziness, blurred vision, headache, fever, hypoxia, cyanosis, paralysis, and respiratory or cardiac arrest resulting in death [1]. Chronic exposure to low cyanotoxin concentration leads to liver damage [155] and the development of primary liver cancer, which is proven in China [15, 160], and colorectal cancer in the town of Haining [161], and recently, in a small clinical study, where MC/NOD and CYN were detected in all patients with hepatocellular carcinoma [162].
4. How to prevent the cyanobacterial blooms in water bodies and how to protect yourself and your companion animals
Preventing the appearance of cyanobacterial blooms is the most effective method for avoiding contamination of water with cyanotoxins. To help reduce cyanobacterial blooms from forming, it is important to:
reduce the amount of nutrients flowing into nearby water bodies by using only the recommended amounts of fertilizers on the farm, yard, and garden;
prevent wastewater from leaking into nearby water bodies by ensuring proper maintenance of the septic system;
reduce discharges from municipal and industrial wastewater treatment plants through biological, physical, or chemical measures.
Considering all that has been stated before, some precautionary steps need to be taken to prevent illness in your family and companion animals.
If you see signs of a bloom (e.g., smells bad—earthy odors, such as rotting plants; looks discolored; has foam, scum on the surface; has dead fish/other animals on its shore, etc), stay out of the water. Avoid eating fish and shellfish from water suspected of being contaminated with cyanobacteria. People should consult with a healthcare provider before taking food supplements containing cyanobacteria or giving them to a child. Do not fish, swim, boat, or play water sports in that area. Also, protect your pets and livestock from getting sick by keeping them away from water with possible cyanobacteria. Do not let animals drink the water, get into the water, lick or eat mats (of cyanobacteria), or eat dead fish, shells, and shrimps on the shore.
Nonetheless, if you or your companion animals do go in water possibly contaminated with cyanobacterial bloom, rinse yourself and your pets immediately afterward with tap water. Do not let pets lick their fur until they have been rinsed.
Cyanobacteria are charging ahead forcefully, supported by climate change, global warming, increased industrialization, and urban and farm pollution—eutrophication. This continues to affect human health as well as causing wildlife and domestic animal deaths through ingestion, inhalation, or dermal pathways. The infrequent research on cyanotoxins (aside from MCs) despite the high risks of human and animal intoxication cases, highlights the growing need for the development and application of effective water monitoring and management strategies. This is crucial for preventing cyanobacterial bloom occurrence and should be affordable for all geographic regions. In future research, it is important to share knowledge of this potential risk and how to take appropriate precautions to safeguard human health and companion animals and the health of the environment. Further, developing robust, precise, and inexpensive analytic techniques for the early detection of cyanotoxins should be one of the main aims of modern research. Given unequally distributed investigations and scientists, but equally distributed cyanotoxins in water bodies worldwide, we recommend introducing projects and workshops that would connect different countries and provide knowledge to both, the scientific community and those with a lower level of education. Because—Every little step is a huge step forward.
This work was supported by the Ministry of Science, Technological Development and Innovation of the Republic of Serbia (Grants No. 451-03-66/2024-2103/200125 & 451-03-65/2024-2103/200125).
I would like to express my deepest appreciation to my dear colleague Dr. Gorenka Bojadžija Savić for helpful contributions, constructive advice, and insightful suggestions.
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Written By
Dijana Lalić
Submitted: 27 April 2024Reviewed: 02 May 2024Published: 13 August 2024
Open access peer-reviewed chapter
