Shellfish, such as mussels, can accumulate these toxins, making people who eat them sick with various symptoms, including the following 1 , 2 , 5 :. Diarrhetic Shellfish Poisoning DSP is caused by eating shellfish contaminated with okadic acid and dinophysistoxins, toxins produced by the dinoflagellates Dinophysis and Procentrum 1 , 2.
DSP produces stomach and intestinal symptoms that usually begin 30 minutes to a few hours after eating contaminated shellfish and include 1 , 2 :. Recovery occurs within about 3 days, with or without medical treatment. DSP is generally not life-threatening 1. AZP is believed to be caused by a dinoflagellate that produces toxins that have been found in Ireland, the Netherlands, Belgium, Morocco, and eastern Canada Eating contaminated shellfish can result in symptoms including :.
Contact exposures to marine HABs have been fatal for aquatic animals. Affected birds that came into direct contact with the bloom were covered in a slimy material produced by the algae. This material coated their feathers, affecting their natural water repellency. There were no confirmed reports of human illness related to this HAB, although there were anecdotal reports of illness from local surfers.
Marine HABs have also caused neurologic effects in animals including aquatic animals and birds 1 , 2. Over sea lions, seals, and birds died or were affected by a HAB produced by the diatom Pseudonitzschia australis near Monterey Bay, California. The HAB produced domoic acid, a neurotoxin, which was also detected in mussels, anchovies, and sardines that were likely eaten by the sea lions 3. Section Navigation.
Marine Environments Minus Related Pages. On This Page. Skin Contact and Inhalation. Literature review of Florida red tide: implications for human health effects. External Harmful Algae. Occupational exposure to aerosolized brevetoxins during Florida red tide events: effects on a healthy worker population.
External Environ Health Perspect. Initial evaluation of the effects of aerosolized Florida red tide toxins brevetoxins in persons with asthma. Environmental exposures to Florida red tides: Effects on emergency room respiratory diagnoses admissions. External Harmful algae. When these fish are eaten, the ciguatoxins can cause stomach and intestinal symptoms, including the following 2 , 4 : Diarrhea Abdominal pain Nausea Vomiting These symptoms often start within 12—24 hours of eating the contaminated fish and might last for up to 4 days 2.
Stomach and intestinal symptoms might be followed by or accompanied by symptoms related to the heart, blood vessels, and nerves, including 5 : Numbness and tingling in the extremities Dizziness Muscle aches Decreased heart rate Low blood pressure Weakness Heightened response to hot or cold temperatures Symptoms have been reported to last anywhere from a few weeks to years 2 , 6. Ciguatera fish poisoning: Treatment, prevention and management.
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External Woods Hole Oceanographic Institute. Distribution of HABs in the U. Ciguatera fish poisoning. External JAMA. Cyanobacterial poisoning in livestock, wild mammals and birds—an overview. External Adv Exp Med Biol. Cetinkaya F, Mus TE. Shellfish poisoning and toxins. Symptoms begin 1—3 hours after eating the contaminated shellfish and can include the following 3 : Numbness Tingling in the mouth, arms and legs Loss of coordination Vomiting Diarrhea Heightened response to hot or cold temperatures Symptoms usually resolve in 2—3 days 2. References Woods Hole Oceanographic Institute.
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Neurotoxic shellfish poisoning. Symptoms are generally mild and can include the following 1 : Numbness or tingling of the face, arms, and legs Headache Dizziness Nausea Loss of coordination A floating sensation Muscle paralysis and respiratory failure can occur in severe cases In cases of severe poisoning, muscle paralysis and respiratory failure can lead to death in 2—25 hours 1. With no direct information regarding the human health risks of cyanobacterial toxins in seafood as a function of degree of exposure dose-response , it is necessary to extrapolate information from animal toxicity studies.
There are several different types of animal studies used to identify hazards and to assess the dose-response.
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They include acute, sub-chronic, chronic, reproductive and developmental toxicity, as well as genotoxicity studies [ 8 ]. As only oral exposure is relevant when considering toxin exposure from seafood, animal studies in the published literature that were conducted in accordance with the OECD Guideline for the Testing of Chemicals for sub-chronic oral toxicity were assessed [ 8 , 9 ]. Where possible, experimental data from two species, one rodent and one non-rodent, was used.
To determine the safe dose of potentially toxic materials in the diet, toxicological data is used to calculate a Tolerable Daily Intake TDI. This is an estimate of the intake of a substance which is without appreciable health risk to consumers over their lifetime.
Types and Examples of Toxicity
However, as the cyanobacterial toxins are acutely toxic and consumers may eat large portion sizes on occasions, it is also appropriate to consider establishing an acute reference dose ARfD. The ARfD is used to assess the dietary risk for those consumers who eat high levels of seafood in a single meal or over a single day, while the TDI is used to assess the dietary risk for those consumers that eat the average level of seafood over a lifetime.
Uncertainty factors are applied to the NOAEL to allow for variations in individual sensitivity, extrapolation between human and animal studies and to account for uncertainties in data. The standard factors are 10 for intraspecies within human variability, 10 for interspecies rodent compared to human variability, and an additional third variable factor for limitations in data.
Limitations in the data that this additional factor may account for include: the use of only one sex or species of animal; possibility of mutagenicity or carcinogenicity; teratogenicity or reproductive toxicity. In the derivation of all health guideline values for cyanobacterial toxins in seafood refer to Section 3 below this additional factor was assigned a value of 2. For each of the toxins the limitations in the data that necessitated this value of 2 varied see below. It should be noted, however, that for none of the toxins did this value aim to allow for the fact the toxicity trials were sub-chronic rather than lifetime.
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For these toxins this was not regarded as a limitation in the data because the seasonality and irregularity of toxic cyanobacterial blooms mean that human exposure to the toxins will be acute to sub-chronic. To convert the TDI or ARfD into a health guideline value in seafood it is necessary to undertake an exposure assessment to incorporate information including the bodyweight of consumers; the quantity of seafood consumed; and whether the consumer may be exposed to the toxin via other sources for example, through drinking water or through recreational activities.
Average body weights for specific age groups that is 17 years or above and 2—16 years were sourced from recent national nutritional surveys [ 11 , 12 ]. For acute dietary risk assessment purposes and to protect consumers of high levels of seafood, data on the high-level consumption of fin fish, prawns and molluscs It is not possible to establish generic health guideline values which would be applicable to other regions of the world because seafood consumption patterns can vary considerably.
However, if average bodyweights and high-level consumption data are available then it is possible to use the outlined procedure to derive relevant health guideline values for other countries where seafood consumption patterns differ substantially from Australia and New Zealand. The survey used two hr recalls for all respondents.
For the purposes of estimating acute dietary exposures only a single day hour recall is used [ 12 ]; 3 Diadromous and freshwater fish consumption excluding all marine fish; 4 The food consumption data outlined in the table includes the amount consumed alone and as an ingredient in mixed foods. There were only 11 consumers of mussels in the 2—16 year age group dataset. In the context of this report the allocation factor is defined as the proportion of toxin exposure gained through the consumption of seafood. The only likely route of public exposure to cyanobacterial toxins would be through the consumption of seafood.
Drinking water is not sourced from the Gippsland Lakes and recreational use of the lakes is strongly advised against as soon as a significant cyanobacterial bloom occurs, as per the Guidelines for Managing Risks in Recreational Water [ 13 ]. It is appropriate to consider the acute dietary risks posed by the presence of cyanobacterial toxins in seafood as they are acutely toxic and consumers may eat large portion sizes on occasions.
Therefore, the establishment of maximum levels MLs for seafood should ideally be based on an acute dietary risk characterisation, which would be suitably protective of excessive chronic exposures as the target organ is the same following either a single or repeated dietary exposure.
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There is a paucity of data on the thresholds of acute oral toxicity for cyanobacterial toxins and therefore limited potential to establish an ARfD for cylindrospermopsin and microcystins. On this basis, a conservative approach has been taken where the high-level intake the Two population groups have been assessed; 17 years and above and 2—16 year olds. For the saxitoxins STXs , no acute dietary risk characterisation has been undertaken because the current Australian and New Zealand ML has proven to be an effective risk management limit.
By integrating the hazard identification, dose-response and exposure assessment information, health guideline values for cylindrospermopsin and microcystins in seafood can be derived. The steps are as follows:.
Harmful Algal Blooms
Health guideline values need to be derived for each cyanobacterial toxin separately using specific TDI or ARfD values and then for each seafood fish, prawns and mussels or molluscs separately using different average consumption values. Cylindrospermopsin CYN occurs in fresh and brackish waters worldwide, due to the presence of the cyanobacterial genera Cylindrospermopsis , Aphanizomenon , Anabaena , Raphidiopis , Lyngbya and Umezakia [ 14 ]. Studies of bioaccumulation of cylindrospermopsin in gastropod snails, bivalves [ 15 ], crustaceans [ 16 ], amphibian tadpoles and fish [ 17 ] demonstrated that this toxin is concentrated into tissues from free solution and from toxic Cylindrospermopsis cells.
Cylindrospermopsin appears in muscle tissue as well as viscera, increasing the possibility of consumption in these seafoods. Human poisoning from CYN has been previously recorded. In Palm Island in , for example, people received hospital treatment for an unusual hepatoenteritis after drinking water from a reservoir that was treated with copper to remove a Cylindrospermopsis algal bloom [ 18 ]. The absence of toxin exposure information, however, makes this case unusable for the purposes of deriving a TDI.
There have, however, been several published accounts of the oral toxicity of cylindrospermopsin in animals, with the majority of studies using a single dose [ 19 , 20 , 21 ]. Repeat oral dosing after a two week interval showed unexpectedly enhanced toxicity, indicating residual damage to the animals from the first dose [ 22 ].
A study by Humpage and Falconer [ 23 ], following the protocols set out by the OECD for subchronic oral toxicity assessment in rodents, exposed male Swiss Albino mice to cylindrospermopsin through drinking water and through gavage dosing by mouth [ 9 ]. The first trial used a cylindrospermopsin-containing extract from cultured Cylindrospermopsis raciborskii , supplied in drinking water for 10 weeks. The animals were examined clinically during the trial and showed no ill effects other than a small dose-related decrease in body weight compared to controls after 10 weeks.
Liver and kidney weights were significantly higher with increasing dose.