Algal toxins do not enter the marine environment from an external source but are generated during blooms of particular naturally occurring marine algal species. Such blooms have been referred to as toxic algal blooms, harmful algal blooms (HABs) and red tides. For example Gyrodiunium aureolum causes a red discolouration of the water (a red tide) and has been associated with shellfish and fish mortalities, particularly in marine fish farms. Chaetoceros, another alga, has spines which can physically clog and damage fish gills, leading to the death of cage-reared salmon and other species. Other algal species, such as Alexandrium and Dinophysis can cause poisoning through the food chain when shellfish ingest these algae (and their toxins) and are then subsequently consumed by fish, birds and potentially humans (Environment Agency 1998). The occurrence of blooms of these and other so-called toxic algae is perfectly natural but there are concerns that increases in the supply of essential nutrients (such as nitrogen, phosphorus) to the marine environment as a result of Man's activities may be contributing to the increased frequency and magnitude of these events.

Algal toxins can give rise to a number of different poisoning syndromes:

• NSP - neurotoxic shellfish poisoning;
• PSP - paralytic shellfish poisoning;
• ASP - amnesic shellfish poisoning;
• DSP - diarrhoetic shellfish poisoning;

All are caused by toxins synthesized by dinoflagellates, except for ASP, which is produced by diatoms of the genus Pseudonitzschia (WHOI 1995). Some species of microflagellates may also produce toxins, e.g. Chrysochromalina sp. A fifth human illness, ciguatera fish poisoning (CFP), is caused by benthic dinoflagellate toxins in coral reef communities. However, this does not represent a problem in UK waters.

The principal concern about the effects of algal toxins in the environment has been the contamination of sea food for human consumption and consequently much of the research and monitoring is directed at protecting humans from these effects. There must also be concerns on the effects of these toxins on natural populations of consumers (fish, birds and marine mammals).

Monitoring for the occurrence of toxic algae and their effects is carried out routinely by the Centre for the Environment, Fisheries and Aquatic Sciences (CEFAS) on behalf of MAFF in England and Wales, by Fisheries Research Services in Aberdeen on behalf of SERAD in Scotland and by DANI in Northern Ireland. The results of this monitoring is reported annually (e.g. Howard and Kelly 1997 and MAFF 1998).

Monitoring takes the form of the analysis of water samples for the presence and concentration of toxic algal species and the measurement of concentrations of algal toxins in samples of shellfish flesh. Standards for concentrations of algal toxins in shellfish flesh (so-called end product standards) have been set in The Food Safety (Fishery Products and Live Shellfish) Regulations 1998 as a requirement of the Shellfish (Hygiene) Directive. Breaches of these standards can result in the closure of a particular fishery for a period of time.

It is very difficult with current knowledge to determine the likelihood of toxic algal bloom occurrence, since bloom occurrence appears to be only loosely linked to nutrient levels (if at all), although it has been suggested by a number of authors that changes in salinity can stimulate either the growth or decline of toxic blooms. Other factors that have been cited for the reported increased occurrence of harmful algal blooms include increased awareness and monitoring (especially in relation to the effects on aquaculture), climate change and the transport of toxic algal species in the ballast tanks of vessels. Toxic dinoflagellate species also overwinter by forming spores which settle on the sea bed. These germinate and provide the inoculum for bloom development in future years. Consequently, once a toxic bloom has occurred for the first time, there is an increased risk of toxic bloom development at the same site in future years. Dinoflagellate spores remain viable for a relatively long period of time (certainly several, and perhaps tens, of years).

Algal toxins are naturally occurring compounds that are released into the environment, either when algal cells are ingested by filter feeding animals, or when algal cells are broken down after a bloom crashes. The fate and behaviour of these toxins in the marine environment is not well known but they will undergo microbial biodegradation when released into the environment.

Some dinoflagellate species of toxic algae form cysts that can accumulate in the sediment and act as an inoculum for a new population when conditions favour germination of the cysts.

An exhaustive literature review on the effects of algal toxins to marine organisms has not been carried out for the purposes of this profile. The information provided in this section is taken from existing general information and selected references.

The direct effects of blooms of toxic algae on marine organisms include:

• sub-lethal and lethal toxicity, especially to fish, birds and sea mammals;
• physical damage to fish gills.

Toxic phytoplankton can be filtered from the water by shellfish, such as clams, mussels, oysters, or scallops, which then accumulate the algal toxins to levels which can be lethal to consumers, including humans (Shumway 1990, Ahmed 1991). Typically, the shellfish are only marginally affected, even though a single clam can sometimes contain sufficient toxin to kill a human. Fish and shellfish can also be subject to sub-lethal effects, including increased susceptibility to disease and reduced growth.

Fish can be affected by algal toxins, either by direct uptake from the water column (planktivorous fish) or by bioaccumulation through the food chain (zooplankton and macroinvertebrates). In turn, these fish can then endanger whales, porpoises, seabirds, and other animals.

In addition to toxin production, algae have also been implicated in fishkills by the following direct methods:

• Mechanical damage to gills by algal spines, notably the serrated spines of Chaetoceros spp. (e.g. Yang and Albright 1992).
• Irritation of gills resulting in over-production of mucilage within the gills leading to suffocation (WHOI 1995).
• Physical blocking of the secondary lamellae of fish gills (Jones and Rhodes 1994).
• Increased water viscosity due to the secretion of polysaccharides (e.g. Hallegraeff 1992).

The principal indirect effects arise from changes in the oxygen balance of the water column associated with the presence of the bloom during its growth phase (supersaturation with oxygen during the day and oxygen depletion during the night) and the decay of the algal cells when the bloom has crashed (oxygen depletion of parts of the water column and possibly the sediments).

Algae have been implicated in fishkills by the following indirect methods:

• Asphyxiation caused by oxygen depletion (e.g. Brooker et al 1977). This can occur as a result of the oxygen demand generated by a senescent bloom, or at night due to extreme diurnal fluctuations in dissolved oxygen levels which may occur during algal blooms.
• Gas bubble trauma from extreme oxygen supersaturation (Renfro 1963).

Many algal toxins readily bioaccumulate in marine animals and significantly biomagnify through food chains posing a hazard to consumers at higher trophic levels (fish, birds and sea mammals).

Potential effects include:

• bioaccumulation and sub-lethal and lethal toxicity of a range of algal toxins to consumers at higher trophic levels (fish, birds and sea mammals). A precautionary approach to determining the scale of possible impacts of algal toxins should be adopted if the presence of toxic algal species or algal toxins is detected in a European marine site ;
• adverse physical effects on fish because of the presence of harmful algal blooms;
• hazards to all marine organisms resulting from changes to the oxygen balance of the water column, and potentially the sediments, both during and after a harmful algal bloom.

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