Cyanobacteria have
often been observed to be toxic: numerous fatalities of wild and domestic
animals after ingestion of cyanobacteria from drinking scum-contaminated water
are documented. A number of case studies of human illness after exposure
through drinking-water or recreation implicate cyanobacteria to be the cause of
symptoms such as dermal, gastrointestinal, respiratory, eye or ear irritation
and inflammation as well as nausea, diarrhoeae, vomiting, muscular pains, and
allergic reactions. Two epidemiological studies demonstrated an elevated rate
of symptom occurrence after exposure to cyanobacterial cells.
Some of the
substances causing these effects are known: Cyanobacteria contain a large
variety of oligopeptides, alkaloids, lipopolysaccharides and potentially other
substance groups. Depending on the substance, their effects include
hepatotoxicity, neurotoxicity, inflammations and dermal irritation, and for
some, there is limited evidence of tumour promotion and/or genotoxicity (for an
overview, see http://www.who.int/water_sanitation_health/dwq/chemicals/en/index.html
and www.cyanonet.org). Among these,
neurotoxic cyanobacterial blooms may cause high toxin levels that have been
implicated in some cases of acute animal poisoning, though these appear to
occur only occasionally. The cytotoxic alkaloid cylindrospermopsin, particularly
causing liver damage but also affecting kidneys and other organs, has been
found in high concentrations in some localities, particularly in warmer
climates. In freshwaters of temperate as well as tropical climates, the
currently available data indicate that the hepatotoxic peptides – i.e.
microcystins – are the most frequently occurring cyanotoxins, although
detection of cylindrospermopsin is also increasingly being reported. The
related peptide hepatotoxin – nodularin – is common in some brackish waters
worldwide.
For most of the
neurotoxins, microcystins, nodularin and for cylindrospermopsin, results of
toxicological experiments characterise mechanisms of toxicity and quantify at
least their acute toxicity (i.p. mouse LD50). Experiments with microcystins
showed substantial, dose-related liver tissue damage, at chronic exposure also
at low concentrations. Microcystins occur in the majority of the field
populations investigated so far, particularly of the genera Microcystis and Planktothrix. They are largely cell-bound, although cell death and
lysis in water-bodies or in drinking-water treatment may lead to release and
thus to high concentrations of dissolved microcystins. The World Health
Organisation gives a provisional Guideline-value for one of the structural
variants of microcystin, i.e. microcystin-LR, of 1 µg/L.
In water-bodies
with major cyanobacterial population development, microcystin concentrations in
the range of 10-100 µg/L may readily be found, particularly in surface scums.
If Planktothrix rubescens dominates,
such concentrations may also occur in deeper layers. In heavy blooms (“pea
soup”), concentrations reach the range of >1000 or even >10000 µg/L.
Microcystin
concentrations in water depend on the cell density or biomass per water volume
of the microcystin-containing cyanobacterial species. This in turn depends on
the “carrying capacity” for biomass in a given water-body as determined by
nutrient concentrations, in most cases phosphorus. Further environmental
factors, particularly water-body mixing and light conditions in the water, also
influence cyanobacterial proliferation. They determine the extend to which
cyanobacteria will be able make use of the carrying capacity and to dominate,
or whether other phytoplankton taxa have a better chance to win this
competition.
However, results
of a variety of bioassays indicate that cyanobacterial crude extracts often
show more toxicity than their content of known cyanotoxins accounts for. Vice versa, a large range of metabolites
is found in cyanobacteria, many of which show some enzyme inhibition or other
effects if tested in vitro, but whose effect on entire cells, tissues or
organisms has not yet been investigated. Current research, e.g. in the
EU-Project PEPCY (PEPtides in CYanobacteria; see www.PEPCY.de),
is endeavouring to reduce this knowledge gap. While possibly the known
cyanotoxins (see cyanotoxin overview)
comprise those most important to human health, hazard assessment should include
consideration of further effects of cyanobacteria – i.e. beyond those caused by
the known cyanotoxins.
For hazard
analysis and risk management, microcystins and other known cyanotoxins may
serve as indicators of cyanotoxin hazard occurrence and of system performance
in controlling the cyanotoxin hazard (somewhat in analogy to E. coli for pathogen contamination of
water). I.e. systems optimised towards minimising cyanobacterial proliferation
and/or eliminating known cyanotoxins – e.g. through sufficiently stringent
protection of the water-body and its catchment, or through drinking-water
treatment – are likely to be protective of unknown cyanotoxins as well.
However, just as some pathogens behave differently from E. coli in the natural environment, some cyanobacterial metabolites
will show transport and attenuation patterns which differ from those fairly
well-studied for microcystins. Validation of assumptions based on microcystin
monitoring may therefore be critical to ensure safety of water for human use.
For more
information about health hazard analysis for cyanotoxins č cyanotoxin literature