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Newsletter and Technical Publications
Freshwater Management Series No. 5
Guidelines for the Integrated Management of
the Watershed
- Phytotechnology and Ecohydrology -
B. Modification of algal succession to limit toxic algal blooms
Problems with toxic cyanobacterial bloom formation
The storage of good quality water is the
primary objective of the reservoir management. Drinking water supplies
especially have a requirement for high water quality. But even when reservoir
waters are impounded for industrial use, fisheries, or recreation, the
impounded water have greater utility if they are relatively clean. The design
features of reservoirs, such as surface area and volume of reservoirs relative
to river flows and the locations of inlet and outflow structures, can influence
these water quality conditions.
Small (volume = 106- 08
m3), shallow lowland reservoirs, especially those used as sources of
drinking water, and for fish cultivation, irrigation, and recreation, are
sometimes characterised by long water retention times. These reservoirs are
ecosystems that are especially susceptible to eutrophication (Taub 1984,
Staskraba et al. 1999a, Zalewski
1999). This is caused by:
- runoff of agrochemicals from
agricultural land uses in catchment;
- high catchment area to reservoir area ratios, and high nutrient inputs;
- intensive sedimentation of both particulate and dissolved matter
in the reservoir;
- disruption
of the biotic structure as a consequence of frequent and/or significant changes
in water levels during a year; and
- the
absence of a properly working littoral zone as a consequence of the water level
fluctuations.
Eutrophication in reservoirs leads to the
formation of intensive phytoplankton blooms. During recent years, both the
incidence and intensity of such blooms appear to be increasing, when examined
at the global scale. This increasing severity of algal blooms may be a
consequence of increasing levels of nutrient enrichment as a result of sewage
disposal, increased agricultural runoff, and changes in hydrological regimes
potentially related to climate change.
The term, "bloom," describes a phytoplankton biomass
significantly higher than the average biomass during a year. According to
Nebaeus (1984), phytoplankton biomass greater than 3 mg/l,
or chlorophyll-a concentrations above 20 mg/m3,
constitute a bloom. Cyanobacterial, or blue-green algal, blooms can occur in
different portions of the water column (Figure 8.2). In tropical water bodies,
blooms also can take place throughout the year. In temperate regions, however,
there is often a characteristic seasonal development of bloom-forming algal
populations. These blooms usually comprise one or two species identified by the
dominant phytoplankton type or genera; e.g., diatom blooms, cyanobacterial
blooms, Microcystis blooms, Scenedesmus blooms, etc.
Phytoplankton blooms can degrade water quality in
several ways by:
- decreasing water
column transparency,
- affecting the
taste and odour of the water,
- depleting deep
water oxygen concentrations1,
- changing fish
community composition,
- decreasing the
abundance of submerged macrophytes and shifting aquatic plant communities
toward those dominated by a few species of bloom-forming algae,
- producing toxic
compounds that pose an health hazard to people and animals.
One of the most dangerous effects of cyanobacterial
blooms is the release of secondary metabolites, many of which are very toxic
(Carmichael 1992, Codd and Bell 1998, Chorus and Bertram 1999), into the
environment. This consequence is often exacerbated by water treatment
techniques that cause the algal cells to lyse, releasing the cell contents
including the toxins into the treated water. In addition, when these compounds
are chlorinated, some can produce trihalomethanes, which are human carcinogens.
Cyanobacterial biotoxins fall into four classes:
hepatotoxins, neurotoxins, dermatotoxins, and lipopolysaccharides (Table 8.1).
These substances are often algal genera, species-, or strain-specific.
Hepatotoxic microcystins are the most common of the cyanobacterial toxins. They
have the form of cyclic peptides, and can cause death through haemorrhages of
the liver. Mortality can occur over a time period ranging from a few minutes to
a few days after intoxication. Microcystins also are carcinogens, which have
tumour-causing properties, primarily leading to liver cancers (Ueno
et al. 1996). Hepatotoxic cyanobacterial
extracts can induce chromosomal aberrations in human cells (Figure 8.3), and
can occur as a consequence of long-term, chronic exposure of humans to
cyanobacterial toxins. Such exposure can occur via drinking water, as
conventional water treatment processes are ineffective in removing toxins
during water purification process (Chorus and Bertram 1999).
1 Note: Many tropical systems
naturally stratify as a consequence of the temperature-density relationships
pertaining within those systems, and often develop anoxic or anaerobic
hypolimnia as a consequnce of this stratification, whereas temperature systems
generally develop anoxic or anaerobic hypolimnia as a consequence of the
decomposition or oxidation of organic matter settling into the hypolimnion as a
consequence of high levels of biological production resulting from the
eutrophication of those systems. For this reason, Ryding and Rast (1989) suggest
that hypolimnetic deoxygenation alone not be considered a eutrophication
indicator in tropical lakes and reservoirs. Rather, a combination of indicators
is recommended to support the diagnosis of eutrophic conditions in these lakes.
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Fig. 8.2. Typical locations of
phytoplankton blooms in thermally-stratified, shallow lakes or reservoirs:
1 - shoreline scums; 2 - planktonic scums on open water; 3 - phytoplankton
scums in or on the lake sediments; 4 - dispersed populations of phytoplankton
within the epilimnion; 5 - homogeneous populations of phytoplankton dispersed
throughout the water column during well-mixed, non-stratified conditions; 6 -
scums under ice; 7 - sub-surface or metalimnetic phytoplankton maxima (modified
from Lindholm and Meriluoto 1989) |
Toxic
cyanobacterial blooms have caused massive mortalities among wild and domestic
animals (Codd et al. 1997), and have
constituted a hazard to human health principally through gastric upsets and
diarrhoea arising from the ingestion of polluted water and contaminated foods,
and skin irritations. Many data concerning the effects of poisoning from
cyanobacterial toxins in humans comes from tropical and subtropical areas in
Australia, Africa, and South America (Falconer 1994). The first well-documented
human fatalities, in which cyanobacterial toxins were implicated, were
described in Brazil in 1996. More then 50 patients died after displaying
hepatotoxic and neurotoxic symptoms following treatment in a haemodialysis
centre (Puoria et al. 1998). Because
of the epidemiological character of cyanobacterial toxins, the World Health
Organization recommended safety guidelines for the maximum concentrations of
microcystin in drinking water is 1 µg/l (WHO 1998).
Tab. 8.1. Cyanobacteria reported in the literature as having toxic properties |
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Toxin classes |
Cyanobacterial genera |
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| Hepatotoxins |
microcystins |
Microcystis, Anabaena, Plantotrix (Oscillatoria),
Nostoc, Anabaenopsis |
nodularins |
Nodularia |
cylindrospermopsins |
Cylindrospermopsis,
Aphanizomenon, Umezakia |
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| Neurotoxins |
anatoxin-a |
Anabaena, Plantotrix (Oscillatoria), Cylindrospermum,
Aphanizomenon Anabaena |
anatoxin-a(s) |
Aphanizomenon, Anabaena, Cylindrospermopsis, Lyngbya |
saxitoxins |
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| Dermatotoxins |
lyngbyatoxin-a |
Lyngbya |
aplysiatoxins |
Lyngbya,
Plantotrix (Oscillatoria), Schizothrix |
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| Lipopolysaccharides |
many cyanobacteria |
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| Fig. 8.3. Chromosomal aberrations induced by extracts from
cyanobacterial blooms in in vitro human
lymphocytes: A - chromatid breakdowns, B - chromatid exchanges, and C - dicentric chromosomal and acentric fragmentation (Kontek et al. 1997) |
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