CYANOBACTERIAL TOXINS - Cyanobacteria - page 555

Human health risk assessment could be possible by determining the toxin levels in potable
and recreational water bodies. Knowledge on the nutrient status, periodicity in the development of
HABs, the prevalence of toxic cyanobacterial species, nature and types of toxins produced and the
level of toxins in these waters is very important. It is diffi cult to predict the concentration of toxins
in the cells or in water during a bloom because of differences in the proportion of toxin-producers
and non-toxin-producers within cyanobacterial populations. Despite this, the cellular contents of
cyanobacterial toxins visa-vis the level of toxins present in water bodies per unit volume have been
determined. Of the cyanobacterial toxins, nodularins were present to a maximum of 18 mg g -1 dry
weight (Sivonen and Jones, 1999). On the basis of the number of cyanobacterial cells ml -1 water, three
levels of adverse health effects have been recognised. Relatively low adverse health effects can be
expected if the number of cyanobacterial cells ml -1 are about 20,000 or in otherwords on the basis
of chlorophyll content if it is nearly 10 µg chlorophyll a L -1 . Moderate adverse health effects can
result when the cell number is around 100,000 cyanobacterial cells ml -1 or equivalent to 50 µg
chlorophyll a L -1 . High adverse health effects can arise due to scum formation by HABs. If in potable
or recreational water bodies, a situation favouring moderate risk prevails and if bloom samples
are predominantly represeted by Microcystis spp., then the MC level is likely to be 20 µg MC L -1
with average cellular MC content of 0.2 pg cell -1 or 0.4 µg MC µg chlorophyll a -1 . If the bloom
sample contains P . agardhii , then the levels of MCs can be 1-2 µg MC µg chlorophyll a -1 attaining
concentrations of 200-400 µg MC L -1 . As per WHO (1998) guidelines the value of permissible MC-LR
concentration in drinking water is 1 µg MC-LR L -1 . Moreover, the transition from moderate risk to
high risk level due to the formation of scums is found to be achieved very swiftly in a short period
of few h. Thus it becomes more obligatory to monitor the levels of toxic cyanobacteria on a day
to day basis as the toxin concentrations may be enhanced 1000 times or more than the guidelines
prescribed by WHO.
The conventional water treatment processes employ chlorination or ozonation and also use
ferric chloride and potassium permanganate and it is very likely the fi nished waters may contain
increased concentrations of MCs due to lysis of cyanobacterial cells (Lam et al ., 1995). The application
of copper sulphate or the use of organic copper-chelated algicide caused lysis of bloom samples
increasing concentrations of MCs from 4.7 µg L -1 to 1110 µg L -1 within 4 h post-treatment (Jones
and Orr, 1994). Human illness attributed to toxic cyanobacterial lysis following copper sulphate
treatment of drinking water sources has been reported from Charleston, West Virginia (Tisdale,
1931), Palm Island, Queensland, Australia (Bourke et al ., 1983) and Armidale, New South Wales,
Australia (Falconer et al ., 1983).
Occurrence of toxic blooms : Toxic blooms have been reported from almost all quarters of the
world.
Africa : The river Nile (used as drinking water source) at Sohag Province of Egypt supported the
development of blooms of O . tenuis which is a known producer of MCs (Brittain et al ., 2000). Many
fresh water bodies of Morocco developed toxic cyanobacterial blooms of the genera Microcystis ,
Synechocystis , Pseudoanabaena and Oscillatoria (Oudra et al ., 2002; Sabour et al ., 2002). Drinking water
contamination of toxic M . aeruginosa led to the poisoning of livestock in S. Africa (Van Halderen et
al ., 1995).
America : The development of toxic blooms in Canada, North America and South America is
described here. Majority of the Lakes and rivers in Northern America develop extensive blooms.
The magnitude of the development of a mixed bloom of M . aeruginosa and A . circinalis in St. Johns