Environmental Engineering Reference
In-Depth Information
only to the high density of microscopic algal cells that colorize water, but also
includes blooms of highly toxic cells that can cause problems even at low cell densities,
i.e., a few hundred cells L
−1
. Therefore, the term Harmful Algal Blooms (HABs)
has been introduced to describe blooms of both toxic and non-toxic algae that
potentially have negative effects on humans and the environment (Anderson
2009
).
The reported global incidence of paralytic shellfi sh poisoning (PSP) that has been
associated with HABs has been increasing annually (Anderson
1989
). However, it
is still unclear whether the increase results from elevated public awareness and
reporting of HABs, or from an increase in anthropogenic factors, like increasing
marine pollution incidents.
Under normal conditions, HAB cells in aquatic environments exist at a negligible
concentrations, and therefore, are harmless. However, certain conditions trigger
harmful algal cell blooms, resulting in the secretion of high concentrations of potent
toxins, e.g., saxitoxin (STX) (Deeds et al.
2008
). All aquatic organisms are vulnerable
to saxitoxin except bivalves (e.g., mussels, clams, scallops, oysters, and butter clams).
This is because bivalves are fi lter feeders that consume plankton, which are then
transferred from gills to digestive organs wherein the toxins are concentrated (Soon
and Ransangan
2014
; Bricelj and Shumway
1998
).
Prolonged exposure to PSTs may produce mutations that increase the resistance of
shellfi sh to the toxin (Brivelj et al.
2005
). When this occurs, the mutated shellfi sh are
capable of accumulating toxins to a fatal concentration. PSP is caused by ingestion
of shellfi sh that are contaminated with one or more PST chemicals. Clinical symp-
toms of PST intoxication include numbness of the lips, tongue and fi ngertips, within
minutes after consumption, followed by numbness of neck, legs and arms, combined
with a feeling of lightness, dizziness and headache (Acres and Gray
1978
). Death by
respiratory failure can occur within 1-24 h post-ingestion (Rodrigue et al.
1990
).
However, for those who survive intoxication, no lasting effect remains after 24 h.
Several countries have established a regulatory action limit of 80
ʼ
g STXeg/100 g of
shellfi sh fl esh, which is equivalent to 0.2 g STXeq MU
−1
for STX in consumed food
(AOAC
1995
).
2
Paralytic Shellfi sh Toxins
PSTs are typically comprised of STX and STX-related compounds, and these are the
toxins that cause fatal PSP. The PSTs are water soluble neurotoxins that are respon-
sible for causing 50,000-500,000 human intoxications annually, and are estimated to
cause a 1.5% mortality rate (Wang et al.
2008
). PSTs cause a highly reversible and
specifi c sodium channel blockage of ion transport when present at an equimolar
ratio. The blockage is proposed to result from the binding of a positively charged
7,8,9-guanidinium group of STX to the negatively charged carboxyl groups at site 1 of
the sodium channel (Cestele and Catterall
2000
). This binding prevents conductance
of neuronal signals and causes muscular paralysis. In severe cases, death may result
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