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not reveal local patterns of residue accumulation in which grain-eating birds as well
as predatory ones sometimes contained lethal concentrations of cyclodienes.
5.3.4 T
of x i c i T y
o f
c
y c l of d i e n e s
There is strong evidence that the primary target for dieldrin, heptachlor epoxide,
endrin, and other cyclodienes in the mammalian brain is the gamma aminobutyric
acid (GABA) receptor, against which they act as inhibitors (Eldefrawi and Eldefrawi
1990). In insects, too, cyclodiene toxicity is attributed, largely or entirely, to the
interaction with GABA receptors of the nervous system. Toxaphene and gamma
HCH also act on this receptor. GABA receptors are found in the brains of both ver-
tebrates and invertebrates, as well as in insect muscle; they possess chloride channels
that, when open, permit the flow of Cl
−
with consequent repolarization of nerves and
reduction of excitability. They are particularly associated with inhibitory synapses.
In vertebrates, the action of cyclodienes can lead to convulsions.
Given this mode of action upon the central nervous system (CNS), it is not sur-
prising that cyclodienes can have a range of sublethal effects. These have been
observed in humans occupationally exposed to aldrin or dieldrin (Environmental
Health Criteria 91, Jaeger 1970). The symptoms observed included headache, dizzi-
ness, drowsiness, hyperirritability, general malaise, nausea, and anorexia. Sublethal
effects included characteristic changes in electroencephalogram (EEG) patterns,
and were observed over a wide range of blood concentrations. At the early stage
of intoxication, muscle twitching and convulsions sometimes occurred. According
to various authors, patients showing these symptoms had blood dieldrin levels in
the range 8-530 μg/L (Environmental Health Criteria 91). The relationship between
blood levels and the toxic effects of dieldrin in humans is shown in Figure 5.6. With
increasing tissue levels of dieldrin, severe convulsions occurred, leading eventually
1.0
Lethal poisoning (one individual)
0.8
Threshold for lethal intoxication
0.6
0.4
Threshold for convulsions
Threshold for clinical signs, e.g.,
hyperirritability
Subclinical effects, e.g., enzyme induction
No effect level
0.2
0.105
0
fIgure 5.6
Dieldrin intoxication in humans and its relationship to blood levels. The
hatched area represents the sublethal effects seen at 15-30% of lethal threshold concentration
in blood (after Jager 1970).
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