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shell thinning caused by
p,p
′-DDE residues of 19-30 ppm in eggs. Subsequently,
pollution of the St. Lawrence river by DDT was reduced. The
p,p
′-DDE levels in
the gannets fell, and by the mid- to late-1970s, shells became thicker, reproductive
success increased, and the population recovered (Elliott et al. 1988). Taken overall,
these findings illustrate very clearly the ecological risks associated with the wide
dispersal of a highly persistent pollutant that can have sublethal effects.
Evidence for effects of
p,p
′-DDE on eggshell thickness and productivity has also
come from studies on Golden eagles (
Aquila chrysaetos
) conducted up to the late
1990s in Western Norway (Nygard and Gjershaug 2001). Their evidence suggests
that this species may be particularly sensitive to DDE-induced eggshell thinning,
and the results are broadly comparable to those from earlier work on this species
conducted in Scotland (Ratcliffe 1970).
Before leaving the question of effects of DDT and its derivatives upon popula-
tions, brief mention should be made of indirect effects. Sometimes insect populations
increase in size because an insecticide reduces the numbers of a predator or parasite
that keeps the insects' numbers in check. Such an effect was found in a controlled
experiment where DDT was applied to a brassica crop infested with caterpillars of
the cabbage white butterfly (
Pieris brassicae
; see Dempster in Moriarty 1975). Field
applications of DDT severely reduced the population of carabid beetles, which prey
upon and control the numbers of
Pieris brassicae
larvae. The infestation of the crop
was initially controlled by DDT but, as the residues declined on the crop, the caterpil-
lars eventually returned to reach much higher numbers than on control plots untreated
by DDT, where natural predators maintained control of the pest. Thus the long-term
indirect effect of DDT was to increase the numbers of the pest species. When DDT
was used as an orchard spray, it was implicated, together with certain other insec-
ticides, in the triggering of an epidemic of red spider mites (Mellanby 1967). The
insecticides successfully controlled the capsid bugs (e.g.,
Blepharidapterus angula-
tus),
which normally keep down the numbers of red spider mites, and this led to
a population explosion of the latter—and to a new pest problem! These examples
illustrate well a fundamental difference between ecotoxicology and normal medical
toxicology. The well-established test procedures of the latter may tell us very little
about what will happen when toxic chemicals are released into ecosystems.
5.2.5.2 effects on Population genetics (gene frequencies)
DDT had not been in general use for very long before there were reports of DDT resistance
in insect populations that were being controlled by the insecticide. Examples included
resistant strains of houseflies (
Musca domestica
) and mosquitoes (Georghiou and Saito
1983; Oppenoorth and Welling 1976). For further discussion, see Brown (1971). Two
contrasting resistance mechanisms have been found in resistant strains of housefly. The
first is metabolic resistance, usually due to enhanced levels of DDT dehydrochlorinase.
In one resistant strain of housefly, enhanced monooxygenase activity was found, which
might cause increased rates of detoxication to kelthane and other oxidative metabolites
(Oppenoorth and Welling 1976). By contrast, some houseflies showed “knockdown”
resistance (“kdr” or “super kdr”), due to nerve insensitivity. It now seems clear that this
is the consequence of the appearance of a mutant form (or forms) of the Na
+
channel
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