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TECHNICAL


usually toxic to a broader range of organisms and also persist in the environment. The problem is made more difficult with chlorinated hydrocarbons especially, because of their susceptibility to biomagnification: an increasing concentration of insecticide in organisms at higher trophic levels, as a result of a repeated cycle of concentration of the insecticide in particular tissues in a lower trophic level, consumption by the trophic level above, further concentration, further consumption, and so on, until top predators which were never intended as targets, suffer extraordinary high doses. Figure 2 shows the process of biomagnification in the context of DDT. The DDT concentration is in parts per million. As the trophic level increases in a food chain, the amount of toxic build up increases. The x represent the amount of toxic build up accumulating as the trophic level increases. Toxins build up in organism's fat and tissue. Predators accumulate higher toxins than prey. The broadly toxic effects of herbicides have generally not been considered as great a problem as those of insecticides. One important reason is that many herbicides have a quite specific effect on plant physiology which has no exact equivalent in animal physiology. There are, though, a number of herbicides, for instance diquat and paraquat, which have high mammalian toxicity and where great care is therefore required in handling (especially in these cases there are no known antidotes). Furthermore, in the 1960s, a controversy began over the possible effects to human health of 2,4,5-T and 2,4-D, which were used in combination (‘Agent Orange’) between 1962 and 1970 to defoliate swamps and forests in South Vietnam. Of course, most weed-control practices affect a wider range of plants than the target species. The result has been the disappearance of many attractive ones that have never been serious weeds. Species such as wild delphinium (Delphinium ajacis), pheasant’s eye (Adonis annua), corn cockle, (Agrostemma githago)and cornflower (Centaurea cyanus), have come to the verge of extinction in Britain and can now only be found in abundance in the peasant agricultural systems of Eastern Europe.


Target pest resurgence


Of particular importance are the effects of insecticides on the natural (arthropod) enemies of an insect pest. This, in itself, may not appear too serious, apart from the regrettable loss in the natural diversity of harmless species. However, it can - and often has - had two extremely serious consequences.


The first, target pest resurgence, refers to the rapid increase in pest numbers following some time after the initial drop in pest abundance caused by an application of insecticide. This rebound effect occurs when treatment kills not only large numbers of the pest, but large numbers of their natural predators too (with any survivors likely to starve to death because there are insufficient pests on which to feed). Then, any pest


PC February/March 2019 129


Figure 2. Illustrating the problem of biomagnification that some of the early pesticides created by Øystein Paulsen - https://commons.wikimedia.org/wiki/File:Meganyctiphanes_norvegica2.jpg, CC BY-SA 3.0, https://commons.wikimedia.org/w/index.php?curid=69446831


individuals that survive (either because of resistance or good luck) or that migrate into the area, find themselves with a plentiful food resource but few if any natural predators. A population explosion is the likely outcome because the predator requires the pest to be present to support population growth, but the pest certainly doesn’t need the predator. Another reason is tied into what makes a pest: they are likely to be able to reproduce rapidly when food resource becomes available and they have the ability to locate these resources, i.e. good dispersal ability. Hence, pests are likely to be good at resurging.


Secondary pest outbreaks


When the natural predator cycle is broken, it is not only the target pest that might resurge.


Alongside any actual pest are likely to be a number of potential pest species, which are not pests only because they are kept in check by their natural enemies. Thus, if a primary pest is treated with an insecticide that destroys a wide range of predators and parasitoids, other species may realise their potential and become ‘secondary’ pests. A dramatic example of this took place in Central America in 1950; when mass dissemination of organic insecticides began, there were two primary pests within cotton production: the boll weevil and the Alabama leafworm. Organochlorines and organophosphates applied fewer than five times per year initially had apparently miraculous results and yields soared. By 1955, however, three further pests had emerged, cotton bollworm, cotton aphid and


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