Within the context of ecotoxicology, the importance of the bioaccumulation (used in a general sense to describe situations where organisms acquire higher concentrations in their body than are present in their food and/or the ambient medium in which they live) of persistent pollutants in ecosystems became very clear in the late 1950s and early 1960s when populations of birds of prey were severely affected by residues of organochlorine insecticides. Sharp declines in population of sparrowhawk (Accipiter nisus) and peregrine (Falco peregrinus) in Western Europe were associated with residues of dieldrin and heptachlor epoxide originating from seed dressings (Ratcliffe 1980; Newton & Haas, 1984). The thinning of eggshells of raptors and fish-eating birds was associated with residues of pp'DDE (Cooke, 1973; Ratcliffe, 1980; Newton & Haas, 1984). During the same period in Sweden, birds of prey were affected by organomercury compounds used as fungicides (Brinck, 1967). In all these cases there was evidence of marked bioaccumulation of the compounds with movement along food chains. With the withdrawal of aldrin, dieldrin, heptachlor and DDT from most countries of Western Europe and North America, recoveries of populations of certain birds of prey (e.g. sparrowhawk and peregrine) were subsequently documented (Ratcliffe, 1980; Newton & Haas, 1984). Following these events there was a tendency to feel that the problem of bioaccumulation had been solved. Subsequent events were to prove that this was not the case. In 1969, a large kill of fish-eating sea birds (mainly guillemots [Uria aalge] and razorbills [Alca torda]) occurred in the Irish sea, and the birds were found to contain high levels of polychlorinated biphenyls (PCBs). A subsequent investigation implicated PCBs in the disaster but suggested that they were not the primary cause, although a substantial proportion of birds contained residues in liver sufficiently high to cause death in cormorants (Phalacrocorax aristotelis) (NERC Report, 1971; Koeman et al., 1973; Walker, 1990). More recently several studies have shown that high levels of some 15-20 PCB congeners are still to be found in top predators, despite the withdrawal of PCB mixtures from the market (Norstrom, McKinnon & de Freitas, 1976; Borlakoglu, Wilkins & Walker, 1988). Significant levels of certain highly toxic polychlorodibenzodioxins (PCDDs) and polychlorinated dibenzofurans (PCDFs) have also been reported in fish-eating sea birds (Van den Berg et al., 1987). Organotin compounds have been shown to be effectively bioaccumulated by shellfish. Their implication in the decline of oyster populations when used as antifouling agents in marine paints was a factor leading to their withdrawal from the British Market. Finally, there is evidence that second generation anticoagulant rodenticides (e.g. brodifacoum, bromadiolone and difenacoum) may be bioaccumulated in the livers of predators (e.g. owls) and scavengers (e.g. corvids) which feed upon rats and mice. Why do these lipophilic compounds undergo bioaccumulation in ecosystems? This is not simply an academic question, since an understanding of the critical processes leading to bioaccumulation is fundamental to the solution of an important practical question -how can the risks of bioaccumulation in ecosystems be predicted? How can the potential hazards of new pesticides be assessed? Because of the complexity of ecosystems, there is no single answer to this question and there is no single model or system that will predict all cases of bioaccumulation. In the following account, bioaccumulation will be considered in two distinct situations: 1 Aquatic systems. 2 Terrestrial organisms. In each case model systems will be discussed which may be useful for the prediction of risks of bioaccumulation of lipophilic pollutants.
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