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follow. These have included cases where the recovery of populations followed the
reduction of pollutant levels in the environment. Examples include the declines of
predatory birds caused by cyclodiene insecticides and p,p ′-DDE, and the decline
of dog whelks caused by tributyl tin. Here, other stress factors were evidently not
implicated in either the declines or the recoveries. However, now that action has
been taken to rectify problems such as these in most parts of the world, the effects of
pollutants are less easy to detect and may increasingly need to be seen in relation to
stress factors more generally.
From a toxicological point of view, stress needs to be seen in relation to the toxic
process as a whole (Figure 4.4). As the dose of a toxicant increases, organisms move
from a homeostatic state through a stressed state to a reversible disease state, before
finally reaching an irreversible disease state. Thus, although the impact of stress
needs to be taken into consideration in the early stages of intoxication, the more
serious effects in terms of health tend to come later when moving beyond stress to
fundamental disturbances of function that may lead to starvation, infertility, and
death. Indeed, it was effects of the latter kind that led to the population declines
referred to previously.
4.6
effectS of cHemIcaLS at tHe PoPuLatIon LeVeL
4.6.1 p o p u l a T i o n d y n a m i c s
In environmental risk assessment, the objective is to establish the likelihood of a
chemical (or chemicals) expressing toxicity in the natural environment. Assessment
is based on a comparison of ecotoxicity data from laboratory tests with estimated
or measured exposure in the field. The question of effects at the level of population
that may be the consequence of such toxicity is not addressed. This issue will now
be discussed.
Toxic effects upon individuals in the field may be established and quantified in a
number of assays. Lethal effects can be assessed by collecting and counting corpses
found in the field following the application of a chemical, as in field trials with new
pesticides. This is an imprecise technique because many individual casualties will
escape detection, especially with mobile species such as birds. With very stable pol-
lutants such as dieldrin, heptachlor epoxide, p,p ′-DDT, and p,p ′-DDE, the determina-
tion of residues in carcasses found in the field can provide evidence of lethal toxicity
in the field. Such data may also be used to obtain estimates of the effects of chemi-
cals upon mortality rates of field populations, which can then be incorporated into
population models (see Chapter 5, Section 5.3.5.1). Mechanistic biomarker assays
can also be used to quantify toxic effects in the field. Even when investigating cases
of lethal poisoning, relatively stable biomarker assays such as cholinesterase inhibi-
tion may be used to establish the cause of death so long as carcasses are relatively
fresh. Of particular interest is the use of biomarker assays to monitor the effects
of chemicals on living organisms in the field. Here, biomarker assays can provide
measures of sublethal toxic effects. Ideally, these should be nondestructive, to allow
serial sampling of individuals.
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