Neurotoxicity and Behavioral Effects of Environmental Chemicals - Organic Pollutants: An Ecotoxicological Perspective - page 294

Claviceps purpurea . Indeed, these natural toxins have given many useful leads in the
design of new pesticides, biocides, or drugs.
In earlier chapters, many examples were given of lethal effects and associated neu-
rotoxic or behavioral effects or both caused by pesticides in the field. These included
effects of organomercury fungicides upon birds (Chapter 8, Section 8.2.5), organo-
chlorine insecticides on birds, and both organophosphorous and carbamate insecti-
cides upon birds (Chapter 10, Section 10.2.4). Also, a retrospective analysis of field
data on dieldrin residues in predatory birds in the U.K. suggested that sublethal neu-
rotoxic effects were once widespread and may have contributed to population declines
observed at that time (Chapter 5, Section 5.3.5.1). Lethal and sublethal effects of neu-
rotoxic insecticides upon bees is a long-standing problem (see Chapter 10, Section
10.2.5). Speaking generally, it has been difficult to clearly identify and quantify neuro-
toxic and behavioral effects caused by pesticides to wild populations, especially where
the compounds in question have been nonpersistent (e.g., OP, carbamate, or pyrethroid
insecticides), and where any sublethal effects would have been only transitory.
It is very clear, therefore, that there have been many examples of neurotoxic effects,
both lethal and sublethal, caused by pesticides in the field over a long period of time.
Far less clear, despite certain well-documented cases, is to what extent these effects,
especially sublethal ones, have had consequent effects at the population level and
above. Interest in this question remains because neurotoxic pesticides such as pyre-
throids, neonicotinoids, OPs, and carbamates continue to be used, and questions con-
tinue to be asked about their side effects, for example, on fish (Sandahl et al. 2005),
and on bees and other beneficial insects (see, for example, Barnett et al. 2007).
The present account will consider, in a structured way, how neurotoxic com-
pounds may have effects upon animals, and how these effects can progress through
different organizational levels, culminating in behavioral and other effects at the
“whole animal” level. Emphasis will be placed upon the identification and quanti-
fication of these effects using biomarker assays, and upon attempts to relate these
biomarker responses to consequent effects at the population level and above, refer-
ring to appropriate examples. The concluding discussion will focus on the use of this
approach to identify and quantify existing pollution problems and on its potential in
environmental risk assessment.
In the first place, there are a number of different sites of action for toxic chemicals
within the central and peripheral nervous system of both vertebrates and inverte-
brates. When studying the effects of neurotoxic compounds, it is desirable to monitor
the different stages in response to them using appropriate biomarker assays, begin-
ning with initial interaction at the target site (site of action), progressing through
consequent disturbances in neurotransmission, and culminating in effects at the level
of the whole organism, including effects upon behavior. Thus, in concept, a suite of
biomarker assays can be used to measure the time-dependent sequence of changes
that follows initial exposure to a neurotoxic compound—changes that constitute the
process of toxicity. From integrated studies of this kind should come principles and
techniques that can be employed to develop and validate new approaches and assays
for the purpose of environmental monitoring and environmental risk assessment. In
reality, however, only a very limited range of biomarker assays are available at the
time of writing, and much work still needs to be done to realize this objective.