Environmental Engineering Reference
In-Depth Information
Despite the partial or total regulation of most OC pesticides, they are still ubiquitously
present in the environment. All these recalcitrant POPs are organohalogen compounds (as
also are some newly added pesticides to the list of new or potentially new POPs such as
chlordecone, endosulfan, and α-, β-hexachlorocyclohexane (HCH) and lindane (γ-HCH))
(Lohmann et al. 2007; Bhatt et al. 2009; Muir et al. 2010), which allow a sensitive detection
by means of the electron capture detector (ECD). Coupled to a gas chromatograph (GC),
the GC/ECD instrumentation played an important role in demonstrating the extent of
the contamination with these substances since mid-1960s (Lovelock 1991). Resolution of
analytes later improved with the introduction of the open tubular columns (“capillary
columns”) and selectivity with the substitution of the ECD by a single-quadrupole mass
spectrometer (MS). In the last few years, more sophisticated and powerful detection tech-
niques, such as tandem MS (MS
2
) or MS-time of flight (MS-TOF), and at present, some of
the current methods of choice to detect and quantify POPs and other pesticide residue con-
taminants and/or their transformations products became available, and the combination
with liquid chromatography (LC) allows even a larger-scale screening, identification, and
quantitation of pesticides in environmental samples (Barceló and Petrovic 2007; Margariti
et al. 2007; Muir and de Wit 2010; El-Shahawi et al. 2010; Petrovic et al. 2010).
Analytical chemistry and therefore chemical monitoring were and continue to be a cor-
nerstone for the assessment of wildlife exposure to POPs and other pesticides using resi-
due determination in the tissues and other biological material such as eggs, milk, or feces
(Peakall 1992; Keith 1996). However, biomarkers of response or toxic effect (Walker et al.
1996; Timbrell 1998) and thus biological monitoring are increasingly used in environmental
sciences to identify the impact of exposure to, and effects caused by, pesticides (Hoffman
et al. 1990; Walker 1995). A classic example was the work by Ratcliffe (1967), in which
he described decreases in eggshell thickness in peregrine falcons (
Falco peregrinus
) and
Eurasian sparrowhawks (
Accipiter nisus
) in Britain from 1946 onward. Eggshell thinning
related to DDT, and specifically its metabolite 1,1-bis-(4-chlorophenyl)-2,2-dichloroethene
(p,pʹ-DDE), is now well documented and has been considered the cause of reproductive
failure in raptors and fish-eating birds in the past (Hickey and Anderson 1968; Blus et al.
1972; Bignert et al. 1995; Blus 1996, 2003; Keith 1996; Newton 1998; Gervais et al. 2000; Giesy
et al. 2003; Kendall and Smith 2003; Henny et al. 2008b; Rattner 2009). Nevertheless, studies
on Canadian peregrine falcon, for example, suggest that eggshell thinning due to the high
DDE content in the eggs continued to be a problem until recently (Johnstone et al. 1996).
Acetylcholinesterase (AChE) (EC 3.1.1.7) activity is another frequently used biomarker to
verify, in this case, OP and CB exposure and effects (Newton 1998; Walker 1995; Mineau
and Tucker 2002; Berny 2007). These pesticides, mainly applied as insecticides, have been
widely used in agriculture since the ban on OCs in the 1970s. They are neurotoxicants
that inactivate AChE, which is the enzyme responsible for the breakdown of acetylcholine
into acetate and choline, through the inhibition by phosphorylation or carbamylation. The
neurotransmitter is present at the cholinergic nerve endings and myoneural junctions, and
accumulation in the synaptic cleft leads to cholinergic toxicity, characterized by tremors,
convulsions, and eventually death from respiratory failure. As chemical detection requires
GC or HPLC equipment with an appropriate and selective (but also expensive) detector
such as an MS, usually exposure to anticholinesterase agents determining the parent com-
pounds or their metabolites (there is the additional problem that some OPs and CBs are
rapidly metabolized) is substituted in many laboratories by the measurement of the AChE
activity in brain or the cholinesterase activity in the blood, plasma, or serum (Peakall 1992;
Keith 1996; Maul and Farris 2005; Berny 2007). Although the toxic effects of these com-
pounds are associated with the inhibition of AChE activities in the central nervous system
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