Pesticide Residues in Birds and Mammals - Pesticides: Evaluation of Environmental Pollution - page 397

label, they can also represent a hazard, especially under some circumstances (Swiggart
et al. 1972; Guitart et al. 1996b; Goldstein et al. 1999; Berny 2007; Martínez-Haro et al. 2008;
Anadón et al. 2009). For example, in a retrospective study of the US Geological Survey
National Wildlife Health Center (NWHC) mortality database from 1980 to 2000, in which
335 mortality events attributed to anticholinesterase poisoning involving 8877 carcasses
of 103 different avian species were analyzed, 14% of the mortality events were associated
with pesticide use, 10% with misuse, and 76% with undetermined use (Fleischli et al. 2004).
In another survey carried out in Spain in the period 1990-2006 with the cinereous vulture
( Aegypius monachus ), an endangered species worldwide that inhabits Mediterranean for-
ested areas, in which 241 incidents affecting 464 vultures were examined, the approved
use of pesticides was responsible for only 1.3% of the incidents, whereas up to 98% of them
were considered intentional poisonings (Hernández and Margalida 2008).
Lethal and sublethal exposures of animals to pesticides may result either from primary
consumption of the toxic bait (or solid or liquid formulations of pesticides) or, less com-
monly, from direct inhalation or dermal contact with the substance, or through secondary
contamination or poisoning (Vermeer et al. 1974; Newton 1998; de Snoo et al. 1999; Smith
et al. 2007; Vyas et al. 2007). Tertiary (and quaternary) expositions are also possible: a great
horned owl ( Bubo virginianus ) was found dead in Oregon under a tree after it fed on a red-
tailed hawk ( Buteo jamaicencis ) that died following ingestion of a black-billed magpie ( Pica
pica ) that obtained the insecticide famphur from the hair of dusted cattle (Henny et al.
1987).
Exposure to environmental pesticide contaminants can also be through transfer from
gravid females into the eggs in birds and through transplacental and lactational pathways
in mammals (Wolkers et al. 2004; Smith et al. 2007; Haraguchi et al. 2009; Miranda Filho
et al. 2009; Van den Steen et al. 2009b; Mwevura et al. 2010).
Short-term exposure is more often associated with acute or single ingestion, inhalation,
or topical contact with the pesticide. Secondary exposure can also occur with fast-acting
toxicants and thus also with short-term exposures, but is usually related to highly or mod-
erately persistent compounds, such as the organochlorine (OC) fungicide, hexachloroben-
zene (HCB), and several OC insecticides, or the ARs, and consequently, with long-term
or chronic exposures (Brakes and Smith 2005). As many OC pesticides are now banned
worldwide and their environmental levels are declining (Bignert et al. 1995; Addison and
Stobo 2001; Braune et al. 2001, 2005; Damstra et al. 2002; Herkert 2004; Aguilar and Borrell
2005; Verreault et al. 2005; Borrell and Aguilar 2007; Bustnes et al. 2007; Helgason et al.
2008; Walker et al. 2008a; Leonel et al. 2010; Rigét et al. 2010), there is growing concern
about the risk of secondary poisoning to valued wildlife populations due to ARs, and this
is manifested by an increasing number of reported studies in the scientific literature of the
last 15-20 years (Newton et al. 1990; Eason and Spurr 1995; Eason et al. 2002; Mineau and
Tucker 2002; Fournier-Chambrillon et al. 2004; Hoare and Hare 2006; Dowding et al. 2010).
On the other hand, there are some cases that pose problems in the distinction between
primary and secondary poisonings. Zinc phosphide, for example, is a rodenticide that is
hydrolyzed in the acidic environment of the stomach, liberating phosphine gas, which is
responsible for the inhibition of oxidative phosphorylation and the production of reactive-
oxygen free radicals (Plumlee 2004). As undigested zinc phosphide residues have been
shown to be localized almost entirely in the gastrointestinal tract of the target small
rodents, predators, and scavengers, consuming such poisoned animals can be a risk in fact
of primary hazard (Srterner and Mauldin 1995; Mauldin et al. 1996). Even the attending
veterinarians of poisoned animals can be at risk if phosphine is inhaled during nasogastric
intubation (Drolet et al. 1996), and care should be taken also during necropsy procedures.