57
During the early 1950s, organochlorines, the earliest generations of synthetic
pesticides, were used in huge quantities in farms and forests. Organochlorines like
dichlorodiphenyltrichloroethane (DDT), cyclodienes, and hexachlorocyclohexanes
(HCHs) have the property to remain unchanged in the environment for long time.
Due to their lipophilic nature or high octanol-water (Kow) and octanol-air partition
(Koa) coefficients, warm-blooded organisms (i.e. birds and mammals) cannot
excrete easily through, instead getting accumulated in adipose tissue and undergoing biological magnification (Odabasi and Cetin 2012). The book ‘Silent Spring’
authored by Rachel Carson (Carson 1962) raised the issue of the environmental
risks of use of organochlorines especially DDT. The book elucidated publicly for
the first time how indiscriminate application of pesticides and other chemicals is
polluting water bodies, impairing birds and animals, and causing health problems in
humans (Carson 1962). Although most toxic organochlorines (DDT and several
cyclodiene compounds) were restricted and banned in many countries, gradually
(since 1980), the second-generation, less persistent pesticides like organophosphates and carbamates and synthetic pyrethroids become the popular agriculture
pesticides replacing DDT and cyclodienes. Both organophosphates and carbamates
exert their effect to both invertebrates and vertebrates through inhibition of acetylcholinesterase at the cholinergic synapses in the nerve endings (Bishop et al. 1998).
Accumulation of the neurotransmitter acetylcholine at nerve terminals and neuromuscular junctions leads to incessant transmission having consequences like seizures, respiratory failure, and, eventually, death (Pope et al. 1995; Marrs 1996;
Testai et al. 2010) (Fig. 3.1). In human, organophosphate exposure at sublethal
doses for longer duration can lead to cancer, diabetes, and neuronal disorders like
Alzheimer’s and Parkinson’s disease (Amani et al. 2016). As organophosphate and
carbamates are easily metabolised and readily excreted from the body, they were
once considered safe to nontarget organisms. But unfortunately, a number of reports
have shown an alarming decline of birds (namely, sparrow-hawk, mallard, and
brown pelicans) in the last five decades due to pesticide toxicity (Mineau 1993;
Mineau et al. 1999, 2005; Pain et al. 2004; Mineau and Palmer 2013). The secondgeneration pesticides have the potential to cause lethal effect in birds as birds are
more sensitive to cholinesterase inhibitors than other vertebrates (Table 3.1)
(predicted LD 50 (lethal dose) values in sensitive birds are below 1 mg kg
−1
body
weight, whereas in rat this value is <10 mg kg
−1
body weight) (Mineau et al. 2001;
Health and welfare Canada 1987). The rate of binding of cholinesterase inhibitors
like organophosphate and carbamates to acetylcholinesterase is more rapid than
other vertebrates (Westlake et al. 1983; Hill 1992) because acetylcholinesterase
has higher activity in the brains of bird. In different species of avian fauna brain
acetylcholinesterase activity ranges from 7.4 to 19.8 μmol/min/g tissue (Shimshoni
et al. 2012). As Mineau (2009) described, the abrupt deactivation of the critical
cholinesterase in bird’s brain and peripheral nervous system leads to ‘shortcircuiting’ neural connections having a multitude of fatal consequences.
As birds play a central role in ecosystem functioning, healthy avian populations
are symbolized for ecological stability because they are highly potential for rapid
detection of environmental damages (Wayland et al. 2001; Smits and Fernie 2013).
3 Toxic Effects of Pesticides on Avian Fauna
During the early 1950s, organochlorines, the earliest generations of synthetic
pesticides, were used in huge quantities in farms and forests. Organochlorines like
dichlorodiphenyltrichloroethane (DDT), cyclodienes, and hexachlorocyclohexanes
(HCHs) have the property to remain unchanged in the environment for long time.
Due to their lipophilic nature or high octanol-water (Kow) and octanol-air partition
(Koa) coefficients, warm-blooded organisms (i.e. birds and mammals) cannot
excrete easily through, instead getting accumulated in adipose tissue and undergoing biological magnification (Odabasi and Cetin 2012). The book ‘Silent Spring’
authored by Rachel Carson (Carson 1962) raised the issue of the environmental
risks of use of organochlorines especially DDT. The book elucidated publicly for
the first time how indiscriminate application of pesticides and other chemicals is
polluting water bodies, impairing birds and animals, and causing health problems in
humans (Carson 1962). Although most toxic organochlorines (DDT and several
cyclodiene compounds) were restricted and banned in many countries, gradually
(since 1980), the second-generation, less persistent pesticides like organophosphates and carbamates and synthetic pyrethroids become the popular agriculture
pesticides replacing DDT and cyclodienes. Both organophosphates and carbamates
exert their effect to both invertebrates and vertebrates through inhibition of acetylcholinesterase at the cholinergic synapses in the nerve endings (Bishop et al. 1998).
Accumulation of the neurotransmitter acetylcholine at nerve terminals and neuromuscular junctions leads to incessant transmission having consequences like seizures, respiratory failure, and, eventually, death (Pope et al. 1995; Marrs 1996;
Testai et al. 2010) (Fig. 3.1). In human, organophosphate exposure at sublethal
doses for longer duration can lead to cancer, diabetes, and neuronal disorders like
Alzheimer’s and Parkinson’s disease (Amani et al. 2016). As organophosphate and
carbamates are easily metabolised and readily excreted from the body, they were
once considered safe to nontarget organisms. But unfortunately, a number of reports
have shown an alarming decline of birds (namely, sparrow-hawk, mallard, and
brown pelicans) in the last five decades due to pesticide toxicity (Mineau 1993;
Mineau et al. 1999, 2005; Pain et al. 2004; Mineau and Palmer 2013). The secondgeneration pesticides have the potential to cause lethal effect in birds as birds are
more sensitive to cholinesterase inhibitors than other vertebrates (Table 3.1)
(predicted LD 50 (lethal dose) values in sensitive birds are below 1 mg kg
−1
body
weight, whereas in rat this value is <10 mg kg
−1
body weight) (Mineau et al. 2001;
Health and welfare Canada 1987). The rate of binding of cholinesterase inhibitors
like organophosphate and carbamates to acetylcholinesterase is more rapid than
other vertebrates (Westlake et al. 1983; Hill 1992) because acetylcholinesterase
has higher activity in the brains of bird. In different species of avian fauna brain
acetylcholinesterase activity ranges from 7.4 to 19.8 μmol/min/g tissue (Shimshoni
et al. 2012). As Mineau (2009) described, the abrupt deactivation of the critical
cholinesterase in bird’s brain and peripheral nervous system leads to ‘shortcircuiting’ neural connections having a multitude of fatal consequences.
As birds play a central role in ecosystem functioning, healthy avian populations
are symbolized for ecological stability because they are highly potential for rapid
detection of environmental damages (Wayland et al. 2001; Smits and Fernie 2013).
3 Toxic Effects of Pesticides on Avian Fauna