Birds pesticide toxicity

Luttik R, Aldenberg T. 1997. Extrapolation factors for small samples of pesticide toxicity data Special focus on LD50 values for birds and mammals. Environ Toxicol Chem 16 1785-1788. 

Walker CH, Johnston GO. 1993. Potentiation of pesticide toxicity in birds role of cytochrome P-450. Biochem Soc Trans 21 1066-1068. 

Diazinon, the active ingredient in products such as Diazinon, Basudin, and Knox Out. is a nonsystemic OP insecticide. Diazinon has a half-life in soil of 2-4 weeks (Pesticide Information Profiles, 1996). In water, diazinon s half-life is related to pH, with faster breakdown related to increasing pH, whereas in neutral conditions, half-life can be as long as 6 months (Pesticide Information Profiles, 1996). Although use of diazinon on golf courses and. sod farms in the United States was banned in 1988, primarily due to its high toxicity and lethality to birds (Pesticide Information Profiles, 1996), diazinon is still widely used in Canada, although several bird deaths have been reported (Frank et ui, 1991). 

The effects of pollution can be direct, such as toxic emissions providing a fatal dose of toxicant to fish, animal life, and even human beings. The effects also can be indirect. Toxic materials which are nonbiodegradable, such as waste from the manufacture of insecticides and pesticides, if released to the environment, are absorbed by bacteria and enter the food chain. These compounds can remain in the environment for long periods of time, slowly being concentrated at each stage in the food chain until ultimately they prove fatal, generally to predators at the top of the food chain such as fish or birds. 

Walker, C.H. (1983). Pesticides and birds— mechanisms of selective toxicity. Agriculture, Environment, and Ecosystems 9, 211-226. 

Just like mammals, birds have a delayed reaction to lipotropHc pesticides such as OCPs and their metabolites. These toxic substances dissolve and accumulate in the fatty tissues of well-fed birds, and are comparably harmless in this form. However, once the bird starts using the stored fat (at the end of a long flight or when laying eggs), the substances are carried through the bloodstream to the brain, liver, or yolk of the egg, and poison all the systems [1]. In particular, well-fed raptors have lower DDE concentrations in their liver (0.5 mg/kg) than less well-fed (3.5 mg/kg) and emaciated birds (7.3 mg/kg) [6]. 

Schafer, E.W. 1972. The acute oral toxicity of 369 pesticidal, pharmaceutical and other chemicals to wild birds. Toxicol. Appl. Pharmacol. 21 315-330. 

Tucker, R.K. and M.A. Haegele. 1971. Comparative acute oral toxicity of pesticides to six species of birds. Toxicol. Appl. Pharmacol. 20 57-65. 

Table 1 Acute toxicity of SPs to birds and earthworms (http //ec.europa.eu/ sanco pesticides/public/ index.cfin)...

Endrin was introduced in the United States in 1951 as an avicide, rodenticide and insecticide. Its principal use to control the cotton bollworm and tobacco budworm peaked in the early 1970s. In 1979, the EPA canceled some uses of endrin and indicated its intent to cancel all uses of endrin (EPA 1979f USDA 1995). By 1986, all uses were voluntarily canceled (Bishop 1984, 1985, 1986 EPA 1993e USDA 1995), except for its use as a toxicant on bird perches, which was canceled in 1991 (USDA 1995). Endrin also was a contaminant in dieldrin (Verschueren 1983) however, all uses of this pesticide have been canceled since the mid-1980s (EPA 1992b). Consequently, there are no longer any significant releases of endrin to the environment in the United States. 

The big advantage of this type of insecticide is its relatively rapid degradation and low toxicity to applicators, fish, birds, beneficial insects, and other wildlife. The price is competitive with more conventional pesticides. No doubt more third generation insecticides will be developed in the future. 

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