Avian testing

This book indudes 67 ASTM test methods, practices, and guides, covering field sampling, toxidty of water, sediment toxidty, fate related procedures, uses of data, avian test procedures, and genotoxicity tests. 

Ecotoxicological Prolonged fish toxicity (including reproduction) Avian acute/subacute toxicity Accumulation, degradation and mobility tests... 

Specifications for nest box placement and predator guards should also be included. Specifics of nest box placement will depend on the behavior of avian species being monitored. Inter-box distances and orientation to test areas are two parameters that may vary widely with the organism being smdied. Predators vary from area to area, and if nest boxes are near tree canopies, predation from above may in fact be the dominant route of predator intrusion rather than the standard access from the ground. 

Distributions of pesticide concentrations in potential food items for avian species are required to estimate the contribution of food to exposure of birds in different regions where the test chemical may be used. On treated fields, detectable CEF residues were found in 102 of 207 earthworm samples. No earthworm samples collected from control fields (N = 28) contained detectable CEF. Average CEF concentrations in earthworms reached maxima 1-4 days post-application (Table 3). Mean CEF residues in earthworms fell below 0.1 qg g after 8 days post-application. This... 

Veit, H.P., R.J. Kendall, and P.F. Scanlon. 1983. The effect of lead shot ingestion on the testes of adult ringed turtle doves (Streptopelia risoria). Avian Dis. 27 442-452. 

In birds, mortality occurred in young individuals of sensitive species when rations contained more than 500 mg Ni/kg (Outridge and Scheuhammer 1993). Nickel accumulated in avian tissues at dietary loadings as low as 0.7 to 12.5 mg Ni/kg ration (Cain and Pafford 1981 Eastin and O Shea 1981 Stoewsand et al. 1984) however, nickel intoxication in some species tested was not always reflected by elevated tissue nickel concentrations (Outridge and Scheuhammer 1993). 

No data were found on the effects of silver compounds on avian or mammalian wildlife. All controlled studies with silver were with domestic poultry, livestock, or small laboratory mammals. Signs of chronic silver ion intoxication in tested birds and mammals included cardiac enlargement, vascular hypertension, hepatic necrosis, anemia, lowered immunological activity, altered membrane permeability, kidney pathology, enzyme inhibition, growth retardation, and a shortened life span (Smith and Carson 1977 Freeman 1979 Fowler and Nordberg 1986 USPHS 1990). 

No studies have been conducted with silver and avian or mammalian wildlife, and it is unreasonable to extrapolate the results of limited testing with domestic poultry and livestock to wildlife to establish criteria or administratively enforced standards. Research on silver and avian and terrestrial wildlife merits the highest priority in this subject area. No silver criteria are available for the protection of avian and mammalian health, and all criteria now proposed are predicated on human health (Table 7.8). As judged by the results of controlled studies with poultry and small laboratory mammals, safe concentrations of silver ion were less than 250 pg/L in drinking water of mammals, less than 100 mg/L in drinking water of poultry, less than 6 mg/kg in diets of mammals, less than 10 mg/kg in copper-deficient diets of poultry, less than 200 mg/kg in copper-adequate diets of poultry, and less than 1.8 mg/kg in chicken eggs. The proposed short-term (10-day) allowable limit of 1142 pg Ag/L in drinking water for human health protection (Table 7.8) should... 

Pharmacologically, carbofuran inhibits cholinesterase, resulting in stimulation of the central, parasympathetic, and somatic motor systems. Sensitive biochemical tests have been developed to measure cholinesterase inhibition in avian and mammalian brain and plasma samples and are useful in the forensic assessment of carbamate exposure in human and wildlife pesticide incidents (Bal-lantyne and Marrs Hunt and Hooper 1993). Acute toxic clinical effects resulting from carbofuran exposure in animals and humans appear to be completely reversible and have been successfully treated with atropine sulfate. However, treatment should occur as soon as possible after exposure because acute carbofuran toxicosis can be fatal younger age groups of various species are more susceptible than adults (Finlayson et al. 1979). Carbofuran labels indicate that application is forbidden to streams, lakes, or ponds. In addition, manufacturers have stated that carbofuran is poisonous if swallowed, inhaled, or absorbed through the skin. Users are cautioned not to breathe carbofuran dust, fumes, or spray mist and treated areas should be avoided for at least 2 days (Anonymous 1971). Three points are emphasized at this juncture. First, some carbofuran degradation... 

Hill, E.F. and M.B. Camardese. 1982. Subacute toxicity testing with young birds response in relation to age and intertest variability of LC50 estimates. Pages 41-65 in D.W. Lamb, and E.E. Kenaga (eds.). Avian and Mammalian Wildlife Toxicology Second Conference. Am. Soc. Testing Mater. ASTM STP 757. 

Gile, J.D. and S.M. Meyers. 1986. Effects of adult mallard age on avian reproductive tests. Arch. Environ. Contam. Toxicol. 15 751-756. 

McCrady, J.K., Johnson, D.E., and Turner, L.W. Volatility of ten priority pollutants from fortified avian toxicity test diets, Bull. Environ. Contam. Toxicol, 34(5) 634-644, 1985. 

Tests and refinements of a general structure-activity model for avian repellents. Journal of ChemicalEcology 20,321-339. 

Avian Toxicity Testing. Pensacola, Florida, 4 to 7 Dec 1994. Co-sponsored by Organisation for Economic Co-operation and Development. Published by OECD, 1996. 

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