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Lead contamination and associated disease in captive and reintroduced red kites Milvus milvus in England

Pain, D.J., Carter, I., Sainsbury, A.W., Shore, R.F., Eden, P., Taggart, M.A., Konstantinos, S., Walker, L., Meharg, A.A. and Raab, A. (2007) Lead contamination and associated disease in captive and reintroduced red kites Milvus milvus in England. Science of The Total Environment, 376 (1-3). pp. 116-127.

Link to Published Version: http://dx.doi.org/10.1016/j.scitotenv.2007.01.062
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Abstract

Since 1989, a red kite Milvus milvus reintroduction programme has been underway in the United Kingdom, with 4-6 week old nestlings brought into captivity and held for 6-8 weeks before reintroduction. As scavengers, red kites may consume unretrieved game, and ingest shot or lead (Pb) fragments in their prey's flesh. We evaluated exposure to Pb in captive and wild red kites by taking blood samples from 125 captive young red kites prior to release, through analysing 264 pellets (regurgitated by wild birds) collected from under a roost site, and analysing Pb concentrations in livers and/or bones of 87 red kites found dead between 1995 and 2003. Lead isotope analyses of livers were also conducted in an effort to identify Pb exposure routes. Forty-six (36.8%) kites sampled prior to release had elevated blood Pb concentrations (201-3340 μg l- 1). The source of this Pb was probably small fragments of lead ammunition in the carcasses of birds or mammals either fed to the nestlings by their parents or, more likely, subsequently whilst in captivity. Once released, kites were also exposed to lead shot in their food, and a minimum of 1.5-2.3% of regurgitated pellets contained Pb gunshot. Seven of 44 red kites found dead or that were captured sick and died within a few days had elevated (> 6 mg kg- 1 dry weight [d.w.]) liver Pb concentrations, and six of these (14%) had concentrations of > 15 mg kg- 1 d.w., compatible with fatal Pb poisoning. Post-mortem analyses indicated that two of these birds had died of other causes (poisoning by rodenticide and a banned agricultural pesticide); the remaining four (9%) probably died of Pb poisoning. Bone samples from 86 red kites showed a skewed distribution of Pb concentration, and 18 samples (21%) had Pb concentrations > 20 mg kg- 1 d.w., indicating elevated exposure to Pb at some stage in the birds' life. Lead isotopic signatures (Pb 208/206; Pb 206/207) in liver samples of the majority of kites were compatible with those found in lead shot extracted from regurgitated pellets. Lead isotope ratios found in the livers of kites with very low Pb concentrations were distinct from UK petrol Pb isotopic signatures, indicating that birds were exposed to little residual petrol Pb. We conclude that the primary source of Pb to which red kites are exposed is lead ammunition (shotgun pellets or rifle bullets), or fragments thereof, in their food sources; in some cases exposure appears sufficient to be fatal. We make recommendations to reduce Pb poisoning in both captive and wild red kites and other scavenging species.

Publication Type: Journal Article
Murdoch Affiliation: School of Veterinary and Biomedical Sciences
Publisher: Elsevier BV
Copyright: © 2007 Elsevier B.V.
URI: http://researchrepository.murdoch.edu.au/id/eprint/10188
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