Pain D J, Carter I, Sainsbury A W, Shore R F, Eden P, Taggart M A, Konstantinos S, Walker L A, Meharg A A, Raab A
Royal Society for the Protection of Birds, The Lodge, Sandy, Bedfordshire SG19 2DL, UK.
Sci Total Environ. 2007 Apr 15;376(1-3):116-27. doi: 10.1016/j.scitotenv.2007.01.062. Epub 2007 Feb 16.
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 microg 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.
自1989年以来,英国一直在开展一项赤鸢重新引入计划,将4至6周大的雏鸟圈养起来,饲养6至8周后再放归自然。作为食腐动物,赤鸢可能会食用未被找回的猎物,并在其猎物的肉中摄入铅弹或铅(Pb)碎片。我们通过在125只圈养的幼年赤鸢放归前采集血样、分析从栖息地收集的264颗食丸(野生鸟类反刍的)以及分析1995年至2003年间发现死亡的87只赤鸢的肝脏和/或骨骼中的铅浓度,来评估圈养和野生赤鸢的铅暴露情况。还对肝脏进行了铅同位素分析,以确定铅暴露途径。46只(36.8%)放归前采样的赤鸢血铅浓度升高(201 - 3340微克/升)。这种铅的来源可能是鸟类或哺乳动物尸体中的铅弹药小碎片,这些碎片要么是由亲鸟喂给雏鸟的,要么更有可能是在圈养期间摄入的。一旦放归,赤鸢在食物中也会接触到铅弹,至少1.5 - 2.3%的反刍食丸含有铅弹。在44只发现死亡或捕获后生病并在几天内死亡的赤鸢中,7只肝脏铅浓度升高(干重>6毫克/千克),其中6只(14%)浓度>15毫克/千克,符合致命铅中毒的情况。尸检分析表明,其中两只鸟死于其他原因(杀鼠剂和一种禁用的农用杀虫剂中毒);其余四只(9%)可能死于铅中毒。86只赤鸢的骨骼样本显示铅浓度分布不均,18个样本(21%)铅浓度>20毫克/千克,表明这些鸟类在生命的某个阶段铅暴露水平升高。大多数赤鸢肝脏样本中的铅同位素特征(Pb(208/206);Pb(206/207))与从反刍食丸中提取的铅弹中的特征相符。铅浓度极低的赤鸢肝脏中发现的铅同位素比率与英国汽油中的铅同位素特征不同,表明鸟类很少接触到残留的汽油铅。我们得出结论,赤鸢接触铅的主要来源是其食物来源中的铅弹药(霰弹或步枪子弹)或其碎片;在某些情况下,暴露似乎足以致命。我们提出了减少圈养和野生赤鸢以及其他食腐物种铅中毒的建议。