Rattner Barnett A, McKernan Moira A, Eisenreich Karen M, Link William A, Olsen Glenn H, Hoffman David J, Knowles Kathy A, McGowan Peter C
U.S. Geological Survey, Patuxent Wildlife Research Center, Laurel, Maryland, USA.
J Toxicol Environ Health A. 2006 Feb;69(3-4):331-51. doi: 10.1080/15287390500398265.
A recent Canada goose (Branta canadensis) die-off at a petroleum refinery fly ash pond in Delaware was attributed to vanadium (V) toxicity. Because of the paucity of V toxicity data for wild birds, a series of studies was undertaken using the forms of V believed to have resulted in this incident. In 7-d single oral dose trials with mallard drakes (Anas platyrhynchos), the estimated median lethal dose (LD50) for vanadium pentoxide was 113 mg/kg body weight, while the LD50 for sodium metavanadate was 75.5 mg/kg. Sodium metavanadate was found to be even more potent (LD50 = 37.2 mg/kg) in male Canada geese. The most distinctive histopathological lesion of both forms of V was lympho-granulocytic enteritis with hemorrhage into the intestinal lumen. Vanadium accumulation in liver and kidney was proportional to the administered dose, and predictive analyses based on these data suggest that V concentrations of 10 microg/g dry weight (dw) in liver and 25 microg/g dw in kidney are associated with mortality (>90% confidence that exposure is >LD50) in mallards acutely exposed to sodium metavanadate. Chronic exposure to increasing dietary concentrations of sodium metavanadate (38.5 to 2651 ppm) over 67 d resulted in V accumulation in liver and kidney (25.2 and 13.6 microg/g dw, respectively), mild intestinal hemorrhage, blood chemistry changes, and evidence of hepatic oxidative stress in mallards, although some of these responses may have been confounded by food avoidance and weight loss. Dietary exposure of mallards to 250 ppm sodium metavanadate for 4 wk resulted in modest accumulation of V in liver and kidney (<5 microg/g dw) and mild intestinal hemorrhage. Based on these data and other observations, it is unlikely that chronic low-level dietary exposure to V poses a direct lethal hazard to wildlife. However, point sources, such as the V-laden fly ash pond encountered by geese at the petroleum refinery in Delaware, may pose a significant hazard to water birds.
最近,特拉华州一家炼油厂粉煤灰池发生的加拿大黑雁(Branta canadensis)死亡事件被归因于钒(V)中毒。由于野生鸟类的钒毒性数据匮乏,因此开展了一系列研究,使用的是据信导致此次事件的钒形态。在对绿头雄鸭(Anas platyrhynchos)进行的7天单次口服剂量试验中,五氧化二钒的估计半数致死剂量(LD50)为113毫克/千克体重,而偏钒酸钠的LD50为75.5毫克/千克。结果发现,偏钒酸钠对雄性加拿大黑雁的毒性更强(LD50 = 37.2毫克/千克)。两种钒形态最显著的组织病理学损伤都是淋巴细胞性粒细胞性肠炎,并伴有肠腔出血。肝脏和肾脏中的钒蓄积量与给药剂量成正比,基于这些数据的预测分析表明,急性暴露于偏钒酸钠的绿头鸭中,肝脏钒浓度为10微克/克干重(dw)、肾脏钒浓度为25微克/克dw与死亡率相关(暴露高于LD50的置信度>90%)。在67天内让绿头鸭长期暴露于浓度不断增加的偏钒酸钠日粮(38.5至2651 ppm)中,导致肝脏和肾脏中钒蓄积(分别为25.2和13.6微克/克dw)、轻度肠道出血、血液化学变化以及绿头鸭出现肝脏氧化应激迹象,不过其中一些反应可能因拒食和体重减轻而受到混淆。让绿头鸭日粮暴露于250 ppm偏钒酸钠4周,导致肝脏和肾脏中钒适度蓄积(<5微克/克dw)以及轻度肠道出血。基于这些数据和其他观察结果,长期低水平日粮暴露于钒不太可能对野生动物构成直接致命危害。然而,像特拉华州炼油厂中大雁遇到的富含钒的粉煤灰池这样的点源,可能会对水鸟构成重大危害。