Gilbertson M, Kubiak T, Ludwig J, Fox G
International Joint Commission, Windsor, Ontario.
J Toxicol Environ Health. 1991 Aug;33(4):455-520. doi: 10.1080/15287399109531538.
Several species of colonial fish-eating birds nesting in the Great Lakes basin, including herring gulls, common terns and double-crested cormorants, have exhibited chronic impairment of reproduction. In addition to eggshell thinning caused by high levels of DDT and metabolites, the reproductive impairment is characterized by high embryonic and chick mortality, edema, growth retardation, and deformities, hence the name Great Lakes embryo mortality, edema, and deformities syndrome (GLEMEDS). The hypothesis has been advanced that GLEMEDS in colonial fish-eating birds resembles chick-edema disease of poultry and has been caused by exposure to chick-edema active compounds that have a common mode of action through the cytochrome P-448 system. Detailed evidence has been collected from the following three groups of studies on herring gulls in the lower Great Lakes during the early 1970s; Forster's terns in Green Bay, Wisconsin in 1983; and double-crested cormorants and Caspian terns in various locations in the upper Great Lakes from 1986 onwards. It has proved difficult to establish not only the onset of the disease in the various species at various locations but also the period in which chick-edema active compounds were released. Anecdotal evidence suggested that serious egg mortality in Lake Ontario herring gulls first occurred in 1966, through the signs of chick-edema disease were not looked for until 1974. Only indirect evidence is available on the date of the release of one of the presumed causal agents, 2,3,7,8-tetrachlorodibenzo-p-dioxin, but highest levels may have occurred in the early to mid 1960s. More reliable data show that the onset of the improvement of reproduction of Lake Ontario herring gulls coincided with the declines in organochlorine compounds and particularly 2,3,7,8-TCDD and PCB. Similarly, information on the onset of the disease and exposures in the Forster's tern and double-crested cormorants in Green Bay is uncertain but bird banders did not observe deformities until the 1970s, which corresponds with the onset of high levels of PCB. If the disappearance of the Caspian tern from Saginaw Bay in the mid 1960s corresponds with the onset of GLEMEDS at that location, then there is a close temporal relationship to the onset of high PCB levels. Chick-edema disease is difficult to diagnose because there is no specific lesion, but rather there is a suite of lesions.(ABSTRACT TRUNCATED AT 400 WORDS)
几种在五大湖流域筑巢的群居食鱼鸟类,包括银鸥、普通燕鸥和双冠鸬鹚,都出现了繁殖能力的慢性损害。除了高浓度滴滴涕及其代谢产物导致蛋壳变薄外,繁殖能力受损还表现为胚胎和雏鸟死亡率高、水肿、生长发育迟缓以及畸形,因此得名五大湖胚胎死亡、水肿和畸形综合征(GLEMEDS)。有人提出假说,认为群居食鱼鸟类的GLEMEDS与家禽的雏鸡水肿病相似,是由于接触了通过细胞色素P - 448系统具有共同作用模式的雏鸡水肿活性化合物所致。在20世纪70年代初,从以下三组关于五大湖下游银鸥的研究中收集了详细证据;1983年在威斯康星州绿湾对福斯特燕鸥的研究;以及从1986年起对五大湖上游不同地点的双冠鸬鹚和里海燕鸥的研究。事实证明,不仅难以确定不同物种在不同地点疾病的发病时间,也难以确定雏鸡水肿活性化合物的释放时间。轶事证据表明,安大略湖银鸥的严重卵死亡率首次出现在1966年,但直到1974年才开始寻找雏鸡水肿病的迹象。关于一种假定的致病因子2,3,7,8 - 四氯二苯并 - p - 二恶英的释放日期,只有间接证据,但最高浓度可能出现在20世纪60年代初至中期。更可靠的数据表明,安大略湖银鸥繁殖能力改善的开始时间与有机氯化合物,特别是2,3,7,8 - TCDD和多氯联苯的减少相吻合。同样,关于绿湾福斯特燕鸥和双冠鸬鹚疾病的发病时间和接触情况的信息也不确定,但鸟类环志者直到20世纪70年代才观察到畸形,这与多氯联苯浓度升高的开始时间相符。如果20世纪60年代中期里海燕鸥从萨吉诺湾消失与该地点GLEMEDS的发病时间相对应,那么这与多氯联苯浓度升高的开始时间存在密切的时间关系。雏鸡水肿病难以诊断,因为没有特定的病变,而是有一系列病变。(摘要截取自400字)