Cook Philip M, Robbins John A, Endicott Douglas D, Lodge Keith B, Guiney Patrick D, Walker Mary K, Zabel Erik W, Peterson Richard E
Mid-Continent Ecology Division, National Health and Environmental Effects Research Laboratory, U.S. Environmental Protection Agency, 6201 Congdon Boulevard, Duluth, Minnesota 55804, USA.
Environ Sci Technol. 2003 Sep 1;37(17):3864-77. doi: 10.1021/es034045m.
Lake trout embryos and sac fry are very sensitive to toxicity associated with maternal exposures to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) and structurally related chemicals that act through a common aryl hydrocarbon receptor (AHR)-mediated mechanism of action. The loading of large amounts of these chemicals into Lake Ontario during the middle of the 20th century coincided with a population decline that culminated in extirpation of this species around 1960. Prediction of past TCDD toxicity equivalence concentrations in lake trout eggs (TEC(egg)s) relative to recent conditions required fine resolution of radionuclide-dated contaminant profiles in two sediment cores; reference core specific biota--sediment accumulation factors (BSAFs) for TCDD-like chemicals in lake trout eggs; adjustment of the BSAFs for the effect of temporal changes in the chemical distributions between water and sediments; and toxicity equivalence factors based on trout early life stage mortality. When compared to the dose-response relationship for overt early life stage toxicity of TCDD to lake trout, the resulting TEC(egg)s predict an extended period during which lake trout sac fry survival was negligible. By 1940, following more than a decade of population decline attributable to reduced fry stocking and loss of adult lake trout to commercial fishing, the predicted sac fry mortality due to AHR-mediated toxicity alone explains the subsequent loss of the species. Reduced fry survival, associated with lethal and sublethal adverse effects and possibly complicated by other environmental factors, occurred after 1980 and contributed to a lack of reproductive success of stocked trout despite gradually declining TEC(egg)s. Present exposures are close to the most probable no observable adverse effect level (NOAEL TECegg = 5 pg TCDD toxicity equivalence/g egg). The toxicity predictions are very consistent with the available historical data for lake trout population levels in Lake Ontario, stocking programs, and evidence for recent improvement in natural reproduction concomitant with declining levels of persistent bioaccumulative chemicals in sediments and biota.
湖鳟胚胎和初孵仔鱼对母体接触2,3,7,8-四氯二苯并对二恶英（TCDD）及通过共同的芳烃受体（AHR）介导作用机制起作用的结构相关化学物质所产生的毒性非常敏感。20世纪中叶，大量此类化学物质排入安大略湖，与此同时湖鳟种群数量下降，最终在1960年左右该物种灭绝。要预测湖鳟鱼卵中过去的TCDD毒性当量浓度（TEC(egg)）相对于近期状况，需要精确解析两个沉积物岩芯中放射性核素测年的污染物分布；湖鳟鱼卵中TCDD类化学物质的参考岩芯特定生物群 - 沉积物积累因子（BSAF）；针对水和沉积物之间化学物质分布随时间变化的影响对BSAF进行调整；以及基于鳟鱼早期生命阶段死亡率的毒性当量因子。与TCDD对湖鳟明显的早期生命阶段毒性的剂量反应关系相比，所得出的TEC(egg)预测出一段湖鳟初孵仔鱼存活率可忽略不计的延长时期。到1940年，由于鱼苗投放减少以及成年湖鳟因商业捕捞而减少，导致种群数量下降了十多年，仅由AHR介导的毒性所预测的初孵仔鱼死亡率就解释了该物种随后的灭绝。1980年后出现了鱼苗存活率降低的情况，这与致死和亚致死的不利影响相关，并且可能因其他环境因素而变得复杂，尽管TEC(egg)逐渐下降，但仍导致放流鳟鱼缺乏繁殖成功。目前的暴露水平接近最可能的无明显不良效应水平（NOAEL TECegg = 5 pg TCDD毒性当量/克鱼卵）。毒性预测与安大略湖湖鳟种群水平、放流计划的现有历史数据以及近期自然繁殖改善的证据非常一致，同时沉积物和生物群中持久性生物累积化学物质的水平也在下降。
