A large number of toxicity studies report abnormalities in early life-stage (ELS) fish that are described here as a sublethal toxicity syndrome (TxSn_FELS) and generally include a reduced heart rate, edemas (yolk sac and cardiac), and a variety of morphological abnormalities. The TxSn_FELS is very common and not diagnostic for any chemical or class of chemicals. This sublethal toxicity syndrome is mostly observed at high exposure concentrations and appears to be a baseline, non-specific toxicity response; however, it can also occur at low doses by specific action. Toxicity metrics for this syndrome generally occur at concentrations just below those causing mortality and have been reported for a large number of diverse chemicals. Predictions based on tissue concentrations or quantitative-structure activity relationship (QSAR) models support the designation of baseline toxicity for many of the tested chemicals, which is confirmed by observed values. Given the sheer number of disparate chemicals causing the TxSn_FELS and correlation with QSAR derived partitioning; the only logical conclusion for these high-dose responses is baseline toxicity by nonspecific action and not a lock and key type receptor response. It is important to recognize that many chemicals can act both as baseline toxicants and specific acting toxicants likely via receptor interaction and it is not possible to predict those threshold doses from baseline toxicity. We should search out these specific low-dose responses for ecological risk assessment and not rely on high-concentration toxicity responses to guide environmental protection. The goal for toxicity assessment should not be to characterize toxic responses at baseline toxicity concentrations, but to evaluate chemicals for their most toxic potential. Additional aspects of this review evaluated the fish ELS teratogenic responses in relation to mammalian oral LD50s and explored potential key events responsible for baseline toxicity.

大量毒性研究报告了生命早期 (ELS) 鱼的异常，这里将其描述为亚致死毒性综合征 (TxSn _FELS )，通常包括心率减慢、水肿（卵黄囊和心脏）以及各种形态异常。TxSn _FELS很常见，不能诊断任何化学品或任何类别的化学品。这种亚致死毒性综合征主要在高暴露浓度下观察到，并且似乎是一种基线、非特异性毒性反应；然而，它也可以通过特定作用在低剂量下发生。这种综合征的毒性指标通常发生在略低于导致死亡的浓度下，并且已经报告了大量不同的化学物质。基于组织浓度或定量-结构活性关系 (QSAR) 模型的预测支持指定许多测试化学品的基线毒性，这由观察值证实。鉴于导致 TxSn _FELS的不同化学物质的绝对数量以及与 QSAR 派生分区的相关性；这些高剂量反应的唯一合乎逻辑的结论是非特异性作用引起的基线毒性，而不是锁和钥匙型受体反应。重要的是要认识到，许多化学物质既可以作为基线毒物，也可以作为可能通过受体相互作用的特定作用毒物，并且不可能根据基线毒性来预测这些阈值剂量。我们应该寻找这些特定的低剂量反应进行生态风险评估，而不是依靠高浓度毒性反应来指导环境保护。毒性评估的目标不应是表征基线毒性浓度下的毒性反应，而是评估化学品的最大毒性潜力。