N-(1,3-Dimethylbutyl)-N′-phenyl-p-phenylenediamine-quinone, also known as 6PPD quinone, was recently identified as a toxic chemical that causes acute mortality in coho salmon following exposure to urban runoff. Despite its potential occurrence in receiving waters worldwide, there is no information about the toxicity of 6PPD quinone to other aquatic species. In this study, to assess the aquatic toxicity of 6PPD quinone to freshwater fish and crustacean species, we performed standardized 48−96 h acute toxicity tests of 6PPD quinone with four species (Danio rerio, Oryzias latipes, Daphnia magna, and Hyalella azteca). In contrast to the high toxicity observed in coho salmon in a previous study (24 h LC 50 of 0.79 μg/L), 6PPD quinone did not exhibit acute lethal toxicity to any species at its maximum water solubility. The absence of acute lethality of 6PPD quinone to tested species indicates that the urban runoff toxicity observed for the species can be attributed to other chemicals. The observed large discrepancy in toxicity (by a factor of ∼100) might be due to the specific toxicity of 6PPD quinone to coho salmon. Further research is needed to reveal the underlying mechanisms of the observed difference, which will be useful for both urban runoff management and aquatic toxicology.

The human thyroid receptor (hTR)-agonist activities of 796 compounds were evaluated using a yeast two-hybrid assay in this study. A total of 17 compounds exhibited agonist activity at tenfold the effective concentration (EC × 10 ) [0.0083 -7,500 nM]. Additionally, TRIAC, TETRAC, and GC-1, which exhibited 30 -200 times higher activities than T3 and T4, may cause thyroid-hormone receptors (TR) activity at extremely low concentrations in real environmental water. Moreover, 3-chloro-3',5,5'-triiodo-L-thyronine exhibited high TR-agonist activity for the first time. Chemicals with a structure equivalent to thyroid hormones exhibited TR-agonist activity regardless of the TR type. Information on hTR-agonist activity is important because previous studies, such as those involving EDSP21, have focused exclusively on rTR-agonist activity. Therefore, the knowledge gained from the present study will boost chemical regulation strategies benefiting human and wildlife.

3,3′,5-Triiodothyroacetic acid (TRIAC) was identified as a major contributor to the activity of thyroid hormone receptor (TR) agonists in environmental water. TRIAC contributed 60–148% of the TR-agonist activity in effluents from sewage treatment plants (STPs). Meanwhile, the contributions of 3,5,3′-triiodothyronine (T3), 3,3′,5,5′-tetraiodothyronine (T4), and analogues were <1%. TRIAC concentrations in the range of 0.30–4.2 ng/L are likely enough to cause disruption of the thyroid system in living aquatic organisms. The origin of TRIAC in the STP effluents was investigated by analyzing both STP influents and effluents. Relatively high concentrations of T3 and T4 (2.5 and 6.3 ng/L, respectively) were found only in the influents. TRIAC was identified only in the effluents. These findings suggested that T3 and T4 in STP influents were potentially converted into TRIAC during activated sludge treatment or by other means. The evaluation of TRIAC at relevant environmental concentrations by in vivo assays and an appropriate treatment to reduce the TR activity in sewage are needed.

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