Previous studies assessing excessive proliferation of phytoplankton (EPP) in lakes are generally based on single investigation and focused on limited environmental factors; meanwhile, less attention has been paid to lakes susceptibility to EPP. Here, we identify the priority of lakes for EPP control in a basin by assessing EPP in multiple lakes and identify the key factors related to lakes’ vulnerability to EPP. Field measurements, as well as multi-source survey data acquisition were conducted for 63 shallow lakes in the middle-lower Yangtze River basin. Resource-use efficiency by phytoplankton (RUE) was then used to represent lake susceptibility to EPP. Generalized linear models were used to assess the relative importance of environmental factors for RUE. We found that most lakes (76.19 %) were not suitable for recreation, due to health concern attributed to irritative or allergenic risk caused by EPP. Phosphorus was the primary limiting nutrient for EPP (74.60 % of lakes) which should be limited to < 0.09 mg/L. The linear model that included latitude, particulate matter 10, and precipitation explained 27.60 % of the variation of RUETP among lakes. In contrast, the linear model that included ozone, Secchi depth, and wind speed explained 19.41 % of the variation of RUETN among lakes. The key factor related to RUETP and RUETN was particulate matter 10 and ozone, respectively, both of which potentially increase RUE or reflect it. Our results suggest that integrating multiple survey datasets is critical for lakes EPP assessment in a basin, while lakes impacted by air pollution are a high priority for EPP control.

2,4-Dichloro-6-nitrophenol (DCNP) is an environmental transformation product of 2,4-dichlorophenol that has been identified as widespread in effluent wastewater, but little is known about its toxicity because this compound is not regulated. Therefore, to investigate the endocrine disruption potency of DCNP in Chinese rare minnows (Gobiocypris rarus), adult and juvenile fish were exposed to various concentrations of DCNP (2, 20, and 200 μg/L) for 28 d. After 28 d exposure, the plasma vitellogenin (VTG) levels were reduced in females while increased in males and juvenile fish considerably, as compared with the control. These results suggested that DCNP affects the HPG-axis in a sex-dependent way. Testosterone (T) levels in the plasma were significantly lower in adult and juvenile fish and were accompanied by an increased estradiol (E2)/T ratio. Histopathological observation revealed hypertrophy of the hepatocytes and nuclear pyknosis in the liver, the inhibition of spermatogenesis in the testes, and the degeneration of oocytes in the ovaries after DCNP exposure. The expression pattern of selected genes indicated that the nuclear receptor, steroidogenesis and gonadotropin regulation pathways were perturbed after DCNP exposure. Above all, our results demonstrated that DCNP clearly had anti-androgenic activity in both adult and juvenile fish and can therefore be considered as an endocrine-disrupting chemical.

Triclosan has been used as a broad-spectrum antibacterial agent for over 40 years worldwide. Increasing reports indicate frequent detection and broad exposure to triclosan in the natural environment and the human body. Current laboratory studies in various species provide strong evidence for its disrupting effects on the endocrine system, especially reproductive hormones. Multiple modes of action have been suggested, including disrupting hormone metabolism, displacing hormones from hormone receptors and disrupting steroidogenic enzyme activity. Although epidemiological studies on its effects in humans are mostly negative but conflicting, which is typical of much of the early evidence on the toxicity of EDCs, overall, the evidence suggests that triclosan is an EDC. This article reviews human exposure to triclosan, describes the current evidence regarding its reproductive endocrine-disrupting effects, and discusses potential mechanisms to provide insights for further study on its endocrine-disrupting effects in humans.

Phenanthrene (Phe) is a tricyclic polycyclic aromatic hydrocarbon with high bioavailability under natural exposure. However, there are few studies on the reproductive toxicity of Phe in mammals. In this study, male Kunming mice were gavaged once every two days with Phe (5, 50, and 500 ng/kg) for 28 weeks. The accumulation levels of Phe in the testis were dose-dependently increased. Histopathological staining showed that Phe exposure reduced the number of spermatogonia, sperm and Sertoli cells. The percentage of testicular apoptotic cells was significantly increased, which was further verified by the upregulated BAX protein. The expression of the GDNF/PI3K/AKT signaling pathway was downregulated, which might suppress the self-renewal and differentiation of spermatogonial stem cells. Meanwhile, Phe exposure inhibited the expression of Sertoli cell markers (Fshr, WT1, Sox9) and the Leydig cell marker Cyp11a1, indicating damage to the function of Sertoli cells and Leydig cells. Serum estrogen and testicular estrogen receptor alpha were significantly upregulated, while androgen receptor expression was downregulated. These alterations might be responsible for impaired spermatogenesis. This study provides new insights for evaluating the reproductive toxicity and potential mechanisms of Phe in mammals.