Ecological risk assessment of heavy metals in desulfurized seawater discharged from a coal-fired power plant in Qingdao.

Despite the prevalence of discharge of large volumes of heavy-metal-bearing seawater from coal-fired power plants into adjacent seas, studies on the associated ecological risks remain limited. This study continuously monitored concentrations of seven heavy metals (i.e. As, Cd, Cr, Cu, Hg, Pb, and Zn) in surface seawater near the outfall of a coal-fired power plant in Qingdao, China over three years. The results showed average concentrations of As, Cd, Cr, Cu, Hg, Pb, and Zn of 2.63, 0.33, 2.97, 4.63, 0.008, 0.85, and 25.00 µg/L, respectively. Given the lack of data on metal toxicity to local species, this study investigated species composition and biomass near discharge outfalls and constructed species sensitivity distribution (SSD) curves with biological flora characteristics. Hazardous concentrations for 5% of species (HC5) for As, Cd, Cr, Cu, Hg, Pb, and Zn derived from SSDs constructed from chronic toxicity data for native species were 3.23, 2.22, 0.06, 2.83, 0.66, 4.70, and 11.07 µg/L, respectively. This study further assessed ecological risk of heavy metals by applying the Hazard Quotient (HQ) and Joint Probability Curve (JPC) based on long-term heavy metal exposure data and chronic toxicity data for local species. The results revealed acceptable levels of ecological risk for As, Cd, Hg, and Pb, but unacceptable levels for Cr, Cu, and Zn. The order of studied heavy metals in terms of ecological risk was Cr > Cu ≈ Zn > As > Cd ≈ Pb > Hg. The results of this study can guide the assessment of ecological risk at heavy metal contaminated sites characterized by relatively low heavy metal concentrations and high discharge volumes, such as receiving waters of coal-fired power plant effluents.

Long-term bisphenol S exposure aggravates non-alcoholic fatty liver by regulating lipid metabolism and inducing endoplasmic reticulum stress response with activation of unfolded protein response in male zebrafish.

Environmental chemical exposures have been implicated as risk factors for the development of non-alcoholic fatty liver (NAFLD). Bisphenol S (BPS), widely used in multitudinous consumer products, could disrupt lipid metabolism in the liver. This study aimed at examining the hypothesis that long-term exposure to BPS promotes the development of liver fibrosis and inflammation by means of the application of a semi-static exposure experiment that exposed zebrafish to 1, 10, and 100 µg/L BPS from 3 h post fertilization to 120 day post fertilization. Results showed that the 120-d BPS exposure elevated plasma aspartate aminotransferase and alanine aminotransferase activities, increased triacylglycerol (TAG) and total cholesterol levels in male liver, and even induced hepatic apoptosis and fibrosis. Hepatic lipid accumulation observed in the 30-d BPS-exposed zebrafish was recovered after a 90-d depuration phase, thereby indicating that long-term BPS exposure promotes the progression of simple steatosis to non-alcoholic steatohepatitis. Furthermore, BPS exposure for 120-d promoted the synthesis of TAG and lipotoxic free fatty acids by elevating the transcription of srebp1, acc, fasn, and elovl6, induced endoplasmic reticulum (ER) stress with increasing expression levels of unfolded protein response (UPR) genes (perk, hsp5, atf4a, and ddit3), and then stimulated the expression of two key autophagy genes (atg3 and lc3) and inflammatory genes (il1b and tnfα). It is indicated that BPS can induce the development of steatohepatitis via the activation of the PERK-ATF4a pathway of the UPR. Data gathered suggest that environmental pollutants-induced ER stress with the activation of UPR can potentially trigger the NAFLD development in males. Overall, our study provided new sights into understanding of the adverse health effects of metabolism disrupting chemicals.

Carbofuran induces increased anxiety-like behaviors in female zebrafish (Danio rerio) through disturbing dopaminergic/norepinephrinergic system.

Carbofuran, a carbamate pesticide, is widely used in developing countries to manage insect pests. Studies have found that carbofuran posed potential risks for the neurotransmitter systems of non-target species, we speculated that these disruptive effects on the neurotransmitter systems could trigger anxiety-like behaviors. In this study, female zebrafish were exposed to environmental levels (5, 50, and 500 µg/L) of carbofuran for 48 h to evaluate the effects of carbofuran on anxiety-like behaviors. Results showed that zebrafish exhibited more anxiety-like behaviors which proved by the observed higher bottom trend and more erratic movements in the novel tank after carbofuran treatment. In order to elucidate the underlying molecular mechanisms of carbofuran-induced anxiety-promoting effects, we measured the levels of neurotransmitters, precursors, and major metabolites, along with the level of gene expression and the enzyme activities involved in neurotransmitter synthesis and metabolism. The results demonstrated that acute carbofuran exposure stimulated the mRNA expression and enzyme activity of tyrosine hydroxylase, which sequentially induced the increased levels of dopamine and norepinephrine. Tyrosine hydroxylase inhibitor relieved the anxiety-related changes induced by carbofuran, confirming the overactive tyrosine hydroxylase-mediated accumulation of dopamine and norepinephrine in the brain was one of the main reasons for carbofuran-induced anxiety-like behaviors in the female zebrafish. Overall, our study indicated the environmental health risks of carbamate pesticide in inducing neurobehavioral disorders and provided novel insights into the investigation of the relevant underlying mechanisms.

Bisphenol S Induces Ectopic Angiogenesis in Embryos via VEGFR2 Signaling, Leading to Lipid Deposition in Blood Vessels of Larval Zebrafish.

Bisphenol S (BPS), used as a bisphenol A substitute, has been detected in various environments. However, the safety of BPS is still unclear. Here, zebrafish embryos were exposed to BPS (0, 1, 10, and 100 µg/L) for 24, 48, 72, 96 h, and 15 days. BPS induced ectopic sprouting of budding blood vessels in embryos, but the blood flow velocity within these lesions was unchanged at 48 h. At 72 h postfertilization (hpf), by observing the subintestinal venous plexus responsible for yolk absorption, we found that VEGFR2 transduced an angiogenic signal and that the subsequent reduction in blood flow velocity inhibited yolk absorption. At 96 hpf, yolk consumption was still delayed because of the disturbed transportation route, resulting in transient extensive lipid retention in the blood vessels. After feeding, obvious atherogenic lipids were discovered in the blood vessels, especially in bends, bifurcations, and stenoses. This dynamic visualization of the pathogenesis demonstrates a plausible mechanistic link between BPS exposure-induced embryonic vessel overgrowth and an increased atherosclerosis risk.