Mechanisms of Developmental Toxicity of Dioxins and Related Compounds.

Dioxins and related compounds induce morphological abnormalities in developing animals in an aryl hydrocarbon receptor (AhR)-dependent manner. Here we review the studies in which 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) is used as a prototypical compound to elucidate the pathogenesis of morphological abnormalities. TCDD-induced cleft palate in fetal mice involves a delay in palatogenesis and dissociation of fused palate shelves. TCDD-induced hydronephrosis, once considered to be caused by the anatomical obstruction of the ureter, is now separated into TCDD-induced obstructive and non-obstructive hydronephrosis, which develops during fetal and neonatal periods, respectively. In the latter, a prostaglandin E2 synthesis pathway and urine concentration system are involved. TCDD-induced abnormal development of prostate involves agenesis of the ventral lobe. A suggested mechanism is that AhR activation in the urogenital sinus mesenchyme by TCDD modulates the wingless-type MMTV integration site family (WNT)/ß-catenin signaling cascade to interfere with budding from urogenital sinus epithelium. TCDD exposure to zebrafish embryos induces loss of epicardium progenitor cells and heart malformation. AHR2-dependent downregulation of Sox9b expression in cardiomyocytes is a suggested underlying mechanism. TCDD-induced craniofacial malformation in zebrafish is considered to result from the AHR2-dependent reduction in SRY-box 9b (SOX9b), probably partly via the noncoding RNA slincR, resulting in the underdevelopment of chondrocytes and cartilage.

Selenium poisoning of fish by coal ash wastewater in Herrington Lake, Kentucky.

Selenium pollution from the E.W. Brown Electric Generating Station was investigated in Herrington Lake, KY. Coal ash wastewater is discharged as surface water overflow from ash disposal ponds into the lake via a National Pollutant Discharge Elimination System permit issued by the Kentucky Division of Water, but the permit does not restrict or limit the amount of selenium released. Unpermitted discharges occur from seeps and drainage through leaks in ash pond dams. Together, these discharges have resulted in selenium concentrations in water, sediment, benthic macroinvertebrates, and fish that are 2-9 times the level that is toxic for fish reproduction and survival. A large proportion (12.2%, or 25 times background) of juvenile largemouth bass (Micropterus salmoides, the only species examined) exhibited spinal and/or craniofacial malformations that are consistent with selenium poisoning. Teratogenic Deformity Index values indicated a 3.05% population-level impact on the bass fishery, with total selenium-induced mortality (including pre-swimup mortality) estimated to be in excess of 25% per year. These findings confirm that coal ash discharges into Herrington Lake are contributing selenium to the Lake that is poisoning fish.

Teratogenic effects and monetary cost of selenium poisoning of fish in Lake Sutton, North Carolina.

Selenium pollution from coal ash wastewater was investigated in Lake Sutton, NC. This lake has been continuously used as a cooling pond for a coal-fired power plant since 1972. Historic and recent levels of contamination in fish tissues (14-105µg Se/g dry weight in liver, 24-127 in eggs, 4-23 in muscle, 7-38 in whole-body) exceeded toxic thresholds and teratogenic effects were observed in fish collected in 2013. A high proportion (28.9 percent) of juvenile Lepomis spp. exhibited spinal and craniofacial malformations that were consistent with selenium poisoning. Teratogenic Deformity Index values indicated population-level impacts on the fishery. The partially monetized cost of resultant fishery losses was calculated at over $US 8.6 million annually, and over $US 217 million for the entire period of damage, which dates back to 1987 when chemical and biological monitoring began.