Combined exposure to decabromodiphenyl ether and nano zero-valent iron aggravated oxidative stress and interfered with metabolism in earthworms.

Decabromodiphenyl ether (BDE-209) is a common brominated flame retardant in electronic waste, and nano zero-valent iron (nZVI) is a new material in the field of environmental remediation. Little is known about how BDE-209 and nZVI combined exposure influences soil organisms. During the 28 days study, we determined the effects of single and combined exposures to BDE-209 and nZVI on the oxidative stress and metabolic response of earthworms (Eisenia fetida). On day 7, compared to CK, malondialdehyde (MDA) content increased in most combined exposure groups. To remove MDA and reactive oxygen species (ROS), superoxide dismutase (SOD), catalase (CAT), and peroxidase (POD) activities were induced in most combined exposure groups. On day 28, compared to CK, the activities of SOD and CAT were inhibited, while POD activity was significantly induced, indicating that POD plays an important role in scavenging ROS. Combined exposure to BDE-209 and nZVI significantly affected amino acid biosynthesis and metabolism, purine metabolism, and aminoacyl-tRNA biosynthesis pathways, interfered with energy metabolism, and aggravated oxidative stress in earthworms. These findings provide a basis for assessing the ecological impacts of using nZVI to remediate soils contaminated with BDE-209 from electronic waste.

Effects of 17ß-estradiol and 17α-ethinylestradiol on the embryonic development of the clearhead icefish (Protosalanx hyalocranius).

Estrogenic effects of 17ß-estradiol (E2) and 17α-ethinylestradiol (EE2) on animals have been widely reported. The high sensitivity of fish in the early-life stages to xenobiotics can be exploited to evaluate the developmental effects of environmentally relevant levels of E2 and EE2. In this work, clearhead icefish (Protosalanx hyalocranius) embryos (blastula stage) were exposed to E2 or EE2 at concentrations between 0.05 ng/L and 1 mg/L. The toxicity endpoints of mortality, teratogenesis, and hatching retardation were evaluated. The results showed that continuous exposure of the fish embryos/larvae to higher concentrations of E2 and EE2 dramatically increased mortality after 17 days, when the hatching period started. An E2 concentration of 8 µg/L (day 16) and an EE2 concentration of at 0.2 mg/L (day 18) induced maximum teratogenesis rates of 30% and 35%, respectively. Embryos exposed to 0.2 mg E2 or EE2/L had a significantly retarded hatching time compared to the control. Thus, although environmentally relevant concentrations E2 and EE2 are not lethal for P. hyalocranius embryos or larvae, their ability to induce teratogenesis and hatching retardation merits concern.