Read the full story at Environmental Health News.
Fish exposed to low levels of common flame retardants called PBDEs for most of their lives pass the chemicals – and more surprisingly, the associated toxic effects – along to their progeny. While parents’ health effects were minimal, the exposures reduced hatch rates and altered the thyroid hormone system of the next generation.
Effects were worse if the offspring were also exposed to the same low chemical levels as their parents, a situation that would mimic wild fish in a natural environment. The findings – published in the journal Environmental Science and Technology – broadly suggest that the toxic effects of PBDE exposure may magnify in subsequent generations of wild fish.
The study is important because it shows that flame retardants can trigger thyroid hormone disruption in the next generation whether or not the offspring are exposed to the chemicals.
Full citation for the research article: Yu, L, JCW Lam, Y Guo, RSS Wu, PKS Lam and B Zhou. 2011. “Parental transfer of PBDEs and thyroid endocrine disruption in zebrafish”. Environmental Science and Technology http://dx.doi.org/10.1021/es2026592.
Abstract: Polybrominated diphenyl ethers (PBDEs) have the potential to disrupt the thyroid endocrine system. The objective of the present study was to characterize the disrupting effects of long-term exposure on the thyroid endocrine system in adult fish and their progeny following parental exposure to PBDEs. Zebrafish (Danio rerio) embryos were exposed to environmentally relevant concentrations (1, 3, and 10 μg/L) of the PBDE mixture DE-71 for 5 months until sexual maturation. In the F0 generation, exposure to DE-71 significantly increased plasma thyroxine (T4) but not 3,5,3′-triiodothyronine (T3) in females. This increased T4 was accompanied by decreased mRNA levels of corticotropin-releasing hormone (CRH) and thyrotropin β-subunit (TSHβ) in the brain. The F1 generation was further examined with or without continued DE-71 treatment conditions. Exposure to DE-71 in the F0 fish caused significant increases in T4 and T3 levels in the F1 larvae and modified gene expressions in the hypothalamic–pituitary–thyroid axis (HPT axis) under both conditions. Decreased hatching and inhibition of growth in the F1 offspring were observed in the condition without DE-71 treatment. Continued DE-71 treatment in the F1 embryos/larvae resulted in further decreased hatching, and increased malformation rates compared with those without DE-71 exposure. Analysis of F1 eggs indicated that parental exposure to DE-71 could result in a transfer of PBDEs and thyroid hormones (THs) to their offspring. For the first time, we demonstrated that parental exposure to low concentrations of PBDEs could affect THs in the offspring and the transgenerational PBDE-induced toxicity in subsequent nonexposed generations.