Embryo-larval BDE-47 exposure causes decreased pathogen resistance in adult male fathead minnows (Pimephales promelas).

Exposures to polybrominated diphenyl ethers (PBDEs) have been shown to alter immune function in adult organisms across a variety of taxa. However, few if any studies have investigated the long-term consequences of early life stage PBDE exposures on immune function in fish. This study sought to determine the effects of early life stage BDE-47 exposure on pathogen resistance in the fathead minnow (Pimephales promelas) following an extended depuration period (≥180 d). Minnows were exposed to BDE-47 via a combination of maternal transfer and diet through 34 days post fertilization (dpf), raised to adulthood (>215 dpf) on a clean diet, then subjected to pathogen resistance trials. Early life stage exposures to BDE-47 did not affect the ability of females to survive from Yersinia ruckeri infection. However, the survival of BDE-47 exposed males was significantly reduced relative to controls, indicating that developmental exposures to BDE-47 altered male immunity. Because BDE-47 is a known thyroid hormone disruptor and thyroid hormone disruptors have the potential to adversely impact immune development and function, metrics indicative of thyroid disruption were evaluated, as were immune parameters known to be altered in response to thyroid disruption. BDE-47 exposed minnows exhibited signs of thyroid disruption (i.e., reduced growth); however, no alterations were observed in immune parameters known to be influenced by thyroid hormones (i.e., thymus size, expression of genes associated with lymphoid development) suggesting that the observed alterations in immunocompetence may occur through alternative mechanisms. Regardless of the mechanisms responsible, the results of this study demonstrate the potential for early life stage PBDE exposures to adversely impact immunity and illustrate that the immunological consequences of PBDE exposures are sex dependent.