Global climate change is impacting organisms, biological communities and ecosystems around the world. While most research has focused on characterizing how the climate is changing, including modeling future climatic conditions and predicting the impacts of these conditions on biodiversity, it is also the case that climate change is altering the environmental impacts of chemical pollution. Future climate conditions are expected to influence both the worldwide distribution of chemicals and the toxicological consequences of chemical exposures to organisms. Many of the environmental changes associated with a warming global climate (e.g., increased average – and possibly extreme – temperatures; intense periods of drier and wetter conditions; reduced ocean pH; altered salinity dynamics in estuaries) have the potential to enhance organism susceptibility to chemical toxicity. Additionally, chemical exposures themselves may impair the ability of organisms to cope with the changing environmental conditions of the shifting climate. Such reciprocity in the interactions between climate change and chemicals illustrates the complexity inherent in predicting the toxicological consequences of chemical exposures under future climate scenarios. Here, we summarize what is currently known about the potential reciprocal effects of climate change and chemical toxicity on wildlife, and depict current approaches and ongoing challenges for incorporating climate effects into chemical testing and assessment. Given the rapid pace of new man-made chemistries, the development of accurate and rapid methods to evaluate multiple chemical and non-chemical stressors in an ecologically relevant context will be critical to understanding toxic and endocrine-disrupting effects of chemical pollutants under future climate scenarios.

Background: Polybrominated diphenyl ether (PBDE) flame retardants have been implicated as disruptors of the hypothalamic-pituitary-thyroid axis. Animals exposed to PBDEs may show reduced plasma thyroid hormone (TH), but it is not known whether PBDEs impact TH-regulated pathways in target tissues. Objective: We examined the effects of dietary exposure to 2,2′,4,4′-tetrabromodiphenyl ether (PBDE-47)—commonly the highest concentrated PBDE in human tissues—on plasma TH levels and on gene transcripts for glycoprotein hormone α-subunit (GPHα) and thyrotropin β-subunit (TSHβ) in the pituitary gland, the autoinduced TH receptors α and β in the brain and liver, and the TH-responsive transcription factor basic transcription element-binding protein (BTEB) in the brain. Methods: Breeding pairs of adult fathead minnows (Pimephales promelas) were given dietary PBDE-47 at two doses (2.4 μg/pair/day or 12.3 μg/pair/day) for 21 days. Results: Minnows exposed to PBDE-47 had depressed plasma thyroxine (T4), but not 3,5,3′-triiodothyronine (T3). This decline in T4 was accompanied by elevated mRNA levels for TStHβ (low dose only) in the pituitary. PBDE-47 intake elevated transcript for TH receptor αin the brain of females and decreased mRNA for TH receptor β in the brain of both sexes, without altering these transcripts in the liver. In males, PBDE-47 exposure also reduced brain transcripts for BTEB. Conclusions: Our results indicate that dietary exposure to PBDE-47 alters TH signaling at multiple levels of the hypothalamic-pituitary-thyroid axis and provide evidence that TH-responsive pathways in the brain may be particularly sensitive to disruption by PBDE flame retardants.

SUMMARY: Salmon have long been known to imprint and home to natal stream odors, yet the mechanisms driving olfactory imprinting remain obscure. The timing of imprinting is associated with elevations in plasma thyroid hormone levels,with possible effects on growth and proliferation of the peripheral olfactory system. Here, we begin to test this idea by determining whether experimentally elevated plasma levels of 3,5,3′-triiodothyronine (T3)influence cell proliferation as detected by the 5-bromo-2′-deoxyuridine(BrdU) cell birth-dating technique in the olfactory epithelium of juvenile coho salmon (Oncorhynchus kisutch). We also explore how natural fluctuations in thyroxine (T4) relate to proliferation in the epithelium during the parr-smolt transformation. In both studies, we found that BrdU labeled both single and clusters of mitotic cells. The total number of BrdU-labeled cells in the olfactory epithelium was significantly greater in fish with artificially elevated T3 compared with placebo controls. This difference in proliferation was restricted to the basal region of the olfactory epithelium, where multipotent progenitor cells differentiate into olfactory receptor neurons. The distributions of mitotic cluster sizes differed significantly from a Poisson distribution for both T3 and placebo treatments, suggesting that proliferation tends to be non-random. Over the course of the parr-smolt transformation, changes in the density of BrdU cells showed a positive relationship with natural fluctuations in plasma T4. This relationship suggests that even small changes in thyroid activity can stimulate the proliferation of neural progenitor cells in the salmon epithelium. Taken together, our results establish a link between the thyroid hormone axis and measurable anatomical changes in the peripheral olfactory system.