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In this study, we describe remarkable intraspecific variation in sensitivity to the broadly distributed pollutants, polychlorinated biphenyls (PCBs), among wild populations of the nonmigratory estuarine Atlantic killifish (Fundulus heteroclitus). Variation among killifish populations was characterized in 28-day laboratory challenges using embryonic and larval life stages and the highly toxic, dioxin-like PCB congener, 3,3′4,4′,5-hexachlorobiphenyl (PCB126). In summarizing results for 24 populations, we show that killifish populations vary over four orders of magnitude in their sensitivity to PCB126 and that this variation is adaptive to the magnitude of contamination at their residence site. The four least-sensitive killifish populations reside in US Atlantic coast urban harbors >100 km apart from one another: New Bedford, MA, Bridgeport, CT, Newark, NJ, and Norfolk, VA, USA. Prior studies examining all but the CT population have shown that these killifish are relatively insensitive to local contaminants, with mixed evidence concerning the heritability of this trait. We show here that tolerance to PCB126 is extreme, with some mechanistic similarities among these four killifish populations. However, these populations do not respond identically to each other, and in at least one population, tolerance appears to degrade over the F1 and F2 generations tested. Complementary ongoing studies using molecular approaches provide opportunity to identify unique and shared mechanisms of tolerance in these independently evolving populations and explore the adaptive benefits and costs of contemporary evolutionary responses in the wild.

A population of the nonmigratory estuarine fish species Fundulus heteroclitus (mummichog) indigenous to a polychlorinated biphenyl (PCB)-contaminated Superfund site (New Bedford Harbor, MA, USA) demonstrated an inherited tolerance to local, dioxinlike contaminants (DLCs). These findings suggest that DLCs have acted as selective agents, allowing the survival of only the most tolerant individuals, forming DLC-adapted populations. We hypothesized that DLC-tolerant mummichog populations would reside where local conditions are toxic to sensitive individuals, and that toxic environmental conditions could be predicted based on responses of sensitive early life stages to laboratory exposures of DLCs. As a measure of DLC tolerance, progeny of field-collected fish were tested in the laboratory with a dioxinlike PCB congener, 3,3',4,4',5-pentachlorobiphenyl (PCB 126). Mummichog populations were collected from sites with sediment PCB concentrations predicted to range from nontoxic to toxic. Consistent with predictions, tolerant populations were indigenous to sites with elevated sediment PCB concentrations. Also, as predicted, DLC-tolerant populations were resident to sites far less contaminated than the Superfund site. These results suggest that exposures to persistent, bioaccumulative, and toxic contaminants may produce evolutionary effects on a geographic scale larger than previously envisioned. This study presents an approach and describes a model system that may improve understanding of the scale of occurrence for these potentially irreversible ecological effects.

Atrazine (ATR) has recently been shown to activate the hypothalamic-pituitary-adrenal (HPA) axis in rodents. The current study investigated the effect of ATR and two of its chlorinated metabolites, desisopropylatrazine (DIA) and diamino-s-chlorotriazine (DACT), on the HPA axis in the Long-Evans female rat. A single oral gavage administration of 75 mg/kg ATR or 60.2 mg/kg DIA (a dose equimolar to the applied ATR dose) during the morning of proestrus resulted in significant, acute increases in circulating adrenocorticotropic hormone (ACTH), corticosterone, and progesterone. Oral doses of ATR or DIA were given daily over the course of the 4-day ovarian cycle starting on the day of vaginal estrus, resulted in a similar, dose-responsive activation of the HPA axis. The increase in ACTH, corticosterone, and progesterone by these compounds was of a similar magnitude to that produced by 5-min restraint stress. Single or multiple oral exposures to DACT, on the other hand, did not significantly alter pituitary-adrenal hormone release. These results were observed despite plasma levels of DACT being higher than any other metabolite at the time of hormone measurement. Overall, circulating metabolite concentrations following equimolar dosing were much higher than those observed after ATR administration. Additional studies indicated that the activation of the HPA axis by oral exposure to ATR and DIA was not due simply to the stimulation of gastrointestinal afferents. Similar responses were observed in rats which received an oral dose of ATR following bilateral subdiaphramatic vagotomy and following intravenous administration of DIA in jugular vein catheterized animals. We conclude that ATR and the metabolite DIA significantly activate the HPA axis following oral exposure in the female rat. Activation of this endocrine axis by these chlorotriazines could contribute to the induced changes of female reproductive function reported previously.

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