Over the years, Diane Nacci and her group at the Atlantic Ecology division of the EPA, has done some really nice (and tedious) work with many populations, and generations of killifish which strongly suggests evolution in populations along the Atlantic coast, in response to PCBs, dioxins and similar acting chemicals. For a review of Diane’s work see: Adaptation of the Estuarine Fish Fundulus heteroclitus (Atlantic Killifish) to Polychlorinated Biphenyls (PCBs)
Additional studies with Andrew Whitehead at Louisiana State University provide some insight into the mechanism behind such widespread resistance as discussed here. For more, see Common mechanism underlies repeated evolution of extreme tolerance to pollution, published in the Proceedings of the Royal Society B.
Also, Whitehead and others tease apart differences in gene expression associated with plasticity versus adaptation. In their article “Functional genomics of physiological plasticity and local adaptation in killifish” published in Journal of Heredity, 2011, 102:499-511. In killifish, tolerance to rapid changes in salinity (e.g. saltwater populations transferred to freshwater) hundreds of genes respond, according to the authors, enabling fish to undergo “early crisis contol phase followed by a tissue remolding phase.” Yet these changes are drawn from the existing genetic architecture, and as such are considered to be the result of a plastic phenotype. In contrast, resistance or tolerance to contaminants like PCBs and dioxins as discussed above, are the result of changes in the genome which are heritable and which have become fixed within exposed populations. Changes in salinity are thought to be sporadic in contrast to anthropogenic contamination like PCBs and dioxins, which are continuous for local populations, presenting perhaps differences in “spatial and temporal scale[s] at which environmental extremes ae experience in the lifetimes of individuals. For more see: Whitehead et al., 2011.