Ever since the pioneering work of George Burdick in the 1960s on DDT-related mortality affecting early life stages of lake trout, there has been an increased awareness and appreciation of the sensitivity of embryonic stages to environmental stressors. In the 1970s and 1980s, John Gunn’s seminal work on acid precipitation showed the extreme vulnerability of early life stages of lake trout to acidic runoff. In the 1990s still more evidence of the sensitivity of early life stages was provided in the elegant work of Mary Walker and Richard Peterson on the extreme susceptibility of larval lake trout to 2,3,7,8-tetrachlorodibenzo-p-dioxin and its establishment as a prototypical chlorinated organic toxicant. Given this history, we should not be surprised by the elevated occurrence of early mortality syndromes (EMS) now occurring in the progeny of various Great Lakes salmonids; however, it is unusual that these syndromes show so little relationship with anthropogenic toxicants. Indeed, the current mortality syndromes seem to have occurred during a period of reduced contaminant levels, with no direct human involvement, and in contrast seem to have been generated by the very food webs on which the affected species have depended for nourishment for many decades. It is noteworthy that EMS has been present for some time and while the causal factors that have generated the current epizootics of EMS remain to be clearly identified, a threshold has evidently been crossed in recent times. The consequences of this new set of conditions is evident in the high levels of EMS occurring in salmonids throughout the Great Lakes. Yet the problem extends beyond the Great Lakes: it affects salmonids in the New York Finger Lakes where it is called Cayuga Syndrome and the Baltic Sea where it is called M74.