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hazardous to wildlife. The herring collapse was explained by a disease caused by a viral
hemorrhagic septicemia virus, possibly favored by immunological deficiency consecutive
to PAH contamination (Chapter 6). Other factors have been put forward, such as insuffi-
cient food supply, population at carrying capacity, and poor overwintering conditions for
the fish. The tools were not in place at the time of the oil spill and the collapse to validate
any hypothesis. Therefore, the link between the EVO spill and disappearance of the her-
ring population has remained a contentious subject.
Recent papers reanalyzed the question in the light of documented data demonstrating
that the herring decline began earlier than 1992 and was associated with the EVO spill.
Thorne and Thomas (2008) produced comprehensive data on the behavior of adult her-
ring, showing them to be vulnerable to damage from oil spills, which was unknown or
misunderstood at the time of the spill: for instance, the surfacing behavior of herring that
undergo vertical migration and gulp air at the surface, contributing to their exposure to oil
via ingestion and gill coating.
Hulson et al. (2008) confirmed that the population model used overestimated her-
ring biomass from 1990 to 1992, and that back-calculated estimates from hydroacoustic
abundance showed a decline actually starting in 1989. For these authors, there were two
declines, one in 1989 due to the oil spill, and the main one in 1992 when disease affected a
large population that was in weakened condition.
Incardona et al. (2005, 2009) and Hicken et al. (2011) gave mechanistic explanations to the
decline of the Pacific herring in PWS. Fish embryos exposed to low levels of low molecular
tricyclic PAHs in weathered crude oil were shown to develop a syndrome of pericardial
edema, and craniofacial and body axis defects (Incardona et al. 2005). Cardiac syndrome
was the primary response of herring embryos to ANSCO crude oil during weathering
(Incardona et al. 2009). Transient embryonic exposure to very low concentrations of oil
causes sublethal and delayed toxicity: nearly a year after oil embryonic exposure, adult
fishes showed subtle changes in performance, indicative of reduced cardiac output suf-
ficient to compromise survival under stress conditions. These delayed physiological
impacts on cardiovascular performance at later stages provide a potential mechanism
linking reduced individual survival to population-level ecosystem responses of fish spe-
cies to chronic, low-level oil pollution.
The population effects on fish populations after the EVO spill are cause for concern of
the effects of any major spill, including the recent Deepwater Horizon (DWH) event. The
long-term biological consequences of this oil spill are still unknown, especially for resident
organisms, with the exception of evident toxicity on avian species and mortality in wild-
life. Embryotoxicity studies are being conducted. Genomic and physiological footprints
of the DWH oil spill on resident marsh fishes attested to exposure to hydrocarbon-like
chemicals and indicate physiological and reproductive impairment (Whitehead et al. 2011).
13.3.2 Genotoxicity, Population Genetics, and Environmental Contamination
We have not found any experimental ecoepidemiological studies directly answering the
question of the involvement of genomic alterations induced by environmental stressors on
population dynamics. But there are a few studies retrospectively relating genomic changes
and good health of living populations in contaminated environments.
Theodorakis and Shugart (1997) studied these relationships in populations of mosquito
fish (
G. affinis)
) living in four ponds—two noncontaminated (A, B) and two radioactively-
contaminated (C, D)—on or near the Department of Energy Oak Ridge Reservation
(US-TN). Site C was colonized in the late 1970s by the transplantation of approximately
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