Page 950 - The Toxicology of Fishes

930 The Toxicology of Fishes

to stress at the end of the winter as they come into spawning condition. As evidence, viral hemorrhagic
septicemia virus has been isolated several times from adult Pacific herring in Washington, British
Columbia, and Alaska, and these areas were not exposed to oil spills (Meyers and Winton, 1995). In a
detailed study of disease in the Pacific herring population of PWS from 1994 through 2002, both hepatic
necrosis and viral hemorrhagic septicemia virus were common during some years in spring samples but
not fall samples, and these findings were considered to be independent of any direct effects from Exxon
Valdez oil (Marty et al., 2003).
Among adult Pacific herring examined in 1990, fish from oiled sites had significantly greater histo-
pathology scores for pigmented macrophage aggregates. Pigmented macrophage aggregates are irregular
spherical structures that are a normal component of organs such as the liver, kidney, and spleen.
Lipofuscin and iron are the most common non-melanin pigments, and three main functions have been
identified (Wolke, 1992): (1) immunity; (2) storage, destruction, or detoxification of substances produced
inside the fish (tissue components) or outside the fish (e.g., toxins in the water); and (3) iron recycling.
Pigmented macrophage aggregates are rare in Pacific herring before they first spawn, but they increase
in size and number as fish age. In samples from 1990, the age of fish from the oiled site (mean, 5.6
years) was greater than the age of fish from the reference site (mean, 2.3 years); therefore, differences
in pigmented macrophage aggregates were more likely a result of age differences in the sample than
due to oil exposure (Marty et al., 1999; Wolke, 1992). In 1991, no oil-related effects were detected
among adults. In 1992, fish from the 1988 year class that spawned in previously oiled areas had less
reproductive success than fish spawning in reference areas; reproductive success was significantly related
to microscopic lesions but not to oil history of the sites (Kocan et al., 1996b). In the fall of 1992, a
record Pacific herring biomass was predicted for the roe harvest in April 1993. The Pacific herring
population of PWS was considered fully recovered from effects of the spill, and all Pacific herring study
was terminated.
In 1993, the population crashed. More than 700 million adult Pacific herring, 70 to 80% of the
population, disappeared between the fall of 1992 and the spring of 1993. Between 15 and 43% of the
fish that returned to spawn in 1993 had ulcers and hemorrhage of the skin and fins (Meyers et al., 1994);
as soon as the magnitude of the problem was realized, all Pacific herring fisheries were closed. The
cause was probably not directly related to oil exposure but might have been a secondary response to
management decisions that increased the population density after the spill. A detailed analysis of potential
causes of the population crash and a potential link to the oil spill can be found elsewhere (Carls et al.,
2002; Pearson et al., 1999). Viral hemorrhagic septicemia virus was isolated from fish sampled in 1993
(Meyers et al., 1994), and the virus probably contributed significantly to the death of many of the fish.
After another year of population decline, detailed study in 1994 revealed no evidence that fish exposed
to the oil spill in 1989 as larvae or juveniles had increased disease prevalence (Elston et al., 1997; Marty
et al., 1998). The cause of the population crash likely was a complex interaction among the fish,
environment, and the diseases or pathogens to which the fish were exposed. Comprehensive semiannual
disease study of the Pacific herring population of PWS through 2002 clearly demonstrated a significant
link between disease prevalence and changes in population biomass (Marty et al., 2003).

Summary
Oil spilled from the Exxon Valdez caused significant damage to Pacific herring larvae and adults in 1989.
Decreased concentrations of oil in the water column by 1990 were correlated with an absence of
significant effects in Pacific herring in 1990 and beyond. Severe population decline occurred just 4 years
after the spill, but direct links to the spill were not detected. Because Pacific herring commonly are
infected with a potentially deadly virus (viral hemorrhagic septicemia virus), and stress results in virus
outbreaks, Pacific herring are unusually sensitive to spilled oil or other abnormal stressors during
physiologically demanding periods of their life cycle such as spring spawning. As a result, oil spills that
overlap with Pacific herring spawning are likely to cause greater population damage than oil spills that
occur at other times of the year.