Page 949 - The Toxicology of Fishes

Effects of the Exxon Valdez Oil Spill on Pacific Herring in Prince William Sound, Alaska 929

hatch. When Exxon-funded scientists examined the resultant larvae for abnormalities that could be
detected using a dissecting microscope (Pearson et al., 1995), they found no relation between lesions
and egg PAH levels and concluded that 4% of miles of herring spawn were on oiled beaches. By
comparison, Trustee Council-funded scientists examined resultant larvae using gross examination,
cytogenetic analysis (e.g., morphology of mitotic figures in fin epidermal cells), and histopathology
(Hose et al., 1996). They found that significant morphological and cytogenetic abnormalities were
significantly correlated with PAH concentrations in mussels collected from the same area as eggs, and
these results were confirmed with laboratory study (Carls et al., 1999; Kocan et al., 1996a). Trustee
Council-funded scientists concluded that more than 25% of the egg biomass was deposited within the
oil trajectory (Brown et al., 1996; Carls et al., 2002). Eggs deposited in 1990 and beyond had no
evidence of spill-related effects.
Two studies of Pacific herring larvae in 1989 revealed that the spill had several significant effects. In
the first study, staggered plankton trawls in oiled and reference sites in nearshore areas of PWS through
May and June of 1989 provided evidence that larval mortality in oiled areas was two times greater than
in reference areas (McGurk and Brown, 1996). Microscopic analysis of a subset of the trawled larvae
revealed that larvae from oiled sites were shorter, had ingested less food, and had evidence of slower
growth (Marty et al., 1997); the prevalence of fish with cytogenetic damage in this subset was also
greater in fish from oiled areas (oiled, 56 to 84% had damage; reference, 32 to 40% had damage).
Prevalence of ascites (i.e., accumulation of fluid in the coelomic/peritoneal cavity) was greater in fish
from oiled sites (16%) than in fish from reference sites (1%) (Marty et al., 1997). As corroborative
evidence that the spill was responsible for these changes, laboratory study demonstrated that 50% of
Pacific herring developed ascites after continuous exposure to 0.8-µg/L PAH during embryonic and early
larval development (Carls et al., 1999). Ascites and pericardial edema (i.e., accumulation of fluid around
the heart) are probably irreversible lethal lesions in most affected fish.
In a second field study, plankton trawls were done in offshore areas of PWS during May, June, and
July of 1989 (Norcross et al., 1996). Currents in offshore areas had mixed the planktonic larvae such
that the potential oiling history of larvae captured offshore could not be determined; however, many
larvae exhibited symptoms associated with oil exposure in laboratory experiments and other oil spills.
Effects included morphological malformations, genetic damage, and small size. Growth between May
and June 1989 was the lowest ever reported for field-caught larval Pacific herring throughout their
distribution (Norcross et al., 1996). Some of the offshore trawls were repeated 6 years later; in May
1995, jaw and cytogenetic development in Pacific herring larvae were normal and significantly different
from larvae in 1989 (Norcross et al., 1996). Despite very large spawn deposition in 1989, that year’s
class turned out to be one of the smallest to be recruited into the fishery; by comparison, the spawning
biomass of the 1995 year class was less than 25% of the 1989 year class, but recruitment of the 1995
year class into the fishery was above average. Although it is tempting to conclude that the oil spill was
responsible for poor recruitment of the 1989 year class, recruitment of the 1989 year class was also poor
in Sitka Sound (G.D. Marty and Alaska Department of Fish and Game, unpublished data), which was
used as a reference site for the PWS Pacific herring population (Hose et al., 1996; Pearson et al., 1995).
Thus, oceanographic variables probably were more significant in limiting recruitment of the 1989 year
class in PWS than was the oil spill (Marty et al., 1997).
Effects of the oil spill on Pacific herring juveniles were not reported, but significant effects were found
among adults. Unfortunately, small sample size in 1989 prevented the extrapolation of these findings to
the population level. In 1989, 20% of 20 adults sampled from oiled sites had hepatic necrosis (liver cell
death, determined using histopathology), but none of the fish from reference sites had hepatic necrosis
(Marty et al., 1999). Also, fish sampled from oiled sites had fewer herring worms (Anisakidae) in their
visceral cavity than did fish from reference sites, and laboratory study confirmed that parasite numbers
in the visceral cavity significantly decreased after oil exposure (Moles et al., 1993). Hepatic necrosis
was initially thought to be a direct toxic effect of oil; however, subsequent laboratory study revealed
that hepatic necrosis in Pacific herring can be caused by expression of viral hemorrhagic septicemia
virus (Kocan et al., 1997), and expression of viral hemorrhagic septicemia virus can be induced in adults
by dose-dependent exposure to weathered crude oil (Carls et al., 1998). The link between oil exposure
and viral expression is probably a nonspecific complication following stress, and fish are most susceptible