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conspired to create a "worst case" scenario for marine oil pollution.
Therefore, the Amoco Cadiz spill offered a unique opportunity to study
in detail the long-term impact and timecourse of biological recovery
from a catastrophic pollution incident.
While we already know that the immediate biological effects of the
spill were very serious in some areas (Cross et al. , 1978; Chasse, 1978;
Chasse and Morvan, 1978), there was very little information upon which
to base estimates of the rate at which the impacted area would be returned
to pre-spill biological productivity. We have used several biochemical
parameters and histopathological examination in an ongoing biological
survey to assess the health and rate of recovery of marine animals from
the two heavily polluted estuaries.
The primary objective of this research program was to assess the
degree of chronic sublethal pollutant stress experienced by representative
species of benthic fauna from Aber Benoit and Aber Wrac'h. Two
indices of stress were used. These are histopathology and biochemical
composition. We expected the fauna of these severely impacted estuaries
to exhibit an elevated incidence of various histopathological lesions
directly or indirectly related to oil pollution stress. As the estuaries
recovered from the spill the incidence of these lesions was expected to
diminish. Similarly, the concentrations of certain diagnostic biochemical
components of the severely stressed fauna were expected to deviate significantly
from normal. These diagnostic biochemical indices were
expected to return to normal as the estuaries recovered and the resident
fauna became less severely stressed. The results of this investigation
provide valuable information for assessing the biological recovery of
these severely polluted estuaries. They also provide a means of diagnosing,
pollutant stress in other polluted environments.
I. Histopathology of Oysters Crassostrea gigas
Marine animals readily accumulate petroleum hydrocarbons in their
tissues from dispersion or solution in sea water and to a lesser extent
from petroleum-contaminated sediments and food (see recent reviews by
Neff et al., 1976 a,b; Lee, 1977; Varanasi and Malins, 1977; Neff, 1979;
Neff and Anderson, 1981). The accumulated hydrocarbons and in particular
the more toxic aromatic hydrocarbons interact with cellular membranes
and interfere with membrane-mediated biological processes (Roubal and
Collier, 1975). Two types of histopathological lesions may result from
chronic contamination of marine animals with oil.
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