404
changes (Snyder et al. 2019). Similar to red snapper, preliminary microscopic analysis of golden tilefish tissues indicated 99% of individuals exhibited microscopic
changes in hepatic tissue. These changes included glycogen-type vacuolar change
(72%), increased occurrence of pigmented macrophage aggregates (55%), biliary
fibrosis and duplication (37%), lipid-type vacuolar change (35%), granulomas
(25%), hepatocellular atrophy (12%), foci of cellular alteration (9%) and one neoplasm (<1%). The occurrence of neoplasms typically associated with chronic contaminant exposure was rare (n = 1; hepatocellular adenoma); however, approximately
9% of individuals examined exhibited foci of cellular alteration, which are often
considered “preneoplastic lesions.” Preliminary data analysis suggests significant
linear associations between hepatobiliary burdens of PAHs and hepatocellular atrophy, foci of cellular alteration, biliary fibrosis, and glycogen-type vacuolar change
in golden tilefish from the DeSoto Canyon region (Fig. 24.9). However, further
investigation is warranted as many of the observed changes could be normal for the
species or the changes could be related to chronic stress, disease, or starvation, all
of which could potentially be exacerbated by chronic toxicant exposure.
A smaller subset of golden tilefish hepatic tissues collected from offshore Texas
in 2016 (n = 26) and the Bay of Campeche, Mexico, in 2015 (n = 24) were also
analyzed for microscopic changes. Golden tilefish from these regions exhibited
similar hepatic changes to those from the DeSoto Canyon region, with glycogentype vacuolar change being the most common (92% of individuals from Mexico,
85% from Texas). The frequency of occurrence of lesion types was similar across
the three regions, with a notable difference being higher frequency of granulomas in
both the Mexico (88%) and Texas (65%) regions compared to the DeSoto Canyon
(25%). The granulomas observed were likely the result of host response to a parasitic infection, most commonly of larval nematode migration through the tissues.
Higher frequency of parasitic infection in these regions may be due to higher susceptibility of hosts in response to contamination in the environment.
24.7 Conclusions
While massive fish kills and similar evidence of severe impacts were not obvious
from either the DWH or Ixtoc 1, there is nevertheless strong observational and correlative evidence of impacts on fish populations within the boundaries of observed
oil distributions. Many sub-lethal effects were observed in field-caught specimens
that were also apparent in controlled laboratory-based exposure trials. For example,
elevated lesion frequencies in several species (Fig. 24.2; Murawski et al. 2014) were
correlated with PAH exposure; subsequent laboratory trials were able to induce
lesion occurrence when fishes were exposed to oil and elevated bacterial loads, but
not to elevated pathogenic bacteria levels alone (Bayha et al. 2017). This is strong
prima facie evidence for oil exposure being the proximal cause of skin lesions
observed not only in scientific surveys but by fishers. This example demonstrates
E. L. Pulster et al.
changes (Snyder et al. 2019). Similar to red snapper, preliminary microscopic analysis of golden tilefish tissues indicated 99% of individuals exhibited microscopic
changes in hepatic tissue. These changes included glycogen-type vacuolar change
(72%), increased occurrence of pigmented macrophage aggregates (55%), biliary
fibrosis and duplication (37%), lipid-type vacuolar change (35%), granulomas
(25%), hepatocellular atrophy (12%), foci of cellular alteration (9%) and one neoplasm (<1%). The occurrence of neoplasms typically associated with chronic contaminant exposure was rare (n = 1; hepatocellular adenoma); however, approximately
9% of individuals examined exhibited foci of cellular alteration, which are often
considered “preneoplastic lesions.” Preliminary data analysis suggests significant
linear associations between hepatobiliary burdens of PAHs and hepatocellular atrophy, foci of cellular alteration, biliary fibrosis, and glycogen-type vacuolar change
in golden tilefish from the DeSoto Canyon region (Fig. 24.9). However, further
investigation is warranted as many of the observed changes could be normal for the
species or the changes could be related to chronic stress, disease, or starvation, all
of which could potentially be exacerbated by chronic toxicant exposure.
A smaller subset of golden tilefish hepatic tissues collected from offshore Texas
in 2016 (n = 26) and the Bay of Campeche, Mexico, in 2015 (n = 24) were also
analyzed for microscopic changes. Golden tilefish from these regions exhibited
similar hepatic changes to those from the DeSoto Canyon region, with glycogentype vacuolar change being the most common (92% of individuals from Mexico,
85% from Texas). The frequency of occurrence of lesion types was similar across
the three regions, with a notable difference being higher frequency of granulomas in
both the Mexico (88%) and Texas (65%) regions compared to the DeSoto Canyon
(25%). The granulomas observed were likely the result of host response to a parasitic infection, most commonly of larval nematode migration through the tissues.
Higher frequency of parasitic infection in these regions may be due to higher susceptibility of hosts in response to contamination in the environment.
24.7 Conclusions
While massive fish kills and similar evidence of severe impacts were not obvious
from either the DWH or Ixtoc 1, there is nevertheless strong observational and correlative evidence of impacts on fish populations within the boundaries of observed
oil distributions. Many sub-lethal effects were observed in field-caught specimens
that were also apparent in controlled laboratory-based exposure trials. For example,
elevated lesion frequencies in several species (Fig. 24.2; Murawski et al. 2014) were
correlated with PAH exposure; subsequent laboratory trials were able to induce
lesion occurrence when fishes were exposed to oil and elevated bacterial loads, but
not to elevated pathogenic bacteria levels alone (Bayha et al. 2017). This is strong
prima facie evidence for oil exposure being the proximal cause of skin lesions
observed not only in scientific surveys but by fishers. This example demonstrates
E. L. Pulster et al.