![]() ![]() |
NOAA Technical Memorandum NMFS-NWFSC-36
Fish Injury
|
Reference in this document to trade names does not imply endorsement by the National Marine Fisheries Service, NOAA.
Paper copies of this report may be available for a fee from:
National Technical Information Service
5285 Port Royal Road
Springfield, VA 22161
1-800-553-6847
orders@ntis.fedworld.gov
Section 1. Juvenile Salmon Injury Study
Section 2. Flatfish Toxicopathic Injury Study
Section 3. Flatfish Reproductive Injury Study
The following appendices are available only in PDF format - click here to download the Adobe Acrobat reader: Adobe Acrobat
Appendix A - Sampling and Analysis Plan for Hylebos Waterway Fish Injury Studies (42 p.
Appendix B - List of Individual Organic Analytes Measured in Chemical Analyses of
Fish Liver Tssue and Stomach Contents for Hylebos Waterway Fish Injury Studies (4 p.
Appendix C - Case Narratives for Hylebos Water Fish Injury Studies
Appendix E - Commencement Bay Damage Assessment Quality Assurance Plan (35 p.
List of Abbreviations (Included with Appendix E)
SECTION 1. JUVENILE SALMON INJURY STUDY
Figure 1.1 Sampling site locations for the Juvenile Salmon Injury Study
Figure 1.2 Hexachlorobenzene and hexachlorobutadiene in liver of juvenile salmon
Figure 1.3 PCBs in liver of juvenile salmon
Figure 1.4 DDTs, chlordanes, and dieldrin in liver of juvenile salmon
Figure 1.5 Heptachlor, lindane, and aldrin in liver of juvenile salmon
Figure 1.6 Fluorescent aromatic compounds in bile of juvenile salmon
Figure 1.7 Aromatic hydrocarbons in stomach contents of juvenile salmon
Figure 1.8 Hexachlorobenzene and hexachlorobutadiene in stomach contents of juvenile salmon
Figure 1.9 PCBs in stomach contents of juvenile salmon
Figure 1.10 DDTs, chlordanes, and dieldrin in stomach contents of juvenile salmon
Figure 1.11 Heptachlor, lindane, and aldrin in stomach contents of juvenile salmon
Figure 1.12 Cytochrome P4501A activity and DNA adducts in liver of juvenile salmon
Figure 1.13 Comparisons of Hylebos Waterway
juvenile salmon data with historical data from Commencement Bay and the Duwamish Waterway
SECTION 2. FLATFISH TOXICOPATHIC INJURY STUDY
Figure 2.1 Sampling site locations for the Flatfish Toxicopathic Injury Study
Figure 2.2 Aromatic hydrocarbons in English sole and rock sole stomach contents
Figure 2.3 Polychlorinated biphenyls in English sole and rock sole stomach contents
Figure 2.4 Hexachlorobenzene and hexachlorobutadiene in stomach contents of English sole and rock sole
Figure 2.5 DDTs, chlordanes, and dieldrin English sole and rock sole stomach contents
Figure 2.6 Heptachlor, lindane, and aldrin in English sole and rock sole stomach contents
Figure 2.7 Fluorescent aromatic compounds in bile of English sole and rock sole
Figure 2.8 PCBs in English sole and rock sole liver.
Figure 2.9 Hexachlorobenzene and hexachlorobutadiene in English sole and rock sole liver
Figure 2.10 DDTs, chlordanes, and dieldrin in English sole and rock sole liver.
Figure 2.11 Heptachlor, lindane, and aldrin in English sole and rock sole liver
Figure 2.12 Cytochrome P4501A and DNA adducts in English sole and rock sole liver
Figure 2.13 Liver lesions in English sole and rock sole sampled during the Flatfish Toxicopathic Injury Study.
Figure 2.14 Liver lesions in rock sole sampled during the Flatfish Reproductive Injury Study
Figure 2.15 Liver lesions in rock sole sampled during the combined Flatfish Toxicopathic and Reproductive Injury Studies
Figure 2.16 Liver lesions in English sole from the combined Flatfish Injury Studies
Figure 2.17 Liver lesions in English sole and rock sole from the combined Flatfish Injury Studies, compared to historical data
Figure 2.18 Fluorescent aromatic compounds in bile of English sole and rock sole from the Flatfish Toxicopathic Injury Study, compared to historical data
Figure 2.19 DNA adducts in English sole and rock sole from the Flatfish Toxicopathic Injury Study, compared to historical data
Figure 2.20 Cytochrome P4501A in liver of English
sole and rock sole from the Flatfish Toxicopathic Injury Study,
compared to historical data
SECTION 3. FLATFISH REPRODUCTIVE INJURY STUDY
Figure 3.1 Sampling sites for the Flatfish Reproductive Injury Study
Figure 3.2 Contaminants in female English sole stomach contents
Figure 3.3 Hexachlorobenzene in female English sole liver
Figure 3.4 Fluorescent aromatic compound concentrations in bile of female English sole
Figure 3.5 DDTs in female English sole liver
Figure 3.6 Summed PCB congeners in female English sole liver
Figure 3.7 TCDD toxic equivalents in female English sole liver
Figure 3.8 DNA adducts in female English sole liver
Figure 3.9 Liver lesions in female English sole.
Figure 3.10 Mean size at age for female English sole.
Figure 3.11 Length-weight relationships in female English sole.
Figure 3.12 Condition factor in subadult and adult female English sole.
Figure 3.13 Hepatosomatic index in female English sole
Figure 3.14 Percentages of adult female English sole with developing yolked eggs
Figure 3.15 Percentages of female English sole with developing yolked eggs by age class
Figure 3.16 Estimated probability of ovarian development with age in English sole
Figure 3.17 Ovarian lesion prevalences in female English sole.
Figure 3.18 Gonadosomatic index in adult female English sole.
Figure 3.19 Plasma 17ß-estradiol concentrations in adult female English sole.
Figure 3.20 Liver HCB as a risk factor for precocious sexual maturation in subadult female English sole
Figure 3.21 Fluorescent aromatic compounds (FACs) in bile as a risk factor for inhibited gonad development in adult female English sole
Figure 3.22 Projected egg and larval production
by age in female English sole.
SECTION 1. JUVENILE SALMON INJURY STUDY
Table 1.1 Sampling sites and dates for the 1994 Juvenile Salmon Injury Study
Table 1.2 Numbers of composite samples collected
for 1994 Juvenile Salmon Injury Study
SECTION 2. FLATFISH TOXICOPATHIC INJURY STUDY
Table 2.1 Site of capture and age as risk factors for liver lesions in rock sole, Flatfish Toxicopathic Injury Study
Table 2.2 Site of capture and age as risk factors for liver lesions in English sole, Flatfish Toxicopathic Injury Study
Table 2.3 Site of capture and age as risk factors for liver lesions in English sole, combined studies
Table 2.4 Biliary FACs as risk factors for liver lesions in English sole, combined studies
Table 2.5 Chemical risk factors for liver lesions in English sole, combined studies
Table 2.6 Hepatic DNA adducts as risk factors for liver lesions in female English sole, Flatfish Reproductive Injury Study
Table 2.7 Hepatic DNA adducts as risk factors for liver lesions in English sole, combined studies
Table 2.8 Chlorinated hydrocarbons (measured by HPLC/PDA) as risk factors for liver lesions in female English sole on an individual basis, Flatfish Reproductive Injury Study
Table 2.9 Chlorinated hydrocarbons (measured
by HPLC/PDA) as risk factors for liver lesions in female English sole, based on mean
concentrations and prevalence data, Flatfish Reproductive Injury Study
Table 3.1 PCB congeners in female English sole liver
Table 3.2 Chemical risk factors for reproductive abnormalities in female English sole
Table 3.3 Contaminant exposure vs. gonad size and plasma estradiol concentrations in subadult and adult female English sole
Table 3.4 Contaminant exposure vs. precocious
steroid production and gonad growth in subadult female English
sole
The Hylebos Waterway is one of several waterways
included in the Commencement Bay Superfund Site. The Commencement
Bay Natural Resource Trustee Council (the Trustees) is concerned
that hazardous substances present in the sediments of the Hylebos
Waterway have caused and are continuing to cause injury to natural
resources. Members of this council include NOAA, the U.S. Fish
and Wildlife Service, the Washington State Department of Ecology,
the Washington State Department of Natural Resources, the Puyallup
Tribe of Indians, and the Muckelshoot Indian Tribe. As the Trustees
became aware of the severity of the chemical contamination in
the sediments of the Hylebos Waterway, concerns were raised as
to whether the flatfish feeding in the Hylebos Waterway or the
juvenile salmon migrating through it were suffering injury as
a result of their exposure to toxic contaminants. Accordingly,
studies to assess fish injury were designed, approved, and funded,
and these studies are the subject of this publication.
The overall objective of the Hylebos Waterway
fish injury assessment investigation was to document the current
status of contaminant exposure and associated injuries in fish
indigenous to the Hylebos Waterway, to quantify the extent of
these injuries, and to evaluate links between these injuries and
chemical contaminants in this waterway. The basic design of the
studies was derived from substantial previous effort performed
by the National Marine Fisheries Service, documenting several
relationships between exposure of fish to chemical contaminants
and the occurrence of biological impacts. The three specific
objectives were to 1) assess chemical contamination and the potential
for associated injuries in juvenile salmonids, 2) determine toxicopathic
conditions (e.g., liver disease) in flatfish, and 3) determine
contaminant-induced reproductive dysfunction in flatfish. The
field collections for these studies were conducted between May
of 1994 and April of 1995, analyses of samples were completed
by June of 1996, and analysis of data was completed by January
of 1997.
The objective of the Juvenile Salmon Injury
Study was to determine to what degree juvenile chum (Oncorhynchus
keta) and chinook salmon (Oncorhynchus tshawytscha)
captured from the Hylebos Waterway might be exposed to organic
contaminants, and to compare the levels of exposure observed to
previous studies where such exposures have been linked to biological
dysfunction. The results showed that juvenile chum and chinook
salmon from the Hylebos Waterway are being exposed to a wide range
of chemical contaminants, compared to fish from hatcheries or
reference estuaries. These contaminants include high and low
molecular weight polycyclic aromatic hydrocarbons (PAHs), polychlorinated
biphenyls (PCBs, including the toxic congeners 105 and 118), hexachlorobutadiene
(HCBD), hexachlorobenzene (HCB), DDTs, heptachlor, and several
pesticides. Moreover, the concentrations of contaminants in juvenile
chinook and chum salmon from the Hylebos Waterway are comparable
to levels previously shown to be associated with biological injury
in juvenile chinook salmon. For example, contaminant concentrations
similar to those measured in tissues, stomach contents, and fluids
of juvenile salmon from the Hylebos Waterway are associated with
impaired growth, suppression of immune function, and increased
mortality following pathogen exposure in chinook salmon collected
from another contaminated waterway in Puget Sound, the Duwamish
River. To what extent these effects are occurring in juvenile
salmon from the Hylebos Waterway, however, was not specifically
determined in the investigation. Additional research is underway
to further assess injury to these fish, by examining the potential
of the toxicants present in the Hylebos Waterway to elicit biological
dysfunction such as impaired disease resistance and reduced growth.
The objectives of the Flatfish Toxicopathic
Injury Study, were to 1) assess the extent of chemical contaminant
exposure of English sole (Pleuronectes vetulus) and rock
sole (Pleuronectes bilineatus) residing in the Hylebos
Waterway by examining chemical concentrations, early biochemical
responses, and prevalences of liver lesions, and 2) compare liver
lesion prevalences and biochemical responses with historical data
to determine if conditions have changed since the late 1970s and
1980s. Results showed that English sole and rock sole residing
in the Hylebos Waterway are being exposed to several classes of
toxic chemical contaminants, including PAHs, PCBs, DDT (and its
derivatives), HCB, and HCBD. These exposures were also clearly
reflected in elevated levels of DNA adducts and cytochrome P4501A
(CYP1A) activities in liver. Higher prevalences of injury in
the form of toxicopathic liver lesions were detected in English
sole from the Hylebos Waterway, in comparison to the reference
site. The chemical risk factors most commonly associated with
hepatic lesion occurrence in Hylebos flatfish were exposure to
PAHs, PCBs, and DDTs. The frequency of injury in the form of
hepatic lesions closely paralleled levels of DNA damage in liver
in fish from the study sites. In comparing the results of this
investigation with earlier work done in the Hylebos Waterway,
it was found that lesion prevalences and biochemical measures
of early response to contaminant exposure had not changed appreciably
since the late 1970s, and 1980s, respectively. Thus, there has
been little or no improvement in the Hylebos Waterway over the
past decade or more with respect to this particular fish injury.
The Flatfish Reproductive Injury Study was
undertaken to assess contaminant-associated changes in gonadal
development and reproductive steroid concentrations in female
English sole. Because of its potential to impact population growth
and consequently fisheries productivity, reproductive impairment
is potentially one of the most damaging effects of aquatic pollution
on marine fish. Accordingly, considerable effort was expended
on this portion of the Hylebos Waterway fish injury investigation.
Similar to the other portions of the investigation, it was shown
that adult female flatfish from the Hylebos Waterway are being
exposed to several classes of toxic contaminants, including PAHs,
PCBs, pesticides, and HCB. Moreover, this contaminant exposure
was associated with several types of injury in female English
sole from the Hylebos Waterway. Most notably, 40-50% of juvenile
sole in the Hylebos Waterway showed precocious sexual maturation,
and 20-30% of adult sole showed inhibited gonadal development.
Whereas the inhibition of gonadal development was most closely
associated with indicators of exposure to PAHs, the increased
prevalence of precocious sexual maturation was associated with
increased exposure to both chlorinated hydrocarbons and PAHs.
Substantial proportions of fish also exhibited DNA damage and
hepatic lesions. The reproductive injury observed in Hylebos
fish would presumably reduce the number of eggs and larvae contributed
by these animals to the English sole population in Commencement
Bay and southern Puget Sound, and the associated decline in recruitment
could reduce the overall productivity of the sole population and
its resilience to the impacts of other environmental stressors.