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SEDIMENT CONTAMINATION AND MARINE ECOSYSTEMS:
POTENTIAL RISKS TO HUMAN HEALTH
Donald C. Malins
Pacific Northwest Research Foundation
ABSTRACT
It is recognized that exposure of aquatic organ-
isms to contaminated sediments results in the bioaccu-
mulation of toxic chemicals (Capuzzo et al., 1988~.
Toxic ~ ~~ ~ ~ ~ ~~ ~
. responses may occur at the biochem~cal-cellular,
organismal, population, and community levels and range
from metabolic impairment to changes in community
structure and function (Capuzzo et al., 1988; Buhler
and Williams, 19881. The toxic insults are not limited
to the initial organisms impacted, but may extend
throughout the food web and include the human consumer
of seafood.
Contamination of the sediment is especially significant because of
the host of benthic species that inhabit the ocean floor--species that
serve as initial contaminant reservoirs and are food for a variety of
organisms. Thus, the sediment is the starting point for the transfer
of toxic chemicals through wide expanses of the food web (Malins et
al., 1984; U.S. EPA, 1985).
Many gaps exist in our understanding of the far ranging effects of
sediment contamination on the myriad organisms that inhabit rivers,
estuaries, and coastal areas. ~ ~ ~ ~ ~ ~~
iney vary trom a ~ emoted understanding
of synergistic/antagonistic interactions to a shallow perspective of
chronic effects. Knowledge about mechanisms that mediate chemical
accumulations, metabolic changes and biological effects have been
especially elusive. Yet, we know far more about the impacts of
sediment contamination on aquatic species than on the human consumer.
Simply stated, our understanding of events and processes that
lead to potential human health effects from the consumption of
contaminated seafood are virtually unknown, as is the extent of the
impact on human populations (Swain, 1988; Friberg, 1988~.
Many of the chemicals that contaminate fish and shellfish in
polluted environments are transferred to humans through the diet
prawns er a.., troy. Onus, numans are ~og~cai~y viewed as an
intimate part of marine food webs. Metabolically resistant
(refractory) chemicals, such as PCBs, DDT derivatives, and other
halogenated compounds are readily transferred from the sediments to
benthic species, such as worms, clams. and bottom-feeding fish
~ %. ~ ~ . ~ ~ ~ ~ ~ ~ ~ ~ ~ ~ ~ ~ ~
155
r
OCR for page 156
156
(Malins et al., 1984~. Thus, the potential exists for their transfer
and bioconcentration through the food web.
Compounds that are actively metabolized, such as the aromatic
hydrocarbons, are not readily transferred through aquatic food webs,
although they do accumulate in organisms, such as shellfish, that have
a limited ability to metabolize them (Malins et al., 1986~. Thus, with
fish the readily metabolized compounds may be of less concern for the
human consumer than the refractory compounds, some of which are known
to accumulate in the edible muscle (MacLeod et al., 1981; Romberg et
al., 1984; Table 1~. The same conclusion cannot be drawn with respect
to shellfish contaminated with xenobiotics. Overall, however, it is
important to remember, as indicated, that little is known about the
propensity for humans to accumulate and bioconcentrate through the diet
the thousands of different parent chemicals and metabolites arising
from contamination of sediments (Malins et al., 1986~. Also, only a
paucity of information exists about the nature and extent of the human
health effects.
Having broadly delineated some of the complex problems that can be
attributed to one of the "original sins" of chemical contamination--
pollution of the sediments--several specific questions will now be
addressed:
TABLE 1 Concentration (ppm, Wet Weight) of PCBs, DDT and
AHs in Edible Tissues of Striped Bass and Salmon
PCBs EDDT EAHs
Striped bass
(Hudson River, New York) 7.00
Striped bass
(Montauk, Long Island) 0.80
Striped bass
(Orient Point, New York Bight) 3.00 0.73
Chinook salmon
(Denny Way, Seattle) 1.35
Chinook salmon
(Richmond Beach, Seattle)
NOTES:
aTrace
bPhenanthrene identified
SOURCE: MacLeod et al.,
1.01 ta
0.11 t
O . 01 PHNb
0.23 0.01 PHN
1981 and Romberg et al., 1984.
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157
1. What is actually known about the dietary transfer to humans of
toxic chemicals from contaminated fish and shell fish?
2. What are the human health implications?
3. How can the gaps in knowledge be filled?
TRANSFER OF TOXIC CHEMICALS TO HUMAN POPULATIONS
An almost singular emphasis has been placed on PCBs as a "model"
for considering the exposure of humans to contaminants through marine
food webs (U.S. EPA, 1985; Swain, 1988~. These studies suggest that
refractory organic compounds have the potential for being transferred
to human populations through consumption of contaminated sea food (U.S.
EPA, 1985; Swain, 19881. For example, a study was conducted on the
exposure of humans to PCBs through the consumption of fish from Lake
Michigan (Humphrey, 1976~. In the 18 counties that border Lake Michi-
gan, 381, 000 licensed sports fishermen caught 14 million pounds of
trout and salmon annually. As a group, the fishermen and their fami
lies consumed 36.6 pounds of fish per year (Humphrey, 1976, 1983),
which is over three times the national average. Adults were used in a
matched cohort study (MacLeod et al., 1981; Romberg et al., 1984) in
which samples of serum from each group were analyzed for PCBs, then the
results were compared with data obtained from interviews with each indi-
vidual involved in the study. The findings generally revealed an
increase in PCB serum levels with increased fish consumption (Humphrey,
1983; Table 2~. These data also provided evidence that the Michigan
residents were exposed through the diet to levels of PCBs significantly
above those for the average population ~ Swain, 1988 ~ .
TABLE 2 PCBs in Human Serum as a Function of Fish Consumption and
Geographic Location of Fish Source
Amount
consumed Sample Serum PCB (ug/kg)
Source of fish (kg~a N Range Mean Median
No source O 29 NDb-41 17.3 15
Lake St. Clair 5 - 66 . 8 15 ND- 38 19 .4 17
Lake Michigan 0-2.73 39 ND-41 18.5 20
Lake Michigan 10.91-118 90 25-366 72.7 56
NOTES:
aPresumably kg/yr, though not so specified.
bND ~ Not detected; detection limit specified as <5pg/kg.
SOURCE: Humphrey, 1983.
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158
It was reasoned that additional groups especially at risk were
pregnant women and their unborn and newborn offspring. Thus, a longitu-
dinal study was designed to assess the impact of contaminated fish con-
sumption on these groups (Jacobson et al., 1983~. Briefly, the study
revealed that infants were exposed to PCBs in utero, as well as post-
partum via the breast milk, when the mothers consumed contaminated
fish.
The above findings are not surprising. Evidence with rodents
exposed to PCBs revealed essentially the same potential for bioaccu-
mulation (see U.S. EPA, 1985~. In addition, a recent study with seals
(Reijnders, 1988) showed that the consumption of PCB-contaminated fish
resulted in substantial accumulations of these compounds. Comparable
results were also obtained with mink fed PCB-contaminated fish
(Reijnders, 1986~.
The findings with the PCBs add an additional dimension to the con-
cern expressed after the Minamata, Japan, mercury poisoning incident in
the 1950s (Takeuchi, 1972~. ~
, ~ , or ~ ~
IN phi ~ BAND Pi ah were shown to he the
source or methy~mercury exposure in humans seriously afflicted with
neurological and other damage (Takeuchi, 1972~. Unfortunately, little
or no information exists on the transfer to human populations of the
wide variety of xenobiotics that exist together with the PCBs in edible
tissues of aquatic life exposed to pollutants. It is not known, for
r
TABLE 3 DDTa concentrations (pg/gm, ppm Wet Weight) in Uncooked
and Pan Fried White Croaker (Genyonemus lineatus) Fillets
DDT (pg/g)
Composite Percent original Pan fried
number weight Uncooked Pan fried normalized
1 27 .8 0.202 0.247 0.069
2 35.7 0.167 0.184 0.066
3 35.2 1.110 0.844 0.297
4 33.2 1.070 0.531 0.176
5 31.8 0.410 0.506 0.161
Mean + SE 32 . 7 0. 57+0 . 20 0. 46+0 . 12 0 . 15+0 . 04
Mean percent loss of DDT due to frying
74
NOTE:
aRefers to DDT, 000, and DOE.
SOURCE: Puffer et al., 1982.
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159
example, whether synergistic or antagonistic interactions play an impor-
tant part in the disposition in humans of xenobiotics derived from con-
t~minated seafood. Moreover, little is known about the accumulation of
metabolites in edible tissues, especially those compounds that are not
detected by conventional analytical techniques. Although, as stated,
there are indications that metabolites of aromatic hydrocarbons may not
accumulate to a significant degree in the edible tissue of fish (Malins
et al., 1987), substantive information on possible contamination from
many other compounds s imply does not exist (Swain, 1988~. Clearly of
significance is the finding that pan- fried fish tend to have a signi-
ficantly lower concentration of ODT derivatives than the uncooked fish
(Puffer et al., 1982; Table 3~; however, the influence of cooking on
the concentrations of other contaminants is virtually unknown
THE HUMAN HEALTH IMPLICATIONS
Considerations of human health effects from the consumption of
contaminated seafood have focused, for the most part, on the PCBs;
however, some concern has been expressed about inorganic compounds
(e.g. , arsenic) that accumulate in the muscle of fish (Friberg, 1988) .
Some studies, for example, point to a possible threat from arsenic
(Friberg, 1988~. While most of the arsenic in seafood is in the form
of arsenobetaine, which is considered relatively atomic, "extreme
consumption" of seafood may give rise to an intake of several hundred
micrograms of inorganic arsenic per day--an exposure, which over a
lifetime, may be associated with a "significant increase in skin
cancer" (Friberg, 1988~. Unfortunately, related studies that focus
tightly on cause - effect relationships have yet to be conducted. The
daily intake of tin through the consumption of seafood is not particu-
larly high; however, more studies need to be conducted on the potential
toxicity of trimethyltin resulting from biochemical alkylation reac-
tions. Also, despite regulations pertaining to methylmercury, groups
having a "high" fish intake, or an intake of fish with a "high" methyl-
mercury content, may exceed established tolerance levels. In this
regard, a special concern exists about pregnant women (Friberg, 1988~.
Results from the relatively large amount of research on PCBs sug-
gests that these compounds may pose a significant problem for the con-
sumer of fish from polluted areas. In Lake Michigan studies (Jacobson
et al., 1983, 1984; Fein et al. , 1984), for example, effects observed
among infants born to mothers in "high fish consumption" categories in-
cluded delays in developmental maturation at birth (rein et al., 1984~.
The infants were also smaller in physical size, and had a reduced head
circumference and neuromuscular maturity (Table 4~. They also exhi-
bited an altered lability of state, increased startle reflexes, and
were classified by physicians to be within the "worrisome" neonatal
category (Jacobson et al., 1984, 1988~. Swain (1988) makes the point
that these observations suggest "an effect of contaminants upon the
centers of higher integration in infants secondarily exposed via mater-
nal circulation." A study conducted with rats (Hertzler and Daly,
1985) supports the conclusion that PCBs derived from fish indeed have
OCR for page 160
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161
an effect on the nervous system. It was shown, for example, that rats
maintained on a diet of PCB-contaminated salmon from Lake Ontario devel-
oped behavioral anomalies, compared to controls, in relation to brain
concentrations of PCBs. Such a finding can be compared with results
obtained from the previously mentioned study of seals exposed to PCBs
through their fish diet (Reijnders, 1986~. The reproductive process
was shown to be "disrupted in the post-ovulation phase." Another study
with mink (Reijnders, in press, and 1986) also supported the proposi-
tion the PCBs derived from a fish diet have an effect on reproduction
at "very low (25 fig per day) levels."
Overall, a limited number of studies have indicated that signifi-
cant changes in health status may occur in humans consuming contami-
nated fish; however, obviously many factors impinge on the exact nature
of the threat--so many, in fact, that the present findings are best
viewed as a stimulus to study the issue in greater detail through care-
fully controlled field and laboratory investigations.
FILLING THE GAPS IN KNOWLEDGE
Information required for a minimal understanding of the impacts of
toxic environmental chemicals on aquatic species and human health sub-
stantially exceeds the information available. Important areas for
future research include obtaining more knowledge about the nature and
extent of exposure on an individual, population, and geographic bases.
In addition, biochemical/toxicological data on the scores of chemicals
that have the potential to accumulate in edible tissues are also impor-
tant to obtain, as is information on chronic effects. Moreover, pos-
sible human health effects associated with the loss of volatile sedi-
ment chemicals to the atmosphere, such as from contaminated subtidal
areas, is well worth studying.
The problem of human risk assessment is formidable when one consi-
ders that marine life is often exposed to complex mixtures of chemicals
in contaminated areas. Moreover, in some cases, assessments conducted
thus far with contaminated fish have projected clearly unacceptable
human cancer risks (Brown, 1985; Table 5~. In addition, the present
reliance on PCBs and a small number of other compounds for risk assess-
ment is clearly inadequate. More work needs to be undertaken to make
risk assessment more meaningful from a public health point of view,
such as by taking into account the fact that complex mixtures of poten-
tially toxic chemicals are likely to be present in edible tissues of
fish from polluted areas. Studies in which laboratory animals are fed
a diet of contaminated fish tissue or a diet containing extractable,
environmentally derived chemicals may well prove to be a useful
approach.
Finally, one can only hope that future work will consider a variety
of biological end points as indicators of human health effects, rather
than focus on the few (e g., cancer and neurological impairment) that
have been studied thus far.
OCR for page 162
162
TABLE 5 Contaminant Concentration and Risk Assessment
for Consumption of Southern California Fish at Average
U.S. Consumption Ratea
Concentration
(mg/wet kg)
Risk
White Point
White Croakers DDTs 7.6 3.4/10,000
PCBs 0.38 2.2/20.000
Total 8.0 5.6/10,000
Rockfish DDTs 0.44 2.0/100,000
PCBs 0.057 3.3/100.000
Total 0.50 5.3/100,000
P. Mackeral DDTs 0.051 2.3/1,000,000
PCBs 0.014 8.0/1.000. 000
0.065 1.0/100, 000
Santa Monica Bay
White Croakers DDTs 0.57 2 . 6/100, 000
PCBs 0.20 1.1/10. 000
Total 0 . 77 1. 4/10, 000
Rockfish DDTs 0.22 9. 9/1, 000, 000
PCBs 0.12 6 . 9/100. 000
Total 0.34 7 . 9/100, 000
P. Mackeral DDTs 0.057 2 . 6/1, 000, 000
PCBs 0.015 8.6/1.000. 000
0.072 1. 1/100, 000
NOTE:
a9.3 g/day consumption of domestic estuarine and marine fish.
SOURCE: Brown, 1985.
REFERENCES
Brown, D. 1985. Personal Communication. Based on work conducted
while at the Southern California Coastal Water Research Project
(S.C.W.R.P.), Long Beach, CA.
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chemicals in the marine environment: Predictions of impacts from
r
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U.S.
Representative terms from entire chapter:
contaminated fish
