Northeast Fisheries Science Center Reference Document 02-09
A
Compilation of Reported Fish Kills in the Hudson-Raritan
Estuary during 1982 through 2001
by Robert N. Reid1, Paul
S. Olsen2, and John
B. Mahoney1
1National Marine Fisheries Serv., James J. Howard
Marine Sciences Lab., 74 Magruder Rd., Highlands, NJ 07732
2New Jersey Dept. of Environmental Protection,
Bur. of Freshwater &
Biological Monitoring, P.O. Box 427, Trenton, NJ 08625
Print
publication date July 2002;
web version posted July 17,2002
Citation: Reid, R.N.; Olsen, P.S.; Mahoney, J.B. 2002. A compilationof reported fish kills in the Hudson-Raritan Estuary
during 1982 through 2001. U.S. Dep. Commer., Northeast Fish. Sci. Cent. Ref. Doc. 02-09; 16 p.
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Abstract
Concern about
mass fish mortalities in eastern U. S. coastal regions has increased
in recent years. Major kills attributed to the toxic dinoflagellate Pfiesteria
piscicida or related species, primarily in eutrophic estuaries
in the southeast but ranging north to Chesapeake Bay and possibly
to Delaware, have sparked interest in fish kill phenomena in general. We
found that lack of organized information was a hindrance to the
understanding of fish kills in the long-stressed Hudson-Raritan
estuary. To address this we compiled kill reports for 1982 through
2001, with focus on seasonality, causes, incidence, and kill size.
All
reported fish kills in the estuary during 1982-2001, a total of 15,
occurred between mid-June and mid-September. Their causes were uncertain,
as generally is the case with fish kills. Most were attributed to
low dissolved oxygen; decomposing phytoplankton blooms; and seasonal
high water temperatures. A role for toxic substances in one of the
kills was suspected. Reported possible causes of some monospecific
kills of Atlantic menhaden included low dissolved oxygen and spillage
from fishing nets. No pattern for the kills over the 20 years was
evident; incidence data were inadequate for statistical analysis. Sandy
Hook Bay may be a problem locus because seven of the 15 kills were
detected there. With the caveat that mortality assessments likely
were consistently inadequate and low, one kill involved about one
million fish and another was estimated at 3.9 million. These can
be considered major incidents; the other 13 were relatively minor. The
occurrence of two major kills during 20 years does not suggest the
estuary to be a prime center for such phenomena. We believe, nevertheless,
that the problem requires additional examination. We discuss the
need for more comprehensive and unified investigation of fish kills
in the estuary.
KEYWORDS: Hudson-Raritan
estuary, Raritan Bay, Sandy Hook Bay, fish kills, algal blooms,
dissolved oxygen.
Introduction
Most marine
finfish kills occur in estuaries and coastal waters (Brongersma-Sanders,
1957; May, 1973; Swanson and Sindermann, 1979; Lowe et al., 1991). Fish
kills have a wide variety of causes which often manifest strongly
in these waters: physical conditions, e.g., storms, seaquakes, temperature
and salinity changes; chemical conditions, e. g., toxic contaminants,
oxygen depletion, hydrogen sulfide generation; biological phenomena,
e.g., algal blooms, biotoxins, and disease; and combinations of these
factors (Swanson and Sindermann, 1979). Most major kills in United
States coastal waters from 1980 through 1989 were associated with
high summer temperatures, low dissolved oxygen, and low water circulation
(Lowe et al., 1991). Often, it has not been possible to establish
with certainty what caused a given kill, or to what extent the lethal
conditions were natural or anthropogenic.
The dinoflagellate Pfiesteria
piscicida, which produces a highly potent biotoxin, or a closely
related species, has been implicated as the cause of major fish
kills during the last decade in southeastern and mid-Atlantic U.
S. estuaries, particularly eutrophic ecosystems (Burkholder et
al., 1995; U. S. Environmental Protection Agency et al., 1998). Burkholder
et al. (1995) found P. piscicida in eastern U. S. estuarine
waters and sediments as far north as Indian River, DE. The species
is considered the probable cause of a fish kill in the Indian River
(U. S. Environmental Protection Agency et al., 1998). In New York
Bight coastal waters, Rublee (P. Rublee, University of North Carolina
at Greensboro, Greensboro NC, pers. comm., 8/30/99) detected the
species in the Tuckahoe River, NJ, and Long Island, NY, embayments,
but not in a toxic phase or in confirmed association with fish
mortality. There is no indication at present of P. piscicida as
a threat in the New York Bight. Nevertheless, the fish kills to
the south have resulted in increased concern about kills in Bight
coastal waters.
The Hudson-Raritan
estuary, at the apex of the Bight, has a long history of serious
pollution with sewage and industrial wastes (Federal Water Pollution
Control Administration, 1967). Hypoxia episodes and contamination
of the estuary’s sediment with toxic chemicals are two major indirect
or direct consequences of the chronic pollution (Keller and Squibb,
1992). Various metals, petroleum hydrocarbons, pesticides, and halogenated
hydrocarbons were detected in the estuary at levels threatening to
the biota (Breteler, 1984). The estuary has been characterized as
one of those most contaminated with PCBs in the U. S. (Zdanowicz
et al. 1986).
Epizootics
of fin rot disease that affected 23 species of fishes had their focus
in the estuary (Mahoney et al., 1973); outbreaks of fin rot frequently
are associated with environmental stress (Sindermann, 1979). Further
indication of a long-stressed environment, intense phytoplankton
blooms or “red tides” have occurred annually in the Hudson-Raritan
estuary and adjacent waters for decades (Mahoney and McLaughlin,
1977; Olsen and Mahoney, 1986). It has been shown that bloom biomass
can be a major contributor to hypoxia in the estuary (Olsen and Mulcahy,
1991). The estuary remains polluted although abatement measures
appear to have yielded long term improvements in water quality (Brosnan
and O’Shea, 1996) and sediment quality (O’Connor et al., 1998).
Organized
information on fish kills can aid in understanding their causes and
identifying where corrective measures are most necessary (Lowe et
al., 1991). Burkholder et al. (1995) pointed out that there is widespread
lack of such information for U. S. coastal waters, however. We address
that need for a portion of the Hudson-Raritan estuary.
METHODS
This paper
provides a synopsis of information on fish kills in the southeastern
waters of the Hudson-Raritan Estuary: Sandy Hook Bay, the New Jersey
portion of Raritan Bay, and the Shrewsbury and Navesink Rivers, which
drain into Sandy Hook Bay (Table 1, Figure
1). The New York or northern half of the estuary was not considered
because we found no fish kill reports for that region. The reporting
period is 1982 through 2001.
Information
on the kills did not stem from long-term programmed fish mortality
monitoring. Most was from annual reports of the New Jersey Department
of Environmental Protection, Bureau of Freshwater and Biological
Monitoring (NJDEP, BFBM, 1982-2001) on phytoplankton blooms and related
conditions in New Jersey coastal waters. NJDEP, BFBM annually monitored
phytoplankton bloom incidence, late May through early September,
in cooperation with the U.S. Environmental Protection Agency (USEPA),
New York Bight Water Quality Monitoring Program. Kill information
was noted in the reports when available (most often provided by NJDEP
Division of Fish and Wildlife). Some observations were made by NJDEP
and USEPA helicopter surveillance. Information on a July 1990 incident
was from a National Marine Fisheries Service, James J. Howard Marine
Sciences Laboratory investigation; Howard Laboratory (HL) data augmented
NJDEP information on the relatively large July 1992, July 1995 and
July 1999 kills. Monmouth County (NJ) Department of Health (MCDH)
provided information on the June 1990, July 1995, July and September
1999 kills, and the July 2000 kill. The information on the July
2000 kills was provided by NJDEP, Division of Fish and Wildlife. Some
of the June 1988 and July 1989 kill information, and all the September
1999 kill information, was from newspaper accounts. To our knowledge,
these are the only data sources on fish kills in the estuary.
Field methods
were fairly uniform among the several agencies NJDEP, MCDH, Howard
Laboratory). Estimates of numbers of dead fish were obtained by
multiplying the length of affected shoreline by the mean of several
counts of visible carcasses per square meter along the shore. Dissolved
oxygen (DO) was measured using the Winkler technique or a YSI oxygen
meter. Time of day when meter measurements were made, or water samples
for DO analyses were collected, was not necessarily when DO was highest
or lowest for the day. Identification of dominant species in a phytoplankton
bloom was made either by NJDEP, the Howard Laboratory, or MCDH. Phytoplankton
counts by NJDEP, HL or MCDH were routinely done under the microscope
using a Palmer-Maloney or Sedgewick-Rafter chamber; the Howard Laboratory
used a Coulter counter when blooms were monospecific.
RESULTS
AND DISCUSSION
Seasonality
of Kills and Suspected Causes
All fish kills
reported in the Hudson-Raritan estuary during 1982-2001 occurred
between mid-June and early September (Table
1). Greater potential for observation due to increased human
traffic may have been a factor in this apparent seasonality, but
it is reasonable to assume most kills to have occurred in summer. Nationwide,
64% of all fish kills reported during 1980-1989 (accounting for 86%
of the total fish reported killed) occurred from May through September
(Lowe et al., 1991). In addition, the greatest number of fish species
are present at this time in the Hudson-Raritan estuary, with many
species in increased abundance (Wilk et al., 1998); high abundance
can contribute to the magnitude of kills (Bigelow and Schroeder,
1953).
As was the
majority of fish kills reported nationwide during 1980-1989 (Lowe
et al., 1991), most of the kills in the Hudson-Raritan estuary were
attributed to low DO, and high water temperatures (Table
1). Metabolic rates and thus oxygen needs of fish usually increase
with temperature, while oxygen solubility in water decreases. Dissolved
oxygen also can be dramatically reduced by high summer oxygen consumption,
especially by respiration of other components of the biota and large-scale
decomposition of algae.
Seven of the
Hudson-Raritan fish kills were associated with decomposing phytoplankton
blooms. Hypoxic DO levels were detected during four of the bloom-associated
kills; DO data were not obtained or not reported for the other three
kills (Table 1).
Following
multiple kills in 1988, which were attributed in large part to hypoxia
from bloom decomposition, NJDEP and USEPA conducted a joint field
investigation of the problem (Olsen and Mulcahy, 1991). Weekly DO,
phytoplankton composition and chlorophyll assessments were made during
the summer of 1989 for 12 sites in the Hudson-Raritan estuary. An
intense bloom dominated by the dinoflagellate Katodinium rotundatum occurred
from about June 24 to July 2; highest phytoplankton and chlorophyll
concentrations were predominantly in the southeastern portion of
the estuary. Clearly showing bloom/hypoxia association, following
the bloom bottom water DO levels were decreased considerably throughout
the estuary for one to three weeks, with lowest levels (0.84-1.68
ml/l) in Raritan Bay and Sandy Hook Bay. Intense diatom blooms occurred
from late July through early September but did not result in hypoxia. Only
one minor fish kill was reported during the summer. This indicates
that intense phytoplankton blooms in the estuary may or may not result
in hypoxia. Also, even when considerably widespread and prolonged,
hypoxia may not result in a major fish kill. Water temperatures
were not always reported for the Hudson-Raritan fish kills but all
occurred (Table 1) when temperatures are
seasonally at highest levels (Draxler et al., 1984). Winter flounder, Pleuronectes
americanus, becomes inactive at temperatures above 22oC,
and can die at 26-32oC (Buckley, 1989). During the July
1995 kill, which included an estimated 50,000 juvenile winter flounder,
water temperatures as high as 29.5oC were recorded. Temperature
very likely had a role in this kill, at least.
High temperature
and low dissolved oxygen can act in concert with other stressors,
such as toxic chemicals (Keller and Squibb, 1992). They suggested
that interactive effects between hypoxia/anoxia and toxic chemicals
in the Hudson-Raritan estuary, could be important. In this regard,
the second largest recorded kill in the estuary, in June 1988, was
attributed to localized hypoxia, decomposing phytoplankton blooms
etc., and possibly toxic substances (Table 1). According
to Halgren (B. Halgren, NJ DEP, Nacote Creek Research Station, Port
Republic, NJ, pers. comm., 11/18/99) this kill had characteristics
suggesting possible involvement of anthropogenic or biological toxins;
it was spatially limited, of short duration, and involved
species which can usually avoid (e. g., bluefish, Pomatomus saltatrix)
or tolerate (e. g., American eel, Anguilla rostrata) hypoxic
conditions.
We have no
evidence that algal biotoxins caused any of the Hudson-Raritan estuary
fish kills but the possibility should not be ruled out. Phytoplankton
species toxic to humans have not been identified as dominants in
the area; however, the potentially icthyotoxic phytoflagellate Heterosigma
carterae has been a dominant bloom species in the estuary for
many years (Olsen and Cohn, 1979). This species is known to be toxic
to fish in various parts of the world (Whyte et al., 1999). Also,
a biotoxin has been reported in sea lettuce, Ulva lactuca (Johnson
and Welch, 1985), which is the most abundant macroalga locally.
Seven kills
not reported to be associated with algal blooms involved only, or
predominantly, Atlantic menhaden, Brevoortia tyrannus. Three
were in Sandy Hook Bay, one was in the Navesink River, one occurred
in Waackaack and Thorns Creeks which empty into southern Raritan
Bay), one was in Lanes Creek and another in Little Silver Creek,
which both empty into the Shrewsbury River (Table
1, Figure 1). Of the three Sandy Hook
Bay menhaden kills, the likely cause of one was reported to be spillage
of dead fish from pound nets (weirs); this can be deduced from appearance
of the fish, i. e., torn gill opercula, net marks on bodies. Two
kills were ascribed to either low dissolved oxygen or spillage from
pound nets and the cause of one was unreported. A menhaden kill
in the Navesink River in July 1999 occurred at a time when juveniles
were abundant, and were observed being chased into shallows by bluefish
(J. Rosendale, James J. Howard Marine Sciences Laboratory, Highlands,
NJ, pers. comm., 12/30/99); low dissolved oxygen and high water temperatures
were recorded (Table 1). The September
1999 Waackaack and Thorns Creeks kills occurred after heavy rains,
when juvenile menhaden were trapped upstream of floodgates. The
July 2000 major kill of juvenile menhaden in Little Silver Creek,
and a smaller kill of juvenile menhaden the same month were attributed
to low DO.
The Navesink
River, Waackaack Creek, Thorns Creek, Little Silver Creek and Lanes
Creek kills were not necessarily associated with poor ambient water
quality. Atlantic menhaden is a pelagic, schooling species which
swims continuously while filter-feeding (Rogers and Van Den Avyle,
1989). Dense schools of menhaden themselves can significantly lower
dissolved oxygen and raise ammonia levels (Oviatt et al., 1972). Menhaden
sometimes die en masse when they strand themselves in shoal
waters or crowd into small coves or heads of creeks, in attempts
to escape predators or for other reasons (Bigelow and Schroeder,
1953; Reintjes and Pacheco, 1966).
Temporal
Incidence / Water Quality Change
Kills were
reported in ten of the 20 years covered, with multiple kills recorded
only in 1988, 1990, 1999 and 2000 (Table 1). We
note that there were seven incidents in Sandy Hook Bay reported
between 1982 and 1990, and none subsequently to 2001. Given the
limitations of the data, especially irregular monitoring and imprecise
estimates of numbers killed, this may or may not be significant. We
did not attempt trend analysis.
Long-term
trend toward smaller and/or less frequent kills (specifically those
caused by low dissolved oxygen) might be expected because water quality
of the Hudson-Raritan estuary improved significantly following passage
of the Clean Water Act in 1972 (Brosnan and O'Shea, 1996; New York
City Department of Environmental Protection, 1998). However, the
only pertinent long-term uninterrupted data available for the estuary
(for the northern region) (Brosnan and O’Shea, 1996; New York City
Department of Environmental Protection, 1998) suggest that most of
the water quality improvement, in terms of nutrient levels, was before
the period we consider. That is, from 1985 through 1997, concentrations
of nitrite, nitrate, total phosphorus, and orthophosphate in surface
waters decreased significantly at only one of three standard monitoring
stations between the mouth of the Arthur Kill and mid-Raritan Bay;
there were significant reductions in ammonium in surface waters at
two of the three stations (New York City Department of Environmental
Protection, 1998). Data for 1989-1997 from the same three stations
show there were significant increases in chlorophyll at two of the
three stations and dissolved oxygen in bottom waters increased significantly
at all three stations (New York City Department of Environmental
Protection, 1998). This limited evidence suggests that, although
phytoplankton production was not reduced, oxygen demand was lowered
in the northern part of the estuary. Obviously, extrapolation of
this information to the southern half of the estuary where the kills
occurred is problematic.
Spatial
Incidence / Cause and Effect Linkage
Given the
same caveat about the data discussed under temporal incidence, location
of the kills suggests Sandy Hook Bay to be a possible problem locus,
because seven of the 14 kills were detected there. Kills or underlying
water quality conditions may not have originated where the dead fish
were observed, however. Nutrients and blooms from the Shrewsbury
and Navesink Rivers discharge into Sandy Hook Bay. Net water flow
in this estuary region is eastward (Jeffries, 1962), and tends to
move nutrients, phytoplankton blooms, and dead or moribund fish in
that direction. For example, the large June 1988 kill in Sandy Hook
Bay was linked to decay of a phytoplankton bloom which first developed
several km to the west of where the kill occurred (Figure
1). Much of the nutrient loading enters the estuary west
of Sandy Hook Bay. Sources include the Raritan and Hudson Rivers,
the Arthur Kill, and the large Middlesex County sewage outfall, which
discharges a mean of 124 million gallons/day of secondary treated
effluent through an outfall located 1.6 km ESE of the mouth of the
Raritan River [(Figure 1) (Interstate Sanitation
Commission, 1997)]. These rivers and outfall are also major sources
of organic loading which contribute to reduced dissolved oxygen in
the system (Mueller et al., 1982). Perhaps significant, the most
recent non-menhaden kills (7/92 and 7/95) were off Cliffwood Beach
(NJ) in western Raritan Bay, proximal to these pollution sources.
Size
of Mortalities
Lowe et al.
(1991) considered a "major" kill to be of a million or
more fish. They reported 86 major kills nationwide from 1980-89;
the ten largest involving mortality of ten to 50 million fish. Only
the June 1988 kill in Sandy Hook Bay and the July 2000 kill in Little
Silver Creek (Shrewsbury River) would be classified major by this
criterion. Next in numbers, the September 1999 kill in the Waackaack
and Thorns Creeks involved several hundred thousand juvenile menhaden. Assessed
mortalities in all other local kills were under 60,000 (Table
1).
All counts
of dead fish very likely are underestimates of actual numbers killed,
however. Apparently, only shoreline observations were made, and
fish mortalities usually were assessed on single observations, likely
post-peak. Contributing to underestimates when this kind of observation
is made is that some fish are too deep in the water to be visible,
and others may be removed by predators or scavengers; these are common
reasons for underestimates (American Fisheries Society, 1992). During
an August 1988 fish kill investigation in Sandy Hook Bay scavenging
seabirds removed almost all dead fish within two days of the estimated
peak of the kill (Pacheco, Howard Laboratory internal memorandum).
Considerations
in Evaluating Fish Kills
This topic
is discussed thoroughly in two standard references on fish kill investigations
(Meyer and Barclay, 1990; American Fisheries Society, 1992). Some
considerations listed in these guides, and pertinent to our compilation
are: 1) kills are more likely to be observed in warmer weather; 2)
most fish species are more abundant in the warmest months, so larger
kills might be expected then regardless of other factors; 3) most
kill counts are underestimates; 4) causes may be complex, and often
difficult or impossible to establish by observations and sampling
after the fact; 5) some "kills" may be due not to habitat
conditions but to other causes such as commercial fishing activity
or fish behavior (e. g., spillage from nets or stranding); and 6)
locations where kills are observed may not be where the kills or
any underlying water quality problems originate. Another complication
is that, in addition to seasonal trends in abundance, most species
in the study area have cyclic long-term (years) changes in abundance. Long
term population change can also influence incidence or sizes of kills
(as could spatial variations in abundance).
For kills
due to water quality impairments, the often ephemeral nature
of the contributing conditions can increase the difficulty of detecting
causes, and drawing conclusions about water quality trends. For
example, bloom development which can cause precipitous change in
water quality, may be short-term, often on the order of 1-2 weeks. Also,
blooms can cause DO supersaturation during the day, whereas at night
algal respiration can reduce oxygen drastically. Evidence for causes
of kills involving some toxic chemicals may be similarly ephemeral,
e. g., most pesticides are now short-lived and difficult to detect
in water soon after application (Engel and Thayer, 1998).
Critique
of Fish Kill Assessment in the Hudson-Raritan Estuary
Despite the
Hudson-Raritan estuary’s history of environmental perturbation (including
high toxic contaminants burdens; chronic phytoplankton blooms and
hypoxia events) fish kills during the study period with two exceptions
were found to be relatively minor. However, although fish kill investigations
in the area by various agencies have improved greatly in recent years,
most incidents were not assessed in accordance with accepted guidelines
such as developed by the American Fisheries Society (1992). Kill
estimates were based on short term, shoreline sampling, not throughout
the kill duration and over the water body and sub-surface. The investigations
lacked a consistent, complete approach -- including analyses for
toxic contaminants (metals, organics) and pathology examinations
beyond gross external pathology. Sublethal effects of blooms, hypoxia
and other water quality impairments on resident fish were not assessed. Poor
water quality can retard growth of fishes, e. g., juvenile winter
flounder (Bejda et al., 1992), or can cause avoidance of areas that
may otherwise be valuable habitat (Pihl et al., 1991). Most mortality
assessments focused on finfish. However, conditions that cause fish
kills can also be detrimental to other components of the biota including
invertebrates (Pihl, 1994). Large numbers of dead invertebrates
were noted in the July 1992 kill, including blue crabs, Callinectes
sapidus, lady crabs, Ovalipes ocellatus, sand shrimp, Crangon
septemspinosa, grass shrimp, Palaemonetes spp., and soft
clams, Mya arenaria. The varied sources and quality of fish
kill reportage included in our compilation reflect a lack of a central,
organized, fish kill data-base, such as recommended by Burkholder
et al. (1995). The American Fisheries Society (1992) advised that
regular monitoring using established protocols is necessary for documentation
of fish kills and the conditions leading to them. Burkholder et
al. (1999) advised that strong strategies in response to fish kills
and epizootics must incorporate sound field data, experimental testing,
and careful interpretation of data.
Fish kill
studies in our study area would benefit from increased commitment
and coordination among the several agencies with responsibilities
for water quality and marine living resources (e. g., U.S. Environmental
Protection Agency, National Marine Fisheries Service, U.S. Fish and
Wildlife Service, state departments of environmental protection and
county departments of health). One reason particular environmental
agencies may have difficulty in responding to emergency situations
is that funding and personnel are usually committed on the basis
of planned rather than emergency activities. Pooling of responsibilities,
expertise, and resources by several government agencies could alleviate
this.
ACKNOWLEDGEMENTS
We thank A.
Draxler, S. A. Fromm, L. Arlen and L. Stehlik, NMFS, James J. Howard
Marine Sciences Laboratory (HL), W. Andrews, NJDEP, Division of Fish
and Wildlife, E. Cosgrove, Monmouth County, NJ, Department of Health,
and R. Braun and H. Grebe, USEPA, Region 2, Surveillance and Monitoring
Branch, for fish kill investigations data. We also thank B. Phelan
(HL) for data on winter flounder densities; C. Zetlin (HL) for the
map of the Hudson-Raritan estuary showing kill locales; and L. Stehlik,
F. Steimle, and J. Vitaliano (all HL), and G. Wikfors, NMFS, Milford
Laboratory, for helpful comments on the manuscript.
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