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Northeast Fisheries Science Center Reference Document 02-09

A Compilation of Reported Fish Kills in the Hudson-Raritan Estuary during 1982 through 2001

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

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.

Information Quality Act Compliance: In accordance with section 515 of Public Law 106-554, the Northeast Fisheries Science Center completed both technical and policy reviews for this report. These predissemination reviews are on file at the NEFSC Editorial Office.

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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.


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.


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.


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.


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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