The minimum concentration of mercury in the lower Hackensack River (4 ppm) reported by Squibb et 

 al. (1991) exceeded the ERM value ( 1 ppm) listed by Long and Morgan ( 1 990); the maximum concen- 

 tration (50 ppm) exceeded this value by a factor of 50-fold. Maximum concentrations of lead in New- 

 ark Bay and Arthur Kill exceeded the ERM concentration (110 ppm) by factors of about 8- to 10-fold. 

 The concentrations of DDT, PCBs, total PAHs, chlordane, and dieldrin in Newark Bay, Arthur Kill, 

 and/or the Passaic River were very high relative to concentrations previously associated with toxic 

 effects. 



Long and Morgan (1990) reported that in numerous studies the types of biological effects observed in 

 association with exceedances of the effects ranges included high mortality in amphipods, other crusta- 

 ceans, bivalve larvae, polychaetes, and fish in either spiked-sediment bioassays or toxicity tests of 

 ambient sediments; or altered infaunal community structures and/or reduced abundance of infauna; or 

 acute or chronic effects in aquatic species as predicted by equilibrium-partitioning models. 



Both Long and Morgan (1990) and Squibb et al. (1991) recognized the uncertainty in applying the 

 effects ranges as predictors of toxic effects. Many factors control the bioavailability of sediment- 

 associated toxicants and, as a consequence, bulk sediment concentrations often are poor predictors of 

 toxic effects. Both reports recommended that surveys to determine the presence of toxicant-associated 

 effects should be conducted to verify the potential for these effects. 



In more recent studies, the concentrations of a number of different substances, notably total PAHs, 

 mercury, lead, and zinc were found in concentrations that exceeded the ERL and ERM concentrations 

 in samples collected in the lower Passaic River, lower Hackensack River, and Newark Bay (Huntley et 

 al., 1993; Bonnevie et al., 1993). These are areas previously identified as highly contaminated. 



Previously Measured Biological Effects. The adverse biological effects of toxicants in the Hudson- 

 Raritan Estuary have been apparent for many years (Gottholm et al., 1993). Pearce (1988) reported 

 that portions of the estuary were severely degraded as early as the U.S. Civil War. In the early 1900s 

 some fish were unfit to eat because of high contamination and in the 1920s the shellfish populations 

 crashed due to the effects of wastewaters. Based upon the summaries prepared by several contributors 

 to NOAA (1988a), the major categories of toxicant-associated biological effects reported for the estu- 

 ary include: 



•alterations to resident microbial communities, including increased resistance to toxicants through 

 long-term continual exposure; 



•alterations and shifts in phytoplankton community structures and diminished species diversity; 



•reduced densities and species diversity of benthic communities; 



•severely reduced abundances of ampeliscid amphipods in benthic communities; 



•elevated prevalences of fin erosion and other diseases in bottom-dwelling fish; 



•elevated prevalences of tumors and other histopathological disorders of bottom-dwelling fish; 



•elevated prevalences of a variety of diseases in crabs, lobsters and shrimp; 



•tissue contamination leading to closures of fisheries and advisories against fish consumption; 



•increased resistance of resident killifish and soft-shelled clams to the effects of subsequent doses of 



toxicants. 



In Mayer (1982), several contributors reported that diminished commercial landings of some species 

 have occurred in the estuary, and that increased prevalences of histopathological disorders and a num- 

 ber of other diseases in fish in the adjacent New York Bight have been recorded. The causes of some of 

 these conditions are unknown, while the cause of others are known or suspected. 



8 



