Chromium geochemistry and bioaccumulation in sediments from the lower Hackensack River, New Jersey.

Total and hexavalent chromium [Cr(VI)] were measured in sediment and sediment porewater in the lower Hackensack River (NJ) to assess the relationship between sediment geochemistry and chromium speciation, which in turn controls the mobility, bioavailability, and toxicity of chromium. Between 2003 and 2005, >100 surface (0 to 15 cm) sediment samples were tested for total chromium and Cr(VI), acid-volatile sulfides (AVS), ferrous iron (Fe(II)), divalent manganese (Mn(II)), ammonia, and organic carbon. Sediment porewater samples were collected by centrifugation or using in situ samplers colocated with the collection of sediments. In whole sediments, total chromium and Cr(VI) concentrations ranged from 5 to 9190 mg/kg dry weight (dw) and from <0.47 to 31 mg/kg dw, respectively. Sediment porewater concentrations ranged from <10 to 83 microg/l for total chromium; Cr(VI) was not detected in sediment porewater (n = 78). Concentrations of AVS (ranging between <10.6 to 4178 mg/kg) and other geochemistry measurements indicated anoxic, reducing conditions in the majority of sediment samples. In polychaetes (Nereis virens) and clams (Macoma nasuta) exposed in the laboratory for 28 days to sediments contained between 135 and 1780 mg/kg dw total chromium, concentrations in whole tissues after 24-hour depuration ranged between 1.2 and 14.8 mg/kg wet weight (ww; median 1.6 mg/kg ww) total chromium. In whole tissues of indigenous polychaetes collected from the sediment, tissue concentrations of total chromium ranged between 1.0 and 37.5 mg/kg ww (median = 2.1 mg/kg ww). Chromium concentrations in whole tissues of animals exposed in the field or in the laboratory showed no relationship with total chromium or Cr(VI) concentrations in the sediment. There were no statistical differences among animals exposed to sediments from site and reference locations. The results of this study are consistent with sediment studies conducted elsewhere indicating low chromium bioavailability in sediment under reducing conditions. This study also highlights the importance of sediment geochemistry and in situ porewater measurements to understand the ecological significance of chromium in sediment and the potential for human health and ecological exposures.

Screening-level ecological risk assessment of polychlorinated dibenzo-p-dioxins and dibenzofurans in sediments and aquatic biota from the Venice Lagoon, Italy.

Recent monitoring data indicate that portions of Italy's Venice Lagoon ecosystem have been degraded due to biological and chemical pollution from a variety of potential sources. Using polychlorinated dibenzo-p-dioxin (PCDD) and dibenzofuran (PCDF) data collected from sediment, fish and shellfish in the Lagoon, a screening-level ecological risk assessment (ERA) was performed to evaluate the risks to representative aquatic biota and wildlife receptors. Risks to aquatic invertebrates posed by PCDD/Fs in sediment were evaluated by comparing measured tissue concentrations in fish and shellfish to appropriate ecotoxicological reference values. For mammalian and avian receptors, risks posed by theoretical exposures to PCDD/Fs through the food chain were calculated using conservative wildlife exposure models. Results of the screening-level approach indicate that the potential for adverse effects to fish and aquatic invertebrate receptors from PCDD/Fs in surficial sediments are unlikely. Adverse effects to wildlife are possible but highly uncertain, and warrants further investigation in a more comprehensive ERA.

Incorporation of propyphenazone in beard hair of a migraine patient.

The incorporation of propyphenazone in beard hair after consumption of this substance present in the analgesic Migraine-Kranit (Codali) was investigated. Because of a migraine attack a volunteer took four tablets of Migraine-Kranit (one tablet contains 150 mg propyphenazone) the first day and two tablets the second day. Shaved beard hair was collected 48, 72, 96 and 120 h after the first consumption of the analgesic drug. These hair specimens were washed (acetone and water), pulverized and then incubated during 2 h in a thioglycolic solution. After solid-phase extraction on C18 columns, propyphenazone was assayed in these extracts by GC/MS operating in selected ion monitoring mode (m/z 230, 215). Diazepam-d5 was used as an internal standard. In hair specimen 1 (48 h after consumption) the highest concentration was found (170 pg/mg hair). In hair specimen 2 (72 h) and 3 (96 h) the concentration were significantly lower (44 and 18 pg/mg, respectively). After 120 h no propyphenazone could be detected (limit of detection: 5 pg/mg hair). These results show that propyphenazone was already in beard hear 2 days after consumption, whereas no more presence could be shown after 120 h. As the time period of 2 days is too short to allow entrapment into the hair matrix from bloodstream and growing of hair out of the follicle, our results suggest that incorporation of propyphenazone may be mainly due to excretion in sweat and subsequent incorporation into the hair.

A site-specific evaluation of mercury toxicity in sediment.

A site-specific evaluation of mercury toxicity was conducted for sediments of the Calcasieu River estuary (Louisiana, USA). Ten-day whole-sediment toxicity tests assessed survival and growth (dry weight) of the amphipods Hyalella azteca and Leptocheirus plumulosus under estuarine conditions (10 ppt salinity). A total of 32 sediment samples were tested for toxicity, including 14 undiluted site sediment samples and 6 sediment dilution series. All sediment samples were analyzed for total mercury and numerous other chemical parameters, including acid volatile sulfide (AVS) and simultaneously extracted metals (SEM). No toxicity attributable to mercury was observed, indicating that a site-specific threshold for total mercury toxicity to amphipods exceeds 4.1 mg/kg dry weight. Site-specific factors that may limit mercury bioavailability and toxicity include relatively high sulfide levels. Additionally, the chemical extractability of mercury in site sediments is low, as indicated by SEM mercury analyses for three sediment samples containing a range of total mercury concentrations.http://link. springer-ny.com/link/service/journals/00244/bibs/37n4p488.++ +html

Sources of pollution and sediment contamination in Newark Bay, New Jersey.

A review of historical water quality and sediment quality data and chemical body burdens in biota reveals significant levels of a wide range of chemicals and water quality stressors throughout the Newark Bay, New Jersey estuary. The estuary, which encompasses the Passaic River, Hackensack River, Kill van Kull, and the Arthur Kill, has been heavily impacted by both industrial and urban expansion for more than 200 years. The available information was sufficient to identify the major sources of pollution and the contributions of various metals and organic chemicals to the aquatic environment. Mass loadings for several chemicals and water quality parameters were estimated for publicly owned treatment works (POTWs) and combined sewer overflows (CSOs), industrial waste discharged either directly to the estuary or through POTWs, stormwater runoff, and accidental spills of petroleum products and hazardous chemicals. The recent trend toward regionalized waste treatment systems to provide secondary levels of treatment have provided some reductions of overall contaminant mass loadings. However, CSOs remain a significant source of untreated waste in the estuary. Additionally, the magnitude of the major sources relative to the ability of the estuary to absorb and dilute the various waste streams suggests that much more must be done to reduce chemical inputs at the source.

Historical changes in the ecological health of the Newark Bay Estuary, New Jersey.

A review of ecological conditions in the Newark Bay estuary over the past century was conducted to characterize chemical, physical, and biological indices of the health of the estuary and to evaluate the relationship of these trends with past and current urban-industrial influences within the watershed. The available data indicate that both the diversity and the abundance of aquatic species within the estuary have been substantially reduced since the late 1800s due to the intense industrialization and urbanization that occurred throughout the region. Water and sediment quality in major rivers and bays linked to the estuary have also been severely impacted. In addition, significant natural habitat has been destroyed as a result of industrial development, urban expansion, and shoreline modifications. Each of these parameters directly influences the status and condition of the ecological community, and their deterioration has likely been the cause of multiple adverse impacts on the overall health of the ecosystem. Review of more recent studies of sediment and water quality indicates that pollution control measures and the reduction or control of other environmental stressors have produced a gradual improvement in the ecosystem over the past 2 decades.

Assessment of chemical loadings to Newark Bay, New Jersey from petroleum and hazardous chemical accidents occurring from 1986 to 1991.

Newark Bay, New Jersey, is particularly vulnerable to ecological damage from accidental petroleum and chemical spills due to the enclosed nature of the bay and the large volume of chemical and petroleum commerce within the region. A review of the New Jersey Department of Environmental Protection and Energy's database of hazardous chemical spills in New Jersey waterways was conducted to determine the frequency and volume of chemical and petroleum spills in Newark Bay and its major tributaries. Accidents reported from 1986 to 1991 were extracted from the database and summarized. The compilation of records indicated that 1400 incidents, resulting in the release of more than 18 million gallons of hazardous materials to the estuary had been reported to state officials. The bulk of the chemicals released to the aquatic environment were petroleum products, specifically No. 2 Fuel Oil (4,636,512 gallons) and No. 6 Fuel Oil (12,600,683 gallons). The majority of the reported incidents occurred in the Arthur Kill and its tributaries. The results indicate that accidental discharge of petroleum and other hazardous chemicals to Newark Bay represents a significant ongoing source of chemical pollution.

Mercury contamination in the Newark Bay estuary.

As a result of several decades of industrialization, heavy metals, including mercury, have become the focus of ecological and human health concerns in Newark Bay, New Jersey. In this study, concentrations of mercury were determined in 18 surficial sediment samples collected from throughout the estuary. Measured concentrations ranged from nondetectable (0.1 mg/kg) to 9.8 mg/kg (dry weight). These results were compared to data from previous investigations of sediment and biota in the estuary in an effort to characterize the extent of mercury contamination and the potential for toxic effects in humans and biota. Mean concentrations of total mercury were elevated above estimated background levels throughout the estuary. Areas with the highest sediment concentrations included the lower Passaic River and the Arthur Kill. Comparisons to various state and federal sediment quality criteria and guidelines suggest that the presence of mercury poses a toxic hazard to aquatic biota. These data suggest that further investigation of sources is needed to reduce or eliminate this contamination.

Application of pattern recognition techniques to evaluate polychlorinated dibenzo-p-dioxin and dibenzofuran distributions in surficial sediments from the lower Passaic River and Newark Bay.

Isomer-specific determinations of polychlorinated dibenzo-p-dioxins (PCDDs) and dibenzofurans (PCDFs) were performed in 19 surficial sediment samples collected from the lower Passaic River and Newark Bay, New Jersey. Total PCDD and PCDF concentrations ranged from 415 to 23,300 ng/kg (dry wt) and 37 to 8400 ng/kg, respectively. OCDD and OCDF were the predominant congeners in all samples, followed by the hepta-, hexa-, tetra-, and penta-chlorinated compounds. Forty-seven percent (9/19) of the sediment samples contained no detectable levels of 2, 3, 7, 8-TCDD. The concentrations of 2, 3, 7, 8-TCDD and 2, 3, 7, 8-TCDF ranged from nondetect to 510 ng/kg (geometric mean of 5 ng/kg) and from 2.8 to 480 ng/kg (geometric mean of 13 ng/kg), respectively. The composition of PCDD/Fs in sediments was evaluated using chemometric pattern recognition techniques. Principal components analysis and complete linkage:farthest neighbor cluster analysis revealed the presence of at least five distinctive fingerprint patterns in surficial sediments collected from different locations in the Newark Bay estuary. Differences among PCDD/F patterns were attributable to the relative presence or absence of 1, 2, 3, 4, 6, 7, 8-HpCDF and the hepta-, hexa-, and octa-chlorinated congeners. To determine whether the presence of PCDD/Fs in sediments could be associated with a single source, residues in sediments were compared to those found in three soil samples and one sump sediment sample from a former 2, 4, 5-T manufacturing plant. Significant compositional differences were observed between the two data sets. Fingerprint patterns in sediments were dominated by the higher PCDD/F chlorinated congeners and contained significantly lower levels of the tetra-chlorinated congeners, particularly 2, 3, 7, 8-TCDD, than soils from the former 2, 4, 5-T plant. These differences, as well as those observed among surficial sediments from different locations, indicate that there are clearly several different sources of 2, 3, 7, 8-TCDD and other PCDD/Fs to the estuary.

Petroleum and hazardous chemical spills in Newark Bay, New Jersey, USA from 1982 to 1991.

Newark Bay, New Jersey, is particularly vulnerable to ecological damage from petroleum and chemical spills, as a result of the enclosed nature and shallow depth of the bay, the high frequency of shipping traffic, and the numerous chemical and petroleum transfer terminals located alongs its shores. To evaluate the potential impacts to the natural resources of this coastal estuarine ecosystem, chemical and petroleum accidents reported to the US Coast Guard (USCG) between 1982 and 1991 were compiled to determine the frequency and volume of these incidents in Newark Bay and in each of its major tributaries. Records obtained from the USCG National Response Center's computerized database indicated that more than 1453 accidental incidents, resulting in the release of more than 18 million US gallons of hazardous materials and petroleum products, occurred throughout Newark Bay during this period of time. The bulk of the materials released to the aquatic environment consisted of petroleum products, specifically No. 6 Fuel Oil (103 spills, 12 829 272 US gal) and gasoline (207 spills, 48 816 US gal). The majority of the reported incidents occurred in the Arthur Kill and its tributaries, as well as in the Kill Van Kull and the Passaic River. The results of this study indicated that the accidental discharge of petroleum and hazardous chemicals represents a significant source of chemical pollution in Newark Bay. Based on the frequency of spills and the volume of materials released to the aquatic environment, it is likely that these events are having a deleterious effect on the Newark Bay ecosystem.

Recent developments on the hazards posed by 2,3,7,8-tetrachlorodibenzo-p-dioxin in soil: implications for setting risk-based cleanup levels at residential and industrial sites.

Since the publication of the Times Beach risk assessment in 1984, which suggested that residential soils were of concern when the level of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) was in excess of 1 ppb, there has been continued interest in this topic. Studies conducted within the past 5 yr on the environmental and toxicological behavior of TCDD, as well as refinement of parameters regarding human exposure, indicate that previous assessments of the risk to humans posed by TCDD-contaminated soil were overestimated. In this paper, recent information drawn from nearly 100 recently published articles regarding the histopathology interpretation of the Kociba bioassay, environmental fate and half-life of TCDD in soil, and estimates of human exposure via soil ingestion, dermal contact, inhalation, surface runoff, and the consumption of fish were incorporated into a risk assessment. Cleanup levels for TCDD in residential and industrial soils were calculated based on most likely exposure scenarios. Probability distributions of key exposure parameters were incorporated into a Monte Carlo uncertainty analysis to predict the range and probability of TCDD uptake and corresponding cleanup levels in soil. This analysis demonstrated that the most significant route of human exposure to TCDD is through dermal contact with soil, followed by soil ingestion, fish consumption, and inhalation of airborne particulates. At residential sites, soils containing 20 parts per billion (ppb) of TCDD were found to pose a lifetime cancer risk no greater than 1 in 100,000 (10(-5) risk) under typical exposure conditions. Based on the Monte Carlo analysis, soil concentrations for the 75th and 95th percentile person were 12 and 7 ppb (10(-5) risk), respectively. In industrial soils, TCDD concentrations ranged between 131 and 582 ppb (10(-5) risk), depending on the amount of time spent outdoors under typical exposure conditions. Industrial soil concentrations of approximately 93 and 46 ppb (10(-5) risk) were calculated for the 75th and 95th percentile worker, respectively, engaged in outdoor activities. The range of TCDD concentrations in industrial soils was not reduced significantly when the consumption of fish from a neighboring waterway by off-site receptors was considered. While cleanup levels for TCDD should be derived on a site-specific basis, this analysis indicated that soil cleanup standards can be generally higher than those implemented over the past 8 yr.

Potential sources of 1,2,8,9-tetrachlorodibenzo-P-dioxin in the aquatic environment.

A recent study reported elevated levels of 1,2,8,9-tetrachlorodibenzo-p-dioxin (1,2,8,9-TCDD) in crustaceans and finfish collected from Newark Bay, New Jersey (Rappe et al., 1989). The authors suggested that the presence of this compound in biota was due to operations at a former 2,4,5-trichlorophenoxy acetic acid (2,4,5-T) manufacturing facility located on the lower Passaic River. Since 1,2,8,9-TCDD had been identified in two soil samples claimed to be associated with the site, it was concluded that the former manufacturing plant was the source of this compound. A review of the scientific literature was conducted to evaluate whether this isomer is associated with the formulation of 2,4,5-T and to determine whether 1,2,8,9-TCDD is commonly found in the aquatic environment. Measurements and chromatographic data from known sources of polychlorinated dibenzo-p-dioxins indicate that incinerator fly ash, soot from wood-burning chimneys, and the combustion of polychlorinated biphenyls and some chlorophenoxy herbicides are sources of 1,2,8,9-TCDD. This isomer has never been found in samples of 2,4,5-T. We conclude, therefore, that the presence of 1,2,8,9-TCDD in Newark Bay biota is not associated with 2,4,5-T manufacturers but, rather, the result of various commercial, residential, municipal, and industrial combustion processes.

Pathology reevaluation of the Kociba et al. (1978) bioassay of 2,3,7,8-TCDD: implications for risk assessment.

The chronic bioassay of 2,3,7,8-tetrachlorodibenzo-p-dioxin (2,3,7,8-TCDD) reported in 1978 by Kociba et al. has been considered to be the primary evidence supporting its carcinogenicity, and is the basis for most dioxin regulations in North America and Western Europe. Because the histopathological criteria for proliferative lesions in the rat liver have changed significantly since 1978, a reevaluation of the liver slides was conducted recently by an independent panel of pathologists. Using current National Toxicology Program criteria, their study showed, in contrast to the original findings, that about two-thirds fewer tumors were present in the livers of female Sprague-Dawley rats. The no-observed-adverse-effect level (NOAEL) for hepatocellular carcinomas was 0.01 micrograms/kg/d rather than 0.001 micrograms/kg/d, which had been reported in 1978. In light of these significant findings, a quantitative dose-response assessment of 2,3,7,8-TCDD was undertaken to predict the potential carcinogenic risks to humans. Risk-specific doses (RsDs) and cancer potency factors (CPFs) were calculated by applying the linearized multistage (LMS) model to the combined incidences of hepatocellular carcinomas and adenomas, classified in accordance with the 1990 histopathological criteria. Based on the weight of evidence regarding the mechanism of action of 2,3,7,8-TCDD, body weight rather than surface area was selected as the appropriate means for scaling rodent data to predict the human response. Using the survival-adjusted data, the RsD for a 1 in 1,000,000 (10(-6)) plausible upper bound (95%) lifetime incremental cancer risk was 370 fg/kg/d based only on the incidence of hepatocellular carcinomas, and 100 fg/kg/d when hepatocellular carcinomas and adenomas were combined. The corresponding upper-bound (95%) CPFs were 2700 and 9700 (mg/kg/d)-1, respectively. These results indicate that the carcinogenic risk to humans from exposure to 2,3,7,8-TCDD is at least 16-fold lower than previous estimates derived from the Kociba et al. (1978) bioassay.

Risk assessment of 2,3,7,8-TCDD using a biologically based cancer model: a reevaluation of the Kociba et al. bioassay using 1978 and 1990 histopathology criteria.

The Moolgavkar-Venzon-Knudson (M-V-K) two-stage model for carcinogenesis was used to estimate the risk-specific dose (RsD) based on the incidence of tumors reported by Kociba et al. (1978) for Sprague-Dawley rats exposed to 2,3,7,8-tetrachlorodibenzo-p-dioxin (2,3,7,8-TCDD; dioxin). The results from the recently completed (1990) reevaluation of the Kociba et al. study, which used the current National Toxicology Program (NTP) pathology criteria, were also evaluated. Time-to-tumor information for each rat was incorporated into the analysis. Model parameters for the approximate form of the hazard function of the two-stage M-V-K model were determined by maximum likelihood estimation. This simplification was significant but necessary, because laboratory data on the intermediate cell growth rate and the transition rates have not been determined. Estimates of the RsD (10(-6) risk) (based on the original 1978 histopathology results) were 10 fg/kg/d when carcinomas and hyperplastic nodules were combined and 150 fg/kg/d when only carcinomas were considered. In contrast, using the 1990 histopathology data, the RsD (10(-6) risk) was 80 fg/kg/d when adenomas and carcinomas were combined and 25,000 fg/kg/d when only hepatocellular carcinomas were considered. Since the two-stage M-V-K model is intended to predict the occurrence of malignant tumors, the mathematically appropriate RsD is 25,000 fg/kg/d (10(-6) risk). Because the model does not account for pharmacokinetics or the possibility of other toxic effects, the appropriate RsD (10(-6) risk) for humans should be much smaller. Using the carcinoma data only, a sensitivity analysis of key parameters in the model was conducted. Results indicated that the ranges of plausible values for the RsD (10(-6) risk) for the original 1978 and the 1990 reevaluation data were 70-2600 fg/kg/d and 120-50,000 fg/kg/d, respectively. The lowest plausible RsD is, therefore, approximately 10-fold greater than the current U.S. EPA RsD (10(-6) risk) of 6.4 fg/kg/d [which is based on the linearized multistage (LMS) model]. Even though these results must be considered preliminary until some of the values for the model parameters are experimentally determined and a complete physiologically based or receptor-based model is developed, this analysis shows that nearly any plausible laboratory data on tumor progression will yield a much higher RsD than currently embraced by the U.S. EPA.