Geology topics

Paul D. Jones

Publications and source records attributed to Paul D. Jones.

7 recordsLinked to original sources

USGS2002

Effects of chronic dietary exposure to environmentally relevant concentrations to 2,3,7,8-tetrachlorodibenzo-p-dioxin on survival, growth, reproduction and biochemical responses of female rainbow trout (Oncorhynchus mykiss)

Adult female rainbow trout were exposed to dietary 2,3,7,8-tetrachlorodibenzo- p -dioxin (TCDD) at concentrations of 1.8, 18 and 90 ng TCDD/kg (ww) food for up to 300 day. At the end of the exposure fish were spawned and the reproductive outcomes were assessed. TCDD was accumulated into tissues and eggs in a dose-dependent manner with steady state being achieved after 50–100 day of exposure. Biochemical and hematological parameters were monitored at 50, 100, 150, and 200 day after the beginning of exposure. The survival of adult female trout was reduced in a dose-dependent manner by exposure to TCDD in the diet. Fish fed 1.8 ng TCDD/kg, moist weight of diet, showed significantly reduced survival compared with those fed the control diet. TCDD also affected survival of fry from females fed 1.8 ng TCDD/kg. Observed adverse effects in adult fish were as sensitive as early life-stage endpoints. Liver EROD activity was only moderately increased in all exposure groups after 250+ day of exposure. Low rates of edema and deformities were observed in fry from all treatment groups including controls. This study has demonstrated adverse effects of TCDD to both adults and fry at concentrations comparable to current environmental concentrations. This suggests that direct adult toxicity as well as reproductive endpoints need to be incorporated in the current risk assessment paradigm for these compounds.

Aquatic Toxicology↗

USGS2001

Accumulation of 2,3,7,8-tetrachlorodibenzo-p-dioxin by rainbow trout ( Onchorhynchus mykiss ) at environmentally relevant dietary concentrations

Rainbow trout were fed a diet containing 1.8, 18, or 90 pg/g 3H-2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) for up to 320 d. Concentrations of TCDD were determined in muscle, liver, and ovaries at 100, 150, 200, and 250 d. Concentrations of TCDD reached an apparent steady-state concentration in liver after 100 d of exposure, whereas concentrations in other tissues continued to increase until 150 d of exposure. The greatest portion of the total mass of TCDD was present in the muscle tissue with lesser proportions in other organs. As the ovaries developed before spawning, an increase occurred in the total mass of TCDD present in this tissue. The assimilation rate of TCDD during the initial 100 d of the exposure was determined to be between 10 and 30%. This is somewhat less than estimates derived based on both uptake and elimination constants determined during shorter exposures. Biomagnification factors (BMFs) were estimated for all tissues and exposure concentrations, and at all exposure periods. Lipid-normalized BMFs for muscle ranged from 0.38 to 1.51, which is consistent with the value of 1.0 predicted from fugacity theory. Uptake and depuration rate constants were determined and used to predict individual organ TCDD concentrations. Comparison with observed values indicated that the model could be used to predict tissue concentrations from the known concentrations of TCDD in food. This model will allow more refined risk assessments by predicting TCDD concentrations in sensitive tissues such as developing eggs.

Environmental Toxicology and Chemistry↗

USGS1995

Dietary exposure of mink to carp from Saginaw Bay. 3. Characterization of dietary exposure to planar halogenated hydrocarbons, dioxin equivalents, and biomagnification

Mink are known to be very sensitive to the toxic effects of planar polychlorinated biphenyls (pPCBs), polychlorinated dibenzo- p -dioxins (PCDDs), and polychlorinated dibenzofurans (PCDFs), collectively known as planar halogenated hydrocarbons (PHHs). Previously, we reported the reproductive effects in mink fed a diet containing 10, 20, or 40% fish taken from Saginaw Bay, Lake Huron. The present study reports the chemical characterization of the diets and the adult mink livers, along with a comparison of an additive model of toxicity with the results of the H4IIE bioassay on these samples. The assessment of dietary or tissue-based exposure of the mink to 2,3,7,8-tetrachlorodibenzo- p -dioxin (TCDD) and related compounds revealed that TCDD equivalents of the PHH mixtures largely followed an additive model of toxicity as compared with the H4IIE bioassay. Consistent dietary and liver tissue-based threshold concentrations for reproductive toxicity in mink were determined regardless of whether PHHs were quantified as TEQs (additive toxicity) or TCDD-EQs (H4IIE bioassay). Significant reproductive effects were observed in the lowest treatment group (10% fish or 19.4 pg of H4IIE bioassay-derived TCDD-EQs/g). Consumption-normalized mink liver biomagnification factors (BMFs) were 6.4−74.2 for PCDDs, <1−75.8 for PCDFs, <1−15.9 for PCBs, and in general, increased with degree of chlorination within each class. Based on TEQs or TCDD-EQ, this study confirms that mink are among the most, if not the most, sensitive mammalian species to the reproductive toxicity of TCDD and related compounds.

Environmental Science & Technology↗

USGS1995

Development of toxic equivalency factors for PCB congeners and the assessment of TCDD and PCB mixtures in rainbow trout

This study was undertaken to evaluate the relationship between mammalian and piscine 2,3,7,8-tetrachlorodibenzo- p -dioxin (TCDD) toxic equivalency factors (TEFs) for PCBs, based on induction of CYP1A enzyme activity, catalytic protein, and mRNA. Rainbow trout administered a single i.p. injection of TCDD had an average (±SD) ED50 of 0.91 ± 0.14 μg TCDD/kg for induction of ethoxyresorufin O -deethylase (EROD) activity. Ortho-substituted PCB congeners 2,3,3′,4,4′-pentachlorobiphenyl (PCB 105), 2,3′,4,4′,5-pentachlorobiphenyl (PCB 118), 2,3,3′4,4′5-hexachlorobiphenyl (PCB !56), and 2,2′3,4,4′,5-hexachlorobiphenyl (PCB 138) did not induce CYP1A activity in rainbow trout. Only three non-ortho-substituted PCBs, i.e., 3,3′4,4′-tetrachlorobiphenyl (PCB 77), 3,3′,4,4′,5-pentachlorobiphenyl (PCB 126), and 3,3′4,4′5,5′-hexachlorobiphenyl (PCB 169) induced CYP1A enzyme activity, protein, and mRNA. The ED50s for induction of EROD activity were calculated as 134, 5.82, and 93.7 μg/kg for PCB 77, PCB 126, and PCB 169, respectively. The TCDD-TEFs based on EROD activity were 0.0006, 0.0014, and 0.0003 for PCB 77, PCB 126, and PCB 169, respectively. Binary mixtures of TCDD and three PCBs were also evaluated. Based on EROD activity and CYP1A protein, mixtures of TCDD and PCB 77 were slightly greater than additive. Mixtures of TCDD-PCB 156 and TCDD-PCB 126 were slightly less than additive. Results from these studies indicate that mammal-derived TEFs will underestimate the potency of planar chlorinated hydrocarbon mixtures to induce the CYP1A catalytic activity in rainbow trout. Also, while interactions among PCB congeners and TCDD were somewhat equivocal, they did not greatly differ from predicted additive responses.

Environmental Toxicology and Chemistry↗

USGS1993

Uptake of planar polychlorinated biphenyls and 2,3,7,8-substituted polychlorinated dibenzofurans and dibenzo- p -dioxins by birds nesting in the lower Fox River and Green Bay, Wisconsin, USA

The uptake of persistent polychlorinated hydrocarbons (PCHs) by four avian species was investigated at upper trophic levels of two aquatic food chains of the lower Fox River and Green Bay, Wisconsin. Accumulation of total and specific planar polychlorinated biphenyls (PCBs), polychlorinated dibenzofurans (PCDFs), polychlorinated dibenzo-p-dioxin (PCDDs), and H411E rat hepatoma cell bioassay-derived 2,37,8-tetrachlorodibenzop-dioxin equivalents (TCDD-EQ) was evaluated in Forster's tern ( Sterna forsteri ) and common tern ( Sterna hirundo ) chicks, and in tree swallow ( Tachycineta bicolor ) and red-winged blackbird ( Agelaius phoeniceus ) nestlings from colonies nesting in several locations within the watershed. Concentrations of the PCHs were greatest in eggs and chicks of the two tern species, less in the tree swallows and least in the red-winged blackbirds. Young of all four species accumulated total PCBs, PCB congeners 77, 105, 126, and 169, and TCDD-EQ. The young birds also accumulated small concentrations of several 2,3,7,8-sbustituted PCDF and PCDD congeners. Uptake rates for certain of the PCHs for the Forster's tern chicks were: 15 μg/day for total PCBs, 70, 200, 6.5, and 0.14 ng/day for PCB congeners 77, 105, 126, and 169, respectively, and 270 μg/day for TCDD-EQ. Principal components analysis revealed that the patterns of PCH concentrations in the samples were influenced by species of bird, their age (or length of exposure) and nesting location. Collectively, our findings demonstrate that exposure of avian species to contaminants derived from aquatic food chains can be characterized and quantified for the purposes of ecological risk assessment.

Wisconsin↗

USGS1993

2,3,7,8-Tetrachlorodibenzo-p-dioxin equivalents in tissues of birds at Green Bay, Wisconsin, USA

The environment has become contaminated with complex mixtures of planar, chlorinated hydrocarbons (PCHs) such as polychlorinated biphenyls (PCBs), polychlorinated dibenzo- p -dioxins (PCDDs), polychlorinated dibenzofurans (PCDFs) and structurally similar compounds. Because the potencies of individual congeners to cause the same adverse effects vary greatly and the relative as well as absolute concentrations of individual PCH vary among samples from different locations, it is difficult to assess the toxic effects of these mixtures on wildlife. These compounds can cause a number of adverse effects, however, because the toxic effects which occur at ecologically-relevant concentrations such as embryo-lethality and birth defects appear to be mediated through the same mechanism, the potency of individual congeners can be reported relative to 2,3,7,8-tetrachlorodibenzo- p -dioxin (2,3,7,8-TCDD) which is the most toxic congener in the PCH class. The concentations of 2,3,7,8-TCDD Equivalents (TCDD-EQ) were determined in the tissues of aquatic and terrestrial birds of Green Bay, Wisconsin by the H4IIE bioassay system and compared toxic equivalency factors (TEFs) with the concentration predicted by the use of toxic equivalency factors applied to concentrations of PCH, which were determined by instrumental analyses. Concentrations of TCDD-EQ ranged from 0.52 to 440 ng/kg, wet weight. The greatest concentrations occurred in the fish-eating birds. Concentrations of TCDD-EQ, which were determined by the two methods were significantly correlated, but the additive model which used the TEFs with concentrations of measured PCB, PCDD and PCDF congeners underestimated the concentrations of TCDD-EQ measured by the H4IIE bioassay by an average of 57%. This is thought to be due to contributions from un-quantified PCH, which are known to occur in the environment. Of the quantified PCH congeners, PCDD and PCDF contributed a small portion of the TCDD-EQ in the aquatic birds, while most of the TCDD-EQ were due to non-ortho-substituted PCBs. In the terrestrial birds, the proportion of the TCDD-EQ contributed by the PCDD and PCDF was greater. This paper has been reviewed in accord with U.S. Environmental Protection Agency policy. Mention of specific products or trade names does not imply endorsement by the U.S. Government.

Archives of Environmental Contamination and Toxico↗

USGS1993

A comparison of water quality criteria for the Great Lakes based on human and wildlife health

Water quality criteria (WQC) can be derived in several ways. The usual techniques involve hazard and risk assessment procedures. For non-persistent, non-biomagnified compounds and elements, WQC are experimentally derived from their acute and chronic toxicity to aquatic organisms. For those persistent chlorinated hydrocarbons (PCHs) that are bioaccumulated and biomagnified, these traditional techniques have not been effective, partly because effects higher in the food web were not considered. Polychlorinated biphenyls (PCBs) are the bioaccumulative synthetic chemicals of primary toxicological significance to the Great Lakes biota which have caused widespread injury to wildlife. In the Laurentian Great Lakes, the primary emphasis of hazard assessments has been on the potential for adverse effects in humans who eat fish. The primary regulatory endpoint of traditional hazard and risk assessments underlying current WQC are the probabilities of additional cancers occurring in the human population. The analysis presented here indicates that this is not adequate to restore sensitive wildlife species that are highly exposed to PCBs, especially those that have suffered serious population declines. Because WQC are legal instruments, the methods of deriving WQC have large implications for remediation, litigation, and damage assessments. Here WQC are derived for six species based on the responses of wildlife in the field or produced by feeding fish to surrogate species, rather than projecting a potential of increased cancer rates in humans. If the most sensitive wildlife species are restored and protected for very sensitive reproductive endpoints, then all components of the ecosystem, including human health, should be more adequately protected. The management of Great Lakes wildlife requires an understanding of the injury and causal relationships to persistent toxic substances.

Journal of Great Lakes Research↗