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Phytoplankton concentrate mercury from their aqueous surroundings and represent the primary entry point for Hg in aquatic food webs. We used 203Hg to compare the uptake of inorganic mercury, Hg(II), and methylmercury, MeHg, in four phytoplankton species (a diatom, a chlorophyte, a cryptophyte, and a cyanobacterium) in two waters containing different concentrations of dissolved organic carbon (DOC). At steady state, volume concentration factors (VCFs) for Hg(II) in the four species were similar and ranged from 0.5 to 5 x 10(4) for both water types, whereas VCFs for MeHg exceeded those for Hg(II) and ranged from 1.3 to 14.6 x 10(5). The VCFs for MeHg in the three eukaryotic cells in the high DOC water were 2-2.6 times greater than those in the low DOC water, but the VCFs for the prokaryote were similar in both waters. Higher cell surface area to volume ratios correlated with increased MeHg concentrations but not with Hg(II). In both water types, VCFs of Hg(II) were similar for living and heat-killed cells, but the VCFs of MeHg were 1.5-5.0 times greater in living cells, suggesting an active uptake component for MeHg. Hg(II) and MeHg were entirely bound to cell surfaces of the dead cells, whereas 59-64% of the MeHg and 9-16% of the Hg(II) in living cells entered the cytoplasm.

In the present study, we investigated the effects of mercury intoxication on the structure of the posteromedial barrel subfield (PMBSF) in the primary somatosensory cortex (SI) of adult rats, as revealed by histochemical reactivity to the enzyme NADPH diaphorase (NADPH-d). Enzymatic reactivity in the neuropil inside barrels was drastically reduced in intoxicated animals, suggesting that the synthesis and/or transport of the nitric oxide synthase enzyme can be altered in acute mercury intoxication. However, the cell bodies and dendrites of barrel neurons, also strongly reactive to the enzyme, were spared from the mercury's deleterious effects.

The concentration of methylmercury (MeHg) in human hair is an excellent marker for its exposure, since a portion of MeHg is taken up from the blood circulation to the hair protein in a dose-dependent manner. However, a small portion of the mercury in human hair is found in the inorganic form, though the mechanism of its occurrence is not well established. Here, we examined the hair uptake of inorganic mercury in the rat. Male Wistar rats were exposed to MeHg (1 microg Hg/ml) or HgCl(2) (20 microg Hg/ml) for 84 days through drinking water. The hair, grown from 49 to 84 days, was collected from the MeHg-exposed rats, and the hair samples showed 54.5 microg/g hair of the total mercury concentration, 6.1% of which was in the inorganic form. The inorganic mercury in the plasma (0.022 microg/ml), which would probably be formed from MeHg in rat tissues, accounted for as high as 29% of the total mercury (0.076 microg/ml). The hair uptake rate of inorganic mercury estimated from the hair/plasma ratio was about 1/6 lower than that of MeHg. On the other hand, the total hair mercury level in the HgCl(2)-exposed group at the same time point was 2.86 microg/g, with the inorganic portion being as high as 62%. These findings suggest that the inorganic mercury is also taken up by rat hair from the blood circulation, as is the MeHg, irrespective of the consequences of the biotransformation of MeHg or exposure to inorganic mercury itself. Accordingly, a selective quantification of inorganic mercury in human hair may be useful in detecting inorganic mercury exposure.

Striped bass (Morone saxatilis), white perch (Morone Americana), and largemouth bass (Micropterus salmoides) were collected in the Chesapeake Bay mainstem and tributaries and analyzed for total mercury (Hg) and methylmercury (MeHg) content. Striped bass are anadromous, whereas white perch and largemouth bass are resident species, and the largemouth bass are also restricted to the tidal fresh portion of the Bay. Total Hg and MeHg concentrations in striped bass increased with fish size, and large fish (>7.5 kg wet weight) tended to have MeHg concentrations of 300 ng g(-1) or greater. On average, the striped bass MeHg concentration was 120 +/- 100 ng g(-1) and the fraction of the total Hg as MeHg was 65 +/- 22%. Reasons for the lower relative MeHg content are discussed. Otolith strontium/calcium ratios were also determined to examine whether migration had a significant impact on MeHg content in striped bass. Resident fish did appear to have a higher MeHg burden than the more migratory fish of similar size. Largemouth bass and white perch tended to have low MeHg content (respectively, 14 +/- 7 and 13 +/- 11 ng g(-1); all fish <1 kg wet weight), and the white perch also had a low %MeHg (28 +/- 14%), reflecting their mostly planktivorous lifestyle. A comparison of largemouth bass and striped bass MeHg concentrations for the estuarine fish with those of fish in Maryland reservoirs of similar size showed that the estuarine fish have much lower MeHg burdens. Differences in MeHg concentration in the estuarine waters compared to the reservoir waters likely account for much of this difference, although the importance of other factors is also discussed.

Humans are exposed to methylmercury (MeHg) principally by consumption of marine fish. The coastal zone supports the majority of marine fish production, and may therefore be an important source of MeHg to humans; however, little is known about the bioaccumulation of MeHg in near-shore marine ecosystems. We examined MeHg in microseston, zooplankton, a decapod crustacean, and four representative species of finfish that differ in trophic status and/or prey selection in Long Island Sound (LIS), a large coastal embayment in the northeastern United States. MeHg biomagnifies in LIS; levels in microseston were 10(4.2) greater than those in water and 2.3-fold less than zooplankton. MeHg concentrations were related positively to fish length for each species, but often varied considerably among larger individuals. This may be due to differences in the past dietary MeHg exposure of these fish, some of which are migratory. Sedimentary production and mobilization can account for most of the MeHg in microseston of LIS, and by extension, other near-shore locations. Hence, much of the MeHg in higher trophic levels of coastal marine ecosystems, including fishes destined for human consumption, may be attributed to net sedimentary production and dietary bioaccumulation.

High Hg concentrations in freshwater fish are a concern for human health, yet we lack a clear understanding of the mechanisms that produce high Hg concentrations in fish. Controlled studies in natural surface waters that quantify the uptake and retention of Hg in fish tissues following exposures from the aqueous phase and from invertebrate prey diets are rare. Using 203Hg, we contrasted the accumulation of inorganic Hg (HgI) and methylmercury (MeHg) from the dissolved phase and from invertebrate food in mosquitofish (Gambusia affinis) feeding on Daphnia pulex (representing a pelagic food chain) and in redear sunfish (Lepomis microlophus) feeding on amphipods (Hyallela sp., representing a benthic/macrophyte-based chain). Experiments were conducted with environmentally realistic Hg concentrations in two freshwaters from the San Francisco Bay Delta (CA, USA) with significantly different dissolved organic carbon (DOC) concentrations. Mercury uptake rates following aqueous exposures were consistently higher for fish in the water with lower DOC, whereas efflux rates were similar for both water types. Approximately 50% of the ingested Hg, associated with invertebrate prey was lost from mosquitofish, and 90% or more from sunfish, within 48 h. Assimilation efficiencies for ingested MeHg for both fish were 86 to 94%, substantially higher than those for HgI regardless of water type. Biokinetic modeling using the parameters determined in these experiments accurately predicted Hg burdens for fish in the San Francisco Bay Delta system. Despite considerable accumulation of HgI from both aqueous and dietary exposure routes, the high assimilation efficiencies and slow loss of MeHg from dietary sources are the principal determinants of predicted Hg burdens in both fish species.

A cohort of 1022 consecutive singleton births was generated during 1987-1988 in the Faroe Islands, where increased methylmercury exposure occurs from traditional seafood diets that include pilot whale meat. The prenatal exposure level was determined from mercury analyses of cord blood, cord tissue, and maternal hair. At age 14 years, 878 of 1010 living cohort members underwent detailed neurobehavioral examination. Eighteen participants with neurological disorders were excluded. Blood and hair samples obtained from the participants were analyzed for mercury. The neuropsychological test battery was designed based on the same criteria as applied at the examination at age 7 years. Multiple regression analysis was carried out and included adjustment for confounders. Indicators of prenatal methylmercury exposure were significantly associated with deficits in finger tapping speed, reaction time on a continued performance task, and cued naming. Postnatal methylmercury exposure had no discernible effect. These findings are similar to those obtained at age 7 years, and the relative contribution of mercury exposure to the predictive power of the multiple regression models was also similar. An analysis of the test score difference between results at 7 and 14 years suggested that mercury-associated deficits had not changed between the two examinations. In structural equation model analyses, the neuropsychological tests were separated into five groups; methylmercury exposure was significantly associated with deficits in motor, attention, and verbal tests. These findings are supported by independent assessment of neurophysiological outcomes. The effects on brain function associated with prenatal methylmercury exposure therefore appear to be multi-focal and permanent.

Objectives: The subclinical effects of prenatal exposure to methylmercury from fish consumption on the cardiac autonomic function were assessed in 136 Japanese 7-year-old children recruited for this study., Methods: Samples of child's hair and dry umbilical cord preserved were collected, and hair mercury and cord tissue methylmercury concentrations were determined as current and prenatal exposure biomarkers, respectively. Cardiac autonomic indicators of parasympathetic and sympathetic activities were calculated from the electrocardiographic RR intervals measured., Results: In the children, the cord tissue methylmercury (0.017-0.367, median 0.089 microg/g) was not significantly correlated with the hair mercury (0.43-6.32, median 1.66 microg/g). The cord tissue methylmercury was related negatively to parasympathetic components of cardiac autonomic indicators (P < 0.05) and positively to sympathovagal indices (P < 0.05), even after correction for possible confounders such as age and sex, although the hair mercury was not significantly correlated with any cardiac autonomic indicators., Conclusions: Despite the potential limitations involved in the retrospective study, these findings suggest that prenatal methylmercury exposure (median of estimated maternal hair mercury at parturition, 2.24 microg/g) may be associated with reduced parasympathetic activity and/or sympathovagal shift.

The aim of this research was to verify the incidence of endocrine dysfunction associated with mercury intoxication in the hypothalamus-pituitary reproductive system of normally cycling or castrated female rats and the possible protective action of estrogen replacement therapy. We found no differences in the frequency of estrus cycle stages (diestrus I, diestrus II, proestrus, and estrus) in normally cycling female rats during 54 days of daily oral administration of 0.004, 0.02, and 1 mg/kg MeHgCl. Conversely, the higher dose (1 mg/kg) induced a significant decrease in content of luteinizing hormone releasing hormone (LHRH) into the medial hypothalamus when administered daily during 3 days in ovariectomized rats. This effect was associated with increased levels of mercury found in the anterior pituitary gland and medial hypothalamus, rather than the anterior and posterior hypothalamus, striatum or cerebellum. A decrease in plasma levels of luteinizing hormone (LH) was also detected after administration of 7.5 mg/kg MeHgCl. These disturbances in LHRH and LH secretion induced by mercury were abolished or superimposed (respectively) by estrogenic replacement therapy (0.025 mg/kg 17beta estradiol cypionate, intramuscular). These effects were associated with a significant reduction in mercury content of the anterior pituitary gland and medial hypothalamus, suggesting a protective estrogenic effect.

Epidemiologic studies commonly use mercury (Hg) level in hair as a valid proxy to estimate human exposure to methylmercury (MeHg) through fish consumption. This study presents the results yielded by a complete data set on fish consumption habits, Hg levels in edible fish resources, and corresponding Hg accumulation in hair, gathered in three distinct communities of eastern Canada. For one of these communities, the average hair Hg concentration was 14 times less than the expected value based on calculated daily oral exposure and current knowledge of MeHg metabolism. This finding could be explained by differences in specific genetic characteristics and/or interactive effects of other dietary components.

Early life stages of fishes have been shown to be especially susceptible to the toxic effects of heavy metal pollution. In this study, fathead minnow (Pimephales promelas) embryos were exposed in the laboratory to a graded series of aqueous methyl mercury concentrations under continuous-flow conditions. A number of toxicological endpoints were examined including; acute toxicity, bioaccumulation, protein production, impact on mitosis, gross and histopathology. Acute toxicity, reported as LC50 values of methyl mercury, ranged from 221 microg/l (95% C.I. 246-196 microg/l) for 24-h tests to 39 microg/l (95% C.I. 54-24 microg/l) for 96-h exposures. Fathead minnow embryos were shown to rapidly take up mercury from the surrounding water. Mercury levels in embryos reached levels of 2.80 microg/g wet weight after 96 h exposure to 40 microg/l methyl mercury. An initial elevation of total protein in embryo was observed in embryos exposed to 25 microg/l methyl mercury during the first 12 h of development. At later stages, significantly lower levels of protein/microg embryo were observed. Methyl mercury had no effect on mitotic stages (p=0.05) in early, cleaving blastula-stage embryos. Live embryos and serial sections were utilized to characterize changes in embryo morphology and histopathology.

Objective: To probe into the prelude marker of central nervous system injury in response to methyl mercury chloride (MMC) stimulation and the signal transduction molecular mechanism of injury in rat brain induced by MMC., Methods: The expression of c-fos mRNA in brain and the expression of c-FOS protein in cortex, hippocampus and ependyma were observed using reverse transcription polymerase chain reaction (RT-PCR) and immunocytochemical methods. The control group was injected with physiological saline of 0.9%, while the concentrations for the exposure groups were 0.05 and 0.5, 5 mg/kg MMC respectively, and the sampling times points were 20, 60, 240, 1440 min., Results: The expression of c-FOS protein in cortex and hippocampus increased significantly, the accumulation of mercury in the brain induced by 0.05 mg/Kg MMC for 20 min had no significant difference compared with the control group. The mean value was 0.0044 mg/Kg, while the protein c-FOS expression had significant difference compared with the control group (P < 0.01). More sensitive expression occurred in hippocampus and cortex, but not in ependyma. Conclusion The expression of c-FOS protein in cortex and hippocampus can predict the neurotoxicity of MMC in the early time, and immediately early gene (IEG) c-fos participates in the process of brain injury induced by MMC.

Uptake of methylmercury (MeHg) by the alga Selenastrum capricornutum was measured in freshwater batch culture bioassays. The concentration of MeHg in the alga increased rapidly (within 15 min), reached a maximum by 6 h, and then declined because of growth dilution. The alga's rapid growth rate (doubling time, approximately 10 h) contributed to the importance of growth dilution. Conditional first-order rate constants were calculated for uptake (k1 = 6.95 x 10(-9) L/cell/h) and growth (kG = 0.07/h). A competitive synthetic ligand, disodium ethylenediaminetetra-acetate, formed strong complexes with MeHg and reduced MeHg uptake, consistent with the biotic ligand model. A conditional equilibrium formation constant (K) for the MeHg-algae complex was estimated to be approximately 10(16) and was used to model the influence of natural ligands on MeHg bioavailability. Model results suggested MeHg would be most bioavailable at concentrations of dissolved organic matter (DOM) less than 10 mg/L and increasingly unavailable at higher DOM concentrations for the specific humic acid modeled. Similarly, at molar concentrations of sulfide (and, possibly, metal-sulfide clusters) equal to approximately half the MeHg concentration, MeHg was predicted to be unavailable to algae because of the formation of strong 2:1 MeHg-sulfide complexes.

Significant amounts of methylmercury (MeHg) can bioaccumulate in fish and sea mammals. To monitor MeHg exposure in individuals, organic and inorganic mercury are often measured in blood samples or in hair strands, the latter being by far the best integrator of past exposure. With knowledge of the MeHg kinetics in humans, the levels of both biomarkers can be related to MeHg body burden and intakes. In the present study, we use the toxicokinetic model of Carrier et al. (2001) describing the distribution and excretion of MeHg in humans, to reconstruct the history of MeHg intakes of indigenous women of the Inuvik region in Canada starting from total mercury concentrations in hair segments. From these reconstructed MeHg intakes, the corresponding simulated mercury blood concentrations are found to be good predictors of the concentrations actually measured in blood samples. An important conclusion of this study is that, for almost all subjects, the reconstructed history of their MeHg intakes provides much lower intake values than intakes estimated from questionnaires on food consumption and estimated MeHg levels in these foods; the mean value of the reconstructed MeHg intakes is 0.03 microg/kg/day compared with the mean value of 0.20 microg/kg/day obtained from questionnaires. The model was also used to back-calculate the MeHg intakes from concentrations in hair strands collected from aboriginals of the Amazon region in Brazil, a population significantly more exposed than the population of the Inuvik region.

The investigation of mercuric ion and mercuric conjugate inside live specimens has drawn intense attention because of their cytotoxicity. The translocation, transportation, and distribution of Hg2+ inside either mammals or plants, however, are still invisible due to the lack of favorable fluorescent molecular sensors for Hg2+. Here, two sensors, 2,6-bis(4'-peperazino-N'-hydroxylethoxylethylene-1',8'-naphthalimide)dimethylpyridine and 2,6-bis(4'-peperazino-N'-butyl-1',8'-naphthalimide)dimethylpyridine, which were composed of nitrogen atoms of 2,6-bis(aminomethyl)pyridine as the ion receptor and the donor of photoinduced electron transfer, were applied to the cultured mammalian cells and plant cells. Their membrane permeability, low toxicity, slow bleaching/fading, and high selectivity and sensitivity to Hg2+ in a live cell rendered them attractive to become real-time and real-space sensors. For the first time, the transportation of Hg2+ cation and Hg2+ conjugate of cysteine was observed with the help of a fluorescence microscope. The chloroplast location of Hg2+ in transgenic tobacco was also visible.

It is well established that methylmercury (MeHg) and mercury vapor pass the placenta, but little is known about infant exposure via breast milk. We measured MeHg and inorganic mercury (I-Hg) in blood of Swedish mothers (n = 20) and their infants, as well as total mercury (T-Hg) in breast milk up to 13 weeks postpartum. Infant blood MeHg was highly associated with maternal blood MeHg at delivery, although more than twice as high. Infant MeHg decreased markedly until 13 weeks of age. Infant blood I-Hg was associated with, and about as high as, maternal blood I-Hg at delivery. Infant I-Hg decreased until 13 weeks. In breast milk, T-Hg decreased significantly from day 4 to 6 weeks after delivery but remained unchanged thereafter. At 13 weeks, T-Hg in breast milk was associated with infant MeHg but not with maternal MeHg. Conversely, T-Hg in breast milk was associated with maternal I-Hg but not with infant I-Hg. From the findings of the present study in which the exposure to both MeHg and I-Hg was low, we conclude that the exposure to both forms of mercury is higher before birth than during the breast-feeding period, and that MeHg seems to contribute more than I-Hg to infant exposure postnatally via breast milk.

Background: The activity of the organic anion transporter 1 (OAT1) has been implicated recently in the basolateral uptake of thiol conjugates of inorganic mercury in renal proximal tubular cells. However, very little is known about the role of OAT1 in the renal epithelial transport of organic forms of mercury, such as methylmercury (CH(3)Hg(+)), especially when it is in the form of the cysteine (Cys) S-conjugate of methylmercury (CH(3)Hg-Cys), which is believed to be a biologically relevant form of mercury., Methods: Accordingly, the present study, was designed to characterize the transport of CH(3)Hg-Cys in Madin-Darby canine kidney (MDCK) cells transfected stably with the human isoform of OAT1 (hOAT1) and in proximal tubular-derived NRK-52E cells., Results: Data on saturation kinetics, time dependency, substrate specificity, and temperature dependency demonstrate that CH(3)Hg-Cys is transported by hOAT1. Substrate-specificity data from the control cells also show that CH(3)Hg-Cys is a substrate of one or more transporter(s) that is/are not hOAT1. Additional findings indicate that at least one amino acid transport system is involved in the uptake of CH(3)Hg-Cys in MDCK cells. Furthermore, in the presence of cytotoxic concentrations of CH(3)Hg-Cys, rates of survival were lower in hOAT1-transfected cells than in wild-type control cells., Conclusion: The present data demonstrate clearly that CH(3)Hg-Cys is indeed a transportable substrate of OAT1. Moreover, the collective findings from the MDCK cells and NRK-52E cells infer that CH(3)Hg-Cys is a likely transportable mercuric species in proximal tubular epithelial cells that is taken up in vivo by both OAT1 and amino acid transporters.

Breastfeeding has been associated with an advantage to infant neurobehavioral development, possibly in part due to essential nutrients in breast milk. However, breast milk may be contaminated by environmental neurotoxicants, such as methylmercury. In the Faroe Islands, where maternal consumption of pilot whale may cause transfer of marine toxicants into breast milk, a cohort of 1022 consecutive singleton births was generated during 1986-87. Methylmercury exposure was assessed from mercury concentrations in cord blood and in the hair of the child at age 12 months, and the duration of breastfeeding was recorded. At approximately 7 years of age, 917 (90%) of the children underwent detailed neurobehavioral examination. After adjustment for confounders, breastfeeding was associated with only marginally better neuropsychological performance on most tests. These associations were robust even after adjustment for cord-blood and hair mercury concentration at age 1 year. Thus, in this cohort of children with a relatively high prenatal toxicant exposure and potential exposure to neurotoxicants through breast milk, breastfeeding was associated with less benefits on neurobehavioral development than previously published studies though not associated with a deficit in neuropsychological performance at age 7. Although the advantage may be less, Faroese women can still safely breastfeed their children.

We report on the uptake of MeHg in astrocytes and neurons, as well as specific indicators of neurotoxicity. Cerebellar granule neurons and astrocytes separately and in co-culture were cultured in the presence of MeHg and changes in 3-[4, 5-dimethylthiazol-2-yl]-2, 5 diphenyltetrazolium bromide (MTT)-reduction, lactate dehydrogenase (LDH) leakage, and cellular content of glutathione and amino acids were used as indicators of MeHg toxicity. Mitochondria in cortical astrocytes were slightly more sensitive than those in cerebellar astrocytes to the toxic effects of MeHg; furthermore, cellular integrity was better preserved in cerebellar astrocytes. When neurons and astrocytes from cerebellum were incubated in separable co-cultures using inserts, the astrocytes showed cellular damage at lower exposure to MeHg while neurons showed less changes compared to respective cell types in mono-cultures. Mercury uptake studies at 25 microM MeHg (10% serum present) showed that for neurons in co-culture the uptake was 1/3 compared to mono-cultures. In contrast, for astrocytes in co-culture, uptake was increased by 75%. A MeHg concentration-dependent increase of glutamate content in mono-cultures was noted. When MeHg concentration was increased to 10, 25, or 50 microM, neurons in co-cultures decreased their glutamate content, whereas astrocytes showed an increase. Other amino acids, such as glutamine, serine, valine, isoleucine, taurine, and phenylalanine were unaffected by MeHg. Glutathione content showed MeHg concentration-dependent changes in astrocytes and was increased in neurons in co-culture incubated with 5 microM MeHg. In conclusion, astrocytes appear to increase neuronal resistance, indicating a possible protective role for astrocytes in MeHg neurotoxicity.

Recent studies have implicated the activity of the organic anion transporter 1 (OAT1) protein in the basolateral uptake of inorganic mercuric species in renal proximal tubular epithelial cells. However, very little is known about the potential role of OAT1 (and other OATs) in the renal epithelial transport of organic forms of mercury such as methylmercury (CH(3)Hg(+)). The present investigation was designed to study the transport of N-acetyl cysteine (NAC) S-conjugates of both methylmercury (CH(3)Hg-NAC) and inorganic mercury (NAC-Hg-NAC) in renal epithelial cells [Madin-Darby canine kidney (MDCK) cells] stably transfected with the human isoform of OAT1 (hOAT1). These mercuric species were studied because numerous mercapturates have been shown to be substrates of OATs. Data on saturation kinetics, time dependence, substrate specificity, and temperature dependence for the transport of CH(3)Hg-NAC and NAC-Hg-NAC indicate that both of these two mercuric species are indeed transportable substrates of hOAT1. Substrate specificity data also show that CH(3)Hg-NAC is a substrate of a transporter in MDCK cells that is not hOAT1. These data indicate that an amino acid carrier system is a likely candidate responsible for this transport. Furthermore, the rates of survival of the hOAT1-transfected MDCK cells were significantly lower than those of corresponding control MDCK cells when they were exposed to cytotoxic concentrations of CH(3)Hg-NAC or NAC-Hg-NAC. Collectively, the present data support the hypothesis that CH(3)Hg-NAC and NAC-Hg-NAC are transportable substrates of OAT1 and thus potentially transportable mercuric species taken up in vivo at the basolateral membrane of proximal tubular epithelial cells.

Thimerosal is a preservative that has been used in manufacturing vaccines since the 1930s. Reports have indicated that infants can receive ethylmercury (in the form of thimerosal) at or above the U.S. Environmental Protection Agency guidelines for methylmercury exposure, depending on the exact vaccinations, schedule, and size of the infant. In this study we compared the systemic disposition and brain distribution of total and inorganic mercury in infant monkeys after thimerosal exposure with those exposed to MeHg. Monkeys were exposed to MeHg (via oral gavage) or vaccines containing thimerosal (via intramuscular injection) at birth and 1, 2, and 3 weeks of age. Total blood Hg levels were determined 2, 4, and 7 days after each exposure. Total and inorganic brain Hg levels were assessed 2, 4, 7, or 28 days after the last exposure. The initial and terminal half-life of Hg in blood after thimerosal exposure was 2.1 and 8.6 days, respectively, which are significantly shorter than the elimination half-life of Hg after MeHg exposure at 21.5 days. Brain concentrations of total Hg were significantly lower by approximately 3-fold for the thimerosal-exposed monkeys when compared with the MeHg infants, whereas the average brain-to-blood concentration ratio was slightly higher for the thimerosal-exposed monkeys (3.5 +/- 0.5 vs. 2.5 +/- 0.3). A higher percentage of the total Hg in the brain was in the form of inorganic Hg for the thimerosal-exposed monkeys (34% vs. 7%). The results indicate that MeHg is not a suitable reference for risk assessment from exposure to thimerosal-derived Hg. Knowledge of the toxicokinetics and developmental toxicity of thimerosal is needed to afford a meaningful assessment of the developmental effects of thimerosal-containing vaccines.

Samples of copepods (Calanus hyperboreus) and arctic cod (Boreogadus saida) were collected along the SHEBA (Surface HEat Budget of the Arctic) drift track, which commenced in the Canada Basin (October 1997) and finished in the Mendeleev Basin (October 1998). Here, we report total mercury (HgT) and CH3Hg concentrations in these biological samples and examine concentration variability along the drift track in the context of trophic variation, inputs from land, spring mercury depletion events (MDEs), and oceanographic provinces. We find background concentrations of HgT in C. hyperboreus as low as 0.02 microg/g (dw), with the Canada Basin samples exhibiting approximately 2-fold higher mercury concentrations than those from the Chukchi Plateau and Mendeleev Abyssal Plain. This east-to-west trend in mercury concentration is punctuated by two and possibly three intervals of elevated mercury (HgT, 0.10-0.12 microg/g (dw); CH3Hg, 0.023-0.028 microg/g (dw)) along the drift track. One interval of elevated HgT and CH3-Hg levels occurred during and shortly after melt. %CH3Hg reached a maximum of 60% during this time period, three times higher than any other time during the drift. This transient rise in C. hyperboreus CH3Hg concentration seems to strongly point to mercury accumulated in snow during MDEs. However, the alignment of elevated mercury samples with oceanographic fronts and the observed regional differences between basins suggest that variation of mercury concentration is primarily a consequence of ocean structure. Given that large animals such as whales selectively forage in regions of higher food concentration such as fronts, recent change in the ice climate of the western Arctic Ocean, perhaps mediated by changes in heat storage, may provide the means to change their exposure to mercury thus explaining observed increases in mercury concentrations in western beluga whales during the 1990s.

We modeled the flow of methyl mercury, a toxic global pollutant, in the Faroe Islands marine ecosystem and compared average human methyl mercury exposure from consumption of pilot whale meat and fish (cod, Gadus morhua) with current tolerable weekly intake (TWI) levels. Under present conditions and climate change scenarios, methyl mercury increased in the ecosystem, translating into increased human exposure over time. However, we saw greater changes as a result of changing fishing mortalities. A large portion of the general human population exceed the TWI levels set by the World Health Organization [WHO; 1.6 microg/kg body weight (bw)], and they all exceed the reference dose (RfD) of 0.1 microg/kg bw/day set by the U.S. Environmental Protection Agency (EPA; equivalent to a TWI of 0.7 microg/kg bw). As a result of an independent study documenting that Faroese children exposed prenatally to methyl mercury had reduced cognitive abilities, pregnant women have decreased their intake of whale meat and were below the TWI levels set by the WHO and the U.S. EPA. Cod had approximately 95% lower methyl mercury concentrations than did pilot whale. Thus, the high and harmful levels of methyl mercury in the diet of Faroe Islanders are driven by whale meat consumption, and the increasing impact of climate change is likely to exacerbate this situation. Significantly, base inflow rates of mercury into the environment would need to be reduced by approximately 50% to ensure levels of intake below the WHO TWI levels, given current levels of whale consumption.

A connection between loadings of inorganic Hg, especially from the atmosphere, and accumulation of methylmercury (MeHg) in aquatic biota has not been firmly established. Mosquitoes (Diptera: Culicidae) may be a useful indictor of Hg contamination or MeHg accumulation in aquatic ecosystems because they have aquatic life stages, and their ubiquitous distribution permits sampling across wide ranges of climate, biological productivity, and atmospheric Hg deposition. We examined MeHg in adult mosquitoes from subtropical (Florida), maritime (California), continental (Michigan), and arctic (Alaska) regions of North America that span a range in wet atmospheric Hg deposition (1.5-15 microg m(-2) y(-1)). More than 90% of the Hg in mosquitoes was MeHg, and concentrations varied among locations. Levels of MeHg differed among mosquito species at six sites in northwest Florida (Ochlerotatus atlanticus < Culex nigripalpus < Anopheles crucians); this may be related to differences in biogeochemical characteristics of the aquatic habitat that affect dietary accumulation of MeHg during the larval stage. Mosquito MeHg was related positively to wet atmospheric Hg deposition among locations where atmospheric deposition is the principal source of Hg, and it was greatly enhanced in Hg-polluted environs near the Sulphur Bank Mine in Lake County, California. These results suggest that MeHg in mosquitoes may be a useful and sensitive indicator of Hg loadings to aquatic systems, including that derived from atmospheric deposition.

Inorganic mercury and methylmercury concentrations were measured both in guts and remaining carcasses of southern leopard frog (Rana sphenocephala) larvae from 10 Carolina bay wetlands in South Carolina, USA. Significant variation among bays in methylmercury and inorganic mercury concentrations existed both in guts and carcasses. There was a moderate negative correlation between dissolved organic carbon concentration in bays and mean inorganic mercury concentrations in guts. There was also a weak positive correlation between pH in bays and mean methylmercury concentrations in carcasses. The ratio of methylmercury to inorganic mercury decreased with increasing total mercury concentration in guts and in larvae, but the rate of decrease was highly variable among bays. Ratios of concentrations in carcasses to concentrations in guts were inversely related to gut concentration. Mercury concentrations in carcasses in some bays were within the range of concentrations at which adverse effects have been observed in laboratory studies of R. sphenocephala.

An in vivo experiment was conducted to evaluate the effects of sodium selenite, sepiolite, and bentonite on inorganic mercury (Hg) and methylmercury (MeHg) bioaccumulation. For this purpose 160 chickens were fed under different controlled conditions. Chickens were exposed to Hg(II) and MeHg added to feed with or without selenium or clays supplementation. No significant differences were observed in the voluntary intake and feed/gain conversion rates. The target organs of Hg(II) and MeHg in chickens were the liver and kidney, respectively, but the greatest body store was the muscle in both cases. A higher bioaccumulation for MeHg than for Hg(II) was observed. The results showed that addition of sodium selenite, sepiolite, or bentonite induced a decrease of up to 60-100% in the inorganic mercury bioabsorption. Bentonite addition to a MeHg-containing diet also caused a decrease in organic mercury bioaccumulation (29-67%). On the other hand, inorganic selenium and sepiolite did not decrease MeHg accumulation.

Despite the key role microalgae play in introducing toxicants into aquatic food webs, little is known about the effects of environmental factors on metal accumulation by these primary producers. Environmental factors such as light and nutrients alter growth rates and may consequently influence metal concentrations in microalgae through growth dilution. Laboratory experiments suggested that metal uptake and elimination by microalgal biofilms were gradual enough to enable dilution of metals within the biofilms by photosynthetically accrued carbon, and a simple kinetic model of metal accumulation predicted significant variation in metal content due to growth dilution over the natural range of microalgal growth rates. The ratio of metal uptake to carbon uptake by microalgal biofilms decreased exponentially with increasing light in short-term laboratory experiments because photosynthesis was much more sensitive to a light gradient than was metal uptake. The effect of light on biofilm metal concentrations was confirmed in situ with a long-term experiment in which experimental shading of biofilms in a metal-contaminated stream decreased biofilm growth rates and caused a 3x increase in biofilm concentrations of twelve metals, including methylmercury. Slow growth at the primary producer level is a likely contributor to higher biotic metal concentrations in shaded, oligotrophic, or cold ecosystems.

We studied the effect of zooplankton diet on MeHg accumulation in different zooplankton size-fractions from lakes of different trophic status. Using fatty acid biomarkers, we tested the hypotheses that (a) variations of MeHg concentrations are determined bythe taxonomic composition of zooplankton and (b) concentrations of dietary algal and bacterial compounds can predict MeHg concentrations of seston (10-64 microm), micro- (100-200 microm), meso- (200-500 microm), and macrozooplankton (>500 microm) in lakes on Vancouver Island, Canada. MeHg concentrations increased from seston (4-48 ng g dry weight(-1)) to macrozooplankton (94-240 ng g dry weight(-1)), indicating that MeHg accumulated as a function of plankton size. Results from linear regression analysis showed that MeHg concentrations were not significantly related to the taxonomic composition of zooplankton. However, using dietary lipid biomarkers, we demonstrated that bacterial diet (R2 = 0.50; p < 0.01) could better predict variations of MeHg concentrations in zooplankton than essential algal diet (R2 = 0.35; p < 0.01). Because MeHg accumulation within the planktonic food web was higher (20x) than the observed accumulation of total bacterial (6.5x) and algal (4.7x) diet biomarkers, zooplankton retained dietary MeHg more efficiently than bacterial and algal diet compounds. These results indicate that MeHg of macrozooplankton, the preferred prey size of planktivorous fish, is more efficiently transferred than essential diet compounds to organisms at higher trophic levels.

The physical factors controlling total mercury (HgT) and methylmercury (MeHg) concentrations in lakes and streams of northeastern USA were assessed in a regional data set containing 693 HgT and 385 corresponding MeHg concentrations in surface waters. Multiple regression models using watershed characteristics and climatic variables explained 38% or less of the variance in HgT and MeHg. Land cover percentages and soil permeability generally provided modest predictive power. Percent wetlands alone explained 19% of the variance in MeHg in streams at low-flow, and it was the only significant (p < 0.02) predictor for MeHg in lakes, albeit explaining only 7% of the variance. When stream discharge was added as a variable it became the dominant predictor for HgT in streams, improving the model r2 from 0.19 to 0.38. Stream discharge improved the MeHg model more modestly, from r2 of 0.25 to 0.33. Methylation efficiency (MeHg/HgT) was modeled well (r2 of 0.78) when a seasonal term was incorporated (sine wave with annual period). Physical models explained 18% of the variance in fish Hg concentrations in 134 lakes and 55% in 20 reservoirs. Our results highlight the important role of seasonality and short-term hydrologic changes to the delivery of Hg to water bodies.

Methylmercury (MeHg) is a common environmental pollutant due to both natural and anthropogenic sources. Although the central nervous system (CNS) is considered the critical organ for the toxic effect of MeHg, it has recently been suggested that the immune system might be at least as sensitive as the CNS. We have examined the effects of MeHg on the immune system in genetically metal-susceptible mice. Subcutaneous (sc) injections of 2 mg MeHg/kg body weight (bw) every third day (internal dose ca. 540 microg Hg/kg bw/day) to A.SW mice of the H-2(s) haplotype, caused during the first week a 47 and 9% reduction of B- and T-cells, respectively, which indicates immunosuppression. Subsequently, an autoimmune syndrome developed which shared certain features with the syndrome induced by inorganic mercury in H-2(s) mice, including antibodies targeting the 34 kDa nucleolar protein fibrillarin, increased expression of IL-4 mRNA, increase of Th2-type of immunoglobulins (IgE and IgG1), and increased MHC class II expression on B-cells. However, the response using MeHg was attenuated compared with even lower doses of Hg in the form of inorganic mercury, and specifically lacked the increased expression of IL-2 and IFN-gamma mRNA, the polyclonal B-cell activation (PBA), and the systemic immune-complex (IC) deposits which are induced by inorganic mercury. Increasing the dose of MeHg increased the titre of anti-nucleolar antibodies and shortened the induction time, but did not lead to stronger immunostimulation or systemic IC-deposits. The kidney and liver selectively accumulated MeHg, while the blood, spleen and lymph nodes showed lower levels of MeHg. The accumulation of MeHg and Hg(2+) increased throughout the 30-day period. The fraction of Hg(2+) in the kidney varied between 4 and 22%, and the lymph nodes showed a maximum of 30% Hg(2+). We conclude first that MeHg has quantitatively different effect on the immune system compared with inorganic mercury, and secondly that an initial immunosuppression induced by a xenobiotic does not preclude subsequent immunostimulation and autoimmunity.

In 2001, the U.S. Environmental Protection Agency (EPA) adopted a revised reference dose (RfD) for methyl mercury (MeHg) of 0.1 microg/kg/day. The RfD is based on neurologic developmental effects measured in children associated with exposure in utero to MeHg from the maternal diet. The RfD derivation proceeded from a point of departure based on measured concentration of mercury in fetal cord blood (micrograms per liter). The RfD, however, is a maternal dose (micrograms per kilogram per day). Reconstruction of the maternal dose corresponding to this cord blood concentration, including the variability around this estimate, is a critical step in the RfD derivation. The dose reconstruction employed by the U.S. EPA using the one-compartment pharmacokinetic model contains two areas of significant uncertainty: It does not directly account for the influence of the ratio of cord blood: maternal blood Hg concentration, and it does not resolve uncertainty regarding the most appropriate central tendency estimates for pregnancy and third-trimester-specific model parameters. A probabilistic reassessment of this dose reconstruction was undertaken to address these areas of uncertainty and generally to reconsider the specification of model input parameters. On the basis of a thorough review of the literature and recalculation of the one-compartment model including sensitivity analyses, I estimated that the 95th and 99th percentiles (i.e., the lower 5th and 1st percentiles) of the maternal intake dose corresponding to a fetal cord blood Hg concentration of 58 microg/L are 0.3 and 0.2 microg/kg/day, respectively. For the 99th percentile, this is half the value previously estimated by the U.S. EPA.

The distribution of mercury to the brain following an injection of methylmercury (MeHg) or ethylmercury (EtHg) was examined in immature mice. Postnatal day (PND) 16 CD1 mice received MeHg chloride either by IM injection or by gavage. At 24 h and 7 days post-injection, total mercury concentrations were determined in blood, kidney, brain, and muscle by cold vapor atomic fluorescence spectrometry. At 24 h, an IM injection of MeHg chloride (17.4 microg) produced total mercury concentrations in the blood (6.2 +/- 0.9 microg/g), brain (5.6 +/- 1.3 microg; 0.6% delivered dose), and kidney (25.2 +/- 5.6 microg; 1.1%), approximately 30% of that obtained from oral administration (blood: 17.9 +/- 1.0 microg; brain: 16.1 +/- 1.2 microg, 1.5%; kidney: 64.9 +/- 6.3 microg, 2.7%). For comparison, PND 16 mice received an IM injection of concentrated dosing suspensions (2 microl dosing vol.) for EtHg chloride (6 microg) or Thimerosal (15.4 microg). For EtHg, approximately 0.39 +/- 0.06% of the injected mercury was detected in the brain and 3.5 +/- 0.6% in the kidney at 24 h. Thimerosal IM injection resulted in 0.22 +/- 0.04% in the brain, and 1.7 +/- 0.3% in the kidney. By 7 days, mercury levels decreased in the blood but were unchanged in the brain. An acute IM injection to adult mice of each suspension at a 10-fold higher dose resulted an average 0.1% mercury in the brain, and higher levels in the blood, kidney, and muscle as compared to the young. In immature mice, MeHg delivered via oral route of administration resulted in significantly greater tissue levels as compared to levels from IM injection. Comparisons of tissue distribution following IM administration suggest that an oral route of administration for mercury is not comparable to an IM delivery and that MeHg does not appear to be a good model for EtHg-containing compounds.

Temperature is an important environmental variable affecting the physiology and metabolism of aquatic invertebrates and can potentially affect the rate and pathway of the uptake and elimination of contaminants. In this study, we studied the effects of the ambient temperature on the uptake (from water and food) and elimination of inorganic mercury [Hg(II)] and methymercury (MeHg) in a freshwater cladoceran, Daphnia magna, in the laboratory. At different temperatures (i.e., 14, 19 and 24 degrees C), the assimilation efficiencies of both Hg species from ingested alga were not significantly different while the dissolved uptake rates were 32 and 73% lower at 14 degrees C than at 24 degrees C for Hg(II) and MeHg, respectively. The reduced uptake rates of Hg(II) at 14 degrees C could be adequately explained by the reduced filtration rate (40% reduction), but for MeHg, the reduced filtration rate could not completely explain reduction in MeHg uptake rate. Despite the elimination rates of both Hg compounds not being affected by the temperature, the relative importance of different routes of Hg loss (i.e., excretion, egestion, molting and reproduction) was significantly different at various temperatures. The relative importance of excretion to MeHg loss increased from 24 to 14 degrees C (i.e., 52 to 85% of Hg loss) while that of reproduction to MeHg loss decreased from 43 to 11% simultaneously. Using a kinetic model, we showed that the fraction of MeHg accumulated in the daphnids coming from the dietary phase was higher at lower temperature, while there was increased accumulation of both Hg(II) and MeHg in the daphnids at higher temperatures. Nevertheless, the trophic transfer potentials for both Hg species in this algae-daphnids food chain were not influenced by the temperature.

Methylmercury is eliminated from the human body as glutathione (GSH) conjugates. GSH production is mediated by glutamyl-cysteine ligase (GCL) and conjugation by glutathione S-transferases (GST). In this study, the authors tested whether polymorphisms in GCL and GST genes modify methylmercury retention. Erythrocyte mercury concentration (EryHg), plasma polyunsaturated fatty acids (PPUFA), and genotype for GCLC, GCLM, GSTA1, GSTM1, GSTP1, and GSTT1 were determined in 365 individuals. A general linear model was developed for analyzing whether genotype modified the regression of EryHg on PPUFA. The presence of one variant allele for either GCLC-129 or GSTP1-114 was associated with higher EryHg and steeper regression slope. No similar trends were shown for GCLM, GSTA1, GSTM1, or GSTT1. These findings indicate that GCLC polymorphisms that affect GSH production also affect methylmercury retention, and that GSTP1 may play a role in conjugating methylmercury with GSH.

Critical concentration of methylmercuric chloride (MeHgCl) in the nutrient solution to which Spartina plants are tolerant is 15 micromol/L, three times higher than that of tobacco plants. After being treated with methylmercuric chloride, total quantity of organic mercury within plants increased and that of nutrient solution decreased greatly so that total quantity of inorganic mercury rose. It is inferred that Spartina plants absorb organic mercury and partially transform organic into inorganic mercury, and then more inorganic mercury is accumulated in underground parts of plants. In addition, inorganic mercury derived from organic mercury moved to solution by diffusion and permeation. In this way, the features Spartina plants exhibit in mercury accumulation and transformation from organic to inorganic mercury are valuable for phytoremediation of environment pollution.

Objective: The issue of thimerosal-containing vaccines as a possible cause of autistic spectrum disorders (ASD) and neurodevelopmental disorders (NDDs) has been a controversial topic since 1999. Although most practitioners are familiar with the controversy, many are not familiar with the type or quality of evidence in published articles that have addressed this issue. To assess the quality of evidence assessing a potential association between thimerosal-containing vaccines and autism and evaluate whether that evidence suggests accepting or rejecting the hypothesis, we systematically reviewed published articles that report original data pertinent to the potential association between thimerosal-containing vaccines and ASD/NDDs., Methods: Articles for analysis were identified in the National Library of Medicine's Medline database using a PubMed search of the English-language literature for articles published between 1966 and 2004, using keywords thimerosal, thiomersal, mercury, methylmercury, or ethylmercury alone and combined with keywords autistic disorder, autistic spectrum disorder, and neurodevelopment. In addition, we used the "related links" option in PubMed and reviewed the reference sections in the identified articles. All original articles that evaluated an association between thimerosal-containing vaccines and ASD/NDDs or pharmacokinetics of ethylmercury in vaccines were included., Results: Twelve publications that met the selection criteria were identified by the literature search: 10 epidemiologic studies and 2 pharmacokinetic studies of ethylmercury. The design and quality of the studies showed significant variation. The preponderance of epidemiologic evidence does not support an association between thimerosal-containing vaccines and ASD. Epidemiologic studies that support an association are of poor quality and cannot be interpreted. Pharmacokinetic studies suggest that the half-life of ethylmercury is significantly shorter when compared with methylmercury., Conclusions: Studies do not demonstrate a link between thimerosal-containing vaccines and ASD, and the pharmacokinetics of ethylmercury make such an association less likely. Epidemiologic studies that support a link demonstrated significant design flaws that invalidate their conclusions. Evidence does not support a change in the standard of practice with regard to administration of thimerosal-containing vaccines in areas of the world where they are used.

The curious phenomenon of similar levels of methylmercury (MeHg) accumulation in fish from contaminated and pristine environments may be explained by the observation that the proportion of total mercury (HgT) present as MeHg is inversely related to HgT in natural waters. We hypothesize that this "MeHg accumulation paradox" is explained by the quantitative induction of bacterial enzymes that are encoded by the mercury resistance (mer) operon, organomercury lyase (MerB), and mercuric reductase (MerA) by inorganic Hg (Hg[II]). We tested this hypothesis in two ecosystems in New Jersey: Berry's Creek in the Meadowlands (ML) and Pine Barren (PB) lakes. Across all sites, an inverse correlation (r2 = 0.80) between the concentration of HgT (ML, 113-4220 ng L(-1); PB, 0.3-5.4 ng L(-1)) and the proportion of HgT as MeHg (MeHg in ML and PB ranged from 0.08 to 1.6 and from 0.03 to 0.34 ng L(-1), respectively) was observed. The planktonic microbial community in Meadowlands surface waters exhibited adaptation to mercury, the presence of mer genes and mRNA transcripts, and high rates of reductive demethylation (k(deg) = 0.19 day(-1)). In contrast, the microbial community of PB was not adapted to mercury and demonstrated low rates of oxidative demethylation (k(deg) = 0.01 day(-1)). These results strongly support our hypothesis and show that the degradation of MeHg by mer-encoded enzymes by the water column microbiota of contaminated environments can significantly affect the amount of MeHg that is available for entry into the aquatic food web.

Although much is known about the biogeochemical cycling of mercury in the environment, relatively little is known about methylmercury (MeHg) bioaccumulation in fishes and how chronic sub-lethal exposures affect their functioning. Several species of fish in Clear Lake, California have high MeHg tissue levels, including Sacramento blackfish, Orthodon microlepidotus, a large native cyprinid that is fished commercially. We fed juvenile blackfish one of four diets containing MeHg (0.21 mg/kg control; 0.52 mg/kg low; 22.2 mg/kg medium; and 55.5 mg/kg high treatments) for 70 days. There were no statistical differences (P > 0.05) in food consumption among the treatment groups. By 35 days the high treatment group had a significantly depressed growth rate when compared to the control group (P < 0.05) and by 70 days both the medium and the high groups had significantly lower growth rates (P < 0.05). The high-dose group had a significantly (P < 0.05) lower specific growth rate (SGR) compared all other treatment groups at 35 days, although by 70 days these differences were not significant. The wet/dry muscle mass and muscle mass/total mass ratios, condition factor, and resting routine metabolic rates at both 35 and 70 days were statistically indistinguishable (P > 0.05) between treatment groups. All treatment groups assimilated the dietary MeHg into muscle tissue in a dose-dependent fashion. Percent assimilation was significantly lower (P < 0.05) in the high-dose group compared to the low-dose group at 35 days, (control 53%, low-dose 61%, medium-dose 50%, and high-dose 40%) but at 70 days assimilation was lower (35, 43, 42, and 32%, respectively) and statistically indistinguishable (P > 0.05) among the treatment groups. Dietary MeHg concentrations and bioaccumulation rates were correlated (r2 = 0.98 at 35 days, 0.99 at 70 days). These results may contribute to construction of ecosystem mercury models and more informed natural resources management at Clear Lake.

A short-term low level exposure experiment was conducted on rats in order to determine urinary and faecal excretion, accumulation, and biological responses to methylmercury from fish products. Male Wistar rats were fed fish-meal diets containing methylmercury contaminated fish (1.45 or 2.61 mgHg/kg as methylmercury), uncontaminated fish supplemented with methylmercury chloride (CH3HgCl) at similar levels (1.24 and 2.49 mgHg/kg, respectively) or uncontaminated fish as a control (0.052 mgHg/kg) for 4 weeks (n=6 rats per treatment). After 2 and 4 weeks of exposure, rats were placed in metabolic chambers for 48 h to assess overall faecal and urinary excretion of mercury. The overall faecal excretion in rats fed fish supplemented with CH3HgCl (12%) was significantly lower (P <0.05) than rats fed methylmercury in fish muscle (19%) or rats fed control diet (76%). Urinary excretion did not differ among the experimental groups. Rats fed the highest level of CH3HgCl had a significantly higher (P <0.05) blood, liver, kidney and brain mercury contamination compared to rats fed methylmercury contaminated fish or rats fed control diet. Metallothionein levels in kidney were significantly higher in CH3HgCl-fed rats compared to rats fed contaminated fish. The results indicate a higher faecal excretion and lower tissue accumulation, and metallothionein induction in rats following exposure to methylmercury naturally incorporated in fish compared to methylmercury chloride added to the same matrix.

Average methylmercury levels in five Savannah River tributary streams, sampled 11 times over 2 years (0.170 ng/l), were nearly twice as high as in the Savannah River (0.085 ng/l). Total mercury levels in the tributaries (2.98 ng/l) did not differ significantly from the river (2.59 ng/l). All of the tributaries drained extensive wetlands that would be expected to support comparatively high rates of methylation. Mercury concentrations in Asiatic clams (Corbicula fluminea) collected from the discharge plumes of Savannah River tributaries (average of 0.044 microg/g wet weight) were significantly (P<0.001) higher than in Asiatic clams collected from the Savannah River upstream from the tributary mouths (average of 0.017 microg/g wet weight). These results indicate that streams draining wetlands into coastal plain rivers can create localized areas of elevated methylmercury with resulting increases in the mercury levels of river biota., (Copryright 2003 Elsevier B.V.)

During the late 1980s, the upper trophic-level biota of the Everglades (FL, USA) was recognized as being highly contaminated with mercury (Hg). However, the timing and pattern of that increase is poorly known, and no information is available about mercury contamination in Everglades wildlife prior to 1974. We measured methylmercury concentrations in feathers of white ibises (n = 33), great egrets (n = 7), anhingas (n = 21), and great blue herons (n = 12) from museum specimens collected from 1910 through 1980 and combined them with more recent feather samples collected from live birds (1985-2000, n = 98, 37, 49, and 7, respectively). We found no evidence of contamination of museum samples with inorganic mercuric preservatives (0.01-0.28% of total Hg in feathers). All species showed relatively low concentrations of mercury through the 1970s (<5 microl/L dry wt for anhingas, ibises, and egrets, <10 microl/L for herons). Samples from all species taken during the 1990s showed a large and significant increase (4-5X) in MeHg concentration. This evidence suggests that most of the increase in Hg deposition during the 20th century in south Florida occurred during the last two to three decades, which is consistent with information about local source deposition. Contamination levels prior to the 1970s appear to have been associated with normal reproduction in these birds, suggesting partial evidence for a threshold of reproductive impairment.

We examined maternal transfer efficiency, retention by subsequent generations, and transgenerational toxicity of methylmercury (CH3Hg or MeHg) in a population of freshwater zooplankton (Daphnia magna). The effect of dietary MeHg residence time in the daphnids on the efflux system also was quantified. After ingesting a relatively high dosage of MeHg, D. magna exhibited a reduction of live neonates and an increase of undeveloped eggs (or embryos), which reflected the sublethal toxicity of MeHg. The daily maternal transfer efficiency of MeHg to both reproductive outputs ranged from 0.42 to 4.9% over different ages of the parental daphnids, which was dependent on the daily reproductive output. During the lifetime of D. magna, reproduction contributed to 10.8% +/- 1.74% (n = 3) SD of total MeHg loss from the parental daphnids. The percentage of MeHg retention by the second generation (F1) of D. magna (40-60%) was generally higher than that by the parental generation (F0; approximately 25%) after 20 d of depuration. Methylmercury imposed sublethal toxicity to the F0 and F1 generations, but a smaller effect was observed on the F2 generation. Because of the very low MeHg body burden in the subsequent generations, we hypothesized that factors other than MeHg, such as nutritional deficiency in the offspring contributed to the transgenerational toxicity. Different MeHg residence times did not significantly affect the efflux rate of MeHg but did significantly affect the relative importance of reproduction as the elimination pathway for MeHg. Based on the MeHg body burden of neonates, we estimated that MeHg took 2.5 to 3.0 d to be optimally transferred from assimilation (e.g., gut) to the site of egg development (e.g., brood chamber) in D. magna. Our study demonstrated that maternal transfer of MeHg in freshwater zooplankton is an important predictor of MeHg concentration in their offspring and is a time-dependent and highly dynamic process.

We examined the influences of different concentrations and species of Se (selenite, selenate, and seleno-l-methionine) in the ambient environment on the accumulation of inorganic Hg(II) and methylmercury (MeHg) by the diatom Thalassiosira pseudonana and the green mussel Perna viridis. At the experimental concentrations tested (< 500 microgl(-1)), selenite and selenate did not significantly affect the uptake of either mercury species by the diatoms and the green mussels. The assimilation efficiency of Hg(II) and MeHg by the mussels from ingested diatoms was also independent of the inorganic Se loadings in the food particles. In contrast, selenomethionine significantly inhibited the uptake of MeHg and enhanced the uptake of Hg(II) by the diatoms and the mussels, but it did not affect the assimilation from the ingested diatoms. The influence of tissue body burden of Se in the green mussels following pre-exposure to selenite and selenomethionine for different periods (1-5 weeks) on the accumulation of Hg(II) and MeHg was further investigated. Our results showed that tissue Se concentrations did not significantly affect the dietary assimilation of mercury, but the influences on the aqueous uptake were variable. Our study thus, strongly highlights the specificity of the Se-Hg interaction in marine mussels for different Se and Hg species. Both dissolved and dietary uptake appeared to be equally important in the accumulation of Hg(II) and MeHg in the green mussels., (Copyright 2004 Elsevier B.V.)

Mercury (Hg) is an important environmental pollutant due to its highly toxic nature and widespread occurrence in aquatic systems. The biokinetics of Hg in zooplankton have been largely ignored in previous studies. This study examines the assimilation, dissolved uptake, and efflux of inorganic mercury [Hg(II)] and methylmercury (MeHg) in a freshwater cladoceran, Daphnia magna, and models the exposure pathways of Hg(II) and MeHg in the daphnids. The assimilation efficiencies (AEs) of both Hg species decreased significantly with increasing algal carbon concentrations. The dissolved uptake of Hg(II) and MeHg was proportional to the ambient concentration (ranging from environmentally realistic to high concentration over a 3-4 orders of magnitude variation), whereas MeHg had a slightly higher uptake rate constant (0.46 L g(-1) h(-1)) than Hg(II) (0.35 L g(-1) h(-1)). Surprisingly, the efflux rate constants of Hg(ll) and MeHg were rather comparable (0.041 -0.063 day(-1)). The release of both Hg(II) and MeHg via different routes (excretion, egestion, molting, and neonate production) was further examined at different food concentrations. It was found that regeneration into the dissolved phase was important for D. magna to eliminate both Hg species, but maternal transfer of Hg(II) (11-15%) and MeHg (32-41%) to neonates represented another important pathway for the elimination of Hg(II) and MeHg from the mothers. Modeling results suggest that food is an important source for MeHg exposure (47-98%), but water exposure represents 31-96% of Hg(II) accumulation in D. magna, depending on the variation of Hg bioconcentration factor in ingested food. Furthermore, MeHg predominates the bioaccumulation of Hg in D. magna even though MeHg constitutes only a small percentage of the total Hg in the water. The results strongly indicate that maternal transfer of Hg(II) and MeHg in freshwater zooplankton should be considered in manytoxicity testings and risk assessment in aquatic food chains.