Mercury is a metal that has long been used because of its many advantages from the physical and chemical points of view. However, mercury is very toxic to many life forms, including humans, and mercury poisoning has repeatedly been reported. The main chemical forms of mercury are elemental mercury (Hg0), divalent mercury (Hg2+) and methylmercury (CH3−Hg+), the toxicities and metabolisms of which differ from each other. Methylmercury is converted from divalent mercury and is a well-known neurotoxicant, having been identified as the cause of Minamata disease. It bioaccumulates in the environment and is biomagnified in the food web. Human exposure to methylmercury is mainly through fish and seafood consumption. Methylmercury easily penetrates the blood-brain barrier and causes damage to the central nervous system, particularly in fetuses. In this paper, we summarize the global mercury cycle and mercury metabolism, toxicity and exposure evaluation, and the thresholds for the onset of symptoms after exposure to different chemical forms of mercury, particularly methylmercury.
mercury; methylmercury; global cycle; metabolism; toxicity
Mercury is a pervasive environmental pollutant whose toxic effects have not been studied in sea turtles in spite of their threatened status and evidence of immunosuppression in diseased populations.
In the present study we investigate mercury toxicity in loggerhead sea turtles (Caretta caretta) by examining trends between blood mercury concentrations and various health parameters.
Blood was collected from free-ranging turtles, and correlations between blood mercury concentrations and plasma chemistries, complete blood counts, lysozyme, and lymphocyte proliferation were examined. Lymphocytes were also harvested from free-ranging turtles and exposed in vitro to methylmercury to assess proliferative responses.
Blood mercury concentrations were positively correlated with hematocrit and creatine phosphokinase activity, and negatively correlated with lymphocyte cell counts and aspartate amino-transferase. Ex vivo negative correlations between blood mercury concentrations and B-cell proliferation were observed in 2001 and 2003 under optimal assay conditions. In vitro exposure of peripheral blood leukocytes to methylmercury resulted in suppression of proliferative responses for B cells (0.1 μg/g and 0.35 μg/g) and T cells (0.7 μg/g).
The positive correlation between blood mercury concentration and hematocrit reflects the higher affinity of mercury species for erythrocytes than plasma, and demonstrates the importance of measuring hematocrit when analyzing whole blood for mercury. In vitro immunosuppression occurred at methylmercury concentrations that correspond to approximately 5% of the individuals captured in the wild. This observation and the negative correlation found ex vivo between mercury and lymphocyte numbers and mercury and B-cell proliferative responses suggests that subtle negative impacts of mercury on sea turtle immune function are possible at concentrations observed in the wild.
aspartate aminotransferase (AST); blood; creatine phosphokinase (CPK); hematocrit; immunotoxicity; lymphocytes; loggerhead sea turtles; mercury; methylmercury; toxicity
Methylmercury is a hazardous substance that is of interest with regard to environmental health, as inorganic mercury circulating in the general environment is dissolved into freshwater and seawater, condensed through the food chain, ingested by humans, and consequently affects human health. Recently, there has been much interest and discussion regarding the toxicity of methylmercury, the correlation with fish and shellfish intake, and methods of long-term management of the human health effects of methylmercury. What effects chronic exposure to a low concentration of methylmercury has on human health remains controversial. Although the possibility of methylmercury poisoning the heart and blood vessel system, the reproductive system, and the immune system is continuously raised and discussed, and the carcinogenicity of methylmercury is also under discussion, a clear conclusion regarding the human health effects according to exposure level has not yet been drawn. The Joint FAO/WHO Expert Committee on Food Additives proposed to prepare additional fish and shellfish intake recommendations for consumers based on the quantified evaluation of the hazardousness of methylmercury contained in fish and shellfish, methylmercury management in the Korea has not yet caught up with this international trend. Currently, the methylmercury exposure level of Koreans is known to be very high. The starting point of methylmercury exposure management is inorganic mercury in the general environment, but food intake through methylation is the main exposure source. Along with efforts to reduce mercury in the general environment, food intake management should be undertaken to reduce the human exposure to methylmercury in Korea.
Methylmercury; Health effect; Toxicity; Human exposure; Epidemiology
Remote coastal populations that rely on seafood for subsistence often receive unusually high doses of organochlorines and methyl mercury. Immunosuppression resulting from prenatal exposure to organochlorines has been reported in wildlife species and humans. In this study, we assessed lymphocyte activation and associated cytokine secretion in 47 newborns from a remote maritime population living on the Mid and Lower North Shore regions of the St. Lawrence River (Québec, Canada; subsistence fishing group) and 65 newborns from nearby urban settings (reference group). Cord blood samples were collected for organochlorine and mercury analyses and also to isolate cord blood mononuclear cells (CBMCs) for the in vitro assessment of cytokine production and expression of surface markers after mitogenic stimulation (CD4(+)CD45RO(+), CD8(+)CD45RO(+), CD3(+)CD25(+), and CD8(+)HLA-DR(+)). Blood mercury and plasma concentrations of polychlorinated biphenyls (PCBs), 1,1-dichloro-2,2-bis(4-chlorophenyl)ethylene (p,p'-DDE), and hexachlorobenzene (HCB) were significantly higher in the subsistence fishing group than in the reference group (p < 0.001). No difference was observed between the two groups regarding subsets of lymphocytes showing markers of activation. In vitro secretion of cytokines by CBMCs after mitogenic stimulation was lower in the subsistence fishing group than in the reference group (p < 0.05). Moreover, we found an inverse correlation between tumor necrosis factor-alpha (TNF-alpha) secretion and plasma PCB, p,p'-DDE, and HCB concentrations (p < 0.05). Our data support a negative association between TNF-alpha secretion by CBMCs and prenatal organochlorine exposure. If the relationship between organochlorine and TNF-alpha secretion is causal, it would suggest a role for this important proinflammatory cytokine in mediating organochlorine-induced immunotoxicity in infants developmentally exposed to these compounds.
Acute or chronic mercury exposure can cause adverse effects during any period of development. Mercury is a highly toxic element; there is no known safe level of exposure. Ideally, neither children nor adults should have any mercury in their bodies because it provides no physiological benefit. Prenatal and postnatal mercury exposures occur frequently in many different ways. Pediatricians, nurses, and other health care providers should understand the scope of mercury exposures and health problems among children and be prepared to handle mercury exposures in medical practice. Prevention is the key to reducing mercury poisoning. Mercury exists in different chemical forms: elemental (or metallic), inorganic, and organic (methylmercury and ethyl mercury). Mercury exposure can cause acute and chronic intoxication at low levels of exposure. Mercury is neuro-, nephro-, and immunotoxic. The development of the child in utero and early in life is at particular risk. Mercury is ubiquitous and persistent. Mercury is a global pollutant, bio-accumulating, mainly through the aquatic food chain, resulting in a serious health hazard for children. This article provides an extensive review of mercury exposure and children’s health.
The potential danger of natural mercury accumulation in the diet of the Eskimo is evaluated through mercury levels determined in cord blood, placenta, maternal blood, hair, and milk of 38 maternal-infant pairs from Anchorage and the Yukon-Kuskokwim Delta. Although mercury levels are not discernably dangerous, trends to larger accumulations in maternal and fetal RBC and placental tissue with proximity to the sea and consumption of seals during pregnancy provide the basis for considering possible indicators of neonatal involvement. Mercury level in RBC from cord blood appeared as the best potential indicator of this involvement, although relationships with the mother's diet and level of mercury in the placenta also appear useful. In this area, average and maximal mercury levels in cord blood are 39 and 78 ng/ml, respectively, far below the acknowledged toxic level in infants of these mothers who eat seals or fish every day during their pregnancy.
Background: Methylmercury (MeHg) exposure has been linked to an increased risk of coronary heart disease (CHD). Paraoxonase 1 (PON1), an enzyme located in the high-density–lipoprotein (HDL) fraction of blood lipids, may protect against CHD by metabolizing toxic oxidized lipids associated with low-density liproprotein and HDL. MeHg has been shown to inhibit PON1 activity in vitro, but this effect has not been studied in human populations.
Objectives: This study was conducted to determine whether blood mercury levels are linked to decreased plasma PON1 activities in Inuit people who are highly exposed to MeHg through their seafood-based diet.
Methods: We measured plasma PON1 activity using a fluorogenic substrate and blood concentrations of mercury and selenium by inductively coupled plasma mass spectrometry in 896 Inuit adults. Sociodemographic, anthropometric, clinical, dietary, and lifestyle variables as well as PON1 gene variants (rs705379, rs662, rs854560) were considered as possible confounders or modifiers of the mercury–PON1 relation in multivariate analyses.
Results: In a multiple regression model adjusted for age, HDL cholesterol levels, omega-3 fatty acid content of erythrocyte membranes, and PON1 variants, blood mercury concentrations were inversely associated with PON1 activities [β-coefficient = –0.063; 95% confidence interval (CI), –0.091 to –0.035; p < 0.001], whereas blood selenium concentrations were positively associated with PON1 activities (β-coefficient = 0.067; 95% CI, 0.045–0.088; p < 0.001). We found no interaction between blood mercury levels and PON1 genotypes.
Conclusions: Our results suggest that MeHg exposure exerts an inhibitory effect on PON1 activity, which seems to be offset by selenium intake.
Inuit; methylmercury; Nunavik; omega-3 polyunsaturated fatty acids; paraoxonase; PON1; selenium
In the US, exposure to methylmercury, a neurotoxin, occurs primarily through consumption of fish. Data from recent studies assessing the health impact of methylmercury exposure due to consumption of fish and other sources in the aquatic food web (shellfish, crustacea, and marine mammals) suggest adverse effects at levels previously considered safe. There is substantial variation in human methylmercury exposure based on differences in the frequency and amount of fish consumed and in the fish's mercury concentration. Although virtually all fish and other seafood contain at least trace amounts of methylmercury, large predatory fish species have the highest concentrations. Concerns have been expressed about mercury exposure levels in the US, particularly among sensitive populations, and discussions are underway about the standards used by various federal agencies to protect the public. In the 1997 Mercury Study Report to Congress, the US Environmental Protection Agency summarized the current state of knowledge on methylmercury's effects on the health of humans and wildlife; sources of mercury; and how mercury is distributed in the environment. This article summarizes some of the major findings in the Report to Congress and identifies issues of concern to the public health community.
Recent mass mortalities among several marine mammal populations have led to speculation about increased susceptibility to viral infections as a result of contaminant-induced immunosuppression. In a 2.5-year study, we fed herring from either the relatively uncontaminated Atlantic Ocean or the contaminated Baltic Sea to two groups of captive harbor seals and monitored immune function in the seals. Seals fed the contaminated fish were less able to mount a specific immunological response to ovalbumin, as measured by in vivo delayed-type hypersensitivity (DTH) reactions and antibody responses. The skin reaction to this protein antigen was characterized by the appearance of mononuclear cells which peaked at 24 hr after intradermal administration, characteristic of DTH reactions in other animals studied. These DTH responses correlated well with in vitro tests of T-lymphocyte function, implicating this cell type in the reaction. Aryl-hydrocarbon (Ah) receptor-dependent toxic equivalent (TEQ) profiles in blubber biopsies taken from the seals implicated polychlorinated biphenyls rather than dioxins or furans in the observed immunosuppression. Marine mammal populations currently inhabiting polluted coastal environments in Europe and North America may therefore have an increased susceptibility to infections, and pollution may have played a role in recent virus-induced mass mortalities.
Methylmercury is among the most potentially toxic species to which human populations are exposed, both at high levels through poisonings and at lower levels through consumption of fish and other seafood. However, the molecular mechanisms of methylmercury toxicity in humans remain poorly understood. We used synchrotron X-ray absorption spectroscopy (XAS) to study mercury chemical forms in human brain tissue. Individuals poisoned with high levels of methylmercury species showed elevated cortical selenium with significant proportions of nanoparticulate mercuric selenide plus some inorganic mercury and methylmercury bound to organic sulfur. Individuals with a lifetime of high fish consumption showed much lower levels of mercuric selenide and methylmercury cysteineate. Mercury exposure did not perturb organic selenium levels. These results elucidate a key detoxification pathway in the central nervous system and provide new insights into the appropriate methods for biological monitoring.
Methylmercury; methylmercury toxicology; human brain; neurotoxicology; X-ray absorption spectroscopy; X-ray fluorescence imaging
In recent years, population declines related to viral outbreaks in marine mammals have been associated with polluted coastal waters and high tissue concentrations of certain persistent, lipophilic contaminants. Such observations suggest a contributing role of contaminant-induced suppression of cell-mediated immunity leading to decreased host resistance. Here, we assessed the effects of the prototypic polycyclic aromatic hydrocarbon (PAH), benzo[a]pyrene (B[a]P), and two polychlorinated biphenyls (PCBs), CB-156 and CB-80, on the T-cell proliferative response to mitogen in harbor seal peripheral lymphocytes. Despite the variability associated with our samples from free-ranging harbor seals, we observed a clear suppressive effect of B[a]P (10 uM) exposure on T cell mitogenesis. Exposures to 10 uM CB-156 and CB-80, and 1.0 and 0.1 uM B[a]P, did not produce significant depression in lymphoproliferation. Exposure to the model PAH at 10 uM resulted in a 61% (range 34-97%) average reduction in lymphoproliferation. We were able to rule out a direct cytotoxic effect of B[a]P, indicating that observed effects were due to altered T cell function. Based on our in vitro results, we hypothesize that extensive accumulation of PAH by top-trophic-level marine mammals could alter T cell activation in vivo and impaired cell-mediated immunity against viral pathogens.
The nervous system is the principal target for a number of metals. Inorganic compounds of aluminum, arsenic, lead, lithium, manganese, mercury, and thallium are well known for their neurological and behavioral effects in humans. The alkyl derivatives of certain metals--lead, mercury and tin--are specially neurotoxic. Concern over human exposure and in some cases, outbreaks of poisoning, have stimulated research into the toxic action of these metals. A number of interesting hypotheses have been proposed for the mechanism of lead toxicity on the nervous system. Lead is known to be a potent inhibitor of heme synthesis. A reduction in heme-containing enzymes could compromise energy metabolism. Lead may affect brain function by interference with neurotransmitters such as gamma-amino-isobutyric acid. There is mounting evidence that lead interferes with membrane transport and binding of calcium ions. Methylmercury produces focal damage to specific areas in the adult brain. One hypothesis proposes that certain cells are susceptible because they cannot repair the initial damage to the protein sythesis machinery. The developing nervous system is especially susceptible to damage by methylmercury. It has been discovered that microtubules are destroyed by this form of mercury and this effect may explain the inhibition of cell division and cell migration, processes that occur only in the developmental stages. These and other hypotheses will stimulate considerable experimental challenges in the future.
In the past, methylmercury compounds were manufactured as fungicides or appeared as unwanted byproducts of the chemical industry, but today the methylation of inorganic mercury in aquatic sediments and soils is the predominant if not the sole source of methylmercury. This form of mercury is bioaccumulated to a high degree in aquatic food chains to attain its highest concentrations in edible tissues in long-lived predatory fish living in both fresh and ocean waters. It is well absorbed from the diet and distributes within a few days to all tissues in the body. It crosses without hindrance the blood-brain and placental barriers to reach its principal target tissue, the brain. It is eliminated chiefly in the feces after conversion to inorganic mercury. The biological half-time of methylmercury in human tissues is about 50 days, but there is wide individual variation. Adult poisoning is characterized by focal damage to discrete anatomical areas of the brain such as the visual cortex and granule layer of the cerebellum. A latent period of weeks or months may ensue before the appearance of signs and symptoms of poisoning. The latter manifest themselves as paresthesia, ataxia, constriction of the visual fields, and hearing loss. The prenatal period is the most sensitive stage of the life cycle to methylmercury. Prenatally poisoned infants exhibit a range of effects from severe cerebral palsy to subtle developmental delays. Methylmercury is believed to inhibit those processes in the brain specially involved in development and growth such as neuronal cell division and migration.
Experimental studies suggest that selenium (Se) may decrease methylmercury (MeHg) toxicity under certain exposure regimens. In epidemiological studies, the exposure to MeHg occurs from fish and seafood, which are also a source of beneficial nutrients such as selenium. However, little is known about the potential protective effects of dietary Se against MeHg neurotoxicity in humans. The possible interaction was assessed in two birth cohorts in the Faroe Islands, consisting of singleton term births from 1986 to 1987 (N = 1,022), and 1994 to 1995 (N = 182), respectively. Dietary habits in this fishing population included frequent consumption of seafood, including whale meat high in mercury. Both Hg and Se were measured in cord whole blood. Neurodevelopmental outcomes were evaluated at age 7 years in both cohorts, and the smaller cohort also included neurological assessment on several prior occasions. Each outcome was modeled as a function of Hg and Se interactions (with adjustments for potential risk factors) by expressing the effects of log10(Hg) within the lowest 25%, the middle 50%, and the highest 25% of the Se distribution. Surplus Se was present in cord blood, the average being a 10-fold molar excess above MeHg. Regression analyses failed to show consistent effects of Se, or statistically significant interaction terms between Se and MeHg. Overall, no evidence was found that Se was an important protective factor against MeHg neurotoxicity. Prevention, therefore, needs to address MeHg exposures rather than Se intakes. Because of the benefits associated with fish intake during pregnancy, consumers should be advised to maintain a high fish and seafood intake that is low in Hg contamination. Additional research is needed to determine the identity of the nutrients responsible for the beneficial effects.
Methylmercury; Neuropsychological tests; Prenatal exposure delayed effects; Preschool children; Selenium
The dangers associated with the consumption of large amounts of methylmercury in fish are well recognized, and there is some evidence to suggest that methylmercury may be the cause of subtle neurological impairments when ingested at even low to moderate levels, particularly the prenatal and early childhood periods. This concern has prompted a continuing assessment of the risk of methylmercury toxicity among fish consumers in the United States as well as other countries. The toxicokinetics of methylmercury in humans are reviewed and used to estimate body burdens associated with toxic effects. To determine seafood consumption patterns among the continental U.S. population the Food and Drug Administration (FDA) has analyzed data from a diary study commissioned by the Tuna Research Foundation. Mercury residue levels in domestic fish sampled by the FDA were used to determine the level of exposure to methylmercury. Until evidence is presented that substantially lowers the known body burden of methylmercury which causes toxicity, calculations indicate that the current 1.0 ppm regulatory level provides adequate protection for the average fish consumer, for young children, and for a significant number of consumers exceeding the acceptable daily intake. However, additional studies are being carried out in a continuing process to ensure that safe levels of prenatal exposure to mercury residues in fish are maintained.
Methylmercury is an organic form of mercury that is highly toxic to humans. Here, we present and establish a novel method to detect methylmercury concentrations in the blood of Koreans.
Methylmercury concentration was analyzed with an automated methylmercury analytic system (MERX, Brooks Rand Co., USA) using cold vapor atomic fluorescence spectrophotometry (CVAFS). A variety of biological materials were digested in methanolic potassium hydroxide solution. The analysis method was validated by examination of certified reference material (955c, National Institute of Standard and Technology, USA). We randomly selected 30 Korean adults (age 20 yr or older) to analyze total blood mercury and methylmercury concentrations.
The detection limit and methylmercury recovery rate using this method were 0.1 pg/L and, 99.19% (range: 89.33-104.89%), respectively. The mean blood concentration of methylmercury was 4.54±2.15 µg/L (N=30). The mean proportion of methylmercury to the total mercury concentration was 78.27% (range: 41.37-98.80%).
This study is the first report to analyze blood methylmercury concentration using CVAFS in Korea. We expect that this method will contribute to the evaluation of mercury exposure and the assessment of the toxicological impact of mercury in future studies.
Methylmercury; Blood; Limit of detection
Recent policies attempting to reduce adverse effects of methylmercury exposure from fish consumption in the United States have targeted reductions in anthropogenic emissions from U.S. sources.
To analyze the prospects for future North American and international emissions controls, we assessed the potential contributions of anthropogenic, historical, and natural mercury to exposure trajectories in the U.S. population over a 40-year time horizon.
We used models that simulate global atmospheric chemistry (GEOS-Chem); the fate, transport, and bioaccumulation of mercury in four types of freshwater ecosystems; and mercury cycling among different ocean basins. We considered effects on mercury exposures in the U.S. population based on dietary survey information and consumption data from the sale of commercial market fish.
Although North American emissions controls may reduce mercury exposure by up to 50% for certain highly exposed groups such as indigenous peoples in the Northeast, the potential effects of emissions controls on populations consuming marine fish from the commercial market are less certain because of limited measurements.
Despite uncertainties in the exposure pathway, results indicate that a combination of North American and international emissions controls with adaptation strategies is necessary to manage methylmercury risks across various demographic groups in the United States.
biogeochemical cycling; exposure; mercury; seafood
Sources of elemental mercury (Hg0) include old natural gas regulators, manometers, sphygmomanometers, thermometers, and thermostats. Causes of Hg0 spills include improper storage, container breakage, children playing with Hg0, the breakage of devices containing Hg0, and ritualistic use of Hg0. Inhalation is the primary exposure route for Hg0. Mercury released into the environment can enter lakes and streams, where bacteria convert it into methylmercury, which bioaccumulates in fish. Chronic exposure to Hg0 vapors can damage the kidneys and neurologic system. Short-term exposure to high levels of Hg0 vapors may cause lung damage, nausea, vomiting, diarrhea, increases in blood pressure or heart rate, skin rashes, and eye irritation, among other effects. Minimizing Hg0 dispersal is important after an Hg0 spill. Tracking by shoes or apparel or vacuuming can spread Hg0, increasing airborne concentrations and cleanup costs. The Illinois Department of Public Health’s response to an Hg0 spill depends on the size of the spill. Airborne concentrations after large spills are mapped with a mercury vapor analyzer (MVA). The cleanup begins with the spill site and any hot spots that were identified with the MVA. Hard surfaces can usually be cleaned, but contaminated porous items must be discarded. Leaving marginally contaminated items outdoors for a month or more during warm weather may dissipate the Hg0. After a cleanup, clearance sampling is conducted to determine if further cleanup is needed. The best way to prevent Hg0 spills is reduce its use.
cleanup; elemental mercury; health effects; mercury; prevention; remediation; spill; spill management
As methylmercury is excreted in human milk and infants are particularly susceptible to toxicity due to this compound, the purpose of this study was to evaluate the possible transfer of methylmercury to infants via breast-feeding. In a community with a high intake of seafood, 583 children from a birth cohort were followed. The duration of nursing was recorded, and hair samples were obtained for mercury analysis at approximately 12 months of age. The hair mercury concentrations increased with the length of the nursing period, and those nursed throughout the first year showed the highest geometric mean (9.0 nmol/g or 1.8 microg/g). Human milk therefore seems to be an important source of methylmercury exposure in infants. An increasing time interval from weaning to hair sample collection was not associated with any detectable decrease in mercury concentrations. A slow or absent elimination of methylmercury during the first year after birth could explain this finding. In certain fishing communities, infants nursed for long periods may be at increased risk of developing methylmercury toxicity.
Mercury is a very toxic element that is widely spread in the atmosphere, lithosphere, and surface water. Concentrated mercury poses serious problems to human health, as bioaccumulation of mercury within the brain and kidneys ultimately leads to neurological diseases. To control mercury pollution and reduce mercury damage to human health, sensitive determination of mercury is important. This article summarizes some current sensors for the determination of both abiotic and biotic mercury. A wide array of sensors for monitoring mercury is described, including biosensors and chemical sensors, while piezoelectric and microcantilever sensors are also described. Additionally, newly developed nanomaterials offer great potential for fabricating novel mercury sensors. Some of the functional fluorescent nanosensors for the determination of mercury are covered. Afterwards, the in vivo determination of mercury and the characterization of different forms of mercury are discussed. Finally, the future direction for mercury detection is outlined, suggesting that nanomaterials may provide revolutionary tools in biomedical and environmental monitoring of mercury.
determination of mercury; sensors; nanomaterials; mercury pollution; fluorescence
Monomethylmercury is a neurotoxin that poses significant risks to human health1 due to its bioaccumulation in food webs. Sunlight degradation to inorganic mercury is an important component of the mercury cycle that maintains methylmercury at low concentrations in natural waters. Rates of photodecomposition, however, can vary drastically between surface waters2–5 for reasons that are largely unknown. Here, we show that photodegradation occurs through singlet oxygen, a highly reactive form of dissolved oxygen generated by sunlight irradiation of dissolved natural organic matter. The kinetics of degradation, however, depended on water constituents that bind methylmercury cations. Relatively fast degradation rates (similar to observations in freshwater lakes) applied only to methylmercury species bound to organic sulfur-containing thiol ligands such as glutathione, mercaptoacetate, and humics. In contrast, methylmercury-chloride complexes, which are dominant in marine systems, were unreactive. Binding by thiols lowered the excitation energy of the carbon-mercury bond on the methylmercury molecule6–7 and subsequently increased reactivity towards bond breakage and decomposition. Our results explain methylmercury photodecomposition rates that are relatively rapid in freshwater lakes2–4 and slow in marine waters5.
The main forms of mercury (Hg) exposure in the general population are methylmercury (MeHg) from seafood, inorganic mercury (I-Hg) from food, and mercury vapor (Hg0) from dental amalgam restorations. While the distribution of MeHg in the body is described by a one compartment model, the distribution of I-Hg after exposure to elemental mercury is more complex, and there is no biomarker for I-Hg in the brain. The aim of this study was to elucidate the relationships between on the one hand MeHg and I-Hg in human brain and other tissues, including blood, and on the other Hg exposure via dental amalgam in a fish-eating population. In addition, the use of blood and toenails as biological indicator media for inorganic and organic mercury (MeHg) in the tissues was evaluated.
Samples of blood, brain (occipital lobe cortex), pituitary, thyroid, abdominal muscle and toenails were collected at autopsy of 30 deceased individuals, age from 47 to 91 years of age. Concentrations of total-Hg and I-Hg in blood and brain cortex were determined by cold vapor atomic fluorescence spectrometry and total-Hg in other tissues by sector field inductively coupled plasma-mass spectrometry (ICP-SFMS).
The median concentrations of MeHg (total-Hg minus I-Hg) and I-Hg in blood were 2.2 and 1.0 μg/L, and in occipital lobe cortex 4 and 5 μg/kg, respectively. There was a significant correlation between MeHg in blood and occipital cortex. Also, total-Hg in toenails correlated with MeHg in both blood and occipital lobe. I-Hg in both blood and occipital cortex, as well as total-Hg in pituitary and thyroid were strongly associated with the number of dental amalgam surfaces at the time of death.
In a fish-eating population, intake of MeHg via the diet has a marked impact on the MeHg concentration in the brain, while exposure to dental amalgam restorations increases the I-Hg concentrations in the brain. Discrimination between mercury species is necessary to evaluate the impact on Hg in the brain of various sources of exposure, in particular, dental amalgam exposure.
Mercury is a ubiquitous contaminant in aquatic ecosystems, posing a significant health risk to humans and wildlife that eat fish. Mercury accumulates in aquatic food webs as methylmercury (MeHg), a particularly toxic and persistent organic mercury compound. While mercury in the environment originates largely from anthropogenic activities, MeHg accumulation in freshwater aquatic food webs is not a simple function of local or regional mercury pollution inputs. Studies show that even sites with similar mercury inputs can produce fish with mercury concentrations ranging over an order of magnitude. While much of the foundational work to identify the drivers of variation in mercury accumulation has focused on freshwater lakes, mercury contamination in stream ecosystems is emerging as an important research area. Here, we review recent research on mercury accumulation in stream-dwelling organisms. Taking a hierarchical approach, we identify a suite of characteristics of individual consumers, food webs, streams, watersheds, and regions that are consistently associated with elevated MeHg concentrations in stream fish. We delineate a conceptual, mechanistic basis for explaining the ecological processes that underlie this vulnerability to MeHg. Key factors, including suppressed individual growth of consumers, low rates of primary and secondary production, hydrologic connection to methylation sites (e.g. wetlands), heavily forested catchments, and acidification are frequently associated with increased MeHg concentrations in fish across both streams and lakes. Hence, we propose that these interacting factors define a syndrome of characteristics that drive high MeHg production and bioaccumulation rates across these freshwater aquatic ecosystems. Finally, based on an understanding of the ecological drivers of MeHg accumulation, we identify situations when anthropogenic effects and management practices could significantly exacerbate or ameliorate MeHg accumulation in stream fish.
biomagnification; methylmercury; stream fish; trace elements; trophic transfer
The underlying mechanism for the biological activity of inorganic mercury is believed to be the high affinity binding of divalent mercuric cations to thiols of sulfhydryl groups of proteins. A comprehensive analysis of published data indicates that inorganic mercury is one of the most environmentally abundant toxic metals, is a potent and selective nephrotoxicant that preferentially accumulates in the kidneys, and is known to produce cellular injury in the kidneys. Binding sites are present in the proximal tubules, and it is in the epithelial cells of these tubules that toxicants such as inorganic mercury are reabsorbed. This can affect the enzymatic activity and the structure of various proteins. Mercury may alter protein and membrane structure and function in the epithelial cells and this alteration may result in long term residual effects. This research was therefore designed to evaluate the dose-response relationship in human renal proximal tubule (HK-2) cells following exposure to inorganic mercury. Cytotoxicity was evaluated using the MTT assay for cell viability. The Annexin-V assay was performed by flow cytometry to determine the extent of phosphatidylserine externalization. Cells were exposed to mercury for 24 hours at doses of 0, 1, 2, 3, 4, 5, and 6 μg/mL. Cytotoxicity experiments yielded a LD50 value of 4.65 ± 0.6 μg/mL indicating that mercury is highly toxic. The percentages of cells undergoing early apoptosis were 0.70 ± 0.03%, 10.0 ± 0.02%, 11.70 ± 0.03%, 15.20 ± 0.02%, 16.70 ± 0.03%, 24.20 ±0.02%, and 25.60 ± 0.04% at treatments of 0, 1, 2, 3, 4, 5, and 6 μg/mL of mercury respectively. This indicates a dose-response relationship with regard to mercury-induced cytotoxicity and the externalization of phosphatidylserine in HK-2 cells.
Mercury; cytotoxicity; MTT; HK-2 cells; apoptosis; flow cytometry; Annexin V
Methylmercury exposure causes a variety of adverse effects on human health. Per capita estimates of mercury exposure are critical for risk assessments and for developing effective risk management strategies.
This study investigated the impact of natural stochasticity in mercury concentrations among fish and shellfish harvested from the Atlantic Ocean, Pacific Ocean, and foreign shores on estimated mercury exposures.
Mercury concentrations and seafood consumption are grouped by supply region (Atlantic Ocean, Pacific Ocean, and foreign shores). Distributions of intakes from this study are compared with values obtained using national FDA (Food and Drug Administration) mercury survey data to assess the significance of geographic variability in mercury concentrations on exposure estimates.
Per capita mercury intake rates calculated using FDA mercury data differ significantly from those based on mercury concentration data for each supply area and intakes calculated for the 90th percentile of mercury concentrations.
Differences in reported mercury concentrations can significantly affect per capita mercury intake estimates, pointing to the importance of spatially refined mercury concentration data. This analysis shows that national exposure estimates are most influenced by reported concentrations in imported tuna, swordfish, and shrimp; Pacific pollock; and Atlantic crabs. Collecting additional mercury concentration data for these seafood categories would improve the accuracy of national exposure estimates.
Atlantic; fish imports; methylmercury; ocean; Pacific; per capita mercury intake; tuna