Blood MeHg Research Articles

Exposure to methylmercury in non-fish-eating people in Sweden

The extensive use of fish meal as a source of protein for poultry and swine may lead to additional exposure to methylmercury (MeHg). We determined the concentration of MeHg and inorganic mercury (I-Hg) in blood and total mercury (T-Hg) in hair in 27 persons (9 men and 18 women, 20–58 years of age) who stated that they had consumed no fish for a period of 2 years or more. The participants answered a food frequency questionnaire and reported their number of dental amalgam fillings. The MeHg concentrations in blood (median, 0.10 μg/L; range, 0.0–1.0 μg/L) were very low and did not constitute a concern for health effects. We also analyzed selenium (Se) in serum. The median concentration was 76 μg/L (range, 53–103 μg/L), which is in agreement with previous studies of the Swedish general population, indicating that the Se status of non-fish-eating individuals is not substantially lower than that of people who include fish in their diet. We found a significant association ( P=0.002) between the number of dental amalgam fillings and the I-Hg concentration in blood (median, 0.09 μg/L; range, 0.03–0.57 μg/L). The T-Hg in hair (median, 0.06 mg/kg; range, 0.04–0.32 mg/kg) was significantly associated ( R 2=0.89; P<0.001) with the MeHg in blood, but not with the I-Hg in blood. Therefore, the T-Hg in hair seems to reflect MeHg exposure and not I-Hg exposure even in persons with no intake of fish.

Methyl mercury and inorganic mercury in Swedish pregnant women and in cord blood: influence of fish consumption.

We studied exposure to methyl mercury (MeHg) in Swedish pregnant women (total mercury [T-Hg] in hair) and their fetuses (MeHg in cord blood) in relation to fish intake. The women were recruited at antenatal care clinics in late pregnancy to participate in an exposure study of environmental pollutants. Fish consumption was evaluated using food frequency questionnaires including detailed questions on fish consumption. In addition, we determined inorganic mercury (I-Hg) and selenium (Se) in cord blood. On average, the women consumed fish (all types) 6.7 times/month (range 0-25 times/month) during the year they became pregnant. They reported less consumption of freshwater fish--species that might contain high concentrations of MeHg--during than before pregnancy. T-Hg in maternal hair (median 0.35 mg/kg; range 0.07-1.5 mg/kg) was significantly associated (R2 = 0.53; p < 0.001) with MeHg in cord blood (median 1.3 microg/L; range 0.10-5.7 microg/L). Both hair T-Hg and cord blood MeHg increased with increasing consumption of seafood (r = 0.41; p < 0.001 and r = 0.46; p < 0.001, respectively). Segmental hair analysis revealed that T-Hg closer to the scalp was lower and more closely correlated with MeHg in cord blood than T-Hg levels in segments corresponding to earlier in pregnancy. We found a weak association between Se (median 86 microg/L; range 43-233 microg/L) and MeHg in cord blood (r = 0.26; p = 0.003), but no association with fish consumption. I-Hg in cord blood (median 0.15 microg/L; range 0.03-0.53 microg/L) increased significantly with increasing number of maternal dental amalgam fillings.

Inorganic mercury and methylmercury in placentas of Swedish women.

We determined levels of inorganic mercury (I-Hg) and methylmercury in placentas from 119 Swedish women, not selected with respect to high exposure of mercury. Our objective was to relate placental Hg species with maternal and fetal blood concentrations and to evaluate possible associations with selenium. We performed the analyses using automated alkaline solubilization/reduction and cold-vapor atomic fluorescence spectrophotometry. I-Hg levels in placenta increased with an increasing number of maternal dental amalgam fillings (p < 0.001). Despite placental accumulation (median, 1.3 microg/kg; range, 0.18-6.7 microg/kg wet weight), a substantial fraction of maternal blood I-Hg, probably as Hg(0), reached the fetus. Although MeHg transferred easily to the fetus, it also accumulated in the placenta. On average, 60% of placental Hg was in the form of MeHg. The median concentration was 1.8 microg/kg (range, 0-6.2 microg/kg wet weight), more than twice the maternal blood concentration. We found significant associations between MeHg and selenium in both maternal and umbilical cord blood but not in the placenta. The associations were particularly obvious in freshwater fish consumers, probably reflecting that fish is a source of both MeHg and selenium. We found no correlations between I-Hg and selenium. This study increases the understanding of Hg, in its different forms, in human placenta and how they are related to maternal and fetal exposure.

In Vitro Study of Methylmercury in Blood of Bottlenose Dolphins (Tursiops truncatus)

The biochemical behavior of methylmercury (MeHg) in dolphin blood was investigated in vitro. MeHg distribution between plasma and erythrocytes and its release from erythrocytes into plasma or medium without SH group was determined. At the subcellular level its distribution among different thiol-containing molecules was also investigated in erythrocytes and plasma. When blood was treated with 0.1 mM MeHg, about 98.1% was found in red cells and 1.9% in plasma; only 0.6% of MeHg present in the cellular compartment was bound to membranes. Hemoglobin (Hb) and albumin, principal proteins containing SH groups (PSH), and glutathione (GSH) appeared to be the main targets of MeHg in dolphin blood. Gel filtration of stroma-free hemolysate of treated red blood cells (RBCs) revealed that MeHg was almost equally present in high (52.5%) and low (47.5%) molecular weight fractions, whereas in plasma it only eluted with proteins (high molecular weight fractions). Hemoglobin was identified as the main intracellular protein binding MeHg. The exchange reaction of MeHg between GSH and dolphin hemoglobin was also evaluated and the equilibrium constants calculated.

Effects of uncertainties on exposure estimates to methylmercury: a Monte Carlo analysis of exposure biomarkers versus dietary recall estimation.

This article presents a general model for estimating population heterogeneity and "lack of knowledge" uncertainty in methylmercury (MeHg) exposure assessments using two-dimensional Monte Carlo analysis. Using data from fish-consuming populations in Bangladesh, Brazil, Sweden, and the United Kingdom, predictive model estimates of dietary MeHg exposures were compared against those derived from biomarkers (i.e., [Hg]hair and [Hg]blood). By disaggregating parameter uncertainty into components (i.e., population heterogeneity, measurement error, recall error, and sampling error) estimates were obtained of the contribution of each component to the overall uncertainty. Steady-state diet:hair and diet:blood MeHg exposure ratios were estimated for each population and were used to develop distributions useful for conducting biomarker-based probabilistic assessments of MeHg exposure. The 5th and 95th percentile modeled MeHg exposure estimates around mean population exposure from each of the four study populations are presented to demonstrate lack of knowledge uncertainty about a best estimate for a true mean. Results from a U.K. study population showed that a predictive dietary model resulted in a 74% lower lack of knowledge uncertainty around a central mean estimate relative to a hair biomarker model, and also in a 31% lower lack of knowledge uncertainty around central mean estimate relative to a blood biomarker model. Similar results were obtained for the Brazil and Bangladesh populations. Such analyses, used here to evaluate alternative models of dietary MeHg exposure, can be used to refine exposure instruments, improve information used in site management and remediation decision making, and identify sources of uncertainty in risk estimates.

Longitudinal Study of Methylmercury and Inorganic Mercury in Blood and Urine of Pregnant and Lactating Women, as Well as in Umbilical Cord Blood

We have investigated exposure to methylmercury (MeHg) and mercury vapor (Hg0) in pregnant women and their newborns in Stockholm. The women were followed for 15 months post delivery. MeHg, inorganic Hg (I-Hg), and total Hg (T-Hg) in maternal and cord blood were determined by automated alkaline solubilization/reduction and cold vapor atomic fluorescence spectrometry. T-Hg in urine was determined by inductively coupled plasma mass spectrometry. About 72% of the Hg in blood (n=148) in early pregnancy was MeHg (median 0.94 μg/L, maximum 6.8 μg/L). Blood MeHg decreased during pregnancy, partly due to decreased intake of fish in accordance with recommendations to not eat certain predatory fish during pregnancy. Cord blood MeHg (median 1.4 μg/L, maximum 4.8 μg/L) was almost twice that in maternal blood in late pregnancy and was probably influenced by maternal MeHg exposure earlier and before pregnancy. Blood I-Hg (median 0.37 μg/L, maximum 4.2 μg/L) and urine T-Hg (median 1.6 μg/L, maximum 12 μg/L) in early pregnancy were highly correlated, and both were associated with the number of amalgam fillings. The concentrations decreased during lactation, probably due to excretion in milk. Cord blood I-Hg was correlated with that in maternal blood. The results show the importance of speciation of Hg in blood for evaluation of exposure and health risks.

Determination of methyl mercury in whole blood by ethylation-GC-CVAFS after alkaline digestion-solvent extraction.

A method for the determination of methyl mercury in whole blood samples based on ethylation-gas chromatography-cold vapor atomic fluorescence spectrometry after alkaline digestion-solvent extraction is described. The extraction procedure and conditions were optimized, and the matrix interference after extraction was critically investigated. The storage stability of MeHg in blood samples and a series of extracts was determined. The method detection limit was found to be approximately 0.02 ng/g for a 0.5-g blood sample with relative standard deviations of less than 10%. The accuracy and precision were evaluated by summarizing the quality-control (QC) data generated over a one and one half year period. Appropriate procedures for sample collection, transportation, and storage were adapted to the method. Using this method accompanied by explicit QC protocols and procedures, background levels of MeHg and total mercury in blood for 150 8-10-year-old Portuguese children with nonoccupational and nonamalgamal exposure were determined and reported with summarized QC data.

Distribution Kinetics of Dietary Methylmercury in the Arctic Charr (Salvelinus alpinus)

We fed immature 1+ arctic charr with a single dose of methyl[203Hg]mercury (MeHg) and quantified distribution kinetics with a new and simple three-compartment caternary model having well-perfused viscera and blood as the central compartment (VB), whereas gut (G) and the rest of body (R) constituted the peripheral compartments. The model accurately described distribution kinetics of MeHg in the fish, using either data of MeHg content in compartments or blood concentration data. Despite the known fast translocation of MeHg between binding sites at the molecular level, its translocation rate between compartments was surprisingly slow, 27 days being needed to complete 95% of the transfer from gut to blood and 48 days for the subsequent transfer to compartment R. This probably results from a limitation of the stepwise transfer rate of MeHg from red blood cells, which contain most of blood MeHg, to plasma and then to tissues due to low plasmatic concentration of small mobile sulfhydryl ligands. The model presented is a convenient tool that could be used to compare the fate of MeHg and other organometals, such as butyltins and alkylleads, in various aquatic and terrestrial animal species.

Determination of methylmercury in human blood using capillary gas chromatography and selected-ion monitoring

A capillary gas chromatographic method, using selected-ion monitoring in the electron-impact mode, was developed for the analysis of methylmercury (MeHg) in human blood. The samples, spiked with the internal standard propylmercury bromide (PropHgBr), were, after addition of sodium bromide and cupric sulfate, extracted with toluene. The organic phase was extracted with an ethanol—water solution of sodium thiosulfate. After addition of sodium bromide solution, the ethanol—water phase was extracted with toluene. Methylated derivatives (MeHgCH 2Br and PropHgCH 2Br) were formed by the addition of a diethyl ether solution of diazomethane. The chromatographic properties of the derivatives were much better than those of the non-methylated compounds. The m/z 215 fragment of MeHgCH 2Br and the molecular ion m/z 338 of PropHgCH 2Br were monitored. The calibration graphs, with a linear correlation coefficient of 0.992 ( n = 12) in the 1–5 μg/l concentration range, passed through the origin. The detection limit for MeHg in human blood was ca. 0.5 μg/l. Analysis of spiked blood samples at concentrations of about 2 and 10 μg/l gave a relative standard deviation of 4.2 and 5.5%, respectively ( n = 10).

Prenatal Exposure to Methyl Mercury among Greenlandic Polar Inuits

During the period 1982 to 1988, 37 paired samples of blood from Inuit women and their newborn children were collected in North Greenland. The samples were analyzed for whole blood content of total mercury (tot-Hg) and for content of methyl mercury (Me-Hg). In maternal blood, 80% of the tot-Hg was found to be methylated in contrast to 98% in cord blood. Concentrations of Me-Hg in maternal and cord blood were significantly correlated, and the mean ratio between fetal and maternal blood Me-Hg was 1.9. Concentrations of Me-Hg in cord blood were closely related to the marine food intake of the mothers. Eighty-four percent of the mothers had blood concentrations of Me-Hg above 0.11 mumol/l (23 micrograms/l), which corresponds to the provisional limit of tolerable intake set by the World Health Organization. This indicates that the majority of the pregnant woman have an unacceptable high intake of methyl mercury.

Neurobehavioral assessment of Mohawk Indians for subclinical indications of methyl mercury neurotoxicity.

A total of 200 male and 200 adult female Mohawk Indians were examined by means of performance tests as part of a total health evaluation of participants in a medical field survey on the St. Regis Reserve. Age-corrected performance test scores were studied in relation to blood, urinary, and hair methyl mercury (MeHg) levels, and local fish consumption. Males were found to eat more fish than females and had relatively higher MeHg levels than females. Blood and hair MeHg levels were significantly correlated with local fish consumption for both sexes. Biological indicators of MeHg absorption suggested low exposure levels but did not correlate significantly with performance test scores. These findings indicate that the time of examination, St. Regis residents were exposed to almost "background" levels of MeHg and did not exhibit either subclinical or clinical manifestations of MeHg neurotoxicity.

Effect of red-cell-bound mercury on measurements of tissue mercury distribution

Blood is the transport vehicle of methylmereury (MeHg) in the body (GIBLIN and MASSARO, 1974; NORDBERG and SKERFVING, 1972; PASSOW, 1970; WHITE and ROTHSTE!N, 1973), with almost complete binding to the hemoglobin molecule (GARCIA et al., 1974; ROTHSTEIN, 1973). Although some variation in the percentage of mercury contained in red cells has been reported among species, most data indicate that red cells contain over 90% of the total blood MeHg (LUNDGREN et al., 1967; NORDBERG and SKERFVING, 1972; SUZUKI et al., 1971; SWENNSON et al., 1959). Because of the high affinity of the red cell for MeHg, gross errors in tissue content of MeHg could result unless corrections are made for the MeHg in red cells retained in the tissues. This may be particularly true if tissues are examined within a few hours or days after dosing (before equilibration between red cells and tissues occurs). Results from most studies using isotope techniques to show distribution and tissue content of MeHg do not reflect residual red cell MeHg (ANSARI et al., 1973; IVERSON et al., 1973; REYNOLDS and PITKIN, 1975; ULFVARSON, 1969). Few studies (MOFFITT and CLARY, 1974; SOMJEN et al., 1973) have been performed in which such corrections were made for MeHg bound to the hemoglobin of red cells. The purpose of this experiment was to determine whether the relative contribution of red cell MeHg to total tissue MeHg is sufficiently great to-affect the measurement of total tissue MeHg.