High-precision isotopic analysis sheds new light on mercury metabolism in long-finned pilot whales (Globicephala melas).

Whales accumulate mercury (Hg), but do not seem to show immediate evidence of toxic effects. Analysis of different tissues (liver, kidney, muscle) and biofluids (blood, milk) from a pod of stranded long-finned pilot whales (Globicephala melas) showed accumulation of Hg as a function of age, with a significant decrease in the MeHg fraction. Isotopic analysis revealed remarkable differences between juvenile and adult whales. During the first period of life, Hg in the liver became isotopically lighter (δ202Hg decreased) with a strongly decreasing methylmercury (MeHg) fraction. We suggest this is due to preferential demethylation of MeHg with the lighter Hg isotopes and transport of MeHg to less sensitive organs, such as the muscles. Also changes in diet, with high MeHg intake in utero and during lactation, followed by increasing consumption of solid food contribute to this behavior. Interestingly, this trend in δ202Hg is reversed for livers of adult whales (increasing δ202Hg value), accompanied by a progressive decrease of δ202Hg in muscle at older ages. These total Hg (THg) isotopic trends suggest changes in the Hg metabolism of the long-finned pilot whales, development of (a) detoxification mechanism(s) (e.g., though the formation of HgSe particles), and Hg redistribution across the different organs.

Associations between prenatal mercury exposure and early child development in the ALSPAC study.

INTRODUCTION: There is evidence that high levels of mercury exposure to the pregnant woman can result in damage to the brain of the developing fetus. However there is uncertainty as to whether lower levels of the metal have adverse effects on the development of the infant and whether components of fish consumption and/or the selenium status of the woman is protective. METHODS: In this study we analysed data from the Avon Longitudinal Study of Parents and Children (ALSPAC) (n=2875-3264) to determine whether levels of total blood mercury of pregnant women collected in the first half of pregnancy are associated with the development of the offspring at ages 6, 18, 30 and 42 months. The developmental measures used maternal self-reported scales for individual types of development (fine and gross motor, social and communication skills) and total scores. Multiple and logistic regression analyses treated the outcomes both as continuous and as suboptimal (the lowest 15th centile). The statistical analyses first examined the association of prenatal mercury exposure with these developmental endpoints and then adjusted each for a number of social and maternal lifestyle factors; finally this model was adjusted for the blood selenium level. RESULTS: Total maternal prenatal blood mercury and selenium ranged from 0.17 to 12.76 and 17.0 to 324µg/L respectively. We found no evidence to suggest that prenatal levels of maternal blood mercury were associated with adverse development of the child, even when the mother had consumed no fish during pregnancy. In general, the higher the mercury level the more advanced the development of the child within the range of exposure studied. For example, the fully adjusted effect sizes for total development at 6 and 42 months were +0.51 [95%CI +0.05, +1.00] and +0.43 [95%CI +0.08, +0.78] points per SD of mercury. For the risk of suboptimal development the ORs at these ages were 0.90 [95%CI 0.80, 1.02] and 0.88 [95%CI 0.77, 1.02]. In regard to the associations between blood mercury and child development there were no differences between the mothers who ate fish and those who did not, thus implying that the benefits were not solely due to the beneficial nutrients in fish. CONCLUSIONS: We found no evidence of adverse associations between maternal prenatal blood mercury and child development between 6 and 42 months of age. The significant associations that were present were all in the beneficial direction.

Association between body levels of trace metals and glaucoma prevalence.

IMPORTANCE: Abnormal body levels of essential elements and exposure to toxic trace metals have been postulated to contribute to the pathogenesis of diseases affecting many organ systems, including the eye. OBJECTIVE: To investigate associations between body levels of trace metals and the prevalence of glaucoma in a cross-sectional population-based study. DESIGN, SETTING, AND PARTICIPANTS: Blood or urine metallic element levels and information pertaining to ocular disease were available for 2680 individuals 19 years and older participating in the fourth Korea National Health and Nutrition Examination Survey between January 1, 2008, and December 31, 2009, the second and the third years of the survey (2007-2009). Glaucoma diagnosis was based on criteria established by the International Society of Geographic and Epidemiologic Ophthalmology. Demographic, comorbidity, and health-related behavior information was obtained via interview. Multivariable logistic regression analyses were performed to determine associations between blood and urine trace element levels and the odds of glaucoma diagnosis. All analyses were performed between September 2014 and December 2014. MAIN OUTCOME AND MEASURE: The presence or absence of glaucoma. RESULTS: After adjustment for potential confounders, blood manganese level was negatively associated with the odds of glaucoma diagnosis (odds ratio [OR], 0.44; 95% CI, 0.21-0.92). Blood mercury level was positively associated with glaucoma prevalence (OR, 1.01; 95% CI, 1.00-1.03). No definitive association was identified between blood cadmium or lead levels or urine arsenic level and a diagnosis of glaucoma. CONCLUSIONS AND RELEVANCE: These findings in a cross-sectional study of the South Korean population suggest that a lower blood manganese level and a higher blood mercury level are associated with greater odds of glaucoma. For more confidence that trace metals may have a role in the pathogenesis of glaucoma, prospective studies would need to confirm that the presence of such trace metals increases the chance of developing glaucoma.

Procedimiento de validación de un método para cuantificar mercurio en sangre por espectroscopía de absorción atómica con descomposición térmica y amalgamación / Validation procedure of a method for measuring mercury in blood by thermal decomposition, amalgamation and atomic absorption spectrometry

El mercurio es un tóxico ambiental que produce numerosos efectos adversos en la salud humana y en los ecosistemas naturales. La ingesta excesiva de metilmercurio procedente del pescado contaminado produce toxicidad neurológica, reproductiva y cardiovascular. El objetivo de este estudio es validar un método para la medida de mercurio en sangre mediante espectroscopía de absorción atómica con descomposición térmica y amalgamación. Los límites de detección y cuantificación fueron de 0,103 μg/L y 0,313 μg/L, respectivamente. La sensibilidad analítica encontrada fue de 12080 μAbs/ng Hg. La curva de calibración es lineal entre 0 y 100 μg/L. La pendiente obtenida con adiciones estándar de mercurio está incluida dentro del intervalo de confianza de la curva de calibración con patrones acuosos, por tanto no hay efecto matriz. Se comprobó la exactitud y precisión empleando material de referencia Seronorm® Trace Elements Whole Blood. La recuperación media obtenida fue de 97,36%. El método propuesto se considera sensible, robusto, exacto y preciso para biomonitorizar la concentración de mercurio en sangre como indicador de riesgo para la salud (AU)

Mercury is an environmental toxicant that causes numerous adverse effects in human health and natural ecosystems. The excessive methyl-mercury intake due to consumption of contaminated fish leads to neurological, reproductive and cardiovascular toxicity. The aim of this study is to validate a method for measuring mercury in blood samples by thermal decomposition, amalgamation and atomic absorption spectrometry. The detection and quantification limits were 0.103 y 0.313 μg/L, respectively. The analytical sensitivity was 12080 μAbs/ng Hg. The calibration curve is linear between 0 and 100 μg/L. The slope of the standard addition curve is within the confidence interval of the calibration curve using aqueous standards, meaning that there is no matrix effect. The precision and accuracy were tested using Seronorm® Trace Elements Whole Blood reference material. The mean recovery was 97.36%. The proposed method shows to be sensitive, robust, accurate, and precise for biomonitoring the concentration of mercury in blood samples as an indicator of health risk (AU)

Riparian swallows as integrators of landscape change in a multiuse river system: implications for aquatic-to-terrestrial transfers of contaminants.

Recent research has highlighted the transfer of contaminants from aquatic to terrestrial ecosystems via predation of aquatic emergent insects by riparian consumers. The influence of adjacent land use and land cover (LULC) on aquatic-to-terrestrial contaminant transfer, however, has received limited attention. From 2010 to 2012, at 11 river reaches in the Scioto River basin (OH, USA), we investigated the relationships between LULC and selenium (Se) and mercury (Hg) concentrations in four species of riparian swallows. Hg concentrations in swallows were significantly higher at rural reaches than at urban reaches (t=-3.58, P<0.001, df=30), whereas Se concentrations were positively associated with adjacent land cover characterized by mature tree cover (R(2)=0.49, P=0.006). To an extent, these relationships appear to be mediated by swallow reliance on aquatic emergent insects. For example, tree swallows (Tachycineta bicolor) at urban reaches exhibited a higher proportion of aquatic prey in their diet, fed at a higher trophic level, and exhibited elevated Se levels. We also found that both Se and Hg concentrations in adult swallows were significantly higher than those observed in nestlings at both urban and rural reaches (Se: t=-2.83, P=0.033, df=3; Hg: t=-3.22, P=0.024, df=3). Collectively, our results indicate that riparian swallows integrate contaminant exposure in linked aquatic-terrestrial systems and that LULC may strongly regulate aquatic contaminant flux to terrestrial consumers.

Mercury and selenium concentrations in leatherback sea turtles (Dermochelys coriacea): population comparisons, implications for reproductive success, hazard quotients and directions for future research.

Leatherback sea turtles (Dermochelys coriacea) are long-distance migrants that travel thousands of km from foraging grounds to breeding and nesting grounds. These extensive journeys are fueled by ingestion of an estimated 300-400 kg of prey/d and likely result in exposure to high concentrations of environmental toxicants (e.g., mercury compounds). Increased bodily concentrations of mercury and its compounds in nesting female turtles may have detrimental effects on reproductive success. Leatherbacks have relatively low reproductive success compared with other sea turtles (global average hatching success ~50-60%). To assess toxicants and necessary nutrients as factors affecting leatherback turtle reproductive success at Sandy Point National Wildlife Refuge (SPNWR), St. Croix, U.S. Virgin Islands, we collected blood from nesting female leatherbacks and tissues from their hatchlings (blood from live turtles, liver and yolk sac from dead turtles). We compared the concentrations in those tissues to hatching and emergence success. We found that on SPNWR, hatching and emergence success were more closely related to seasonal factors than to total mercury and selenium concentrations in both nesting females and hatchlings. Selenium concentrations of nesting females were positively correlated with those of their hatchlings. Mercury and selenium in the liver of hatchlings were positively correlated with one another. Turtles with greater remigration intervals tended to have higher blood selenium concentrations, suggesting that selenium accumulates in leatherbacks through time. Through hazard quotients, we found evidence that selenium may be at or above concentrations that may cause physiologic harm to hatchlings. We also found evidence that population level differences exist for these trace elements. The concentrations of mercury and selenium established in this manuscript form a baseline for future toxicant studies.

Differences in prenatal exposure to mercury in South African communities residing along the Indian Ocean.

Mercury is a persistent environmental pollutant that has the potential to adversely affect human health, particularly, foetal neurodevelopment. The purpose of the study was to investigate prenatal mercury (Hg) exposure in the population in three sites along the South Africa coast. Study subjects included women (n=350) who were admitted for delivery at the local hospitals. Maternal and cord blood samples were collected to measure total mercury and each participant was required to answer a questionnaire. The 90th percentile of mercury levels in maternal and cord blood of the total population was 1.15 µg/l and 1.67 µg/l, respectively. Site 1 (Manguzi) participants had the highest maternal geometric mean (GM) values of 0.93 µg/l, which was significantly different from Site 2 (Port Shepstone) (0.49 µg/l) and Site 3 (Empangeni) (0.56 µg/l) (ANOVA test, p<0.001). Umbilical cord blood GM Hg level for Site 1 (1.45 µg/l) was more than double the GM Hg level in Site 2 (0.70 µg/l) and Site 3 (0.73 µg/l). Univariate analysis indicated that the following maternal characteristics were positive predictors for elevated umbilical cord Hg levels: maternal blood Hg levels, living with a partner, residing in Site 1, living in informal housing, using wood and gas for cooking, borehole water as a drinking source, and a member of the household being involved in fishing. Maternal dietary predictors of elevated Hg levels in umbilical cord blood included consuming fresh fish, tinned fish, fruit or dairy products, daily. This study provides baseline data and reveals that 2% of the study population were above the EPA's reference value (5.8 µg/l) suggesting low level exposure to mercury in pregnant women and the developing foetus in South Africa. Further research is required to explore the sources of elevated Hg levels in Site 1.

Mercury, APOE, and children's neurodevelopment.

The benefit of the nutritious elements in fish is insufficient for explaining the controversial finding regarding prenatal mercury (Hg) exposure and neurodevelopment; the varying frequency of susceptible genes among these populations may shed light on these observations. However, limited studies have been reported on the association between genetic susceptibility of prenatal Hg exposure and child development. Apolipoprotein E (APOE, protein; Apoe, gene) is a major protein transporter expressed in the brain. The Apoe epsilon 4 (ε4) allele is associated with poor neural repair function and is a risk factor associated with Alzheimer disease. We conducted a prospective cohort study in 2004 and 2005. In this study, 168 subjects were recruited at delivery and followed up at two years of age, and genetic polymorphisms of Apoe were included to assess genetic susceptibility and to determine the relationship between Hg concentrations in cord blood and neurodevelopment. The results showed that adverse effects on neurodevelopment were consistently associated with prenatal Hg exposure in all subtests of Comprehensive Developmental Inventory for Infants and Toddlers (CDIIT) among ε4 carriers as assessed by both simple linear and multiple linear regression models. After controlling for confounding factors, statistical significance was found in the subtests of cognition tests (ß=-8.47, 95% confidence interval (CI)=-16.10 to -0.84), social tests (ß=-11.02, 95% CI=-20.85 to -1.19) and the whole test of CDIIT (ß=-10.45, 95% CI=-17.36 to -3.54) in a multiple linear regression model. Additionally, the interaction effect between gene polymorphisms of Apoe and Hg levels was significant in the whole test CDIIT and subtests of cognition, language and fine motor tests. In conclusion, Apoe modifies the adverse effects of cord blood Hg on neurodevelopment at the age of two years.

Minimal change disease caused by exposure to mercury-containing skin lightening cream: a report of 4 cases.

Mercury is a known cause of nephrotic syndrome and the underlying renal pathology in most of the reported cases was membranous nephropathy. We describe here 4 cases of minimal change disease following exposure to mercury-containing skin lightening cream for 2 - 6 months. The mercury content of the facial creams was very high (7,420 - 30,000 parts per million). All patients were female and presented with nephrotic syndrome and heavy proteinuria (8.35 - 20.69 g/d). The blood and urine mercury levels were 26 - 129 nmol/l and 316 - 2,521 nmol/d, respectively. Renal biopsy revealed minimal change disease (MCD) in all patients. The use of cosmetic cream was stopped and chelation therapy with D-penicillamine was given. Two patients were also given steroids. The time for blood mercury level to normalize was 1 - 7 months, whereas it took longer for urine mercury level to normalize (9 - 16 months). All patients had complete remission of proteinuria and the time to normalization of proteinuria was 1 - 9 months. Mercury-containing skin lightening cream is hazardous because skin absorption of mercury can cause minimal change disease. The public should be warned of the danger of using such products. In patients presenting with nephrotic syndrome, a detailed history should be taken, including the use of skin lightening cream. With regard to renal pathology, apart from membranous nephropathy, minimal change disease should be included as another pathological entity caused by mercury exposure or intoxication.

Cinnabar is different from mercuric chloride in mercury absorption and influence on the brain serotonin level.

The toxicity of cinnabar, a naturally occurring mercury sulphide (HgS), has long been referred to soluble mercury chloride (HgCl2 ). To investigate whether the speciation of mercury plays a role in its disposition and toxicity, we hereby investigated and compared cinnabar with soluble HgCl2 and pure insoluble HgS in mice on mercury absorption, tissue distribution and in relation to the biological effects. The male C57BL/6J mice were treated by oral administration of various doses of cinnabar, with 0.01 g/kg of HgCl2 for comparison, or the same dose of cinnabar or pure HgS (0.1 g/kg), once a day for 10 consecutive days. The total mercury contents in serum and tissue (brain, kidney, liver) were measured by atomic fluorescence spectrometer (AFS). The biological effects investigated involved monoamine neurotransmitters (serotonin, 5-HT) in brain as an indicator of therapeutic function, and serum alanine transaminase (ALT) as a marker of hepatic damage, blood urea nitrogen (BUN) and serum creatinine as markers for renal function. The mercury absorption of cinnabar or HgS was much less than that of HgCl2 . The mercury levels in brains of the cinnabar group were only slightly changed and kept in a steady-state with the dose elevated. Cinnabar or HgS suppressed brain 5-HT levels. HgCl2 could not cause any changes in brain 5-HT although the mercury level increased considerably. The results revealed that cinnabar or HgS is markedly different from HgCl2 in mercury absorption, tissue distribution and influence on brain 5-HT levels, which suggests that the pharmacological and/or toxicological effects of cinnabar undertake other pathways from mercuric ions.

Mercury in non-breeding sparrows of North Carolina salt marshes.

We captured Nelson's, Saltmarsh and Seaside Sparrows (Ammodramus nelsoni, A. caudacutus and A. maritimus) at three salt marsh sites near Wrightsville Beach, North Carolina during five non-breeding seasons (September through April, 2006-2011). We analyzed breast feather samples from all of these seasons and blood and first primary feather (P1) samples from three seasons (2008-2011) for mercury (Hg). Generalized linear models were used to test for the impact of species, season, site and month on blood Hg, species, season and site on P1 Hg and species and season on breast feather Hg. The best-fit model for blood indicated that Hg varied among species, seasons and months. Saltmarsh Sparrows maintain higher blood Hg than Nelson's and Seaside Sparrows during the non-breeding season while they are feeding in mixed flocks. In Nelson's and Seaside Sparrows, blood Hg decreased during mid-winter compared to early fall and late spring. Breast feather and P1 Hg varied among species with Saltmarsh Sparrows exhibiting higher concentrations than the other two species, while Nelson's Sparrows had lower concentrations than the other two species. Breast feather Hg was higher in the final three seasons than in the first two. Our results indicate that Hg exposure on breeding sites may be increasing and that high levels of Hg exposure during the breeding season may affect blood Hg concentrations year-round in Saltmarsh Sparrows. Our data thus provide a baseline for future Hg assessments in these species in NC.

Mercury exposure and oxidative stress in communities of the Brazilian Amazon.

This study was designed to assess possible associations between biomarkers of mercury (Hg) exposure and oxidative stress in fish-eating Amazonian communities. Clinical samples were obtained from riparians living in the Brazilian Amazon. Biomarkers of oxidative stress (glutathione - GSH, glutathione peroxidase - GSH-Px, catalase - CAT, activity and reactivation index of delta-aminolevulinate dehydratase - ALA-D (R%) were determined in blood. Total Hg was measured in whole blood (B-Hg), plasma (P-Hg) and hair (H-Hg). Association between biomarkers of Hg exposure and oxidative stress were examined using multiple regression models, including age, gender, alcohol consumption, smoking status, fish consumption and then stratified for gender. Significant inverse relations were observed between GSH-Px, GSH, CAT, ALA-D activity and B-Hg or H-Hg (p<0.05). ALA-D reactivation index was positively related to B-Hg (p<0.0001). P-Hg was directly related to ALA-D reactivation index and inversely associated with GSH-Px, GSH, and ALA-D activity (p<0.05). When stratified for gender, women showed significant inverse associations between all biomarkers of Hg exposure and CAT (p<0.05) or GSH (p<0.05), while for men only P-Hg showed a significant inverse relation with GSH (p<0.001). Our results clearly demonstrated an association between Hg exposure and oxidative stress. Moreover, for B-Hg, P-Hg and H-Hg gender differences were present.

Differential neurotoxic effects of methylmercury and mercuric sulfide in rats.

Methylmercury (MeHg) is an environmental toxicant, while mercuric sulfide (HgS) is a main active component of cinnabar, a Chinese mineral medicine used as a sedative. Because the neurotoxicological effects of HgS were not clearly understood, in this study, we attempted to compare HgS with MeHg in various physiological responses in Sprague-Dawley rats. After oral administration (2 mg/(kg day)) for consecutive 5 and 14 days, MeHg reversibly decreased both of motor nerve conduction velocity (MNCV) and tail flick response, whereas irreversibly inhibited all of the motor equilibrium performance, recovery of compound muscle action potentials (CMAP) following exhaustic tetanic stimuli and Na+/K+-ATPase activity of the isolated sciatic nerve. These toxic effects of MeHg were found in well correlation of Hg contents of various tissues (blood, cerebral cortex, liver and kidney) in rats. For comparison, a dose of 1g/(kg day) of HgS was orally administered to the rats based on our previous findings on ototoxicity of HgS. The results revealed that HgS only reversibly delayed the recovery of suppressed CMAP and inhibited sciatic nerve Na+/K+-ATPase activity in accordance to the lower Hg contents of the tissues. These findings provide the important information on the differential susceptibility of various nervous tissues to MeHg and HgS. The neruotoxic effects produced by HgS was estimated to be about 1000 of those induced by MeHg found in this study and our previous reports.

The role of phosphoinositide 3-kinase/Akt signaling in low-dose mercury-induced mouse pancreatic beta-cell dysfunction in vitro and in vivo.

The relationship between oxidation stress and phosphoinositide 3-kinase (PI3K) signaling in pancreatic beta-cell dysfunction remains unclear. Mercury is a well-known toxic metal that induces oxidative stress. Submicromolar-concentration HgCl(2) or methylmercury triggered reactive oxygen species (ROS) production and decreased insulin secretion in beta-cell-derived HIT-T15 cells and isolated mouse islets. Mercury increased PI3K activity and its downstream effector Akt phosphorylation. Antioxidant N-acetyl-l-cysteine (NAC) prevented mercury-induced insulin secretion inhibition and Akt phosphorylation but not increased PI3K activity. Inhibition of PI3K/Akt activity with PI3K inhibitor or by expressing the dominant-negative p85 or Akt prevented mercury-induced insulin secretion inhibition but not ROS production. These results indicate that both PI3K and ROS independently regulated Akt signaling-related, mercury-induced insulin secretion inhibition. We next observed that 2- or 4-week oral exposure to low-dose mercury to mice significantly caused the decrease in plasma insulin and displayed the elevation of blood glucose and plasma lipid peroxidation and glucose intolerance. Akt phosphorylation was shown in islets isolated from mercury-exposed mice. NAC effectively antagonized mercury-induced responses. Mercury-induced in vivo effects and increased blood mercury were reversed after mercury exposure was terminated. These results demonstrate that low-dose mercury-induced oxidative stress and PI3K activation cause Akt signaling-related pancreatic beta-cell dysfunction.

Increased oxidative DNA damage, as assessed by urinary 8-hydroxy-2'-deoxyguanosine concentrations, and serum redox status in persons exposed to mercury.

BACKGROUND: Mercury is a ubiquitous and highly toxic environmental pollutant. In this study, we evaluated the relationship between mercury exposure and oxidative stress, serum and urinary mercury concentrations, oxidative DNA damage, and serum redox status in chronically mercury-exposed persons compared with healthy controls. METHODS: We measured urinary 8-hydroxy-2'-deoxyguanosine (8-OHdG), which we used as a biomarker of oxidative DNA damage in the mercury-exposed persons, by HPLC with electrochemical detection (ECD). We evaluated antioxidant status by measuring the activities of superoxide dismutase and glutathione peroxidase and the concentrations of total reduced glutathione and protein-bound thiols in serum. RESULTS: The significant increase in 8-OHdG concentrations in urine indicated that mercury-induced oxidative damage to DNA occurred in vivo. Differences in body mercury burden and antioxidant enzyme activities were statistically significant between the mercury-exposed persons and controls. Serum and urinary mercury concentrations in the mercury-exposed persons were more than 40-fold higher than in controls. CONCLUSIONS: Mercury exposure can induce oxidative DNA damage, whereas the antioxidative repair systems can be expected to minimize DNA lesions caused by mercury. Measurement of urinary 8-OHdG could be useful for evaluating in vivo oxidative DNA damage in mercury-exposed populations.

[Repeated metallic mercury intravenous injections for doping]. / Wielokrotne dozylne wstrzykniecia rteci metalicznej w celach dopingowych.

In this article we described a 24 year-old patient, suffering from nephropathy of unknown origin, who was admitted to the Clinic after having tried to commit suicide for the third time by overusing tricycle antidepressant drugs (TLPD) and ethanol. During toxicological tests the serum TLPD level was 548 micrograms/L and the serum ethanol level was 2.1 g/L. His chest X-ray showed the presence of several metal particles of approx. 1.5 mm in diameter disseminated in both lungs, which could have been particles of metallic mercury. When the state of coma was over the patient admitted that for the past three years he had many times injected intravenously a small amount of metallic mercury (about 0.5 ml/dose) to improve his strength, speed and physical fitness. Tested serum mercury level was 300 micrograms/L and urinary mercury excretion 500 micrograms/L/24 hours.

Adverse health effects related to mercury exposure from dental amalgam fillings: toxicological or psychological causes?

BACKGROUND: Possible adverse health effects due to mercury released by amalgam fillings have been discussed in several studies of patients who attribute various symptoms to the effects of amalgam fillings. No systematic relation of specific symptoms to increased mercury levels could be established in any of these studies. Thus, a psychosomatic aetiology of the complaints should be considered and psychological factors contributing to their aetiology should be identified. METHODS: A screening questionnaire was used to identify subjects who were convinced that their health had already been affected seriously by their amalgam fillings (N = 40). These amalgam sensitive subjects were compared to amalgam non-sensitive subjects (N = 43). All participants were subjected to dental, general health, toxicological and psychological examinations. RESULTS: The two groups did not differ with respect to the number of amalgam fillings, amalgam surfaces or mercury levels assessed in blood, urine or saliva. However, amalgam sensitive subjects had significantly higher symptom scores both in a screening instrument for medically unexplained somatic symptoms (SOMS) and in the SCL-90-R Somatization scale. Additionally, more subjects from this group (50% versus 4.7%) had severe somatization syndromes. With respect to psychological risk factors, amalgam sensitive subjects had a self-concept of being weak and unable to tolerate stress, more cognitions of environmental threat, and increased habitual anxiety. These psychological factors were significantly correlated with the number and intensity of the reported somatic symptoms. CONCLUSIONS: While our results do not support an organic explanation of the reported symptoms, they are well in accord with the notion of a psychological aetiology of the reported symptoms and complaints. The findings suggest that self-diagnosed 'amalgam illness' is a label for a general tendency toward somatization.

Structural basis of the antagonism between inorganic mercury and selenium in mammals.

Mercuric chloride toxicity in mammals can be overcome by co-administration of sodium selenite. We report a study of the mutual detoxification product in rabbit plasma, and of a Hg-Se-S-containing species synthesized by addition of equimolar mercuric chloride and sodium selenite to aqueous, buffered glutathione. Chromatographic purification of this Hg-Se-S species and subsequent structural analysis by Se and Hg extended X-ray absorption fine structure (EXAFS) spectroscopy revealed the presence of four-coordinate Se and Hg entities separated by 2.61 A. Hg and Se near-edge X-ray absorption spectroscopy of erythrocytes, plasma, and bile of rabbits that had been injected with solutions of sodium selenite and mercuric chloride showed that Hg and Se in plasma samples exhibited X-ray absorption spectra that were essentially identical to those of the synthetic Hg-Se-S species. Thus, the molecular detoxification product of sodium selenite and mercuric chloride in rabbits exhibits similarities to the synthetic Hg-Se-S species. The underlying molecular mechanism for the formation of the Hg-Se-S species is discussed.

Inorganic, organic, and total mercury in blood and urine: cold vapor analysis with automated flow injection sample delivery.

A cold vapor atomic absorption technique for blood or urine mercury analysis that uses persulfate oxidation to prepare samples for total mercury analysis and acid permanganate oxidation to prepare samples for inorganic mercury analysis is described. The linearity of the procedures ranged from 0.5 to 25 micrograms/L. Precision ranged from 20% at 1 microgram/L to 7% at 20 micrograms/L. Documentation of accuracy is based on analysis of samples prepared by an international proficiency survey program. The development of a two-step digestion procedure followed by automated flow-injection mercury analysis was a necessary precursor to the assessment of inorganic and alkylmercury exposure in a large unexposed human population. Application of this technique to 902 blood and 902 urine samples collected from a normal human population who had no extraordinary mercury exposure generated mean plus two standard deviation skewed confidence-limit ranges of results as follows: blood total mercury, 0-8.4 micrograms/L; blood inorganic mercury, 0-1.7 micrograms/L; blood organic mercury, 0-7.5 micrograms/L; urine total mercury, 0-9.9 micrograms/L; urine inorganic mercury, 0-8.6 micrograms/L; and urine organic mercury, 0-1.8 micrograms/L.