Bioavailability study of arsenic and mercury in traditional Chinese medicines (TCM) using an animal model after a single dose exposure.

Traditional Chinese medicines (TCM) are increasingly being used as alternative medicines in many countries, and this has caused concern because of adverse health effects from toxic metal bioavailability such as mercury (Hg) and arsenic (As). The aim of this study was to investigate the bioavailability of As and Hg from TCM after a single exposure dose using an animal model of female Sprague-Dawley rats. The rats were divided into 6 groups which included four groups treated with sodium arsenite (NaAsO2), arsenic sulfide (As2S3), mercuric chloride (HgCl2), mercuric sulfide (HgS), and two groups treated with TCM containing high Hg or As (Liu Shen Wan: As 7.7-9.1% and Hg 1.4-5.0%; Niuhang Jie du Pian: As 6.2-7.9% and Hg <0.001%). The samples of urine, faeces, kidney and liver were collected for analysis and histological assay. The results indicated that relatively low levels of As and Hg from these TCM were retained in liver and kidney tissues. The levels of As in these tissues after TCM treatment were consistent with the levels from the As sulphide treated group. With the exception of the mercuric chloride treated group, the levels of Hg in urine from other groups were very low, and high levels of As and Hg from TCM were excreted in faeces. The study showed poor bioavailability of As and Hg from TCM as indicated by low relative bioavailability of As (0.60-1.10%) and Hg (<0.001%). Histopathological examination of rat kidney and liver tissues did not show toxic effects from TCM.

Neuropsychological Effects of Mercury Exposure Among Dentists in Monastir City.

AIMS: The aim of this study is to assess the neuropsychological manifestations of mercury exposure in dentists. METHODS: A cross-sectional study was carried out including 64 dentists matched to a control group according to age and gender. This study protocol included a neurological evaluation, a questionnaire assessing the study groups' general characteristics and personal factors that may affect mercury urinary excretion in both groups. EUROQUEST questionnaire and Hospital Anxiety and Depression scale (HADS) were used to evaluate the neuropsychological symptoms reported during the last 12 months. In both groups, mercury impregnation was assessed by monitoring urinary mercury. RESULTS: In the exposed group, scores of neurological symptoms, memory disturbances and anxiety were found to be significantly higher than those in controls (p < 0.01). Mean scores of HAD Depression's scale were higher in the exposed group than in controls. Most of the neurotoxic manifestations were correlated to the levels of urinary mercury excretion in the exposed group. Mean levels of urinary mercury were significantly higher in the dentists group than in controls, with respective values of 21.1 ± 19.6 µg/g of creatinine and 0.05 ± 0.9 µg/g of creatinine. In nine dentists having urinary mercury levels higher than 35 µg/g of creatinine, neurological examination showed a bilateral and symmetric intentional tremor in both upper limbs. In the exposed group, the neuropsychological manifestations and levels of urinary mercury were found to be significantly correlated. CONCLUSION: Increased levels of urinary mercury observed in dentists suggest that exposure to mercury vapour emissions adversely affects dental professionals, therefore prevention measures should be strengthened, with a special medical supervision program of dentists exposed to mercury vapours should be implemented. We have also outlined some relevant patents in this article.

Mercury Toxicity and Contamination of Households from the Use of Skin Creams Adulterated with Mercurous Chloride (Calomel).

Inorganic mercury, in the form of mercurous chloride, or calomel, is intentionally added to some cosmetic products sold through informal channels in Mexico and the US for skin lightening and acne treatment. These products have led to multiple cases of mercury poisoning but few investigations have addressed the contamination of cream users' homes. We report on several cases of mercury poisoning among three Mexican-American families in California from use of mercury-containing skin creams. Each case resulted in widespread household contamination and secondary contamination of family members. Urine mercury levels in cream users ranged from 37 to 482 µg/g creatinine and in non-users from non-detectable to 107 µg/g creatinine. Air concentrations of up to 8 µg/m³ of mercury within homes exceeded the USEPA/ATSDR health-based guidance and action level of <1.0 µg/m³. Mercury contamination of cream users' homes presented a multi-pathway exposure environment to residents. Homes required extensive decontamination, including disposal of most household items, to achieve acceptable air levels. The acceptable air levels used were not designed to consider multi-pathway exposure scenarios. These findings support that the calomel is able to change valence form to elemental mercury and volatilize once exposed to the skin or surfaces in the indoor environment.

Toxicological significance of renal Bcrp: Another potential transporter in the elimination of mercuric ions from proximal tubular cells.

Secretion of inorganic mercury (Hg(2+)) from proximal tubular cells into the tubular lumen has been shown to involve the multidrug resistance-associated protein 2 (Mrp2). Considering similarities in localization and substrate specificity between Mrp2 and the breast cancer resistance protein (Bcrp), we hypothesize that Bcrp may also play a role in the proximal tubular secretion of mercuric species. In order to test this hypothesis, the uptake of Hg(2+) was examined initially using inside-out membrane vesicles containing Bcrp. The results of these studies suggest that Bcrp may be capable of transporting certain conjugates of Hg(2+). To further characterize the role of Bcrp in the handling of mercuric ions and in the induction of Hg(2+)-induced nephropathy, Sprague-Dawley and Bcrp knockout (bcrp(-/-)) rats were exposed intravenously to a non-nephrotoxic (0.5 µmol · kg(-1)), a moderately nephrotoxic (1.5 µmol · kg(-1)) or a significantly nephrotoxic (2.0 µmol · kg(-1)) dose of HgCl2. In general, the accumulation of Hg(2+) was greater in organs of bcrp(-/-) rats than in Sprague-Dawley rats, suggesting that Bcrp may play a role in the export of Hg(2+) from target cells. Within the kidney, cellular injury and necrosis was more severe in bcrp(-/-) rats than in controls. The pattern of necrosis, which was localized in the inner cortex and the outer stripe of the outer medulla, was significantly different from that observed in Mrp2-deficient animals. These findings suggest that Bcrp may be involved in the cellular export of select mercuric species and that its role in this export may differ from that of Mrp2.

Mercury Exposure and Antinuclear Antibodies among Females of Reproductive Age in the United States: NHANES.

BACKGROUND: Immune dysregulation associated with mercury has been suggested, although data in the general population are lacking. Chronic exposure to low levels of methylmercury (organic) and inorganic mercury is common, such as through fish consumption and dental amalgams. OBJECTIVE: We examined associations between mercury biomarkers and antinuclear antibody (ANA) positivity and titer strength. METHODS: Among females 16-49 years of age (n = 1,352) from the National Health and Nutrition Examination Survey (NHANES) 1999-2004, we examined cross-sectional associations between mercury and ANAs (indirect immunofluorescence; cutoff ≥ 1:80). Three biomarkers of mercury exposure were used: hair (available 1999-2000) and total blood (1999-2004) predominantly represented methylmercury, and urine (1999-2002) represented inorganic mercury. Survey statistics were used. Multivariable modeling adjusted for several covariates, including age and omega-3 fatty acids. RESULTS: Sixteen percent of females were ANA positive; 96% of ANA positives had a nuclear speckled staining pattern. Geometric mean (geometric SD) mercury concentrations were 0.22 (0.03) ppm in hair, 0.92 (0.05) µg/L blood, and 0.62 (0.04) µg/L urine. Hair and blood, but not urinary, mercury were associated with ANA positivity (sample sizes 452, 1,352, and 804, respectively), after adjusting for confounders: for hair, odds ratio (OR) = 4.10 (95% CI: 1.66, 10.13); for blood, OR = 2.32 (95% CI: 1.07, 5.03) comparing highest versus lowest quantiles. Magnitudes of association were strongest for high-titer (≥ 1:1,280) ANA: hair, OR = 11.41 (95% CI: 1.60, 81.23); blood, OR = 5.93 (95% CI: 1.57, 22.47). CONCLUSIONS: Methylmercury, at low levels generally considered safe, was associated with subclinical autoimmunity among reproductive-age females. Autoantibodies may predate clinical disease by years; thus, methylmercury exposure may be relevant to future autoimmune disease risk.

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.

Plasma and urine dimercaptopropanesulfonate concentrations after dermal application of transdermal DMPS (TD-DMPS).

2,3-Dimercaptopropane-1-sulfonate (DMPS) is a metal chelator approved in Europe for oral or intravenous use for heavy metal poisoning. Transdermally applied DMPS (TD-DMPS) is used by some alternative practitioners to treat autism, despite the absence of evidence for its efficacy. We found no literature evaluating the pharmacokinetics of the transdermal route of delivery or the ability of TD-DMPS to enhance urinary mercury elimination. We hypothesized that TD-DMPS is not absorbed. Eight adult volunteers underwent application of 1.5-3 drops/kg of TD-DMPS. Subjects provided 12-h urine collections the day before and day of application. Subjects underwent blood draws at 0, 30, 60,90, 120, and 240 min after TD-DMPS application. Plasma and urine were assayed for the presence of DMPS. Urine was assayed for any change in urinary mercury excretion after DMPS. One control subject ingested 250 mg of oral DMPS and underwent the same urine and blood collections and analyses. No subject had detectable urine DMPS or increased urine mercury excretion after TD-DMPS. One subject had detectable levels of DMPS in the 30-min plasma sample, suspected to be contamination. All other samples for that subject and the other seven subjects showed no detectable plasma DMPS. The control subject had detectable urine and plasma DMPS levels and increased urine mercury excretion. These results indicate that TD-DMPS is not absorbed. There was no increase in urine mercury excretion after TD-DMPS. Our results argue that TD-DMPS is an ineffective metal chelator.

Elemental mercury poisoning presenting as hypertension in a young child.

Mercury intoxication is an uncommon cause of hypertension in children and can mimic several other diseases, such as pheochromocytoma and vasculitis. Mercury intoxication can present as a diagnostic challenge because levels of catecholamines may be elevated, suggesting that the etiology is a catecholamine-secreting tumor. Once acrodynia is identified as a primary symptom, a 24-hour urine mercury level can confirm the diagnosis. Inclusion of mercury intoxication in the differential diagnosis early on can help avoid unnecessary and invasive diagnostic tests and therapeutic interventions. We discuss a case of mercury intoxication in a 3-year-old girl presenting with hypertension and acrodynia, without a known history of exposure. Chelation therapy successfully treated our patient's mercury intoxication. However, it was also necessary to concurrently treat her hypertension and the pain associated with her acrodynia. Because there were no known risk factors for mercury poisoning in this case, and because ritual use of mercury is common in much of the United States, we recommend high clinical suspicion and subsequent testing in all cases of acrodynia.

Human mercury exposure associated with small-scale gold mining in Burkina Faso.

PURPOSE: In Burkina Faso, gold ore is one of the main sources of income for an important part of the active population. Artisan gold miners use mercury in the extraction, a toxic metal whose human health risks are well known. The aim of the present study was to assess mercury exposure as well as to understand the exposure determinants of gold miners in Burkinabe small-scale mines. METHODS: The examined gold miners' population on the different selected gold mining sites was composed by persons who were directly and indirectly related to gold mining activities. But measurement of urinary mercury was performed on workers most susceptible to be exposed to mercury. Thus, occupational exposure to mercury was evaluated among ninety-three workers belonging to eight different gold mining sites spread in six regions of Burkina Faso. Among others, work-related exposure determinants were taken into account for each person during urine sampling as for example amalgamating or heating mercury. All participants were medically examined by a local medical team in order to identify possible symptoms related to the toxic effect of mercury. RESULTS: Mercury levels were high, showing that 69% of the measurements exceeded the ACGIH (American Conference of Industrial Hygienists) biological exposure indice (BEI) of 35 µg per g of creatinine (µg/g-Cr) (prior to shift) while 16% even exceeded 350 µg/g-Cr. Basically, unspecific but also specific symptoms related to mercury toxicity could be underlined among the persons who were directly related to gold mining activities. Only one-third among the studied subpopulation reported about less than three symptoms possibly associated to mercury exposure and nearly half of them suffered from at least five of these symptoms. Ore washers were more involved in the direct handling of mercury while gold dealers in the final gold recovery activities. These differences may explain the overexposure observed in gold dealers and indicate that the refining process is the major source of exposure. CONCLUSIONS: This study attests that mercury exposure still is an issue of concern. North-South collaborations should encourage knowledge exchange between developing and developed countries, for a cleaner artisanal gold mining process and thus for reducing human health and environmental hazards due to mercury use.

Mercury exposure in young children living in New York City.

Residential exposure to vapor from current or previous cultural use of mercury could harm children living in rental (apartment) homes. That concern prompted the following agencies to conduct a study to assess pediatric mercury exposure in New York City communities by measuring urine mercury levels: New York City Department of Health and Mental Hygiene's (NYCDOHMH) Bureau of Environmental Surveillance and Policy, New York State Department of Health/Center for Environmental Health (NYSDOHCEH), Wadsworth Center's Biomonitoring Program/Trace Elements Laboratory (WC-TEL), and Centers for Disease Control and Prevention (CDC). A previous study indicated that people could obtain mercury for ritualistic use from botanicas located in Brooklyn, Manhattan, and the Bronx. Working closely with local community partners, we concentrated our recruiting efforts through health clinics located in potentially affected neighborhoods. We developed posters to advertise the study, conducted active outreach through local partners, and, as compensation for participation in the study, we offered a food gift certificate redeemable at a local grocer. We collected 460 urine specimens and analyzed them for total mercury. Overall, geometric mean urine total mercury was 0.31 microg mercury/l urine. One sample was 24 microg mercury/l urine, which exceeded the (20 microg mercury/l urine) NYSDOH Heavy Metal Registry reporting threshold for urine mercury exposure. Geometric mean urine mercury levels were uniformly low and did not differ by neighborhood or with any clinical significance by children's ethnicity. Few parents reported the presence of mercury at home, in a charm, or other item (e.g., skin-lightening creams and soaps), and we found no association between these potential sources of exposure and a child's urinary mercury levels. All pediatric mercury levels measured in this study were well below a level considered to be of medical concern. This study found neither self-reported nor measured evidence of significant mercury use or exposure among participating children. Because some participants were aware of the possibility that they could acquire and use mercury for cultural or ritualistic purposes, community education about the health hazards of mercury should continue.

Screening for mercury in aqueous environmental samples and urine samples using thin layer chromatography.

A method for screening based on thin layer chromatography (TLC) comprising silica gel 'G' as a stationary phase and benzene as a mobile phase was found to be most suitable for the detection of mercury in aqueous samples and spiked human urine, without digesting the samples. A broad range for the detection of mercury, from 20 microg/L (20 ppb) to 1000 mg/L (1000 ppm), was established, by optimizing the experimental conditions. In urine samples, mercury could be detected also, at levels as low as 50 microg/L (50 ppb) or above. Mercury was detected by complexation with dithizone followed by TLC, also in the presence of other heavy metals, including arsenic, cadmium, lead, copper, iron, zinc, and nickel. The method is simple, cheap, and has no interference of the matrix present in the natural water and aqueous industrial effluent samples obtained from the field. Further, no sophisticated instrument is needed for the detection of mercury.

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.

Mercury poisoning associated with a Mexican beauty cream.

OBJECTIVES: To describe demographic characteristics, patterns of use, and symptoms associated with mercury poisoning among persons who used a Mexican beauty cream containing mercurous chloride and to estimate the prevalence of cream use in Texas near the Mexico border. DESIGN: Case series and cross-sectional survey. SETTING: Border communities of Arizona, California, New Mexico, and Texas. PARTICIPANTS: Persons who used the cream and contacted a health department in response to announcements about the cream and households that participated in the Survey of Health and Environmental Conditions in Texas Border Counties and Colonias, 1997. MAIN OUTCOME MEASURES: Urine mercury concentrations, self-reported symptoms, and prevalence of cream use among households. RESULTS: Of 330 cream users who contacted their health department, 96% were women, and 95% were Hispanic. The mean urine mercury concentration was 146.7 microg/L (reference range : 0-20 microg/L). In 5% of 2,194 randomly selected Texas households near the Mexico border, at least 1 person had used "Crema de Belleza-Manning" (Laboratorios Vida Natural, S.A., Tampico, Tamaulipas, Mexico) in the previous year. CONCLUSIONS: Most cream users had increased urine mercury concentrations. Cream use was common in Texas near the Mexico border. Physicians should consider toxicity in patients with neurologic symptoms of unclear cause and use public health departments when investigating unusual illnesses.

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.

Longitudinal study of workers exposed to mercury vapour at low concentrations: time course of inorganic and organic mercury concentrations in urine, blood, and hair.

Seven Japanese female workers exposed to mercury vapour at a concentration of < 0.02 mg Hg/m3 (8 h/day, 44 h/week) were examined for inorganic (I-Hg) and organic (O-Hg) mercury concentrations in urine, blood, and hair after 0, 4, 8, 17, and 23 months of exposure. Both I-Hg and O-Hg concentrations in urine and hair did not increase significantly even after 23 months of exposure. The concentration of I-Hg and O-Hg in plasma and O-Hg in erythrocytes, however, increased significantly after four months of exposure, and the high concentrations were maintained until the end of the study (23 months of exposure). Absence of a significant increase in the concentration of O-Hg in hair indicates that changes in concentrations of I-Hg and O-Hg in blood could be caused by the occupational exposure to mercury vapour. These results show clearly that mercury concentration in blood indicates the uptake of mercury compared with data from before employment with mercury. Even after 23 months of exposure to mercury vapour, however, urinary mercury concentration was not affected.

Mercury kinetics in a case of severe mercuric chloride poisoning treated with dimercapto-1-propane sulphonate (DMPS).

A case of severe mercuric chloride poisoning with clinical signs of mucosal damage of the gastrointestinal tract and anuric renal failure, is presented. The initial whole blood mercury concentration was 14,300 micrograms l-1. This concentration is supposed to be associated with fatal outcome due to multiple organ failure. Because of anuric renal failure, haemodialysis was necessary. Kidney function returned to normal within 10 days. Haemodialysis proved to be ineffective with regard to total mercury elimination. Treatment with DMPS was started because of very severe poisoning, anuric renal failure and optimistic reports on the "new" chelating agent 2,3-dimercapto-1 propanesulphonic acid (DMPS) in mercury poisoning. DMPS was administered by parenteral route initially and was continued thereafter by oral route, until whole blood and urine mercury concentrations had decreased below a level considered as toxic. Except for a temporary pruritic erythema of the skin, no side effects of DMPS treatment were observed. The clinical course was mild, despite continuing high whole blood mercury concentrations. Recovery was uneventful and complete. DMPS treatment, administered by intravenous and oral route, was shown to be an effective alternative for BAL in life-threatening mercuric chloride intoxication. The pharmacokinetic data presented in this case report suggest that non-renal mercury clearance may considerably exceed renal mercury clearance.