Search

Background: There are no reports on the incidence of chronic mercury poisoning in a large population in China. This study investigated the epidemiology, clinical manifestations, treatment, and follow-up of Chinese patients with chronic mercury poisoning., Methods: Data for 288 mercury poisoning patients were collected at our hospital from July 2014 to September 2019, including sex, age, admission time, blood mercury content, urine mercury content, creatinine, urinary mercury/creatinine ratio, 24-h urinary protein levels, electromyography (EMG) findings, renal biopsy, and follow-up. Patient characteristics were evaluated by statistical and correlation analyses., Results: First, mercury poisoning in China mainly occurred through occupational exposure and the inappropriate use of mercury-containing cosmetics and Chinese folk remedies (CFRs). Second, the most common symptoms were nervous system (50.3 %), kidney (16.4 %) and breathing (8.0 %). Mercury poisoning-induced Nephrotic syndrome (NS) and peripheral neuropathy are common long-term complications. The complications of occupational and cosmetics-induced mercury poisoning are consistent with international belief. However, the NS caused by CFRs is mainly membranous nephropathy and the probability of peripheral neuropathy caused by CFRs is higher than other pathogens. Third, follow-up data shows that 13 patients with EMG-confirmed neurological injury, 10 showed full recovery after 38.50 ± 8.03 months. Furthermore, among 18 patients with NS, 15 had normal urine protein and serum albumin levels after 22.67 ± 10.26 months., Conclusions: Regulation of skin-lightening cosmetic products, safety surveillance of CFRs, and prevention and control of occupational exposure must be improved to decrease the incidence of mercury poisoning in China.

Background: Mercury is an environmental hazard. Organic mercury is biologically more toxic than inorganic mercury. Therefore, we studied recent trends in the blood levels of organic and inorganic mercury in the United States., Methods: A total of 56,445 participants that had blood mercury and urine mercury measurements in National Health and Nutrition Examination Survey (NHANES) 1999-2016 were included. The organic mercury level was obtained by subtracting the inorganic mercury level from the total mercury level. Results were analyzed using SPSS complex sample module version 25. Pregnant women, children ages <20 years, and different ethnicities were analyzed as subgroups., Results: Blood organic mercury level increased from (geometric mean [95% confidence interval]) 0.08 [0.07-0.10] to 0.17 [0.16-0.18] µg/L during 1999-2016. It increased significantly (P <0.001) from 0.03 [0.02-0.03] to 0.07 [0.06-0.07] µg/L in children ages <20 and from 0.14 [0.09-0.21] to 0.36 [0.16-0.83] µg/L in pregnant women in this period (P <0.001). In 2013-2016, non-Hispanic Asians had the highest blood organic mercury level among different ethnicities, 0.93 [0.82-1.05] µg/L (P <0.001). Blood inorganic mercury level decreased from 0.31 [0.31-0.31] in 1999-2000 to 0.21 [0.21-0.22] µg/L in 2015-2016 (P <0.001). Urine mercury level decreased from 0.75 [0.71-0.80] in 1999-2000 to 0.16 [0.16-0.17] µg/L in 2015-2016 (P <0.001)., Conclusion: Blood organic mercury increased over the period 1999-2016 in the US population, including children and pregnant women, whereas there was a steady decline in both blood inorganic mercury and urine mercury levels., (Copyright © 2020 Elsevier Inc. All rights reserved.)

Mercury is the only metal that remains in liquid form at the room temperature. It is a very toxic metal and even short-term exposure can lead to poisoning. Mercury intoxication can affect many systems such as skin, cardiovascular, genitourinary, central and peripheral nervous, respiratory, and musculoskeletal system. Consequently, the diagnosis of mercury intoxication can be challenging due to its non-specific and multisystemic presentation. Herein, we report five pediatric cases with mercury intoxication from two families that were initially misdiagnosed as rheumatic disorders. We also performed a literature review about pediatric cases with mercury intoxication to investigate the clinical findings in children, the source of intoxication, and the current treatment preferences. As in our cases, reported patients were previously misdiagnosed as various infectious and/or rheumatic diseases before the diagnosis of mercury intoxication was established. A delay in diagnosis and treatment can cause serious morbidities and even mortality. We report this case series to emphasize the multisystemic presentation of mercury intoxication, and to remind and provide clues for physicians to recognize this rare toxicologic syndrome.

Mercury is a heavy metal with high toxicity, the level of which depends on the form of the metal. One of the newer techniques for determining trace amounts of total mercury in various materials, including biological samples, is thermal decomposition, amalgamation and atomic absorption spectrometry (TDA AAS). The TDA AAS method was optimized and validated using a mercury analyzer (DMA-80). The limits of detection for mercury were 0.10 and 0.20 μg/L (nickel and quartz boats, respectively). The working range of the calibration curve was at least from 0.6 to 200 ng Hg/mL; the intra-day precision in samples (RSD)-in the range of: 1.66-6.86% (blood), 0.82-1.47% (urine) and 2.01-3.44% (hair); the inter-day precision (over 8 days): 2.51%, and 2.5% (blood spiked with 2.5 and 10 ng Hg, respectively), 5.10% and 3.16% (urine spiked with 2.0 and 6.0 ng Hg, respectively). The accuracy (as relative error, mean value) determined on the basis of the study of reference materials of blood (Seronorm Trace Elements Whole Blood L-1, L-2, L-3), urine (Seronorm Trace Elements Urine, Urine L-2), and hair (Human Hair NIES CRM No. 13) was: 2.00% (blood), 0.50% (urine) and 0.86% (hair); recovery of 2.5 ng Hg (blood): 93-97%. The method was used for the determination of mercury in 76 samples of various biological matrices, including samples of whole blood, urine, hair, bile and vitreous humor. Mercury concentrations in postmortem blood (n = 24) were in the range: 0.61-12.4 μg/L (median 3.02 μg/L); urine (n = 12): 0.16-2.19 μg/L (median 0.81 μg/L); hair (n = 14): 0.08-0.53 μg/g (median 0.22 μg/g); bile (n = 12): 1.15-7.11 μg/L (median 2.41 μg/L and vitreous humor (n = 13): 0.22-1.01 μg/L (median 0.47 μg/L). The method is suitable for the purposes of forensic toxicology analysis., (© The Author(s) 2019. Published by Oxford University Press. All rights reserved. For Permissions, please email: journals.permissions@oup.com.)

Background: Dental staff may be at increased risk of adverse pregnancy outcome secondary to their chronic exposure to mercury., Objective: To investigate obstetric outcome among dental staff and explore the oxidative stress induced by mercury exposure., Methods: A cohort of 64 pregnant dental staff (exposed group) and 60 pregnant employees (non-exposed group) were studied. Urinary mercury level and blood antioxidant activity were measured. Participants were followed to assess their obstetric outcome., Results: The exposed group had a higher mean urinary mercury level and a lower blood antioxidant activity during the three trimesters compared to non-exposed group (p<0.001). Women in the exposed group were experienced more frequently spontaneous abortion and pre-eclampsia (p<0.05). Babies born to the women in the exposed group tended to be smaller for gestational age compared to those of non-exposed group (p<0.001)., Conclusion: Pregnant dental staff suffered higher odds of developing spontaneous abortion and pre-eclampsia and giving birth to babies smaller for gestational age. This may be linked to oxidative stress induced by exposure to mercury.

Rationale: Ingestion of a massive amount of metallic mercury was thought to be harmless until the last century. After that, in a number of cases, mercury ingestion has been associated with appendicitis, impaired liver function, memory deficits, aspiration leading to pneumonitis and acute renal failure. Treatment includes gastric lavage, giving laxatives and chelating agents, but rapid removal of metallic mercury with gastroscopy has not been used., Patient Concerns: An 18-year-old man was admitted to our emergency department after drinking 1000 g of metallic mercury as a suicide attempt., Diagnosis: Except from mild umbilical tenderness, he had no other symptoms. Radiography showed a metallic density in the area of the stomach., Intervention: Gastroscopy was performed to remove the mercury. One large pool and several small droplets of mercury were removed from the stomach., Outcomes: Blood and urine mercury levels of the patient remained low during hospitalization. No symptoms of mercury intoxication developed during the follow-up period., Lessons: Massive mercury ingestion may cause several symptoms, which can be prevented with prompt treatment. We used endoscopy to remove the mercury, which shortened the exposure time and minimized the risk of aspiration. This is the first case where endoscopy was used for the management of mercury ingestion.

The aim of this study is to report ophthalmic findings of acute mercury poisoning in 48 adults referred to emergency department. Full ophthalmologic examination including the best corrected visual acuity, external eye examination, reaction to light, a slit-lamp examination, funduscopy, intraocular pressure measurements, and visual field (VF) and color vision (CV) tests were performed at the presentation and repeated after 6 months. The parametric values of VF test, the mean deviation (MD), and pattern standard deviation (PSD) were recorded in order to compare patients and the 30 healthy controls. The mean parameter of color confusion index in patients was found to be statistically different than controls (p < 0.01). The MD and PSD in patients were different from controls statistically significant (p < 0.01 and p < 0.01, respectively). There was no correlation between the ocular findings and the urine and blood mercury levels. Methyl mercury, held in the school laboratory for experimental purpose, may be a source of poisoning. In this case series, we showed that acute exposure to mercury had hazardous effect on the visual system, especially CV and VF. We propose that emphasizing the public education on the potential hazards of mercury is crucial for preventive community health., (© The Author(s) 2013.)

Background: With the fast growth in the market of fluorescent lamps, particularly compact fluorescent light, the associated risk of mercury exposure, which is an essential component in all types of fluorescent lamps, has received increasing public attention worldwide. Even low doses of mercury are toxic., Objective: To study the health consequences of occupational exposure to mercury in workers of a fluorescent lamp factory., Methods: In a cross-sectional study 138 workers of a fluorescent lamp factory and 151 people who had no occupational exposure to mercury (the comparison group) were studied. Environmental study of mercury and noise levels was done. For all participants a neurobehavioral test battery was administered, spirometry was performed and air conduction audiometry was done. Urinary mercury level was also measured for all participants., Results: Prominent symptoms among workers exposed to mercury included tremors, emotional lability, memory changes, neuromuscular changes, and performance deficits in tests of cognitive function. Among the exposed group, the mean urinary mercury level was significantly higher in those who had personality changes or had manifestations of mercury toxicity. With increasing duration of employment and urinary mercury level, the performance of participants in neurobehavioral test battery and spirometric parameters deteriorated., Conclusion: Neurobehavioral test battery must be used for studying subclinical central nervous system dysfunction in those with chronic exposure to mercury. The test is especially useful for evaluating the severity of mercury effects in epidemiological studies. This study also reinforces the need for effective preventive programs for fluorescent lamp industry workplaces especially in developing countries with the lowest unhygienic work conditions.

Elemental mercury exposure occurs frequently and is potentially a toxic, particularly in children. Children are often attracted to elemental mercury because of its color, density, and tendency to form beads. Clinical manifestations of elemental mercury intoxication vary depending on its form, concentration, route of ingestion, and the duration of exposure. We present data on 179 pediatric cases of elemental mercury poisoning from exposure to mercury in schools in two different provinces of Turkey. Of all patients, 160 children had both touched/played with the mercury and inhaled its vapors, while 26 children had only inhaled the mercury vapor, two children reported having tasted the mercury. The median duration of exposure was 5 min (min 1-max 100), and 11 (6 %) children were exposed to the mercury for more than 24 h at home. More than half of the children (51.9 %) were asymptomatic at admission. Headache was the most common presenting complaint. The results of physical and neurological examinations were normal in 80 (44.6 %) children. Mid-dilated/dilated pupils were the most common neurological abnormality, and this sign was present in 90 (50.2 %) children. Mercury levels were measured in 24-h urine samples daily, and it was shown that the median urinary level of mercury was 29.80 μg/L (min, 2.40 μg/L; max, 4,687 μg/L). A positive correlation was also found between the duration of exposure and urinary mercury levels (r = 0.23, p = 0.001). All patients were followed up for 6 months. On the first follow-up visit performed 1 month after discharge, the neurological examinations of all patients were normal except for those patients with peripheral neuropathy and visual field defects. On the last follow-up visit at the sixth month, only two children still experienced visual field defects. In conclusion, this study is one of the largest case series of mercury intoxication of students in schools. Elemental mercury exposure can be potentially toxic, and its symptomatology is variable, particularly in children. Therefore, school staff and children should be aware of the risk of mercury toxicity. Pediatricians also need to warn parents and children about the hazards of playing with any chemical.

Deliberate poisoning with intentional ingestion of elemental mercury is reported not to result in systemic toxicity due to minimal absorption from the gastrointestinal tract. We report a case of a 43 year old male who intentionally ingested 200 ml elemental mercury which resulted in abdominal pain and vomiting. The patient subsequently aspirated globules of mercury which was confirmed on chest x-ray and his blood mercury levels were markedly raised. He was treated with chelating agents and managed in a negative pressure room to reduce the risk of staff being exposed to exhaled mercury vapour from the patient.

Acute mercury vapor poisoning is a rare but fatal toxicological emergency. People are exposed to mercury in daily life by the way of foods, vaccines, antiseptics, ointments, amalgam or occupation. We present here, the clinical picture and management of four members of the same family who were exposed to elemental mercury. Three of the family members were seen in another hospital with malaise, fever, eritematous rash and pulmonary problems. Their questioning revealed the mercury exposure. Having a suspicion of heavy metal intoxication, blood and urine mercury levels were measured and mercury intoxication was diagnosed. On admission to our hospital, two patients already had chelation therapy. In three of them we found three distinct abnormalities: encephalopathy, nephrotic syndrome and polyneuropathy. The fourth family member had minor symptoms. This family is an example for the inhalation exposure resulting from inappropriate handling of liquid mercury. During the first days, flu like illness ensues. Then, severe pulmonary, neurological, renal, hepatic, hematological and dermatological dysfunctions develop. Blood and urine mercury levels should be tested on suspicion, but it must be kept in mind that blood level is unreliable in predicting the severity of mercury toxicity. The priority in the treatment should be removing the patient from the source of exposure. Then British anti-Lewisite, edetate calcium disodium, penicillamine, Sodium 2,3-dimercaptopropane-1-sulfhonate and 2,3-dimercaptosuccinic acid can be used for binding the mercury. We conclude that since mercury-containing devices are present in daily life, physicians must be able to recognize the clinical manifestations and treatment of mercury poisoning.

Unlabelled: Mercury is a heavy metal found in nature in three forms: metallic mercury, organic and inorganic compounds. It is a general protoplasmatic toxin. The pathophysiology of mercury toxicity is related to its binding to sulfhydryl groups of different receptor proteins and cellular enzymes, interrupting cellular metabolism and in this way causing cell death. In the paper we present a case of 57-year-old woman, who was admitted due to suspicion of metallic mercury parenteral poisoning. The computed tomography (CT) scan of abdomen accidentally revealed multiple disseminated tiny metallic densities. The blood mercury level was high (41.9 microg/l), as well as mercury urine level (85.7 microg/g creatinine which was 42.8 microg/l). Neurologic examination revealed unobtrusive symptoms of cerebellum affection. Psychological examination revealed disturbances of cognitive abilities reliant on the efficiency of vision organ. The results of A. Benton's organic test were abnormal. Psychiatric examination revealed no abnormalities. Results of pulmonary function tests were within normal limits., Conclusions: The intravenous injection of metallic mercury did not cause serious clinical effects. Followup examination in order to reveal chronic toxic effects is necessary. Diagnostics and treatment of metallic mercury intoxications by parenteral injection should be carried out in the clinical toxicology departments.

In this paper we present the long-term follow-up of two patients, after injection of metallic mercury. Case 1. In 1997, 29-years-old man injected himself to left elbow about 20 ml of metallic mercury by mistake (he was heroin abuser for short time). Mercury concentration in the blood was 400 microg/L. X-ray of the chest, abdomen and affected elbow area showed radiopaque foreign material (depots of mercury). Depots of mercury were also visible on the tricuspid valve in echocardiography. Mercury from the soft tissue left elbow pit was partially surgically removed. During 15 years follow-up two times chelating therapy was performed with d-penicyllamine and DMPS. In 2012, he was admitted to hospital next time. The blood and urine mercury concentration was still elevated (55.2 microg/L and 197 microg/L), mercury depots in the lung and abdomen were present. The signs and symptoms of CNS damage, like peripheral polyneuropathy and ataxia, were diagnosed. CT of brain did not revealed any changes, despite head trauma before 6 years. However neurological findings are typical for chronic mercury poisoning, it is not possible to determine whether these changes are directly related to mercury, because head trauma history, Case 2. In 2003, 16-years-old woman injected herself one month before, in suicidal attempts to both elbows several millilitres of metallic mercury. Mercury concentration in the blood was 56.2 microg/L, in urine 906 microg/L and in the hair 1.12 microg/g. Chest Xray showed depots of mercury in the lung. Mercury from the soft tissue was two times surgically removed. During 9 years two times chelating therapy was performed with d-penicyllamine and DMPS. After 9 years there is no symptoms of mercury poisoning. Mercury depots in the lung are still present. The blood and urine mercury concentration is low (13.7 microg/L and 2.53 microg/L). In mean time she gave birth two healthy children. Further patients evaluation is necessary.

Objectives: The aim of this study is to investigate the effect of elemental mercury exposure on renal function and antioxidative enzymes activity as a possible mechanism of renal affection among dental staff., Methods: This study was performed on a group of dental staff exposed to elemental mercury (N = 32) and matched control group (N = 37). Urinary and blood level of mercury, albumin α1 microgloblin in urine, glutathione peroxidase and superoxide dismutase blood level were measured for the exposed and control group., Results: Compared to the control group, urinary and blood mercury were significantly higher in the exposed group. Glutathione peroxidase and superoxide dismutase activities in blood were significantly decreased and were negatively correlated with duration of work., Conclusion: Oxidative stress is an important molecular mechanism for renal dysfunction in mercury exposure, manifested by decreased activities of antioxidant enzymes.

Introduction: Public concern about adverse health effects from mercury exposure from dental amalgams remains a high-profile issue. Patients with nonspecific neuropsychiatric symptoms may incorrectly attribute their complaints to mercury poisoning, and some alternative medical providers diagnose mercury toxicity using nonvalidated tests or without testing at all., Case Report: We report the case of a 37-year-old female who was referred to our outpatient medical toxicology clinic by her family medicine physician after a wellness doctor involved in her care ordered a dimercaptopropanesulfonic acid (DMPS) challenge urine study that revealed an "elevated" mercury level., Discussion: The use of postchelator challenge urine testing to diagnose mercury poisoning has not been validated. Use of such tests may cause falsely elevated urine mercury levels resulting in misdiagnosis of mercury poisoning and unncessary, expensive, and potentially dangerous chelation therapy., Conclusion: Family medicine physicians may encounter patients who are concerned about mercury poisoning after undergoing postchelator challenge urine testing. In patients with a low suspicion for mercury toxicity, reassurance is adequate. In patients with moderate to high suspicion for mercury toxicity, a validated test for mercury, such as a 24-hour urine mercury level, or referral to a medical toxicologist is the most appropriate approach.

Objectives: Due to public concern in Scandinavian countries about the health situation of dental nurses, the Norwegian Ministry of Labor and Social Inclusion initiated a project to look at previous exposure to metallic mercury and its possible effects on dental personnel. The aims of this part of the study were to: (i) describe Norwegian dental personnel's exposure to mercury during the last 50 years, (ii) develop a model for scoring that reflects the cumulative exposure on an individual basis, and (iii) relate the calculated score to earlier measured levels of mercury in urine., Methods: We obtained lists of previous and current dental employees in both the private and public sector and mailed them a questionnaire concerning their working conditions. We received a response from 655 dental nurses and 452 dentists. We also obtained urine mercury levels measured between 1970-1990 for 143 (22%) of the dental nurses and 130 (29%) of the dentists., Results: The results revealed a widespread exposure to mercury in both the individual exposure score and the measured mercury values in urine. For most respondents, however, the level of exposure to mercury seemed to be low. The use of copper amalgam, which is heated before it is applied, is of particular concern as a significant source of mercury exposure in dental personnel., Conclusion: It seems evident that the exposure to mercury among dental personnel varies substantially; this is important to take into account when making exposure assessments for this group of workers.

Background and Objectives: Long-term contact with mercury may induce membranous nephropathy (MN); however, the clinical pathologic features and pathogenesis of mercury-induced MN have not been investigated., Design, Setting, Participants, & Measurements: The present study retrospectively evaluated 11 cases of mercury-induced MN to analyze its causes and its clinical and pathologic features., Results: A total of 10 women and 1 man ages 15 to 45 years were enrolled in the present study. Mercury exposure was caused by mercury-containing pills (five patients), skin lightening cream (four patients), hair-dyeing agents (one patient), and mercury vapor (one patient). The duration of contact with mercury ranged from 2 to 60 months, and the urinary mercury concentrations were 1.5 to 50 times higher than reference values. All patients presented with proteinuria and normal renal function; three had nephrotic syndrome. Light microscopy revealed thickened glomerular basement membrane and mildly proliferative mesangial cells. Acute tubulointerstitial injury occurred in three patients. The immunofluorescence findings showed granular deposits of IgG and C3 along the glomerular capillary wall, mostly accompanied by deposits of C4 and C1q. IgG1 and IgG4 (predominantly IgG1) deposits were observed along the glomerular capillary loops. Nine patients reached complete remission in follow-up after withdrawal from mercury exposure., Conclusions: Deposits of IgG1 subclasses in renal tissues indicated that the pathogenesis of mercury-induced MN differs from that of idiopathic MN. It is important that clinicians are aware that mercury exposure should be considered a possible cause of membranous nephropathy.

Aim: To determine whether patients complaining of oral and medical symptoms perceived to be associated with chronic mercury toxicity have elevated mercury levels in their blood and urine., Methods: The study group in this audit were 56 patients presenting to an oral medicine unit with complaints perceived to be related to chronic mercury toxicity. Their symptoms and co-morbidity were charted and mercury levels in blood and urine were biochemically tested by atomic absorption spectrophotometry., Results: None had elevated mercury levels in blood or urine above the normal threshold level. Subgroup analysis showed subjects with oral lesions, autoimmune disorders and multiple sclerosis had relatively and significantly higher mercury levels within this cohort, but within the threshold values. When tested by multiple logistic regression adjusted for age and gender, mercury levels in blood or urine, numbers of amalgams were not significant for multiple sclerosis or previously diagnosed autoimmune disease., Conclusion: Mercury levels in blood and urine of this cohort of patients with perceived chronic mercury toxicity were within the normal range in accordance with a national laboratory threshold value.

Background: Cardiovascular diseases, including hypertension, are a leading cause of death in developing and developed countries. Mercury can induce hypertension and atherosclerosis in experimental animals and humans. The assessment of the effect of mercury on the occurrence of cardiovascular system disturbances in the population is an essential task. The aim of this study was to assess the association between mercury concentration in urine and the risk of fatal cardiovascular disease during ten coming years., Material and Methods: The study included chemical factory workers who used mercury in the chlorine production., Results: The mean urine concentration of mercury in 154 workers was 4.9 +/- 11.2 microg/g creatinine. The most common disease was hypertension., Conclusions: The cardiovascular risk was higher in workers exposed to small or moderate mercury levels than in workers exposed to mercury vapor in high concentrations. Furthermore, the negative association was observed between mercury exposure and smoking in workers with low urinary excretion of mercury.

Case Report: A 19-year-old male with an unremarkable medical history presented with his father, who requested an evaluation of a pathology specimen from a reported "lump" under the skin in the middle of the son's lower abdomen. The lump had been excised by a surgeon approximately 3 months prior, per parental request. Upon gross inspection, the specimen appeared to contain small metallic droplets. The patient denied self-injection of any metals, including mercury, despite the results of a 24-hour urine heavy-metal screen (without chelation) that revealed an elevated concentration of mercury (87.6 microg/g creatinine; reference range for nonexposed adults: <4 microg/g creatinine). Confirmatory analysis of the tissue sample included gross and microscopic examination, electron microscopy using secondary and backscattered electron imaging modes, and energy dispersive x-ray spectrum analysis of isolated tissue particles. Grossly, the tissue had small silver spherules suggestive of elemental mercury; these droplets were identified histologically with associated foreign body reaction. Numerous smooth, round-to-oval particles scattered randomly throughout the tissue were identified ultrastructurally, which produced an x-ray energy spectrum corresponding to mercury., Discussion: Elemental mercury is liquid at room temperature and may be injected into the body for recreational, psychiatric, and other purposes. Isolated cases of mercury injection following accidents with broken thermometers have been reported, as well as cases of elevated metallothionein concentration following human gingival amalgam tattoos., Conclusion: In cases of surreptitious injection, histology and ultrastructural evidence may be used to confirm the presence of mercury.

An infant presented with failure to thrive and developmental regression. Physical examination revealed an irritable child with swollen, erythematous extremities, and elevated blood pressure. Extensive investigations, including a metabolic work-up and neuroimaging, were unrevealing. Exposure to self-purchased medication was initially denied. The physical signs were suggestive of acrodynia. Mercury poisoning was ultimately established by measuring paired blood and urine mercury levels. On further enquiry, it was revealed that the child had been given a Chinese medicinal product for 4 months. He responded well to a chelating agent. Acrodynia is a childhood disease considered to be of historical interest only, but making a diagnosis of mercury poisoning is rewarding because the response to treatment is good. This case highlights the common misconception that alternative medicines are safe and benign.

Context: Public awareness of methylmercury in fish has caused patients to seek testing for mercury poisoning. In some patients, the diagnosis of mercury poisoning has been made based on urine mercury excretions following oral dosing of meso-dimercaptosuccinic acid (DMSA), a metal chelator. However, studies comparing urine mercury excretion following DMSA in healthy non-fish eaters with healthy fish eaters could not be located., Objectives: To describe urinary mercury excretion before and after DMSA in healthy fish eaters and non-fish eaters, and to determine whether urine mercury excretion after DMSA would rise above baseline levels to a greater extent in fish eaters., Design: A total of 24 healthy physicians were assigned to 1 of 3 groups based on fish consumption: non-fish eaters; 1 to 2 fish servings per week; and 3 or more servings per week. Blood mercury concentrations and 12-hour urine mercury and creatinine excretions were measured before and after oral ingestion of 30 mg of DMSA per kilogram of body weight., Results: A total of 24 subjects completed the study, and 2 subsequently were excluded. No difference in baseline urinary mercury excretion was detected between groups. All groups demonstrated an increase in urinary mercury excretion following DMSA, which was higher in fish eaters (P = .04). Multiple linear regression found that the best predictor of a rise in urine mercury excretion following DMSA challenge was the prechelation blood mercury concentration., Conclusions: In this study of healthy physicians, oral DMSA produced a rise in urine mercury excretion both in non-fish eaters and fish eaters. The increase in chelated mercury excretion was higher in fish eaters. A simple rise in chelated mercury excretion over baseline excretion is not a reliable diagnostic indicator of mercury poisoning.

Objective: To study the early indicators for renal damages in mercury workers and the clinical significance., Methods: Eighty-five mercury workers were divided into 2 experimental groups: the normal & subject-under-surveillance group and the mercury-poisoning group. Sixty-five healthy adults with no mercury exposure history were assigned as the control group. Any subjects with history of renal diseases or concurrent renal diseases were excluded. The results from physical examinations and measurements of HgU, B-Cr, U-Cr, BUN, N-acetyl-beta-D-glucosaminidase (NAG), beta2-microglobulin (beta2-MG), urinary alpha1-microglobulin (alpha1-MG), and retinol-binding protein (RBP) in all the groups were analyzed., Results: The levels of HgU, NAG, alpha1-MG, beta2-MG, and RBP were significantly higher in the experimental groups than in the control group. The levels of NAG, beta2-MG and RBP were significantly higher in the nomal & subject-under-surveillance group than in the control group. However, there was no statistically significant difference between the levels of B-Cr and BUN in the experimental groups and those of the control group., Conclusions: Long-term exposure to mercury can cause renal damages. The level of NAG, alpha1-MG, beta2-MG, and RBP can be used as sensitive indicators for detecting early renal damages caused by mercury.

Two recent studies, from France (Nataf et al., 2006) and the United States (Geier & Geier, 2007), identified atypical urinary porphyrin profiles in children with an autism spectrum disorder (ASD). These profiles serve as an indirect measure of environmental toxicity generally, and mercury (Hg) toxicity specifically, with the latter being a variable proposed as a causal mechanism of ASD (Bernard et al., 2001; Mutter et al., 2005). To examine whether this phenomenon occurred in a sample of Australian children with ASD, an analysis of urinary porphyrin profiles was conducted. A consistent trend in abnormal porphyrin levels was evidenced when data was compared with those previously reported in the literature. The results are suggestive of environmental toxic exposure impairing heme synthesis. Three independent studies from three continents have now demonstrated that porphyrinuria is concomitant with ASD, and that Hg may be a likely xenobiotic to produce porphyrin profiles of this nature.

Porphyrins are derivatives formed in the heme synthesis pathway and porphyrins afford a measure of xenobiotic exposure. The steps in the heme pathway most vulnerable to heavy metal inhibition are uroporphyrin decarboxylase (UROD) and coproporphyrinogen oxidase (CPOX) reactions. Mercury toxicity was associated with elevations in urinary coproporphyrin (cP), pentacarboxyporphyrin (5cxP), and precoproporphyrin (prcP) (also known as keto-isocoproporphyrin) levels. Two cohorts of autistic patients in the United States and France had urine porphyrin levels associated with mercury toxicity. A prospective study of urinary porphyrin testing at LabCorp (United States) and the Laboratoire Philippe Auguste (France) involving 71 autism spectrum disorder (ASD) patients, neurotypical sibling controls, and general population controls was undertaken. ASD patients had significant elevations in urinary levels of cP, 5cxP, and prcP relative to controls, and > 50% of ASD patients had urinary cP levels more than 2 standard deviations above the mean values for neurotypical sibling controls. Significant reductions in urinary 5cxP and cP levels were observed in ASD patients following chelation. A significant correlation was found between urinary porphyrins measured at LabCorp and those measured at the Laboratoire Philippe Auguste on individual ASD patients. The established developmental neurotoxicity attributed to mercury and biochemical/genomic evidence for mercury susceptibility/toxicity in ASDs indicates a causal role for mercury. Urinary porphyrin testing is clinically available, relatively inexpensive, and noninvasive. Porphyrins need to be routinely measured in ASDs to establish if mercury toxicity is a causative factor and to evaluate the effectiveness of chelation therapy.

A 2-year-old girl presented with hypertension, anorexia and vomiting, restlessness, insomnia and acrodynia. Her blood pressure upon arrival was 145/98 mmHg. Ultrasound of the abdomen, CT scan of chest, abdomen and pelvis, and echocardiogram, were normal. Urinary levels of catecholamines were elevated, urine level of mercury was found to be high (33.2 microg/g creatinine), although blood level was normal (>0.5 microg/dl, reference value 0-4 microg/dl). Following a 1-month course of oral treatment with dimercaptosuccinic acid (DMSA) the child's symptoms and signs resolved, and urinary mercury and catecholamines levels normalized. Mercury intoxication should be suspected in a patient with severe hypertension, personality changes and acrodynia. Normal blood levels of mercury do not exclude this diagnosis, and catecholamine levels may serve as a surrogate marker for confirmation of the diagnosis and to evaluate response to treatment.

Objective: We aimed to investigate whether the Prognos device might be a useful tool in the diagnosis of disorders suspected to be due to dental amalgam fillings., Participants and Methods: A diagnostic case-control study was performed in 27 patients who complained about health problems attributed to amalgam (cases), 27 healthy volunteers with amalgam fillings (controls I), and 27 healthy amalgamfree volunteers (controls II). All participants were tested before and after application of 300 mg DMPS (2.3-dimercapto- 1-propanesulfonic acid) with Prognos, a diagnostic device for the energetic measurement of Traditional Chinese Medicine meridians. In addition, mercury was measured in blood, urine, and saliva, and a lymphocyte transformation test (LTT) was performed., Results: Diagnoses derived from the first and second Prognos testing did not agree above chance (Cohen's Kappa = -0.11, 95% confidence interval -0.33 to 0.10; p = 0.30). Agreement for secondary outcome measures was poor, too. Prognos measurements did not differ between cases and controls. Correlations with measurements in urine, blood and saliva were low., Conclusion: In this study Prognos could not be shown to be a useful tool in the diagnosis of disorders suspected to be due to dental amalgam fillings.

Objective: According to a 1997 finding, mercury was available for sale in several Chicago communities for use in spiritual or medicinal practice. Mercury used this way may impact the health of children. The Chicago Department of Public Health (CDPH) and the Centers for Disease Control and Prevention conducted a study to 1) quantify mercury exposure in biological specimens collected from a pediatric clinic or home visit in selected neighborhoods in Chicago, and 2) investigate possible sources of mercury exposure in homes., Methods: An exposure assessment study design was chosen to determine whether children living in Chicago communities that historically sold mercury were exposed to mercury vapor. We enrolled and collected biological samples from 306 children aged 2-10 years. In addition, we enrolled 42 children during a door-to-door survey of community residents. All the urine samples were analyzed for elemental or inorganic mercury. We also analyzed 43 blood samples to assess dietary mercury., Results: Overall geometric mean urine mercury was 0.26 microg/L. Urine mercury levels did not differ among the three clinics or between the various participant groups. We did not find any association between ritualistic mercury use and exposure to mercury., Conclusions: Although pediatric mercury exposure does not appear to be problematic among our study population, mercury remains a potential health threat as long as it is readily available in communities. Healthcare providers should be aware of the potential for mercury exposure. Physicians and patients may call the National Poison Control Centers (1-800-222-1222) for information about diagnosis, testing, and treatment for all types of exposures, including exposure to mercury. Professionals are available 24 hours a day.

In a highly mercury-burdened, small scale gold mining area in the Philippines, spontaneous urine samples were taken from 75 Hg intoxicated volunteers before (U1), and 2-3 hours after (U2) the oral application of 200 mg DMPS (2,3-Dimercapto-1-propanesulfonic acid, Dimaval). In the urine samples, the concentrations of organic and inorganic bound mercury were determined separately by CV-AAS. In U1, median concentrations of 15.7 microg inorganic Hg/g crea. and 2.2 microg organic Hg/g crea. were found. In U2, these values increased to 262 for inorganic Hg and 14.5 for organic Hg. Maximum concentrations (microg/g crea.) as high as 7,593 for inorganic Hg and 2,011 for organic Hg were observed after DMPS. The mean (median) increasing factor (U2/U1) was 16.0 for inorganic Hg and 5.1 for organic Hg. There was a trend that females responded better to DMPS than males. It was concluded that DMPS increases the renal excretion of organic bound Hg as it does for inorganic Hg, but to a lesser extent.

The concentrations of albumin, IgG, transferrin, retinol binding protein (RBP), alpha-1-microglobulin (alpha-1-m) and beta-2-microglobulin (beta-2-m) were determined in urine of 83 males 21 to 60 years old (Mean = 41.2 +/- SD = 10.7) with a history of occupational exposure to metallic mercury vapours from 7 months to 37 years (Mean=16.3 +/- 10.9) and in 30 males without this exposure by using the nephelometry (Behring's antibodies, references and controls). The weighted mean of mercury concentrations in air was from 0.028 to 0.037 mg m(-3). The urinary level of mercury was determined by using the atomic absorption spectrometer Coleman Mercury Analyzer Mas-50, Perkin-Elmer USA, in alpha=253.7nm. The detection limit of the analytical procedure of determination of mercury in urine was 10 microg/dm3 and in blood was 4 microg Hg/dm3. Workers were divided into three groups depending on the duration of exposure: I/. 30 males with a short history of exposure to Hg0 (7 months to 9 years) (4.2 +/- 2.8), II/. 18 males exposed from 10 to 20 years (14.5 +/- 3.3) and III/. 35 males with a history of long exposure (21 to 37 years) (27.5 +/- 4.0) following three groups were divided depending on the degree of exposure: 1/. 32 males with concentrations of mercury in urine < 50 microg Hg/ dm3 (30.5 +/- 10.7) aged 26 to 59 years (45.5 +/- 8.0) and exposed to Hg0 from 7 months to 37 years (18.1 +/- 10.8); 2/. 41 males with concentrations of mercury in urine 51 to 150 microg Hg/dm3 (86.1 +/- 24.3) aged 21 to 60 years (39.8 +/- 10.8) and exposed to Hg0 from 7 months to 35 years (15.9 +/- 10.8) and group 3/. 32 males with concentrations of mercury in urine 151 to 260 microg Hg/dm3 (211.4 +/- 37.1) aged 21 to 56 years (35.5 +/- 13.1) and exposed to Hg0 from 7 months to 30 years (9.1 +/- 8.8). Occupational exposure to mercury vapours influenced urine mercury concentration and urine excretion of determined proteins: albumin, IgG, transferrin, alpha-1-microglubulin and beta-2-microglubulin. In the group of workers exposed to mercury vapours from 7 months to 9 years, statistically significance elevation of alpha-1-m and beta-2-m [alpha-1-m by 67.5% (p<0.05) and beta-2-m by 66.7%] according to the control group was observed. Albumin urine concentrations was highest in the group of exposed workers with mean urine mercury concentration > 150 microg/dm3, 2-times higher (p<0.05) than in the control group as well as in the group workers exposed to mercury with mean urine mercury concentrations 51 to 150 microg/dm3 (p<0.05) and more than 3-times higher than in the workers with mean urine mercury concentrations < or = 50 microg/ dm3. Mean IgG and transferrin urine concentrations were higher [IgG 2.6-times higher (p<0.05), transferrin 7.5-times higher (p<0.05) according to the control group] in the group of workers with urine mercury concentrations > 150 microg/dm3. Mean alpha-1-m and beta-2-m urine concentrations were highest in group of workers with urine mercury concentration > 150 microg/dm3 [alpha-1-m by 82% (p<0.05) and beta-2-m by 289% (p<0.01)]. Moreover, a positive correlation between mercury urine concentration and alpha-1-m (r=0,33), as well as between mercury urine concentration and albumin (r=0,31) and IgG (r=0.30) also were observed. Values of "r" between mercury urine concentration and albumine (r=0.46), IgG (r=0.46) and transferrin (r=0.42) were highest in group of workers exposed to mercury vapours from 10 to 20 years. Albumin, transferrin and IgG urine concentrations, as well as alpha-1-m and beta-2-m urine concentrations were statistically significantly higher in the group of workers with > 150 microg Hg/dM3 urine concentration. In conclusion, determination of urine proteins, as a markers of early subclinical renal damage may be useful in monitoring occupational exposure to mercury vapours, especially in the group of workers with higher values of urine mercury concentrations.

Methylmercury is an environmental toxicant that has been shown to cause neurologic damage in both children and adults if ingested in sufficiently high quantities. Poisoning outbreaks in Japan and Iraq have revealed serious effects on developing fetuses at levels far below those that produced clinical signs or symptoms in the mothers. Therefore, health guidance values for methylmercury, such as the chronic oral minimal risk level (MRL) of the Agency for Toxic Substances and Disease Registry, have been set by governmental agencies at levels that would protect fetuses. Since adults are less sensitive than fetuses, chronic intakes within an order of magnitude of the MRL generally have been considered to represent no health risk to otherwise healthy adults. The present report of suspected mercury intoxication in a 53-year-old female suggests that some individuals might be susceptible to adverse health impacts of methylmercury at intakes just 7 to 15 times the MRL.

The effects of mercury exposure are determined by: (a) chemical form, (b) route of exposure, (c) dose, and (d) patient factors. Patient factors include age, genetics, environmental aspects, and nutritional status, and are responsible for different individual responses to similar doses. When blood and urine are collected to evaluate exposure, the results are influenced by (a) specimen collection, (b) analysis, and (c) the time elapsed from exposure. Interpretation is influenced by the patient's symptoms and is facilitated by comparison to published reports. The ranges reported in the literature are broad, with elevations as high as 16,000 microg/L in blood and 11,000 microg/L in urine. Interpretation is relatively straightforward when the results are massively elevated, but becomes increasingly difficult as concentrations approach the population norms (blood and urine mercury < 10-20 microg/L). Interpretation can be aided by biological markers (eg, urine porphyrins, beta2-microglobulin, and N-acetyl-beta-D-glucosaminidase).

Some people living in Japan have traditionally eaten the internal organs of small cetaceans (toothed whales and dolphins), and a mixed package of boiled liver, kidney, lung, and so on is still marketed for human consumption. Recently, we reported that these organs are highly contaminated with mercury. In this study, we investigated the absorption, distribution, excretion, and biochemical parameters in serum and urine after a single oral administration of boiled whale liver containing 1980 microg/g of total mercury and 23.5 microg/g of methyl mercury to rats (0.2 g boiled liver/100 g rat). The single administration of the boiled liver resulted in marked increases of the mercury concentration in the rat kidney, urinary volume, and the urinary excretion of N-acetyl-beta-D-glucosanidase, albumin, and sodium, suggesting the renal toxicity caused by inorganic mercury. Furthermore, the administration increased lactate dehydrogenase activity and creatinine, potassium, and phosphorus concentrations in serum. About 95% of total mercury dose was excreted in feces and less than 0.05% was excreted in the urine. Thus, the absorption rate of mercury from the boiled whale liver appears to be about 5% or slightly higher. These data indicate that the human consumption of boiled whale liver may cause acute intoxication by the contaminated inorganic mercury.

Skin whitening cream from developing countries is a recognized source of chronic mercury poisoning. The authors report on a 34-year-old Indonesian domestic helper who presented with nephrotic syndrome secondary to membranous nephropathy. It was subsequently found that she used a skin whitening cream regularly that was found to contain a mercury level of almost 2,000 times above the allowable limit. Her blood and urinary mercury levels were both grossly elevated. Her symptoms improved after she stopped using the cream. However, she returned to her home country before chelating therapy could be arranged. Because mercury-containing skin products are still widely available in developing countries, the use of these products should be considered a possible cause of membranous nephropathy in immigrants from those countries., (Copyright 2003 by the National Kidney Foundation, Inc.)

The iso-enzyme profiles of urinary N-acetyl-beta-D-glucosoaminidase (NAG) were studied in the workers from a chloro-alkaline electrolysis plant that had been continuously exposed to elemental mercury. The same workers then had a work break of four months and were later re-exposed to mercury for another five months. The activities of urinary NAG in workers exposed to mercury before and after the work break and in the control group were 2.09 +/- 1.03 IU/L; 0.90 +/- 0.52 IU/L and 1.13 +/- 0.35 IU/L, respectively. The fraction of the dominant A form activity in the total activity, in the workers exposed to mercury after a work break (85.31 +/- 5.32%), was almost equal to the fraction of A in the control group (84.64 +/- 2.75%). The percent fraction of A forms (A and A2) during continuous exposure was almost equal to the sum of the fractions A and A2 in the control group and for exposure after the work break. The fraction of the B form activity in the total activity during exposure to elemental mercury for five months after the work break (7.41 +/- 3.45%) was lower (P < 0.1) than the fraction of the B form in the control group (8.62 +/- 2.19%). The decrease in the fraction of the B form compared with the control group was more significant (P < 0.001) in the case of continuously exposed workers (5.25 +/- 2.55%). Beside the major A and B iso-enzymes of NAG, the A2 form was also isolated, and its fraction in the control group (6.73 +/- 2.15%) was not negligible. For workers exposed to mercury for five months, it was 7.28 +/- 3.52%. It is concluded that mercury affected the increased exocytosis of iso-enzyme A and the inhibition of B iso-enzyme of NAG. The increase in activity of urinary NAG in subjects exposed to mercury was a consequence of the increased excretion of A form. It was established also that the four months work break was sufficient for the repair of renal damages that occurred during continuous exposure, and which were monitored by the activity of NAG. Thus, the effects of mercury seem to have been reversible.

Exposure to mercury can cause serious multiorgan damage affecting the central nervous system, kidneys, liver, lungs, spleen, bone marrow, and skin. At the end of the summer of 1999, the accidental leakage of 4 liters of mercury from a container into the waterway canals resulted in mass exposure to elemental mercury among the residents of a building block of a residential area of the city of Shiraz, in the south of Iran. One hundred and eleven individuals who experienced exposure to elemental mercury were investigated. Twenty-four-hour measurement of the urine mercury level-revealed a toxic level of more than 20 microg/L in 6 children and 3 adults (including a pregnant woman). Despite normal physical and laboratory (CBC, renal and liver function tests, and urinalysis) findings, dimercaprol was prescribed. One month later during the course of the follow-up the urine mercury level in 6 patients, including the pregnant woman from the same family, was found to be again at a toxic level. The pregnant mother from the same family aborted her fetus; however, due to the lack of equipment for measuring the serum mercury level, it was not possible to confirm the relation between the mercury toxicity and the abortion. This family had kept mercury in their kitchen against health workers' instructions. The attractive physical and chemical properties of mercury could explain the continuity of exposure and poisoning in these 6 cases. It is concluded that prophylactic therapy in the presence of toxic levels of mercury, despite the presence of an asymptomatic state in exposed residents, is effective in preventing the development of signs and symptoms, though instruction of high-risk cases is the best way to combat it.

Changes in urinary porphyrin excretion patterns (porphyrin profiles) during prolonged mercury exposure are attributable to mercury accumulation in the kidney and to consequent effects of Hg2+ on renal porphyrin metabolism. In the present study, we evaluated the quantitative relationship of urinary porphyrin concentrations to mobilizable renal mercury content, using the metal chelator 2,3-dimercapto-1-propanesulfonic acid (DMPS) to modulate kidney mercury levels. Rats exposed to methylmercury hydroxide (MMH) at 10 ppm in drinking water for 6 weeks were treated with up to 3 consecutive doses of DMPS (100mg/kg, ip) at 72-h intervals. Consistent with previous findings, the concentrations of pentacarboxyl- (5-) and copro- (4-) porphyrins and of an atypical porphyrin specific to mercury exposure, precoproporphyrin, were significantly elevated in urine of MMH-exposed rats, compared with that of rats exposed to distilled water (dH2O) for the same period. Consecutive DMPS treatments of MMH-exposed rats significantly decreased kidney concentrations of total, as well as Hg2+ and CH3Hg+ species, and promoted increased urinary mercury excretion. Concomitantly, DMPS treatment decreased both kidney and urinary porphyrin concentrations, consistent with depletion of renal mercury levels. Regression analyses demonstrated a high correlation (r approximately 0.9) between prechelation urinary porphyrins and postchelation urinary mercury levels and also between prechelation urinary porphyrins and prechelation kidney mercury concentrations. These findings demonstrate that urinary porphyrin concentrations relate quantitatively to DMPS-mobilizable mercury in the kidney and, therefore, serve as a biochemical measure of renal mercury content.

Tremor is being increasingly evaluated by quantitative computer-based systems to differentiate its causes. In this study, a group of mercury-exposed workers were assessed to determine whether tremor characteristics differed by exposure level. Workers were classified into two groups: those with an average urine mercury concentration below the American Conference of Government Industrial Hygienist Biological Exposure Index of 35 micrograms/g creatinine, and those with an average urine mercury concentration above the Biological Exposure Index. Tremor characteristics (including intensity, harmonic index, center frequency, standard deviation of the center frequency, and tremor index) were measured and recorded with a computer-based tremor system. Sixteen of 17 workers who were potentially exposed to mercury participated in the study. Three workers had a mean urine mercury concentration of 27.0 micrograms/g-creatinine and were assigned to the low-exposure group, and 13 workers had a mean urine mercury concentration of 200.2 micrograms/g-creatinine and were assigned to the high-exposure group. There was a statistically significant difference in the tremor index (which compiles five individual tremor parameters into a single value) between the two groups (P = 0.04; Wilcoxon's rank sum test). Other tremor characteristics did not differ significantly between the groups. Tremor index may be more useful than measures of individual tremor parameters in differentiating normal from subclinical pathological tremors among groups of workers with chronic mercury exposure.

Objectives: Dental amalgam is the major source of inorganic mercury exposure in the general population. Dental amalgam contains approximately 50% mercury, which is a toxic element. Since children are more at risk for mercury toxicity, we aimed to study prospectively the effects of amalgam filling on urinary mercury excretion in 5- to 7-year-old children., Methods: Children admitted to the Pedodontics Department with no previous amalgam filling, and in a good state of health with one or more carious posterior teeth, were selected. All fillings were placed in one session for each child using Sina (Iran) amalgam powder and Degussa (Germany) mercury, which were mixed by an automated electric amalgamator (Dentomate 3, Germany). Urinary mercury concentrations were estimated before and 9-12 days after amalgam filling by atomic absorption using the mercuric hydride system., Results: Forty-three children (20 male, 23 female) aged 5.95+/-0.92 years and weighing 19.09+/-3.10 kg were studied. Urinary mercury concentrations before and after amalgam filling were 3.83+/-2.45 and 5.14+/-3.14 microg/L, respectively (p = 0.001). There were no statistically significant correlations between the urinary mercury concentrations and any other variables, including the number and surfaces of filled teeth, weight, age, and sex., Conclusion: Although there were highly significant increases in urinary mercury concentrations after amalgam filling, no significant correlation was found between the urinary mercury concentration and the amounts of filled amalgam. Additional investigation is required concerning the effects of mercury release from amalgam.

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.

The chelating agent 2,3 dimercaptopropane-1-sulfonate (DMPS) has been used in a mercury mobilization test for diagnoses in illnesses allegedly associated with the presence of amalgam restorations. DMPS is an accepted antidote to heavy metal poisoning. The aim of the present study was to evaluate the diagnostic value of DMPS in patients with symptoms self-related to their amalgam fillings. The subjects consisted of four groups: 19 healthy controls without amalgam experience; 21 healthy controls with amalgam fillings; 20 patients who claimed symptoms of "mercury poisoning" from dental amalgam; and 20 patients who had amalgam fillings removed because of such symptoms. DMPS (2 mg/kg body weight) was injected intravenously, and urine was collected prior to the injection, 30 and 120 min after the injection, and throughout the next 22 hrs. The samples were analyzed for total mercury by cold vapor atomic absorption spectrophotometry. The total median amounts of mercury excreted over 24 hrs for those with complaints allegedly associated with amalgam and for the healthy controls with amalgam fillings were similar. Persons with amalgam fillings excreted about three times more mercury than those without. The controls, who had never had amalgam fillings, and the subjects who had had their fillings removed excreted median amounts of 8.5 microg and 7.2 microg mercury, respectively. The present DMPS challenge test did not differentiate between patients with or those without complaints self-related to their amalgam fillings but did confirm the higher mercury values in patients with dental amalgam.

We investigated discordant urinary mercury testing results from 2 patients with potential mercury exposures. Two patients had mercury levels of 634 and > 1,000 micrograms/L respectively. Although repeat 24 h urine mercury levels were elevated, spot urines were negative. Investigation revealed that technical HCl with high mercury content had been added to the 24 h urine collection containers. Subsequently, 20 hospitals were contacted to determine their heavy metals testing procedure and to analyze the acid used for mercury. Most hospitals contacted used acid in the preparation of their urine heavy metal collection containers. Of 13 HCl samples tested, 5 had low levels of mercury and 1 had heavy mercury content. Acid added to heavy metal collection containers should be of high purity grade to avoid mercury contamination of samples.

The authors report on atomic absorption method determining mercury in urine. Being sensitive, with lower determination threshold of 10 nmole/l and correctness of 95.5%, the method was tested on children living in two districts of Moscow suburb.