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Study of The Role of Mercury Poisoning in Rheumatoid Arthritis Patients and Its Relation with Zinc and Copper Levels
Abstract
Determinations of trace elements in human tissues and fluids were used to obtain information on nutritional status for diagnosis of diseases, indication of systemic intoxication, and to obtain information on environmental toxic exposure. The present study aimed to evaluate the role of mercury intoxication on rheumatoid arthritis patients living in Dakahlia governorate and to investigate the interaction between zinc and copper from one side and mercury from the other side and their relation to disease activity. The present study included 32 patients (test group) suffering from rheumatoid arthritis (RA) attending the rheumatology and rehabilitation out patient clinic, Mansoura university hospital and 30 healthy volunteers (control group) matched according to age, sex, residence and occupation. All patients of test group were evaluated by Disease Activity Score (DAS 28) and accordingly, the test group included 10 patients (31.3%) were mild and moderate DAS and 22 patients (68.7 %) were high DAS (6 patients were with dental filling amalgam and 16 were free from amalgam). Blood mercury, zinc and copper levels were determined using atomic absorption spectrophotometer. The present study observed significant increase in blood mercury level while, blood zinc level was significantly decreased in addition, blood copper level was found to be significantly decreased in test group when compared with control group. As regards the presence of dental amalgam, the present results revealed that the highest mercury levels (13.13±0.58 µg/dl), the lowest zinc level (108.28±7.89 µg/dl) and relatively lowest copper levels (7.26±0.73 µg/dl) were observed in severe RA activity score patient with dental filling amalgam. There were a significant negative correlation between blood mercury and zinc levels and DAS while, there was non-significant negative correlation was found between blood copper level and DAS. In conclusion, the current study provided some support for the hypothesis that dietary intake or inhalation of toxic elements (mercury), most probably through dental filling amalgam, may increase the risk of rheumatoid arthritis.
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Post Minamata incident there has been awareness about mercury toxicity even among the general public. Previous researches contributed a vast amount of data regarding acute mercury exposure, but gradually information about the low dose [Ninomiya, T., Ohmori, H., Hashimoto, K., Tsuruta, K., Ekino, S., 1995. Expansion of methylmercury poisoning outside minamata: an epidemiological study on chronic methylmercury poisoninig outside of Minamata. Environ. Res. 70 (1) 47-50; Lebel, J., Mergler, D., Lucotte, M., Amorim, M., Dolbec, J., Miranda, D., Arantes, G., Rheault, I., Pichet, P., 1996. Evidence of early nervous system dysfunction in Amazonian populations exposed to low-levels of methylmercury. Neurotoxicology 17 (1) 157-167] of mercury toxicity has been trickling in. With mercury contaminating rain-, ground- and sea-water no one is safe. Polluted water leads to mercury laced fish, meat and vegetable. In aquatic environments, inorganic mercury is microbiologically transformed into lipophilic organic compound 'methylmercury'. This transformation makes mercury more prone to biomagnification in food chains. Consequently, populations with traditionally high dietary intake of food originating from fresh or marine environment have highest dietary exposure to mercury. Extensive research done on locals across the globe have already established this, persons who routinely consume fish or a particular species of fish are at an increased risk of methylmercury poisoning. The easy access of the toxicant to man through multiple pathways air, water, food, cosmetic products and even vaccines increase the exposure. Foetus and children are more susceptible towards mercury toxicity. Mothers consuming diet containing mercury pass the toxicant to foetus and to infants through breast milk. Decreased performance in areas of motor function and memory has been reported among children exposed to presumably safe mercury levels. Similarly, disruption of attention, fine motor function and verbal memory was also found in adults on exposure to low mercury levels. It is an occupational hazard for dental staff, chloralkali factory workers and goldminers, etc. Mercury has been found to be a causative agent of various sorts of disorders, including neurological, nephrological, immunological, cardiac, motor, reproductive and even genetic. Recently heavy metal mediated toxicity has been linked to diseases like Alzeihemer's, Parkinson's, Autism, Lupus, Amyotrophic lateral sclerosis, etc. Besides this, it poses danger to wildlife. Therefore, it becomes imperative to spread the information regarding the threat of mercury exposure amongst the scientists and masses.
The aim of the study was to evaluate zinc levels in three biological compartments (serum, erythrocytes and hair) in patients with rheumatoid arthritis (RA) as compared to healthy individuals. Zinc levels in serum, erythrocytes and hair (in 74 patients with RA and 30 healthy individuals) were assessed by atomic absorption spectroscopy. The mean hair zinc content was significantly lower in RA patients as compared to healthy individuals (p < 0.001). Moreover, a positive correlation was observed in the RA patient group between the erythrocyte zinc levels and the prednisone dose (r
s = 0.48, p < 0.05), and a negative correlation was found in this population between the serum zinc levels and disease duration (r
s = −0.42, p < 0.0006). In conclusion, it seems that hair may be a useful complementary study material for evaluating “zinc status” in rheumatoid arthritis patients.
We have previously observed that Brown Norway (BN) rats display a relative resistance to experimental Chlamydia-induced arthritis. In the present study, we examine an environmental toxin, mercuric chloride (HgCl2), as a modulator of this innate resistance to arthritis.
To assess the effect of the heavy metal exposure, one group of rats received two subcutaneous injections of HgCl2 (1 mg/kg) 48 hours apart. Seven days later, the animals received the intra-articular injection of synoviocyte-packaged Chlamydia.
Histopathology revealed that BN rats receiving only Chlamydia had a minimal cellular infiltration in the joint, which was predominantly mononuclear in character. In contrast, mercury-exposed rats had a marked exacerbation of the histopathological severity of the arthritis, and the infiltration was predominantly neutrophilic. Mercury exposure was also associated with marked enhancement in IgE levels and an alteration in IgG2a/IgG1 ratio, reflecting a Th2 shift. The local cytokine profile in the joint was markedly altered after mercury exposure, with a suppression of tumour necrosis factor-alpha and interferon-gamma but an enhancement of vascular endothelial growth factor. This was associated with decreased host clearance capacity reflected in enhanced bacterial load in both the spleen and the joint and was accompanied by enhanced detection of microbial antigens in the synovial tissues by immunohistological staining.
Genetically defined cytokine production in the joint defines the severity of reactive arthritis by dictating the local clearance of the pathogen. This interplay can be altered dramatically by heavy metal exposure, which results in suppression of protective cytokines in the microenvironment of the joint.
Considerable attention has been drawn to the environmental levels of mercury, arsenic, selenium and antimony in the last decade. Legislative and environmental pressure has forced levels to be lowered and this has created an additional burden for analytical chemists. Not only does an analysis have to reach lower detection levels, but it also has to be seen to be correct. Atomic fluorescence detection, especially when coupled to vapour generation techniques, offers both sensitivity and specificity.
Developments in the design of specified atomic fluorescence detectors for mercury, for the hydride-forming elements and also for cadmium, are described in this paper. Each of these systems is capable of analysing samples in the part per trillion (ppt) range reliably and economically. Several analytical applications are described.
An investigation of clinical and laboratory variables which might form the basis for judging disease activity in clinical practice was made by six rheumatologists in a prospective study of up to three years' duration of 113 patients with early rheumatoid arthritis. Decisions to start treatment with slow acting antirheumatic drugs were equated with moments of high disease activity. If treatment with slow acting antirheumatic drugs was not started or if the slow acting antirheumatic drug remained unchanged for at least one year or if treatment was stopped because of disease remission, this was equated with periods of low disease activity. Two groups, one with high and one with low disease activity according to the above criteria, were formed. Factor analysis was performed to enable easy handling of the large number of clinical and laboratory variables without loss of information; this resulted in five factors. Next, discriminant analysis was done to determine to what extent each factor contributed to discrimination between the two groups of differing disease activity. Finally, a multiple regression analysis was carried out to determine which laboratory and clinical variables underlie the factors of the discriminant function, resulting in a 'disease activity score'. This score consisted of the following variables: Ritchie index, swollen joints, erythrocyte sedimentation rate, and general health, in declining importance. The rheumatologists' decisions to prescribe slow acting antirheumatic drugs, or not, were mainly based on articular symptoms.
Amalgam, which has been in use in dentistry for 150 years, consists of 50 % elemental mercury and a mixture of silver, tin, copper and zinc. Minute amounts of mercury vapour are released continuously from amalgam. Amalgam contributes substantially to human mercury load. Mercury accumulates in some organs, particularly in the brain, where it can bind to protein more tightly than other heavy metals (e. g. lead, cadmium). Therefore, the elimination half time is assumed to be up to 1 - 18 years in the brain and bones. Mercury is assumed to be one of the most toxic non-radioactive elements. There are pointers to show that mercury vapour is more neurotoxic than methyl-mercury in fish. Review of recent literature suggests that mercury from dental amalgam may lead to nephrotoxicity, neurobehavioural changes, autoimmunity, oxidative stress, autism, skin and mucosa alterations or non-specific symptoms and complaints. The development of Alzheimer's disease or multiple sclerosis has also been linked to low-dose mercury exposure. There may be individual genetical or acquired susceptibilities for negative effects from dental amalgam. Mercury levels in the blood, urine or other biomarkers do not reflect the mercury load in critical organs. Some studies regarding dental amalgam reveal substantial methodical flaws. Removal of dental amalgam leads to permanent improvement of various chronic complaints in a relevant number of patients in various trials. Summing up, available data suggests that dental amalgam is an unsuitable material for medical, occupational and ecological reasons.
The aim of the present study was to measure the changes in serum selenium, zinc, and copper in patients being treated for rheumatoid arthritis. Thirty-two patients and 52 healthy controls were included in the study. The copper level was higher and those of selenium and zinc were lower in the patients relative to controls. Treatment with methotrexate elevated the zinc levels, but not zinc and selenium. Treatments with salazopyrin, corticosteroids, chloroquine, and non-steroidal anti-inflammatory drugs did not change the levels of any of the elements studied. The decrease in zinc and selenium levels and elevation in copper levels observed in the patients probably resulted from the defense response of organism and are mediated by inflammatory-like substances.
Female SJL/N mice were given either 5.0, 2.5, 1.25, or 0.625 mg mercuric chloride per liter drinking water (ppm HgCl2). Serum antinucleolar antibodies (ANuA) of the IgG class were seen in mice given at least 1.25 ppm HgCl2 for 10 weeks, a dose which corresponded to a mean renal mercury concentration, as measured with atomic absorption spectrophotometry, of 2.4 +/- 0.43 microgram Hg/g wet weight (ppm Hg; means +/- 1 SD). At a dose of 5.0 ppm HgCl2 all mice showed IgG ANuA with a mean titer of 1:846 and a mean renal mercury concentration of 14.8 +/- 3.9 ppm. Significantly increased titers of granular IgG deposits, corresponding to immune-complex (IC) deposits, developed in the renal mesangium of mice given 5.0 ppm HgCl2. Mice with heavy mesangial IgG deposits showed a mild glomerular endocapillary cell proliferation and widening of the mesangium. Renal vessel wall IgG deposits were found only in mice given 5.0 ppm HgCl2, whereas such deposits were seen in splenic and cardiac arteries of mice receiving 1.25 ppm or more of HgCl2. The renal and splenic mercury concentration was significantly increased in all groups of mercuric chloride-exposed mice and correlated with the dose. We conclude that 10 weeks peroral treatment with mercuric chloride in drinking water is able to elicit autoimmunity and IC disease in genetically homogeneous, mercury-sensitive mice at a body burden similar to that reported in some occupationally exposed humans.
Fluoride is known to have biological effects on bone cells as well as physicochemical effects on bone crystals. This review concentrates on the latter. Fluoride increases the stability of the apatite lattice and decreases the solubility of the apatite crystals. In bone mineral, this ion has been shown to affect bone crystal structure by increasing crystallinity and reducing specific surface area. These changes in turn lead to changes in the chemistry of bone mineral. Bone mineral deposition is delayed by fluoride. This ion does not diffuse into bone already formed, but is incorporated during mineralization. Subsequently fluoride tends to accumulate in the most highly mineralized bone. Bone treated with fluoride has been shown to be more resistant to acid dissolution than normal bone, which would explain the reduced rate of resorption of fluoridated bone. The distribution of fluoride in bone is not uniform, but its net effect is to increase bone mineral density probably by an increased packing of bone crystals. Finally, there is a debate as to whether fluoride produces a bone of different quality. Whether these changes in the quality of bone will prove to be helpful or harmful remain to be determined.
Concentrations of Pb, Hg, Cd, Zn, Ni, Cu, and Mn in the hair of subjects from the industrial city of Port Arthur, Texas were determined. Values were compared to published values of subjects living in the eastern United States. Comparable results were obtained; however, higher lead values were found for Port Arthur. There were several subjects containing high lead and/or mercury. These appear to be isolated cases. Copper and zinc values appear to be related to hair pigmentation.
The development and validation of Modified Disease Activity Scores (DAS) that include different 28-joint counts.
These scores were developed by canonical discriminant analyses and validated for criterion, correlational, and construct validity. The influence of disease duration on the composition of the DAS was also investigated.
No influence of disease duration was found. The Modified DAS that included 28-joint counts were able to discriminate between high and low disease activity (as indicated by clinical decisions of rheumatologists).
The Modified DAS are as valid as disease activity scores that include more comprehensive joint counts.
Autoimmune diseases may be induced by physical and/or chemical environmental factors. A review of the available literature on mercuric chloride, iodine, silicone, anilides, L-tryptophan, vinyl chloride, and canavanine suggests three general mechanisms by which they may induce disease. First, oxidative damage probably is a frequent process involved in disease induction and pathogenesis. Second, certain compounds also may generate antigen-specific immune responses that could then cross-react with self-tissues. Other xenobiotics might bind to self-tissues and increase self-tissue immunogenicity. Third, physical and chemical agents may also modulate the immune system. Finally, in response to controversies surrounding the influence of human activities on global climate changes, the immunosuppressive effects of ozone and ultraviolet radiation are discussed.
There are conflicting reports whether patients with rheumatoid arthritis (RA) are at a higher risk for periodontal disease (PD). Analogous mechanisms of tissue destruction have been reported for both diseases. This cross-sectional study should quantify PD in patients with longstanding RA and examine a possible association between the two diseases. It should also be investigated whether PD in RA patients could be the result of reduced functional capacity or be amplified by concomitant medical treatment. 50 RA patients were matched for age, sex, smoking and oral hygiene with 101 healthy controls. Data on the medication over the last three years was obtained by questionnaire. Among the rheumatological parameters recorded were a 28-joint-count, C-reactive protein (CRP), grip strength testing, upper extremity function (Keitel Index) and the Larsen-score of radiological joint destruction. The oral examination included the recording of individual oral hygiene measures and sicca symptoms, a modified Approximal Plaque- and Sulcus-Bleeding-Index (SBI), probing depths and clinical attachment loss and the Community Periodontal Index of Treatment Needs. The mean duration of RA was 13 (+/- 7.9) years. RA patients under treatment with disease modifying antirheumatic drugs (DMARDs, n = 46; 92%), corticosteroids (n = 38; 76%) and non steroidal antirheumatic drugs (NSAIDs, n = 43; 86%) had a higher rate of gingival bleeding (+ 50%), probing depth (+ 26%), clinical attachment loss (+ 173%) and number of missing teeth (+ 29%) compared with controls. While no correlation between the rheumatological variables (radiological destruction, functional capacity, grip strength) and the periodontal measurements (SBI, probing depth, clinical attachment loss) could be demonstrated, a positive correlation was observed between the CRP and the periodontal attachment loss (r = 0.32; p <0.05). In spite of a strong correlation between the duration of DMARD- and cortisone-medication and the Larsen-score (r = 0.48 and 0.64; p = 0.0005 and 0.0001, rsp.), no correlation between the duration of pharmacotherapy and the periodontal parameters could be established. Patients with long-term active RA present a substantially higher degree of PD including loss of teeth compared with controls. Functional impairment of the upper extremity might amplify present PD. The longterm use of NSAIDs, corticosteroids and DMARDs shows no connection with the severe PD observed in these patients. Oral hygiene amplifies PD severity and treatment need. Intensive prophylactic measures are required to prevent or reduce the damage of the periodontal tissues in RA patients.
In past years, consensus has been reached on the assessment of rheumatoid arthritis in clinical trials. Next to a core set of disease activity variables, response criteria have been developed and validated. These criteria are, however, of limited value in daily clinical practice. In this situation, emphasis should be paid to accurate measurement of disease activity on a continuous scale using the lowest possible number of core set variables. Different studies have shown that the DAS28 is a valuable instrument for this purpose. Many factors have been identified to possess a prognostic value; however, the IgM rheumatoid factor is still the only one which is of any importance in daily clinical practice.
Potentially damaging species (reactive oxygen, nitrogen and chlorine species) arise as by-products of metabolism and as physiological mediators and signalling molecules. Levels of these species are controlled by the antioxidant defence system. Several components of this system are micronutrients (e.g. vitamins C and E) or are dependent upon dietary micronutrients (e.g. CuZn and Mn superoxide dismutase). The antioxidant defences act as a coordinated system where deficiencies in one component may affect the efficiency of the others. Oxidative stress may be an important factor in infection if micronutrients are deficient.
Mercury is a toxic metal that is widely used in everyday life. It has organic and inorganic forms that are both toxic. As acute mercury poisoning is uncommon, diagnosis is difficult if the exposure is not manifest. It has usually a slow onset and non-specific symptoms. In this paper we report a patient who developed polyarthritis after mercury exposure.
Mercury is well known to adversely affect the immune system; however, little is known regarding its molecular mechanisms. Macrophages are major producers of nitric oxide (NO) and this signaling molecule is important in the regulation of immune responses. The present study was designed to determine the impact of mercury on NO and cytokine production and to investigate the signaling pathways involved. The murine macrophage cell line J774A.1 was used to study the effects of low-dose inorganic mercury on the production of NO and proinflammatory cytokines. Cells were treated with mercury in the presence or absence of lipopolysaccharide (LPS). Mercury (5-20 microM) dose-dependently decreased the production of NO in LPS-stimulated cells. Concomitant decreases in the expression of inducible nitric oxide synthase (iNOS) mRNA and protein were detected. Treatment of J774A.1 cells with mercury alone did not affect the production of NO nor the expression of iNOS mRNA or protein. Interestingly, mercury alone stimulated the expression of tumor necrosis factor alpha (TNFalpha), and increased LPS-induced TNFalpha and interleukin-6 mRNA expression. Mercury inhibited LPS-induced nuclear translocation of nuclear factor kappaB (NF-kappaB) but had no effect alone. In contrast, mercury activated p38 mitogen-activated protein kinase (p38 MAPK) and additively increased LPS-induced p38 MAPK phosphorylation. These results indicate that mercury suppresses NO synthesis by inhibition of the NF-kappaB pathway and modulates cytokine expression by p38 MAPK activation in J774A.1 macrophage cells.
Reactive oxygen species, such as superoxide radicals, are thought to underlie the pathogenesis of various diseases. Almost 3 to 10% of the oxygen utilized by tissues is converted to its reactive intermediates, which impair the functioning of cells and tissues. Superoxide dismutase (SOD) catalyzes the conversion of single electron reduced species of molecular oxygen to hydrogen peroxide and oxygen. There are several classes of SOD that differ in their metal binding ability, distribution in different cell compartments, and sensitivity to various reagents. Among these, Cu, Zn superoxide dismutase (SOD1) is widely distributed and comprises 90% of the total SOD. This ubiquitous enzyme, which requires Cu and Zn for its activity, has great physiological significance and therapeutic potential. The present review describes the role of SODs, especially Cu, Zn SOD, in several diseases, such as familial amyotrophic lateral sclerosis (FALS), Parkinson's disease, Alzheimer's disease, dengue fever, cancer, Down's syndrome, cataract, and several neurological disorders. Mutations in the SOD1 gene cause a familial form of amyotrophic lateral sclerosis. The mechanism by which mutant SOD1 causes the degeneration of motor neurons is not well understood. Transgenic mice expressing multiple copies of FALS-mutant SOD1s develop an ALS-like motor neuron disease. Vacuolar degeneration of mitochondria has been identified as the main pathological feature associated with motor neuron death and paralysis in several lines of FALS-SOD1 mice. Various observations and conclusions linking mutant SOD1 and FALS are discussed in this review in detail.
Serum levels of acute phase reactants (APR) were measured in patients with rheumatoid arthritis (RA) and the correlations of these parameters with the disease activity score (DAS28) were investigated. The study included 47 patients with RA and 50 healthy controls. Laboratory tests included erythrocyte sedimentation rate (ESR), serum C-reactive protein (CRP), haptoglobin (Hp), ferritin, and plasma fibrinogen. Disease activity was assessed using the DAS28 score. The means (+/- SD) of ESR, CRP, Hp, ferritin, and fibrinogen levels were respectively 36.0 +/- 23.5 mm/hr, 2.4 +/- 1.9 mg/dl, 121.3 +/- 34.2 mg/dl, 67.7 +/- 36.2 ng/ml, and 371.2 +/- 96.0 mg/dl in the patients with RA, vs 16.4 +/- 11.3 mm/hr, 0.4 +/- 0.3 mg/dl, 104.0 +/- 35.3 mg/dl, 50.9 +/- 23 ng/ml, and 332.2 +/- 58.5 mg/dl in the controls. All of the APR levels were significantly higher in patients vs controls (p < 0.001 for ESR and CRP; p < 0.05 for Hp, ferritin, and fibrinogen). There were significant correlations between serum APR levels and disease activity based on DAS28 score in RA patients (for CRP, r = 0.650, p <0.01; for Hp, r = 0.331, p < 0.05; for ferritin, r = 0.299, p < 0.05; for fibrinogen, r = 0.373, p < 0.01). This study indicates that serum CRP, among the various ARP tests, is the most useful biochemical marker for evaluating the disease activity of patients with RA.
In recent years, a great number of studies have investigated the possible role of trace elements in the etiology and pathogenesis of rheumatoid arthritis (RA) and osteoartritis (OA). We studied synovial fluid and plasma concentrations of selenium (Se), zinc (Zn), copper (Cu), and iron (Fe) in patients with RA and OA and compared them with sex- and age-matched healthy subjects. Plasma albumin levels were measured as an index of nutritional status. Plasma Se, Cu, and Zn concentrations were determined by atomic absorption spectrophotometry and Fe concentrations were determined by the colorimetric method. Although plasma and synovial fluid Se concentration were found to be significantly lower (p < 0.05, and p < 0.05, respectively), Cu concentrations were significantly higher in patients with RA than those of healthy subjects and OA (p < 0.05 and p < 0.05, respectively). There were no significant differences in plasma and synovial fluid Zn concentrations and albumin levels among three groups (p > 0.05). On the other hand, synovial fluid Cu and Fe concentrations were significantly higher in patients with OA than those of healthy subjects (p < 0.05). There was a significantly positive correlation between synovial fluid Se-Cu values and Zn-Fe values in patients with RA. Our results showed that synovial fluid and plasma trace element concentrations, excluding Zn, change in inflammatory RA, but not in OA. These alterations in trace element concentrations in inflammatory RA might be a result of the changes of the immunoregulatory cytokines.
Zinc is required for multiple cellular tasks, and especially the immune system depends on a sufficient availability of this essential trace element. During the last decades, many studies attempted to affect the outcome of various diseases by zinc supplementation. These efforts either aimed at supporting immunity by zinc administration or at correcting a loss of zinc secondary to the disease to restore the zinc-dependent functions of the immune system. This review aims to summarize the respective findings and to discuss possible molecular mechanisms by which zinc could influence viral, bacterial, and parasitic infections, autoimmune diseases, and the response to vaccination. Zinc supplementation in diseases such as diarrhea, chronic hepatitis C, shigellosis, leprosy, tuberculosis, pneumonia, acute lower respiratory infection, and leishmaniasis seems beneficial. In contrast, the results for the common cold and malaria are still not conclusive, and zinc was ineffective in most vaccination and rheumatoid arthritis studies. For AIDS and type 1 diabetes, zinc supplementation may even be a risk factor for increased mortality or deterioration of the glucose metabolism, respectively. In these cases, zinc supplementation should be used with care and limited to clearly zinc-deficient individuals.
Mercury is a major toxic metal ranked top in the Toxic Substances List. Cinnabar, which contains mercury sulfide, has been used in Chinese traditional medicines for thousands of years as an ingredient in various remedies, and 40 cinnabar-containing traditional medicines are still used today. Little is known about toxicology profiles or toxicokinetics of cinnabar and cinnabar-containing traditional medicines, and the high mercury content in these Chinese medicines raises justifiably escalations of public concern. This minireview, by searching the available database of cinnabar and by comparing cinnabar with common mercurials, discusses differences in their bioavailability, disposition, and toxicity. The analysis showed that cinnabar is insoluble and poorly absorbed from the gastrointestinal tract. Absorbed mercury from cinnabar is mainly accumulated in the kidneys, resembling the disposition pattern of inorganic mercury. Heating cinnabar results in release of mercury vapor, which in turn can produce toxicity similar to inhalation of these vapors. The doses of cinnabar required to produce neurotoxicity are 1000 times higher than methyl mercury. Following long-term use of cinnabar, renal dysfunction may occur. Dimercaprol and succimer are effective chelation therapies for general mercury intoxication including cinnabar. Pharmacological studies of cinnabar suggest sedative and hypnotic effects, but the therapeutic basis of cinnabar is still not clear. In summary, cinnabar is chemically inert with a relatively low toxic potential when taken orally. In risk assessment, cinnabar is less toxic than many other forms of mercury, but the rationale for its inclusion in traditional Chinese medicines remains to be fully justified.
Environmental Health Criteria
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- P L Van Riel
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