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Toxicological Effects of Methylmercury 2 CHEMISTRY, EXPOSURE, TOXICOKINETICS, AND TOXICODYNAMICS THIS chapter presents background information that serves as a foundation for understanding the toxicology of MeHg. The chemical, toxicokinetic, and toxicodynamic properties of MeHg are presented. There is extensive literature on MeHg, and this review is not meant to be exhaustive. Although the primary emphasis of this report is on MeHg, this chapter includes discussions of other Hg species to provide a general review of the sources of exposure and toxicological properties of different Hg species. The emphasis is on human Hg data. Animal data are also discussed. PHYSICAL AND CHEMICAL PROPERTIES Chemical species of Hg that are of toxicological importance include the inorganic forms, elemental or metallic Hg (Hg0), mercurous Hg (Hg1+), and mercuric Hg (Hg2+), and the organic forms, MeHg and ethylmercury. Although there are many organic Hg compounds, the emphasis in this chapter is on MeHg. The structure, chemical formula, and physical and chemical properties of some Hg-containing compounds are shown in Table 2-1. A more complete table of physical and chemical properties of some Hg compounds can be found in the Agency of Toxic Substances and Disease Registry (ATSDR) Toxicological Profile for Mercury (Update) (ATSDR 1999). Table 2-2 summarizes the informa-
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Toxicological Effects of Methylmercury TABLE 2-1 Physical and Chemical Properties of Some Toxicologically Relevant Mercury Compounds Chemical Name Elemental Mercurya Mercuric Chloride Mercurous Chlorideb Methylmercuric Chloridec Dimethylmercury Molecular formula Hg0 HgCl2 Hg2Cl2 CH3HgCl C2H6Hg Molecular structure Cl-Hg-Cl Cl-Hg-Hg-Cl CH3-Hg-Cl CH3-Hg-CH3 Molecular weight 200.59 271.52 472.09 251.1 230.66 Solubility 5.6 × 10-5 g/L at 25°C 69 g/L at 20°C 2.0 × 10-3 g/L at 25°C 0.100 g/L at 21°C 1 g/L at 21°C Density 13.534 g/cm3 at 25°C 5.4 g/cm3 at 25°C 7.15 g/cm3 at 19°C 4.06 g/cm3 at 20°C 3.1874 g/cm3 at 20°C Oxidation state +1, +2 +2 +1 +2 +2 aAlso known as metallic mercury. bAlso known as calomel. cMethylmercuric chloride is used experimentally to investigate the effects of methylmercury. tion on some toxicologically relevant Hg compounds discussed later in this chapter. At 25° C, elemental Hg has a water solubility of 5.6×10-5 g/L. Mercuric chloride is considerably more soluble, having a solubility of 69 g/L at 20° C. In comparison, an organic Hg compound, such as methylmercury chloride, is much less water soluble, having a solubility of 0.100 g/L at 21° C. Dimethylmercury, a very toxic by-product of the chemical synthesis of MeHg (Nierenberg et al. 1998), also has a relatively low water solubility (1.0 g/L at 21° C). Due to its low water solubility, MeHg chloride is considered to be relatively lipid soluble. As discussed later in this chapter, the solubility of the different forms of Hg might play a role in their differential toxicity.
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Toxicological Effects of Methylmercury TABLE 2-2 Summary Table Comparing Toxicologically Relevant Mercury Species Methylmercury (CH3Hg+) Elemental Mercury (Hg0) Mercuric Mercury (Hg2+) Sources of Exposure Fish, marine mammals, crustaceans, animals and poultry fed fish meal Dental amalgams, occupational exposure, Caribbean religious ceremonies, fossil fuels, incinerators Oxidation of elemental mercury or demethylation of MeHg; deliberate or accidental poisoning with HgCl2 Biological Monitoring Hair, blood, cord blood Urine, blood Urine, blood Toxicokinetics Absorption Inhalation: Vapors of MeHg absorbed Inhalation: Approximately 80% of inhaled dose of Hg0 readily absorbed Inhalation: Aerosols of HgCl2 absorbed Oral: Approximately 95% of MeHg in fish readily absorbed from GI tract Oral: GI absorption of metallic Hg is poor; any released vapor in GI tract converted to mercuric sulfide and excreted Oral; 7-15% of ingested dose of HgCl2 absorbed from the GI tract; absorption proportional to water solubility of mercuric salt; uptake by neonates greater than adults Dermal: In guinea pigs, 3-5% of applied dose absorbed in 5 hr Dermal: Average rate of absorption of Hg0 through human skin, 0.024 ng/cm2 for every 1 mg/m3 in air Dermal: In guinea pigs, 2-3% of applied dose of HgCl2 absorbed Distribution Distributed throughout body since lipophilic; approximately 1-10% of absorbed oral dose of MeHg distributed to blood; 90% of blood MeHg in RBCs Rapidly distributed throughout the body since it is lipophilic Highest accumulation in kidney; fraction of dose retained in kidney dose dependent
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Toxicological Effects of Methylmercury MeHg-cysteine complexa involved in transport of MeHg into cells Half-life in blood, 50 d; 50% of dose found in liver; 10% in head. Half-life in blood, 45 d (slow phase); half-life appears to increase with increasing dose Half-life in blood, 19.7-65.6 d; 1st phase, 24 d, 2nd phase, 15-30 d Readily crosses blood-brain and placental barriers Readily crosses blood-brain and placental barriers Does not readily penetrate blood-brain or placental barriers In neonate, mercuric Hg not concentrated in kidneys; therefore, more widely distributed to other tissues In fetus and neonate, blood-brain barrier incompletely formed, so mercuric Hg brain concentrations higher than those in adults Biotransformation MeHg slowly demethylated to mercuric Hg (Hg2+) Hg0 in tissue and blood oxidized to Hg2+ by catalase and hydrogen peroxide (H2O2); H2O2 production the rate-limiting step Hg0 vapor exhaled by rodents following oral administration of mercuric Hg Tissue macrophages, intestinal flora, and fetal liver are sites of tissue demethylation Mercuric Hg not methylated in body tissues but GI microorganisms can form MeHg
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Toxicological Effects of Methylmercury Mechanisms of demethylation unknown; free radicals demethylate MeHg in vitro; bacterial demethylation enzymes studied extensively, none has been characterized or identified in mammalian cells Does not bind or induce metallothionein Binds and induces metallothionein Excretion Daily excretion, 1% of body burden; major excretory route is bile and feces; 90% excreted in feces as Hg2+; 10% excreted in urine as Hg2+ Excreted as Hg0 in exhaled air, sweat, and saliva, and as mercuric Hg in feces and urine Excreted in urine and feces; also excreted in saliva, bile, sweat, exhaled air, and breast milk Lactation increases clearance from blood; 16% of Hg in breast milk is MeHg Half-Life limination (Whole body) 70-80 d; dependent on species, dose, sex, and animal strain 58 d 1-2 mo Toxicodynamics Critical target organ Brain, adult and fetal Brain and kidney Kidney Causes of Toxicity Demethylation of MeHg to Hg2+ and the intrinsic toxicity of MeHg Oxidation of Hg0 to Hg2+ Hg2+ binding to thiols in critical enzyme (e.g., cysteine) and structural proteins
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Toxicological Effects of Methylmercury Latency period In Iraq, from weeks to month; in Japan, more than a year; differences suggested to be caused by Se in fish; no toxic signs during latency period Mobilization DMPS, DMSA After oxidation to Hg2+: DMPS, DMSA DMPS, DMSA Possible Antagonists Selenium, garlic, zinc aMeHg-cysteine complex is structurally analogous to methionine. Abbreviations: HgCl2, mercuric chloride; DMPS, 2,3-dimercapto-1-propane sulfonate; DMSA, meso 2,3-dimercaptosuccinic acid; GI, gastrointestinal tract; RBC red blood cells.
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Toxicological Effects of Methylmercury METHODS OF CHEMICAL ANALYSIS The methods used for analyzing Hg in biological samples include atomic absorption spectrometry (AAS), atomic fluorescence spectrometry (AFS) (Vermeir et al. 1991a, b), X-ray fluorescence (XRF) (Marsh et al. 1987), gas chromatography (GC)-electron capture (Cappon and Smith 1978), and neutron activation analysis (NAA) (Fung et al. 1995). Anodic stripping voltammetry (ASV) has also been used (Liu et al. 1990). Of those procedures, GC-electron capture is able to distinguish MeHg from other species, but only cold vapor (CV)-AAS will detect Hg at parts per billion. CV-AAS, AFS, XRF, and NAA have all been used to analyze Hg content in hair (Zhuang et al. 1989). To measure total Hg in biological samples, the Hg must first be reduced to the elemental form. CV-AAS is most frequently used to measure Hg in urine (Magos and Cernik 1969) and blood (Magos and Clarkson 1972). For example, CV-AAS, the most commonly used method for analyzing Hg in biological samples, involves reduction of the Hg in the sample with stannous chloride to elemental Hg. To measure inorganic Hg, the analysis is carried out without chemical reduction of the sample. The difference between the total Hg concentration and the inorganic Hg concentration represents the concentration of organic Hg that was present in the sample. Biological samples containing MeHg can also be analyzed using Pseudomonas putida strain FB1. That bacteria converts MeHg to methane gas and elemental Hg (Baldi and Filippelli 1991). This method is one of the most reliable and specific methods for MeHg quantification, because chemical interference is negligible. It can detect 15 ng of MeHg in 1 g of biological tissue with a coefficient of variation of 1.9%. New methods for analyzing Hg in biological samples have been developed such as inductively coupled plasma-mass spectrometry (ICPMS) (Kalamegham and Ash 1992). Most of the new methods are expensive and beyond the reach of most laboratories. The cost is approximately $150,000-250,000 for the instrument and more than $35,000 a year for gases and maintenance costs. Regardless of the analytical method used, care must be taken to eliminate or prevent contamination of the sample by Hg during preparation and analysis. All glassware and plasticware used for collection and analysis of the specimen must be acid washed. In addition, care must
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Toxicological Effects of Methylmercury be taken to avoid losses due to volatilization of elemental Hg and MeHg, especially when preserving or concentrating the samples. Many procedures require the digestion of the sample before reduction. When attempting to quantify Hg content, especially in biological samples, data are needed to validate the procedures and their use in a given laboratory. All the methods of analysis are prone to large variations. Biological monitoring of inorganic Hg, including elemental Hg, requires measurement of Hg concentrations in blood, urine, or both (Clarkson et al. 1988). Biological monitoring for MeHg usually involves measuring Hg content in scalp hair, blood, or both. The MeHg incorporated into hair is stable and can be used for longitudinal timing (historical record) of exposure to MeHg by analyzing segments of hair (Phelps et al. 1980; IPCS 1990; Grandjean et al. 1992; Suzuki et al. 1992). One source of error in hair Hg analysis is the presence of Hg on the hair surface due to external deposition. Adequate washing of the hair sample before analysis minimizes that error (Francis et al. 1982). An excellent summary of the analytical methods for determining various species of Hg in biological specimens, including blood, urine, hair, breath, and tissues, as well as in environmental samples can be found in Table 6-1 in Toxicological Profile for Mercury (Update) (ATSDR 1999) and in the World Health Organization (WHO) report Methylmercury (IPCS 1990). EXPOSURES TO MeHg IN THE U.S. POPULATION The major source of MeHg exposure in humans is consumption of fish, marine mammals, and crustaceans. Because exposure to MeHg occurs almost entirely through fish consumption and varies according to the types of fish consumed, variations in exposure to MeHg in the U.S. population are based on individual characteristics of fish consumption. Exposure also varies according to the characteristic amounts and types of fish consumed in different regions of the United States. Hg concentrations in commercial fish and seafood in the United States span about two orders of magnitude. For example, herring contains Hg at approximately 0.01 ppm and shark contains Hg at greater than 1 ppm (EPA 1997a). Limited data suggest that coastal regions generally have
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Toxicological Effects of Methylmercury higher rates of fish consumption (Rupp et al. 1980). In addition, specific ethnic and cultural subgroups, as well as recreational fishermen, can have increased exposures (EPA 1997a). Population-based estimates of MeHg exposure in the United States have been made on the basis of dietary assessment studies, which provide information on fish consumption by species and by portion size. The combination of intake frequency by species and portion size by species for each individual consumer provides an estimate of the average mass of fish consumed (in grams per day). Summaries of such studies giving national data are provided in EPA's report to Congress (EPA 1997a). Another such dietary assessment study was conducted in New Jersey (Stern et al. 1996). To estimate population-based MeHg exposure from such studies, the gram-per-day amount of each species consumed by each individual is multiplied by the characteristic MeHg concentration of each species (microgram per gram) and then is summed across species to give the average intake of MeHg by each individual (microgram/day). The distribution of individual intakes for the study sample can then provide an estimate of MeHg intake in the underlying population. Uncertainties in such assessments include those in recall and recording of intake frequency and portion size, misidentification of the species consumed, extrapolation of short-term dietary studies to long-term average exposure, and the outdated and incomplete national database on average MeHg concentrations of different fish species. Estimates also typically vary depending on the length of time over which the fish-intake data was obtained (e.g., 1-day recall versus 1-week recall). These uncertainties are discussed by EPA (1997a) and Stern et al. (1996). Table 2-3 presents the EPA (1997c) analysis of MeHg intake for the general population and for the population of women of childbearing age based on fish-consumption data for month-long consumption. Estimates based on intake from such data are generally lower than those based on 1-day dietary data. Table 2-3 also presents data from New Jersey based on a 7-day recall survey. These data, along with the study by Rupp et al. 1980, suggest that the population in that region of the United States has higher intakes than the U.S. population in general. Estimates of population exposure and risk based on the average exposure of the U.S. population might, therefore, underestimate exposure to large subpopulations. Upon completion, data from Continuing Survey of Food Intakes by Individuals (CFSII) and National Health and Nutrition Examination
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Toxicological Effects of Methylmercury TABLE 2-3 Estimated Average MeHg Intake for the U.S. Population and for New Jersey Fish Consumers Average Daly Intake of MeHg (µg/day)a Percentiles of the Population General Population Women of Childbearing Age U.S.b,c New Jerseyd U.S.b,e New Jerseyc,f 50th 1.4 3.1 0.6 3.2 75th 3.5 5.8 1.8 5.4 90th 9.1 13.1 4.8 10.8 95th 15.6 21.1 7.8 15.7 99th 49.9 22.2 26.5 aAssuming body weight of 70 kg for the general population and 60 kg for women of childbearing age. bData from EPA 1997a. cUnweighted average across ethnic groups. dData from Stern et al. 1996. eWomen 15-45 years old. fWomen 18-40 years old. Survey (NHANES IV) might provide information on regional fish consumption. NHANES IV is also designed to provide information on MeHg exposure in U.S. populations. Consumption of animals or poultry fed fish meal might increase the exposure to MeHg, but data are not available. The use of organic Hg compounds as preservatives in vaccines and medical preparations is also a source of exposure and is of particular importance in young children who might be more sensitive to those mercurials than adults. As many as 219 such products are in use (FDA 1999). Thimerosal (TM) (sodium ethylmercurithiosalicylate) and phenylmercuric acetate (PMA) are the most frequently used compounds, at concentrations of 0.01% and 0.0002%, respectively. The FDA estimates that 75-80 kg of Hg compounds are used annually by the manufacturers of those vaccines and medical preparations. The risks associated with thimerosal use in vaccines have been discussed in an interim report to clinicians (American Academy of Pediatrics 1999). Small amounts of MeHg can be formed in the gut by intestinal bacte-
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Toxicological Effects of Methylmercury ria. A.O. Summers (University of Georgia, personal commun., Dec. 1999) estimated that 9 µg of MeHg can be formed per day in the gut of humans. That estimate is based on the bacterial species reported to occur in the human gut and assumes that there are 454 g of feces in the lower bowel of an adult human. However, not all the MeHg that is synthesized would be absorbed. Some of the methylation would occur in the colon, where absorption is less. In addition, intestinal flora can demethylate MeHg to inorganic Hg, which is poorly absorbed by the GI tract (Nakamura et al. 1977; Rowland et al. 1980). The major source of exposure to elemental Hg in the general U.S. population is due to Hg vapor released from dental amalgams (Goering et al. 1992; Halbach 1994; Lorscheider et al. 1995). Approximately 300 metric tons of Hg are used annually by dentists for amalgams (Arenholt-Bindslev and Larsen 1996). Most amalgams used in the United States contain approximately 50% Hg (IPCS 1991; Aposhian et al. 1992a; Lorscheider et al. 1995). In a study of college students who have dental amalgams, two-thirds of the Hg excreted in the urine appeared to be derived from the Hg vapor released from their amalgams (Aposhian et al. 1992a). Evidence shows that Hg vapor from dental amalgams enters tissues, including the brain, where it is oxidized to inorganic Hg. Pregnant sheep given amalgam fillings labeled with radioactive Hg accumulated radioactivity in maternal and fetal tissues within a few days (Vimy et al. 1990). Significant positive correlations between the number of amalgams in the mouth and the mercury content of human tissues, including the brain, are also seen (Drasch et al. 1994). The mean concentration of total Hg in whole blood (in the absence of consumption of fish with high concentrations of MeHg) is probably of the order of 5-10 µg/L (IPCS 1991; Mahaffey and Mergler 1998). This concentration is most likely due to exposure to Hg vapors from amalgams, because retention of inorganic Hg is very low compared with retention of organic and elemental Hg. Furthermore, exposure to MeHg from non-fish sources is also very low (IPCS 1991). Occupational exposure to elemental Hg has occurred because of accidents in chloralkali plants (Bluhm et al. 1992). However, there are other potential occupational exposures to elemental Hg. In addition, some Caribbean religions use elemental Hg in religious ceremonies (Wendroff 1995). Children have been known to play with elemental Hg because of its fascinating physical properties (i.e., liquid silver), possibly
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Toxicological Effects of Methylmercury Aposhian. 1992a. Urinary mercury after administration of 2,3-dimercaptopropane-1-sulfonic acid: Correlation with dental amalgam score. FASEB J. 6(7):2472-2476. Aposhian, H.V., R.M. Maiorino, M. Rivera, D.C. Bruce, R.C. Dart, K.M. Hurlbut, D.J. Levine, W. Zheng, Q. Fernando, D. Carter, and M.M. Aposhian. 1992b. Human studies with the chelating agents DMPS and DMSA. Clin. Toxicol. 30(4):505-528. Aposhian, H.V., R.M. Maiorino, D. Gonzalez-Ramirez, M. Zuniga-Charles, Z. Xu, K.M. Hurlbut, P. Junco-Munoz, R.C. Dart, and M.M. Aposhian. 1995. Mobilization of heavy metals by newer, therapeutically useful chelating agents. Toxicology 97(1-3):23-28. Aposhian, M.M., R.M. Maiorino, Z. Xu, and H.V. Aposhian. 1996. Sodium 2,3-dimercapto-1-propanesulfaonte (DMPS) treatment does not redistribute lead or mercury to the brain of rats. Toxicology 109(1):49-55. Arenholt-Bindslev, D., and A.H. Larsen. 1996. Mercury levels and discharge in waste water from dental clinics. Water Air Soil Pollut. 86(1-4):93-99. Aschner, M., N.B. Eberle, and H.K. Kimelberg. 1991. Interactions of methylmercury with rat primary astrocyte cultures: Methylmercury efflux. Brain Res. 554(1-2):10-14. Atchison, W.D., and M.F. Hare. 1994. Mechanisms of methylmercury-induced neurotoxicity. FASEB J. 8(9):622-629. ATSDR (Agency for Toxic Substances and Disease Registry). 1999. Toxicological Profile for Mercury. (Update). U.S. Department of Health & Human Services, Agency for Toxic Substances and Disease Registry , Atlanta, GA. Bakir, F., S.F. Damluji, L. Amin-Zaki, M. Murthadha, A. Khalidi, N.Y. Al-Rawi, S. Tikriti, H.I. Dhahir, T.W. Clarkson, J.C. Smith, and R.A. Doherty. 1973. Methylmercury poisoning in Iraq. Science 181:230-241. Baldi, F., and M. Filippelli. 1991. New method for detecting methylmercury by its enzymic conversion to methane. Environ. Sci. Technol. 25(2):302-305. Ballatori, N. 1991. Mechanisms of metal transport across liver cell plasma membranes. Drug Metab. Rev. 23(1-2):83-132. Ballatori, N., and T.W. Clarkson. 1982. Developmental changes in the biliary excretion of methylmercury and glutathione. Science 216(4541):61-63. Baron Jr, S., N. Haykal-Coates, and H.A. Tilson. 1998. Gestational exposure to methylmercury alters the developmental pattern of trk-like immuno-reactivity in the rat brain and results in cortical dysmorphology. Dev. Brain Res. 109(1):13-31. Begley, T.P., A.E. Walts, and C.T. Walsh. 1986. Bacterial organomercurial lyase: Overproduction, isolation, and characterization . Biochemistry 25(22): 7186-7192. Berlin, M. 1986. Mercury. Pp. 387-445 in Handbook on the Toxicology of
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