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-



The National Academies | 500 Fifth St. N.W. | Washington, D.C. 20001
Copyright © National Academy of Sciences. All rights reserved.
Terms of Use and Privacy Statement



Below are the first 10 and last 10 pages of uncorrected machine-read text (when available) of this chapter, followed by the top 30 algorithmically extracted key phrases from the chapter as a whole.
Intended to provide our own search engines and external engines with highly rich, chapter-representative searchable text on the opening pages of each chapter. Because it is UNCORRECTED material, please consider the following text as a useful but insufficient proxy for the authoritative book pages.

Do not use for reproduction, copying, pasting, or reading; exclusively for search engines.

OCR for page 31
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-

OCR for page 31
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.

OCR for page 31
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

OCR for page 31
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

OCR for page 31
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

OCR for page 31
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.

OCR for page 31
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

OCR for page 31
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

OCR for page 31
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

OCR for page 31
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-

OCR for page 31
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

OCR for page 31
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

OCR for page 31
Toxicological Effects of Methylmercury Metals, 2nd Ed., L. Friberg, G.F. Nordberg, and V.B. Vouk, eds. New York: Elsevier. Bernard, S., and P. Purdue. 1984. Metabolic models for methyl and inorganic mercury. Health Phys. 46(3):695-699. Bluhm, R.E., R.G. Bobbitt, L.W. Welch, A.J.J. Wood, J.F. Bonfiglio, C. Sarzen, A.J. Heath, and R.A. Branch. 1992. Elemental mercury vapour toxicity, treatment, and prognosis after acute, intensive exposure in chloralkali plant workers: Part I: History, neuropsychological findings and chelator effects. Hum. Exp. Toxicol. 11(3):201-210. Bornmann, G., G. Henke, H. Alfes, and H. Mollmann. 1970. Intestinal absorption of metallic mercury. [in German]. Arch. Toxicol. 26(3):203-209. Brown, N.L., S.J. Ford, R.D. Pridmore, and D.C. Fritzinger. 1983. Nucleotide sequence of a gene from the Pseudomonas transposon Tn501 encoding mercuric reductase. Biochemistry 22(17):4089-4095. Burbaker, P.E., R. Klein, S.P. Herman, G.W. Lucier, L.T. Alexander, and M.D. Long. 1973. DNA, RNA and protein synthesis in brain, liver and kidneys of symptomatic methylmercury treated rats. Exp. Mol. Pathol. 18(3):263-280. Cappon, C.J., and J.C. Smith. 1978. A simple and rapid procedure for the gas-chromatographic determination of methylmercury in biological samples. Bull Environ. Contam. Toxicol. 19(5):600-607. Carty, A.J., and S.F. Malone. 1979. The chemistry of mercury in biological systems. Pp. 433-470 in The Biogeochemistry of Mercury in the Environment, J.O. Nriagu, ed. Amsterdam: Elsevier. Cernichiari, E., R. Brewer, G.J. Myers, D.O. Marsh, L.W. Lapham, C. Cox, C.F. Shamlaye, M. Berlin, P.W. Davidson, and T.W. Clarkson. 1995. Monitoring methylmercury during pregnancy: Maternal hair predicts fetal brain exposure. Neurotoxicology 16(4):705-710. Chang, L.W., and M.A. Verity. 1995. Mercury neurotoxicity: Effects and mechanisms. Pp. 31-59 in Handbook of Neurotoxicology, L.W. Chang, and R.S. Dyer, eds. New York: Marcel Dekker. Chang, L.W., M. Gilbert, and J. Sprecher. 1978. Modification of methylmercury neurotoxicity by vitamin E. Environ. Res. 17(3):356-366. Chen, R.W., H.E. Ganther, and K.G. Hoekstra. 1973. Studies on the binding of methylmercury by thionein. Biochem. Biophys. Res. Commun. 51(2):383-390. Cherian, M.G., J.B. Hursh, T.W. Clarkson, and J. Allen. 1978. Radioactive mercury distribution in biological fluids, and excretion in human subjects after inhalation of mercury vapor. Arch. Environ. Health 33(3):109-114. Clarkson, T.W. 1997. The toxicology of mercury. Crit. Rev. Clin. Lab. Sci. 34(4):369-403. Clarkson, T.W., L. Friberg, G. Nordberg, and P.R. Sager, eds. 1988. Biological Monitoring of Toxic Metals. New York: Plenum Press.

OCR for page 31
Toxicological Effects of Methylmercury Clarkson, T.W., L. Magos, C. Cox, M.R. Greenwood, L. Amin-Zaki, M.A. Majeed, and S.F. al-Damluji. 1981. Tests of efficacy of antidotes for removal of methylmercury in human poisoning during the Iraq outbreak. J. Pharmacol. Exp. Ther. 218(1):74-83. Cotton, F.A., and G. Wilkinson. 1988. Advanced Inorganic Chemistry, 5th Ed. New York: John Wiley & Sons. Cox, C., T.W. Clarkson, D.O. Marsh, L. Amin-Zaki, S. Tikriti, and G.G. Myers. 1989. Dose-response analysis of infants prenatally exposed to methyl mercury: An application of a single compartment model to single-strand hair analysis. Environ. Res. 49(2):318-332. Davis, L.E., M. Kornfeld, H.S. Mooney, K.J. Fiedler, K.Y. Haaland, W.W. Orrison, E. Cernichiari, and T.W. Clarkson. 1994. Methylmercury poisoning: Long-term clinical, radiological, toxicological, and pathological studies of an affected family. Ann. Neurol. 35(6):680-688. Denny, M.F., and W.D. Atchison. 1994. Elevations in the free intrasynaptosomal concentration of endogenous zinc by methylmercury. [Abstract]. Toxicologist 14:290. Dey, P.M., M. Gochfield, and K.R. Reuhl. 1999. Developmental methylmercury administration alters cerebellar PSA--NCAM expression and Golgi sialytransferase activity. Brain Res. 845(2):139-151. Divine, K.K., F. Ayala-Fierro, D.S. Barber, and D.E. Carter. 1999. Glutathione, albumin, cysteine, and cys-gly effects on toxicity and accumulation of mercuric chloride in LLC-PK1 cells. J. Toxicol. Environ. Health 57(7):489-505. Doi, R. 1991. Individual difference of methylmercury metabolism in animals and its significance in methylmercury toxicity. Pp. 77-98 in Advances in Mercury Toxicology, T. Suzuki, N. Imura, and T.W. Clarkson, eds. New York: Plenum Press. Drasch, G., I. Schupp, H. Hofl, R. Reinke, and G. Roider. 1994. Mercury burden of human fetal and infant tissues. Eur. J. Pediatr. 153(8):607-610. Dunn, J.D., and T.W. Clarkson. 1980. Does mercury exhalation signal demethylation of methylmercury? Health Phys. 38(3):411-414. Elinder, C.G., L. Gerhardsson, and G. Oberdörster. 1988. Biological monitoring of toxic metals — Overview. Pp. 1-72 in Biological Monitoring of Toxic Metals, T.W. Clarkson, L. Friberg, G.F. Nordberg, and P. R. Sager, eds. New York: Plenum Press. EPA (U.S. Environmental Protection Agency). 1997a. Mercury Study Report to Congress. Vol. IV: An Assessment of Exposure to Mercury in the United States . EPA-452/R-97-006. U.S. Environmental Protection Agency, Office of Air Quality Planning and Standards and Office of Research and Development. EPA (U.S. Environmental Protection Agency). 1997b. Mercury Study Report for Congress. Volume V: Health Effects of Mercury and Mercury Com

OCR for page 31
Toxicological Effects of Methylmercury pounds. EPA-452/R-97-007. U.S. Environmental Protection Agency, Office of Air Quality Planning and Standards and Office of Research and Development. EPA (U.S. Environmental Protection Agency). 1997c. Mercury Study Report to Congress. Volume VII: Characterization of Human Health and Wildlife Risks from Mercury Exposure in the United States. EPA-452/R-97-009. U.S. Environmental Protection Agency, Office of Air Quality Planning and Standards and Office of Research and Development. Fang, S.C., and E. Fallin. 1974. Uptake and subcellular cleavage of organomercury compounds by rat liver and kidney. Chem. Biol. Interact. 9(1):57-64. FDA (Center for Drug Evaluation and Research). 1999. List of Drug and Food that Contain Intentionally Introduced Mercury Compounds. Updated November 17, 1999. Online. Available:http://www.fda.gov/cder/fdama/mercury300.htm Fox, B., and C.T. Walsh. 1982. Mercuric reductase. Purification and characterization of a transposon-encoded flavoprotein containing an oxidation-reduction-active disulfide. J. Biol. Chem. 257(5):2498-2503. Fox, B.S., and C.T. Walsh. 1983. Mercuric reductase: Homology to glutathione reductase and lipoamide dehydrogenase. Iodoacetamide alkylation and sequence of the active site peptide. Biochemistry 22(17):4082-4088. Francis, P.C., W.J. Birge, B.L. Roberts, and J.A. Black. 1982. Mercury content of human hair: A survey of dental personnel. J. Toxicol. Environ. Health 10(4-5):667-672. Fredriksson, A., L. Dahlgren, B. Danielsson, P. Eriksson, L. Dencker, and T. Archer. 1992. Behavioural effects of neonatal metallic mercury exposure in rats . Toxicology 74(2-3):151-160. Fredriksson, A., L. Dencker, T. Archer, and Danielsson. 1996. Prenatal coexposure to metallic mercury vapour and methylmercury produce interactive behavioural changes in adult rats. Neurotoxicol. Teratol. 18(2):129-134. Friberg, L., and N.K. Mottet. 1989. Accumulation of methylmercury and inorganic mercury in the brain. Biol. Trace Elem. Res. 21:201-206. Fujiyama, J., K. Hirayama, and A. Yasutake. 1994. Mechanism of methylmercury efflux from cultured astrocytes. Biochem. Pharmacol. 47(9):1525-1530. Fung, Y.K., A.G. Meade, E.P. Rack, A.J. Blotcky, J.P. Claassen, M.W. Beatty, and T. Durham. 1995. Determination of blood mercury concentrations in Alzheimer's patients. Clin. Toxicol. 33(3):243-247. Gage, J.C. 1975. Mechanisms for the biodegradation of organic mercury compounds: The actions of ascorbate and of soluble proteins. Toxicol. Appl. Pharmacol. 32(2):225-238. Goering, P.L., W.D. Galloway, T.W. Clarkson, F.L. Lorscheider, M. Berlin, and

OCR for page 31
Toxicological Effects of Methylmercury A.S. Rowland. 1992. Toxicity assessment of mercury vapor from dental amalgams. Fundam. Appl. Toxicol. 19(3):319-329. Gonzalez-Ramirez, D.M., M. Zuniga-Charles, A. Narro-Juarez, Y. Molina-Recio, K.M. Hurlbut, R.C. Dart, and H.V. Aposhian. 1998. DMPS (2,3-dimercapto-propane-1-sulfonate, dimaval) decreases the body burden of mercury in humans exposed to mercurous chloride. J. Pharmacol. Exp. Ther. 287(1):8-12. Gosselin, R.E., R.P. Smith, H.C Hodge. 1984. Clinical Toxicology of Commercial Products, 5th Ed. Baltimore: Williams & Wilkins. Grandjean, P., P.J. Jørgensen, and P. Weihe. 1994. Human milk as a source of methylmercury exposure in infants. Environ. Health Perspect. 102(1):74-77. Grandjean, P., P. Weihe, P.J. Jørgensen, T.W. Clarksen, E. Cernichiari, and T. Viderø. 1992. Impact of maternal seafood diet on fetal exposure to mercury, selenium, and lead. Arch. Environ. Health 47(3):185-195. Halbach, S. 1994. Amalgam tooth fillings and man's mercury burden. Hum. Exp. Toxicol. 13:496-501. Hall, L.L., P.V. Allen, H.L. Fisher, and B. Most. 1995. The kinetics of intravenously-administered inorganic mercury in humans . Pp. 265-280 in Kinetic Models of Trace Elements and Mineral Metabolism During Development , K.N.S. Subramanian, and M.E. Wastney, eds. Boca Raton, FL: CRC Press. Harada, M. 1995. Minamata disease: Methylmercury poisoning in Japan caused by environmental pollution. Crit. Rev. Toxicol. 25(1):1-24. Henderson, R., H.P. Shotwell, and L.A. Krause. 1974. Analyses for total, ionic and elemental mercury in urine as a basis for biological standard. Am. Ind. Hyg. Assoc. J. 35:576-580. Hursh, J.B. 1985. Partition coefficients of mercury (203Hg) vapor between air and biological fluids. J. Appl. Toxicol. 5(5):327-332. Hursh, J.B., M.G. Cherian, T.W. Clarkson, J.J. Vostal, and P.V. Mallie. 1976. Clearance of mercury (Hg-197, Hg-203) vapor inhaled by human subjects . Arch. Environ. Health 31(6):302-309. Hursh, J.B., T.W. Clarkson, T.V. Nowak, R.C. Pabico, B.A. McKenna, E. Miles, and F.R. Gibb. 1985. Prediction of kidney mercury content by isotope techniques. Kidney Int. 27(6):898-907. Hursh, J.B., T.W. Clarkson, E.F. Miles, and L.A. Goldsmith. 1989. Precutaneous absorption of mercury vapor by man. Arch. Environ. Health 44(2):120-127. IPCS (International Programme on Chemical Safety). 1990. Environmental Health Criteria Document 101: Methylmercury. Geneva: World Health Organization. IPCS (International Programme on Chemical Safety). 1991. Environmental Health Criteria Document 118: Inorganic Mercury. Geneva: World Health Organization.

OCR for page 31
Toxicological Effects of Methylmercury Jakubowski, M., J. Piotrowski, and B. Trojanowska. 1970. Binding of mercury in the rat: Studies using 203HgCl2 and gel filtration . Toxicol. Appl. Pharmacol. 16(3):743-753. Kägi, J.H., and M. Nordberg. 1979. Metallothionein. International Meeting on Metallothionein and Other Low Molecular Weight Metal Binding Proteins. Basel, Switzerland: Birkhäuser. Kalamegham, R., and K.O. Ash. 1992. A simple ICP-Ms procedure for the determination of total mercury in whole blood and urine. J. Clin. Lab. Anal. 6(4):190-193. Kerper, L.E., N. Ballatori, and T.W. Clarkson. 1992. Methylmercury transport across the blood-brain barrier by an amino acid carrier. Am. J. Physiol. 262(5):R761-R765. Kershaw, T.G., T.W. Clarkson, and P.H. Dhahir. 1980. The relationship between blood-brain levels and dose of methylmercury in man. Arch. Environ. Health 35(1):28-36. Klaassen, C.D. 1996. Heavy metals and heavy-metal antagonists. Pp. 1649-1671 in The Pharmacological Basis of Therapeutics, J.G. Hardman, L.E. Limbird, P.B. Molinoff, R.W. Ruddon, and A.G. Gilman, eds. New York: McGraw-Hill. Klimova, L.K. 1958. Pharmacology of a new Unithiol antidote [in Russian]. Farmakol. Toksikol. ( Moscow) 21:53-59. Komsta-Szumska, E., J. Chmielnicka, and J.K. Piotrowski. 1976. Binding of inorganic mercury by subcellllar fractions and proteins of rat kidneys. Arch. Toxicol. 37(1):57-66. Kromidas, L., L.D. Trombetta, and I.S. Jamall. 1990. The protective effects of glutathione against methylmercury cytotoxicity . Toxicol. Lett. 51(1):67-80. Kudsk, F.N. 1965. The influence of ethyl alcohol on the absorption of methyl mercury vapor from the lungs of man. Acta Pharmacol. Toxicol. 23:263-274. Lefevre, P.A., and J.W. Daniel. 1973. Some properties of the organomercury-degrading system in mammalian liver. FEBS Lett. 35(1):121-123. Lind, B., L. Friberg, and M. Nylander. 1988. Preliminary studies on methylmercury biotransformation and clearance in the brain of primates: II. Demethylation of mercury in brain. J. Trace Elem. Exp. Med. 1(1):49-56. Liu, K.Z., Q.G. Wu, and H.I. Liu. 1990. Application of a Nafion-Schiff-base modified electrode in anodic-stripping voltammetry for the determination of trace amounts of mercury. Analyst 115(6):835-837. Lorscheider, F.L., M.J. Vimy, and A.O. Summers. 1995. Mercury exposure from “silver” tooth fillings: Emerging evidence questions a traditional dental paradigm. FASEB J. 9(7):504-508. Magos, L., and W.H. Butler. 1972. Cumulative effects of methylmercury dicyandiamide given orally to rats. Food Cosmet. Toxicol. 10(4):513-517.

OCR for page 31
Toxicological Effects of Methylmercury Magos, L., and A.A. Cernik. 1969. A rapid method for estimating mercury in undigested biological samples . Br. J. Ind. Med. 26(2):144-149. Magos, L., and T.W. Clarkson. 1972. Atomic absorption determination of total, inorganic, and organic mercury in blood. J. Assoc. Off. Anal. Chem. 55(5):966-971. Magos, L., and M. Webb. 1980. The interaction of selenium with cadmium and mercury. Crit. Rev. Toxicol. 8(1):1-42. Magos, L., A.W. Brown, S. Sparrow, E. Bailey, R.T. Snowden, and W.R. Skipp. 1985. The comparative toxicology of ethyl- and methylmercury. Arch. Toxicol. 57(4):260-267. Mahaffey, K.R., and D. Mergler. 1998. Blood levels of total and organic mercury in residents of the upper St. Lawrence River basin, Quebec: Association with age, gender, and fish consumption. Environ. Res. 77(2):104-114. Marsh, D.O., T.W. Clarkson, C. Cox, G.J. Myers, L. Amin-Zaki, and S. Al-Tikriti. 1987. Fetal methyl mercury poisoning: Relationship between concentration in single strands of maternal hair and child effects. Arch. Neurol. 44(10):1017-1022. Matsuo, N, T. Suzuki, and H. Akagi. 1989. Mercury concentration in organs of contemporary Japanese. Arch. Environ. Health 44(5):298-303. Matsuo, N., M. Takasugi, A. Kuroiwa, and H. Ueda. 1987. Thymic and splenic alterations in mercuric chloride-induced glomerulopathy . Pp. 333-334 in Toxicology of Metals: Clinical and Experimental Research, S.S. Brown, and Y. Kodama, eds. Chichester, UK: Ellis Horwood Limited. Miettinen, J.K. 1973. Absorption and elimination of dietary (Hg++) and methylmercury in man. Pp. 233-246 in Mercury, Mercurial, and Mercaptans, M.W. Miller, and T.W. Clarkson, eds. Springfield, IL: C.C. Thomas. Miettinen, J.K., T. Rahola, T. Hattula, K. Rissanen, and M. Tillander. 1971. Elimination of 203Hg-methylmercury in man. Ann. Clin. Res. 3(2):116-122. Miura, K., and T.W. Clarkson. 1993. Reduced methylmercury accumulation in a methylmercury resistant rat pheochromocytoma PC12 cell line. Toxicol. Appl. Pharmacol. 118(1):39-45. Miura, K., and N. Imura. 1987. Mechanism of methylmercury cytotoxicity. Crit. Rev. Toxicol. 18(3):161-188. Mobley, H.L., and B.P. Rosen. 1982. Energetics of plasmid-mediated arsenate resistance in Escherichia coli. Proc. Natl. Acad. Sci. U.S.A. 79(20):6119-6122. Naganuma, A., N. Oda-Urano, T. Tanaka, and N. Imura. 1988. Possible role of hepatic glutathione in transport of methylmercury into mouse kidney. Biochem. Pharmacol. 37(2):291-296. Nakamura, I., K. Hosokawa, H. Tamura, and T. Miura. 1977. Reduced mercury excretion with feces in germfree mice after oral administration of methylmercury chloride. Bull. Environ. Contam. Toxicol. 17(5):528-533.

OCR for page 31
Toxicological Effects of Methylmercury NESCAUM (Northeast States for Coordinated Air Use Management), NEWMOA (Northeast Waste Management Officials' Association), NEIWPCC (New England Interstate Water Pollution Control Commission) , and EMAN ( Canadian Ecological Monitoring and Assessment Network). 1998. Mercury in Northeastern freshwater fish: current level and ecological impacts. Pp. IV.1-IV.21 in Northeast States/Eastern Canadian Provinces Mercury Study — A Frame Work for Action. February, 1998. Nielsen, J.B. 1992. Toxicokinetics of mercuric-chloride and methylmercuric chloride in mice. J. Toxicol. Environ. Health 37(1):85-122. Nierenberg, D.W., R.E. Nordgren, M.B. Chang, R.W. Siegler, M.B. Blayney, F. Hochberg, T.Y. Toribara, E. Cernichiari, and T. Clarkson. 1998. Delayed cerebellar disease and death after accidental exposure to dimethylmercury. N. Engl. J. Med. 338(23):1672-1676. Norseth, T., and T.W. Clarkson. 1970. Studies on the biotransformation of 203Hg-labeled methylmercury chloride in rats. Arch. Environ. Health 21(6):717-727. Okawa, K., H. Saito, I. Kifune, T. Ohshina, M. Fujii, and Y. Takizawa. 1982. Respiratory tract retention of inhaled air pollutants. 1. Mercury absorption by inhaling though the nose and expiring through the mouth at various concentrations. Chemosphere 11(9):943-951. Ostlund, K. 1969. Studies on the metabolism of methyl mercury in mice. Acta Pharmacol. Toxicol. 27(Suppl.1):1-132. Perry, R.D., and S. Silver. 1982. Cadmium and manganese transport in Staphylococcus aureus membrane vesicles. J. Bacteriol. 150(2):973-976. Phelps, R.W., T.W. Clarkson, T.G. Kershaw, and B. Wheatley. 1980. Interrelationships of blood and hair mercury concentrations in a North American population exposed to methylmercury. Arch. Environ. Health 35(3):161-168. Ponce, R.A., T.J. Kavanagh, N.K. Mottet, S.G. Whittaker, and E.M. Faustman. 1994. Effects of methyl mercury on the cell cycle of primary rat CNS cells in vitro. Toxicol. Appl. Pharmacol. 127(1):83-90. Rahola, T., T. Hattula, A. Korolainen, and J.K. Miettinen. 1973. Elimination of free and protein-bound ionic mercury (20Hg2+) in man . Ann. Clin. Res. 5(4):214-219. Robinson, J.B., and O.H. Tuovinen. 1984. Mechanisms of microbial resistance and detoxification of mercury and organomercury compounds: Physiological, biochemical, and genetic analyses. Microbiol. Rev. 48(2):95-124. Rowland, I., M. Davies, and J.G. Evans. 1980. Tissue content of mercury in rats given methylmercuric chloride orally: Influence of intestinal flora. Arch. Environ. Health 35(3):155-160. Rowland, I., M. Davies, and P. Grasso. 1977. Biosynthesis of methylmercury compounds by the intestinal flora of the rat. Arch. Environ. Health 32(1):24-28.

OCR for page 31
Toxicological Effects of Methylmercury Rupp, E.M., F.I. Miller, and C.F. Baes III. 1980. Some results of recent surveys of fish and shellfish consumption by age and region of U.S. residents. Health Phys. 39(2):165-175. Sager, P.R., M. Aschner, and P.M. Rodier. 1984. Persistent, differential alterations in developing cerebellar cortex of male and female mice after methylmercury exposure. Brain Res. 314(1):1-11. Sarafian, T., and M.A. Verity. 1991. Oxidative mechanisms underlying methylmercury neurotoxicity. Int. J. Dev. NeuroSci. 9(2):147-153. Sherlock, J., J. Hislop, D. Newton, G. Topping, and K. Whittle. 1984. Elevation of mercury in human blood from controlled chronic ingestion of methylmercury in fish. Hum. Toxicol. 3(2):117-131. Silver, S., and D. Keach. 1982. Energy-dependent arsenate efflux: The mechanism of plasmid-mediated resistance. Proc. Natl. Acad. Sci. U.S.A. 79(20):6114-6118. Skerfving, S. 1988. Mercury in women exposed to methylmercury through fish consumption, and in their newborn babies and breast milk. Bull. Environ. Contam. Toxicol. 41(4):475-482. Stern, A.H., L.R. Korn, and B.E. Ruppel. 1996. Estimation of fish consumption and methylmercury intake in the New Jersey population. J. Expo. Anal. Environ. Epidemiol. 6(4):503-525. Stopford, W., S.D. Bundy, L.J. Goldwater, and J.A. Bittikofer. 1978. Micro-environmental exposure to mercury vapor. Am. Ind. Hyg. Assoc. J. 39(5):378-384. Suda, I., and K. Hirayama. 1992. Degradation of methy- and ethylmercury into inorganic mercury by hydroxyl radical produced from rat liver microsomes. Arch. Toxicol. 66(6):398-402. Sugano, H., S. Omata, and H. Tsubaki. 1975. Methylmercury inhibition of protein synthesis in brain tissue. I. Effects of methylmercury and heavy metals on cell-free protein synthesis in rat brain and liver. Pp. 129-136 in Studies on the Health Effects of Alkylmercury in Japan, Environmental Agency, Japan. Summers, A.O. 1985. Bacterial resistance to toxic elements. Trends Biotechnol. 3(5):122-125. Summers, A.O., and S. Silver. 1978. Microbial transformations of metals. Annu. Rev. Microbiol. 32:637-672. Sundberg, J., and A. Oskarsson. 1992. Placental and lactational transfer of mercury from rats exposed to methylmercury in their diet: Speciation of mercury in the offspring . J. Trace Elem. Exp. Med. 5(1):47-56. Sundberg, J., S. Jonsson, M.O. Karlsson, I.P. Hallen, and A. Oskarsson. 1998. Kinetics of methylmercury and inorganic mercury in lactating and nonlactating mice. Toxicol. Appl. Pharmacol. 151(2):319-329. Suzuki, T., T. Hongo, N. Matsuo, H. Imai, M. Nakazawa, T. Abbe, Y. Yama

OCR for page 31
Toxicological Effects of Methylmercury mura, M. Yoshida, and H. Aoyama. 1992. An acute mercuric mercury poisoning: Chemical speciation of hair mercury shows a peak of inorganic mercury value. Hum. Exp. Toxicol. 11(1):53-57. Syversen, T.L. 1974. Distribution of mercury in enzymatically characterized subcellular fractions from the developing rat brain after injections of methylmercuric chloride and diethylmercury. Biochem. Pharmacol. 23(21):2999-3007. Takeuchi, T., and E. Komyo. 1977. Pathology and pathogenesis of Minamata disease. Pp. 103-142 in Minamata Disease, T. Tsubake and K. Irukayama, eds. New York: Elsevier. Takeuchi, T., K. Eto, and H. Tokunaga. 1989. Mercury level and histochemical distribution in a human brain with Minamata Disease following a long-term clinical course of 26 years . Neurotoxicology 10(4):651-657. Takizawa, Y. 1979. Epidemiology of mercury poisoning. Pp. 325-366 in The Biogeochemistry of Mercury in the Environment, J.O. Nriagu, ed. Amsterdam: Elsevier/North-Holland Biomedical Press. Thomas, D.J., H.L. Fisher, L.L. Hall, and P. Mushak. 1982. Effects of age and sex on retention of mercury by methylmercury-treated rats. Toxicol. Appl. Pharmacol. 62(3):445-454. Vahter, M., N.K. Mottet, L. Friberg, B. Lind, D.D. Shen, and T. Burbacher. 1994. Speciation of mercury in the primate blood and brain following long-term exposure to methyl mercury. Toxicol. Appl. Pharmacol. 124(2):221-229. Vahter, M.E., N.K. Mottet, L.T. Friberg, S.B. Lind, J.S. Charleston, and T.M. Burbacher. 1995. Demethylation of methyl mercury in different brain sites of Macaca fascicularis monkeys during long-term subclinical methyl mercury exposure. Toxicol. Appl. Pharmacol. 134(2):273-284. Vermeir, G., C. Vandecasteele, and R. Dams. 1991a. Atomic fluorescence spectrometry combined with reduction aeration for the determination of mercury in biological samples. Anal. Chim. Acta 242(2):203-208. Vermeir, G., C. Vandecasteele, and R. Dams. 1991b. Atomic fluorescence spectrometry for the determination of mercury in biological samples. Pp. 29-36 in Trace Elements in Health and Disease, A. Aitio, A. Aro, J. Jarvisalo, and H. Vainio, eds. Cambridge, UK: The Royal Society of Chemistry. Vimy, M.J., D.E. Hooper, W.W. King, and F.L. Lorscheider. 1997. Mercury from maternal “silver” tooth fillings in sheep and human breast milk. A source of neonatal exposure. Biol. Trace Elem. Res. 56(2):143-152. Vimy, M.J., Y. Takahashi, and F.L. Lorscheider. 1990. Maternal-fetal distribution of mercury (203Hg) released from dental amalgam fillings. Am. J. Physiol. 258(4):R939-R945. Wendroff, A.P. 1995. Magico-religious mercury use and cultural sensitivity. Am. J. Public Health 85(3):409-410.

OCR for page 31
Toxicological Effects of Methylmercury WHO (World Health Organization). 1976. Mercury. Environmental Health Criteria 1. Geneva: World Health Organization. Wisniewska, J.M., B. Trojanowska, J. Piotrowski, and M. Jakubowski. 1970. Binding of mercury in the rat kidney by metallothionein. Toxicol. Appl. Pharmacol. 16(3):754-763. Yoshida, M., H. Satoh, T. Kishimoto, and Y. Yamamura. 1992. Exposure to mercury via breast milk in suckling offspring of maternal guinea pigs exposed to mercury vapor after parturition. J. Toxicol. Environ. Health 35(2):135-139. Yoshino, Y., T. Mozai, and K. Nakao. 1966. Distribution of mercury in the brain and its subcellular units in experimental organic mercury poisoning. J. Neurochem. 13:397-406. Zhuang, G., Y. Wang, M. Zhi, W. Zhou, J. Yin, M. Tan, and Y. Cheng. 1989. Determination of arsenic, cadmium, mercury, copper and zinc in biological samples by radiochemical neutron-activation analysis. J. Radioanal. Nucl. Chem. 129(2):459-464.