Biomonitoring Summary


CAS No. 7439-97-6

General Information

Mercury is a naturally occurring metal that has elemental (metallic), inorganic, and organic forms. Elemental mercury is a shiny, silver-white liquid (quicksilver) obtained predominantly from the refining of mercuric sulfide in cinnabar ore. Elemental mercury is used to produce chlorine gas and caustic soda for industrial applications. Other major uses include electrical equipment (e.g., thermostats and switches), electrical lamps, thermometers, sphygmomanometers and barometers, and dental amalgam. Inhalation of elemental mercury volatilized from dental amalgam is a major source of mercury exposure in the general population (Halbach, 1994; Kingman et al., 1998; Woods et al., 2007). Accidental spills of elemental mercury, which create an episodic potential for volatization and inhalation of mercury vapor, have often required public health intervention (Zeitz et al., 2002).Also, elemental mercury is used in rituals practiced in some Latin American and Caribbean communities.

Elemental mercury is released into the air from the combustion of fossil fuels (primarily coal), solid-waste incineration, and mining and smelting. Atmospheric elemental mercury can be deposited on land and water. In addition, water can be contaminated by the direct release of elemental and inorganic mercury from industrial discharges. Metabolism of mercury by microorganisms in aquatic sediments creates methyl mercury, an organic form of mercury, which can bioaccumulate in aquatic and terrestrial food chains. The ingestion of methyl mercury, predominantly from fish and other seafood, constitutes the main source of dietary mercury exposure in the general population. Apart from methyl mercury, synthetic organomercury compounds were once used in pharmaceutical applications of organomercury, and mercury compounds are still used as preservatives (e.g., thimerosal, phenylmercuric acetate) or topical antiseptics (e.g., merbromin).

Inorganic mercury exists in two oxidative states (mercurous and mercuric) that combine with other elements, such as chlorine (e.g., mercuric chloride), sulfur, or oxygen, to form inorganic mercury compounds or salts. Inorganic mercury compounds such as mercuric oxide are used in producing batteries and pigments and in synthesizing many organic chemicals. Some cosmetic skin creams from countries other than the U.S. may contain inorganic mercury. Imported folk and alternative medicines occasionally are contaminated with inorganic mercury.

The kinetics of the different forms of mercury vary considerably. Poorly absorbed from the gastrointestinal tract, elemental mercury is absorbed mainly by inhaling volatilized vapor, undergoes distribution to most tissues, with the highest concentrations in the kidneys (Barregard et al., 1999; Hursh et al., 1980; IARC, 1993). After elemental mercury is absorbed, it is oxidized in the tissues to inorganic forms.Blood concentrations decline initially with a rapid half-life of approximately 1-3 days followed by a slower half-life of approximately 1-3 weeks (Barregard et al., 1992; Sandborgh-Englund et al., 1998). The slow-phase half-life may be several weeks longer in persons with chronic occupational exposure (Sallsten et al., 1993). After exposure to elemental mercury, excretion of mercury occurs predominantly through the kidney (Sandborgh-Englund et al., 1998), and peak urine levels can lag behind peak blood levels by days to a few weeks (Barregard et al., 1992); thereafter, for both acute and chronic exposures, urinary mercury levels decline with a half-life of approximately 1-3 months (Jonsson et al., 1999; Roels et al., 1991).

Less than 15% of inorganic mercury is absorbed from the human gastrointestinal tract (Rahola et al., 1973). Lesser penetration of inorganic mercury occurs through the blood-brain barrier than occurs with either elemental or methyl mercury (Hattula and Rahola, 1975; Vahter et al., 1994). The half-life of inorganic mercury in blood is similar to the slow-phase half-life of mercury after inhalation of elemental mercury. Excretion occurs by renal and fecal routes.

The fraction of methyl mercury absorbed from the gastrointestinal tract is about 95% (Aberg et al., 1969; Miettinen et al., 1971). Methyl mercury enters the brain and other tissues (Vahter et al., 1994) and then undergoes slow dealkylation to inorganic mercury. Human pharmacokinetic studies indicate that methyl mercury declines in blood and the whole body with a half-life of approximately 50 days, with most elimination occurring through in the feces (Sherlock et al., 1984; Smith et al., 1994; Smith and Farris, 1996). Methyl mercury is incorporated into growing hair, a measure of accumulated dose (Cernichiari et al., 1995; Suzuki et al., 1993), and which has served as a useful marker of exposure in epidemiologic studies (Grandjean et al., 1992 and 1999; McDowell et al., 2004; Myers et al., 2003).

Transplacental transport of methyl mercury and elemental mercury has been demonstrated in animals (Kajiwara et al, 1996; Vimy et al, 1990). Mercury levels in the cord blood are higher than in the mother’s blood (Stern and Smith, 2003), and the newborn’s levels decline gradually over several weeks (Bjornberg et al., 2005).Inorganic mercury and methyl mercury are distributed into human breast milk in relatively low concentrations; the transfer may be more efficient for inorganic mercury (Grandjean et al., 1995; Oskarsson et al., 1996). Mercury levels in breast milk also decline in the weeks after birth (Bjornberg et al., 2005; Drexler and Schaller 1998; Sakamoto et al., 2002; Sakamoto et al., 2004).

The health effects of mercury are diverse and can depend on the form of the mercury to which a person is exposed and the dose and the duration of exposure. Acute, high-dose exposure to elemental mercury vapor may cause severe pneumonitis. At levels below those that cause acute lung injury, overt signs and symptoms of chronic inhalation may include tremor, gingivitis, and neurocognitive and behavioral disturbances, particularly irritability, depression, short-term memory loss, fatigue, anorexia, and sleep disturbance (Bidstrup et al., 1951; Smith et al., 1970; Smith et al., 1983). Low-level exposure from dental amalgams has not been associated with neurologic effects in children or adults (Bates et al., 2004; Bellinger et al., 2006; DeRouen et al., 2006; Factor-Litvak et al., 2003). Occupational exposure to elemental mercury vapor has been associated with subclinical effects on biomarkers of renal dysfunction (Cardenas et al., 1993).

Inorganic mercury exposure usually occurs by ingestion. Large amounts may cause irritant or corrosive effects on the gastrointestinal tract (Sanchez-Sicilia et al., 1963). Once absorbed, the most prominent effect is on the kidneys where mercury accumulates and may lead to renal tubular necrosis. Acrodynia is a sporadic and predominantly pediatric syndrome historically associated with calomel (mercuric oxide) in teething powders and occasionally other inorganic forms of mercury.The constellation of findings may include anorexia, insomnia, irritability, hypertension, maculopapular rash, pain in the extremities, and pinkish discoloration of the hands and feet (Tunnessen et al., 1987).

Overt poisoning from methyl mercury primarily affects the central nervous system, causing parasthesias, ataxia, dysarthria, hearing impairment, and progressive constriction of the visual fields, typically after a latent period of weeks to months. High-level prenatal exposure may result in a constellation of developmental deficits that includes mental retardation, cerebellar ataxia, dysarthria, limb deformities, altered physical growth, sensory impairments, and cerebral palsy (NRC, 2000). In recent epidemiologic studies, lower levels of prenatal exposure due to maternal seafood consumption have been associated with an increased risk for abnormal neurocognitive test results in children (NRC, 2000; Rice, 2004). Although recent investigations have suggested a possible link between chronic ingestion of methyl mercury and an increased risk for cardiovascular disease, the existence of a causal relation is unresolved (Chan and Egeland, 2004; Rissanen et al., 2000; Salonen et al, 1995; Stern 2005; Vupputuri et al., 2005).

Workplace standards for inorganic mercury exposure have been established by OSHA and ACGIH, and a drinking water standard for inorganic mercury has been established by U.S. EPA.IARC considers methylmercury to be a possible human carcinogen and elemental and inorganic mercury to be unclassifiable with regard to human carcinogenicity.Information about external exposure (i.e., environmental levels) and health effects is available from the U.S. EPA at icon and from ATSDR at

Biomonitoring Information

In the general population, the total blood mercury concentration is due mostly to the dietary intake of organic forms, particularly methyl mercury. Urinary mercury consists mostly of inorganic mercury (Cianciola et al., 1997; Kingman et al., 1998). These distinctions can help interpret mercury blood levels in people. Total blood mercury levels increase with greater fish consumption (Dewailly et al., 2001; Grandjean et al., 1995; Mahaffey et al, 2004; Sanzo et al., 2001; Schober et al., 2003).Urine mercury levels increase as more occlusal surfaces of teeth are filled with mercury-containing amalgams (Becker et al., 2003).

In Germany the geometric mean for blood mercury was 0.58 µg/L for 4645 adults, aged 18 to 69 years, who participated in a 1998 representative population survey (Becker et al., 2002). From 1996 through 1998, Benes et al. (2000) studied 1216 blood donors in the Czech Republic (896 men and 320 women, average age 33 years; 758 children, average age 9.9 years); the median concentration of blood mercury was 0.78 µg/L for adults and 0.46 µg/L for children. A cohort of 1127 U.S. military veterans (mean age 52.8 years, range 40 years to 78 years) had an average total blood mercury concentration of 2.55 µg/L. These men had no occupational exposure to mercury but previously had received dental amalgams at military facilities (Kingman et al., 1998).

Over the NHANES 1999-2006 survey periods, total blood mercury geometric mean levels in females aged 16-49 years did not change, although non-Hispanic black females had higher levels than non-Hispanic white or Mexican American females. Among the three racial/ethnic groups, total blood mercury increased with age, and the age-related changes differed across the groups (Caldwell et al., 2009). During the same survey periods, total blood mercury levels declined slightly in non-Hispanic black and Mexican American children, and increased slightly in non-Hispanic white children (Caldwell, et al., 2009). In NHANES 1999-2002, slightly higher total blood mercury levels were found in U.S. adult women in several ethnic subgroups (Hightower et al., 2006).

Clinically observable signs of ataxia and paresthesias may occur when blood mercury levels increase to approximately 100 µg/L after methyl mercury poisoning. However, the developing fetus may be the most susceptible to the effects of ongoing methyl mercury exposure (NRC, 2000). A cord blood mercury level of 85 µg/L (lower 95% confidence bound = 58 µg/L) is associated with a 5% increase in the prevalence of an abnormal Boston Naming Test (NRC, 2000). Levels in U.S. women of childbearing age have generally been much lower than these levels (CDC, 2012). ACGIH recommends that the blood levels due to inorganic mercury exposure in workers not exceed 15µg/L.Blood mercury levels of women and children in NHANES 1999-2006 were also below levels established as occupational exposure guidelines (Caldwell, et al., 2009). Information about the biological exposure indices is provided here for comparison, not to imply a safety level for general population exposure.

Urinary mercury levels in recent German (Becker et al., 2003), Czech (Benes et al., 2002), and Italian (Apostoli et al., 2002) adult population surveys were similar to those in a U.S. representative sample of women aged 16-49 years reported in NHANES 1999-2006 (Caldwell, et al., 2009). In the study of U.S. military veterans with dental amalgams, mean urinary mercury was 3.1 µg/L. Urine mercury and the number of dental amalgams were correlated, and on average, the urine mercury increased by approximately 0.1 µg/L for each surface with a dental amalgam (Kingman et al., 1998). Recent studies in children with dental amalgams and urinary levels less than 5 µg/g of creatinine did not have changes in cognitive-behavioral testing when followed for 5-7 years (Bellinger et al., 2006; DeRouen et al., 2006).An expert panel report prepared for the U.S. Department of Health and Human Services noted that several studies have observed a modest, reversible increase in urinary N-acetyl-glucosaminidase, a biomarker of perturbation in renal tubular function, among workers with urinary mercury concentrations of 25-35 µg/L or greater (Barregard et al., 1988; Langworth et al., 1992). The ACGIH (2007) currently recommends that urinary inorganic mercury in workers not exceed 35 µg/g of creatinine.

Finding a measurable amount of mercury in blood or urine does not imply that the level of mercury causes an adverse health effect. Biomonitoring studies provide physicians and public health officials with reference ranges so that they can determine whether people have been exposed to higher levels of mercury than are found in the general population. Biomonitoring data will also help scientists plan and conduct research on exposure and health effects.


Aberg B, Ekman L, Falk R, Greitz U, Persson G, Snihs JO. Metabolism of methyl mercury (203Hg) compounds in man. Arch Environ Health 1969;19:478-84.

ACGIH. 2007 TLVs and BEIs. Based on the Documentation of the Threshold Limit Values for Chemical Substances and Physical Agents and Biological Exposure Indices. Cincinnati (OH): Signature Publications.

Apostoli P, Cortesi I, Mangili A, Elia G, Drago I, Gagliardi T, et al. Assessment of reference values for mercury in urine: the results of an Italian polycentric study. Sci Total Environ 2002;289:13-24.

Barregard L, Hultberg B., Schuzt A, Sallsten G. Enzymuria in workers exposed to inorganic mercury. Int Arch Occup Environ Health 1988;61:65-9.

Barregard L, Sallsten G, Conradi N. Tissue levels of mercury determined in a deceased worker after occupational exposure. Int Arch Occup Environ Health 1999;72:169-73.

Barregard L, Sallsten G, Schutz A, Attewell R, Skerfving S, Jarvholm B. Kinetics of mercury in blood and urine after brief occupational exposure. Arch Environ Health 1992;7(3):176-84.

Bates MN, Fawcett J, Garrett N, Cutress T, Kjellstrom T. Health effects of dental amalgam exposure: a retrospective cohort study. Int J Epidemiol 2004;33:1-9.

Becker K, Kaus S, Krause C, Lepom P, Schulz C, Seiwert M, et al. German Environmental Survey1998 (GerES III): environmental pollutants in blood of the German population. Int JHyg Environ Health 2002;205:297-308.

Becker K, Schulz C, Kaus S, Seiwert M, Seifert B. German environmental survey 1998 (GerES III): environmental pollutants in the urine of the German population. Int J Hyg Environ Health 2003; 206:15-24.

Bellinger DC, Trachtenberg F, Barregard L, Tavares M, Cernichiari E, Daniel D, McKinlay S. Neuropsychological and renal effects of dental amalgam in children: a randomized clinical trial. JAMA 2006;295(15):1775-83.

Benes B, Spevackova V, Smid J, Cejchanova M, Cerna M, Subrt P, et al. The concentration levels of Cd, Pb, Hg, Cu, Zn, and Se in blood of the population in the Czech Republic. Cent Eur J Public Health 2000;8(2):117-9.

Bidstrup PL, Bonnell JA, Harvey DG, Locket S. Chronic mercury poisoning in men repairing direct-current meters. Lancet 1951;2:856-61.

Bjornberg KA, Vahter M, Berglund B, Niklasson B, Biennow M, Sandborgh-englund B. Transport of methylmercury and inorganic mercury to the fetus and breast-fed infant. Environ Health Perspect 2005;113(10):1381-5.

Caldwell KL, Mortensen ME, Jones RL, Caudill SP, Osterloh JD. Total blood mercury concentrations in the U.S. population: 1999-2006. [online May 29, 2009] Int J Hyg Environ Health 2009;212:588-98.

Cardenas A, Roels H, Bernard AM, Barbon R, Buchet JP, Lauwerys RR,et al. Markers of early renal changes induced by industrial pollutants. I. Application to workers exposed to mercury vapour. Br J Ind Med 1993;50:17-27.

Cernichiari E, Brewer R, Myers GJ, Marsh DO, Lapham LW, Cox C, et al. Monitoring methylmercury during pregnancy: maternal hair predicts fetal brain exposure. Neurotoxicology 1995;16(4):705-10.

Centers for Disease Control and Prevention (CDC). Fourth National Report on Human Exposure to Environmental Chemicals. Updated Tables, 2012. [online] Available at URL: 10/26/12

Chan JM, Egeland FM. Fish consumption, mercury exposure, and heart diseases. Nutr Rev 2004;62(2):68-72.

Cianciola ME, Echeverria D, Martin MD, Aposian HV, Woods JS. Epidemiologic assessment of measures used to indicate low-level exposure to mercury vapor (Hgo). J Toxicol Environ Health 1997; 52:19-33.

DeRouen TA, Martin MD, Leroux BG, Townes BD, Woods JS, Leitão J, Castro-Caldas A, Luis H, Bernardo M, Rosenbaum G, Martins IP. Neurobehavioral effects of dental amalgam in children: a randomized clinical trial. JAMA 2006;295(15):1784-92.

Dewailly E, Ayotte P, Bruneau S, Lebel G, Levallois P, Weber JP. Exposure of the Inuit population of Nunavik (Arctic Quebec) to lead and mercury. Arch Environ Health 2001;56(4):350-7.

Drexler H, Schaller KH. The mercury concentration in breast milk resulting from amalgam fillings and dietary habits. Environ Res 1998;77(2):124-9.

Factor-Litvak P, Hasselgren G, Jacobs D, Begg M, Kline J, Geier J, et al. Mercury derived from dental amalgams and neuropsychologic function. Environ Health Perspect 2003;111:719-23.

Grandjean P, Budtz-Jorgensen E, White RF, Jorgensen PJ, Weihe P, Debes F, et al. Methylmercury exposure biomarkers as indicators of neurotoxicity in children aged 7 years. Am J Epidemiol 1999;149:301-5.

Grandjean P, Weihe P, Jorgensen PJ, Clarkson T, Cernichiari E, Videro T. Impact of maternal seafood diet on fetal exposure to mercury, selenium, and lead. Arch Environ Health 1992;47(3):185-95.

Grandjean P, Weihe P, Needham LL, Burse VW, Patterson DG Jr, Sampson EJ, et al. Relation of a seafood diet to mercury, selenium, arsenic, and polychlorinated biphenyl and other organochlorine concentrations in human milk. Environ Res 1995;71(1):29-38.

Halbach S. Amalgam tooth fillings and man’s mercury burden. Hum Exp Toxicol 1994;13:496-501.

Hattula T, Rahola T. The distribution and biological half-time of 203Hg in the human body according to a modified whole-body counting technique. Environ Physiol Biochem 1975;5:252-7.

Hightower JM, O’Hare A, Hernandez GT. Blood mercury reporting in NHANES: Identifying Asian, Pacific Islander, Native American, and multiracial groups. Environ Health Perspect 2006;114(2):173-5.

Hursh JB, Greenwood MR, Clarkson TW, Allen J, Demuth S. The effect of ethanol on the fate of mercury vapor inhaled by man. J Pharmacol Exp Ther 1980;214(3):520-7.

International Agency for Research on Cancer (IARC). IARC Monographs on the Evaluation of Carcinogenic Risks to Humans. Volume 58. Beryllium, Cadmium, Mercury, and Exposures in the Glass Manufacturing Industry. 1993. Available at URL: icon. 10/26/12

Jonsson F, Sandborgh-Englund G, Johanson G. A compartmental model for the kinetics of mercury vapor in humans. Toxicol Appl Pharmacol 1999;155(2):161-8.

KajiwaraY, Yasutake A, Adachi T, Hirayama K. methylmercury transport across the placenta via neutral amino acid carrier. Arch Toxicol 1996;70(5):310-4.

Kingman A, Albertini T, Brown LJ. Mercury concentrations in urine and whole blood associated with amalgam exposure in a US military population. J Dent Res 1998;77(3):461-7.

Langworth S, Elinder CG, Sundquist KG, Vesterberg O. Renal and immunological effects of occupational exposure to inorganic mercury. Br J Ind Med 1992;49(6):394-401.

McDowell MA, Dillon CF, Osterloh J, Bolger PM, Pellizzari E, Fernando R, et al. Hair mercury levels in U.S. children and women of childbearing age: reference range data from NHANES 1999-2000. Environ Health Perspect 2004;112(11):1165-71.

Mehaffey KR, Clickner RP, Bodurow CC. Blood organic mercury and dietary intake: National Health and Nutrition Examination Survey, 1999 and 2000. Environ Health Perspect 2004;112(5):562-70.

Miettinen JK, Rahola T, Hattula T, Rissanen K, Tillander M. Elimination of 203Hg-methyl mercury in man. Ann Clin Res 1971;3(2):116-122.

Myers GJ, Davidson PW, Cox C, Shamlaye CF, Palumbo D, Cernichari, et al. Prenatal methylmercury exposure from ocean fish consumption in the Seychelles child development study. Lancet 2003;361:1686-92.

National Research Council (NRC). Toxicological effects of methylmercury. National Academy Press. Washington (DC). 2000.

Oskarsson A, Schultz A, Skerfving S, Hallen IP, Ohlin B, Lagerkvist BJ. Total and inorganic mercury in breast milk and blood in relation to fish consumption and amalgam fillings in lactating women. Arch Environ Health 1996;51(3):234-241.

Rahola T, Hattula T, Korolainen A, Miettinen JK. Elimination of free and protein-bound ionic mercury (203Hg2+) in man. Ann Clin Res 1973;5:214-219.

Rice DC. The US EPA reference dose for methyl mercury: sources of uncertainty. Environ Res 2004;95:406-13.

Rissanen T, Voutilainen S, Nyyssonen K, Lakka TA, Salonen JT. Fish oil-derived fatty acids, docosahexenoic acid and docosapentaenoic acid, and the risk of acute coronary events—The Kuopio Ischaemic Heart Disease Risk Factor Study. Circulation 2000;103:2766-2679.

Roels HA, Boeckx M, Ceulemans E,Lauwerys RR. Urinary excretion of mercury after occupationalexposure to mercury vapor and influence of the chelating agent meso-2,3-dimercaptosuccinic acid (DMSA). Br J Ind Med 1991;48:247-53.

Sakamoto M, Kubota M, Matsumoto S, Nakano A, Akagi H. Declining risk of methylmercury exposure to infants during lactation. Environ Res 2002;90:185-189.

Sakamoto M, Kubota M, Liu XJ, Murata K, Nakai K, Satoh H. Maternal and fetal mercury and n-3 polyunsaturated fatty acids as a risk and benefit of fish consumption to fetus. Environ Sci Technol 2004;38:3860-3863.

Salonen JT, Seppanen K, Nyyssonen K, Korpela H, Kauhanen J, Kantola M, et al. Intake of mercury from fish, lipid peroxidation, and the risk of myocardial infarction and coronary, cardiovascular, and any death in eastern Finnish men. Circulation 1995;91:645-655.

Sallsten G, Barregard L, Schutz A. Decrease in mercury concentration in blood after long term exposure: a kinetic study of chloralkali workers. Br J Ind Med 1993;50(9):814-821.

Sanchez-Sicilia L, Seto DS, Nakamoto S, Kolff WJ. Acute mercurial intoxication treated by hemodialysis. Ann Intern Med 1963;59(5):692-706.

Sandborgh-Englund G, Elinder CG, Langworth S, Schutz A, Ekstrand J. Mercury in biological fluids after amalgam removal. J Dent Res 1998;77(4):615-624.

Sanzo JM, Dorronsoro M, Amiano P, Amurrio A, Aguinagalde FX, Azpiri MA. Estimation and validation of mercury intake associated with fish consumption in an EPIC cohort of Spain. Public Health Nutr 2001;4(5):981-988.

Schober SE, Sinks TH, Jones RL, Bolger PM, McDowell M, Osterloh J, et al. Blood mercury levels in US children and women of childbearing age, 1999-2000. JAMA 2003;289(13):1667-1674.

Sherlock J, Hislop D, Newton G, Topping G, Whittle K. Elevation of mercury in human blood from controlled ingestion of methyl mercury in fish. Hum Toxicol 1984;2:117-131.

Smith JC, Allen PV, Turner MD, Most B, Fisher HL, Hall LL. The kinetics of intravenously administered methyl mercury in man. Toxicol Appl Pharmacol 1994;128(2):25125-6.

Smith JC, Farris FF. Methyl mercury pharmacokinetics in man: a reevaluation. Toxicol Appl Pharmacol 1996;37:245-252.

Smith PJ, Langolf GD, Goldberg J. Effects of occupational exposure to elemental mercury on short term memory. Br J Ind Med 1983;40:413-419.

Smith RG, Vorwald AJ, Patil LS, Mooney TF. Effects of exposure to mercury in the manufacture of chlorine. Am Ind Hyg Assoc J 1970;31:687-700.

Stern AH. A review of the studies of the cardiovascular health effects of methylmercury with consideration of their suitability for risk assessment. Environ Res 2005;98(1):133-142.

Stern AH, Smith AE. An assessment of the cord blood: maternal blood methyl mercury ratio: implications for risk assessment. Environ Health Perspect 2003;111(12):1465-1470.

Suzuki T, Hongo T, Yoshinaga J, Imai H, Nakazawa M, Matsuo N, et al. The hair-organ relationship in mercury concentration in contemporary Japanese. Arch Environ Health 1993;48(4):221-229.

Tunnessen WW, McMahon KJ, Baser M. Acrodynia: exposure to mercury from fluorescent light bulbs. Pediatrics 1987;79:786-789.

Vahter M, Mottet NK, Friberg L, Lind B, Shen DD, Burbacher T. Speciation of mercury in the primate blood and brain following long-term exposure to methyl mercury. Toxicol Appl Pharmacol 1994;124:221-229.

Vimy MJ, Takahashi Y, Lorscheider FL. Maternal-fetal distribution of mercury (203Hg) released from dental amalgam fillings. Am J Physiol 1990;258(4 Pt 2):R939-945.

Vupputuri S, Longnecker MP, Daniels JL, Guo S, Sandler DP. Blood mercury level and blood pressure among US women: results from the National Health and Nutrition Examination Survey 1999-2000. Environ Res 2005;97(2):195-200.

Woods JS, Martin MD, Leroux BG, DeRouen TA, Leitao JG, Bernardo MF, et al. The contribution of dental amalgam to urinary mercury excretion in children. Environ Health Perspect 2007;115(10):1527-1531.

Zeitz P, Orr MF, Kaye WE. Public health consequences of mercury spills: hazardous substances emergency events surveillance system, 1993-1998. Environ Health Perspect 2002;110:129-132.

Page last reviewed: April 7, 2017