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Biomonitoring Summary

Mercury

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 http://www.epa.gov/mercury and from ATSDR at http://www.atsdr.cdc.gov/toxprofiles/index.asp.

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.

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