The US Centers for Disease Control (CDC) has published its biannual report of toxins found in the a representative sample of the US population. The section on mercury, which some people link to autism, is very informative and gives information on how mercury gets into the environment and into our bodies. Its on page 45 of the full report [PDF 3mb] but I’ve copied the text below for convenience.
The results themselves do not point to an alarming level of mercury. Only 5.7% of adults were anywhere near the level known to cause neurological problems and none where over it. None of the children tested exhibited notably high-levels of mercury either. If there was a major problem with mercury causing autism it is likely that a least one child out of the 1500 tested would have notably high levels of mercury in their blood. This does not mean mercury is not connected with autism. It could be that some children have peaks of mercury poisoning due to environmental hot-spots or eating fish with unusually high levels of mercury. Childern are also not created equal. Some are more susceptible to heavy metal poisoning that others.
However, wide-scale mercury poisoning as a cause of the rise in autism is less likely.
CAS No. 7439-97-6
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. 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 the production of batteries and pigments.
Pharmaceutical applications of mercury have been declining, although certain organomercury compounds are still used as preservatives (e.g., thimerosal, phenylmercuric acetate) or topical antiseptics (e.g., merbromin). Some cosmetic skin creams from countries other than the U.S. may contain mercury. Folk medicines may contain mercury compounds, and elemental mercury is used ritually 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. Through biogeochemical cycling, some atmospheric elemental mercury is deposited on land and water. In addition, water can be contaminated by the direct release of elemental and inorganic mercury from industrial processes. Metabolism of mercury by microorganisms in sediments creates methyl mercury, an organomercurial compound, which can bioaccumulate in terrestrial and especially aquatic 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.
Using the 1999-2000 NHANES data, it was estimated that women 16 to 49 years of age ingest a geometric mean of 1.22 micrograms of mercury per day from fish/seafood (approximately 85% as methyl mercury) (Mahaffey et al., 2004). Inhalation of mercury volatilized from dental amalgam is another major source of mercury exposure in the general population and is estimated to result in a daily intake of 1-5 µg per day (U.S. DHHS, 1993). Accidental spills of elemental mercury, which create the potential for subsequent volatization and inhalation of mercury vapor, have often required public health intervention (Zeitz et al., 2002). The kinetics of the different forms of mercury vary considerably. Elemental mercury, absorbed mainly through inhalation of volatilized vapor, undergoes distribution to most tissues, with the highest concentrations occurring in the kidney (Hursh et al., 1980; Barregard et al., 1999). After absorption of elemental mercury, blood concentrations decline initially with a rapid half-life of approximately 1-3 days followed by a slower half-life of approximately 1 week to 3 weeks (Barregard et al., 1992; Sandborgh- Englund et al., 1998). The slow-phase half-life may be several weeks longer in people 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 mercury 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 (Roels et al., 1991; Jonsson et al., 1999).
About 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 absorped 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 (Sherlock et al., 1984; Smith et al., 1994; Smith and Farris, 1996). After exposure to methyl mercury, greater than two-thirds of the mercury is excreted via the feces, with a relatively minor amount eliminated as inorganic mercury in the urine (Smith et al., 1994; Smith and Farris, 1996). Small fractions of inorganic mercury and methyl mercury are incorporated into hair (Suzuki et al., 1993), which has been used in epidemiologic studies as a biomarker of exposure to methyl mercury (McDowell et al., 2004).
Inorganic mercury and methyl mercury are also distributed into human breast milk, although the process may be more efficient for inorganic mercury (Grandjean et al., 1995; Oskarsson et al., 1996). Transplacental transport of methyl mercury and elemental mercury has been demonstrated in animal models. In a recent human study, concentrations of mercury in umbilical cord blood were correlated with mercury concentrations in maternal hair, maternal
fish/seafood consumption, and maternal dental amalgam (Bjornberg et al., 2003). A recent metaanalysis of human studies of the ratio of mercury in umbilical cord blood to maternal blood produced an estimate of 1.7 (Stern and Smith, 2003). The health effects of mercury are diverse and can depend on the form of the mercury to which a person is exposed and the severity and length 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).
Subclinical neurological effects of low-level occupational exposure to elemental mercury have been found in some investigations (Chapman et al., 1990; Bittner et al., 1998), but an impact of low-level environmental exposure, such as that resulting from dental amalgam, has not been established (Factor- Litvak et al., 2003; Bates et al., 2004a).
Exposure to inorganic mercury usually occurs by ingestion. The most prominent effect is on the kidneys, where mercury accumulates, and leads to tubular necrosis. In addition, there may be an irritant or corrosive effect on the gastrointestinal tract (Sanchez-Sicilia et al., 1963). Occupational exposure to elemental mercury vapor has been associated with subclinical effects on biomarkers of renal dysfunction (Cardenas et al., 1993). Acrodynia, a sporadic and predominantly pediatric syndrome in which the constellation of findings may include anorexia, insomnia, irritability, hypertension, maculopapular rash, pain in the extremities and pinkish discoloration of the hands and feet, has been associated with a variety of exposures to elemental mercury and inorganic mercury compounds (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. Methyl mercury has wellcharacterized adverse reproductive effects. High-level prenatal exposure may result in a constellation of developmental deficits that include mental retardation, cerebellar ataxia, dysarthria, limb deformities, altered physical growth, sensory impairments, and cerebral palsy (National Research Council, 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 (National Research Council, 2000; Rice et al., 2003). Although recent investigations have suggested a possible link between chronic ingestion of methyl mercury and an increased risk for myocardial infarction (Guallar et al., 2002; National Research Council, 2000), the existence of a causal relation is unresolved. Information about external exposure (i.e., environmental levels) and
health effects is available from the U.S. EPA’s IRIS Web site at http://www.epa.gov/iris, the U.S. EPA’s mercury homepage at http://www.epa.gov/mercury, and from ATSDR’s Toxicological Profiles at http://www.atsdr.cdc.gov/toxprofiles.
Interpreting Levels of Mercury in Blood and Urine Reported in the Tables
Blood mercury levels were measured in a subsample of NHANES participants aged 1-5 years and in females aged 16-49 years. Participants were selected within the specified age range to be a representative sample of the U.S. population. The measurement of total blood mercury includes both inorganic and organic forms. In the general population, the total blood mercury concentration is due mostly to the dietary intake of organic forms, particularly of methyl mercury. Little organic mercury is excreted in the urine. Urinary mercury consists mostly of inorganic mercury (Cianciola et al., 1997; Kingman et al., 1998). These distinctions can assist in interpreting mercury blood levels in people. Total blood mercury levels are known to increase with greater fish consumption (Grandjean et al., 1995; Mahaffey and Mergler, 1998; Sanzo et al., 2001; Dewailly et al., 2001), and urine levels will increase with the number of teeth filled with mercurycontaining amalgams (Becker et al., 2003). The data in this Report are similar or slightly lower than levels found in other population studies. In Germany, for example, the geometric mean for blood mercury was 0.58 µg/L for 4,645 adults aged 18 to 69 years participating in a 1998 representative population survey (Becker et al., 2002). During the years 1996 through 1998, Benes et al. (2000) studied 1,216 blood donors in the Czech Republic (896 men and 320 women; average age 33 years) and 758 children (average age 9.9 years). The median concentration of blood mercury for adults was 0.78 µg/L and 0.46 µg/L for the juvenile population. A cohort of 1,127 U.S. men (mean age 52.8 years, range 40 years to 78 years) with no occupational exposure to mercury, but who received dental care at military facilities during the mid to late 1990s, had an average blood mercury concentration of 2.55 µg/L (Kingman et al., 1998). Blood mercury levels in both the 1999-2000 and 2001- 2002 subsamples are below levels considered associated with known health effects. When blood mercury levels rise to about 100 µg/L following recent inorganic or elemental mercury poisoning, abnormal renal function tests may occur with low frequency.
Total blood mercury levels in this Report were also well below levels established as occupational exposure guidelines. ACGIH recommends that the blood levels of inorganic mercury in workers not exceed 15 µg/L (six participants in the survey had higher levels, although these levels were unlikely to be due to inorganic forms of mercury). Information about the biological exposure indices (BEIs) is provided here for comparison, not to imply that the BEI is a safety level for general population exposure.
Clinically observable signs of ataxia and paresthesias occur with low frequency when blood mercury levels rise to about 100 µg/L following recent methyl mercury poisoning. However, the developing fetus may be the most susceptible to the effects of ongoing methyl mercury exposure (National Research Council, 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). Report data for the period 1999-2002 show that all women of childbearing age had levels below 58 µg/L, a concentration associated with neurologic effects in the fetus. These data show that 5.7% of women of childbearing age had levels between 5.8 and 58 µg/L; that is, levels within a factor of 10 of those associated with neurological effects. Better defining safe levels of mercury in maternal blood is a priority area for additional research. EPA has set an oral reference dose (RfD, a daily dose considered to be safe) for methyl mercury of 0.1µg/kg/day, derived in part from this and other associated blood levels in outcome studies. A specific value for the blood mercury concentration that corresponds to the RfD has not been established (Rice, 2004).
Urinary mercury levels in recent German (Becker et al., 2003), Czech (Benes et al., 2002), and Italian (Apostoli et al., 2002b) adult population surveys were roughly similar to the values found for women in the 2001–2002 NHANES subsample. An expert-panel report recently prepared for the U.S. Department of Health and Human Services (U.S. DHHS) 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 greater than or equal to 25-35 µg/L (Life Sciences Research Office, 2004). The ACGIH (2001) currently recommends that urinary inorganic mercury in workers not exceed 35 µg/gram of creatinine.
Comparing Adjusted Geometric Means Geometric mean levels of blood mercury for the demographic groups were compared after adjusting for the covariates of race/ethnicity, age, gender, creatinine, and log serum cotinine (data not shown). In NHANES 2001-2002, non-Hispanic black females aged 16-49 years had higher levels than non-Hispanic white and Mexican-American females aged 16-49 years. Non- Hispanic white females aged 16-49 years had higher levels than Mexican American females aged 16-49 years. It is unknown whether these differences associated with age or race/ethnicity represent differences in exposure, pharmacokinetics, or the relationship of dose per body weight.
For urinary mercury levels, there were no differences of the adjusted geometric means among the three race/ethnicity groups.
Finding a measurable amount of mercury in blood or urine does not mean that the level of mercury causes an adverse health effect. These data provide physicians with a reference range so that they can determine whether or not people have been exposed to higher levels of mercury than are found in the general population. These data will also help scientists plan and conduct research about mercury exposure and health effects.