Mercury

Elevated blood Hg indicates higher than average exposure to the metal, but does not provide information about net bodily retention of Hg. Whole blood constitutes both organic (RBC) and inorganic (serum) Hg. However, blood Hg is not indicative of past exposures if the Hg has cleared the blood and deposited in other tissues.

The biological half-lives of inorganic and organic Hg in blood are about 3 days and 60 days, respectively. Blood Hg levels are typically higher than average in ”high-end” fish consumers.

The symptomatology of Hg excess can depend on many factors:

- the chemical form of absorbed Hg and its transport in body tissues,

- presence of other synergistic toxics (Pb and Cd have such effects),

- presence of disease that depletes or inactivates lymphocytes or is immunosuppressive,

- organ levels of xenobiotic chemicals and sulfhydryl-bearing metabolites (e.g. glutathione),

- and the concentration of protective nutrients, (e.g. zinc, selenium, vitamin E).

Early signs of excessive Hg exposure include:

- decreased senses of touch, hearing, vision and taste,

- metallic taste in the mouth,

- fatigue or lack of physical endurance,

- and increased salivation.

Symptoms may progress with moderate or chronic exposure and retention include:

anorexia, numbness and paresthesias, headaches, hypertension, irritability and excitability, and immune suppression, possibly immune dysregulation.

Advanced disease processes from Hg toxicity include:

tremors and incoordination, anemia, psychoses, manic behaviors, possibly autoimmune disorders, renal dysfunction or failure.

Mercury is commonly used in:

dental amalgams, explosive detonators, in elemental or liquid form for thermometers, barometers, and laboratory equipment; batteries and electrodes; and in fungicides and pesticides.

The use of Hg as a funcicial/pesticide (including that in paints) has declined somewhat due to environmental concerns, but mercury residues persist from past use.

Methylmercury, the common, most neurotoxic form, results from methylation of hg in aquatic biota or sediments, both freshwater and ocean sediments. Methylmercury accumulates in aquatic animals and fish and is concentrated up the food chain reaching high concentrations in large fish and predatory birds. Except for fish, the intake of dietary mercury is negligible unless food is contaminated with one of the previously listed forms/sources.

Measurement of fecal Hg provides an indication of exposure to inorganic mercury from dental amalgams.

Net retention of Hg in the body can be assessed by comparison of pre- and post-provocation urinalysis using DMPS, DMSA or Dpenicillamine.

Mercury intoxication is associated with a triad of symptoms: (1) mental changes, (2) spontaneous tremor and deficits in psychomotor performance, and (3) stomatitis and gingivitis. The toxic effects of mercury have been associated with neurological dysfunction, dementia, and autoimmune diseases. Although research suggests that the etiology of autism is multifactorial, numerous reports demonstrate that aspects of mercury toxicity appear similar to autism symptomatology.

According to the CDC, mercury released from amalgams may comprise up to 75% of an individual’s mercury exposure. Methylmercury from seafood is considered to be the most important source of non-occupational human mercury exposure. Blood mercury has revealed low level chronic and acute exposure from work environments. Significant exposure is evident when whole blood alkyl mercury is greater than 50 μg/L, or when inorganic mercury (Hg2+) exposure is greater than 200 μg/L. Children’s reference values for whole blood mercury from 1.5 to 1.0 μg/L have been proposed. Risk of Attention Deficit Hyperactivity Disorder (ADHD) was found to be nearly 10 times higher when blood mercury was above 29 nmol/L. The quantity of mercury assayed in blood and hair, but not urine, correlates with the severity of toxicity symptoms.