Mercury can affect previously healthy individuals who ingest the muscles of sea- and fresh water fish that harbor toxic amounts of mercury, and others exposed to toxic dust and fumes at work sites tainted by old paint. Mercury-related neurotoxicity starts with acute or chronic exposure and proceeds through a series of steps that pass the blood brain barrier (BBB) where immune system activation occurs before incurring neuronal changes. This includes heightened production by brain supporting cells, termed microglial cells, of two molecules, tumor necrosis factor (TNF)-α and glutamic acid, both of which are potentially toxic to neurons. Microglial cells expressing TNF-α increase the level of glutamic acid while its reuptake into astrocytes is inhibited by mercury-related suppression of Na+-dependent transporters, further adding to the initial insult. Glutamic acid production, mediated by mercury-induced TNF-α, explains some, but not all, of the brain-selective changes associated with mercury neurotoxicity. Glial cell-mediated immune mechanisms are also of notable importance in the progression and exacerbation of several neurodegenerative disorders including Alzheimer disease, amyotrophic lateral sclerosis, and Parkinson disease.
Although there is a limited literature regarding mercury toxicity and neurological infectious illness, exposure to sub-toxic doses of elemental mercury has been employed experimentally in two disorders where it alters cell and humor-mediated immune responses: zoonotic cutaneous Leishmaniasis due to infection by Leishmania (L.) major, a parasitic intracellular pathogen that infects macrophages and dendritic cells of the immune system; and Lyme disease caused by spirochete vector, Borrelia (B.) burgdorferi. Resistance to L. major in experimental mice depends upon an adequate initial interferon (IFN)-γ production, whereas an early interleukin (IL)-4 production results in a non-healing phenotype. Treatment with mercury chloride prior to L. major infection is associated with increased parasite. In a particular strain of mice known to eradicate B. burgdorferi infection and resultant arthritis due to a strong initial T-helper cell (Th)-like responses, exposure to sub-toxic doses of mercury chloride is associated with less severe histological arthritis and delayed eradication of spirochetes in exposed, Borrelia-infected (BbHg) mice compared to unexposed, Bb mice. Both the numbers of Th1 and Th2 cytokine-secreting cells are reduced in BbHg mice, with an alteration in the balance of Th2-induced levels of IgE and IgG2a. These findings raise the intriguing possibility that symptoms of chronic Lyme disease in humans may be due in part, to aberrant cell-and humoral-mediated host immune responses in the setting of mercury exposure, similar to experimental animals.
In general, the decision to proceed with chelation therapy is guided by a history of toxic exposure such as ingestion of contaminated fish, breathing contaminated workplace air, skin contact with mercury, or dental amalgam fillings; combined with clinical and laboratory findings of increased mercury in analysis of blood, urine, hair and nails. Conventional chelation therapy to enhance the elimination of mercury from the body employs 2, 3-Dimercapto-1-propanesulfonic acid (DMPS) and its sodium salt, Unithiol. Integrative interventions employ vitamin and herbal preparations.