Detecting mercury toxicity
Mercury (Hg) is essentially nontoxic in its elemental form. If Hg(0) is chemically modified to the ionized, inorganic species, Hg(+2), it becomes toxic. Further bioconversion to an alkyl Hg, such as methyl Hg (CHHg[+]), yields a species of mercury that is highly selective for lipid-rich tissue such as neurons and is very toxic. The relative order of toxicity is:
Not Toxic - Hg(0) < Hg(+2) << CH(3)Hg(+) -- Very Toxic
Mercury can be chemically converted from the elemental state to the ionized state. In industry, this is frequently done by exposing Hg(0) to strong oxidizing agents such as chlorine.
Hg(0) can be bioconverted to both Hg(+2) and alkyl Hg by microorganisms that exist both in the normal human gut and in the bottom sediment of lakes, rivers, and oceans. When Hg(0) enters bottom sediment, it is absorbed by bacteria, fungi, and small microorganisms; they metabolically convert it to Hg(+2), CH(3)Hg(+), and (CH)(+2)Hg. Should these microorganisms be consumed by larger marine animals and fish, the mercury passes up the food chain in rather toxic form.
Mercury expresses its toxicity in 3 ways:
-Hg(+2) is readily absorbed and reacts with sulfhydryl groups of protein, causing a change in the tertiary structure of the protein-a stereoisomeric change-with subsequent loss of the unique activity associated with that protein. Because Hg(+2) becomes concentrated in the kidney during the regular clearance processes, this target organ experiences the greatest toxicity.
-With the tertiary change noted previously, some proteins become immunogenic, eliciting a proliferation of T lymphocytes that generate immunoglobulins to bind the new antigen; collagen tissues are particularly sensitive to this.
-Alkyl Hg species, such as CH(3)Hg(+), are lipophilic and avidly bind to lipid-rich tissues such as neurons. Myelin is particularly susceptible to disruption by this mechanism.
Members of the public will occasionally become concerned about exposure to mercury from dental amalgams. Restorative dentistry has used a mercury-silver amalgam for approximately 90 years as a filling material. A small amount of mercury (2-20 mcg/day) is released from a dental amalgam when it was mechanically manipulated, such as by chewing. The habit of gum chewing can cause release of mercury from dental amalgams greatly above normal. The normal bacterial flora present in the mouth converts a fraction of this to Hg(+2) and CH(3)Hg(+), which was shown to be incorporated into body tissues. The World Health Organization safety standard for daily exposure to mercury is 45 mcg/day. Thus, if one had no other source of exposure, the amount of mercury released from dental amalgams is not significant.(1) Many foods contain mercury. For example, commercial fish considered safe for consumption contain <0.3 mcg/g of mercury, but some game fish contain >2.0 mcg/g and, if consumed on a regular basis, contribute to significant body burdens.
Therapy is usually monitored by following urine output; therapy may be terminated after urine excretion is <50 mcg/day.
Normal: 0-9 ng/mL
Reference values apply to all ages.
The quantity of mercury (Hg) found in blood and urine correlates with degree of toxicity. Hair analysis can be used to document the time of peak exposure if the event was in the past.
Normal whole blood mercury is usually <10 ng/mL.
Individuals who have mild exposure during work, such as dentists, may routinely have whole blood mercury levels up to 15 ng/mL.
Significant exposure is indicated when the whole blood mercury is >50 ng/mL if exposure is due to alkyl Hg, or >200 ng/mL if exposure is due to Hg(+2).
To avoid contamination during specimen collection, it is essential to follow collection procedures as outlined in Trace Metals Analysis Specimen Collection and Transport in Special Instructions.
High concentrations of gadolinium and iodine are known to interfere with most metals tests. If either gadolinium- or iodine-containing contrast media has been administered, a specimen should not be collected for 96 hours.
Clinical Reference Provides recommendations for further in-depth reading of a clinical nature
1. Lee R, Middleton D, Calwell K, et al: A review of events that expose children to elemental mercury in the United States. Environ Health Perspect 2009;117:871–878
2. Bjorkman L, Lundekvam B, Laegreid T, et al: Mercury in human brain, blood, muscle and toenails in relation to exposure: an autopsy study. Environmental Health 2007;6:30-44
3. deBurbure C, Buchet J-P, Leroyer A, et al: Renal and neurologic effects of cadmium, lead, mercury, and arsenic in children: evidence of early effects and multiple interactions at environmental exposure levels. Environ Health Perspect 2006;114:584–590