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Trace Elements in Abiotic and Biotic Environments
The toxicity of Hg salts varies with their solubility. Inorganic Hg salts are water
soluble, irritate the gut, and cause severe kidney damage. Following oral exposure,
inorganic Hg salts show limited absorption, which is related to their water solubility.
Inorganic Hg compounds are not lipid soluble and do not readily cross the blood–
brain barrier or placenta membranes. Ionic species of inorganic Hg readily bind to
sulfhydryl groups of various thiol-containing compounds, such as glutathione, cysteine, and metallothionein. Kidneys exhibit the greatest concentration of Hg following
exposure to inorganic Hg compounds (WHO 2011b).
Ingestion of other common forms of Hg, such as the salt HgCl 2 , which damages
the gastrointestinal tract and causes kidney failure, is unlikely from environmental
sources.
Exposure to elemental Hg is hazardous because of its potential release of toxic
Hg vapor, which is readily absorbed into the body through inhalation. If elemental
Hg is ingested, it is absorbed relatively slowly and may pass through the digestive
system without causing damage. The vapor pressure at room temperature is about
100 times the safe amount, so poisoning can occur if Hg metal is spilled into crevices
or cracks in the floorboards, so that heating metallic Hg greatly increases the associated risks, as inhalation is the usual route of toxicity. Dentists are occasionally
poisoned this way. Inhalation of Hg vapor may cause respiratory, cardiovascular,
kidney, and neurological effects (Health Canada 2010).
Inhaled Hg vapor accumulates in the body, in particular the central nervous
system, which is the site of its major toxic actions. Approximately 70%–80% of
Hg vapor is absorbed in humans. Once absorbed, a proportion of Hg is taken up
by the red blood cell, while some remains in the bloodstream, allowing its rapid
distribution around the body, including the central nervous system. Within the red
blood cells, liver, and central nervous system, the metal is oxidized through the
catalase–peroxide pathway to Hg 2+ oxide. Mercury excretion from the body starts
almost immediately after absorption, following a variety of routes, though principally by the kidneys. Chronic poisoning markedly affects the central nervous
system and kidney.
The organic Hg compounds are very lipid soluble: 90%–100% of an oral dose
is absorbed. Organic Hg compounds, which are fat soluble, can cross the blood–
brain barrier and cause neurological damage, but inorganic Hg salts are not lipid
soluble, and do not cross this barrier in significant amounts. Usually Hg 1+ compounds are of low solubility and significantly less toxic than Hg 2+ compounds.
Inorganic Hg salts present a far greater hazard than elemental Hg if ingested
orally, owing to their greater water solubility. For Hg 2+ chloride, the lethal dose
may be as small as 0.5 g, compared with 100 g Hg metal. Mercury salts are usually nonvolatile solids, so poisoning by inhalation is rare, though toxicity may
arise if aerosols are deposited in the lungs. Once adsorbed, the Hg 1+ form will
readily react with the thiol groups of amino acids such as cysteine. The majority of the dose of an ingested inorganic Hg salt accumulates either in the liver,
where it is excreted in the bile, or in the kidney, where it is excreted in the urine
(Langford and Ferner 1999).
Following absorption, organic Hg is distributed to all tissues, including hair,
with highest accumulation in the kidneys. Organic Hg is demethylated in the body
Trace Elements in Abiotic and Biotic Environments
The toxicity of Hg salts varies with their solubility. Inorganic Hg salts are water
soluble, irritate the gut, and cause severe kidney damage. Following oral exposure,
inorganic Hg salts show limited absorption, which is related to their water solubility.
Inorganic Hg compounds are not lipid soluble and do not readily cross the blood–
brain barrier or placenta membranes. Ionic species of inorganic Hg readily bind to
sulfhydryl groups of various thiol-containing compounds, such as glutathione, cysteine, and metallothionein. Kidneys exhibit the greatest concentration of Hg following
exposure to inorganic Hg compounds (WHO 2011b).
Ingestion of other common forms of Hg, such as the salt HgCl 2 , which damages
the gastrointestinal tract and causes kidney failure, is unlikely from environmental
sources.
Exposure to elemental Hg is hazardous because of its potential release of toxic
Hg vapor, which is readily absorbed into the body through inhalation. If elemental
Hg is ingested, it is absorbed relatively slowly and may pass through the digestive
system without causing damage. The vapor pressure at room temperature is about
100 times the safe amount, so poisoning can occur if Hg metal is spilled into crevices
or cracks in the floorboards, so that heating metallic Hg greatly increases the associated risks, as inhalation is the usual route of toxicity. Dentists are occasionally
poisoned this way. Inhalation of Hg vapor may cause respiratory, cardiovascular,
kidney, and neurological effects (Health Canada 2010).
Inhaled Hg vapor accumulates in the body, in particular the central nervous
system, which is the site of its major toxic actions. Approximately 70%–80% of
Hg vapor is absorbed in humans. Once absorbed, a proportion of Hg is taken up
by the red blood cell, while some remains in the bloodstream, allowing its rapid
distribution around the body, including the central nervous system. Within the red
blood cells, liver, and central nervous system, the metal is oxidized through the
catalase–peroxide pathway to Hg 2+ oxide. Mercury excretion from the body starts
almost immediately after absorption, following a variety of routes, though principally by the kidneys. Chronic poisoning markedly affects the central nervous
system and kidney.
The organic Hg compounds are very lipid soluble: 90%–100% of an oral dose
is absorbed. Organic Hg compounds, which are fat soluble, can cross the blood–
brain barrier and cause neurological damage, but inorganic Hg salts are not lipid
soluble, and do not cross this barrier in significant amounts. Usually Hg 1+ compounds are of low solubility and significantly less toxic than Hg 2+ compounds.
Inorganic Hg salts present a far greater hazard than elemental Hg if ingested
orally, owing to their greater water solubility. For Hg 2+ chloride, the lethal dose
may be as small as 0.5 g, compared with 100 g Hg metal. Mercury salts are usually nonvolatile solids, so poisoning by inhalation is rare, though toxicity may
arise if aerosols are deposited in the lungs. Once adsorbed, the Hg 1+ form will
readily react with the thiol groups of amino acids such as cysteine. The majority of the dose of an ingested inorganic Hg salt accumulates either in the liver,
where it is excreted in the bile, or in the kidney, where it is excreted in the urine
(Langford and Ferner 1999).
Following absorption, organic Hg is distributed to all tissues, including hair,
with highest accumulation in the kidneys. Organic Hg is demethylated in the body