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Mercury (Hg) is a naturally occurring volatile metal. In its elemental form is considered non-toxic when consumed as it is not absorbed by the gut (~0.01% absorbed) (Klaassen 2008, ASTDR 1999). Mercury has been used throughout history in medicine, but now is only used as an antiseptic (Brandenberger et al 1997); it is also used in dental amalgams and some traditional folk medicines. These exposures are at very low levels and are at limited risk to public and these practices are being reduced (Shaw 2001, ATSDR 1999). The usage of mercury in pharmaceuticals has now been nearly completely abandoned and its main application is now agricultural. The main route of exposure leading to toxicity is through seafood diets (Klaassen 2008, Brandenberger et al 1997). The reason for this type of exposure leading to high levels of toxicity is the accumulation of mercury within the food chain in forms that are absorbable by the gut, for example methyl-mercury (MeHg or CH3Hg+) (ASTDR 1999, Booth et al 2005, Clarkson et 2003, Klaassen 2008). Methyl-mercury is considered the most toxicologically significant form of mercury (Klaassen 2008, ASTDR 1999).
Organic mercury derivatives have been designed for plant protection, for example fungicides (Brandenberger et al 1997,Trasande et al 2005) . The toxicity of the compound is dependent on the organic group (R) of the structure R-Hg-X, if this R is a methyl group (MeHg) the bond is very stable and the compound is volatile, the X subgroup has little significance on the toxicity of the compound (Brandenberger et al 1997). Microorganisms found within the organic sediment of the sea and fresh water can also methylate inorganic mercury compounds forming methyl-mercury and ethyl-mercury (Brandenberger et al 1997, Booth et al 2005, Klaassen 2008). When mercury containing agricultural residues run-off into the groundwater it will enter the sea and fresh water systems and enter the aquatic food chain starting with plankton (Booth et al 2005, Klaassen 2008). It will slowly accumulate, reaching concentrations up to 80,000 times higher than in the surrounding water in the upper predators such as swordfish (Booth et al 2005, Clarkson et al 2003). These fish are consumed by humans giving a high exposure rate and there are more than 1300 active hazardous waste sites in the US giving rise to higher risk of toxicity (US EPA 2001).
The neurotoxicity of methyl-mercury was highlighted firstly in 1956 in Japan and was named Minamata disease after the place it was first observed (Harada 1995, Klaassen 2008). All subjects commonly exhibited sensory disturbances, ataxia (gross lack of coordination of muscles), dysarthria (slurred speech), and tremor (Harada 1995, Takeuchi et al 1962). Correlation occurred to a chemical plant that had been contaminating the water with waste containing methyl-mercury (Harada 1995, Takeuchi et al 1962, Klaassen 2008). Since this disaster there have been many studies on the toxicity and exposure of mercury and mercury-containing compounds, although other high incident accidents have occurred, such as Iraq in 1960 due to grain contamination with methyl-mercury containing fungicides (Rustam et al 1974, Klaassen 2008).
When methyl-mercury is orally consumed 95% will be absorbed by the gut (Ballatori et al 1998, ATSDR 1997), which will be immediately distributed equally between all tissues and then will quickly start to accumulate in the brain, kidney and muscle (Shaw 2001, Takeuchi et al 1961, Klaassen 2008). This toxicity presents itself as ataxia, constriction of the visual fields leading to blindness and paresthesis (prickling, tingling sensation of the extremities) (Klaassen 2008, ATDSR 1997) but these only become apparent after a long latent period of up to 2 months (Ballatori et al 1998). This is due to neuronal degeneration in the visual cortex, cerebellum and ganglia (Klaassen 2008, ATSDR 1997). As well as the neurotoxicity, there has also been correlation of methyl-mercury toxicity with gastrointestinal and renal symptoms but there have been limited studies (ATSDR 2011). Methyl-mercury is a non-carcinogenic compound (ATSDR 2011). Due to the high lipid solubility the methyl-mercury can easily pass the placental barrier and accumulate in the foetus if oxidised to the inorganic mercury as unable to cross back, thus showing methyl-mercury as a major teratogen (Trasande et al 2005, Clarkson et al 2003). The children born of these infected parentsâ€™ exhibit mental retardation, motor disturbances and paralysis (Brandenberger et al 1997, Trasande et al 2005 Clarkson et al 2003, Klaassen 2008)As well as foetal CNS damage, developing children are also at high risk. The differences in severity of symptoms due to exposure age can also be observed in animal studies (ATSDR 1997, Trasande et al 2005). It is assumed to be due to the immature development of the blood brain barrier (BBB) allowing for a more generalised distribution within the brain and also due to the inhibition of division and migration of neuronal cells and disruption of the cytoarchitecture of the developing brain (Trasande et al 2005, Clarkson et al 2003). The toxicity observed is due to high affinity of mercury and for thiol and sulfhydrl groups. Proteins containing these groups are bound by the mercury-containing compound therefore affecting membrane structure and enzyme function, particularly in CNS due to accumulation due to lipophillicity giving rise to neurological symptoms (Nordberg et al 2007, Trasande et al 2005, Klaassen 2008, ASTDR 1997, Harada 1995, Takeuchi et al 1962 ).
Due to the obvious toxicity there are strict guidelines set by both the Food and Drug Administration (FDA) and the United States Environmental Protection Agency (EPA). The FDA limits methyl-mercury concentration in commercial fish at 1ppm (Shaw 2001, FDA 1984). But concentrations exceeding as high as 1mg/L were observed on the Pacific coasts (Shaw 2001, Oâ€™Connor et al 1995). The EPA recommended a maximum daily intake of 0.1ug/kg day from various sources, this value is formed from a no observed adverse effect level (NOAEL) of more than 5ug/L in whole blood (Shaw 2001, ASTDR 1997, US EPA 2001). In children and pregnant women this value should be decreased due to the susceptibility to toxicity (ASTDR 1997, Trasande et al 2005, Clarkson et al 2003, Nordberg et al 2007). Therefore leading to worries for subjects with high fish diets including pescatarians as will lead to accumulation. If methyl-mercury poisoning is suspected, concentrations can be assessed using hair and urine samples (Brandenberger et al 1997). Hair analysis has a sensitivity of 1.0Î¼g/g and being preferred due to the ease of collection, transportation and storage. (Brandenberger et al 1997,Katz et al 1992).
If toxicity does occur, treatment includes removal of source and contamination, supportive care and chelation therapy (Shaw 2001, Risher et al 2005). The first choice of chelation agent is DMPS but others can be employed. Chelation will not reverse the effects of the toxicity but will halt further neuronal damage and should be started even with suspected poisoning (Shaw 2001, Risher et al 2005, Ballatori et 1998).
Methyl-mercury is a potent neurotoxin and teratogen with the ability to cross the placenta and BBB giving rise to in worst case scenarios irreversible blindness, mentally retarded children, paralysis and encephalitis. There are widespread hazardous sites with high levels of contaminated ecosystems as mercury is environmentally persistent. The ability of the microorganisms to bioactivate to methyl-mercury increases contamination level, as well as run-off from fungicides. The accumulation within the food chains increases possible exposure levels, especially with consumption of ultimate predators such as swordfish. High fish diets are considered to be healthy due to essential oils, low fat and high protein content, but concentration of methyl-mercury cannot be certain although some legislation (FDA/EPA) tries to manage it. At risk groups such as pregnant women and developing children should limit amount of fish in diet.