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Mercury is present in the environment in several forms, for example as inorganic mercury—elemental mercury (Hg⁰), mercurous mercury (Hg¹⁺), mercuric salts (Hg²⁺)—and in organic compounds (methylated mercury). In its elemental form, metallic mercury is the only metal that exists in a liquid state at ambient temperatures. It is also known as quicksilver (Clarkson and Magos 2006). Mercury vapors released from elemental mercury occur naturally in the environment as a consequence of the removal of gases from the earth’s crust, volcanic eruptions, and evaporation from oceans and soils. Anthropogenic sources such as metal mining, smelting (with mercury, gold, copper, and zinc), coal combustion, municipal incinerators, and the chloralkaline industry contribute significantly to atmospheric mercury, and mercury vapors are stable within the atmosphere for about one year (Tokar et al. 2013). Once released into the environment, the various forms of mercury undergo complex oxidation-reduction and methylation-demethylation reactions known as the mercury cycle, which further gives rise to inorganic or organic species that become globally distributed.

Exposure to inorganic mercury can occur through inhalation and through oral or dermal routes, but inhalation is the most biologically relevant owing to its high absorbance potential in the lungs (up to 80%; see Risher et al. 2003). Inorganic mercury poisoning often occurs as a result of the inhalation of mercury vapor from industrial sources, dental amalgams, or the continued use of mercury compounds in consumer products (Clarkson and Magos 2006). The inhalation of mercury vapor from the use of liquid mercury can follow from occupational exposure in the chloroalkali industry, in the manufacture of scientific instruments, in fluorescent lightbulb manufacturing, in small-scale gold mining, and in dentistry where mercury amalgams are used as fillings for tooth decay (Clarkson and Magos 2006; Risher et al. 2003). Mercury poisoning can also result from inorganic mercury, which is most commonly found as calomel or mercurous chloride (Hg₂Cl₂) and was used widely in diuretics, antiseptics, skin products, laxatives, and teething powder in the twentieth century (Clarkson and Magos 2006; Klaassen 2013). Additionally, the use of phenylmercuric compounds as antifungal agents in paints, although banned in the United States, still continues in other countries (Risher et al. 2003).

Ding et al. (2016) investigated the plasma miRNA expression profile for female workers in eastern China who were occupationally exposed to inorganic mercury and found that four miRNAs (miR-16-5p, miR-30c-3p, miR-181a-5p, and let-7e-5p) were downregulated and four miRNAs (miR-92a-3p, miR-122-5p, miR-451a, and miR-486-5p) were upregulated, as measured by microarray. Validation of these miRNAs by TaqMan-based RT-qPCR revealed that two miRNAs, namely miR-92a-3p and miR-486-5p, were consistently upregulated when measured by both methods.

Both metallic and organic mercury compounds are oxidized to inorganic mercury in the blood and in the liver, which plays a key role in animal toxicity (Tchounwou et al. 2003). However, organomercurial compounds are generally more toxic to animals than inorganic mercury on account of their high bioaccumulation potential, and methyl mercury (MeHg) is toxicologically the most important organic form. In humans, consumption of methyl mercury-contaminated fish is the predominant route of exposure to organomercury, but other consumables such as drinking water, cereals, vegetables, and meat can also be sources of exposure (Holmes et al. 2009; Karagas et al. 2012; Yang et al. 2020). Early stages of life are generally more sensitive to mercury, such that exposure to high-level elemental, inorganic, and organic mercury results in severe developmental and neurological defects, depending on the length and dose of this exposure (Yang et al. 2020). However, to date, no literature exists that has examined circulating miRNAs that are due to the consumption of methylmercury-containing food sources.