23 C HAPTER 3 Properties Mercury, a silver-white metal that is liquid at room temperature and highly volatile, can exist in three oxidation states: elemental mercury (Hg o ), mercurous ion (Hg 2 2+ ), and mercuric ion (Hg 2+ ). It can be part of both inorganic and organic compounds (USEPA, 1980; Clarkson et al., 1984). All mercury compounds interfere with thiol metabolism, causing inhibition or inactivation of proteins containing thiol ligands and ultimately to mitotic disturbances (Das et al., 1982; Elhassani, 1983; Hook and Hewitt, 1986). The mercuric species is the most toxic inorganic chemical form, but all three forms of inorganic mercury may have a common molecular mechanism of damage in which Hg 2+ is the toxic species (Clarkson and Marsh, 1982). Mercury poisoning and treatment is discussed in more detail in Chapter 4. 3.1 PHYSICAL Pure mercury is a coherent, silvery-white mobile liquid with a metallic luster (Anon., 1948). In thin layers it transmits a bluish-violet light. It freezes at about minus 39 °C with contraction, forming a white, ductile, malleable mass easily cut with a knife, and with cubic crystals. When heated, the metal expands uniformly, boiling at 357.01°C at 760 mm, and vaporizing at about 360.0 ° C. The vapor is colorless. Mercury forms two well-defined series of salts: the mercurous salts derived from the oxide Hg 2 O, and the mercuric salts from the oxide HgO. Mercuric oxide occurs in two forms: a bright red crystalline powder and as an orange-yellow powder. The yellow form is the most reactive and is transformed into the red when heated at 400.0 ° C. Heating the red form results in a black compound, which regains its color on cooling; on further heating to 630.0 ° C, it decomposes to mercury and oxygen (Anon., 1948). Mercurous and mercuric chloride, known respectively as calomel and corrosive sublimate, are two of the most important salts of mercury (Table 3.1). Other halogenated mercury salts include mercurous bromide, Hg 2 Br 2 , a yellowish-white powder insoluble in water; mercuric bromide, HgBr 2 , comprised of white crystals sparingly soluble in cold water but readily soluble in hot water; mercurous iodide, Hg 2 I 2 , a yellowish-green powder; and mercuric iodide, which exists in two crystalline forms. Other mercuric and mercurous compounds include nitrates, nitrites, sulfides, sulfates, phosphides, phosphates, and ammonium salts (Anon., 1948). 3.2 CHEMICAL Elemental mercury is relatively inert in dry air, oxygen, nitrous oxide, carbon dioxide, ammonia, and some other gases at room temperatures (Anon., 1948). In damp air, it slowly becomes coated © 2006 by Taylor & Francis Group, LLC 24 MERCURY HAZARDS TO LIVING ORGANISMS with a film of mercurous oxide. When heated in air or oxygen, it is transformed into the red mercuric oxide, which decomposes into mercury and oxygen on continued heating at higher temperatures. Mercury dissolves many metals to form compounds called amalgams (Anon., 1948). Chemical speciation is probably the most important variable influencing mercury toxicity, but mercury speciation is difficult to quantify, especially in natural environments (Boudou and Ribeyre, 1983). Mercury compounds in an aqueous solution are chemically complex. Depending on pH, alkalinity, redox, and other variables, a wide variety of chemical species are liable to be formed, having different electrical charges and solubilities. For example, HgCl 2 in solution can speciate into Hg(OH) 2 , Hg 2+ , HgCl + , Hg(OH) - , HgCl 3 - , and HgCl 4 2- ; anionic forms predominate in saline environments (Boudou and Ribeyre, 1983). In the aquatic environment, under naturally occurring conditions of pH and temperature, mercury may also become methylated by biological or chemical processes, or both (Beijer and Jernelov, 1979; USEPA, 1980; Ramamoorthy and Blumhagen, 1984; Zillioux et al., 1993; Figure 3.1) — although biological methylation is limited (Callister and Winfrey, 1986). Methylmercury is the most hazardous mercury species due to its high stability, its lipid solubility, and its possession of ionic properties that lead to a high ability to penetrate membranes in living organisms (Beijer and Jernelov, 1979; Hamasaki et al., 1995). In general, essentially all mercury in freshwater fish tissues is in the form of methylmercury; however, meth- ylmercury accounts for less than 1.0% of the total mercury pool in a lake (Regnell, 1990). All mercury discharged into rivers, bays, or estuaries as elemental (metallic) mercury, inorganic divalent mercury, or phenylmercury or alkoxyalkyl mercury can be converted into methylmercury compounds by natural processes (Jernelov, 1969; Figure 3.1). Mercury methylation in ecosystems depends on mercury loadings, microbial activity, nutrient content, pH and redox conditions, sus- pended sediment load, sedimentation rates, and other variables (USNAS, 1978; Compeau and Bartha, 1984; Berman and Bartha, 1986; Callister and Winfrey, 1986; Jackson, 1986). Net meth- ylmercury production was about 10 times higher in reduced sediments than in oxidized sediments (Regnell, 1990). The finding that certain microorganisms are able to convert inorganic and organic forms of mercury into the highly toxic methylmercury or dimethylmercury has made it clear that any form of mercury is highly hazardous to the environment (USEPA, 1980, 1985). The synthesis of methylmercury by bacteria from inorganic mercury compounds present in the water or in the sediments is the major source of this molecule in aquatic environments (Boudou and Ribeyre, 1983; Nakamura, 1994). This process can occur under both aerobic and anaerobic conditions (Beijer and Jernelov, 1979; Clarkson et al., 1984), but seems to favor anaerobic conditions (Olson and Cooper, 1976; Callister and Winfrey, 1986). Transformation of inorganic mercury to an organic form by © 2006 by Taylor & Francis Group, LLC Table 3.1 Some Properties of Mercury and Its Compounds a Property Elemental Mercury Mercurous Chloride Mercuric Chloride Methylmercury Chloride Empirical formula Hg Hg 2 Cl 2 HgCl 2 CH 3 HgCl Molecular weight 200.59 472.09 271.52 251.09 c Chlorine, % 0 15.02 26.12 14.12 c Mercury, % 100 84.98 73.88 79.89 c Melting point, ° C −38.87 Sublimes at 400–500 277 170 c Density 13.534 7.15 5.4 4.063 c Solubility, mg/L (ppm) in water 0.056 2.0 74,070 1,016 d in benzene 2.387 b Insoluble 5,000 6,535 e a All data from Merck Index (1976), except where indicated. b Spencer and Voigt (1961). c Weast and Astle (1982). d Eisler (unpublished), 72-h equilibrium value. e Eisler (unpublished), 24-h equilibrium value. PROPERTIES 25 bacteria alters its biochemical reactivity and hence its fate (Windom and Kendall, 1979; Figure 3.1). Methylmercury is decomposed by bacteria in two phases. First, hydrolytic enzymes cleave the C–Hg bond, releasing the methyl group. Second, a reductase enzyme converts the ionic mercury to the elemental form, which is then free to diffuse from the aquatic environment into the vapor phase. These demethylating microbes appear to be widespread in the environment; they have been isolated from water, sediments, and soils and from the gastrointestinal tract of mammals, including humans (Clarkson et al., 1984). Some strains of microorganisms contain mercuric reductase, which transforms inorganic mercury to elemental mercury, and organomercurial lyase, which degrades organomercurials to elemental mercury (Baldi et al., 1991). Humic substances can reduce inorganic divalent mercury (Hg 2+ ) to elemental mercury (Hg o ). In aquatic environments, Hg o was highest under anoxic conditions, in the absence of chloride, and at pH 4.5 (Allard and Arsenie, 1991). Under these conditions, about 25.0% of 400.0 µg Hg 2+ /L was reduced to Hg o in 50 h. Production of Hg o was reduced in the presence of europium ions and WATER AND BENTHIC REGION AIR ELEMENTAL SHELLFISH MERCURIC MERCUROUS METHYL DIMETHYL inorganic and organic complexes FISH CH 4 Hg 2+ Hg 0 Hg 0 Hg 2+ Hg 2+ 2 HgS (CH 3 ) 2 Hg (CH 3 ) 2 Hg CH 3 SHgCH 3 CH 3 Hg + C 2 H 6 CH 3 Hg + © 2006 by Taylor & Francis Group, LLC Figure 3.1 Major transformations of mercury in the environment. (Modified from Beijer and Jernelov, 1979; Nakamura, 1994; and Eisler, 2000.) 26 MERCURY HAZARDS TO LIVING ORGANISMS by methylated carboxyl groups in the humic substances (Allard and Arsenie, 1991). Mercury is efficiently transferred through wetlands and forests in a more reactive form relative to other land use patterns, resulting in an increased uptake by organisms inhabiting these rivers or downstream impoundments and drainage lakes (Hurley et al., 1995). The behavior and accumulation of mercury in forest soils of Guyana, South America, is related to the penetration of humic substances and the progressive adsorption onto iron oxy-hydroxides in the mineral horizons; flooding of these soils may lead to a release of 20.0% of the mercury initially present (Roulet and Lucotte, 1995). Methylmercury is produced by methylation of inorganic mercury present in both freshwater and saltwater sediments, and accumulates in aquatic food chains in which the top-level predators usually contain the highest concentrations (Clarkson and Marsh, 1982). The percent of total mercury accounted for by methylmercury generally increases with higher trophic levels, confirming that methylmercury is more efficiently transferred to higher trophic levels than inorganic mercury compounds (Becker and Bigham, 1995). Organomercury compounds other than methylmercury decompose rapidly in the environment, and behave much like inorganic mercury compounds (Beijer and Jernelov, 1979). In organisms near the top of the food chain, such as carnivorous fishes, almost all mercury accumulated is in the methylated form, primarily as a result of the consumption of prey containing methylmercury; methylation also occurs at the organism level by way of mucus, intestinal bacteria, and enzymatic processes, but these pathways are not as important as diet (Huckabee et al., 1979; Boudou and Ribeyre, 1983). In tissues of marine flounders, inorganic mercury compounds are strongly bound to metallothioneins and high-molecular-weight ligands; however, methylmercury has a low affinity for metallothioneins and is strongly lipophilic (Barghi- giani et al., 1989). 3.3 BIOLOGICAL The biological cycle of mercury is delicately balanced, and small changes in input rates, geophysical conditions, and the chemical form of mercury can result in increased methylation rates in sensitive systems (USNAS, 1978). For example, the acidification of natural bodies of freshwater is statisti- cally associated with elevated concentrations of methylmercury in the edible tissues of predatory fishes (Clarkson et al., 1984). Acidification has a stronger effect on the supply of methylmercury to the ecosystem than on specific rates of uptake by the biota (Bloom et al., 1991). In chemically sensitive waterways, such as poorly buffered lakes, the combined effects of acid precipitation and increased emissions of mercury to the atmosphere (with subsequent deposition) pose a serious threat to the biota if optimal biomethylation conditions are met (USNAS, 1978). In remote lakes of the Adirondack mountain region in upstate New York, fish contain elevated mercury concentra- tions in muscle; mercury loadings in fish were directly associated with decreasing water column pH and increasing concentrations of dissolved organic carbon (DOC), although high DOC concen- trations may complex methylmercury, thus diminishing its bioavailability (Driscoll et al., 1995). At high concentrations of monomeric aluminum, the complexation of methylmercury with DOC decreases, enhancing the bioavailability of methylmercury (Driscoll et al., 1995). Mercury excretion in mammals is through the urine and feces, and depends on the form of mercury, dose, and time postexposure (Goyer, 1986). With mercury vapor, there is minor initial loss from exhalation and major loss via fecal excretion. With inorganic mercury, fecal loss is predominant after initial exposure, and renal excretion increases with time. With methylmercury, about 90.0% is excreted in feces after acute or chronic exposure and does not change over time (Goyer, 1986). Based on animal studies, all forms of mercury can cross the placenta to the fetus (Goyer, 1986). Fetal uptake of elemental mercury in rats — possibly due to its high solubility in lipids — is 10 to 40 times higher than uptake after exposure to inorganic mercury salts. Concentrations of mercury in the fetus after exposure to alkylmercuric compounds, when compared to elemental mercury, are © 2006 by Taylor & Francis Group, LLC PROPERTIES 27 twice those found in maternal tissues, and methylmercury levels in fetal red blood cells are 30.0% higher than in maternal cells. The positive fetal maternal gradient and increased mercury concen- tration in fetal erythrocytes enhance fetal toxicity to mercury, especially after exposure to alkyl- mercury. Maternal milk contains about 5.0% of the mercury concentration of maternal blood; however, neonatal exposure to mercury may be greatly augmented by nursing (Goyer, 1986). Elemental or metallic mercury is oxidized, probably via catalases, to divalent mercury after absorption into body tissues (Goyer, 1986). Most inhaled mercury vapor absorbed into erythrocytes is transformed into divalent mercury, but some is also transported as metallic mercury to the brain, where biotransformation may occur. Some metallic mercury may cross the placenta into the fetus. Oxidized metallic mercury is then accumulated by brain and fetus. Organomercurials also undergo biotransformation to divalent mercury compounds in tissues by cleavage of the carbon–mercury bond, with no evidence of organomercury formation by mammalian tissues. Phenylmercurials are converted to inorganic mercury more rapidly than the shorter-chain methylmercurials. Phenyl and methoxyethyl mercurials are excreted at about the same rate as inorganic mercury, whereas methyl- mercury excretion is slower (Goyer, 1986). The half-time persistence of methylmercurials in mammalian tissues is about 70 days and seems to follow a linear pattern. For inorganic mercury salts, the biological half-time is about 40 days. And for elemental mercury or mercury vapor, the half-time persistence in tissues ranges between 35 and 90 days and also appears to be linear (Goyer, 1986). 3.4 BIOCHEMICAL Mercury binds strongly with sulfhydryl groups, and has many potential target sites during embryo- genesis; phenylmercury and methylmercury compounds are among the strongest known inhibitors of cell division (Birge et al., 1979). In mammalian hepatocytes, the L-alanine carrier contains a sulfhydryl group that is essential for its activity and is inhibited by mercurials (Sellinger et al., 1991). In the little skate (Raja erinacea), HgCl 2 inhibits Na + -dependent alanine uptake and Na + /K + - ATPase activity, and increases K + permeability. Inhibition of Na + -dependent alanine in skate hepa- tocytes by HgCl 2 is attributed to three different concentration-dependent mechanisms: (1) direct interaction with the transporters; (2) dissipation of the Na + gradient; and (3) loss of membrane integrity (Sellinger et al., 1991). Organomercury compounds, especially methylmercury, cross pla- cental barriers and can enter mammals by way of the respiratory tract, gastrointestinal (GI) tract, skin, or mucus membranes (Elhassani, 1983). When compared with inorganic mercury compounds, organomercurials are more completely absorbed, are more soluble in organic solvents and lipids, pass more readily through biological membranes, and are slower to be excreted (Clarkson and Marsh, 1982; Elhassani, 1983; Greener and Kochen, 1983). Biological membranes, including those at the blood–brain interface and placenta, tend to discriminate against ionic and inorganic mercury, but allow relatively easy passage of methylmercury and dissolved mercury vapor (Greener and Kochen, 1983). As judged by membrane model studies, it appears that electrically neutral mercurials are responsible for most of the diffusion transport of mercury, although this movement is modified significantly by pH and mercury speciation. It appears, however, that the liposolubility of meth- ylmercury is not the entire reason for its toxicity and does not play a major role in its transport. This hypothesis should be examined further in studies with living membranes (Boudou et al., 1983). In liver cells, methylmercury forms soluble complexes with cysteine and glutathione, which are secreted in bile and reabsorbed from the GI tract. In general, however, organomercurials undergo cleavage of the carbon–mercury bond, releasing ionic inorganic mercury (Goyer, 1986). Mercuric mercury induces synthesis of metallothioneins, mainly in kidney cells. Mercury within renal cells becomes localized in lysosomes (Goyer, 1986). The finding of naturally elevated mercury concentrations in marine products of commerce is worrisome to regulatory agencies charged with protection of human health. This topic is discussed © 2006 by Taylor & Francis Group, LLC 28 MERCURY HAZARDS TO LIVING ORGANISMS later in Chapter 6 and Chapter 12. At this time, however, many authorities argue that mercury–sele- nium interactions are the key to methylmercury bioavailability in human diets. In the case of marine mammals and seabirds, for example, mercury is accumulated from the diet mainly as methylmercury and then transformed into the less toxic inorganic mercury. Accordingly, most of the tissue mercury found in high concentrations of these two marine groups is inorganic mercury (Itano et al., 1984; Thompson, 1990; Law, 1996; Yang et al., 2002). Many authorities aver that selenium detoxifies inorganic mercury by forming complexes in a 1:1 molar ratio (Koeman et al., 1973; Ping et al., 1986; Palmisano et al., 1995). Field studies on marine mammal livers corroborate the equimolar ratio of mercury and selenium (Koeman et al., 1973; Pelletier, 1985; Cuvin-Aralar and Furness, 1991; Kim et al., 1996); moreover, mercuric selenide (HgSe) — an inert end product of mercury detoxification in marine mammals — was found in the livers of marine mammals and birds (Martoja and Berry, 1980; Rawson et al., 1995; Nigro and Leonzio, 1996). A proposed mercury detoxification model in higher-trophic marine animals involves transformation of dietary methylmercury to inor- ganic mercury by reactive oxygen species (Suda et al., 1992; Hirayama and Yasutake, 2001; Yasutake and Hirayama, 2001); gut microflora (Rowland et al., 1984; Rowland, 1988); and selenium (Iwata et al., 1982). Inorganic mercury binds to metallothioneins or forms an equimolar Hg–Se complex, and subsequently combines with high molecular weight compounds in liver (Ikemoto et al., 2004). Glutathione molecules solubilize HgSe; the complex then binds to a specific protein (Gailer et al., 2000). The protein-bound Hg–Se complex is thought to be the precursor of mercuric selenide, which occurs in macrophages of marine mammals (Nigro, 1994; Rawson et al., 1995; Nigro and Leonzio, 1996). 3.5 MERCURY TRANSPORT AND SPECIATION The global mercury cycle involves mercury release from geological and industrial processes into water and the atmosphere, followed by sedimentation via rainfall and by microbial metabolism that releases mercury from soil and sediments and transforms mercury from one chemical form to another (WHO, 1976, 1989, 1990, 1991; Fitzgerald, 1986; Fitzgerald and Clarkson, 1991; Barkay, 1992). Atmospheric-borne mercury, including anthropogenic mercury, is deposited everywhere, includ- ing remote areas of the globe, hundreds of kilometers from the nearest mercury source, as evidenced by its presence in ancient lake sediments (Fitzgerald et al., 1998) and glacial ice (Schuster et al., 2002). In Amituk Lake in the Canadian Arctic, recent annual deposition of mercury was estimated at 15.1 kg, about 56.0% from snowpack and the rest from precipitation (Semkin et al., 2005). This represents a dramatic increase from historic annual burdens of 6.0 kg mercury annually in this remote area (Semkin et al., 2005); the effects of this increase on Arctic watersheds is unknown. Many important sources affecting global mercury cycles emit elemental metallic mercury (Hg o ) in gaseous form, and to a lesser extent gaseous and particulate species of Hg 2+ (USEPA, 1997; Pacyna et al., 2001). Gaseous and particulate Hg 2+ are removed from the atmosphere through rainfall and dry deposition, thus limiting long-range transport (Lindberg and Stratton, 1998; Ebinghaus et al., 2002). Inorganic Hg 2+ can be readily reduced to Hg o by natural processes in terrestrial and aquatic ecosystems (Nakamura, 1994; Zhang and Lindberg, 2001). Elemental mercury can be oxidized in the atmosphere to Hg 2+ , which is removed through wet and dry deposition (Lindberg et al., 2002). About 67.0% of the mercury in global fluxes is a result of human activities and the rest from natural emissions (Mason et al., 1994). Soils and sediments are the primary sinks for atmospherically derived mercury; however, these enriched pools can be remobilized through vol- atilization, leaching, and erosion (Wiener et al., 2003). Mercury speciation varies in atmospheric, aquatic, and terrestrial environments. In the atmo- sphere, mercury is in the form of gaseous elemental Hg o (95.0%), Hg 2+ (called reactive gaseous © 2006 by Taylor & Francis Group, LLC PROPERTIES 29 mercury), and trace amounts of methylmercury (Lindberg and Stratton, 1998; Schroeder and Munthe, 1998). Particulate and reactive mercury in the atmosphere travels short distances, usually less than 50 km, and has a residence time of about 1 year (Mason et al., 1994). Reactive gaseous mercury is assumed to be HgCl 2 , with some Hg(NO 3 ) 2 •H 2 O in the gas phase (Stratton et al., 2001). Reactive gaseous mercury may comprise a majority of atmospheric gaseous mercury at some locations (e.g., springtime in Alaska) and this component is rapidly removed from the atmosphere by wet and dry deposition (Lindberg et al., 2002; Munthe et al., 2001) and available for methylation once deposited (Lindberg et al., 2002). Mercury point sources and rates of particle scavenging are key factors in atmospheric transport rates to sites of methylation and subsequent entry into the marine food chain (Rolfhus and Fitzgerald, 1995). Airborne soot particles transport mercury into the marine environment either as nuclei for raindrop formation or by direct deposition on water (Rawson et al., 1995). In early 1990, both dimethylmercury and monomethylmercury species were found in the subthermocline waters of the equatorial Pacific Ocean; the formation of these alkyl- mercury species in the low oxygen zone suggests that Hg 2+ is the most likely substrate (Mason and Fitzgerald, 1991). In aquatic environments, Hg o and methylmercury species are the most common, with concen- trations low, usually in the picogram-per-liter to microgram-per-liter range, except in the vicinity of anthropogenic or natural mercury sources (Wiener et al., 2003). The speciation of mercury in water is influenced by redox, pH, and ligands (Gill and Bruland, 1990). In most aerated surface waters near pH 7.0, ion-pair formation for CH 3 + and Hg 2+ is dominated by dissolved organic matter and chloride (Ravichandran et al., 1999). Under anoxic conditions, Hg 2+ and CH 3 + are present mainly as sulfide and sulfhydryl ion pairs (Benoit et al., 1999a; Gill et al., 1999). Complexed Hg 2+ sulfides are less available for methylation (Benoit et al., 1999b). Concentrations of total mercury in uncontaminated, unfiltered freshwater samples range from 0.3 to 8.0 ng/L, but range from 10.0 to 40.0 ng/L near mercury sources (Wiener et al., 2003), and up to 1000.0 ng/L in waters contam- inated by mercury tailings from gold mines (Eisler, 2004). Sulfate-reducing bacteria are the most important mercury-methylating agents in aquatic envi- ronments (Gilmour et al., 1992, 1998), with the most important site of methylation at the oxic–anoxic interface in sediments (Pak and Bartha, 1998); a similar pattern is documented for wetlands (Krabbenhoft et al., 1995; Branfireum et al., 1996; Gilmour et al., 1998). In sediments, microbial methylation of mercury is fastest in the upper profiles where the rate of sulfate reduction is greatest (Hines et al., 2000; King et al., 2001). Methylcobalamin, produced by bacteria, is the active methyl donor to the Hg 2+ ion; methylcobalamin reacts with Hg 2+ to form CH 3 Hg + (Choi et al., 1994). Methylation also occurs, but to a lesser degree, in aerobic freshwater and seawater, in aquatic plants, and in mucosal slime and intestines of fish (Wiener et al., 2003). Abiotic formation of CH 3 Hg + compounds in sediments is documented; however, amounts formed are small when compared to biotic processes (Nagase et al., 1988; Falter and Wilken, 1998). Demethylation occurs via abiotic and biotic processes in the near-surface sediments and in the water column (Winfrey and Rudd, 1990; Oremland et al., 1991; Sellers et al., 1996). An oxidative demethylation pathway similar to that of the degradation of methanol or monomethylamine by methanogens has been proposed for methylmercury degradation (Marvin-DiPasquale et al., 1998, 2000). Photodegradation of methylmercury in surface waters of freshwater lakes is documented at rates up to 18.0% daily and is quantitatively important in mercury budgets of that ecosystem (Sellers et al., 1996, 2001; Branfireun et al., 1998; Krabbenhoft et al., 2002); the end products of mercury photodemethylation are not known with certainty (Krabbenhoft et al., 1998). Frequently, however, methylmercury concentrations in aerobic lakewater surfaces increase during sunlight hours or remain unchanged (Sicialiano et al., 2005). This phenomenon is linked to dissolved organic matter (DOM) and solar radiation — specifically to certain fractions of DOM that generates methylmercury when exposed to sunlight, especially in water from lakes with logged watersheds. The mechanism to account for © 2006 by Taylor & Francis Group, LLC 30 MERCURY HAZARDS TO LIVING ORGANISMS methylmercury production is not clear at present; however, it corrects the conventional wisdom that methylmercury is rapidly photodegraded (Sicialiano et al., 2005). Terrestrial soils are a significant contributor of mercury to surface waters (Mason et al., 1994; Cooper and Gillespie, 2001; Grigal, 2002; Gabriel and Williamson, 2004). Moreover, up to 60.0% of the atmospherically deposited mercury that reaches lakes originates from the associated terrestrial watershed (Krabbenhoft and Babiarz, 1992; Lorey and Driscoll, 1999; Grigal, 2002). The main biogeochemical reactions affecting the transport and speciation of mercury in the terrestrial water- shed include formation of mercury ligands, mercury adsorption and desorption, and elemental mercury reduction and volatilization (Gabriel and Williamson, 2004). In terrestrial environments, OH − , Cl − , and S − ions have the greatest impact on inorganic mercury–ligand formation. Under oxidized surface soil conditions, Hg(OH) 2 , HgCl 2 , HgOH + , HgS (cinnabar), and Hg 0 are the dominant inorganic mercury forms and usually bind to organic and mineral ions. Under reducing conditions, common mercury forms are HgSH + , HgOHSH, and HgClSH, and many are further bound to both inorganic and organic ligands. The following organomercurials predominated in terrestrial soils: CH 3 HgCl > CH 3 HgOH > free CH 3 Hg + (Gabriel and Williamson, 2004). In upland soils, mercury is mostly in the form of Hg 2+ species sorbed to organic matter in the humus layer and a lesser extent to soil minerals (Kim et al., 1997). The overall adsorption of mercury to mineral and organic particles is positively correlated, in order of importance, with surface area, organic content, cation exchange capacity, and grain size (Gabriel and Williamson, 2004). Mercury adsorption and desorption to mineral and organic surfaces is strongly influenced by pH and dissolved ions; for example, increased Cl −− −− and decreased pH — alone or together — can decrease mercury adsorption, and clays and organic soils have the highest capability of adsorbing mercury (Gabriel and Williamson, 2004). Common forms of methylated mercury in soils depend on pH (Reimers and Krenkel, 1974; Jackson, 1998). At pH 2 to about 4.7, the most common forms were CH 3 HgCl > free CH 3 Hg + > CH 3 HgOH; at pH 4.7 to about 7.5, the most common forms were CH 3 HgCl > CH 3 HgOH > free CH 3 Hg + ; and at pH 7.5 to 10, this order was CH 3 HgOH > CH 3 HgCl >> free CH 3 Hg + (Reimers and Krenkel, 1974; Jackson, 1998). Reduction of abiotic inorganic mercury increases with increasing electron donors, low redox potential, and sunlight intensity (Gabriel and Williamson 2004). Factors that increase mercury volatilization from soils include increased soil permeability, higher temperatures, and increased sunlight intensity; therefore, increased volatilization is expected in tropical climates. A decrease in mercury adsorption and an increase in soil moisture can also increase volatilization (Gabriel and Williamson, 2004).Gabriel and Williamson (2004) recommend that additional research be conducted on inorganic mer- cury–ligand formation in water and runoff and its effects on methylmercury formation in soils, and on quantification of the sources and transport characteristics of methylmercury in terrestrial envi- ronments. The mercury–ligand form exiting the terrestrial watershed will strongly influence the mercury/methylmercury bioaccumulation potential in surface waters. Accordingly, more analyses are needed to determine the mercury forms in terrestrial watershed runoff in dissolved and partic- ulate fractions (Gabriel and Williamson, 2004). 3.6 MERCURY MEASUREMENT Techniques for analysis of different mercury species in biological samples and abiotic materials include atomic absorption, cold vapor atomic fluorescence spectrometry, gas-liquid chromatography with electron capture detection, neutron activation, and inductively coupled plasma mass spectrom- etry (Takizawa, 1975; Lansens et al., 1991; Schintu et al., 1992; Porcella et al., 1995). Methyl- mercury concentrations in marine biological tissues are detected at concentrations as low as 10.0 µg Hg/kg tissue using graphite furnace sample preparation techniques and atomic absorption spec- trometry (Schintu et al., 1992). © 2006 by Taylor & Francis Group, LLC PROPERTIES 31 3.7 SUMMARY Physical, chemical, biological, and biochemical properties of mercury are briefly reviewed; mercury transport and speciation processes are summarized; and analytical techniques listed for mercury measurement. In mammals, all forms of mercury can cross the placenta to the fetus and interfere with thiol metabolism. Chemical speciation is probably the most important variable influencing mercury toxicity; however, speciation is difficult to quantify. In freshwater lakes, for example, mercury speciation depends, in part, on pH, alkalinity, redox, and microbial activity. Most authorities agree that all mercury species discharged into natural bodies of water can be converted into methylmer- curials — the most toxic form — at rates influenced, in part, by mercury loadings, nutrient content, sedimentation rates, and suspended sediment loadings. Bioavailability of methylmercury to aquatic biota is highly dependent on lake chemistry, mercury deposition rates, dissolved organic carbon, and other variables. Methylmercury, in turn, is decomposed abiotically and by bacteria containing mercuric reductase and organomercurial lyase; these demethylating strains of bacteria are common in the environment and have been isolated from water, sediments, soils, and the GI tract of humans and other mammals. Other mechanisms can reduce inorganic Hg 2+ to Hg o in freshwater, with Hg o production higher under anoxic conditions, in a chloride-free environment, and at pH 4.5. Methylmercury concentrations in tissues of marine fishes can now be detected at levels greater than 10.0 µg/kg tissue using graphite furnace sample preparation techniques and atomic absorption spectrometry. REFERENCES Allard, B. and I. Arsenie. 1991. Abiotic reduction of mercury by humic substances in aquatic system — an important process for the mercury cycle, Water Air Soil Pollut., 56, 457–464. Anon. 1948. Mercury, Encylop. Brittanica, 15, 269–272. Baldi, F., F. Semplici, and M. Filippelli. 1991. Environmental applications of mercury resistant bacteria, Water Air Soil Pollut., 56, 465–475. Barghigiani, C., D. Pellegrini, and E. Carpene. 1989. Mercury binding proteins in liver and muscle of flat fish from the northern Tyrrhenian Sea, Comp. Biochem. Physiol., 94C, 309–312. Barkay, T. 1992. Mercury cycle. In Encyclopedia of Microbiology, Vol. 3, p. 65–74. Academic Press, San Diego. Becker, D.S. and G.N. Bigham. 1995. 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