Mercury Toxicity in the Chesapeake Bay and Its Watershed
In recent years concern regarding the mercury content in fish harvested from the Chesapeake Bay and its tributaries has escalated. Mercury is one of the most common heavy metals found in Earth’s environment. Throughout history it has been used therapeutically as a cathartic, diuretic, anti-inflammatory, vermifugan, anti-parasitic and in dental amalgams (Peraza et el 1998). Mercury is anthropogenically released into the environment in a variety of ways, including mining and industrial combustion. It is then globally cycled through the atmosphere, land, and oceans. Elemental mercury can be converted into methyl mercury, a compound that bioaccumulates in ecosystems such as the Chesapeake Bay. Methyl mercury, like most organo-mercury compounds, is highly toxic and has no known commercial value (Environmental Protection Agency 2009).
Methylation & Demethylation of Mercury
Methyl mercury is produced by redox reactions catalyzed by sulfate-reducing bacteria and involving mercury species in two unique oxidation states. Oxidation and reduction of mercury occurs in the water column as well as in the benthos and both processes are thought to be (at least partially) photochemically mediated. Elemental mercury concentrations in natural saline waters decrease significantly when the system is exposed to ultraviolet light. Studies suggest that the dominant oxidants of elemental mercury are hydroxide free radicals, which are photochemically produced (Whalin et el 2007). The demethylation of organic mercury to inorganic mercury occurs simultaneously with the methylation of inorganic mercury compounds. Methyl mercury is constantly accumulating in and being released from the sediment. Abiotic methylation of mercury in benthic habitats is dependent upon temperature, pH and the relative concentrations of humic acid, fulvic acid and inorganic mercury compounds (Boszke et el 2003).
Since they are the primary producers of methyl mercury in the Chesapeake Bay, sulfate-reducing bacteria are important in mediating the concentration of organic mercury in the environment. The rate of conversion of mercury to methyl mercury in coastal sediments is important for estimating the bioaccumulation of mercury in coastal organisms (Benoit et el 1998, Sunderland et el 2006). Sulfur, organic carbon, and sediment structure/composition can all affect methyl mercury production by changing the amount of bioavailable inorganic mercury and by stimulating the activity of methylating microbes (Sunderland et el 2006). Mercury in its second oxidation state can be consumed by microorganisms such as plankton and bacteria and converted to its toxic form. The oxidation of Hg(II) to methyl mercury occurs only in anoxic conditions, which are prevalent in the Chesapeake Bay (Whalin et el 2007).
It is thought that halides enhance the oxidation rate of elemental mercury in natural bodies of water. Halides react with hydroxide free radicals, producing more oxidants. Halides readily form stable compounds with different mercury species. This decreases the rate of reduction, which ultimately increases net oxidation (Whalin et el 2007).
In anaerobic conditions mercury has a strong affinity for sulfur, so sulfur content in sediment strongly influences the chemistry of mercuric compounds in the benthos. Metal sulfides in anoxic conditions, including mercury sulfide, are useful in controlling the toxicity of many metals (Benoit et el 1998). This is because mercury sulfides are non-polar and precipitate in sediment, where they are no longer bioavailable. When mercuric sulfide concentrations are high, organic mercury content is low. Cinnabar is the common name for mercuric sulfide compounds, and is mercury in its ore form (Boszke et el 2003). In such form, mercury is non-toxic to aquatic organisms and is insoluble (Environmental Protection Agency 2009). The solubility of cinnabar and cinnabar-like compounds increases considerably as sulfide ion content increases. This property is responsible for the great concentrations of soluble mercury species in the anaerobic zones of the Chesapeake Bay and other estuarine habitats. When appropriate concentrations of sulfide ions are present, sulfide and disulfide complexes are formed. Disuflide mercury compounds tend to be the dominant mercury species that occur under anaerobic conditions, suggesting it is also the most stable (Boszke et el 2003, Benoit et el 1998).
The complexation of methyl mercury to methyl mercury-bisulfide decreases the phytoplankton uptake rate, and thus decreases the amount of methyl mercury entering the food chain (Lawson & Mason 1999).
Mercury in Sediment
The sediment is where mercury methylation and demethylation occur. It is also where mercuric sulfides precipitate. Mercury can undergo many chemical reactions in the benthos, depending on the composition of the sediment. The net production of methyl mercury in Chesapeake Bay sediment exceeds net accumulation of mercury in its non-toxic form. The sediment provides a potential source of mercury compounds that could be released into the water column. In the Chesapeake Bay area the concentration of methyl mercury in bottom sediments is between one and 1.5 percent of the total mercury contained in waters leading to the Bay (Boszke et el 2003, Benoit et el 1998).
Mercury & Organic Matter
Organic matter plays a key role in the mobility of mercury in the environment and can bind to up to 95 percent of all divalent mercury species (Boszke et el 2003). Due to these properties, organic matter content is thought to play a large role in controlling the mercury content of sediments (Benoit et el 1998). It is theorized that reduction of mercury in its second oxidized form is correlated with organic matter content. Organic matter in aquatic conditions can act as a photosynthesizing manner, creating the hydroxide radicals that bind to mercury and form the reactive intermediate compound in the process of methylation (Whalin et el 2007).
Elemental mercury acts as a neurotoxin that is especially detrimental to developing embryos (Chesapeake Bay Foundation 2009). Elemental mercury is poorly absorbed through dermal contact and the gastrointestinal tract, but can be toxic if inhaled. Neurotoxic effects of elemental mercury are caused by the increasing of the permeability of cell plasma membranes to calcium, leading to hypercalcemia. Symptoms of hypercalcemia range from extreme lethargy to kidney disease (Peraza et el 1998).
Inorganic mercury salts, such as cinnabar, can cause nephrotoxicity, On a cellular level, mercury sulfides impair mitochondrial function by creating membrane leakage. Inorganic mercury compounds can also stimulate the production of excess hydrogen peroxide in the system, which exacerbates mercury toxicity (Peraza et el 1998). Elemental and inorganic mercury toxicity are of little concern in the Chesapeake Bay, but are worth noting as a reference for the different mechanisms through which mercury species can be harmful.
Methyl mercury is the species of mercury that is of most concern in the Chesapeake Bay, and is the form of mercury most commonly consumed by humans. Methyl mercury is lipophilic, so it is readily absorbed into fatty tissue via dermal contact, inhalation or ingestion. Within a few days of exposure, methyl mercury distributes to all tissues within the body, and stays in the system for an average of fifty days. It is then excreted in the urine. Microscale effects of methyl mercury toxicity include microtubule damage, inhibition of the uptake of serotonin and glutamate and the suppression of specific calcium channels as well as specific amino acid pathways. This type of toxicity is also known as oxidative-like toxicity and is resultant of the exposure of tissues to oxidative stressors (Peraza et el 1998).
The exact mechanism of toxicity is unknown for methyl mercury, although it is thought that the cleavage of methyl mercury compounds creates oxygen radicals. These oxygen radicals take part in chemical reactions that lead to lipid peroxidation and neuronal cell damage (Peraza et el 1998).
Micronutrient intake has a large effect on the toxicity and carcinogenesis caused by various chemicals and metals, including mercury. At several points in the body micronutrients can affect the chemical pathways of different toxins. Absorption, binding, secretion and sequestration are all methods by which micronutrients interact with the metabolism of potentially toxic compounds (Peraza et el 1998).
As the mechanism for mercury toxicity is
unknown, the mechanism for toxicity resistance is also unknown. Some
microorganisms are not affected by the metal in any quantifiable way, but how
this is possible remains undiscovered (Boszke et el 2003). Methionine, an essential amino acid, can prevent
neurotoxic effects of methyl mercury by blocking the transport of the toxic
complex into the brain. Vitamin E, an anti-oxidant, can prevent free radical
injury to cells by initiating a process in which free radicals break down the
methyl mercury. The natural content of selenium found in foodstuffs can modify
methyl mercury toxicity by reducing the organic mercury to mercuric iron
(Peraza et el 1998).
Bioaccumulation & Contamination of the Food Chain
Mercury is the only metal that bioaccumulates through all levels of the aquatic food chain. Lower trophic levels are especially important in determining the bioaccumulation rate of mercuric compounds (Lawson & Mason 1999). Methyl mercury is the only form of mercury that bioaccumulates to significant amounts in aquatic animal tissues and cells (Sunderland et el 2006). Mercury increases in concentration as it moves up trophic levels, and concentrations of mercury in fish tissues can be millions of times greater than concentrations in the surrounding water. (Chesapeake Bay Foundation 2009). This biomagnification makes methyl mercury a toxin of essential concern.
The uptake of mercury by phytoplankton increases
with the complexation of methyl mercury to methyl mercury-cysteine and methyl
mercury-thiourea; different ligands influence organic mercury uptake by
microorganisms. The accumulation rate of mercury and methyl mercury within
planktonic cells is a function of many variables, including water pH, salinity
and ligand concentrations. The trophic transfer of mercury is higher for
contaminated systems with low pH levels because phytoplankton have higher
loadings of mercury under such conditions (and this mercury is transferred up
the food chain) (Lawson & Mason 1999).
Despite efforts to reduce mercury emissions in the United States, worldwide emissions of mercury are increasing (Peraza et el 1998). The coastal zone and areas like the Chesapeake Bay play an integral role in the worldwide mercury cycle, so studying them is imperative to understanding mercury toxicity. Fifty to 80 percent of the total mercury that flows into the Chesapeake Bay stays there- it is very persistent in the environment. Treatment options are limited and include sorption and precipitation techniques, but such methods are only effective on a small scale (Whalin et el 2007, Environmental Protection Agency 2009). Any transformation or transport of mercuric compounds away from zones of methylation would lead to lower contamination of the aquatic food web, but no comprehensible method for doing this has been presented (Whalin et el 2007). The most effective way to combat mercury pollution is by not releasing any more mercury into the environment and avoiding the use of any technology that emits mercury as a byproduct.
Thanks for Reading! Literature Consulted:
Benoit, J., C. Gilmour, R. Mason, G.S. Riedel and G.F. Riedel. 1998. “Behavior of Mercury in the Patuxent River Estuary.” Biogeochemistry. 40: 249-265.
Boszke, L., A. Kowalski, G. Glosinska, R. Szarek and J. Siepak. 2003. “Environmental Factors Affecting Speciation of Mercury in the Bottom Sediments; An Overview.” 12(1): 5-13.
Chesapeake Bay Foundation. “Bad Water 2009: The Impact on Human Health in the Chesapeake Bay Region.” July 2009. Washington, DC.
Lawson, N. and R. Mason. 1998. “Accumulation of Mercury in Estuarine Food Chains.” Biogeochemistry. 40: 235-247.
Peraza, M., F. Ayala-Fierro, D. Barber, E. Casarez and L. Rael. 1998. “Effects of Micronutrients on Metal Toxicity.” Environmental Health Perspectives. 106: 203-216.
Sunderland, E., F. Gobas, B. Branfireun and A. Heyes. 2006. “Environmental Controls on the Speciation and Distribution of Mercury in Costal Sediments.” Marine Chemistry. 102: 111-123.
United States Environmental Protection Agency. “Report to Congress: Potential Export of Mercury Compounds from the United States for Conversion to Elemental Mercury.” 14 Oct 2009. Washington, DC.
Whalin, L., E. Kim and R. Mason. 2007. “Factors Influencing the Oxidation, Reduction, Methylation and Demethylation of Mercury Species in Coastal Waters.” Marine Chemistry. 107: 278-294.
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