Mercury Toxicity
Introduction
Mercury can exist either in elemental inorganic form or as organic compounds like methylmercury and enthylmercury (“Exposure to Mercury: A Major Public Health Concern” 1). Elemental mercury naturally exists in mineral forms such as in cinnabar (Schweiger, Stadler, and Bowes 5). These various forms of mercury have different levels of toxicity and adverse effects on living organisms. In elemental form, mercury is a silvery liquid that can readily vaporize into the atmosphere, incorporate in rain formation and fall during precipitation, and transported into the earth’s waters and lands (“Exposure to Mercury: A Major Public Health Concern” 1). Also, through natural processes like volcanism and weathering, or anthropogenic activities such as burning of coal and industrial production, mercury is released into the environment (Schweiger, Stadler, and Bowes 5). Then, in the environment, transported mercury can be absorbed by the planktons in bodies of water and transform this from inorganic mercury into organic methyl or ethyl mercury. As fishes ingested these planktons, bioaccumulation occurs, wherein the organic form of mercury accumulate in their tissues (Schweiger, Stadler, and Bowes 5). As this process continues, biomagnification of organic mercury spontaneously arises in the food chain. Finally, the biomagnified organic mercury is acquired by humans and other land organisms by consumption of fishes and other marine organisms (Schweiger, Stadler, and Bowes 5).
Literature Review
The inhalation or ingestion of either elemental or methylmercury adversely affects the central and nervous systems. This may lead to a fatal condition due to brain, kidney and other internal organ failures (“Exposure to Mercury: A Major Public Health Concern” 3). In the same manner, the inorganic salts of mercury causes irritation on eyes, skin, and even to gastrointestinal tract. As such, neurological damage and behavioral effects like cognitive impairment, loss of muscular control, memory loss, and anxiety are observed in mercury cases of intoxication (“Exposure to Mercury: A Major Public Health Concern” 3). Meanwhile, when mercury in its elemental form is discharged into the environment through incineration, burning of coal, and other industrial processes, it is transform into an organic form methylmercury through the metabolism of anaerobic or marine organisms (Freeman A36). Methylmercury is a bioactive compound that has adverse effects even to the nervous system of humans (Brown A212). By means of fish consumption, humans can acquire MeHg and intoxication leads to behavioral disorder and cognitive impairment.
The consumption of mercury-contaminated fishes of pregnant women poses a great risk to the fetal development. This may lead to mental retardation, impairment of the senses, memory loss, and delayed development of infants and children (“Exposure to Mercury: A Major Public Health Concern” 3). The Environmental Protection Agency of the United States in 2004 set the daily standard of MeHg exposure at 0.1 μg/kg and advised pregnant women to limit their fish consumption to six to twelve ounces due to possible MeHg contamination (Brown A212). As a matter of fact, the integration of findings of the studies conducted in New Zealand, and Faroe and Seychelles Islands revealed a 0.18-point decrease in childhood intelligence quotient, IQ, for every apparent increase of mercury in the maternal hair (Brown A212).
Exposure to inorganic form of mercury through dental amalgam is a common case. The possibility of ingestion or inhalation of elemental mercury through its evaporation from the amalgam has been theorized (McGovern A129) and the effects of inorganic form of mercury on the nervous system and kidney has been noted. Based on the longitudinal research conducted in England regarding dental exposure to mercury, the dental amalgam has negligible effect on the renal function (McGovern A129).
Ravneet and Paradiso (2008) reported that neuropsychiatric symptoms such irritability, fatigue, insomnia, and anxiety as were observed in a 47-year old woman after taking two cans of tuna in her everyday diet for seven years. The patient was diagnosed with 74 mcg/dl mercury plasma which is an elevated level of the tolerable 10 mcg/dl (Ravneet and Paradiso 11).
Medical studies showed a significant relationship of inorganic mercury exposure with autoimmune disease in animal models (Hood A538). The weakening brought by this group of illness may lead to incurable condition. A group of science investigators in Maryland found that mice can acquire autoimmune disease even at low-level environmental mercury exposure. Based on the results of their study, researchers suggested that autoimmune disease may develop in humans by means of low-level mercury exposure (Hood A539).
Mechanism of Toxicity
The liver, macrophages, and intestinal flora are typical sites of MeHg degradation (“Toxicological Effects of Methylmercury” 48). The analyses made on the family members died due to consumption of mercury-contaminated pork showed the MeHg sensitivity of cerebrum and cerebellum parts of the brain (“Toxicological Effects of Methylmercury” 45). The burden of the damages on their brains was attributed to the high concentration of inorganic mercury in different regions including calcarine and parietal cortices that are responsible for coordination and sensations (“Toxicological Effects of Methylmercury” 45). This indicated the transformation of MeHg into inorganic mercury.
Demethylation of MeHg converts it to inorganic mercury in tissues. Besides from the role of enzymatic reactions, it is also potulated that free radical mechanism has a crucial role in this transformation. Also, gamma-globulin and serum albumin as stimulated by glutathione contribute to methyl group removal from MeHg (“Toxicological Effects of Methylmercury” 48). Even though MeHg is highly toxic, the accurate mechanism of neurotoxicity is not yet known (“Toxicological Effects of Methylmercury” 4).
After the absorption of MeHg through the gastrointestinal tract, it is transformed into inorganic mercury in the brain (“Toxicological Effects of Methylmercury” 4). The MeHg travels through the blood stream and enters into the red blood cells and bind with the hemoglobin (“Toxicological Effects of Methylmercury” 42). Additionally, MeHg can also bind with proteins (“Toxicological Effects of Methylmercury” 43). About ten percent of MeHg is transported into the brain where it is converted into inorganic form (“Toxicological Effects of Methylmercury” 43). Based on rat experiments, MeHg is carried into the brain by MeHg-L-cysteine complex through the levorotatory isomers of amino acid or L-amino acid. By the action of gamma-glutamyltransferase, MeHg-cysteine complex is exuded from MeHg-glutathione complex (“Toxicological Effects of Methylmercury” 43). This portrays the possible role of glutathione in the absorption of MeHg by the endothelial cells. Since both MeHg-cysteine and MeHg-glutathione complexes are water soluble, the solubility of MeHg to lipids present in tissues and fluids enhances its absorption in brain cells (“Toxicological Effects of Methylmercury” 45).
Medical Treatment
Around one percent of MeHg body burden can be excreted in daily basis. Human excretion of the demethylated form through bile and feces is possible. In addition, inorganic mercury can also be traced in urine while the organic form, MeHg, in the bile is remained (“Toxicological Effects of Methylmercury” 49). Nonetheless, MeHg can also be excreted through breast feeding while vapor of mercury in elemental form can possibly be incorporated in saliva, sweat, feces and urine (“Toxicological Effects of Methylmercury” 50).
Chelating agent has been used to increase the excretion of mercury from the body both in its organic and inorganic forms. Commonly use complexing agents are 2,3-dimercapto-1-propane sulfonate or DMPS and meso 2,3-dimercaptosuccinic acid or DMSA (“Toxicological Effects of Methylmercury” 51). These compounds are water soluble, less toxic and can be introduced orally. Moreover, several clinical reviews concerning DMPS revealed its efficacy in sequestering mercury from the body tissues. It has been used in the treatment of mercury poisoning in Iraq that proved its high potentiality over D-penicillamine N-acetyl-DL-penicillamine or a thiolated resin in the reduction of inorganic mercury in blood (“Toxicological Effects of Methylmercury” 51). Also, in the United States, studies concerning DMPS revealed its efficacy in the treatment of dental amalgam toxicity and increasing mercury excretion through urine. Nonetheless, in rat experiments, DMPS deterred the conversion of MeHg into inorganic form of mercury (“Toxicological Effects of Methylmercury” 51). Medical studies also confirmed the feasibility of N-acetylcysteine or NAC in the treatment of methyl mercury (MeHg) toxicity (Freeman A36). Through metal chelation, MeHg can be excreted; however, other minerals necessary for the functions of the cells are also eliminated (Freeman A36). By means of NAC chelating complex, the loss of essential minerals can be prevented.
Conclusion
Natural exposure to mercury such as in volcanic eruption and rock weathering is tolerable to humans, however, anthropogenic activities has tremendously increased the amount of mercury in the environment. This resulted to the incorporation of mercury to the ecological food chain. As such, spontaneous consequences like bioaccumulation and biomagnification aggravated the scenario. Since humans are at the top of the ecological food pyramid, we ultimately suffer the nature’s vengeance. Although, medical treatment may assuage the adverse effects of mercury intoxication but the most upright solution can be done by eradicating the anthropogenic sources of the pollutant.
References
Brown, Valerie. “Methylmercury and IQ.” Environmental Health Perspectives 115, 4 (2007): A212.
Exposure to Mercury: A Major Public Health Concern. Switzerland: World Health Organization, Public Health and Environment, 2007.
Freeman, Kris. “Mitigating Methylmercury Exposure.” Environmental Health Perspectives 116, 1 (2008): A36.
Hood, Ernie. “Setting the Stage for Illness, Mercury Exposure and Autoimmune Disease.” Environmental Health Perspectives 111, 10 (2003): A538-A539.
McGovern, Victoria. “Taking a Bite Out of Amalgam Concerns?” Environmental Health Perspectives 116, 3 (2008): A129.
Ravneet, Dhaliwal and Paradiso, Sergio. “Anorexia Nervosa and Mercury Toxicity.” The American Journal of Psychiatry 165 (2008): 11.
Schweiger, Larry, Stadler, Felice, and Bowes, Catherine. Poisoning Wildlife: The Reality of Mercury Pollution. Reston, VA 20190: National Wildlife Federation, 2006.
Toxicological Effects of Methylmercury. Washington, DC: National Academy Press, 2000.
