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Methyl (Organic) Mercury


Lead author

Case Studies


Minamata, Japan: Mercury and Fish

In the late 1950s the subtle and serious consequences of methyl mercury exposure became evident in Minamata, Japan. Initially, health experts were baffled by early signs of uncoordinated movement and numbness around the lips and extremities, followed by constriction in visual fields in fishermen and their families. Developmental effects were clearly evident in infants who exhibited subtle to severe disabilities. This spectrum of adverse effects was finally related to methyl mercury exposure from consumption of contaminated fish. Minamata Bay was contaminated with mercury and methyl mercury from a factory manufacturing the chemical acetaldehyde. Mercury was used in the manufacturing process, and both mercury and methyl mercury were discharged into Minamata Bay. The fish in the bay accumulated increasing amounts of methyl mercury, which was subsequently passed to the fish-consuming residents of the area. This was one of the first modern lessons of the consequences of the bioaccumulation of methyl mercury.

Mercury-coated Seed Grain in Iraq

The toxic antifungal properties of organic mercury compounds were beneficial when applied to seed grain, but when humans consumed these seeds there were tragic consequences. During much of the 20th century, seeds were coated with organomercury compounds to reduce their destruction by fungus in the soil. Often these seeds were colored pink to indicate they were coated with an antifungal agent and were for planting only, not consumption. During the early 1970s, a severe drought in Iraq resulted in a loss of seed grain and people struggled with malnutrition. Pink-colored mercury-coated seed grain was shipped to Iraq for planting. Unfortunately, the local population could not read the foreign language on the seed bags nor recognize the pink seeds as hazardous. Bread made from these seeds was pink, tasty, and toxic, particularly to the developing child. Many people died or were tragically disabled for life, giving the world another lesson in communication and mercury toxicity.

Introduction and History


(For a general overview of mercury, see our Mercury page.)

The first reported use of organic mercury compounds in chemical research occurred in 1863. Their synthesis immediately led to the recognition of their extremely high toxicity relative to inorganic mercury forms, and by 1866 two chemists had died from organic mercury poisoning. Therapeutic applications of organic mercurials in the treatment of CNS syphilis, which began in 1887, led to non-occupational poisoning; the use of organic mercury-based medicines ceased soon after because of their extremely high toxicity. The use of synthetic organic mercurials as antifungal dressings for agricultural seeds began in 1914. Their use in this industry has resulted in scattered case reports of acute poisoning associated with the chemical manufacture, application, and inadvertent consumption of either the treated grain or of animals fed with the treated grain. The use of organic mercurials in agriculture has resulted in large-scale poisoning episodes worldwide, such as occurred in Iraq.

Both elemental mercury and inorganic mercury are used in chemical manufacture, including vinyl chloride and acetaldehyde synthesis (inorganic mercury), and chlor-alkali production (elemental mercury). For example, the Minamata factory used mercuric oxide dissolved into sulfuric acid as a catalyst for the hydration of acetylene to acetaldehyde. In addition, vinyl chloride production at the Minamata factory used mercuric chloride absorbed onto activated carbon for the production of vinyl chloride from acetylene and hydrogen chloride. These processes directly led to the contamination of Minamata Bay and the Agano River, Niigata with mercury effluent. This discharge caused large-scale human methyl mercury exposure and toxicity during the 1950s and 1960s and led to our present-day appreciation of mercury's environmental cycling, biomethylation, and food chain transfer.

Organic mercury compounds have also been used in latex paint to extend the shelf life, though such uses are currently restricted in the United States following the recognition of the potential hazard to children. Subsequent evaluation of interior rooms of homes painted with mercury-containing latex paint found that mercury vapor concentrations were elevated and in several cases were above the 0.5 µg/m3 concentration recommended by the Agency for Toxic Substances and Disease Registry.

 

(Image taken from EPA's Mercury website)

Biological Properties


While there are many synthetic organic mercury compounds, the most important organic mercury is the naturally occurring form methyl mercury (MeHg). In the environment, inorganic mercury is biotransformed to MeHg primarily through microbial methylation in sediments of fresh and ocean waters. Once produced, MeHg readily enters the aquatic food chain and bioaccumulates in tissues of aquatic organisms. Because MeHg is stored throughout the life of aquatic organisms, it is transferred up the food chain and results in the highest concentrations in larger, long-lived, predatory species such as swordfish, pike, and ocean tuna. The bulk of mercury in fish is stored in muscle, and almost all of the mercury in muscle is MeHg. The concentration of MeHg in fish depends on the age and trophic level of the particular fish, and can be quite substantial (> 1000 µg/kg (ppb or 1 ppm)). For example, the total mercury in the edible tissues of shark and swordfish can average as high as 1200 µg/kg (1.2 ppm). The use of organomercurials as fungicides and paint preservatives and in medicinal applications has ceased; therefore, fish and marine mammal consumption is the primary source of human MeHg exposure.

Health Effects


The devastating health consequences of methyl mercury (MeHg) exposure were well documented from several tragic incidents (see the case studies section). Historically, MeHg exposure played a very important role in drawing worldwide attention to the consequences of industrial pollution, not just for workers but also for the general public. In the 1950s, the consequences of MeHg exposure to the people of Minamata and Niigata, Japan were recognized. In both cases MeHg exposure resulted from consumption of fish from waters receiving industrial effluent discharge containing mercurials, which demonstrated conclusively that MeHg poisoning could occur through food-chain transfer of MeHg. By 1974 over 2,150 cases of what was then called Minamata disease had been established in the Minamata region alone. Observations of an abnormally high incidence of cerebral palsy-like symptoms with involvement of the visual, sensory, and auditory systems among children from the Minamata region also heralded a new concern over the potential developmental toxicity of industrially derived MeHg. However, as with the adult cases of MeHg poisoning, establishing a causal relationship between environmental MeHg and cases of observed infantile developmental toxicity was difficult because the affected children had not eaten fish and there were no identified neurological effects in their mothers, based on evaluations at that time. The susceptibility and the sensitivity of the fetus to MeHg-induced neurotoxicity were later documented in other studies.

A tragic incident in Iraq clearly documented the fetal effects of maternal methyl mercury exposure (see case study section). During the winter of 1971 some 73,000 tons of wheat and 22,000 tons of barley were imported into Iraq. This grain, intended for planting, was treated with various organic mercurials. Unfortunately, this grain was made into flour and consumed throughout the country, resulting in the hospitalization of some 6,530 people and the death of 459 at the time of the study.

The accumulated evidence leaves no doubt that MeHg is a serious developmental toxicant in humans, especially to the nervous system. While the toxicological and behavioral outcomes resulting from high-concentration in utero exposures are not in debate, questions regarding risks and mechanisms of action following low-concentration, chronic in utero exposures remain.

A US National Research Council report states that "over 60,000 newborns annually might be at risk for adverse neurodevelopmental effects from in utero exposure to MeHg (methyl mercury)." This report clearly makes the point that many infants are exposed to mercury above levels considered safe.

One of the complications with diagnosing MeHg exposure is that presentation of symptoms appears to occur after a latency period during which no effects are observed. The period of latency appears to be related to the level of exposure, with higher exposure concentrations resulting in a shorter latency period. The exact biological mechanisms underlying this latency period are unclear. Some researchers have suggested that latency not only reflects the time to reach accumulation of MeHg in the brain, but also reflects achievement of a threshold wherein enough tissue is destroyed that the capacity of the CNS to compensate for the damage is overwhelmed. Observation of long latencies following cessation of MeHg administration in animals and humans, however, may also derive from long-term demethylation of MeHg to inorganic mercury in the brain.

Reducing Exposure


The primary concern with organic mercury is methyl mercury in fish. Children and women of childbearing age should be cautious about consuming fish known to accumulate mercury, such as tuna, shark, swordfish, and pike. Local fish consumption advisories should be followed.

Regulatory Standards


The primary human exposure to methyl mercury is from consumption of contaminated fish. The most sensitive population is the developing fetus or infant due to the effects of methyl mercury on the nervous system and on development. Exposure limits and fish consumption advisories are directed at pregnant women, women of childbearing age, and children. All agencies also recognize that fish has many nutritional benefits and is an important part of many people's diet. Below is a list of some of these recommendations, but it is very important to consult the local fish consumption advisories.

  • FDA: 1 ppm in commercially harvested fish (i.e. tuna fish)

  • FDA Action level: 0.47 µg/kg/day

  • ATSDR Minimal Risk Levels (MRLs): 0.30 µg/kg/day

  • Washington State Total Daily Intake: 0.035-0.08 µg/kg/day

  • EPA Reference Dose (RfD): 0.1 µg/kg/day (In 1997 the EPA estimated that 7% of the women of childbearing age in the United States exceed the established RfD of 0.1 µg/kg/day.)
  • Children under six should eat less than one half a can of tuna (three ounces) per week. Specific weekly limits for children under six range from one ounce for a twenty pound child, to three ounces for a child weighing about sixty pounds.

  • Women of childbearing age should limit the amount of canned tuna they eat to about one can per week (six ounces). A woman who weights less than 135 pounds should eat less than one can of tuna per week.

Additional Resources


Slide Presentation and Online Material

• A Small Dose of Mercury presentation material and references. Website contains presentation material related to the health effects of mercury.

European, Asian, and International Agencies

• United Nations Environment Program. Reducing Risk from Mercury. This program aims to develop a global assessment of mercury and its compounds, including an outline of options for addressing any significant global adverse impacts of mercury. [accessed April 5, 2009]

• World Health Organization (WHO). Elemental Mercury and Inorganic Mercury: Human Health Aspects. Document on human health aspects of inorganic and organic mercury. [accessed April 5, 2009]

North American Agencies

• Health Canada. Mercury. Health Canada provides information on the health effects and environmental distribution of mercury. [accessed April 5, 2009]

• US Food and Drug Administration (FDA). Advisory on Methyl Mercury and Fish. Site has recent FDA consumer information on methyl mercury. [accessed April 5, 2009]

• US Environmental Protection Agency (EPA). Mercury. [accessed April 5, 2009]

• US Environmental Protection Agency (EPA). What You Need to Know about Mercury in Fish and Shellfish. [accessed April 5, 2009]

• US Environmental Protection Agency (EPA). Mercury Study Report to Congress. [accessed April 5, 2009]

• US Environmental Protection Agency (EPA). Integrated Risk Information System.

• US Agency for Toxic Substance Disease Registry (ATSDR). Toxic Substances - Mercury. ATSDR produces toxicology profile documents on many compounds including mercury. [accessed April 5, 2009]

• US Agency for Toxic Substance Disease Registry (ATSDR). Minimal Risk Levels for Hazardous Substances. ATSDR's list of minimal risk levels. [accessed April 5, 2009]

• US Geological Survey (USGS). Mercury in the Environment. Site has maps and supply information on mercury. [accessed April 5, 2009]

• US National Research Council (NRC). Toxicological Effects of Methylmercury. The full NRC report on mercury. [accessed April 5, 2009]

• Washington State Department of Health. Fish. Site has information on Washington State's advisory of fish consumption and mercury. [accessed April 5, 2009]

• Washington State Department of Ecology. Mercury Reduction in Washington. Comprehensive information on uses and release of mercury in Washington and efforts to reduce mercury use and release. [accessed April 5, 2009]

Non-Government Organizations

The Mercury Policy Project (MPP). "MPP works to raise awareness about the threat of mercury contamination and promote policies to eliminate mercury uses, reduce the export and trafficking of mercury, and significantly reduce mercury exposures at the local, national, and international levels." [accessed April 5, 2009]

• Sea Turtle Restoration Project. Got Mercury?. A calculator that estimates mercury intake from fish and shellfish. [accessed May 26, 2010]

American Conference of Governmental Industrial Hygienists (ACGIH). "ACGIH is a member-based organization and community of professionals that advances worker health and safety through education and the development and dissemination of scientific and technical knowledge." [accessed April 5, 2009]

References


Clarkson, T. "Methylmercury and fish consumption: Weighing the risks". Can Med Assoc J 158 (1998): 1465-1466.

Clarkson, T. W. "The three modern faces of mercury". Environ Health Perspect 110, Suppl 1 (2002): 11-23.

Gilbert, S. G. and K. S. Grant-Webster, K. S. "Neurobehavioral effects of developmental methylmercury exposure". Environ Health Perspect, 6 (1995): 135-142.

Kales, S. N., & R. H. Goldman. "Mercury exposure: current concepts, controversies, and a clinic's experience". J Occup Environ Med 44, 2 (2002): 143-154.

 

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