Toxicity of Organic Mercury, Research Paper Example

Abstract

There has been much attention given to the affects of mercury toxicity on the human body. Evidence suggests that all forms of mercury, both organic and inorganic, are toxic to the human body. However, toxicity depends on the route of entry, exposure limits and environmental setting as well as a host of biological factors. Organic mercury, in particular methylmercury, is the mercury compound that most people, including workers in occupational settings, are exposed to on a regular basis. It is also recognized that MeHg is one of the most toxic forms of mercury, and that it can, at sufficient levels, have devastating effects on human health. A review of the literature revealed ample evidence to suggest that organic mercury is toxic to the human body even at low levels, and can lead to toxicity of the central nervous system, damage to the kidneys and cause autoimmune response. While there are limits to how much of any mercury species workers are exposed to in occupational settings, organic mercury can undergo synthesis such as demethylation in the body and be up-taken into various tissues and organs where it is further broken down to its elemental form and stored indefinitely. When exposed to low levels over time, toxic levels can be built up in the body, with serious consequences to health.  A review of the current scientific literature on organic mercury toxicity reveals that organic mercury is of occupational concern for workers and that steps should be taken to limit their exposure to organic mercury.

Introduction

Mercury (Hg) is a  naturally occurring metal that has been used by humans for thousands of years. Despite its usefulness, mercury, both inorganic and organic, is a poison and is toxic to the human body in even small amounts. Mercury toxicity has been well known and studied over the years. The phrase “mad as a hatter” was coined because of the chronic exposure of mercury that hat makers endured often left them riddled with psychotic illness (Dinner and Brenner, 2009). While humans have found it useful for a number of applications, from making hats to making pharmaceuticals such as vaccines, it is, unlike many metals, not essential for any biological functions (Gochfeld, 174).  Mercury’s historical use by humans goes back to at least the time of the Egyptians, where it has been found in early Egyptian tombs dated to 1500 BC (Diner and Brenner, 2009). It was widely used in the late 18^th century in anti-syphilitic agents and also extensively in the 1800’s for working felt for the making of hats. It is still widely used today in a variety of technical and medical applications, such as in the making of batteries, light bulbs, pesticides, fungicides, medicines and in the manufacturing of other chemicals. In modern times, mercury’s unique physical properties have allowed it to be used in technical applications such as thermostats, thermometers and other instruments as a mercury switch (Gochfeld, 174). It is also used extensively in the field of dentistry, where it is used in the filling of cavities in teeth (Gochfeld, 174).  Mercury is important in the mining industry as it is very useful in mining metals such as gold and silver since it easily amalgamates these metals making them easier to separate out of the bedrock matrix.

Due to the fact that mercury is prevalent in the environment and is already a major public health concern, it is of especial concern for those who work in occupational settings where they are regularly exposed to various species of mercury. Despite the fact that exposure levels are regulated to what are considered safe levels, mercury has a tendency to be stored in the body, making it more dangerous the longer the exposure occurs. A review of the literature reveals an abundance of information on mercury toxicity but there is still room for further research since the direct pathways of mercury metabolism within the body are still poorly understood.

Species of Mercury

Mercury can be found in the environment in both organic and inorganic forms, both naturally as a part of biological processes and due to anthropogenic processes. Mercury (Hg) in its elemental form is a liquid at room temperature and is the only metal that has this property. Also called quicksilver, it does not appear to be toxic in this form (Clarkson and Magos, 612). However, liquid mercury vaporizes at room temperature and is easily absorbed at rates up to 80% by inhalation (Dinner and Brenner, 2009) and it is the vapor that has toxic and adverse affects on the body.  Mercury ore, called cinnabar, is a brilliant red color has been used since ancient times as ink and dye. Other inorganic mercury compounds are typically in the form of mercurial salts.

Organic mercury is most often found in two forms, ethylmercury and methylmercury.  Organic mercury readily combines with chlorine, sulfur, phosphorus and other elements in the environment  to form inorganic compounds. In addition, micro-organisms combine inorganic mercury with carbon to form organic mercury compounds, of which methylmercury is the most abundant (Risher et al, 109).  According to Gardner, Nyland and Silbergeld (182) “there are also important transformations among mercury compounds in biological systems. MeHg is demethylated to iHg (Hg²⁺) in situ in mammalian tissues such as liver, brain, and phagocytic cell population by an unknown mechanism.” However, while organic mercury can ready decompose to inorganic mercury, the opposite has never been observed. Elevated levels of methylmercury in the body have never been reported after exposure to inorganic mercury (Clarkson, 629).

Diethylmercury is an especially toxic organic mercury compound that is used by workers in chemical laboratories. It is used in the calibration of some laboratory equipment, as a reagent and in the manufacture of other chemicals. According to Risher et al (110), “It is used in some chemistry laboratories as a reference material in nuclear magnetic resonance spectroscopy, which has resulted in one lethal exposure through extremely small dermal contact.” Workers in occupational settings where dimethylmercury is used are at added risk for serious toxicity as even a minute amount of this mercurial compound can cause serious, if not deadly, effects. Unlike other forms of organic mercury, where toxic effects can be delayed for weeks if not years, the toxic effects of dimethylmercury are practically instantaneous. Toxicity can occur through the skin or by inhalation, as this compound is easily vaporized in minute, and toxic, amounts at room temperature. “Dimethylmercury can cause delayed permanent brain damage and death with little or no warning during exposure. As there is a paucity of toxicity and other information concerning this particular chemical, extreme caution should be exercised by those using dimethylmercury and other dialkyl mercury compounds (Risher et al, 111).”

Since mercury is easily able to switch forms from organic to inorganic, both in the environment and inside the human body through natural biological functions, it is impossible to simply address the toxicity of organic mercury without also addressing the toxicity of inorganic mercury. “The intact organomercurial cations believed to be the proximate toxic agent responsible for damage to the central nervous system, and the mercuric cation released from ethylmercury plays this role in kidney damage (Clarkson and Magos, 624).” Introduced organic mercury can also react with inorganic mercury that is already in the body. According to Ishitobi et al, (2010), Hg vapor that is introduced into the human body “is trapped and oxidized to divalent inorganic Hg in erythrocytes, part of the Hg vapor remains in the bloodstream long enough for it to be distributed to other tissues and reach the blood-brain barrier.” Thus, inorganic mercury can accumulate in the body where it can then interact with introduced organic mercury and cause additional hazards to the human body (Ishitobi et al, 2010).  A review of the literature reveals an abundance of information on the toxicity of organic mercury in the environment and occupational settings and the potential affects that it can have on public health.

Human Exposure to Mercury

Organic mercury in occupational settings is entirely man-made, but organic mercury in the environment is both anthropogenic and naturally occurring. Anthropogenic organic mercury comes from both mercury manufacture and disposal as well as fossil fuel combustion (Gochfeld, 174). When organic mercury in encountered by humans it is typically by inhalation, ingestion (typically by the eating of fish) or by passing through the skin. Organic mercury tends to build up on surface waters where it bioaccumulates in fish, moving slowly up the food-chain. Methylmercury is the organic mercury compound most widely found in nature and it is the form which most humans are exposed to.

Most people encounter methylmercury through the consumption of fish. Of the mercury encountered in fish, 75-95% is in the MeHg form (Gochfeld, 175). Over time, MeHg builds up in the body and can cause an outbreak of Minamata disease, mercury poisoning usually from organic mercury found in fish due to high levels of industrial mercurial pollutants in the water, mostly in the form of MeHg.  This disease is most commonly encountered in populations who consume a largely fish based diet, such as people who live in the Amazon and Japan, but MeHg can accumulate in the body of anyone. Pregnant women should be especially concerned with the amount of MeHg that they are ingesting as they can transfer amounts of MeHg to their fetus in amounts that is sufficient to impair nervous system development (Gotchfeld, 175). Once inside the body, organic mercury has a half life of about 90 days.

People also regularly encounter methylmercury by exposure to certain pharmaceuticals. For example, ethlylmercury is another form of organic mercury that is often used, along with methylmercury, in the preparation of certain medicines including some vaccines. Ethylmercury, which is used in thimerosal, is more extensively dealkylated to inorganic mercury compared to methylmercury. “Once metabolized, the presence of inorganic mercury in brain and other body tissues is persistent (Gardner et al, 183).”  Thus, exposure to organic mercury can lead to a build up of inorganic mercury in the body, where it is difficult to flush. Occupational workers who are exposed to even low levels of mercury on a daily basis can potentially build up large levels of mercury in their body over time, leading to toxic effects.

Occupations settings where workers are regularly exposed to methylmercury include the mining industry, industrial settings where coal is burned, battery factories, medical settings such as laboratories that produce medications using mercury and workers in the dental industry who use mercury for dental fillings.  Workers who are exposed to organic mercury in the workplace are typically exposed to organic mercury in the environment was well, such as from eating fish. Workers in these fields then are subject to additional risk factors for mercury toxicity.

Pathways of Absorption in the Body

The most recognized target organs for mercury toxicity and damage are the kidneys, central nervous system and the thyroid glands (Holmes, James and Levy, 171). Inorganic mercury that is inhaled in its vapor form can cross the blood brain barrier where it is stored and can cause damage to the central nervous system (Clarkson and Magos, 613).

“The high mobility of inhaled mercury vapor in the body is assumed to be due to its physical properties as an uncharged, monatomic gas that can readily diffuse through the lipid monolayers of the cell membrane. The mechanisms of transport of mercurous and mercuric cations are not well understood. Mercuric mercury is known to exit liver cells into bile as a complex with reduced glutathione. Mercuric mercury has a limited capacity to cross the blood–brain and placental barriers but is avidly accumulated by the kidneys. (Clarkson and Magos, 613).”

Organic mercury has primarily neurological toxic effects, although a number of other organs and bodily systems can be affected, including gastrointestinal, respiratory, hepatic, immune, dermal and renal (Risher et al, 109). “The intact organomercurial cation is believed to be the proximate toxic agent responsible for damage to the central nervous system, and the mercuric cation released from ethylmercury plays this role in kidney damage (Clarkson and Magos, 624).  Methylmercury forms a complex with the amino acid cysteine which accounts for its high rate of mobility within the body. Once the complex is formed, it gains entry into the cells through a neutral amino acid carrier due to the fact that it resembles the neutral amino acid methionine (Clarkson and Magos, 625). Other organomercurials such as phenylmercury and methoxyethylmercury, are quickly converted to inorganic mercury within the body so their toxic effects are similar to mercuric mercury compounds. However, these compounds are still more efficiently absorbed into the body compared to inorganic mercury (Clarkson and Magos, 625).

Below are some of the most common types of mercury encountered and their route of exposure.

^? Some organic mercury compounds involve two carbon atoms attached to mercury, such as dimethylmercury (CH3-Hg-CH3).

Table 1: Mercury species encountered in the environment (Clarkson and Magos, 611)

Mercury enters the human body either through inhalation, ingestion, or, more rarely, through dermal contact. The amount of mercury that enters into the body depends primarily on the route of entry. “When vapors of metallic mercury are inhaled, as much as 80% is absorbed. Following ingestion, absorption is less than 0.01% for metallic mercury, less than 10% for inorganic mercury, and greater than 95% for organic mercury (Argonne National Laboratory).” Once inside the body, organic mercury is quickly up-taken by various body tissues, where some of it is broken down by demethylation into inorganic mercury. It may also bind to sulfhydryl groups where it can then be transported by amino acid carriers across the blood-brain barrier, where it readily accumulates; a similar process also results in placental transfer (Holmes, James, and Levey,173).” Organic mercury has a half life of about 90 days. When it is released from the body mainly from the feces and urine (Argonne National Laboratory).

Table 2: Absorption of mercury species by routes (Gotchfeld, 175).

One of the issues regarding the confusion over organic mercury toxicity is due to the delayed response that toxicity can have. According to Gardner et al, (182), both methylmercury and ethylmercury have been found to induce “autoimmune disease in susceptible mouse strains, through the induction of autoimmune responses by organic species of Hg is slower and somewhat attenuated as compared to iHg.” The pathway by which MeHg causes auto-antibodies starts when MeHg is introduced into the body. It is taken up withing the lymphoid tissue and is followed by progressive demethylation to iHg withing the lymph nodes. Studies have proven that the production of auto-antibodies was positively correlated with demethylation (Gardner et al, 182).” According to the same researchers (183), exposure to inorganic mercury has also been shown to have a positive correlation to the level of auto-antibodies in blood serum levels.

Signs of Mercury Toxicity

There are several visible symptoms of mercury toxicity. Some mercury compounds, including  organomercurcials and mercuric mercury, cause hypersensitivity which shows as a pronounced rash,  profuse sweating and red and swollen hands and feet that are extremely sensitive to touch. Other symptoms include insomnia, loss of speech, shaking, neurological disorders, loss of hearing, progressive weight loss and photophobia (Clarkson and Magos, 614).

Biological Indicators of Organic Mercury Toxicity

The most efficient way to determine the amount of organic mercury in the human body is through blood samples or by examining scalp hair. These are both good indicators of the amount of organic mercury that has reached the target organ, the brain. For testing of prenatal exposure, the cord blood and maternal hair can both be used as efficient indicators (Clarkson and Magos, 629).  The mercury found in hair will typically be 80% methylmercury sp. with the remainder being inorganic mercury. However, since it has been shown that inorganic mercury does not accumulate in hair, the inorganic percentage in hair is due from demethylation of organic mercury within the hair follicle itself, meaning that hair is an indicator solely of the organic mercury exposure.

Organic mercury is typically excreted from the body via the feces. This route of exit accounts for as much as 90% of organic mercury excretion, according to animal analysis . Inorganic mercury that is formed by demethylation in the intestines is also excreted in the feces (Clarkson and Magos, 628).

Mercury Metabolization in the Body

Once a person has been exposed to mercury, it is taken up into the body through the blood. It is then absorbed through various parts of the body. Some organic mercury is released from the body with urine, and this can be a way to tell the amount of exposure a person has had. Yet, as much as  “Methylmercury is readily absorbed by both the GI tract and the lungs and once in the bloodstream, mercury is subject to a very complex and inadequately understood process involving binding and redox cycling, both extracellulary and intracellulary. Physiologically based pharmacokinetic models have been applied to mercury, to estimate the exchange among organ compartments. In vivo methylation and demethylation may also occur, typically in the intestines. These complex processes influence the amounts of mercury exchanged between the blood compartment and various organs, including the brain (internal bio-availability). (Gochfeld, 175).” Methylmercury is also produced from coal burning power stations, municipal incinerators and automobiles when they are recycled, and this accounts for the majority of MeHg that enters the body through inhalation (Clarkson and Magos, 625).

It has been known for years that both chronic and acute affects can arise in occupational workers who are often exposure high levels of various forms of mercury (Holmes and Levy, 172). However, the effects and possible toxicities of  low level exposure were not as well known. In order to ascertain the effects of low level environmental exposure and its concern to human health, a review of the literature was conducted by Holmes, and Levy in 2009.  Studies published from 1998 to 2008 that were published by authoritative experts in the field were reviewed by the authors and judged for credibility and reliability of results. Their review revealed that due to the toxic effects observed in the literature, contact with mercury in all of its forms, organic and inorganic, should be minimized when possible. “For MeHg, the primary focus of concern regarding low-level environmental exposure remains the potential for in utero or early post-natal exposure to cause neurological developmental impairments, including decrements in attention, language, verbal memory, motor speed, visuo-spatial function and IQ impairment (Holmes and Levy, 180).”

Once mercury has been taken up by the body, it is distributed in various areas of the body. Studies have shown that inorganic mercury is stored in neruons, glial cells and lysosomes. Concentrations in neurons are typically more in motor than in sensory neruons with the highest concentrations found int eh motor nuclei of the rhombencephalon. Inorganic mercury has also been found accumulated in the cells of the choriod plexus.  However, while studies can show researchers where the mercury eventually ends up in the body, the exact mechanisms for its transformation and storage are still poorly understood (Clarkson and Magos, 615).

In order to determine the difference in toxicity between inorganic and organic mercury species to humans, a study was under taken by  Gardner et al that compared human cells in vitro at environmentally relevant, sub-cytotoxic concentrations. Human peripheral blood mono-nuclear cells (PBMCs) in the presence and absence of the immune stimulant lipopolysaccharide (LPS) were used for the study. The release of cytokine was used as the evaluation marker for the indicator of the immune response to Hg. Results indicated that all species of mercury act as an “immunotoxicant by dysregulating physiologically appropriate responses to stimuli, suggesting that Hg exposure may lead to similar dysreguation of the immune response to pathogens in exposed person (Gardner et al, 189).”

Examples of Mercury Toxicity

There are many historic cases of occupational organic mercury poisoning. The first case of occupational poisoning of workers from methylmercury was reported in the 1940’s from a factory where fungicides containing methylmercury was being produced. The first victim died of complications 15 years after the initial exposure. The autopsy revealed damage to the brain, including cerebellar cortical atrophy selectively involved at the granule-cell layer of the neo-cerebellum (Clarkson, 631). Another large outbreak of occupational poisoning from organic mercury compounds took place in Minamata, Japan in the 1950’s. Fisherman from the area, and their families, consumed fish from a bay that was being polluted by runoff from a chemical plant manufacturing acetaldehyde, where inorganic mercury was being used as a catalyst. Methylmercury was created as a byproduct of the catalytic reaction and was dumped in to the bay. An estimated 14.6  tons of methylmercruy was released into the bay over several years (Clarkson, 631). The methylmercury poisoning was given the name Minimata disease, which is still used today to describe poisoning by methylmercury that has been released into the environment by anthropogenic means.

A recent example of environmental mercury poisoning through fish and contaminated water in Ontario is the case of members of the First Nation’s communities of Grassy Narrows and Wabaseemoong from northeast Ontario. The mercurial contamination of the river occurred when a pulp mill dumped more than 9,000 kilograms of mercury into the Wabigoon River between 1962 and 1970. The native people who depend on the river for their main source of food, fish, have been suffering severe health problems for decades. Research done by Masazumi Harada, a scientist who researched the mercury poisoning incident in Minamata, Japan in the 1950’s, in 2004 revealed that even those that had been born after the river had been deemed safe were beginning to show symptoms of illness due to mercury toxicity and those whose symptoms were minor 40 years ago have worsened. Diseases  among those affected included mental retardation, muscular dystrophy, cerebral palsy and other forms of mental deficiency. “Eighty nine percent of people who had tested below the level of mercury contamination in 1975 were found to have more severe symptoms 30 years later (Barber).”

Potential Health Effects of Mercury Toxicity and Exposure       

In 1994, a study was undertaken in Japan to determine the effects of mercury exposure to workers in a mercury battery factory (Ishihara and Urushiyama). The test subjects, seven Japanese female workers, were exposed to mercury vapor at levels of less than 0.02 mg Hg/m³ for 8 hours a day, approximately 44 hours a week. In order to determine the amount of inorganic and organic mercury was held in the body, hair, blood and urine samples were taken from workers at 4 months, 8 months, 17 months and 23 months of exposure. While the study found that the levels of inorganic and organic mercury did not increase in hair and urine samples, even after 23 months of exposure, levels in red blood cells and plasma were found to increase significantly after 4 months and remained high for the entire study. This study clearly demonstrated that there was a clear uptake of mercury due to occupational exposure in the workers (Ishihara, and Urushiyama, 660). Results of the study are listed below in Table 3.

Table 3: Mean inorganic and organic mercury concentrations in urine, plasma, erythrocytes and hair after workers exposure to organic mercury (Ishihara and Urushiyama).

Risher et al. (114) report the findings of a 2002 study by Yoshizawa et al. that investigated the link between the intake of mercury from fish, being mainly methylmercury, and the risk of coronary heart disease. Toenails from male health professionals, aged 40 to 75 who had no previous history of cardiovascular disease or cancer, were examined for mercury content. “During a five-year follow-up of the 33,737 enrollees, 470 cases of coronary heart disease were reported. The cases included non-fatal MI, coronary artery surgery, and fatal coronary heart disease. In this study, it was found that mercury level was significantly correlated with fish consumption. In addition, the mean mercury level was found to be higher in dentists than in non dentists (Risher et al, 114).” The occupational risk for mercury toxicity, then, appears from this study to be greater for those health professionals that work with mercury on a regular basis.

Existing Guidelines and Policies Limiting Occupational Exposure in Ontario, Canada

Each country and state has specific regulations regarding the limits that workers can be safely exposed to in occupational settings. In Ontario, Canada, the limits of mercury to which workers can be exposed is clearly defined in Regulation 833, and limits are given in the table below.

These levels are at or below the Chemical Toxicity Values of mercury for a non-cancerous effect, as defined by the Human Health Fact Sheet presented by the Argonne National Laboratory, listed in Table 4 below.

Table 4: Chemical toxicity values of mercury species (Argonne National Laboratory, EVS)

While occupational workers may be exposed to low levels of MeHg while working, levels that are below the toxic levels as defined by official guidelines, workers face the effects that occur when MeHg from multiple pathways builds up to toxic levels in the body. Workers who are exposed to organic mercurial compounds from pharmaceuticals, pesticides, fish and other environmental factors in their normal day to day lives are at a disadvantage because they already have a build up of mercury in their systems. Exposure to added levels of mercury in the workplace, then, can put them over the acceptable daily limit for mercury exposure.

While guidelines exist for the amount of mercury that workers are allowed to be subjected to in occupational settings, limitations do not take into effect the interaction between the various species of mercury, or the breakdown of organic mercury into inorganic mercury in the human body once  workers are exposed to it initially. For example, the U.S. Food and Drug Administration estimates that, on average, each person intakes 50 to 100 nanograms/kg of body weight per day from the environment and diet. Of that, approximately 80 to 90% is in the form of methylmercury. If the person is a heavy fish eater, then that average is increased an additional 36 ng/kg per day (Risher et al, 110). In a study conducted by Ishitobi et al, (242), results indicated that “co-exposure to MeHg and Hg vapor at levels relevant to human exposure might elevate neurotoxic risks.” Co-exposure can worsen adverse behavioral performance and has considerable implications for both public and occupational health. The study by Ishitobi et al (245) also found that “Hg levels were increased by Hg vapor at low MeHg doses, a finding relevant to human exposures, which typically occur at low concentrations.” Studies such as this indicate that the current limits of inorganic and organic mercury that workers are allowed to be exposed to in occupational settings may not be sufficient to protect them against toxicity.

 Discussion

Toxicity from methylmercury can have dramatic effects long after a toxic level of exposure takes place, which makes the process of understanding limits in occupational settings difficult. Clarkson (630) provides a good example of this in the report “The Toxicology of Mercury and its Chemical Compounds.” A female professor at Dartmouth College was working in her lab when she accidentally spilled a few drops of liquid dimethylmercury onto her latex gloves in a fume cupboard.  According to her notes, this occurred in August, 1997. She experienced no immediate ill effects and continued on with her work. However, on January 20, 1998 she was admitted to the hospital after a 5-day history of progressive deterioration in balance, gait and speech. She has been losing weight (15 pounds over 2 months) and had experienced symptoms such as nausea, diarrhea and abdominal discomfort. Clinical symptoms included difficulty with speech, hearing and vision. Neurologic symptoms occurred on February 6, 1998, 176 days after exposure to the dimethylmercury. She became unresponsive to all visual, verbal and light touch stimuli and died several months later despite intensive medial support. Postmortem analysis of the patients hair reveled that she had only had that one exposure to the methylmercuy, as confirmed in her lab notebook. This example reveals the need for studies regarding the toxicity of organic mercury compounds must be done over sufficient periods of time in order to completely understand the long term toxic effects of these compounds.

While the immediate effects of toxicity by organic mercury may be slow in coming, it has been shown to have dramatic long term effects, especially on reproduction. The literature reveals that mercury can build up in the body and be passed by a mother to her unborn child. Mercury toxicity can also cause sterilization in both males and females.  Winker and Rudiger (1) note that “Since the beginning of the twentieth century, there has been a consistent increase in the number of involuntarily childless marriages in nearly all industrialized countries.” The researchers used PubMed to search for possible adverse affects on reproductive toxicology from chemicals used in occupational settings as a possible culprits behind the sterility. The literature revealed that “Only a few substances…are proven to influence fertility in occupational medicine: These are lead, organic mercury compounds, manganese, carbon disulfide, 2-bromopropane and dibromochloropropane (DBCP) (Winker and Rudiger,1).”

Pregnant women are able to freely pass organic mercury to their unborn child in levels that exceed their own levels of MeHg. The literature reveals that “cord blood levels of methylmercury closely follow those in the mother at the time of delivery. Animal data including primates indicate that brain levels in the newborn may be as high as five times the corresponding levels in the mother (Clarkson, 627).”  In addition to passing organic mercury to their child through the blood cord and placenta, organic mercury can also be passed to the child through breast-milk, along with inorganic mercury (Clarkson, 627).

Summary

Toxicity from organic mercury toxicity is a major threat to public health today. Organic mercury is easily taken up from sources in the environment and in occupational settings, where it undergoes biological reactions, reducing it to inorganic mercury, and storing it in various bodily tissues. It has both short term and long term effects on health and thus contact with it should be minimized and avoided if possible. Workers who are regularly exposed to organic mercury in occupational settings are at an added risk of mercury toxicity since they are exposed to additional organic mercury in addition to that which they encounter in the environment.

A review of the scientific literature reveals that there is ample evidence to confirm that those who work in occupations where they are regularly exposed to organic mercury compounds are at a greater risk for both long term health problems. While limits are strictly enforced by governmental standards, the limits do not take into account the organic mercurial compounds that workers encounter on a daily basis outside of the workplace. On a daily basis, most people  are exposed to organic mercury from fish, pesticides and other environmental sources. Since most effects of mercury toxicity occur from the build up of mercury in the body over time, it is important  to take this into account when discussing the use and safety of mercury and exposure to workers in the occupational environment.

Workers should also be aware of the potential long term affects of mercury toxicity. Due to its effects on reproductive health, and the known effect of organic mercury to be readily passed to the fetus, women who are pregnant, or plan to become pregnant, should be especially caution around mercury in the occupational setting, and avoid it if possible. Workers who have a history of cancer, heart conditions, kidney or autoimmune dysfunction should also be cautious with regards to their daily exposure to organic mercury, since these conditions can make them more prone to toxic effects.

By limiting the amount of mercury encountered in the environment, workers would be at less risk for mercury toxicity from exposure to organic mercury in their workplace. Educating workers of the potential hazards of organic mercury, where it is encountered in the environment and its points of entry into the body can help them to avoid unnecessary exposure and reduce the risk of ill health effects from mercury toxicity.  More research into the long term effects of organic mercury on occupational workers will continue to shed light on the toxic effects of mercury and help to shape policy to protect workers from ill health affects due to occupational exposure.

References

Barber, Mike “Mercury Poisoning Lingers Decades after Ontario River Deemed Safe” The Montreal Gazette Web. Retrieved 16 November 2010 http://www.montrealgazette.com/health/Mercury+poisoning+lingers+decades+after+Ontario+river+deemed+safe/2772880/story.html

Clarkson, Thomas W. and Magos, Laszlo (2006) “The Toxicology of Mercury and Its Chemical Compounds” Critical Reviews in Toxicology 36, 609-662.

Diner, Barry M., Brenner, Barry E. (2009) “Toxicity, Mercury” e Medicine Web. Retrieved 12 November, 2010 from http://emedicine.medscape.com/article/819872-overview

Gardner, Renee M., Nyland, Jennifer F., Silbergeld, Ellen K. (2010) “Differential Immunotoxic Effects of Inorganic and Organic Mercury Species  In Vitro” Toxicology Letters 198, 182-190.

Gochfeld, Michael (2003) “Cases of Mercury Exposure, Bioavailability and Absorption” Ecotoxicology and Environmental Safety 56(1), 174-179.

Holmes, P., James, K.A.F., Levey, L.S. (2009) “Is Low-Level Environmental Mercury Exposure of Concern to Human Health?” Science of the Total Environment 408(2), 171-182.

“Human Health Fact Sheet” (2005) Argonne National Laboratory, EVS Web. Retrieved 16 November 2010 http://www.ead.anl.gov/pub/doc/mercury.pdf

Ishihara, Nobuo, and Urushiyama, Kenji (1994) “Longitudinal Study of Workers Exposed to Mercury Vapour at Low Concentrations: Time Course of Inorganic and Organic Mercury Concentrations   in Urine, Blood and Hair” Occupational and Environmental Medicine 51, 660-662.

Ishitobi, H., Stern, S., Thurston, SW., Zareba, G., Langdon, M., Gelein, R., Weiss, B. (2010) “Organic and Inorganic Mercury in Neonatal Rat Brain after Prenatal Exposure to Methylmercury and   Mercury Vapor” Environmental Health Perspectives 118(2), 242-248.

“Occupational Exposure Limits for Ontario Workplaces” (2010) Ontario Ministry of Labour Web. Retrieved 12 November 2010 from http://www.labour.gov.on.ca/english/hs/pubs/oel_table.php

Risher, John F., Murray, H. Edward, Prince, George, R. (2002) “Organic Mercury Compounds: Human Exposure and Its Relevance to Public Health” Toxicology and Industrial Health 18, 109-160.

Winker, R., Rudiger, H.W. (2006) “Reproductive Toxicology in Occupational Settings: An Update”  International Archives of Occupational and Environmental Health 79, 1-10