As outlined above, one of the first steps in a risk assessment is to identify and characterise the risks associated with exposure to a particular chemical or compound. The health effects associated with mercury are dependant on how a person is exposed to mercury (either via inhalation, ingestion or dermal absorption) and the chemical form of mercury when exposure occurs. The toxicity of mercury is highly dependant on its chemical form, the exposure pathway, and the vulnerability of specific body organs. This section details the health effects associated with the three main forms of mercury (elemental, inorganic and organic mercury compounds), the main target organ or organs that mercury can impact and the health effects associated with exposure to the different chemical forms of mercury (both acute and chronic exposures).
Elemental mercury is the most volatile form of mercury. The major human exposure pathway for elemental mercury is via inhalation (WHO, 2003; Clarkson and Magaos, 2006). Inhaled elemental mercury vapour easily crosses from the lung into the blood stream (Tchounwou, 2003). Approximately 80% of inhaled mercury is absorbed into the blood stream, while only 0.01% of elemental mercury is absorbed though the gastrointestinal tract (WHO, 2003). Once in the blood stream, elemental mercury readily crosses the placental barrier and developing foetus can be exposed to mercury (WHO, 2003).
Some dermal adsorption may occur from skin contact with elemental mercury but it is thought to be only a minor exposure route (WHO, 2003).
The symptoms of acute metallic vapour toxicity include dyspnea (difficulty in breathing) which may be followed by coughing, chest pains, nausea and vomiting, however, exposure at this level is usually only seen in an occupational setting.
The main effects of chronic toxicity of mercury inhalation are tremors and psychological disturbances. The principal psychological symptoms include excessive timidity, diffidence, increasing shyness, loss of self confidence, anxiety, and a desire to remain unobserved and unobtrusive (Clarkson and Magos, 2006).
Although the actual fatal level of mercury vapour is not known, exposure of more than 1 to 2 mg/m3 of elemental mercury vapour for a few hours can cause acute chemical bronchiolitis (bronchial infections) and pneumonities (inflammation of lung tissue) (Asano et al, 2000). If the amount of mercury inhaled is large enough, renal failure will develop (Satoh, 2000). Moderate and repeated exposures (lower than a few mg/m3, but higher than 0.05 mg/m3) causes tremors in hands, gingivitis (bleeding from the gums), excessive salivation and mercurial erethism (Satoh, 2000). Mercurial erethism is a term to describe the classic neurological symptoms associated with mercury poisoning, these include behavioural and personality changes such as extreme shyness, excitability, loss of memory, and insomnia (Satoh, 2000).
Lower and long-term exposure to mercury vapours can result in micromercurialism, which includes such symptoms as weakness, fatigue, anorexia, loss of weight and disturbances in the gastrointestinal tract (Satoh, 2000).
Some of the most important salts of mercury (inorganic mercury) are mercurous chloride (Hg2Cl2, or calomel), occasionally used in medicines, mercuric fulminate (Hg(CNO)2, which is used as a detonator in explosives; and mercuric sulphide (HgS, or vermillion), which is used as a paint pigment (Tchounwou et al, 2003).
Generally, the adsorption of inorganic mercury compounds is low, including via the lungs (WHO, 2003). The extent of adsorption of inorganic mercury though the gastrointestinal tract may depend on the solubility of the mercury compound and/or how easily the compound dissociates in the intestine to become available for absorption (WHO, 2003). There is indirect evidence that some inorganic mercury compounds may be absorbed through the skin.
Acute inorganic mercury exposure may give rise to lung damage. Chronic poisoning is characterized by neurological and psychological symptoms, such as tremor, changes in personality, restlessness, anxiety, sleep disturbance and depression. Ingestion of inorganic mercury compounds may cause kidney damage. The symptoms described above are reversible after cessation of exposure. Ingestion of very high concentrations of inorganic mercury, however, can be fatal (Asano et al, 2000).
Methylmercury is the most toxic of the organic forms of mercury and is taken up by terrestrial and aquatic organisms. Bacteria in lakes, streams and ocean sediment can convert elemental mercury into organic mercury compounds (Tchounwou et al, 2003).
Organic mercury, particularly methylmercury, is a cumulative toxin that can cause disruption of the developing central nervous system. Part of the reason why organic mercury, in particular methylmercury, is so toxic to humans is that the gastrointestinal absorption efficiency of methylmercury is in the order of 90 to 95% (Castro-Gonzalez and Mendez-Armenta, 2008). Organic mercury compounds (especially methylmercury) can be readily transformed into other chemical forms which allows them to pass through the blood-brain and placental barriers. Once the organic mercury compound has passed though the brain it can be oxidised into inorganic mercury, inhibiting its removal from the brain. The ability of organic mercury compounds to pass though the placental barrier means that developing foetus are particularly vulnerable to the effects of organic mercury (WHO, 2008). Infants and new born babies are also susceptible to the impacts of organic mercury compounds as they can be transferred from the mother during breast feeding.
Infants born to mothers exposed to methylmercury during pregnancy display a wide range of neurological effects including delayed onset of walking and talking, birth defects, cerebral palsy, lower IQ and reduced neurological test scores (Diez, 2008; Counter and Buchanan, 2004; Harada, 1995).
Exposure to high concentrations of organic mercury can result in a range of symptoms including tingling and numbness in the fingers and toes, loss of coordination, difficulty in walking, generalised weakness, impairment of hearing and vision, tremors and finally loss of consciousness leading to death (Diez, 2008).
Human exposure to methylmercury is almost exclusively due to the consumption of fish and marine mammals (Diez, 2008). The biological half-life of methylmercury in humans is approximately 65 days. Because the biological half-life of methylmercury is so long, it may take up to two years before the methylmercury accumulated in the body from one exposure is excreted. Given that consumption of fish is the predominant pathway of exposure to methylmercury for most people, and that most people will consume a fish meal more than once every two years, methylmercury is likely to accumulate in people.
Other potential exposure to organic mercury is thimerosal (also known as thiomersal) in vaccines. Thimerosal was used as a preservative in vaccines to prevent fungi growth (Clarkson et al, 2003). Thimerosal has the same general toxicity characteristics as ethyl mercury, however early toxicological studies found no adverse effects of using it in a vaccine. However, this has been re-evaluated based on new toxicity data and thimerosal has now been removed from vaccines in the United States but the World Health Organisation (WHO) advisory committee has recently concluded that it is safe to continue using thimerosal in vaccines (Clarkson et al, 2003).
Toxic effects from a substance may arise from both short and long-term exposure. Acute mercury poisoning is that which occurs via exposure to a high concentration of mercury over a relatively short time period. In its mercury toxicological profile, the Agency for Toxic Substance and Disease Registry (ATSDR) (1999) defines acute exposure as being a period of 14 days or less. Acute toxicity usually occurs as a result of accidental exposure (e.g. a broken thermometer).
By contrast, chronic poisoning occurs as a result of exposure to a low concentration of mercury over an extended time period, until the tissue concentration is sufficient to induce a toxic reaction of one sort or another. The ATSDR defines chronic exposure as being a period greater than 365 days. Long-term occupational or food exposure could cause chronic effects.
Table III-2 outlines the major causes of mercury poisoning and the cause and type of exposure.
|Form of mercury||Type of exposure||Cause of exposure|
|Elemental||acute-chronic||Spills (including broken thermometers, barometers, CFLs)|
|Elemental||acute-chronic||Medicinal applications (including ethnic/folk remedies)|
|Inorganic||acute-chronic||Use in medications (e.g., merthiolate)|
|Inorganic||acute-chronic||Use in cosmetic products (e.g., skin-lightening creams)|
|Inorganic||acute||Inks and dyes (including use in tattooing)|
|Organic Mercury||Chronic||Fish consumption|
Note: Adapted from Risher et al (2003).
Several instances of large scale mercury poisoning incidents have occurred overseas, resulting in serious illness and multiple deaths. Incidents have included in Minnamata Bay in Japan in the 1950s and 60s, where industrial discharges cause contamination of sea food (Hazarda, 1995) and in Iraq in the 1970s and 80s, due to contamination of the food supply (Diez, 2008). Such large scale poisoning incidents have not occurred in New Zealand, where mercury poisoning incidents have been either as a result of occupational exposure or exposure as a result of accidental spills.
Historically, mercuric salts were used to make felt hats. As the felt had to be heated to make the hats, the workers were exposed to mercury vapours (Satoh, 2000). Early symptoms amongst hatters included insomnia, forgetfulness, loss of appetite, and mild tremors. Continual exposures led to increased tremors, excitability, memory loss, timidity and sometimes delirium (Tchounwou et al, 2003). The term “as mad as a hatter” is thought to have arisen as a result of mercury exposure amongst hatters.
The historic use of grey powder (a mixture of chalk and metallic mercury) resulted in several cases of chronic mercury poisoning occurring among fingerprint officers. In accord with the symptoms of erethism, some detectives became progressively more shy and bashful, weeping in corners and refusing to arrest people (N. Kim, 1995).
Dental professionals are among the largest group of workers who are occupationally exposed to mercury. During the 1970s, air concentrations in some dental surgeries reached 20 mg/m3, but since then levels have generally fallen to about one-tenth of those concentrations (Lars Järup, 2003).
A study of 43 former New Zealand School Dental Nurses, who were chronically exposed to high levels of mercury vapour and direct skin contact with elemental mercury, found that the nurses do not appear to display any neurological symptoms of mercury exposure. However, the study did find that unfavourable reproductive outcomes (conception difficulties, miscarriages, still births, low weight babies, children with birth defects) were twice as high as the control group. There was also a statistically higher incidence of hysterectomy (Jones et al, 2007). Research conducted by Olfert (2006) found limited evidence linking exposure to elemental mercury and spontaneous abortion, congenital abnormalities and reduced fertility.
In a review of the literature examining the effects of mercury exposure on dental professionals, Clarkson and Magos (2006) noted that some studies have found evidence of decreased hand steadiness and suffering from moods of tension, fatigue, confusion and hostility in dental professionals, with elevated mercury urinary levels compared to control groups. However, Clarkson and Magos (2006) concluded it was uncertain whether the apparent symptoms were the results of mercury exposure or whether dental professionals with those personality traits might spill mercury which resulted in higher mercury exposure.
In order to assess the risk to individuals from mercury exposure, it is necessary to establish what exposure is acceptable. This is typically expressed as a mass (in micrograms or milligrams) per kilogram body weight (kg bw) per day, or in some cases per week or month. Average exposure above the standard indicates a potential for effects whereas exposure below the standard suggests no effects. With respect to inhalation exposure, a health standard is often expressed as an allowable concentration in air (mg/m3).
As noted previously, different forms of mercury have different toxicity, with organic forms (methylmercury) being much more toxic than inorganic forms. In addition, the route of exposure has an effect on toxicity; with metallic mercury having lower toxicity by the oral route (i.e. if swallowed) than via inhalation.
A variety of authorities around the world have considered the toxicity of the various forms of mercury (ASTDR, 1999; US EPA, 1997; WHO, 1972; and WHO, 2008). In New Zealand, the Ministry of Health (MoH), in setting the drinking-water standard for mercury, used a provisional tolerable weekly intake (PTWI) for methylmercury of 3.3 µg/kg bw/week from the report of the 1972 WHO/FAO Joint Expert Committee on Food Additives (JECFA). This is the equivalent of 0.47 µg/kg bw/day or 0.00047 mg/kg bw/day. This value has been used by MoH (2005) to conservatively calculate the drinking-water standard for inorganic mercury.
In 2003, the JECFA revised the PTWI for methylmercury downward to 1.6 µg/kg bw/week (WHO, 2008). Vannoort and Thomson (2005) adopted this value when considering food residue measurements for the 2003/04 New Zealand Total Diet Survey (NZTDS) conducted for the New Zealand Food Safety Authority (NZFSA). Thus, 1.6 µg/kg bw/week can be considered the most recent PTWI for organic mercury officially recognised in New Zealand. This is the equivalent of 0.23 µg/kg bw/day. This value is considered protective of developing foetuses, the most sensitive sub-group in the population.
For inorganic mercury, Vannoort and Thomson (2005) adopted the PTWI for total mercury of 5 µg/kg bw/week set by JEFCA in 1972. This is the equivalent of 0.71 µg/kg bw/day. More recently, a study carried out for MfE to support the derivation of contaminated land soil guidelines (Cavanagh, in prep), which has been reviewed by toxicologists from MoH, ERMA New Zealand and NZFSA, has recommended an oral intake for inorganic mercury of 2 µg/kg bw/day.
Chronic inhalation exposure has been assessed by the US EPA. The US EPA’s recommended inhalation reference concentration (RfC), based on occupational studies, is 0.3 µg/m3 (US EPA, 1995). The US ATSDR has developed a chronic minimum risk level (MRL) for inhalation of elemental mercury of 0.2 µg/m3. The WHO ambient air quality air quality guideline for mercury is 1 µg/m3 (annual average) (WHO, 2000).