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    MONOGRAPH FOR UKPID




    MERCURY




    ST Kolev
    N Bates

    National Poisons Information Service (London Centre)
    Medical Toxicology Unit
    Guy's & St Thomas' Hospital Trust
    Avonley Road
    London
    SE14 5ER
    UK


    This monograph has been produced by staff of a National Poisons
    Information Service Centre in the United Kingdom.  The work was
    commissioned and funded by the UK Departments of Health, and was
    designed as a source of detailed information for use by poisons
    information centres.

    Peer review group: Directors of the UK National Poisons Information
    Service.


    1.  SUBSTANCE/PRODUCT NAME

    1.1  Origin of the substance

    Naturally occurring. Mercury occurs in the Earth's crust, mainly in
    the form of sulphides. The red sulphide, cinnabar, is the main
    component of the mercury ores. It may contain up to 70% mercury.
    Mercury is also released into the environment by human activities e.g.
    combustion of fossil fuels, waste disposal and industrial activities.
    Organic mercury compounds released into the environment are often
    broken down to elemental mercury or mercuric compounds (Berlin, 1986).

    1.2  Name

    Elemental mercury. Inorganic mercury compounds.

    1.2.1  Main brand names/main trade names

    1.2.2  Generic name

    Mercury (Hg).
    Inorganic mercury compounds include: mercuric chloride (HgCl2),
    mercurous chloride (Hg2Cl2), mercuric iodide red (HgI2), mercuric
    oxide red, yellow (HgO), mercuric sulphide black, red (HgS), mercuric
    nitrate (Hg(NO3)2, mercuric cyanide (Hg(CN)2)

    1.2.3  Synonyms

     Metallic mercury: hydrargyrum, hydrargyrum depuratum, mercure
    (French), mercurio (Spanish, Italian), quecksilber (German),
    quicksilver.

     Synonyms of some inorganic mercuric compounds are:
     Mercuric chloride (HgCl2): corrosive sublimate, mercury
    bichloride, quecksilber chlorid (German), Sublimat (Czech), mercuric
    bichloride, mercuric dichloride, mercury bichloride, mercury
    dichloride, mercury (II) chloride, bichlorure de mercure (French),
    bichloride of mercury, chloride rtutnaty (Czech), chlorure di
    mercurique (French), cloruro di mercurio (Italian), cloruro mercurio
    (Spanish), dichloromercury, mercury perchloride.
     Mercurous chloride (Hg2Cl2): calomel, calomelanos, mild mercurous
    chloride, mercury monochloride, mercury protochloride, mercury
    subchloride, white precipitate.
     Mercuric iodide, red: mercury biniodide.
     Mercuric oxide red, yellow (HgO): red precipitate, yellow
    precipitate.
     Mercuric sulphide black, red (HgS): chinese red, cinnabar,
    vermilion.

    1.2.4  Common names/street names

    Quicksilver.

    1.3  Chemical group/family

    Elemental mercury. Inorganic mercury compounds

    1.4  Substance identifier and/or classification by use

    1.5  Reference numbers

    Metallic mercury              CAS       7439-97-6
                                  RTECS     OV 4550000
                                  EINECS    2311067
                                  NCI       C60399
                                  UN        2809

    Mercuric chloride (HgCl2)     CAS       7487-94-7
                                  RTECS     OV 9100000
                                  UN        1624
                                  EINECS    2312998
                                  NCI       C60173

    Mercurous chloride (HgCl2)    CAS       7546-30-7
                                  RTECS     OV 8750000
                                  EINECS    2314309

    Mercuric iodide red (HgI2)    CAS       7774-29-0
                                  RTECS     OW 5250000
                                  UN        1638
                                  EINECS    2318738

    Mercuric oxide yellow (HgO)   CAS       21908-53-2
                                  RTECS     OW 875000
                                  UN        1641
                                  EINECS    2446547

    Mercuric sulphide red (HgS)   CAS       1344-48-5
                                  RTECS
                                  EINECS    2156963

    1.6  Supplier/importer/agent/ licence holder

    Mercury and mercury compounds importers as listed in the UK importers
    database (UKIM) are:
    Seasafe Marine Clothing Ltd.
    Tomita UK Ltd.
    Alarmexpress Ltd
    Philips Components Ltd Durham c/o Philips Impex Ltd
    Hughes Microelectronics Europe Ltd
    Sharp Manufacturing Company UK

    1.7  Presentation

    Some mercuric compounds used in laboratories are listed.

    Mercuric iodide, red
    Form crystalline
    Mercurous mercury as Hg < 0.1%, Soluble mercury salts < 0.05 as Hg.
    Pack sizes available: 25, 100 and 500 g.

    Mercuric chloride
    Form crystalline
    Pack sizes available: 25, 100, 500 g and 1 kg.

    Mercuric nitrate
    Standardised solution 0.010 milliequivalents per ml
    Pack sizes available: 100 ml.

    1.8  Physico-chemical properties

    Molecular weight

    Mercury                       Hg = 200.59
    Mercuric chloride             HgCl2 = 271.5
    Mercurous chloride            Hg2Cl2 = 236.0
    Mercuric iodide red           HgI2 = 454.4
    Mercuric oxide red            HgO = 216.6
    Mercuric sulphide red         HgS = 232.7

    Physical state

    Metallic mercury: shiny, silvery white very mobile liquid, easily
    divisible into globules, which readily volatiles on heating.

    Mercuric chloride: crystals, powder of granules.
    Mercurous chloride: powder.
    Mercuric iodide, red: powder. 
    Mercuric oxide, red: crystalline powder of scales.
    Mercuric oxide, yellow: powder.
    Mercuric sulphide, red: powder, lumps, hexagonal crystals.

    Colour

    Metallic mercury: shiny, silvery white very mobile liquid.
    Mercuric chloride: white.
    Mercurous chloride: white.
    Mercuric iodide, red: red.
    Mercuric oxide, red: bright red or orange red.
    Mercuric oxide, yellow: yellow or orange yellow.
    Mercuric sulphide, red: bright red.

    Odour

    Odourless.

    Solubility in water and organic solvents

    Solubility in lipids in the order of 5-50 mg/L. Solubility in water
    approximately 60 mg Hg/L at 24C. Solubility of the inorganic mercury
    salts is influenced by valence state and anionic component (Goyer,
    1980). Mercuric salts like halides, sulphates and nitrates are water
    soluble, sulphide and oxides are not (Berlin, 1986).

    Metallic mercury: 20-30g/L in water, soluble in nitric acid, insoluble
    in dilute hydrochloric acid, hydrogen bromide, hydrogen iodide and
    cold sulphuric acid.
    Mercuric chloride: 69g/L in water, 476g/L in boiling water, soluble in
    ethanol, benzene, ether, glycerol, acetic acid, methanol, acetone,
    ethyl acetate, slightly soluble in carbon disulphide and pyridine.
    Mercurous chloride: 2 x 10-3 g/L in water, insoluble in alcohol and
    ether.
    Mercuric iodide, red: 0.06g/L, soluble in alcohol, ether, acetone,
    ethyl acetate, carbon disulphide, alkali iodides and chloroform.
    Mercuric oxide, red yellow: practically insoluble in water, soluble in
    dilute hydrochloric acid and nitric acid, alkali cyanides or iodides,
    slowly in solutions of alkali bromides, insoluble in alcohol.
    Mercuric sulphide, red: practically insoluble in water.

    Autoignition temperature

    Not relevant.

    Boiling point

    Metallic mercury:        356.6C
    Mercuric chloride:       302C
    Mercurous chloride:      NA
    Mercuric iodide, red:    about 300C, sublimes
    Mercuric oxide, red:     NA
    Mercuric oxide, yellow:  NA
    Mercuric sulphide, red:  NA

    Density

    Metallic mercury:        13.59 g/cm2
    Mercuric chloride:       5.4 g/cm2
    Mercurous chloride:      7.15 g/cm2
    Mercuric iodide, red:    6.28 g/cm2
    Mercuric oxide, red:     11.14 g/cm2

    Vapour pressure

    Metallic mercury 2 x 10-3 mm at 25C.

    Relative vapour density

    Metallic mercury volatile. A saturated atmosphere of mercuric vapour
    contains approximately 18 mg Hg/m3 at 24C.

    Reactivity

     Metallic mercury: reacts with ammonia, amines, acetylene and oxalic
    acids to form compounds that are sensitive to mechanical shock. Reacts
    with many metals except iron to form amalgams.
     Mercuric chloride: incompatible with formates, sulphites,
    hypophosphites, phosphates, sulphides, albumin, gelatin, alkalies,
    alkaloid salts, ammonia, antimony and arsenic, bromides, borax,
    carbonates, iron, copper, lead, silver salts.
     Mercurous chloride: incompatible with bromides, iodides, alkali
    chlorides, sulphates, sulphites, hydroxides, ammonia, cocaine,
    cyanides, copper salts, hydrogen peroxides, iodine, lead salts, silver
    salts and sulphides.
     Mercuric oxide, yellow: incompatible with reducing agents.

    Many mercury compounds decompose in light and should therefore be
    stored in the dark.

    1.9  Hazard/risk classification

    1.10  Uses

    Approximately 25% of the annual production of mercury is consumed by
    the chloralkali industry, 20% is used in electrical equipment, 15% in
    paints, 10% in measurement and control systems such as thermometers
    and sphygmomanometers, 5% in agriculture, 3% in dentistry (dental
    amalgam), and 2% in laboratories. The remaining 20% includes military
    uses such as detonators, mercury containing catalysts, preservatives
    in the paper-pulp industry, pharmaceuticals, in photography as an
    intensifying agent and others (Korringa and Hagel, 1974).

    Mercury was replaced as a preservative in emulsion paint in the UK by
    substances such as ammonia and subsequently organic based
    preservatives, over a period of years from the mid-fifties to the late
    seventies.

    Inorganic mercury compounds have been used in medicine for centuries,
    but their use has been greatly reduced because of their toxicity.
    Mercuric chloride was used as a laxative and applied topically as an
    antibacterial agent. It was also used in the treatment of syphilis
    before the advent of antibiotics. Mercury compounds have been used as
    an irrigation solutions in the management of carcinoma. Mercurials
    have also been used as spermicides. Mercurius solubilis (Merc. Sol.) a
    nitrated oxide of mercury is used in homoeopathic medicine.

    Mercury compounds (particularly mercuric iodide) have been used in
    skin lightening creams and soaps. Such products are banned but may be
    found in imported products or those intended for sale overseas.

    1.11  Toxicokinetics

    1.11.1  Absorption

     Oral: Metallic mercury is poorly absorbed after ingestion at a rate
    related to the vaporisation (0.01%) and it is generally thought to be
    of no toxicological consequence (Goyer, 1980), unless there is
    significant delay in passage through the gastrointestinal tract or the
    patient is exposed chronically. Inorganic soluble mercuric compound
    are readily absorbed into the circulation e.g. mercurous chloride (up
    to 10%) (WHO, 1991). A considerable proportion can remain fixed to the
    intestinal mucosa and intestinal contents. Insoluble compounds undergo
    oxidation to soluble absorbable compounds (Winship, 1985). Some
    compounds which are particularly insoluble are poorly absorbed e.g.
    cinnabar. However, chronic low dose exposure to these compounds may
    lead to mercury intoxication (Kang-Yum and Oransky, 1992).

     Inhalation: Mercury vapour is efficiently absorbed from the alveolar
    air (about 80%) (WHO, 1991) due to the rapid diffusion of the vapour
    through the alveolar membrane.

     Dermal: Elemental mercury may be readily absorbed if applied to the
    skin in suitable form. When applied as ointment, up to 31% of the
    amount applied was excreted (Oehme, 1972). In animal studies up to 8%
    of mercuric chloride applied to the skin was absorbed within 5 hours
    (Berlin, 1986).

     Vaginal: Mercury compounds presented in vaginal jellies are easily
    absorbed and retained in the body (Oehme, 1972).

    1.11.2  Distribution

    Absorbed mercury passes into the circulation where about half of it is
    bound to albumin in the plasma (in combination with sulphydryl
    groups), the other half enters red blood cells. It is then rapidly
    distributed to the tissues and within a few hours the highest
    concentration is found in the kidneys. The liver, blood, spleen,
    respiratory mucosa, small and large intestine, skin, salivary glands,
    heart, skeletal muscle, brain and lungs contain decreasing amounts.
    Mercury is stored in the bone, bone marrow and liver for a short time.
    A special affinity for absorbed mercury in the frontal and basal
    cerebral regions of the brain has been noted. A week after exposure
    85-95% of all mercury in the body is stored in the kidney. With
    continued absorption the concentration in the kidney increases.
    Further absorption results in higher levels in other organs without
    affecting renal levels (Winship, 1985).

    Since organic mercury is concentrated in the erythrocytes and
    inorganic is not, the ratio of the amount in the red blood cells and
    plasma will indicate whether the patient has been exposed to organic
    or inorganic mercury.

    Mercury vapour crosses cell membranes much more rapidly than divalent
    compounds, a significant amount of the vapour reaches the brain before
    it is oxidised. Exposure to mercury vapour results in concentrations
    in the brain which are 10 times higher than those following an
    equivalent dose of inorganic mercuric salts (Winship, 1985).

    The concentration of mercury in hair is about 300 times that in the
    blood, and the most recent growth of hair reflects past blood mercury
    levels.

    All forms of mercury cross the placenta to the foetus. Foetal uptake
    of elemental mercury in rats has been shown to be 10-40 times higher
    than uptake after exposure to inorganic compounds probably because of
    lipid solubility of mercury vapour (Goyer, 1980).

    1.11.3  Biological half-life

    Biological half-life for inorganic mercury is about 40 days. For
    elemental mercury or mercury vapour the biological half-life is linear
    with a range of values from 35 to 90 days. The biological half-life is
    different for different organs. A fraction of the absorbed mercury
    will remain in the body for a longer time (e.g. years in the brain)
    (WHO, 1991).

    1.11.4  Metabolism

    Metallic mercury is oxidised to divalent mercury after absorption to
    tissues and this is probably mediated by catalases. Inhaled mercury
    vapour absorbed into red blood cells is transformed to divalent
    mercury. However a proportion is also transformed as metallic mercury
    to more distal tissues, particularly to the brain where
    biotransformation may occur.

    1.11.5  Elimination

    Mercury is excreted mainly in the urine but considerable amounts are
    also passed in the faeces through secretion by the gastrointestinal
    tract, particularly in the colon, bile and saliva, gastric and
    intestinal fluid. Mercuric mercury is also excreted by sweat,
    lachrimal and mammary glands (Berlin, 1986). Excretion begins soon
    after absorption and continues rapidly, with the tissue concentration
    falling at different rates. The best mathematical model seems to be a
    multicompartment model with at least two or more excretion rates and
    with one small compartment including the brain. Most of the mercury is
    excreted within a week but low levels may be found in the urine and
    faeces for months. Small amounts may be retained in the brain for a
    long period. Renal tissue tends to retain mercury, one week after
    exposure 60-70% of mercury is still present. 60-70% of the mercury is
    excreted as a sulphydryl mercury compound. The kinetics of clearance
    from the body have shown three distinct phases. In the first, 35% of
    the absorbed mercury with the half-time 3-4 days, accumulated in the
    liver and was excreted into the faeces and transported into the 

    kidneys. In the second phase, 50% of the dose had a half-time of 30
    days and was excreted in the urine following renal accumulation. The
    remaining 15%, with a half time of 100 days, was accounted for by
    renal excretion.

    1.11.6  Special populations

    No data available.

    2.  SUMMARY

    3.  EPIDEMIOLOGY OF POISONING

    Occupational

    Human exposure to inorganic mercury is mainly occupational, most
    commonly associated with mercury vapour. It is often related to
    specific working conditions e.g. mining, spillage of mercury compounds
    on work clothes or in the working environment, handling of mercury
    salts in the chemical industry and laboratories (Berlin, 1986; Bluhm
    et al, 1992; Wide, 1986).

    Accidental

    Illicit gold extraction using mercury has also resulted in mercury
    poisoning in adults and children (Shamley and Sack, 1989; Moromisato
    et al, 1994). The mercury is mixed with quartz and gold, an amalgam is
    formed with the gold and this is then heated until the mercury
    evaporates off. Elevated levels of mercury were reported in 8 students
    following exposure to mercury vapour during an experiment. Fourteen
    others and the teacher had mercury levels below the normal
    concentration (Anon, 1988).

    There are several cases in the literature of mercury poisoning from
    spillage of metallic mercury in the home and inappropriate cleaning up
    of the chemical, particularly using a vacuum cleaner (Schwartz et al,
    1992; McNeil et al, 1984; Muhlendahl, 1990; Bonhomme et al, 1996).
    Mercury poisoning has also occurred from ingestion of a button battery
    containing mercury (Mant et al, 1987). Toxicity has been reported
    following exposure to mercury vapour from a broken mercury expansion
    switch in a heating unit of an infant incubator (McLaughlin et al,
    1980).

    Medicinal and cosmetic use

    Toxicity and deaths have occurred from the medicinal use of inorganic
    mercury compounds (Rajagopal and Hamilton,1984; Laundy et al, 1984).
    Poisoning has been reported following the use of mercury-containing
    skin lightening creams and soaps (Lauwerys et al, 1987; Dept of
    Pharmacology-Drug and Toxicology Information Service, 1990). Poisoning
    has also been reported following the use of traditional remedies (Kew
    et al, 1993; Perharic et al, 1994; Kang-Yum and Oransky, 1992).

    There are rare reports of mercury poisoning following aspiration of
    metallic mercury (Zimmerman, 1969). In some case only mild symptoms
    have developed (Wallach, 1972; Janus and Klein, 1982; Tsuji et al,
    1970).

    Intentional

    Metallic and inorganic salts of mercury have also been used as a means
    of suicide (Winship, 1985), including deliberate intravenous,
    intra-arterial injection (Vale and Proudfoot, 1995) and subcutaneous
    injection (Hill, 1967).

    Dental amalgam

    Dental amalgam and the risk to human health has been the subject of
    several reviews (Goering et al, 1992; Fung and Molvar, 1992; Enwonwu,
    1987; Mjor, 1994; Halbach, 1994; Aposhian et al, 1992). As well as
    mercury poisoning, dental amalgam has been claimed to cause multiple
    sclerosis, leukaemia, rheumatoid arthritis and numerous other
    disorders.

    Dental amalgam contains about 50% mercury with silver, copper, zinc
    and some other metals in small quantities. It has been used in
    dentistry for over 150 years. Amalgam is manufactured to be inert and
    biological inactive, but it is known that mercury vapour is given off
    with chewing and brushing of teeth. This vapour is then inhaled and
    swallowed. Uptake of mercury from dental amalgam has been demonstrated
    in sheep (Boyd et al, 1991) and monkeys (Hahn et al, 1990). In man
    postmortem studies have shown a higher concentration of mercury in the
    brain and kidney of subjects with amalgam fillings than in those
    without.

    One of the most important points raised by these reviews is that the
    effect of chronic low dose mercury exposure on man is not known. The
    currently available evidence suggests that when reasonable precautions
    are used dental amalgam is not a significant health hazard to dental
    workers or patients. There is however a need for more research.

    Table 1 gives the daily mercury retention in the general population
    (WHO, 1991). This includes organic mercury but it is clear that dental
    amalgam is the primary source of mercury in the general population.

    Table 1.

                                                  
    Exposure source         g Hg/day absorbed
                                                  
    Dental amalgam          3.0-17.0
    Fish or seafood         2.34
    Other food              0.25
    Water                   0.0035
    Air                     0.001
                                                  

    Daily mercury retention in the general population (WHO, 1991)

    4.  MECHANISM OF ACTION/TOXICITY

    4.1  Mechanism

    Mercury compounds are highly potent but non-specific cellular poisons,
    that influence many vital processes involving proteins. Mercury ions
    are protein precipitants and as a result cause severe necrosis on
    direct contact with tissue. They have affinity for a number of
    cellular components essential for the function and survival of the
    cell such as enzymes, membrane proteins, nucleic acids and mitotic
    apparatus. Mercury interacts with sulphydryl groups and disulphide
    bonds of the membrane, as a result of which specific membrane
    transport is blocked and selective permeability of the membrane
    altered. Mercuric compounds are also immunotoxic and some have been
    shown to be strong sensitisers (Winship, 1985).

    Table 2 outlines the differential characteristics of inorganic and
    elemental exposure (from Young-Jin, 1994).

    Table 2

                                                                        
                                  Elemental mercury   Inorganic mercury
                                                                        
    Primary route of exposure     Inhalation          Oral, dermal
    Primary tissue distribution   CNS, kidney         Kidney
    Clearance                     Renal, GI           Renal, GI
    Clinical effects                                  
     CNS                          Tremor              Tremor, erethism
     Pulmonary                    +++                 -
     Gastrointestinal             +                   +++ (corrosive)
     Renal                        +                   +++
     Acrodynia                    +                   ++
                                                                        

    Differential characteristics of inorganic and elemental mercury
    exposure (from Young-Jin, 1994)

    4.2  Toxic dose

    Ingestion of 0.5 g mercuric chloride usually results in serious
    illness but rarely proves fatal. Doses of 1 g cause death in about 50%
    of cases and more than 1.5 g in nearly all cases. The prognosis has
    improved since the introduction of chelating agents (Bidstrup, 1964).
    Toxic effects are usually evident within 10-15 minutes of ingestion
    (Reynolds, 1983). Troen et al (1951) reported 18 cases of human
    poisoning after oral ingestion of a single dose of mercuric chloride,
    nine of which resulted in death. The lethal doses ranged from 29 mg/kg
    body weight to at least 50 mg/kg body weight. The most common autopsy
    findings in these cases were gastrointestinal lesions (ranging from
    mild gastritis to severe necrotic ulceration of the mucosa) and renal
    lesions that had resulted in renal failure.

    Clinical features of mercury poisoning did not occur following
    ingestion of 204g (15ml) of metallic mercury and all the mercury was
    passed in the faeces within 3 days (Wright et al, 1980). An adult who
    ingested about 3kg (220ml) of metallic mercury had elevated blood and
    urine levels of mercury but he developed only mild effects; six months
    later he returned with mild jaundice and impaired LFTs. In this case
    the mercury was cleared from the gut within 10 days (Lin and Lim,
    1993).

    Acute mercury intoxication has been described after using 1/500 to
    1/1000 solutions of mercuric chloride for peritoneal lavage (Laundy et
    al, 1984).

    A 17-year old woman developed acute mercury intoxication with renal
    failure after inserting 1 g mercuric chloride tablet into her vagina
    in order to induce abortion (Page et al, 1983).

    Micromercuralism has been reported after long term exposure to mercury
    concentration in the air of 0.05 mg/m3 (Berlin, 1986).

    5.  FEATURES OF POISONING

    5.1  Acute poisoning

    5.1.1  Ingestion

    Critical organs are the kidney and the intestinal tract.

    The corrosive effect of concentrated mercury salt solutions on the
    mucous membranes of the gastrointestinal tract causes extensive
    precipitation of proteins. Gastric pain and vomiting may ensue. As the
    compound passes to the lower regions of the gut, general abdominal
    pain and bloody diarrhoea with necrosis of the intestinal mucosae may
    occur. This may lead to circulatory collapse and death. If the patient
    survives the gastrointestinal tract damage renal failure due to
    necrosis of the proximal tubular epithelium occurs within 24 hours.
    Apart from the corrosive damage there may be also be local vasospasm
    due to activation of the angiotensin system (Berlin, 1986).

    5.1.2  Inhalation

    Inhalation of mercury vapour is the most important route of uptake for
    elemental mercury. The lung is the critical organ upon accidental
    exposure to high concentrations of mercury vapour. Mercury vapour
    causes erosive bronchitis and bronchiolitis with interstitial
    pneumonitis. Victims usually develop respiratory insufficiency. These
    symptoms may be combined with signs caused by effects on the CNS, such
    as tremor or increased excitability. Workers acutely exposed (4-8 h)
    due to an accident exhibited chest pain, dyspnoea, cough, haemoptysis,
    and evidence of interstitial pneumonitis. The calculated elemental
    mercury concentration was 1.1 to 44 mg/m3 (WHO, 1991).

    5.1.3  Skin exposure

    The soluble inorganic compounds of mercury are irritating to the skin
    and mucous membranes; this effect is particularly marked with mercuric
    chloride. Concentrations of 1-5% cause irritation, vesiculation and
    corrosion of the skin. Dilute solutions may produce irritation of
    sensitive skin. The water insoluble mercury compounds do not cause
    immediate skin reactions, but this may develop slowly as the compound
    is absorbed and the mercury ionised in the tissues.

    Mercurous salts are less corrosive than mercuric compounds.

    5.1.4  Eye contact

    Mercurous and mercuric salts are corrosive to the eyes (Atterbury and
    Olson, 1990), the latter more so.

    5.1.5  Parenteral exposure

    A 21 year old female injected metallic mercury subcutaneously into
    both thighs. Her blood concentration of mercury was elevated but she
    did not develop features of mercury poisoning (Hill, 1967).

    Acute mercury intoxication has been described after using 1/500 to
    1/1000 solutions of mercuric chloride for peritoneal lavage (Laundy et
    al, 1984).

    5.1.6  Other

    No data.

    5.2  Chronic poisoning

    5.2.1  Ingestion

    Cases of chronic poisoning with calomel (mercurous chloride) have been
    described. Signs and symptoms similar to those of poisoning with mixed
    exposure to mercury vapour and mercuric mercury were described. With
    chronic exposure to inorganic mercury the kidney is the critical
    organ. Symptoms such as increased salivation and inflammatory changes
    in the gums and black lines on the teeth, due to precipitation of
    mercuric sulphide can also appear. Two type of renal damage can occur:
    1) a glomerular injury caused by the toxic effect of mercury on the
    cells of the basal membrane of the glomeruli. An autoimmune reaction
    is induced due to formation of antigen against the glomerular tissue,
    and a nephrotic syndrome develops with proteinuria and the classical
    signs of glomerulonephritis.
    2) the other type of renal injury is tubular damage. Mercury
    accumulation causes necrosis and damage of the distal and middle
    portion of the proximal tubuli (Berlin, 1986).

    5.2.2  Inhalation

    Chronic inhalation of mercury vapour the major effects are on the
    central nervous system. Early signs are not specific and have been
    termed asthenic-vegetative syndrome or micromercuralism, with symptoms
    such as weakness, fatigue, forgetfulness, anorexia, loss of weight,
    and disturbance of gastrointestinal tract function. At higher exposure
    levels, the characteristic mercurial tremor appears as a fine
    trembling of the muscles, interrupted by coarse shaking movements
    every few minutes. This begins peripherally in the fingers, eyelids,
    and lips and has the characteristics of intentional tremor. In
    progressive cases it may develop into generalised tremor involving the
    entire body, with intermittent violent chronic spasms of the
    extremities. This is often accompanied by changes in personality and
    behaviour, with loss of memory, increased excitability (erethism)
    severe depression, and even delirium and hallucinations. Another
    characteristic feature of mercury vapour intoxication is severe
    salivation and gingivitis (Goyer, 1980). Sporadic instances of
    proteinuria and even nephrotic syndrome may occur.

    EEG changes together with changes in visually evoke response in
    chronically exposed workers have been reported. ALA D hydratase
    activity in blood cells decreases and the cholinesterase activity in
    plasma markedly decreases with the increasing mercury excretion in
    urine. An increased frequency of aneuploidy in lymphocytes from
    workers exposed to mercury vapour has been described. Symptoms of
    poisoning may regress and disappear when exposure has ceased. However,
    in severe cases with long term exposure, persistent sequelae related
    to the nervous system are common. A long term exposure to mercury
    concentration in the air of 0.1 mg/m3 or higher, the probability of
    developing mercuralism increase.

    Exposure to metallic mercury may rarely produce sensitation, for
    example from amalgam teeth fillings.

    5.2.3  Skin exposure

    Typical manifestations are erythema and contact dermatitis. Ammoniated
    mercury is a common cause. Mercury compounds give rise to a type IV
    cell-mediated delayed hypersensitivity reaction. There have been a few
    cases of allergic dermatitis among dental personnel (WHO, 1991).

    An idiosyncratic hypersensitivity reaction has been described,
    particularly in children. This syndrome called acrodynia or pink
    disease, is characterised by a generalised body rash. Other symptoms
    are: chills, swelling and irritation of the hands, feet, cheeks and
    nose, usually followed by desquamation, loss of hair and ulceration,
    hyperplasia and hyperkeratosis, irritability, sleeplessness, and
    profuse perspiration which may lead to dehydration. The perspiration
    is accompanied by dilated and enlarged sweat glands and desquamation
    of the sole and palms. Once mercury exposure ceases, the signs
    gradually disappear. Patients with acrodynia usually have increased
    levels of mercury in the urine (> 50 mg/L) (Berlin, 1986).

    In certain circumstances skin absorption may be responsible for the
    occurrence of systemic chronic toxicity. When applied as ointment, up
    to 31% of the amount applied was excreted (Oehme, 1972). In animal
    studies up to 8% of the mercuric chloride applied to the skin was
    absorbed within 5 hours (Berlin, 1986).

    5.2.4  Eye contact

    Mercurialentis is the name given to an unusual appearance of the
    anterior surface of the lens seen in people exposed to mercury. The
    change in the lens consists of greyish or light-to-coffee brown
    granular discoloration, detected by slit-lamp examination. The change
    is bilateral and symmetrical, and the visual activity is unaffected.
    It has been seen in people who have had prolonged exposure. It was
    suggested that mercury is absorbed through the cornea circulates in
    the aqueous humour, and precipitates on the anterior surface of the
    lens. Mercurialentis is a manifestation of exposure but not necessary
    of toxic absorption (Winship, 1985).

    5.2.5  Other

    Subcutaneous injection of metallic mercury resulted in the development
    of tender fluctuant abscess with surrounding erythema. Between 0.5 and
    1 ml mercury was recovered in each side of injection. No symptoms or
    signs of mercury poisoning developed. However, the blood and urine
    mercury concentration were within the range encountered in chronic
    mercury poisoning (Hill, 1967).

    5.3  Systematic description of clinical effects

    5.3.1  Cardiovascular

     Acute:
    Tachycardia with dull heart sounds and a gallop rhythm have been
    reported secondary to severe pneumonitis after acute exposure to
    mercury vapour (Berlin, 1986).

     Chronic:
    EEG changes have been recorded in chronically exposed workers (Berlin,
    1986).

    5.3.2  Respiratory

     Acute:
    The lung is the critical organ in acute accidental exposure to high
    concentrations of mercury vapour. Mercury vapour causes erosive
    bronchitis and bronchiolitis with interstitial pneumonitis. Chest
    pain, dyspnoea, cough, haemoptysis, and evidence of interstitial
    pneumonitis have been reported (WHO, 1991), atelectasis, emphysema,
    haemorrhage and pneumothorax often follow (Winship, 1985). The cause
    of death is progressive respiratory failure. The mortality rate is
    higher in children than adults (Moutinho et al, 1981; Moromisato et
    al, 1994).

    Aspiration of metallic mercury may result in severe pulmonary toxicity
    or death (Zimmerman, 1969). In some case only mild symptoms have
    developed (Wallach, 1972; Janus and Klein, 1982; Tsuji et al, 1970).

    5.3.3  Neurological

     Chronic:
    Most information focuses on effects on the CNS following occupational
    exposure. Characteristic signs are tremor, motor disturbances and
    mental deterioration. The most common psychiatric signs and symptoms
    are depression, irritability, and exaggerated response to stimulation,
    with excessive shyness, loss of confidence, vague fears, insomnia,
    emotional instability, forgetfulness and confusion. In advanced cases
    there may be loss of memory, hallucinations or intellectual
    deterioration, suicidal melancholia, or even manic-depressive
    psychoses. Tremors are common, a fine static tremor of the fingers,
    eyelids, lips and tongue develops and may progress to the arms and
    legs. The tremor may cause deterioration of the handwriting and the
    ability to perform other manipulative tasks. Intention tremor have
    also been reported. Slurred speech may developed.

    Four out of nine workers exposed to mercury vapour had clinical signs
    suggesting involvement of the peripheral nervous system in addition to
    the features of chronic poisoning. Electromyographic changes
    consistent with denervation were demonstrated in eight. Sensory
    effects are uncommon with poisoning by inorganic salts. However,
    constriction of visual fields, difficulties in counting objects at a
    low illumination and poor depth and colour perception have been
    reported in a patient with chronic mercury poisoning.

    5.3.4  Gastrointestinal

     Acute:
    The gastrointestinal system is usually affected after acute exposure
    to inorganic mercury compounds (e.g. mercuric chloride). One of the
    earliest symptoms is metallic taste, followed by thirst, severe
    abdominal pain, vomiting and diarrhoea. The toxic effects are usually
    evident within 10-15 minutes of ingestion (Reynolds, 1983). Ashen
    discoloration of the mouth and pharynx are seen. Stomatitis develops
    in about 24 hours. Colitis with prolonged haemorrhagic diarrhoea may
    also occur.

     Chronic:
    Excessive salivation with loosening of the teeth is a sign of advanced
    poisoning, as is a blue line along the gum margin (Winship, 1985).

    5.3.5  Hepatic

     Chronic:
    Disturbed liver function with raised serum alkaline phosphatase have
    been reported in 6 out of 70 patients following chronic use of
    ammoniated mercury ointment (Klaassen, 1980).

    5.3.6.1  Renal

     Acute:
    Renal failure due to necrosis of the proximal tubular epithelium
    typically occurs within 24 hours after acute exposure to inorganic
    mercury compounds. Apart from the corrosive damage there may also be a
    local vasospasm due to activation of the angiotensin system (Berlin,
    1986).

     Chronic:
    With chronic exposure to inorganic mercury the kidney is the critical
    organ. Symptoms such as increased salivation and inflammatory changes
    in the gums and black lines on the teeth, due to precipitation of
    mercuric sulphide can also appear. Two type of renal damage can occur:
    1) a glomerular injury caused by the toxic effect of mercury on the
    cells of the basal membrane of the glomeruli. An autoimmune reaction
    is induced due to formation of antigen against the glomerular tissue,
    and a nephrotic syndrome develops with proteinuria and the classical
    signs of glomerulonephritis.
    2) tubular damage may also occur. Mercury accumulation causes necrosis
    and damage of the distal and middle portion of the proximal tubuli
    (Berlin, 1986).

    WHO (1976) states that effects of elemental mercury on the kidney had
    been reported only at doses higher than those associated with the
    onset of the CNS toxicity sign and symptoms. Since then several new
    studies have been carried out, and kidney effects have been seen at
    lower exposure levels (WHO, 1991).

    5.3.7  Endocrine and reproductive systems

    Enlargement of the thyroid gland has been reported but the incidence
    in relation to exposure to mercury is uncertain (Winship, 1985).

    5.3.8  Dermatological

    The soluble inorganic compounds of mercury are irritating to the skin
    and mucous membranes; this effect is particularly marked with mercuric
    chloride. Concentrations of 1 to 5% cause irritation, vesication, and
    corrosion of the skin and mucous membranes, and much more diluted
    solutions may produce irritation to sensitive skin. Typical
    manifestations are erythema and contact dermatitis. Ammoniated mercury
    is commonly implicated (WHO, 1991).

    5.3.9  Eye, nose, throat: local effects

     Acute:
    Mercurous and mercuric salts are corrosive to the eyes (Atterbury and
    Olson, 1990), the latter are more corrosive. Concentrations of 1 to 5%
    cause irritation, vesication, and corrosion of the skin and mucous
    membranes, and much more diluted solutions may produce irritation.

     Chronic:
    Mercurialentis is the name given to an unusual appearance of the
    anterior surface of the lens seen in people exposed to mercury. The
    change in the lens consists of greyish or light-to-coffee brown
    granular discoloration, detected by slit-lamp. The change is bilateral
    and symmetrical, and the visual activity is unaffected. It has been
    seen in people who have had prolonged exposure. It has been suggested
    that mercury is absorbed through the cornea circulates in the aqueous
    humor, and precipitates on the anterior surface of the lens.
    Mercurialentis is a manifestation of exposure but not necessary of
    toxic absorption (Winship, 1985).

    5.3.10  Haematological

     Chronic:
    Anaemia may follow chronic exposure to inorganic and metallic mercury.
    Leucopenia, eosinophilia and thrombocytopenia have been reported
    rarely. Aplastic anaemia and death from bone marrow suppression have
    also been described (Winship, 1985).

    5.3.11  Immunological

    Experimental studies on animals have shown that inorganic mercury may
    induce auto-immune glomerulonephritis in all species tested but not in
    all strains, indicating a genetic predisposition (WHO, 1991).

    5.3.12  Metabolic

     Acute:
    Metabolic, acid base and fluid and electrolyte disturbances may
    developed secondary to severe vomiting and diarrhoea, or to acute
    renal failure after acute poisoning with inorganic mercury salts.

    5.3.12.3  Others

    No data.

    5.3.13  Allergic reactions

    Erythema and contact dermatitis may occur. Ammoniated mercury is
    commonly implicated. Mercury compounds give rise to a type IV
    cell-mediated delayed hypersensitivity reaction. There have been a few
    cases of allergic dermatitis among dental personnel (WHO, 1991).

    Allergic reactions have been reported with dental amalgam. Symptoms
    may occur within hours to several days after placement of amalgam
    restorations. Symptoms may be limited to areas of contact or be
    generalised, including eczema, urticaria and wheals on the face. Other
    symptoms reported include dryness and soreness of the throat and
    mouth, fever, hives, swelling of lips, tongue and mucosa. Most effects
    are self-limiting and resolve within 2 weeks (Fung and Molvar, 1992).

    5.13.14  Other

    An idiosyncratic hypersensitivity reaction has been described,
    particularly in children. This syndrome called acrodynia or pinks
    disease, is characterised by generalised erythematous body rash. Other
    symptoms are chills, swelling and irritation of the hands, feet,
    cheeks and nose, usually followed by desquamation, loss of hair and
    ulceration, hyperplasia and hyperkeratosis, irritability,
    sleeplessness and profuse perspiration which may lead to dehydration.
    The perspiration is accompanied by dilated and enlarged sweat glands
    and desquamation of the sole and palms. Once mercury exposure ceases,
    the signs gradually disappear. Patients with acrodynia usually have
    increased levels of mercury in the urine (> 50 mg/L) (Berlin, 1986).

    5.4  At risk groups

    5.4.1  Elderly

    No special risk as human exposures are mainly occupational.

    5.4.2  Pregnancy

    Sikorski et al (1987) reports a high frequency of foetal malformations
    among the children of dental staff. Of 117 pregnancies in the mercury
    exposed group, 28 pregnancies in 19 women led to spontaneous abortion
    (19 cases) and stillbirth (3 cases) and congenital malformations (5
    cases of spina bifida and one case of intra-atrial defect). In non
    exposed controls, there were 7 cases of adverse pregnancy outcome in
    five women out of a total 63 pregnancies (30 women). Another study
    investigated the Swedish National registers for birth records. There
    was no tendency towards an elevated rate of malformations, abortions
    or stillbirth among dentists dental nurses and dental technicians.
    On balance it would seem likely that there is risk of teratogenicity
    or foetal toxicity following maternal exposure to mercury vapour or
    inorganic salts.

    5.4.3  Children

    Acute mercury vapour inhalation is reported to have a higher mortality
    rate in children than in adults (Moutinho et al, 1981; Moromisato et
    al, 1994).

    In addition to the features of acute and chronic poisoning recorded in
    adults, an idiosyncratic reaction has been described in children. This
    syndrome called acrodynia or pink disease, is characterised by general
    body rash. Other symptoms are chills, swelling and irritation of the
    hands, feet, cheeks and nose, usually followed by desquamation, loss
    of hair and ulceration, hyperplasia and hyperkeratosis, irritability,
    sleeplessness, and perfuse perspiration which may lead to dehydration.
    The perspiration is accompanied by dilated and enlarged sweat glands
    and desquamation of the sole and palms. Once mercury exposure ceases,
    the signs gradually disappear. Patients with acrodynia usually have
    increased levels of mercury in the urine (> 50 mg/L) (Berlin, 1986).

    Renal tubular acidosis has been described in children. This disorder
    was caused by exposure to mercuric salts from application of an
    ointment containing ammoniated mercury. (Berlin, 1986).

    5.4.4  Enzyme deficiencies

    No data available.

    5.4.5  Enzyme induced

    No data available.

    5.4.6  Occupations

    Exposure to mercury vapour occurs in a variety of industries: in
    mercury mining, levels as high as 5mg/m3 have been reported (Berlin,
    1986), chloralkali factories range 10-50mg/m3, (WHO, 1991)
    instrument manufacturing, physics and medical laboratories, some
    exposure may also occur in dental surgeries.

    Common operations in which exposure to inorganic mercury may occur are
    as follows:
    1) During use as a liquid cathode in electrolytic production of
    chlorine and caustic soda from brine.
    2) During manufacture of inorganic and organic compounds for use as
    pesticides, antiseptics, germicides. Also miscellaneous applications
    as chemical intermediate.
    3) Preparation of amalgams in dentistry, in chemistry processing and
    jewellery manufacture.
    4) Manufacturing of mildew-proof paints and marine anti-fouling
    agents.
    5) Manufacturing of batteries, lamps (fluorescent and mercury), power
    tubes, tungsten-molybdenum wire and rods.
    6) Manufacturing of inorganic salts for use as catalysts in the
    production of urethanes, vinyl chloride monomers and other chemicals.
    7) Manufacturing of instruments (e.g. thermometers, barometers with
    mercury as a working fluid).
    8) Manufacturing of explosives and fireworks.
    9) During use as a conductor during construction and maintenance of
    military and nuclear power systems, in mercury-stem boilers, and in
    air rectifiers.
    10) During use and manufacturing of compounds for the pulp and paper
    industry as a control for biological growths.
    11) During roasting and smelting operations, extraction of silver and
    gold, mining and subsequent refining of ore containing cinnabar
    (Aronow, 1990).

    5.4.7  Others

    No data available.

    6  MANAGEMENT

    6.1  Decontamination

    Inhalation

    Immediately remove victim from exposure and give oxygen if available.

    After spill of metallic mercury, carefully clean up all liquid and
    discard contaminated carpeting or porous tile, or arrange for
    professional toxic cleanup with self contained vacuum system.  Do 
     not vacuum with home vacuum cleaner; this may disperse liquid
    mercury, increasing its airborne concentration.

    Ingestion of liquid mercury

    Because liquid mercury usually passes through the gastrointestinal
    tract system without being absorbed gut decontamination is not
    required. Following a very large intentional ingestion, particularly
    in a patient with multiple blind loops of bowel or intestinal
    perforation, there is a risk of chronic intoxication. Whole gut
    lavage, or even surgical removal may be necessary depending on X-ray
    evidence of large pockets of mercury.

    Ingestion of inorganic mercuric salts

    Perform gastric lavage. Do not induce emesis because of risk of
    serious corrosive injury. Whole bowel irrigation may be considered.

    Arrange for endoscopic examination if corrosive injury is suspected.

    6.2  Supportive care

    Inhalation of mercury vapour

    Give supplemental oxygen and observe closely for several hours for
    development of acute pneumonitis and pulmonary oedema.

    Ingestion of mercuric salts

    Anticipate severe gastroenteritis and treat shock aggressively with IV
    fluid replacement. Treat renal failure supportively; it is usually
    reversible, but haemodialysis may be required for 1-2 weeks.

    Allergic reactions to dental amalgam

    Allergic reactions from dental amalgams usually respond to
    antihistmines. In patients unresponsive to antihistamine therapy
    removal of the fillings is recommended.

    6.3  Monitoring

    With acute mercury vapour inhalation symptoms of pneumonitis may be
    delayed for several hours; a chest X-ray and arterial blood gases may
    show early signs of toxicity.

    Monitor electrolytes, fluid balance and renal function. Obtain blood
    and urine mercury levels. Collection of 24 hour urine mercury is
    useful in determining body burden.

    6.4  Antidotes

     Chelation therapy should not be started until the gut has been 
     emptied of mercury or it may enhance mercury absorption. 

    For serious systemic intoxication DMPS (dimercaptopropanesulphonic
    acid) is the treatment of choice. It should be given IV in seriously
    ill patients and orally in those with less severe effects or in those
    with chronic mercury toxicity.

    Dosage - adults:
     Parenteral - slow injection over 3-5 minutes
    Day 1: 250mg IV every 3-4 hours,
    Day 2: 250mg every 4-6 hours,
    Day 3: 250mg every IV/IM every 6-8 hours,
    Day 4: 250mg every IV/IM every 8-12 hours.
    Following days: according to patient's clinical condition 250-750mg
    parenterally or change to oral medication.

    Children:
     Parenteral - slow injection over 3-5 minutes
    Day 1: 5mg/kg 6 times daily,
    Day 2: 5mg/kg 6 times daily,
    Day 3, 4, etc: 5mg/kg 1-3 times daily.

     Oral - acute poisoning
    Adults: 1.2-2.4g daily in divided doses (e.g. 12 times 100-200mg/24
    hours).
    Children: 5mg/kg daily in divided doses.

     Oral - chronic poisoning
    Adults: 300-400mg/day in divided doses. The dose can be increased in
    severe poisoning.
    Children: 5mg/kg daily in divided doses.

    DMSA (succimer, 2-3 dimercaptosuccinic acid) has been used
    successfully as an oral chelating agent in a limited number of
    patients with mercury poisoning (Bluhm et al, 1992; Fournier et al,
    1988; Graziano, 1986) and could be used in patients sensitive to DMPS.

    Dosage: Orally 30 mg/kg body weight daily for 5 days, then 20 mg/kg
    for 14 days.

    Dimercaprol (BAL) is another alternative. Dosage: 3-5 mg/kg IM every
    4-6 hours for several days. Decisions on tapering the dose or ending
    the administration will depend on blood and 24-hour urine mercury
    concentration. After initial course of BAL, a oral chelating agent may
    be used. BAL injections are said to be painful.

    Penicillamine has also been used. Dosage: 100 mg/kg 24 hr (up to 1 g)
    in 4 divided doses. If treatment is to continue longer, the dose
    should be reduces to 35 mg/kg/24 hr. Animal experiments and some
    clinical experience indicate that N-acetyl-D, L-penicillamine (NAP) is
    more specific chelating agent for mercury. There is little human
    experience to support this finding.

    6.5  Elimination techniques

    There is no role for dialysis, haemoperfusion, or repeat dose
    activated charcoal in mercury poisoning. However, dialysis may be
    required for supportive treatment of renal failure, and it may
    slightly enhance removal of the mercury-chelator complex in patients
    with renal failure. Haemodialysis clearance of the mercury-BAL complex
    is about 5 mL/minute (Atterbury and Olson, 1990).

    6.6  Management controversies

    The use of dimercaprol (BAL) has been questioned in recent years with
    the advent of the less toxic hydrophilic BAL analogues DMSA and DMPS.
    Enhanced brain deposition may result from BAL treatment due to
    lipophilicity of the metal complex formed with dimercaprol. This has
    been described with inorganic arsenic and mercury. Experimental models
    using oral administration of mercuric mercury in mice showed that DMPS
    was superior to the other chelators in preventing mortality. Both DMSA
    and DMPS were superior to dimercaprol and NAP in alleviating acute
    toxicity, especially in the brain. Another study compared the
    potential to mobilise mercury and the incidence of drug induced
    toxicity of two chelating agents, DMSA and NAP (N-acetyl-D,
    L-penicillamine), after acute exposure to metallic mercury in man.
    DMSA was able to increase the excretion of mercury to a greater extent
    than NAP. In animal studies, DMSA was also shown to have greater
    activity than NAP in mobilising mercury from a toxic site (Houeto et
    al, 1994)

    A number of reports have indicated that in the treatment of acute
    mercury poisoning by dialysis little mercury is removed even with
    prior use of dimercaprol, except in the first few hours after
    exposure, therefore dialysis has usually been employed only in cases
    with renal failure. Other records, however, indicate then when
    potentially toxic doses have been taken, haemodialysis concurrent with
    dimercaprol administration may remove 10 to 15% of the ingested
    mercury and, even more importantly, relieve the kidneys and treat any
    uraemia caused by reversible kidney damage. Limited experience
    suggests an advantage of starting dialysis within the first 24 hr
    before maximal renal concentration can occur on the second day. This 

    also may assist in controlling fluid and electrolyte imbalance as
    circulatory collapse accentuates the toxic tubular lesions (Aronow,
    1990).

    7  CASE DATA

    Case 1: Intentional ingestion - mercury salts

    A 17-year-old woman with psychological problems leading to four
    previous drug overdoses deliberately ingested a mouthful of mixed
    chemicals which she obtained as pure crystals from the laboratory
    where she worked. They were thought to comprise aniline hydrochloride
    and salts of barium, cadmium, lead, mercury, selenium and thallium in
    unknown proportions. She presented 7 hours later with vomiting and
    corrosive oral damage. Her face was flushed but there were no other
    abnormalities. She was treated with BAL and calcium disodium edetate,
    but became anuric within 16 hours. Her blood pressure remained normal.
    Haemodialysis was started at 24 hours in an attempt to remove chelated
    heavy metal. The results of the analysis taken during the first day of
    admission were available after 4 days and showed an extremely high
    mercury concentration in whole blood (1200 mg/L) measured by the cold
    vapour atomic absorption method. No other heavy metal was found at a
    concentration above normal. Calcium disodium edetate was therefore
    withdrawn, and BAL and dialysis was continued. The dose of BAL used
    was 100 mg IM 4 hourly during the first day, followed by 75 mg twice
    daily for the next 24 days. The patient then declined to accept the
    drug for 10 days, after which she was given 75 mg daily for a further
    3 days. A renal biopsy showed severe tubular necrosis. She remained
    virtually anuric for 31 days and received a total of 180 hours
    dialysis during this period. Her renal function improved and the
    plasma mercury fell, dialysis became unnecessary, when the level had
    reached a concentration of approximately 100 mg/L. There were no other
    manifestations of mercury poisoning except for a mild normochromic
    anaemia and a transient elevation of her serum transaminase
    concentrations. Three months later her creatinine clearance was 56
    ml/min (Newton et al, 1983).

    Case 2 and 3: Acute occupational inhalation - mercury vapour

    Two men, aged 35 and 50 years old weighing 75 and 108 kg, were exposed
    to mercury at work. They were jewellers and accidentally inhaled smoke
    containing mercury vapour produced during the melting of a gold block.
    The patients were exposed to the vapour for about half an hour. They
    presented with moderate headache, spreading pain, nausea, lumbar pain,
    gingival pain and shortness of breath at rest. The EEGs were
    characterised by slow alpha activity. The ECGs were normal. No CNS,
    EEG or nerve conduction velocity changes nor urological and
    cardiovascular symptoms were found. The patients had no evidence of
    any chronic respiratory disorder and arterial blood gas analysis was
    normal. Chelation therapy was given for 10 days. BAL was given
    initially (50 mg in the first injection, then 3 mg/kg 4 hourly for 2 

    days and then 3 mg/kg 6 hourly for 2 days). This was followed with
    oral DMSA (30 mg/kg), due to the painful nature of the intramuscular
    injections of BAL. Samples of plasma and urine were taken from the
    patients every 24 hour over a period of 10 days. The maximum plasma
    concentrations in the first sample were 239.5 mg/L and 93.3 mg/L in
    patient 1 and 2 respectively. They remained at a plateau of about 50
    mg/L (patient 1) and 25 mg/L (patient 2). The serum creatinine and
    urea remained normal. In spite of the fact that high concentrations of
    mercury persisted in the plasma, no further symptoms were observed at
    any time in either patient during the 10 days BAL and DMSA were given.
    Observations were not made after the 10 day period (Houeto et al,
    1994).

    Case 4: Chronic accidental inhalation - mercury vapour

    A 33 month old girl was admitted for anorexia, weight loss, light
    sensitivity and eczema, starting 4 months previously. She had
    widespread severely itching eczema and pink, sweating and scaling
    palms. She was ill-tempered and preferred to lie in bed or to be taken
    around in a small buggy. Acrodynia was suspected, and raised mercury
    concentrations was found in the urine. After 2 weeks of chelation
    therapy with DMPS (30 mg twice daily) the child's eczema and mood
    began to improve. After 4 months of therapy all symptoms had
    disappeared and mercury excretion was normal. Subsequently it was
    discovered that the mercury poisoning in this child was caused by
    mercury from a broken thermometer spilled on the carpet (Muhlendahl,
    1990).

    Case 5: Accidental ingestion - mercuric chloride

    A 23 month old boy ingested an unknown quantity of mercuric chloride
    powder (a skin preparation) that he found on the lower shelf of a
    chemist's shop. Vomiting was induced (method not stated) and within 5
    minutes his tongue and lips were seen to be swollen. On admission
    within an hour of ingestion the oedema and ulceration were so
    extensive that there was a risk of compromising the airway. However, a
    tracheostomy was not thought necessary. He was treated with
    dimercaprol 6mg/kg IM every 6 hours for 48 hours then half that dose
    for a further 48 hours. He was also given antibiotic cover and
    hydrocortisone. On admission the urea was 8.7mmol/L and creatinine
    43mol/L. The blood mercury level on admission was 4.5 mg/L (urine
    30.4 mg/L). This had decreased to 0.95 mg/L (urine 8.5 mg/L) by the
    next day, 0.69 mg/L (urine 0.4 mg/L) on day 5 and 0.30 mg/L (urine
    0.24 mg/L) by day 8. He suffered only mild renal impairment, this may
    have been due to prompt treatment. By day 8 he was able to swallow
    soft food without difficulty. He made a full recovery but the blood
    mercury level only returned to normal after more than 100 days (Stack
    et al, 1983).

    Case 6: Chronic dermal absorption - acrodynia

    A baby boy (2.15kg) developed nappy rash at the age of two weeks. The
    rash did not improve with cream prescribed by the family doctor and
    the mother began using Conotrane (hygraragaphen 0.05%). The baby
    became fretful and refused feeds. He began to vomit and his stools
    became watery. There was considerable erythema of the whole body with
    irritability, photophobia and watering of the eyes. Once it was
    discovered that the cream contained a mercury compound it was realised
    that he was suffering from acrodynia (pink disease). The urine mercury
    concentration was 120 g/ml (Rajagopal and Hamilton, 1984).

    Case 7: Chronic accidental inhalation - mercury vapour

    A three year old boy was admitted to hospital with weight loss (2kg in
    2 months) and acrodynia. A few days before admission he began to
    experience difficulty in walking. High mercury levels were found in
    the blood and urine. His parents and older and younger sisters all had
    elevated mercury levels. His two year old sister had been admitted to
    hospital 2 months earlier with a nephrotic syndrome of unknown cause.
    The only symptom in his 6 year sister was aesthenia. His parents were
    asymptomatic. According to the parents no mercury containing objects
    had been broken in the house. An ozone analyser was used to determine
    the source of the mercury. There was widespread contamination, with
    the highest concentration in hose of the vacuum cleaner and in the
    carpet of the children's room. Very high levels were found in the dust
    of the vacuum cleaner (3020 and 5984 g/g of dust). Dust in the garage
    at ground level and the children's room at air level were 40 g/g and
    4.24 g/m3 respectively. Extensive decontamination of the house was
    undertaken and 4 months later the mercury levels were decreased. All
    the family had at least one course of chelation therapy with DMSA and
    the clinical signs disappeared (Bonhomme et al, 1996).

    Case 8: Fatal accidental aspiration - metallic mercury

    A 48 year old man was admitted to hospital for reevaluation and
    treatment of Hodgkin's disease. Radiation therapy was begun on the
    retroperitoneal area and was well tolerated. However, during the sixth
    week of therapy he became unwell with nausea, vomiting, diarrhoea,
    fever, cramping and abdominal pain and abdominal distension. X-ray
    examination revealed distended, small bowel loops with multiple
    air-fluid levels. A Miller-Abbott tube was passed into the proximal
    ileum and 10ml of metallic mercury was placed in the bag. He began to
    improve over the following 4 days. The tube was then removed but the
    mercury bag ruptured while in the nasopharynx. The patient immediately
    began to cough and expectorated about 4ml of mercury. X-ray
    examination revealed considerable amounts of mercury in the stomach,
    duodenum and throughout the trachea, major bronchi and over both lung
    fields. An additional 5ml of mercury was removed by postural drainage,
    chest tapping and forced coughing. A repeat X-ray 3.5 hours later
    showed an increased amount of mercury in the left lung and a more
    diffuse alveolar spread in the right lung. The patient remained well 

    for 12 hours, but then became pyrexial and irritable. By the next day
    he was incontinent of urine and faeces with weakness and abdominal
    pain. A mild cough produced small amounts of mercury-containing
    sputum. There was no mercury excretion in the 24 hour urine specimen.
    During the following 48 hours his temperature rose, he became confused
    and continued to complain of weakness and abdominal pain. A repeat
    urinary mercury determination was negative. He developed leucocytosis
    and albuminuria. Dimercaprol was started 72 hours after aspiration
    occurred. Four days after aspiration his symptoms persisted and he
    developed hypotension which responded to volume expansion. He
    developed an increasingly severe cough which produced bloody sputum.
    This was eventually produced in such large amounts that the airway
    could not be kept clear. He became tachypnoeic, cyanotic and comatose,
    and died 110 hours after aspiration of the mercury. During this time
    only 8.2ml of the mercury had been recovered. Permission for a
    postmortem was denied (Zimmerman, 1969).

    Case 9: Intentional ingestion - metallic mercury

    A 17 year male ingested approximately 205g (15ml) of metallic mercury
    and presented to hospital about 2 hours later. He was well on
    admission and a gastric lavage was performed. All investigations were
    normal. An X-ray 4 hours after ingestion showed mercury in the stomach
    and small intestine. By three weeks all the mercury had been passed in
    the faeces. He remained well and serial urine mercury levels were
    normal (all less than 15 g) (Wright et al, 1980).

    Case 10: Chronic inhalation exposure plus acute intentional
    ingestion - metallic mercury

    A 42 year old man presented to hospital after ingesting approximately
    3kg (220ml) of metallic mercury. He had worked since the age of 13
    repairing thermometers, barometers, sphygomanometers and related
    instruments. In the last 2 years he had developed mild hand tremor,
    forgetfulness, fatigue and irritability. He was given a gastric lavage
    and cathartics. He complained of abdominal discomfort. An X-ray
    revealed mercury in the stomach and small intestine. By 2 weeks most
    of the mercury had passed in the faeces. An ophthalmological
    examination was normal. Neuropsychiatric and psychological evaluation
    revealed poor concentration and a defect in recent memory. An EEG
    showed diffuse cortical dysfunction. He was treated with penicillamine
    for 7 days. Blood and urine mercury levels 3 days after chelation
    therapy were 116.9 g/L and 22.9 g/L. Six months after ingestion he
    returned to hospital with mild jaundice and impaired liver function
    which resolved over the next 6 months (Lin and Lam, 1993).

    Case 11: Acute ingestion - button battery

    A two year old girl arrived in hospital within two hours of ingestion
    of a button battery containing mercury. The battery was visible on
    X-ray in the upper stomach. An X-ray the following day was unchanged
    but on the second day the battery was observed to be in two halves 

    surrounded by radiopaque material. More radiopaque material was
    visible in the small bowel. The child remained asymptomatic. A
    gastrotomy was performed to remove the mercury salts from the stomach,
    areas of ulceration and bleeding were observed. The two halves of the
    battery casing were removed via an enterotomy from 60 cm beyond the
    pylorus. A blood mercury concentration at this time was 95 L (normal
    <4 g/L) and the urine mercury concentration 60 g/L (normal <20
    g/L). Two days later the blood concentration was 230 g/L and the
    urine 100 g/L. Dimercaprol by IM injection was used as a chelating
    agent. Six days post-operatively the blood mercury concentration was
    340 g/L (urine 600 g/L). At this time she had been vomiting
    intermittently but this became more persistent at nine days and an
    abdominal X-ray revealed small bowel obstruction. Radiopaque material
    was visible in the caecal region. A laparoptomy was performed and the
    obstruction was found to be due to adherence of the proximal jejunum
    to the abdominal wall. Multiple small ulcers were seen in the caecum.
    One week after the second operation no mercury was seen on X-ray and
    the blood mercury concentration was 25 g/L. She was discharged and
    six weeks later the blood mercury concentration was down to 7 g/L
    (Mant et al, 1987).

    Case 12: Acute fatal inhalation in a child- mercury vapour

    A 7 month old girl, her 3.5 year old brother and her father were
    admitted to hospital with a 12 history of fever, vomiting and
    dyspnoea. The family's six month old kitten had died the previous
    evening. Postmortem examination of the cat revealed diffuse pleural
    effusions and pneumonitis. The father and brother recovered over a 2-3
    day period but the girl became increasingly dyspnoeic and was
    transferred to another hospital. On admission coarse breathing sound
    were heard bilaterally and heart sound were dull with a gallop rhythm.
    On the evening of the onset of effects the patient's father had been
    heating a metal thought to be lead on the kitchen stove. The kitten,
    brother and sister were all playing in the kitchen at the time. Black
    fumes were produced and the windows were opened. Analysis of the
    melted metal revealed it to be an amalgam of mercury and tin with
    smaller amounts of lead and zinc. The child was started in oxygen
    therapy but over the following three days the oxygen requirement was
    gradually increased. She had persistent metabolic acidosis and the
    pulmonary interstitial marking became more prominent. Blood mercury on
    the fourth day after exposure was 35 g/L. Urine mercury excretion on
    the same day was 400 g/24 hours, on the 5th day 130 g/24 hours and
    on the 6th day 230 g/24 hours. She was given methylprednisolone,
    sodium bicarbonate and penicillamine. On the 7th hospital day she
    developed increasing dynspnoea leading to apnoea. A chest X-ray
    revealed bilateral pneumonthorax with complete collapse of the right
    upper and left lower lobe. Despite adequate reexpansion, severe
    acidosis, coma and convulsions occurred and she died six hours later.
    At postmortem abnormalities were almost exclusively confined to the
    lungs. The mercury level in the brain was 2.9 g/L, lung 5.2 g/L,
    liver 5.1 g/L and kidney 12.2 g/L. In the family cat the level of
    mercury in the lung was 18 g/L and in the kidney 12 g/L (Moutinho et
    al, 1981).

    8  ANALYSIS

    8.1  Agent/toxin/metabolite

    Mercury can be measured in blood and urine. For inorganic and
    elemental mercury urine mercury determination is preferred.

    8.2  Sample containers to be used

    Blood (10ml) in hard plastic or glass container with anticoagulant
    (heparin or EDTA).
    Urine (20ml) for random sample use sterile universal, for 24 hour
    sample collect in acid washed (nitric acid) hard plastic bottle.

    8.3  Optimum storage conditions

    8.4  Transport of samples

    8.5  Interpretation of data

    Normal levels: Blood <10g/L (<50nmol/L)
                   Urine <20g/L (<100nmol/L)

    Toxic levels:  Blood >35g/L (>175nmol/L)
                   Urine >150g/L (>750nmol/L)

    8.6  Conversion factors

    Metallic mercury 1 mg3 = 0.12ppm
    1g/L = 4.985nmol/L

    8.7  Other recommendations

    9  OTHER TOXICOLOGICAL DATA

    9.1  Carcinogenicity

    Inorganic mercury is generally not considered to be carcinogenic in
    humans (WHO, 1991). However, some data have suggested possible
    carcinogenicity of mercury in some occupationally exposed groups.

    9.2  Genotoxicity

    WHO (1976) did not report any studies showing that inorganic mercury
    was genotoxic in humans. However, some data have since been reported
    suggesting possible genotoxic effects of inorganic mercury.

    9.3  Mutagenicity

    DNA synthesis in animals exposed to mercury leads to the accumulation
    of the metal in the cell nuclei. The affinity of mercury for nuclear
    material was found to be considerable, binding largely to the
    chromatin. Mercuric chloride has been shown to cause depression of 

    mouse leukaemic cells (Nakazawa et al, 1975). Reduction of DNA
    replication in Chinese hamster ovary cells has also been observed.
    Treatment of mice with mercuric chloride  in vivo did not demonstrate
    an increased frequency of chromosomal aberrations in bone marrow cells
    or in spermatogonia (Poma et al, 1981). It seems likely that mercury
    poses a risk of mutagencity in heavily exposed individuals.

    9.4  Reprotoxicity

    Six out of nine male workers accidentally exposed to mercury vapour
    (concentration 44.3 mg/m3 for less than 8 hours) developed acute
    mercury poisoning. During a follow up lasting several years they
    showed signs of chronic poisoning. A loss of libido which persisted
    for at least several years, was reported in all six cases. In a study
    carried out at a US Department of Energy plant that used very large
    quantities of metallic mercury, reproductive outcomes were studied
    among 247 male workers exposed to mercury vapour. No association was
    demonstrated between mercury exposure and decreased fertility,
    increased rates of major malformations of the offspring, or serious
    childhood diseases (WHO, 1991).

    There have been reports of menstrual disturbances in women exposed
    industrially or in dentistry to mercury vapour. A number of reports
    suggested that inorganic mercury compounds cause spontaneous abortion.
    During a 4 year period 17% of 168 exposed workers in a mercury ore
    smelting plant had experienced spontaneous abortion (average exposure
    80 mg mercury/m3), compared with 5% among 178 controls. Toxaemia
    during pregnancy was reported in 35% of the exposed and 2% of the
    unexposed workers. On the other hand, De Rosis et al (1985), revealed
    no difference in the age standardised rate of spontaneous abortions
    between mercury exposed and unexposed females. Two other studies on
    female dental staff also reported no increased abortion rate when
    compared with age standardised controls.

    9.5  Teratogenicity

    Studies on animals revealed that after brief exposure to elemental
    mercury vapour the mercury easily penetrates the placentar barrier
    (Greenwood et al, 1972). After equal exposure of pregnant rats, the
    foetal uptake was 10-40 times higher after exposure to mercury vapour
    than to mercury salts. In contrast, the placentar content of mercury
    after exposure to elemental mercury was only 40% of that after
    injected inorganic salts. The teratogenic effects of inorganic mercury
    has been investigated in the rat: increased resorption and abnormality
    rates were found, the malformations consisted of limbs and eye
    defects. Embryological, teratogenic and foetotoxic effects have also
    been demonstrated in the hamster; resorption rates were increased and
    growth retardation was seen in surviving foetuses. Malformations
    included: exencephaly, encephalocoele, anophthalmia, cleft lip and
    palate, rib fusions and syndactyly (Gale et al, 1982).

    Sikorski et al (1987) revealed a high frequency of malformations among
    dental staff. Of 117 pregnancies in the mercury exposed group, 28
    pregnancies in 19 women led to reproductive failure, with spontaneous
    abortion (19 cases) and stillbirth (3 cases) and congenital
    malformations (5 cases of spina bifida and one case of intra-atrial
    defect). In non exposed controls, there were 7 cases of adverse
    pregnancy outcome in five women out of a total 63 pregnancies (30
    women). Another study investigated the Swedish National registers for
    birth records. There was no tendency towards an elevated rate of
    malformations, abortions or stillbirth among dentists dental nurses
    and dental technicians.

    On balance it would seem likely that there is risk of teratogenicity
    or foetal toxicity following maternal exposure to mercury vapour or
    inorganic salts.

    9.6  Acceptable daily intake (ADI)

    The Food and Agriculture Organisation WHO Expert Committee allocated a
    provisional tolerable weekly intake for adults of 0.3 mg/person or
    0.005 mg/kg.

    9.7  AOEL

    In the UK the occupational exposure standards of mercury and mercury
    compounds (except mercury alkyls) are 0.05 mg (as Hg) per m3 long
    term and 0.15 mg (as Hg) per m3 short term.

    In the USA the permissible and recommended exposure limits for
    inorganic mercury are 0.1 mg/m3 (maximum long term) and 0.05 mg/m3
    (long term).

    9.8  Relevant animal data

    Evidence of damage to brain, kidney, heart and lungs in rabbits
    exposed acutely to metallic mercury vapour at a concentration of 29
    mg/m3 have been reported. The LD50 for inorganic mercury lies
    between 10 and 40 mg/kg body weight for all compounds tested. For
    mercuric chloride, a value of about 10 mg/kg body weight has been
    observed after parenteral administration to mice. The features of
    acute toxicity usually consisted of shock, cardiovascular collapse,
    acute renal failure and severe gastrointestinal damage (WHO, 1991).

    WHO (1976) in evaluating a number of experimental studies on animals,
    concluded that both reversible and irreversible effects may be caused
    by mercury and its compounds. Microscopically detectable changes have
    been seen in the organs of dogs, rabbits and rats exposed to
    concentrations of mercury vapour ranging from about 100 to 30 000
    mg/m3 for different period of time. Severe damage was noted in
    kidneys and brains at mercury concentration of about 900 mg/m3 after
    an exposure period of about 12 weeks. After exposure of dogs to 100 mg
    mercury/m3 for 7 days, 5 days /week, over a period of 83 weeks, no
    microscopically detectable effects were seen, and tests revealed no 

    abnormalities in the kidney function. In two studies tremor and
    behavioural effects were observed in rabbits and rats after several
    weeks exposure to mercury vapour at levels of several mg/m3,
    although there were no morphological changes in the brain.

    During the last 10-20 years, great attention has been paid to effects
    of inorganic mercury on the immune system. A number of studies have
    been evaluated and it is concluded that depending on the animal strain
    tested, either auto-immunity or immunosupression may be observed (WHO,
    1991).

    Selenium has been found to affect the distribution of mercuric mercury
    in many animal species. As a consequence of this redistribution
    decreased toxicity has also been observed. Mercury forms a
    mercury-selenium protein complex with selenium. This complex can be
    identified in plasma and blood cells. Given together with selenium,
    mercury is retained longer in the blood, and as a consequence lessens
    accumulation in the kidney. The mercury taken up by the kidney is
    bound to the protein-selenium complex, binding to metallothionein is
    diminished or negligible on administration of equivalent amounts of
    selenium. Studies of selenium interaction with mercury have mainly
    been done on animals. Selenium metabolism in man is different from
    that in most animals. Observations in workers exposed to mercury
    vapour indicate, however, that there is a remarkable relationship
    between selenium concentrations and mercury concentrations in organs
    such as brain, thyroid and pituitary. Transport of mercury over the
    placental membranes is also inhibited (Berlin, 1986).

    9.9  Relevant  in vitro data

    Mercuric chloride has been shown to cause depression of mouse
    leukaemic cells (Nakazawa et al, 1975). Reduction of DNA replication
    in Chinese hamster ovary cells has also been established. Treatment of
    mice with mercuric chloride  in vivo did not demonstrate an increased
    frequency of chromosomal aberrations in bone marrow cells or in the
    spermatogonia (Poma et al, 1981).

    10.  ENVIRONMENTAL DATA

    10.1  Ecotoxicological data

    Solubility in water

    Elemental mercury: approximately 60 mg Hg/L at 24C.

    Volatilisation

    Metallic mercury is rather volatile. A saturated atmosphere of
    mercuric vapour contains approximately 18 mg Hg/m3 at 24C.

    LC50

    The 96 hour LC50 varies between 33 and 400 mg/L for freshwater fish
    and are higher for seawater fish.

    10.2  Behaviour

    Adsorption onto soil

    In an experimentally set-up, the pH and chloride concentration in
    soils was changed and the effect on the sorption of mercury
    determined. With no chloride there was only a small effect of pH
    between 4 and 6; sorption decreased at higher pH. Addition of chloride
    had minimal effect at higher pH and decreased sorption at low pH.
    Between pH 4 and 5.8, the effect of mercury sorption was entirely due
    to changes in the HgOH+ concentration in solution.

    Heavy metals were found in 2 to 5 fold higher concentrations near
    roadside soils than in soils some distance removed from the road. The
    typical roadside concentration of mercury was 0.12 mg/kg of soil
    (Poisindex, 1995).

    10.3  Biodegradation

    Environmental fate

    Mercury vapour is converted to soluble forms and deposited by rain
    into soil and water. The atmospheric residence time for mercury vapour
    is up to 3 years, where soluble forms have a residence time of only a
    few weeks. The change in specification of mercury from inorganic to
    methylated forms is the first step in the aquatic biotransformation
    process. This can occur non-enzymatically or through microbial action
    (WHO, 1991).

    Abiotic transformation

    The change in specification of mercury from inorganic to methylated
    forms is the first step in the aquatic biotransformation process.
    Experiments performed without the presence of any bacteria showed that
    transfer of methyl groups occurs non-enzymatically.

    Aerobic/anaerobic

    It has been shown that cell extracts of a strictly anaerobic
    methanogenic bacterium effectively converted inorganic mercury into
    methylmercury .

    Microbial

    About 37 consortia were isolated in the presence of mercury chloride.
    These strains retained between 82 and 90% of the total mercury
    influent in fixed bed experiments. The retention mechanism was the
    reduction in ionic mercury to metallic mercury (Poisindex, 1995).

    Half-life in water, soil and vegetation

    Water: The half-life of mercury can vary considerably, depending on
    whether biological and non-biological mechanisms are involved.
    Artificial decontamination of bottom sediments has cleaned up Minimata
    Bay and the nearby Yatsushiro Sea, to a large extend accelerating the
    natural process by an estimated 31.5 years. The natural
    decontamination of the Yatsushiro Sea is estimated to have a half-life
    of 9.5 years. The decontamination of the Ottawa River, where only
    natural processes were involved, was found to have a half-life of 1.5
    years.

    Vegetation: Low levels of uptake of inorganic mercury from the soil by
    plants have been reported.

    10.4  Environmentally important metabolites

    The change in specification of mercury from inorganic to methylated
    forms is the first step in the aquatic biotransformation process. This
    can occur non-enzymatically or through microbial action (WHO, 1991).

    10.5  Hazard warnings

     Aquatic life

    Fish take up metallic mercury and retain it in the tissues,
    principally as methylmercury, although most of the environmental
    mercury to which they are exposed is inorganic. The source of
    methylation is uncertain, but there is strong indication that
    bacterial action leads to methylation in aquatic systems. Elimination
    time is slow in fish (with half lives in the order of months or years)
    and from other aquatic organisms (WHO, 1991).

    10.5.1  Bees

    No data available.

    10.5.2  Birds

    Sea birds and those feeding in estuaries are most at risk of mercury
    poisoning. The form of retained mercury is variable and depends on the
    species, organ and geographical site.

    10.5.3  Mammals

    Bioaccumulation: An experimental study was carried out with six sheep
    which were given 4 mg inorganic mercury in their feed for 28 days. The
    results suggest that the long term ingestion of mercury leads to a
    chronic effect on the production of farm animals. High tissues
    concentrations of mercury have been found in a number of wild animals.

    10.5.4  Plants

    Barley was used to assess plant-availability, tissue concentration and
    genotoxicity of mercury from the solid waste deposited of a
    chloralkali plant. Roots were found to take up most of the mercury,
    bioconcentration in the straw was minimal and accumulation of mercury
    in the grain did not increase with increased mercury in the soil,
    indicating a restriction of transport function (Poisindex, 1995).

    10.5.6  Protected species

    Inorganic mercury is toxic to micro-organisms, aquatic life, insects,
    birds and mammals, therefore, a number of protected species would be
    at risk if exposed to toxic doses. High tissues concentrations of
    mercury have been found in a number of wild animals.

    AUTHORS

    ST Kolev
    N Bates

    National Poisons Information Service (London Centre)
    Medical Toxicology Unit
    Guy's & St Thomas' Hospital Trust
    Avonley Road
    London
    SE14 5ER
    UK

    This monograph was produced by the staff of the London Centre of the
    National Poisons Information Service in the United Kingdom. The work
    was commissioned and funded by the UK Departments of Health, and was
    designed as a source of detailed information for use by poisons
    information centres.

    Peer review was undertaken by the Directors of the UK National Poisons
    Information Service.

    March 1996

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