COLLOIDAL MERCURY

HYDRAGYRUM

HYDRARGYRUM

KWIK (Dutch)

LIQUID SILVER

MERCURE (French)

MERCURIO (Italian)

MERCURY

MERCURY, ELEMENTAL

MERCURY LIQUID

MERCURY METAL

MERCURY, METALLIC

MERCURY VAPOR

METALLIC MERCURY

QUECKSILBER (German)

QUICK SILVER

QUICKSILVER

RTEC (Polish)

QUECKSILBER

RTEC

7439-97-6(Mercury, elemental)

OV4550000

2809-Mercury

2809-Mercury metal

4944325 (mercury, metallic)

4923269 (mercury compound, solid)

IMO CLASSIFICATION:6.1 - Mercury compounds, liquid or solid, not otherwise specified

STANDARD INDUSTRIAL TRADE CLASSIFICATION NUMBER:52227

Hg

172-GALLIUM and MERCURY(for UN/NA Number2809)

Elemental mercury is used in:

REFERENCES: (Tae et al, 2015; (HSDB, 2002); (OHM/TADS, 2002); (ATSDR, 1999); Budavari, 2000; Harbison, 1998a; Lewis, 1998; IARC, 1997; ITI, 1995).

BULLETS - Bullets which have been illegally hollowed out and filled with mercury have been used for animal control in some rural areas (Villalobos & Snodgrass, 1991).

DENTAL AMALGAMS - The amalgam used in dental fillings contains approximately 50% metallic mercury ((ATSDR, 1999)). The World Health Organization estimated in 1991 that dental amalgams comprised 3 percent of the total use of mercury in industrialized countries (IARC, 1997).

INSTRUMENTS OR DEVICES - Elemental mercury is also used in electrical apparatus, thermometers, sphygmomanometers, barometers, Miller Abbott tubes, and other instruments or devices (Hathaway et al, 1991; Lewis, 1998).

PAINTS - Although mercury-containing interior latex paint has not been manufactured in the United States since 1990, and production of exterior mercury-containing paints was discontinued in 1991, these paints may still be available in some households. Mercury-containing paints, joint compounds, plasters, and adhesives manufactured in the US must have a warning label (US DHHS, 1992).

FOLK MEDICINE - In some Mexican-American communities, elemental mercury is used as a folk medicine to treat "empacho," a chronic stomach disorder ((ATSDR, 1999); Geffner & Sandler, 1980).

RELIGIOUS PRACTICES - Elemental mercury is sold under the name "azogue" for use in various religious, ethnic or ritualistic practices ((ATSDR, 1999)).

Elemental mercury is a silvery liquid that is heavy, mobile, non-wetting, slightly volatile and odorless (Bingham et al, 2001; Budavari, 2000; Lewis, 1998). In its solid state, mercury is a tin-white, ductile metal that is malleable enough to be cut with a knife (Budavari, 2000).

Near its boiling point of 356.9 degrees Celsius, mercury is slowly oxidized to mercuric oxide in the presence of oxygen (Bingham et al, 2001; Budavari, 2000).

Mercury is available in the following grades: commercial, instrument, redistilled, technical and triple distilled. Standard commercial grade contains 99.9 percent mercury ((HSDB, 2002)).

Alpha mercuric sulfide (i.e., red mercury, cinnabar, cinnabarite) is the primary ore from which mercury is extracted and processed (Harbison, 1998a; IARC, 1997). Mercury ore is also found in rocks of many varieties, including: limestone, calcareous shales, sandstone, serpentine, chert andesite, basalt and rhyolite ((HSDB, 2002)).

Mercury exists naturally in the earth's crust at 0.5 ppm (Budavari, 2000).

The primary source of atmospheric mercury is from degassing of mercury from soil and surface waters. Fossil fuel burning, the disposal of solid wastes which contain mercury, and the use of mercury containing fungicides, pesticides, paints and other products, also contribute to atmospheric mercury concentrations (Harbison, 1998a; US DHHS, 1992). It is also released into the atmosphere from volcanoes and hot springs (Harbison, 1998a; (HSDB, 2002)).

SOURCES OF EXPOSURE

INGESTION: Ingestion is generally nontoxic in an intact gastrointestinal tract, but mucosal breaks and prolonged contact may increase absorption. Symptoms may resemble inorganic mercury poisoning.

INHALATION: Adverse effects mainly result from vapor inhalation and primarily affect the lungs. Pulmonary pathology includes pneumonitis, necrotizing bronchiolitis, pulmonary edema, acute lung injury, and death. Central nervous system effects, renal damage, gingivitis, and stomatitis can also develop. Within a few hours of high concentration of mercury vapor exposure, weakness, chills, metallic taste, nausea, vomiting, diarrhea, abdominal pain, headache, tremor, visual disturbances, dyspnea, cough, and chest tightness may develop.

INTRAVENOUS OR INTRAMUSCULAR: IV injection may rarely result in pulmonary embolism, and IM injection may lead to renal dysfunction and chronic absorption; signs and symptoms are usually mild, but may be similar to inorganic mercury toxicity.

CHRONIC: Chronic mercury poisoning (mercurialism) usually results from inhalation of elemental mercury vapor or particles. Evidence of chronic poisoning may occur within weeks of an extreme acute exposure or may develop insidiously over many years. Chronic inhalation leads to the classic triad of neuropsychiatric disturbances (ie, personality changes, hallucinations, delirium, insomnia, irritability, fatigue, memory loss, erethism), tremor (fine intention tremor of fingers that progresses to choreiform movements of limbs), and gingivostomatitis. Children and some adults develop acrodynia associated with severe leg cramps, irritability, insomnia, diaphoresis, hypertension, miliarial rash, and peeling erythematous skin on the fingers, hands, and feet. Renal dysfunction has been reported.

Inhalation of vapors or contact with substance will result in contamination and potential harmful effects.

Fire will produce irritating, corrosive and/or toxic gases.

TOXICOLOGY: Mercury covalently binds the sulfur moiety in sulfhydryl groups throughout the body disrupting enzymes, membranes, structural proteins, and transport mechanisms. Toxicity develops as elemental mercury is oxidized to the mercurous (Hg+) and mercuric (Hg2+) forms that interact with these entities causing multiorgan dysfunction.

EPIDEMIOLOGY: Mercury thermometer exposures are not uncommon, but people rarely get sick. Other elemental mercury poisonings are uncommon, but deaths occur.

EXPOSURE

HYPERTENSION: Hypertension has been reported in children with intoxication from exposure to elemental mercury (eg, playing with metallic mercury found in barometers or sphygmomanometers that had broken) (Setz et al, 2008; Celebi et al, 2008; van der Linde et al, 2009). Mercury-induced hypertension increases levels of epinephrine and norepinephrine due to inhibition of catechol-O-methyltransferase. Therefore, first-line antihypertensive agents may not be effective (Koyun et al, 2004).

TACHYCARDIA: Tachycardia has been reported in children with intoxication from exposure to elemental mercury (eg, playing with metallic mercury found in barometers or sphygmomanometers that had broken) (Setz et al, 2008; Celebi et al, 2008; van der Linde et al, 2009).

EMBOLUS: Embolization has occurred following intravenous mercury injection (Kedziora & Duflou, 1995; Eyer et al, 2006; McFee & Caraccio, 2001), and in one case, a repeat CT scan 66 days later revealed right ventricular deposits after initial CT detection in the right ventricle and coronary artery (Eyer et al, 2006).

SKIN ABSORPTION: Liquid elemental mercury and mercury vapors can be absorbed through the skin to a limited degree. However, skin absorption of mercury is much less than absorption which may occur through the lungs (Hursh et al, 1989; US DHHS, 1992).

ERUPTION, ACUTE AND CHRONIC: Erythematous macular or papular rashes are common with mercury vapor poisoning. The rash usually involves the hands and feet. The trunk, axillae, popliteal and antecubital fossae may also be affected (Bluhm et al, 1992; Fuortes et al, 1995; Bartolo & Brandao, 1988). Rashes are common with chronic dermal exposure to elemental mercury (Pambor & Timmel, 1989).

CONTACT DERMATITIS: Allergic contact dermatitis following mercury handling has been reported (Goh & Ng, 1988; Kanerva et al, 1993; Faria & De Freitas, 1992), including a dermatitis with papular erythema following skin exposure to liquid mercury (US DHHS, 1992).

ACRODYNIA, SUBCHRONIC OR CHRONIC: Acrodynia (painful extremities) may rarely result following subchronic or chronic mercury poisoning. The syndrome is characterized by severe leg cramps, pink, painful, and peeling skin of the fingers, hands, feet, and nose (van der Linde et al, 2009; Celebi et al, 2008; US DHHS, 1992), and it occurs more commonly in children (US DHHS, 1992; Karagol et al, 1998).

ALOPECIA: Mild hair loss has been reported following peritoneal contamination from elemental mercury (Lu et al, 1998).

GRANULOMA, ACUTE AND CHRONIC: Granuloma formation with fibrosis and inflammation has developed after intravenous mercury injection (Schaumburg et al, 2009; Netscher et al, 1991).

NECROSIS: In 2 different instances, Injection site necrosis has followed subcutaneous administration of metallic mercury (Soo et al, 2003; Ramdial et al, 1999).

DIAPHORESIS, CHRONIC: Excessive sweating, particularly on the palms and soles of the feet, may occur (Gosselin et al, 1984; Yang et al, 1994).

HYPERTHYROIDISM: Two cases of hyperthyroidism associated with mercury vapor intoxication have been reported (Karpathios et al, 1991; McCann et al, 1991).

PHEOCHROMOCYTOMA: Signs and symptoms of pheochromocytoma (diaphoresis, tachycardia, hypertension, tremor, irritability, insomnia) have been reported in individuals exposed to mercury through various means (Henningsson et al, 1993; Beck et al, 2004; Kosan et al, 2001).

GASTROINTESTINAL DISTRESS: Nausea, vomiting, and diarrhea or constipation can occur after acute mercury vapor inhalation (Sevketoglu et al, 2011; Koyun et al, 2004; Bluhm et al, 1992).

ABDOMINAL PAIN: Abdominal pain and anorexia have also been reported following acute exposure (Florentine & Sanfilippo, 1991; Koyun et al, 2004; Anon, 2005).

LOSS OF APPETITE: Decreased appetite, vague complaints of abdominal distress and mild diarrhea are commonly reported with chronic mercury vapor exposure (Setz et al, 2008; van der Linde et al, 2009).

HEMORRHAGIC COLITIS: In one report, a 46-year-old man presented with symptoms of fever, sharp abdominal pain, bloody diarrhea, and tachycardia 5 days after exposure to mercury vapor during purification of gold from a mercury-containing ore in his home. An abdominal CT revealed diffuse colonic wall thickening and thumbprinting, especially in the ascending colon, consistent with colitis. Following supportive treatment, including dimercaprol therapy for 3 weeks, his symptoms improved gradually (Heise et al, 2009).

PROTEINURIA, ACUTE AND CHRONIC: Proteinuria has been reported after mercury vapor exposure (Snodgrass et al, 1981; Karagol et al, 1998; El-Safty et al, 2003).

RENAL TUBULAR DISORDER: Reversible renal tubular defects were found in 11 men acutely exposed to mercury vapor and in miners chronically exposed to mercury vapor for an average of 15 years. Hyperchloremia, low normal serum bicarbonate, a normal serum anion gap and an elevated urine anion gap were found in these patients (Franko et al, 2005; Bluhm et al, 1992). However, a study of 49 chloralkali workers with previous occupational mercury exposure found no difference in renal function compared to controls. Mercury exposure had ceased an average of 4.8 years prior to the study in these workers (Efskind et al, 2006).

DYSURIA: Dysuria and ejaculatory pain without concomitant evidence of urologic disease developed in workers acutely exposed to toxic levels of mercury vapor (Bluhm et al, 1992a).

RENAL LAB ABNORMALITIES: In one report, minor elevations in BUN (28 mg/dL), serum creatinine (2 mg/dL) and decreased urine output developed in a man after the intravenous injection of 3 mL of elemental mercury and ingestion of 3 mL in a suicide attempt (McFee & Caraccio, 2001).

DYSMENORRHEA: Dysmenorrhea may occur in woman exposed to mercury vapor. A retrospective epidemiological Chinese study of 296 female workers (18 to 44 years of age) exposed to mercury vapor and 394 female workers (control group) from food processing plants showed a significantly higher prevalence of dysmenorrhea (odds ratio (OR) = 1.66, 95% CI 1.07 to 2.59) and abdominal pain (OR = 1.47, 95% CI 1.03-2.11) in the exposed group compared to the control group. The workplace air concentration of mercury ranged from 0.001 to 0.2 mg/m(3) (Yang et al, 2002).

Chronic exposure to mercury may lead to the following adverse effects: lens discoloration and impaired vision, nasal irritation, epistaxis, gingivitis, stomatitis, tremor of the tongue, discolored gums, speech defects (severe cases), and disturbances in taste and smell (Gosselin et al, 1984; Holland et al, 1994). Other effects associated with long-term exposure include band keratopathy and corneal opacity (Grant, 1986).

Specifically to the throat, side effects following acute exposure to vapors may include: respiratory tract irritation, coughing, a metallic taste, swelling of the salivary glands, gingivitis, and stomatitis (Setz et al, 2008; Snodgrass et al, 1981; Bluhm et al, 1992a).

MERCURIALENTIS: Mercurialentis (brownish discoloration of lens) may result following either eye exposure to mercury vapors or systemic mercury poisoning. Mercurialentis usually indicates chronic exposure to elemental mercury rather than toxicity. Diagnosis is made by slit lamp examination (Rosenmann et al, 1986; Winship, 1985).

BLINDNESS: Injection of mercury into the arterial circulation during cardiac catheterization has caused retinal artery embolism and blindness(Grant, 1986).

COLOR DISTURBANCES: Workers exposed to elemental mercury had subclinical color vision loss, mainly in the blue-yellow range compared with controls (Cavalleri et al, 1995). In a follow-up study, subclinical color discrimination impairment was observed in workers exposed to mercury at an exposure level (a limit of 35 mcg/g creatinine based on renal effects has been proposed) below the current biological limit for occupational exposure to mercury (Urban et al, 2003). Another study reported that color discrimination impairment (mainly blue-yellow and red-green) can be found years (6.8 +/- 4.2 years; range 1 to 15 years) after cessation of mercury vapor exposure and may be irreversible (Feitosa-Santana et al, 2008).

TOOTH LOOSENING: Teeth may become loose due to gum inflammation. However, poor dental health is not always associated with chronic exposure to mercury vapor as observed among chloralkali workers (Holland et al, 1994).

THROMBOCYTOPENIA: Thrombocytopenia has been reported in children and adults exposed to elemental mercury vapors (Schwartz et al, 1992; Fuortes et al, 1995).

ANEMIA: Anemia and lymphopenia developed in one woman who, as a folk medicine practice, inhaled smoke from burning dried lime which contained elemental mercury (Mohan et al, 1994). In another case, a 30-year-old woman presented with mercury toxicity after self-injection of approximately 500 g of mercury. Anemia (hemoglobinemia less than 7.1 g/dL) developed among other symptoms, and the woman died 30 days after presentation (DePalma et al, 2008).

ERYTHROCYTE ENZYME DEFICIENCIES: Chronic mercury exposure in exposed workers resulted in changes in glucose-6-phosphate dehydrogenase (G6PD), acetylcholinesterase, glutathione reductase, and superoxide dismutase, as well as increases in hematocrit and decreases in MCV, MCHC, and ferritin (Zabinski et al, 2000).

ABNORMAL LIVER FUNCTION TESTS: Mild jaundice and abnormal liver function tests developed in an adult male six months after ingestion of metallic mercury who was also chronically exposed to mercury in his occupation. Authors proposed a contribution of slowly absorbed mercury to delayed hepatic dysfunction (Lin & Lim, 1993).

CHOLECYSTITIS, CASE REPORT: A 53-year-old man underwent cholecystectomy for a suspected gall bladder wall mass. Biopsy noted droplets of elemental mercury within chronically inflamed tissue. The patient had previously attempted suicide by intravenous injection of elemental mercury at the age of 18 (Zippel et al, 2006).

Reviews of contrasting studies have shown both the presence of immunoglobulin changes (Ellingsen et al, 1993c; Bencko et al, 1990) and the absence of any immunological profile changes (Langworth et al, 1992a).

AUTOANTIBODY DEVELOPMENT: There have been reported increases in the levels of autoantibodies to the glomerular basement membrane (alpha-GBMs) in the blood of workers exposed to mercury vapors (Lauwerys et al, 1983), but these have not been confirmed by later reports (Bernard et al, 1987).

TNF ALPHA DECREASE: A decrease in serum tumor necrosis factor alpha has been reported (Ellingsen et al, 2000).

CIRCULATING MONOCYTES : Subtle changes in circulating monocyte function (impaired chemotaxis) and natural killer (NK) cell function have been reported in mercury exposed workers (Vimercati et al, 2001). Changes in T lymphocyte and NK cell populations have also been reported in chloralkali workers (Park et al, 2000).

MUSCLE WEAKNESS, CHRONIC EXPOSURE: Muscle weakness, particularly limb weakness, can occur following chronic exposure to elemental mercury vapors (Yeates & Mortensen, 1994; Gosselin et al, 1984).

ACRODYNIA: Acrodynia (painful extremities) may result following subchronic or chronic mercury poisoning (Yeates & Mortensen, 1994; Gosselin et al, 1984).

Neurological signs and symptoms are chiefly associated with chronic exposure, (Mohan et al, 1994) and these effects could include personality changes and tremors, (Schaumburg et al, 2009; Celebi et al, 2008) headache, short term memory loss, poor appetite, shyness, insomnia, emotional lability, paresthesias, weakness (Abbaslou & Zaman, 2006; Yeates & Mortensen, 1994) and nerve conduction delays (Rosenmann et al, 1986; US DHHS, 1992).

Symptoms including poor concentration, loss of appetite, gastrointestinal disturbances, nervousness, sleep disturbances, memory disturbances, and tiredness were greater among 89 chloralkali workers exposed to mercury than 75 unexposed controls (Langworth et al, 1992).

FATIGUE: Fatigue has been reported following mercury exposure (Florentine & Sanfilippo, 1991), and in one case-control study, significantly higher symptoms of fatigue and confusion were reported by workers in a fluorescent lamp factory compared to controls (Liang et al, 1993).

CONFUSION: Confused mental status has been reported following acute mercury vapor exposure (Mohan et al, 1994).

SHORT-TERM MEMORY LOSS: Persistent short-term memory defects, increased reaction time, and defects in motor coordination were seen in case-control study where 18 years had passed since the last exposure (Kishi et al, 1994).

VISUAL-MOTOR FUNCTION: Neurological changes involving visual-motor function have been associated with elemental mercury exposure (Haut et al, 1999).

NEUROPSYCHOLOGICAL TEST DEFICITS: In a case-control study comparing 26 former fluorescent plant workers to 20 control subjects, workers previously exposed to mercury had increased depression and anxiety symptoms, slower information processing speed, inferior performance in psychomotor speed, verbal spontaneous recall memory, and manual dexterity in both hands. Workers were exposed for an average of 10.2 +/- 3.8 years and had stopped 6 +/- 4.7 years prior to the study (Zachi et al, 2007).

CEREBELLAR DISORDER, ACUTE AND CHRONIC: Tremor, ataxia and loss of coordination have been reported in workers chronically exposed to mercury vapor (Donoghue, 1998; Albers et al, 1988).

PERIPHERAL NEUROPATHY: Peripheral neuropathy, characterized by decreased strength and sensation, may develop after chronic elemental mercury exposure (Celebi et al, 2008; Florentine & Sanfilippo, 1991).

HYPERREFLEXIA: Abnormal reflexes, including snout and Babinski reflexes, were increased in workers with higher urinary mercury excretion compared with their co-workers (Albers et al, 1988).

TREMOR, CHRONIC EXPOSURE: Tremors are characteristic of chronic exposure to elemental mercury and typically disappear after exposure has ceased (Schaumburg et al, 2009). In one case, a Parkinsonian syndrome with resting and intention tremor, bradykinesia and cogwheel rigidity was reported after long term exposure to elemental mercury vapors (Finkelstein et al, 1996).

EEG ABNORMALITIES: EEG abnormalities have been observed following mercury poisoning, although significant subjective symptoms may not be present (Piikivi & Hanninen, 1989).

Psychiatric changes, both acute and chronic, commonly reported by workers exposed to mercury vapors include insomnia, depression, anger, irritability, aggressiveness, nervousness, loss of self confidence, shyness, and impatience (Rosenmann et al, 1986), Ngim et al, 1992 (Bluhm et al, 1992a). There was an association between the number of neuropsychological symptoms reported and the mean urinary excretion of mercury and N-acetyl glucosaminidase in a study of chronically exposed workers (Rosenmann et al, 1986).

PSYCHOLOGICAL DISTRESS: Tests of psychological distress were markedly abnormal in 11 men acutely exposed to mercury vapor (Bluhm et al, 1992a).

Hemoptysis, cyanosis, cough, chest tightness, pneumonitis, necrotizing bronchiolitis and pulmonary edema have occurred following vapor inhalation (Anon, 2005; Mohan et al, 1994; US DHHS, 1992).

ACUTE RESPIRATORY DISTRESS SYNDROME: Acute respiratory distress syndrome and fatal respiratory failure have occurred following mercury vapor exposure (Rowens et al, 1991; Taueg et al, 1992; Solis et al, 2000).

ASPIRATION: Chronic respiratory disease may occur as a result of mercury aspiration. Radiographs may show mercury droplets at the lung bases (Janus & Klein, 1982). In one case, a 49-year-old ingested 200 mL (2709 g) of elemental mercury and aspirated during gastric lavage. Multiple mercury droplets were detectable on chest x-ray but no significant respiratory symptoms were reported (Lech & Goszcz, 2006).

PULMONARY EMBOLISM: Pulmonary embolization from intravenous injection of mercury has resulted in dyspnea, hemoptysis and metallic densities on chest radiograph and CT (Oliver et al, 1987; Maniatis et al, 1997). Pulmonary emboli have been reported to persist 21 to 66 days following IV injection (Eyer et al, 2006; McFee & Caraccio, 2001).

FIBROSIS, ACUTE AND CHRONIC: Severe, acute mercury exposure may result in residual restrictive pulmonary disease and fibrosis (Sue, 1994).

IMPAIRED PULMONARY FUNCTION: Permanent impairment of pulmonary function may occur following elemental mercury inhalation despite chelation therapy (Lilis et al, 1985; Levin et al, 1988).

FEVER: Fevers are often reported in both children and adults following elemental mercury exposure, and may be misinterpreted as infectious illness or metal fume fever (Sevketoglu et al, 2011; Wale et al, 2010; McFee & Caraccio, 2001).

Although less than 5 percent of a short-term exposure to methylmercury reaches the brain, subsequent demethylation traps it in the brain; oxidation of absorbed elemental mercury vapor to the ionic form also traps it in the brain (Clayton & Clayton, 1994).

The kidney is the target organ for mono- and divalent mercury salts. Moreover, after exposure to mercury vapor or inorganic salts, 50 to 90 percent of the mercury body burden is in the kidney (Clayton & Clayton, 1994).

Mercury is taken up by the brain, peripheral nerves, kidneys, liver, myocardium, intestinal mucosa, testis, skin, bone marrow, and placenta. It tends to be retained in the body for long periods. The half-life of mercury is 64 days in the kidney, 54 days in the whole body, and approximately 1 year in the brain. Concentrations of mercury in the brain thus may accumulate to high levels, which may still be present even 10 years after cessation of exposure (Blum & Manzo, 1985).

The tremor first begins as a fine tremor in the hands, tongue, and eyelids, later progressing to an intention tremor of the hands (O'Donaghue, 1985). The progression of the tremor can be often tracked by comparing samples of handwriting made over a period of time (ILO, 1983). Ataxia may also be present (O'Donaghue, 1985).

Subclinical tremor can occur from chronic exposure to airborne concentrations of approximately 0.026 mg/m(3) (Fawer et al, 1983). It is probable that a tremor will develop with exposure to airborne levels of 0.1 mg/m(3) (Hathaway et al, 1996).

Alterations in motor function and attention were noted in a group of former chloralkali workers after a mean time of 12.7 years since the cessation of exposure (Mathiesen et al, 1999).

After at least ten years of exposure, impairment of memory is more severe and is associated with lower verbal intelligence scores (Piikivi et al, 1984). Older dentists scored more poorly on memory tests than age-matched controls. Psychomotor testing may reveal subclinical signs of chronic mercury exposure (Ritchie et al, 1995).

However, in another reported case, cognitive and personality defects had recovered by 1.5 years after removal from chronic elemental mercury exposure (Hua et al, 1996).

After almalgam removal, there is a decrease in the levels in blood and urine, which slowly approach those of subjects without any history of amalgam fillings (Langworth & Shamburg, 1996; (Sandborgh-Englund et al, 1998).

Chewing gum on a regular basis can release mercury from dental amalgam: In one study, average levels of plasma and urinary mercury were 27 nmol/L and 6.5 nmol/mmol creatinine, respectively, in gum chewers, compared with 4.9 nmol/L and 1.2 nmol/mmol creatinine in controls (Sallsten et al, 1996).

Persons with oral lichen planus adjacent to amalgam fillings had higher lymphocyte reactivity to inorganic mercury relative to controls (Stejskal et al, 1996).

Mercury in the drinking water can induce autoimmunity in susceptible mice; this reaction is strictly dependent on T-helper (CD4(+)) cells and persists indefinitely after cessation of mercury exposure (Hultman et al, 1995).

Exposure to mercury as mercuric chloride induced autoimmunity in mice. Induction of IgG antibodies against nucleolar fibrillarin was determined by the H-2 genotype, whereas the response against chromatin and/or histones was determined by other genetic factor(s) (Hultman et al, 1996).

ELEMENTAL (METALLIC) MERCURY - is usually not absorbed, and usually does not produce acute toxicity unless a GI fistula or another inflammatory process is present or the mercury is retained for a long period in the GI tract. Decontamination is not necessary in normal patients after small ingestions.

Move victim to fresh air.

Call 911 or emergency medical service.

Give artificial respiration if victim is not breathing.

Administer oxygen if breathing is difficult.

Remove and isolate contaminated clothing and shoes.

In case of contact with substance, immediately flush skin or eyes with running water for at least 20 minutes.

Keep victim warm and quiet.

Ensure that medical personnel are aware of the material(s) involved and take precautions to protect themselves.

FIRST AID

INHALATION EXPOSURE

DERMAL EXPOSURE

EYE EXPOSURE

ORAL EXPOSURE

The amount of ingested mercury that would be fatal to a man is estimated at 100 grams (1429 mg/kg) ((HSDB, 2002)). A daily dose of 75 mg mercury in drinking water is also thought to be fatal ((OHM/TADS, 2002)).

A 30-year-old woman presented with mercury toxicity after self-injection and ingestion of approximately 500 g of mercury from 37 broken fever thermometers. Despite supportive treatment, she developed lung embolization complicated by acute respiratory distress syndrome (ARDS), toxic dermatitis, anemia, and mild hepato-renal impairment, and died 30 days after presentation (DePalma et al, 2008).

Patients having mercury concentrations in the blood and urine of 0.4 to 0.9 mg/L and 0.5 to 1.6 mg/L, respectively, died from acute mercury vapor poisoning (Baselt, 2000).

Four adults (2 men and 2 women, ranging in age from 40 to 88 years old) died following exposure to mercury vapors while smelting silver from dental amalgam in their home (Kanluen & Gottlieb, 1991). Measurements of the ambient air in the home eleven to eighteen days after the initial exposure revealed mercury concentrations ranging from 786 to 912 mg/m(3) (ACGIH, 1996).

Systemic mercury toxicity and death followed rupture of a mercury-containing Miller-Abbott intestinal decompression tube (Bredfeldt & Moeller, 1978; Kurt, 1984).

A three year old girl died approximately 2 months after playing with elemental mercury. The mercury concentrations in her tissues at the time of death were: brain, 1.3 mg/kg; lung, 3.7 mg/kg; liver, 3.9 mg/kg; kidney, 14 to 30 mg/kg; antemortem urine, 0.16 to 0.86 mg/L (Baselt, 2000).

CASE REPORT: A 55-year-old man presented to the ED after ingesting 500 g (66 mL) of elemental mercury (quicksilver). Before presentation, he also drank an unknown amount of alcohol and attempted suicide by inhaling propane from a gas bottle. Abdominal x-ray radiographs revealed a large amount of radio-opaque liquid in his stomach. He received a bowel evacuation regimen, containing polyethylene glycol and activated charcoal, and his serum mercury concentrations peaked at 511 nM (occupational exposure safety limit: less than 75 nM, based on inhalational exposure) about 24 hours postingestion. At this time, he also received a single daily oral dose of succimer (10 mg/kg). Because of difficulties with GI evacuation, fluoroscopy was used for bowel emptying and abdominal x-ray radiographs revealed new mercury globules, suggesting the reingestion of fecal mercury. Following further supportive care, including psychiatric treatment to discontinue the fecal mercury reingestion, his mercury levels gradually decreased and he was discharged on day 5 (Mitenko, 2014).

CASE REPORT: A 43-year-old man presented to the ED with severe abdominal pain and persistent vomiting following the ingestion of 200 mL of elemental liquid mercury in a suicide attempt. His chest x-ray revealed small amounts of mercury in lower lung fields bilaterally, indicating aspiration. He was treated with IV fluids, opioid analgesics, and antiemetic medications before being transferred to a negative pressure side room to reduce the risk of mercury inhalation by hospital staff. A nasogastric tube was inserted and 115 mL of mercury was aspirated from his stomach leading to significant improvement in patient's symptoms and resolution of vomiting. The patient's blood mercury concentrations continued to rise by day 2 (675 nmol/L on admission and 934 nmol/L on day 2), suggesting continual systemic absorption from the lungs and his 24-hour urine mercury concentration was also elevated (14365 nmol/day). At this time, he was treated with IV 2,3-dimercaptopropane-1-sulfonate (DMPS, Dimaval; 30 mg/kg/day in 8 divided doses for 6 days), leading to improved blood and urinary mercury concentrations that continued to decrease 5 days later. The patient was subsequently discharged home after psychiatric review (Dawson et al, 2013).

Fluorescent light bulbs contain a very small amount (4 to 6 mg) of mercury inside a glass tubing. In contrast, a glass thermometer contains about 500 mg of mercury (US Environmental Protection Agency, 2007; US Environmental Protection Agency, 2007). Health effects are not expected from acute exposure to a broken bulb.

A man ingested as much as 204 grams of elemental mercury with little effect (Wright et al, 1980).

After a 20 mL IV injection of mercury, a 14-year-old boy experienced emboli in both lung fields, metal densities in the abdomen, and small mercury pools in the right ventricle. He also endured an elevated temperature, difficulty breathing, general malaise, and pleuritic chest pain with shortness of breath ((HSDB, 2002)).

After working for three years at a thermometer plant, nine workers experienced tremors, rigidity, loss of memory, blurred vision, and auditory and visual hallucinations. Permanent defects in recent memory, thought to be related to generalized cerebral cortical dysfunction, were severe in two workers and moderate in seven (ACGIH, 1991).

Deliberate intravenous injection of 20 mL mercury by a 14-year-old boy resulted in mercury emboli in both lungs, severely reduced pulmonary function, elevated temperature and general malaise, but was not fatal ((HSDB, 2002)).

The toxic threshold of mercury through parenteral exposure is estimated at 40 to 270 g ((HSDB, 2002)).

Large quantities of mercury have been accidentally released into the gastrointestinal tract during surgical manipulations without serious effect. Nonpersistent fistulous tracts were the only reported reaction ((HSDB, 2002)).

Toxicity may be evident in populations exposed to mercury vapor concentrations of greater than 1.0 mg/m(3) for extended periods of time (Bingham et al, 2001).

Blood mercury levels of 0.02 mg/L are considered acceptable (Baselt, 2000).

Chlor-alkali workers exposed to mercury vapor concentrations from 0.05 to 0.10 mg/m(3) exhibited no overt signs of mercury intoxication. No abnormalities in perceptual, motor, memory or learning abilities were seen in workers chronically exposed to average concentrations of 25 mcg/m(3) mercury vapor (ACGIH, 1996).

AMALGAMATION: Occupational exposures have been recognized by color changes on gold jewelry (amalgamation).

Fluorescent light bulbs contain a very small amount (4 to 6 mg) of mercury inside a glass tubing. In contrast, a glass thermometer contains about 500 mg of mercury (US Environmental Protection Agency, 2007; US Environmental Protection Agency, 2007). Health effects are not expected from acute exposure to a broken bulb.

An 8-month-old girl was successfully treated for acute mercury vapor intoxication with oxygen, IV injections of nafcillin sodium (100 mg/kg/day) ((HSDB, 2002)).

An elemental mercury spill (0.5 to 1 ounce) in the home resulted in a mercury blood level of less than 1 mcg/dL and a urine level of 120 mcg/24 hours in a 4-year-old. Symptoms associated with these levels were severe (fever, insomnia, headache, ataxia, hallucinations, irritability) requiring treatment with BAL and NAP (Florentine & Sanfilippo, 1991).

An 11-month-old and a 6-year-old developed rash, neurologic toxicity and hypertension 2 weeks after a thermometer was broken in their bedroom resulting in mercury spilling on the carpet (Velzeboer et al, 1997).

The kidneys, liver, brain, heart, lung, and colon of rabbits have been severely damaged after exposure to 28.8 mg/m(3) mercury vapor for one four hour period ((HSDB, 2002)).

Inhalation of mercury vapor by sheep and cattle is extremely toxic, causing dyspnea and coughing, nasal discharge, fever, loss of appetite and, at times, bleeding of oral mucosa, dermatosis and nephritis ((HSDB, 2002)).

ACGIH (American Conference of Governmental Industrial Hygienists, 2010): A4 ; Listed as: Mercury, elemental and inorganic forms, as Hg

ACGIH (American Conference of Governmental Industrial Hygienists, 2010): A4 ; Listed as: Mercury, as Hg

ACGIH (American Conference of Governmental Industrial Hygienists, 2010): Not Listed ; Listed as: Mercury, alkyl compounds, as Hg

ACGIH (American Conference of Governmental Industrial Hygienists, 2010): Not Listed ; Listed as: Mercury, alkyl compounds

ACGIH (American Conference of Governmental Industrial Hygienists, 2010): Not Listed ; Listed as: Mercury, aryl compounds, as Hg

EPA (U.S. Environmental Protection Agency, 2011): D ; Listed as: Mercury, elemental

IARC (International Agency for Research on Cancer (IARC), 2016; International Agency for Research on Cancer, 2015; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010a; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2008; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2007; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2006; IARC, 2004): 3 ; Listed as: Mercury and inorganic mercury compounds

NIOSH (National Institute for Occupational Safety and Health, 2007): Not Listed ; Listed as: Mercury compounds [except (organo) alkyls, as Hg]

NIOSH (National Institute for Occupational Safety and Health, 2007): Not Listed ; Listed as: Mercury (organo) alkyl compounds (as Hg)

MAK (DFG, 2002): Category 3B ; Listed as: Mercury (metallic mercury and inorganic mercury compounds)

MAK (DFG, 2002): Category 3B ; Listed as: Mercury, organic compounds

NTP (U.S. Department of Health and Human Services, Public Health Service, National Toxicology Project ): Not Listed

Oral:

Inhalation:

Drinking Water:

References: ITI, 1995 Lewis, 2000 RTECS, 2002

Editor's Note: The listed values are recommendations or guidelines developed by ACGIH(R) to assist in the control of health hazards. They should only be used, interpreted and applied by individuals trained in industrial hygiene. Before applying these values, it is imperative to read the introduction to each section in the current TLVs(R) and BEI(R) Book and become familiar with the constraints and limitations to their use. Always consult the Documentation of the TLVs(R) and BEIs(R) before applying these recommendations and guidelines.

Not Listed

Listed as: Mercury compounds [except (organo) alkyls, as Hg]

REL:

Listed as: Mercury (organo) alkyl compounds (as Hg)

REL:

IDLH:

IDLH:

Listed as: Mercury (aryl and inorganic) (as Hg)

Table Z-1 for Mercury (aryl and inorganic) (as Hg):

Listed as: Mercury (organo) alkyl compounds (as Hg)

Table Z-1 for Mercury (organo) alkyl compounds (as Hg):

Listed as: Mercury (vapor) (as Hg)

Table Z-1 for Mercury (vapor) (as Hg):

Table Z-2 for Mercury (Z37.8-1971):

Not Listed

Listed as: Mercury (D009)

Final Reportable Quantity, in pounds (kilograms):

Additional Information: Unlisted Hazardous Wastes Characteristic of Toxicity

Listed as: Mercury

Final Reportable Quantity, in pounds (kilograms):

Additional Information:

Listed as: Mercury and compounds

Additional Information:

Listed as: Mercury Compounds

Additional Information:

Not Listed

Listed as: Mercury

P or U series number: U151

Footnote:

Editor's Note: The D, F, and K series waste numbers and Appendix VIII to Part 261 -- Hazardous Constituents were not included. Please refer to 40 CFR Part 261.

Not Listed

Listed as: Mercury compounds

Effective Date for Reporting Under 40 CFR 372.30:

Lower Thresholds for Chemicals of Special Concern under 40 CFR 372.28: 10

Listed as: Mercury Compounds: Includes any unique chemical substance that contains mercury as part of that chemical's infrastructure

Effective Date for Reporting Under 40 CFR 372.30: 1/1/87

Lower Thresholds for Chemicals of Special Concern under 40 CFR 372.28:

Listed as: Mercury

Effective Date for Reporting Under 40 CFR 372.30:

Lower Thresholds for Chemicals of Special Concern under 40 CFR 372.28: 10

Listed as: Mercury

Effective Date for Reporting Under 40 CFR 372.30: 1/1/87

Lower Thresholds for Chemicals of Special Concern under 40 CFR 372.28:

Listed as Mercury (I) (mercurous) compounds (pesticides)

Severe Marine Pollutant: Yes

Listed as Mercury (II) (mercuric) compounds (pesticides)

Severe Marine Pollutant: Yes

Listed as Mercury based pesticide, liquid, flammable, toxic

Severe Marine Pollutant: Yes

Listed as Mercury based pesticides, liquid, toxic

Severe Marine Pollutant: Yes

Listed as Mercury based pesticides, liquid, toxic, flammable

Severe Marine Pollutant: Yes

Listed as Mercury based pesticides, solid, toxic

Severe Marine Pollutant: Yes

Listed as Mercury compounds, liquid, n.o.s.

Severe Marine Pollutant: Yes

Listed as Mercury compounds, solid, n.o.s.

Severe Marine Pollutant: Yes

Listed as: Mercury

Hazardous materials descriptions and proper shipping name: Mercury

Hazardous materials descriptions and proper shipping name: Mercury contained in manufactured articles

Proper Shipping Name: Mercury

UN Number: 2809

Proper Shipping Name: Mercury contained in manufactured articles

UN Number: 2809

Not Listed

Store small quantities of mercury in polyethylene bottles. To prevent evaporation, cover the surface with water. Keep containers tightly closed ((HSDB, 2002); ITI, 1995).

Ambient storage temperatures and open venting are recommended ((HSDB, 2002)).

Mercury may oxidize slowly in moist air, forming mercurous oxide ((HSDB, 2002)).

Floors should be non-porous and washed regularly with dilute calcium sulfide, or other suitable reactant ((HSDB, 2002)).

Keep containers of mercury separate from azides, nitrates, chlorates, oxidants, acetylenic compounds, metals, and the following in particular: 3-bromopropyne; alkynes plus silver perchlorate; ethylene oxide; lithium; methylsilane plus oxygen (explodes when shaken); peroxyformic acid; chlorine dioxide; tetracarbonylnickel plus oxygen; ammonia; boron diiodophosphide; chlorine; chlorine dioxide; methyl azide; sodium acetylide; and nitromethane (DOT 2002a; ((HSDB, 2002); ITI, 1995; Lewis, 2000) Urben, 1999).

Also keep separate from heat, sparks, or ignition (ITI, 1995).

Mercury may react explosively with ammonia (Lewis, 2000).

It is incompatible with tetracarbonylnickel and oxygen ((HSDB, 2002)).

Mercury reacts violently with dry bromine (Urben, 1999). It also reacts with nitric acid and hot, concentrated sulfuric acid (Budavari, 2000).

Ground mixtures of sodium carbide and mercury can react vigorously (NFPA, 1997).

Mercury attacks copper and copper alloys (ILO , 1998; Pohanish & Greene, 1997).

Mercury is slightly volatile at normal temperatures ((HSDB, 2002)).

Wear positive pressure self-contained breathing apparatus (SCBA).

Structural firefighters' protective clothing will only provide limited protection.

All data are compiled from published sources and are NOT recommended specifically by Truven Health Analytics. The appearance of specific manufacturers or products in this section does not represent an endorsement by Truven Health Analytics. No attempt has been made to verify the data presented. All product recommendations should be confirmed with the specific manufacturer for verification of product performance.

CLOTHING

FOOTWEAR

GLOVES

GENERAL INFORMATION

COMPANY INFORMATION

REFERENCES

POTENTIAL FIRE OR EXPLOSION HAZARDS - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 172 (ERG, 2004)

Mercury is noncombustible and not flammable (CHRIS , 2002; NIOSH , 2002).

Not Listed

Use extinguishing agent suitable for type of surrounding fire.

Do not direct water at the heated metal.

Not Listed

When heated to decomposition, mercury emits toxic fumes ((OHM/TADS, 2002); Lewis, 2000).

3-Bromopropyne

Chlorine dioxide

Ethylene oxide

Lithium

Peroxyformic acid

Alkynes + silver perchlorate

Methylsilane + oxygen (explodes when shaken)

Tetracarbonylnickel + oxygen

Methyl azide

Chlorine

Chlorine dioxide

Sodium acetylide

Nitromethane

Acetylenic compounds (e.g., acetylene, 2-butyne- 1,4-diol + acid)

Metals (e.g., aluminum, calcium, potassium, sodium, rubidium, exothermic formation of amalgams)

Consider initial downwind evacuation for at least 100 meters (330 feet).

When any large container is involved in a fire, consider initial evacuation for 500 meters (1/3 mile) in all directions.

CALL Emergency Response Telephone Number on Shipping Paper first. If Shipping Paper not available or no answer, refer to appropriate telephone number:

For additional details see the section entitled "WHO TO CALL FOR ASSISTANCE" under the ERG Instructions.

As an immediate precautionary measure, isolate spill or leak area for at least 50 meters (150 feet) in all directions.

Stay upwind.

Keep unauthorized personnel away.

Listed as Mercury vapor

ERPG-1 (units = ppm): Not appropriate

ERPG-2 (units = ppm): 0.25

ERPG-3 (units = ppm): 0.5

Under Ballot, Review, or Consideration: No

Definitions:

Listed as Mercury vapor

TEEL-0 (units = mg/m3): 0.025

TEEL-1 (units = mg/m3): 0.25

TEEL-2 (units = mg/m3): 1.7

TEEL-3 (units = mg/m3): 8.9

Definitions:

Listed as: Mercury vapor

Proposed Value:

Listed as: Mercury vapor

Proposed Value:

Listed as: Mercury vapor

Proposed Value:

IDLH: 10 mg Hg/m3 (as Hg)

Note(s): Not Listed

IDLH: 2 mg Hg/m3 (as Hg)

Note(s): Not Listed

SPILL OR LEAK PRECAUTIONS - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 172 (ERG, 2004)

RECOMMENDED PROTECTIVE CLOTHING - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 172 (ERG, 2004)

Avoid skin contact with liquid mercury and avoid breathing its vapors (AAR, 2000; CHRIS , 2002). Remove all personnel from area of the spill. Protective clothing and equipment should be worn by all persons decontaminating the area (Sittig, 1991).

Do not attempt vacuum clean-up of spilled mercury; do not sweep or use compressed air to move mercury droplets as these methods can increase mercury vapor concentrations ((ATSDR, 1999); Sittig, 1991). Do not attempt to absorb spilled liquid mercury with a paper towel or cloth, as this will only serve to spread the mercury ((ATSDR, 1999)).

Because droplets can proliferate, spills may be toxic hazards; clean-up requires special care (Lewis, 1997).

Do not use steel or alumunium tools or equipment to clean up a mercury spill ((HSDB, 2002)).

Collect and store the spilled mercury immediately by using a suction pump and aspirator bottle with long capillary tube. For small drops of mercury in less accessible areas, treat with calcium polysulfide and excess sulfur (ITI, 1995).

Small amounts of mercury spilled into cracks should be covered in zinc dust to form an amalgam (Sittig, 1991).

Once the material is cleaned up, store in a tightly stoppered bottle or vapor-tight container for later reclamation (ITI, 1995; Sittig, 1991). Contaminated spill areas can then be treated with calcium sulfide or sodium thiosulfate wash to neutralize any residual mercury ((HSDB, 2002)).

Spilled liquid mercury should be covered in a paste of sulfur and lime; water soluble compounds should be dissolved and water-insoluble compounds converted to nitrates. Adjust the pH and precipitate as mercuric sulfide ((OHM/TADS, 2002)).

In case of a large spill, consider initial downwind evacuation for at least 100 meters (330 feet) (ERG, 2000).

In surface waters with a pH of 4 to 9, a normal sulfide concentration will cause mercury to form mercuric sulfide. In water, this compound is nearly insoluble and thus will precipitate out, removing mercury ions from the water ((ATSDR, 1999)).

Mercury removal in wastewater can be accomplished in following ways ((HSDB, 2002)):

Sodium borohydride is a reducing agent that can be used to precipitate metals from solution as the insoluble elemental metal. It has been used advantageously for recovery of metals such as mercury from waste solutions (Freeman, 1989).

The mercury content of wastewater streams was reduced to less than the permitted level of 10 ppb using Duolite(TM) GT-73 ion exchange resin. With proper precautions this system will routinely reduce mercury input concentrations of 0.2 to 70 ppm to between 1 to 5 ppb. Pre-filtering to remove particulate iron aided the reliability of the process (Ritter & Bibler, 1992).

In mining and primary metal recovery operations, mercury spills often are dusted with large amounts of microcrystalline sulfur or calcium polysulfide. This causes a surface coating of mercuric sulfide to form, which reduces mercury vapor loss during cleanup ((HSDB, 2002)).

The ligand, 1,3-benzenediamidoethanethiol (BDETH2), may be able to reduce mercury concentrations in solution by as much as 99.97 percent (Matlock et al, 2001).

Several treatment processes have proven effective for clean up of mercury spills: clarification/sedimentation results in greater than 99 percent removal; clarification/sedimentation with chemical addition results in greater than 62 percent removal with alum, 88 percent removal with alum polymer, greater than 96 percent removal with lime, 87 percent removal with BaCl2, and 99 percent removal with polymer ((HSDB, 2002)).

ENVIRONMENTAL RECYCLING OF MERCURY: Elemental mercury in soils and waters may be methylated to organic methyl mercury by microbes ((HSDB, 2002)). The methyl mercury is accumulated by aquatic organisms and degraded to dimethylmercury gases. The dimethylmercury gases are released into the air, and decomposed by acid rain to monomethyl mercury. The monomethyl mercury then re-enters the surface waters (IARC, 1997).

Waste management activities associated with material disposition are unique to individual situations. Proper waste characterization and decisions regarding waste management should be coordinated with the appropriate local, state, or federal authorities to ensure compliance with all applicable rules and regulations.

The mercury-resistant bacterium Pseudomonas putida FB1 was used to remove mercury from a continuous axenic culture. The removal efficiency ranged from 99.2 to 99.8%, leaving a residual Hg concentration of less than 5 mcg/L (Baldi et al, 1993).

Pseudomonas putida Spi3 was used to remove mercury from chloralkali plant effluent. Mercury retention rate be the bacteria ranged from 90 to 98 percent; it was found that mercury concentrations of up to 7 mg/L could be treated in this manner without loss of activity (von Canstein et al, 1999).

Peat has proven effective in adsorbing mercury from wastewater. For wastewater with a mercury concentration of approximately 1 mg/L, 71.6% was adsorbed by peat. Maximum mercury adsorption occurred in the pH range of 5.0 to 5.5. Experiments were conducted between 5 and 21 degrees C and indicate that peat's adsorption capacity increases slightly with temperature. Advantages of peat use include its availability and cost effectiveness as compared to activated carbon (Viraraghavan & Kapoor, 1995).

Preliminary studies have been done to test the effectiveness of ground up, discarded automobile tires of absorbing mercury in aqueous solutions. The rubber particles in the tire material were found to have a strong affinity for ionic mercury. This process may be an effective means of removing mercury from contaminated waters while providing a useful end for discarded tires (Gunasekara et al, 2000).

Criteria for land treatment or burial (sanitary landfill) disposal practices are continually subject to change. Prior to implementing land disposal of waste containing mercury residue (including waste sludge), consult with local environmental regulatory agencies for guidance on acceptable disposal practices ((HSDB, 2002)).

Mercury is a poor candidate for incineration ((HSDB, 2002)).

Peanut hull charcoal was 7 times more effective at removing mercury ions from aqueous solutions than a commercial granular activated charcoal. Seventy milligrams of the charcoal would completely remove 20 mg/dm(3) of mercury from a 100 mL solution (Namasivayam & Periasamy, 1993).

Cleanup can be performed with an industrial vacuum cleaner that is specially equipped with a "mercury trap." Once the bulk of the metal is recovered, a fine copperwire or plated carbon fiber brush is recommended as the cleanup utensil (particularly when the spill occurs on metal surfaces susceptible to amalgamation). This can be followed, if necessary, by washes with dilute nitric acid (~1 M), concentrated sulfuric acid, or bleach washes (depending on the type of surface on which the spill occurred), and then by clear water rinses ((HSDB, 2002)).

A vacuum trap that is aspirator-driven and has an amalgamated copper roller that operates in a tin-plate "mercury scoop" may be effective for mercury cleanup ((HSDB, 2002)).

NATURAL SOURCES

INDUSTRIAL SOURCES

Biological reduction is largely responsible for mercury transport into the atmosphere from natural waters. Positive correlations between elemental mercury concentrations and biological productivity can be found in the nutrient-rich waters along latitudinal transects near the equator (Barkay et al, 2003).

Metallic mercury, when released to the atmosphere in vapor form, is often transported far from the release site before wet and dry deposition processes begin (ATSDR, 2003).

Atmospheric mercury can be oxidized/reduced with dissolved ozone, hydrogen peroxide, hypochlorite entities, or organoperoxy compounds or radicals (ATSDR, 2003).

Abiotic oxidation of elemental mercury can enhance atmospheric mercury deposition since particulates, rain, and snow rapidly absorb ionic (+2) mercury (Barkay et al, 2003).

Wet deposition removes approximately 66% of atmospheric mercury. This process accounts for nearly all mercury in surface waters that do not receive mercury from other sources (ATSDR, 2003).

Fifty percent of volatile mercury is in vapor form, with the remainder largely occurring as mercury (+2) form and methyl mercury. Mercury is deposited and revolatilized in the environment many times. Its atmospheric residence time is typically a few days. In its volatile phase, mercury can be transported hundreds of kilometers (HSDB, 2005; ATSDR, 2003).

Estimated residence times for elemental mercury in the atmosphere range from 6 days to 2 years. Rapid oxidation, however, may occur in a matter of hours if elemental mercury contacts ozone (ATSDR, 2003).

An investigation of gas-phase reactions between ozone and elemental mercury showed mercury concentrations decreased and oxidized mercury formation increased when ozone concentrations exceeded 20 ppm, . Specific results indicated a gas phase rate constant of 3 x 10(-20) cm(3)/molec/s at 20 degrees C. At a mean global ozone concentration of 30 ppb, the atmospheric mercury half-life thus averages about 1 year (Hall, 1995).

Field studies performed in Canada and Sweden during 1986, 1988, and 1989 examined the extent of mercury volatilization. The investigations involved simultaneous determination of total vapor-phase mercury in air samples over water surfaces versus over nearby land surfaces. Volatilization rates ranged from 3 to 10 ng/m(2)/H during daytime. Daytime fluxes were about 2.5 times higher than night fluxes. No flux occurred during winter, when lake temperatures hovered just above freezing (Schroeder et al, 1992).

SURFACE WATER

GROUND WATER

TERRESTRIAL

Atmospheric deposits of mercury onto land usually revaporize within 1 or 2 days under sunlit-heated conditions (HSDB, 2005).

Solar activity and the presence of ice crystals reportedly enhance mercury transformation from its elemental to its divalent form. The resultant depositional increase, which occurs from March to June, is referred to as the "polar sunrise mercury depletion incidence" (UNEP, 2002).

Atmospheric mercury can be oxidized/reduced with dissolved ozone, hydrogen peroxide, hypochlorite entities, or organoperoxy compounds or radicals. Elemental mercury may remain in the atmosphere for up to 2 years. However, rapid oxidation can occur in a few hours upon contact with ozone in clouds (ATSDR, 2003).

A recent study attributes the Mer protein in some bacteria to mercury metalloregulation, transport, enzyme catalysis, and reduction of reactive organic and ionic mercury forms to inert elemental mercury. The Mer-mediated demethylation process dominates in aerobic environments with high mercury concentrations, while oxidative methylation dominates in anaerobic environments with low mercury concentrations (Barkay et al, 2003).

At soil pH levels >4, mercury strongly sorbs to humic matter, sesquioxides, and surficial peat layers. Mercury also readily volatilizes from acidic soil surfaces (Dragun, 1988).

In aquatic systems (rivers and streams) where the residence time for water is low, the half-life for mercury can be greater than 1 year (HSDB, 2005).

Mer-mediated demethylation dominates in aerobic environments with high mercury concentrations. Oxidative methylation is more apt to occur in anaerobic environments with low mercury concentrations (Barkay et al, 2003).

Certain bacteria, especially that of the genus Pseudomonas, can convert divalent mercury into metallic mercury (HSDB, 2005).

Sulfur-reducing bacteria can convert most mercury forms in surface water to methylmercury under anaerobic conditions. Under low pH conditions, the yeasts, Candida albicans and Saccharomyces cerevisiae, can both methylate mercury and reduce mercury to its elemental form (ATSDR, 2003).

A group of 395 subjects with varying fish consumption habits were evaluated for mercury levels in whole blood (B-Hg), and selenium levels in plasma (P-Se). There was a statistically significant relationship between fish consumed and B-Hg. The average B-Hg was 1.8 ng/g for subjects who never ate fish and 6.7 ng/g for subjects who ate at least two fish meals per week (Svensson et al, 1992).

Japanese school children (ages 3 to 18) were monitored for mercury in their urine, dental amalgam fillings, and the amount of fish consumed. The geometric mean level of urinary mercury was 1.9 mcg/L for boys and 2.1 mcg/L for girls. Only 1.5% of the data variance was attributed to dental fillings and fish eating frequency (Suzuki et al, 1993).

Consumption of sportfish from the St. Lawrence River has been associated with elevated blood mercury levels in residents of Montreal, Canada. Those consuming sportfish at least once weekly had mean blood mercury levels of 3.03 (+/- 2.43) mcg/L, compared to 1.44 (+/- 2.23) mcg/L in those eating sportfish less than once per week (Kosatsky et al, 2000).

Survey results on marine organisms (17 fish spp, 4 bivalve spp, 2 cephalopod spp, 3 crustacean spp) from the Adriatic and Ionian seas showed the following (Marcotrigiano & Storelli, 2003):

Princess Royal Harbour received mercury contaminated effluents from a superphosphate plant for over 30 years. While the sediment mercury level was not high (~1.7 mg/kg), fish from the harbor had mercury levels up to 10.3 mg/kg. The authors attributed the wide variation among different fish species' mercury content to dietary differences (Francesconi & Lenanton, 1992).

From 1985 to 1990, mercury content was monitored in cod, flounder, spotted dogfish, brown shrimp, and blue mussel. A positive correlation was found between fish length (cod and flounder) and fish mercury content. Mercury concentrations in cod, flounder, and dogfish were 0.11, 0.22, and 0.87 mg/kg, respectively. Mercury concentrations in shrimp and mussel were 0.1 and 0.14 mg/kg, respectively (Guns et al, 1992).

Mercury levels in 29 species of marine fish and three shellfish ranged from 0.01 to 0.48 mcg/g of dry tissue (Joseph & Srivastava, 1993).

A study investigating mercury content in different water fractions of 76 Swedish lakes showed that humic matter in the water was a significant carrier of mercury. A positive correlation was found between the water color and mercury content in pike and perch in deep lakes (average depth greater than 5 meters). It is suggested that the bioavailability of mercury attached to humic matter increases due to anoxic conditions in deep lakes (Nilsson & Hakanson, 1992).

Researchers analyzed mercury in muscle and organ tissues of deep-water shark from the eastern Mediterranean (1280 to 1500 meters depth). Results showed a positive correlation between shark size and mercury content in muscle, kidney, and liver tissues (Hornung et al, 1993).

The mean mercury concentration of 562 muscle tissue samples from sand flathead collected in Port Phillip Bay, Australia was 23 (+/- 0.18) mcg/g wet weight (Fabris et al, 1992).

Total mercury concentrations in largemouth bass (Micropterus salmoides) muscle tissue collected from 53 Florida lakes ranged from 0.04 to 2.04 mcg/g net weight. Lakes with pH levels below 7 produced fish with higher mercury concentrations (Lange et al, 1993).

Mercury concentrations in liver and kidney samples from harbor porpoises of the Norwegian coast varied from 0.15 to 9.9 mcg/g (Teigen et al, 1993).

Mercury accumulation was monitored in brown trout at 25 lakes in Norway. Elevated mercury levels in fish showed a positive correlation to lakes having high atmospheric mercury deposition and high humic material content in sediment (Fjeld & Rognerud, 1993).

The mean mercury level in flesh from 48 black cardinalfish (Epigonus telescopus) caught off New Zealand's east coast in 1990 was 1.47 mg/kg (Tracey, 1993).

Acidification of a body of water may increase mercury residues in fish even in the absence of additional mercury input, possibly because lower pH increases ventilation rate and membrane permeability, accelerates the rates of methylation and uptake, affects partitioning between sediment and water, or reduces growth or reproduction of fish (HSDB, 2005).

Mercury, pesticides, and PCBs levels in French flounder muscle are strongly correlated according to findings from the French Mussel Watch Program. The study concluded that flounder muscle is a valid tool for monitoring chemical contamination in coastal areas. Mercury was the only metal shown to accumulate in flounder muscle tissue in this study (Cossa et al, 1992).

Mercury's biological half-life in fish is approximately 2 to 3 years (HSDB, 2005).

Mercury concentrations in waterfowl (duck and geese) kidney and liver often exceed 0.5 ppm (the FDA limit). Levels in waterfowl muscle tissues are generally lower (CHRIS, 2005).

Results from a worldwide heron and cattle egret study showed mercury concentrations were twelve times higher in egrets at the Aswan versus Cairo sites. Results suggest feather analysis is a sensitive method for monitoring metals in local breeding colonies of cattle egrets (Burger et al, 1992).

Liver and visceral fat samples from 86 cormorants on Lake Kariba in 1986 had as much as 13.6 mg/kg of mercury. These levels did not increase mortality risk (Douthwaite et al, 1992).

Researchers monitored mercury and PCBs in livers from five predatory bird species over a 28-year period (1963 to 1990) in Britain. Test species included two raptors (sparrowhawk, kestrel) and three piscivores (heron, kingfisher, great-crested grebe). Findings showed sparrowhawks had higher contaminant levels than kestrels, and herons and great-crested grebes had the highest PCB and mercury levels (Newton & Wyllie, 1992).

Adult bald eagles in the Columbia River estuary had higher mercury concentrations than juvenile birds, suggesting mercury accumulates over an eagle's lifetime (Anthony et al, 1993).

One study used breast feathers from common terns to compare heavy metal exposure in their summer versus winter habitats. Mercury levels in tern feathers from their northeastern U.S. habitat were higher than those from their South America wintering grounds (Burger et al, 1992).

According to one study, mercury concentrations are much higher in albatrosses than other seabirds. The higher mercury levels were attributed to natural sources and not industrial or agricultural emissions (Thompson et al, 1993).

Researchers measured mercury in body feathers from common terns of the North Sea German coast from the 1940s to the 1980s. During this time, mercury concentrations increased 380% in adult birds and 140% in young birds (Thompson et al, 1993).

AQUATIC

TERRESTRIAL

Aquatic Mammals

Terrestrial Mammals

INVERTEBRATES

Reported bioconcentration factors (BCFs) for mercury include 63,000 for freshwater fish, 100,000 for marine and freshwater invertebrates, and 10,000 for saltwater fish (HSDB, 2005).

Reported bioaccumulation factors for the mushroom, Pleurotus ostreatus, range from 65 to 140 when grown on compost with mercury levels up to 0.2 mg/kg (ATSDR, 2003).

Studies involving alligators of the Florida Everglades determined BCFs for adult alligators of 10.5 x 10(7) and 9.34 x 10(7) for juveniles. BCFs specific to liver and kidney tissues were calculated at 39.9 x 10(7) and 32.9 x 10(7), respectively. Adult alligators (aged 7 to 14 years) had approximately 70% more mercury in their kidney and liver tissues and 40% more mercury in their muscle tissue than juveniles (<4 years old) living under identical conditions (Khan & Tansel, 2000).

A field study on Great tit (Parus major) nestlings examined possible toxic effects from heavy metals exposure on bird condition and health. Sampling occurred along a pollution gradient (0-4000 m) near a large non-ferrous smelter in Belgium over three consecutive breeding seasons. Nestlings' excrement from nest sites nearest the smelter had significantly higher mercury, arsenic, cadmium, lead, and silver concentrations than that from farther nest sites (Janssens et al, 2003).

Researchers used Brassica rapa to monitor plant mercury contamination from a sandy soil. Bloom initiation was slowed at soil mercury levels below 10 mg/kg (Sheppard et al, 1993).

Western grebe (Aechmophorus occidentalis) mortality occurred at Lake Berryessa, Napa County, California in 1982 and 1986. Residue analyses on bird kidney and liver tissues indicated mercury was present at hazardous levels (>20 ppm, wet weight) (Littrell, 1991).

The 50% inhibitory concentration (IC50) of mercury for the bacterium, Pseudomonas fluorescens, was calculated from bioassay data. IC50 values varied between 1.48 and 14.54 mcg/L of mercury (+2) ions (Farrell et al, 1993).

The marine annelid, Nerilla antennata, was used in short term tests at various levels of mercury. Teratogenic effects were found and included morphological anomalies of the cephalic appendages (Magagnini, 1993).

Soil mercury concentrations at 50 ppm impede plant growth. Soil mercury levels >1000 ppm are considered toxic (HSDB, 2005).

FRESHWATER TOXICITY

SALTWATER TOXICITY

OTHER

13.6 (metal) (NIOSH , 2002)

13.59 ((OHM/TADS, 2002))

13.546 (Bingham et al, 2001)

(25 degrees C; 77 degrees F and 760 mmHg)

13.534 g/cm(3) (at 25 degrees C) (Budavari, 2000; Lewis, 2000)

13.59 g/cm(3) (Lewis, 1997)

-38.9 degrees C (-38.0 degrees F; 234.3 K)(CHRIS , 2002; NIOSH , 2002)

-38.85 degrees C(Lewis, 1997)

-39 degrees C (-38.2 degrees F)(Harbison, 1998)

-38.87 degrees C (ACGIH, 1996a; Budavari, 2000; OHM/TADS, 2002; Zenz, 1994a)

-38.88 degrees C (ITI, 1995)

-38.89 degrees C (Lewis, 2000a)

-39 degrees C (Ashford, 1994)

Not applicable (NIOSH , 2002)

Not applicable (NIOSH , 2002)

Mercury is only slightly soluble in water. Solubility in water is 0.28 micromoles/L (at 25 degrees C) (Budavari, 2000).

56 micrograms/L (at 25 degrees C) (Bingham et al, 2001)

Mercury is insoluble in water (ITI, 1995; NIOSH , 2002).

0.28 umoles/l (at 25 degrees C) ((HSDB, 2002))

Mercury is insoluble in alcohol and ether ((HSDB, 2002); ITI, 1995; Lewis, 1997).

2.7 mg/L in pentane ((HSDB, 2002))

It is readily soluble in nitric acid, lipids, and is soluble in boiling sulfuric acid and lipids ((HSDB, 2002); ITI, 1995; Lewis, 1997).

Mercury is insoluble in hydrochloric acid, hydrogen bromide, hydrogen iodide, cold sulfuric acid (ITI, 1995; Lewis, 1997).

odorless ((HSDB, 2002))

23,300 psia (1587 atm; 160.8 MN/m(2)) (CHRIS , 2002; (HSDB, 2002))

1462 degrees C (2664 degrees F; 1735 K) (CHRIS , 2002; (HSDB, 2002))

2.7 cal/g (CHRIS , 2002; (HSDB, 2002))

1.6 to 1.9 (at 20 degrees C) ((HSDB, 2002))

1.55 mPa.sec (15.5 millipose) (at 20 degrees C) ((HSDB, 2002))