a) Elemental mercury is not used as a therapeutic agent, but may occur in some medical instruments or in dental settings in which mercury vapor from dental amalgams may occur. Inhalation of elemental mercury vapor can result in toxicity. Acute toxicity is less likely to occur from other common routes of exposure unless the mercury is converted to an ionized form by acids or strong oxidants.
b) Elemental mercury (vapor) is a RESPIRATORY TRACT, CNS, and RENAL HAZARD. Adverse effects involving the eyes, skin, gingiva, and other organs may occur.

a) MERCURY VAPOR - exposure can result from breaking of mercury fluorescent light bulbs (Yang et al, 1994; Tunnessen et al, 1987), heating of mercury-gold amalgams in order to extract gold (Kanluen & Gottlieb, 1991), and the use of mercury-containing latex paint (Agocs et al, 1990) or building materials and vacuuming of carpet contaminated with mercury ((ATSDR, 1999)). Ingestion or handling of liquid mercury following breakage of thermometers or other mercury-containing devices are other sources of exposure ((ATSDR, 1999)).
b) Insertion or removal of dental amalgam restorations can generate mercury vapor or respirable particulates (Nimmo et al, 1990; Eley & Cox, 1993; Powell et al, 1994; US DHHS, 1992). Mercuric ions may also be produced during the life of a restoration (Eley & Cox, 1993) or with the use of whitening agents (Hummert et al, 1993). Bruxism, chewing (food or gum {in particular long-term use of nicotine chewing gum} and tooth brushing may increase amalgam release of mercury vapor (Goering et al, 1992; Clarkson et al, 2003).
c) FLUORESCENT LIGHT BULBS - Fluorescent light bulbs contain a very small amount (4 to 6 mg) of mercury inside a glass tubing. In contrast, a thermometer contains about 500 mg of mercury. Health effects are not expected from acute exposure to a broken bulb.The EPA recommends the following clean-up and disposal guidelines if these bulbs are dropped or broken (US Environmental Protection Agency, 2007; US Environmental Protection Agency, 2007):
d) THERMOMETERS/INADVERTENT EXPOSURE - Elevated urine mercury levels have been seen in children of thermometer plant workers, presumably because of contamination of workers' clothing with elemental mercury which was then brought home (Hudson et al, 1987).
e) THERMOSTATS: Elevated blood and urine concentrations (55 mcg/L and 15 mcg/mL, respectively) were reported in a man who injected himself with mercury obtained from a thermostat or thermometer (Tae et al, 2015).
f) OCCUPATIONAL/DENTAL WORKERS - The use of silver amalgams can result in exposure to mercury vapor. Various studies over the past several decades have analyzed the potential health effects of long-term exposure. The potential risks of long-term low dose exposure continues to be debated in the literature. A recent concern is that long-term exposure to low concentrations of mercury vapor from amalgams can either cause or exacerbate degenerative diseases, such as amyotrophic lateral sclerosis, Alzheimer's disease, multiple sclerosis, and Parkinson's disease. At present, reviews of epidemiological evidence do not indicate an association (Bates, 2006; Clarkson et al, 2003). A more recent study of dental nurses exposed to silver amalgam 30 years previously found no differences in neurobehavioral test scores compared to controls. Overall, self-reported health status was similar between groups (Jones et al, 2007).
g) BAROMETERS - Several children developed mercury poisoning after exposure to mercury containing devices (barometers that had been broken) found in school settings (Koyun et al, 2004).
h) INTENTIONAL INGESTION of mercury occurs when it is used by some religious practitioners as a folk remedy for "empacho," a chronic stomach disorder or for other religious, ethnic or ritualistic practices ((ATSDR, 1999); Geffner & Sandler, 1980).
i) MEDICAL EQUIPMENT/FEEDING TUBE - Peritoneal exposure to elemental mercury from the use of intestinal feeding tubes (rupture of the weighted portion has resulted in spillage of mercury into the peritoneal cavity) has occurred rarely (Haas et al, 2003).
j) DOMESTIC EXPOSURE/INHALATION - In recent years, power companies in the US have attempted to replace pressure-control devices for domestic gas supply and inadvertent spills of liquid mercury have occurred in several incidences. Quicksilver (liquid metallic mercury), may still be found in homes in developing countries. It is used in cultural and religious ceremonies within the home (sprinkling mercury on floors or a car, burning it in candles or mixing it with perfume) (Hryhorczuk et al, 2006; Clarkson et al, 2003).
k) MEDICAL PROCEDURE - Mercury emboli have occurred during some cardiac catheterization procedures (Gosselin et al, 1984).
l) INHALATION of smoke from heated lime bricks which contained elemental mercury has also been reported (Mohan et al, 1994).
m) An estimated 70,000 to 150,000 workers in the United States are exposed to mercury (various forms) on a regular basis. Occupations which have the greatest exposure to mercury vapors include mining and processing of cinnabar ore, the chlor-alkali industry, and occupations in which mercury-containing instruments or materials are manufactured or handled (Bingham et al, 2001; IARC, 1997).
n) Dietary exposure to mercury (in the form of methyl mercury {organic mercury exposure}) occurs mainly from consumption of fish, shellfish and marine mammals ((ATSDR, 1999); IARC, 1997). Edible mushrooms may also contribute to dietary mercury exposure ((ATSDR, 1999)). See MERCURY, ORGANIC topic for further information.

1) Barometers, thermometers, thermostats, hydrometers, pyrometers, sphygmomanometers
2) Boilers, propellant, Miller Abbott tubes
3) Electrolytic production of chlorine and caustic soda (chlor-alkali industry)
4) Fluorescent lamps, mercury arc lamps, switches, dry-cell batteries
5) Gold mining, coolant, mirror coating, and as a neutron absorber in nuclear power plants
6) Laboratory, agricultural and pharmaceutical chemicals (as an ingredient in many pharmaceuticals, diuretics, antiseptics)
7) Manufacture of mercury cells and all mercury salts
8) Pesticide and fungicide production

1) 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.
2) 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.
3) 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.
4) 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.

1) INGESTION: Ingestion usually does not result in acute toxicity since elemental mercury is poorly absorbed. Obtain an x-ray to document its presence and course. Whole bowel irrigation may assist in cases of large volume ingestion, prolonged retention, mucosal inflammation, or fistula. Surgical removal is almost never needed. Postural drainage or suctioning may aid in the removal of aspirated elemental mercury.
2) INHALATION: Inhalation is the prime source of significant toxicity, especially after vaporization from heating or vacuuming spills. Ventilate the area for 15 minutes and pick up mercury globules with cardboard or duct tape. If vacuuming is required, discard the bag in 2 sealed plastic bags immediately after use. Thermometers contain about 500 mg of mercury and can cause significant injury if vaporized by vacuuming. Move the patient to fresh air. Monitor for respiratory distress and hypoxia. Give 100% humidified oxygen, intubate, and assist ventilation as needed. Administer beta-2 adrenergic agonists for bronchospasm. Severe pulmonary toxicity may mandate admission to an intensive care unit for meticulous supportive care and respiratory management.
3) INTRAVENOUS or INTRAMUSCULAR: IV or IM injection usually requires only supportive care.

1) PREHOSPITAL: Irrigate the eyes and ski, if exposed. Remove contaminated clothing. Move the patient to fresh air. No charcoal is needed.
2) HOSPITAL: Whole bowel irrigation may assist in cases of large volume ingestion, prolonged retention, mucosal inflammation, or fistula. Surgical removal is almost never needed.

1) Manage the airway as needed. Inhalational exposure is the main determinant of pulmonary disease.

1) Chelation has been used to facilitate elemental mercury removal, but clear data showing improved clinical outcomes are lacking. Chelation should be performed in patients with severe symptoms after acute exposure, and should be considered in patients who are symptomatic after chronic exposure. Asymptomatic patients with elevated urinary mercury concentrations probably do not warrant chelation. Mercury chelators include primarily succimer (given orally and most often used for chronic poisoning), dimercaprol (administered IM, used in patients with severe acute poisoning), and unithiol (used in Europe and available from compounding pharmacies in the United States, can be given IV for severe acute poisoning or orally for less severe or chronic poisoining), but D-penicillamine, and N-acetyl penicillamine have also been used.
2) Parenteral chelation (intramuscular Dimercaprol (BAL) or intravenous unithiol) therapy should be initiated in patients with significant acute exposures (acute inhalation with pulmonary, GI or neurologic effects). BAL is given in decreasing doses over 10 days if the patient is unable to take oral medications. The dosing schedule is as follows: 5 mg/kg initially, followed by 2.5 mg/kg 1 or 2 times daily for 10 days. When the patient is improving and able to tolerate oral medications, BAL can be replaced with succimer with no waiting period between treatments. Succimer may given based on the following dosing schedule: 1) 10 mg/kg orally 3 times daily for 5 days then 2) 10 mg/kg 2 times daily for 14 days. Succimer may be used alone in chronically exposed patients. Unithiol (2,3-dimercaptopropanol-sulfonic acid, DMPS) is available through compounding pharmacies in the United States. It is a water-soluble analog of BAL, and can be given orally or parenterally. It is considered a better mercury chelator than succimer. Unithiol is dosed as follows: IV: Day one 250 mg/kg every 3 to 4 hours, day two 250 mg every 4 to 6 hours, day three 250 mg every 6 to 8 hours, day four 250 mg every 8 to 12 hours, days five and six: 250 mg every 8 to 24 hours. Depending on the patient's clinical status, therapy may be changed to the oral route after the fifth day: 100 to 300 mg 3 times daily. ORAL: Initially 1200 mg to 2400 mg every 24 hours divided (100 mg or 200 mg every 2 hours), reduce to 100 mg to 300 mg every 8 hours as tolerated. Patients should be treated for 14 days or until there is no mercury detected in the urine.

1) There is no role for hemodialysis or hemoperfusion.

1) HOME CRITERIA: Asymptomatic patients with brief, , low-dose vapor exposures, tract may be observed at home. Patients with unintentional ingestion of less than the amount of mercury in a fever thermometer who do not have abdominal pain can be observed at home. They may be referred to their physician at a convenient time for an x-ray to document the mercury's course after ingestion. If a small mercury spill has been vacuumed or swept the health department should be notified to perform environmental monitoring and the patient referred for evaluation if ambient concentrations are high.
2) OBSERVATION CRITERIA: The following patients should be referred to a healthcare facility for observation and treatment: patients with suspected self-harm, abuse, or malicious use of elemental mercury; patients with symptoms of acute (eg, cough, dyspnea, chest pain) or chronic (eg, rash, tremor, weight loss) exposure to elemental mercury; exposure to recently heated (eg, stove top, oven, furnace) elemental mercury; patients exposed to documented high air mercury concentrations; patients who ingested more mercury than in a household fever thermometer or those with abdominal pain after ingestion; patients with elemental mercury deposited or injected into soft tissue. Observe patients with inhalation exposure for 6 to 12 hours for respiratory disease progression. The results of blood and urine mercury concentrations (usually require an outside laboratory analysis) will not influence acute care.
3) ADMISSION CRITERIA: Any symptomatic patient (dyspnea, hypoxia, wheezes, gastrointestinal complaints) should be admitted to the intensive care unit. Patients with chronic exposure should be removed from exposure and chelated if symptomatic; this may require admission.
4) CONSULT CRITERIA: Consult a toxicologist for assistance in managing patients with mercury toxicity.

1) Misidentification of the type of mercury exposure (elemental, inorganic, organic). Recent seafood consumption will elevate urinary mercury concentration.

1) Absorption is negligible (0.1%) in a normal gastrointestinal tract, but increases with mucosal breaks and with prolonged contact due to increased chances for oxidation to more readily absorbed inorganic forms. It is well absorbed via inhalation. It distributes to the kidneys and CNS, and is cleared by renal and gastrointestinal routes with an elimination half-life of about 30 to 60 days.

1) Occupational exposure, hobbies involving gold extraction, and folk medicine may predispose to toxicity.

1) Pheochromocytoma; Kawasaki's disease; brucellosis; Creutzfeldt-Jakob disease.

1) Allergic contact dermatitis may result from repeated or prolonged skin contact. Skin absorption of elemental mercury is limited.

1) CHRONIC EXPOSURE: Discoloration of the lens, corneal opacity, band keratopathy, and impaired vision may occur with chronic exposure. Nasal irritation, epistaxis, gingivitis, stomatitis, tremor of the tongue, and disturbed sense of taste and smell may develop. Speech defects may occur in severe cases of chronic mercury exposure (Gosselin et al, 1984; Yang et al, 1994).

1) MERCURY DEPOSITION
2) CONJUNCTIVITIS
3) EYELID TREMORS
4) MERCURIALENTIS
5) PAPILLEDEMA
6) EFFECTS OF LONG TERM EXPOSURE
7) EFFECTS OF INJECTED MERCURY
8) CHRONIC EXPOSURE
9) COLOR VISION DISTURBANCE
10) INTRAOCULAR MERCURY INJECTION

1) Dark spots or dark bluish lines along the gums may develop (Gosselin et al, 1984; Yang et al, 1994).
2) CASE REPORT: A 15-month-old girl with severe mercury poisoning developed gingivitis and premature exfoliation of her primary teeth associated with necrotic mandibular bone (Martin et al, 1997).
3) Oral hypersensitivity to mercury in amalgams may mimic lichen planus (Camisa et al, 1999; Laine et al, 1999).

1) WITH POISONING/EXPOSURE

1) WITH POISONING/EXPOSURE

1) WITH POISONING/EXPOSURE

1) Mercury embolization to the lungs and heart and cardiac granulomas were reported at autopsy in a 24-year-old man who had intravenously injected elemental mercury 5 months prior to his death from narcotic overdose (Kedziora & Duflou, 1995).
2) Mercury emboli were detectable (via CT scan) in the right ventricle and coronary artery of a 27-year-old man following intravenous injection of 1.5 mL elemental mercury. The right ventricular deposits were still present on repeat CT 66 days later (Eyer et al, 2006).
3) CASE REPORT: A 40-year-old man developed dyspnea, fever, tachycardia, and mild gastrointestinal disturbances after the intravenous injection of 3 mL of elemental mercury and ingestion of 3 mL in a suicide attempt. Chest X-ray showed scattered pulmonary infiltrates and embolized mercury bilaterally. In addition, he had minor elevations in BUN and serum creatinine and decreased urine output. Following chelation therapy, his pulmonary and renal functions improved over the next 36 hours (McFee & Caraccio, 2001).

1) WITH POISONING/EXPOSURE

1) Hemoptysis, cyanosis, cough, chest tightness, pneumonitis, necrotizing bronchiolitis and pulmonary edema have occurred following vapor inhalation (Zimmerman, 1969; Tsuji et al, 1970; Tennant et al, 1961; Kanluen & Gottlieb, 1991; US DHHS, 1992; Mohan et al, 1994; Anon, 2005).
2) Children less than 30 months of age may be at increased risk of adverse pulmonary effects following vapor exposure (US DHHS, 1992).
3) CASE REPORT: A 62-year-old man developed cough, dyspnea, and lethargy after attempting to extract gold from an amalgam containing mercury by heating the amalgam in an aluminum pan. He was exposed for 3 hours via fumes and through direct skin contact. A chest x-ray revealed extensive alveolar shadowing indicating pneumonitis. Laboratory findings revealed blood mercury concentration of 5933 nmol/L (level of concern: greater than 70 nmol/L), an elevated white cell count (16.3 x 10(9)/L, reference interval [RI]: 4 to 11 x 10(9)/L), a platelet count of 617 x 10(9) (RI 150 to 400 x 10(9)/L), an abnormal serum albumin concentration (21 g/L, RI: 34 to 48 g/L), and mildly elevated liver enzymes. A urinalysis revealed a mercury concentration of 7556 nmol/L and the mercury:creatinine ratio of 2519 nmol/mmol (level of concern: greater than 5.8 nmol/mmol). Following supportive care, including treatment with dimercaptosuccinic acid (DMSA) (800 mg 3 times daily for 7 days followed by a dose reduction to 800 mg twice daily for an additional 14 days) and prednisolone (50 mg daily with a gradual dose taper down to zero over 3 weeks), his symptoms gradually resolved. A 3-week re-assessment showed ongoing elevated blood mercury concentrations (blood mercury 418 nmol/L), therefore he was re-challenged with DMSA 800 mg 3 times daily for 34 days (starting 66 days after exposure). Despite the improvement of symptoms following prolonged course of DMSA, he re-presented with fatigue, increasing peripheral edema, nausea, and vomiting. Biochemical analysis revealed severe nephrotic syndrome and he was subsequently treated with prednisolone, regular infusions of concentrated albumin, diuretics, and was restricted to 1.2 L of fluids daily. His condition gradually normalized over the next 4 months (Saleem et al, 2013).

1) Acute lung injury may occur following an acute inhalation of fumes from heated elemental mercury. Patients may present with fever, cough, dyspnea, chest pain, erythematous rash, itching, chills, gastrointestinal complaints, metallic taste, headache, and weakness (Cicek-Senturk et al, 2014).
2) CASE REPORT: One study reported bilateral pneumothoraces, and pulmonary findings similar to those of ARDS, in a 3-month-old following inhalation of mercury vapors. The infant's grandfather had been heating mercury over the kitchen stove in order to extract gold from gold ore. The infant developed tachypnea and irritability 4 hours after the gold extraction process (Moromisato et al, 1994).
3) ARDS and fatal respiratory failure developed in 4 adults exposed to heated mercury vapor after trying to extract silver from dental amalgam in their home (Rowens et al, 1991; Taueg et al, 1992).
4) CASE SERIES: A family, including 2 adults (ages of 38 years and 58 years) and 6 children (ranging in ages of 45 days to 14 years), developed respiratory symptoms, becoming subsequently fatal in two cases, after inhaling mercury vapors resulting from home gold ore processing. The spot urine mercury levels in the 8 family members ranged from 27 mcg/L to 682 mcg/L. The blood mercury levels in 4 of the 8 family members ranged from 117 mcg/L to 322 mcg/L (Solis et al, 2000).
5) CASE REPORT: A 2.5-year-old boy developed lethargy and respiratory distress after exposure to mercury vapor. On presentation, he had mild dyspnea, tachypnea (a respiratory rate of 45/min) and an oxygen saturation of 88%. Blood gas analysis showed mild respiratory acidosis. His blood mercury level was 512 mcg/L and random urine mercury level was 165 mcg/L. A chest x-ray showed bilateral paracardiac infiltration with hyperinflation. Following supportive care, including treatment with D-penicillamine, NAC, and multivitamins, he recovered gradually (Sevketoglu et al, 2011).
6) CASE REPORT: A 14-year-old boy presented with a 2-week history of fever, body rash, nausea, and vomiting. His vital signs included a body temperature of 39 degrees C, heart rate of 104 beats/min, respiratory rate of 30 breaths/min, and a blood pressure of 110/55 mmHg. Physical examination revealed a widespread maculopapular rash on his trunk and all limbs, pink and swollen palms and soles, desquamation of his fingertips, and bilateral nonpurulent conjunctivitis. He was admitted for concerns of respiratory failure and received ceftriaxone and clarithromycin; however, his condition deteriorated over the next 5 days. At this time, his mother was also hospitalized with similar symptoms. Laboratory results revealed a blood mercury concentration of 311 mcg/L (reference range, 0.1 to 20 mcg/L) and a 24-hour urine mercury concentration of 130 mcg/L (reference range, 0.6 to 59 mcg/L). At this time, he admitted to bringing mercury from school chemistry laboratory to his home. Initially, he was treated with d-penicillamine (30 mg/kg/day), but his blood and urine mercury concentrations remained high. Following treatment with dimercaptosuccinic acid (DMSA), his blood and urine mercury concentrations normalized and his symptoms resolved (Tezer et al, 2012).

1) Aspiration of elemental mercury may result in hemoptysis, cyanosis, pneumonitis and respiratory distress.
2) Chronic respiratory disease may occur as a result of mercury aspiration. Radiographs may show mercury droplets at the lung bases (Janus & Klein, 1982).

1) INTRAVENOUS INJECTION: 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).
2) CASE REPORT: A 20-year-old man presented with chest pain, fever, and hemoptysis 3 months after injecting approximately 5 mL of elemental mercury subcutaneously into his left forearm and 7 days after injecting 8 to 10 mL of elemental mercury intravenously. Multiple tiny metallic densities in the soft tissues at the site of the subQ injection were observed in the plain radiography of the left forearm. A chest radiograph showed multiple tiny, discrete, metallic densities throughout the lung parenchyma bilaterally, predominantly at the lung bases, as well as at both pulmonary hila and at both cardiophrenic angles. He was treated with penicillamine for a few months. Six weeks after presentation, a chest radiograph revealed some diminution in the quantity of mercury deposits in the lungs (Wale et al, 2010).

1) Severe, acute exposures may result in residual restrictive pulmonary disease and fibrosis (Sue, 1994).

1) Intravenous injection of mercury with microemboli was associated with normal ventilatory function but decreased diffusing capacity of carbon monoxide and arterial oxygen tension in one patient (dell'Omo et al, 1996).
2) INHALATION: Permanent impairment of pulmonary function may occur following elemental mercury inhalation despite chelation therapy (Lilis et al, 1985; Levin et al, 1988).
3) CASE REPORT: A 40-year-old man developed dyspnea and tachypnea 24 hours after IV injection of approximately 40 g (3 mL) elemental mercury and the ingestion of 3 mL of mercury in a suicide attempt. The patient was hypoxic (pO2 60.9 mm Hg) and pulmonary function testing was consistent with a restrictive lung disease pattern (McFee & Caraccio, 2001).
4) CASE REPORT: A 23-year-old woman presented with dyspnea after injecting herself with 5 mL of elemental mercury. All pulmonary function tests were normal. Following treatment with D-penicillamine for 12 days, she was discharged. She developed disabling generalized myoclonus of cortical origin and gait ataxia 2 years after the initial exposure. At this time, her serum mercury was 6 mcg/dL (normal, 0.06 to 5.9 mcg/dL) and urinary mercury levels were markedly high (80.0 mcg/L; normal, less than 20 mcg/L). The pulmonary function tests showed a restrictive lung disease. Her symptoms progressed over the next 2 years. A chest radiograph 4 years after the initial exposure revealed multiple radiopaque specks in the lungs and a chest CT revealed that elemental mercury was finely deposited along the pulmonary vessels. Her symptoms improved after the mercury deposits were cleared surgically from the injection site (Ragothaman et al, 2007).

1) WITH POISONING/EXPOSURE

1) Confused mental status has been reported following acute mercury vapor exposure. Neurological signs and symptoms are chiefly associated with chronic exposure (Mohan et al, 1994).
2) Effects include personality changes, tremors (Schaumburg et al, 2009; Celebi et al, 2008; van der Linde et al, 2009; Chapman et al, 1990), headache, short term memory loss, poor appetite, shyness, insomnia, emotional lability, paresthesias, weakness (Gencpinar et al, 2015; Abbaslou & Zaman, 2006; Yeates & Mortensen, 1994; Lu et al, 1998) and nerve conduction delays (Rosenmann et al, 1986; US DHHS, 1992).
3) CASE REPORT: Behavioral disturbances (periodic confusion, aggression, confabulations, and secondary encopresis, alternating with normal behavior) developed in an 11-year-old girl who also experienced extensive gingival ulceration, loss of 6 teeth, acrodynia, back pain, anorexia, weight loss, fatigue, tremor, and hypertension following exposure to mercury from a broken industrial thermostatic clock. All laboratory results were normal except for a C-reactive protein of 98 mg/L. Following chelation therapy with DMPS for 9 weeks, she recovered gradually (van der Linde et al, 2009).
4) CASE REPORT: A 2.5-year-old boy developed lethargy and respiratory distress after exposure to mercury vapors. Following supportive care, including treatment with D-penicillamine, NAC, and multivitamins, he recovered gradually (Sevketoglu et al, 2011).

1) NEUROPSYCHOLOGICAL - Subtle neurological changes in visual-motor function have been associated with elemental mercury exposure (Bluhm et al, 1992a; Lu et al, 1998). Irritability, fatigue, insomnia (Gencpinar et al, 2015; Florentine & Sanfilippo, 1991; Piikivi et al, 1984; Yeates & Mortensen, 1994), depression, and short term auditory memory impairment (Soleo et al, 1990) have been reported.
2) Self-reported symptoms of 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). The differences in reported tiredness and memory disturbances were statistically significant.
3) Significantly higher symptoms of fatigue and confusion were reported by workers in a fluorescent lamp factory, when compared to controls (Liang et al, 1993). Individuals in the mercury exposed group had statistically significant decrements in performance of some tasks which involved mental arithmetic, two digit searching, attention switching, visual skills, and finger tapping.
4) Persistent short-term memory defects, increased reaction time, and defects in motor coordination were seen in a group of former mercury miners, compared with a matched control group, approximately 18 years after the last exposure (Kishi et al, 1994).
5) Two adolescent children, aged 13 and 15 years, developed more severe neuropsychological symptoms from a 3-month exposure to mercury vapor than did adults under the same circumstances. Defects persisted for at least 1 year (Yeates & Mortensen, 1994).
6) Mercury poisoning from peritoneal contamination (rupture of a distal balloon weighted with elemental mercury, 10 mL) is reported in a 68-year-old female. Deficits in visuospatial functioning and hand/eye coordination was reported 27 months post exposure. Neurologic symptoms have shown a progression with increased fatigue, decreased memory, insomnia and mild tremor (Lu et al, 1998).
7) CASE REPORT: A 22-year-old woman presented with a 2-hour history of chest discomfort after injecting herself in the arm with an unknown amount of elemental mercury from 3 thermometers mixed with alcohol. Radiography and CT scans showed radiopaque deposits of mercury mainly in the middle and lower lobes of the lungs bilaterally and in the pericardium, intestine, kidneys, and liver. Laboratory results revealed urine mercury concentrations greater than 60 mcg/L (nontoxic levels: less than 10 mcg/L) and blood concentrations greater than 35 mcg/L (nontoxic levels: less than 6 mcg/L). Despite normal vital signs for 2 to 3 hours, her mental status deteriorated with confusion, disorientation, tremor, and finally stupor (GCS score of 9). She also developed seizures and was treated with diazepam and valproate acid. Following supportive care, including treatment with a dimercaptosuccinic acid (DMSA)/succimer (800 mg orally 3 times daily for 5 days and 600 mg orally 3 times daily for 14 days) and phenytoin (125 mg IV 3 times daily), her mental status improved 2 hours after the initiation of treatment. CT scans of the thorax, abdomen, and brain revealed multiple radiopaque nodes in both lungs, a small pleural effusion, a few mercury deposits on the pericardium, and multiple deposits on the liver, left kidney, spleen and paraspinal muscles. She was discharged 20 days after presentation, but experienced several seizures during the next 6 months. On a 2-year followup, she was stable without additional seizures (Karatapanis et al, 2015).
8) DIFFERENTIAL DIAGNOSIS (CREUTZFELDT-JAKOB DISEASE): A 42-year-old man presented with a 5-month history of progressive memory disturbance (difficulty in recalling recent conversations), irritability, numbness and tingling in the limbs, slow movement, and sleepiness. Three months before presentation, an MRI of the brain revealed striking, relatively symmetric, high-intensity, diffusion-weighted imaging signals in the cortex without gadolinium enhancement. Slow overall activity was observed in an electroencephalograph. Despite normal results on CSF studies with normal 14-3-3 protein levels, a diagnosis of Creutzfeldt-Jakob disease was made. Although he was treated with IV methylprednisolone and oral prednisone, his condition worsened. On this visit, physical examination revealed prominent cognitive impairment and extrapyramidal features, with bilateral symmetric bradykinesia, cogwheel rigidity in the upper limbs, and impaired finger-nose coordination. A second MRI of the brain showed hyperintense diffusion-weighted imaging signals and hypointense apparent diffusion coefficient signals in the caudate nucleus and the frontal, temporal, and occipital cortices. Laboratory results revealed a blood mercury concentration of 76.3 nmol/L and a urinary mercury concentration of 109.2 nmol/L (reference range, 0 to 12.5 nmol/L). During questioning, it was revealed that the patient cleaned a broken mercury sphygmomanometer in his bed with a whisk broom several days before his symptoms started. Following treatment with sodium 2,3-dimercapto-1-propanesulfonic acid, his numbness and tingling decreased substantially, but memory and movement improved only slightly and no improvement was observed in a follow-up MRI. Persistent cognitive impairment and bradykinesia were observed on a follow-up visit 2 years later. At that time, he had a blood mercury concentration of 2.5 nmol/L and a urinary level of 5.5 nmol/L. An MRI continued to show damage (Tang et al, 2015).

1) WITH POISONING/EXPOSURE

1) WITH POISONING/EXPOSURE

1) WITH POISONING/EXPOSURE

1) WITH POISONING/EXPOSURE

1) WITH POISONING/EXPOSURE

1) WITH POISONING/EXPOSURE

1) WITH POISONING/EXPOSURE

1) INHALATION
2) INGESTION
3) INJECTION

1) WITH POISONING/EXPOSURE

1) Mild jaundice and abnormal liver function tests developed in an adult male six months after ingestion of metallic mercury. The individual was also chronically exposed to mercury in his occupation. The authors propose a contribution of slowly absorbed mercury to delayed hepatic dysfunction (Lin & Lim, 1993).
2) Hepatomegaly developed in a A 52-year-old woman after exposure to mercury fumes (Cicek-Senturk et al, 2014).

1) WITH POISONING/EXPOSURE

1) Proteinuria has been reported after acute mercury vapor exposure (Snodgrass et al, 1981; Karagol et al, 1998).

1) 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).
2) LACK OF EFFECT: 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).

1) WITH POISONING/EXPOSURE

1) 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).

1) WITH POISONING/EXPOSURE

1) WITH POISONING/EXPOSURE

1) WITH POISONING/EXPOSURE

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

1) 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).
2) CASE REPORT: 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 (hemoglobinemia less than 7.1 g/dL), and mild hepato-renal impairment, and died 30 days after presentation (DePalma et al, 2008).

1) 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).

1) WITH POISONING/EXPOSURE

1) WITH POISONING/EXPOSURE

1) WITH POISONING/EXPOSURE

1) WITH POISONING/EXPOSURE

1) WITH POISONING/EXPOSURE

1) WITH POISONING/EXPOSURE

1) WITH POISONING/EXPOSURE

1) CASE REPORT: A 41-year-old female with a history of schizophrenia intentionally subcutaneously injected metallic mercury into her wrist and antecubital fossa. The presence of mercury was confirmed by radiography and ultrasound scan and soft tissue injury was evident within 3 days of injection. Treatment included surgical intervention to remove the mercury streaks contained in the muscle belly and brachialis, as well as friable necrotic tissue that developed along the tract. Chelation therapy with dimercaprol and 2,3-dimercaptosuccinic acid was also performed due to elevated blood and urine levels. Blood mercury levels decreased from 101 to 151 nmol/L in the first two weeks of exposure to 42 nmol/L approximately 3 months later (Soo et al, 2003).
2) CASE REPORT: Membranous fat necrosis has been reported in an individual with intentional subcutaneous mercury injection (Ramdial et al, 1999).

1) WITH POISONING/EXPOSURE

1) Elevated blood and urinary mercury levels have been reported following intramuscular injection of metallic mercury (Makalinao et al, 1995).

1) WITH POISONING/EXPOSURE

1) WITH POISONING/EXPOSURE

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

1) WITH POISONING/EXPOSURE

1) GLOMERULONEPHRITIS
2) ANTINUCLEAR FACTOR TEST POSITIVE
3) WBC ABNORMAL

1) The possible effects on the human fetus as a result of elemental mercury exposure have not been thoroughly studied (US DHHS, 1992). The evidence linking elemental mercury exposure to developmental or teratogenic effects in humans is less clear than in the cases of organic mercury exposure. Many of the human studies have involved exposure to other chemicals in addition to elemental mercury.
2) There is evidence that mercury can cross the placenta and is excreted in breast milk. There have been some reports of adverse reproductive effects in human females and males exposed to elemental mercury.

1) Some animal studies have shown that vapors may cause embryotoxicity, fetotoxicity, and other adverse reproductive outcomes. The relevance of these studies to humans is unclear (US DHHS, 1992). There is little evidence of teratogenic effects due to elemental mercury. Several animal studies report adverse effects on male and female fertility or reproductive organs as a result of elemental mercury exposure.
2) Animal studies have reported adverse reproductive effects as a result of organic or inorganic (e.g. salts) mercury exposure.

1) SUMMARY - Studies concerning the effects of occupational exposure to elemental mercury during pregnancy have conflicting results.
2) A Finnish national study listed mercury among the substances associated with CNS defects, cleft palate, and skeletal defects (Kurppa et al, 1983).
3) A study of 209 mercury-exposed workers failed to find significant neuropathies associated with prenatal exposure (Klimkova-Deutschov, 1977).
4) A woman was exposed in the home to mercury vapor prior to pregnancy and through the 17th week of gestation (Thorp et al, 1992). Mercury concentrations in the home were 20 to 60 mcg/m(3).
5) Lien et al (1983) reported a case of acute mercury toxicity following vapor inhalation by a pregnant woman. Twenty-six days after the exposure, a child was born without clinical abnormalities, but with serum mercury levels comparable to those of the mother.
6) LIMITATIONS OF HUMAN STUDIES

1) CASE STUDIES
2) TRANSPLACENTAL HG TRANSFER
3) HUMAN STUDY LIMITATIONS
4) RISK FACTORS
5) ANIMAL STUDIES

1) RATS
2) MOUSE
3) MONKEYS

1) CASE REPORTS

1) Women exposed to mercury reportedly had anemia, early toxicosis, bleeding, prolonged labor, and lower birth weights (Vasileva, 1975; Mishonova et al, 1980; Gelbier & Ingram, 1989). Complicated pregnancies have been reported in another study of women with combined exposures to mercury, lead, benzene and carbon disulfide (Vasileva, 1975).

1) LIMITATIONS OF HUMAN STUDIES - Many of the human studies involve exposure to other chemicals in addition to mercury. The contribution of mercury alone to the adverse reproductive effects is difficult to determine.
2) The occupational studies reporting effects of mercury on the female reproductive system and on abortion incidence need further clarification as to the nature and extent of exposures (Barlow & Sullivan, 1982).

1) CASE REPORTS

1) Exposure of rats on day 7 to 20 of pregnancy has resulted in increased resorption of fetuses, pup growth retardation and 100% mortality of pups prior to weaning (Baranski, 1973).
2) Mercury vapor exposure resulted in changes in estrus cyclicity but no other changes in reproductive performance in rats (Davis et al, 2001). These changes occurred only at the highest dose tested (4 mg/m3 for 2 hours per day for 11 consecutive days) and was associated with weight loss.

1) In a study of 155 lactating Saudi mothers, the mean concentration of mercury in breast milk was 1.19 mcg/L (range, 0.012 to 6.44 mcg/L), with 57.4% (n=89) of mothers having mercury levels at or above 1 mcg/L, which is the background level for mercury in human milk. All mothers had total blood mercury concentrations below the US Environmental Protection Agency's maximum reference dose of 5.8 mcg/L. Mercury in breast milk was significantly correlated with mercury in maternal blood (p less than 0.001), suggesting efficient transfer of mercury from blood to milk. Measured as biomarkers of oxidative stress, urinary 8-hydroxy-2'-deoxyguanosine (8-OHdG) and malondialdehyde (MDA) increased with increasing levels of mercury in breast milk and urinary mercury levels in infants in a dose-related manner. Thus, the exposure to mercury in breastfed infants may induce oxidative stress and lead to pathogenesis of health problems, especially during neurodevelopment, in these infants (Al-Saleh et al, 2013).

1) Mercury has been found in human milk of exposed and unexposed women at about the same concentration found in cord blood (Mattison et al, 1983).
2) Gonzalez et al (1985) reported a significant correlation between total mercury concentrations measured in the hair of nursing neonates and the mercury levels determined in maternal samples.

1) GUINEA PIGS - Elemental mercury vapor at an airborne concentration of 6 to 9 mg/m(3) was transferred in the milk of guinea pigs to the offspring. Although speciation of the mercury present in the milk was not performed, tissue distribution made it likely that the mercury was inorganic rather than elemental (Yoshida et al, 1992).

1) IARC Classification

1) Mercury is classified as Group D (not classifiable as to human carcinogenicity) by IRIS, based on inadequate human and animal data ((IRIS, 2001)). It is listed with an A4 notation by the ACGIH, indicating it is not classifiable as a human carcinogen (ACGIH, 2000).

1) A borderline excess of lung cancer incidence was reported in Norwegian chloralkali workers exposed to mercury (Ellingsen et al, 1993a). Exposure to inorganic mercury in mines and mills does not seem to be strongly associated with cancer risk, with the possible exception of liver cancer (Boffetta et al, 1998).

1) There is sufficient evidence in experimental animals for the carcinogenicity of methylmercury chloride; methylmercury compounds are classified as Group 2B (possibly carcinogenic to humans)(IARC, 1997).

1) Mercury at a dose of 5 ppm in the drinking water was not carcinogenic in mice (Schroeder & Mitchener, 1975). Mercury given intraperitoneally to rats produced tumors at the site of application ((RTECS, 2001)).
2) Methylmercury chloride given in the diet produced renal tumors in male mice and no tumors in female mice. Mercuric chloride showed some evidence of carcinogenicity in male rats, but not in female mice; results in female rats and male mice were equivocal (Clayton & Clayton, 1994).

1) Blood level of mercury is a good indicator of recent exposure, as concentrations of mercury in whole blood rapidly rise after exposure (Barregard, 1993; Aks et al, 1995). The half-life for mercury in the blood is approximately 3 days (US DHHS, 1992).
2) LIMITATIONS : Blood analysis is useful only for detecting acute exposure immediately after it has occurred. Blood mercury levels often do not correlate well with clinical signs of toxicity (Aks et al, 1995). Some analytical methods do not distinguish between inorganic and organic mercury in biological samples (Knight, 1988).
3) NORMAL CONCENTRATIONS IN UNEXPOSED: Normal whole blood mercury levels rarely exceed 1.5 mcg/dL in unexposed adults (US DHHS, 1992).
4) CONCENTRATIONS ASSOCIATED WITH SYMPTOMS: Symptoms of toxicity may occur in some individuals at blood mercury concentrations of 5 mcg/dL or greater. Many individuals with high blood mercury levels do not exhibit clinical symptoms.
5) SEAFOOD: The use of blood mercury levels after acute exposure should be considered with the knowledge that a single seafood meal will elevate levels for 20 to 30 hours (Kershaw et al, 1980; Sherlock et al, 1984).
6) OTHER SERUM/BLOOD ASSAYS: The measurement of glomerular basement antibodies (alpha-GBMs) in serum is being studied as a biological indicator of chronic elemental mercury vapor exposure and effects (Ellingsen et al, 1993).

1) URINARY MERCURY is the best biological marker for chronic elemental or inorganic mercury exposure.
2) LIMITATIONS: Urinary mercury levels often do not correlate with clinical signs and symptoms of toxicity.
3) NORMAL CONCENTRATIONS IN UNEXPOSED INDIVIDUALS: Normal urine excretion rarely exceeds 15 mcg/L (74.7 nmol/L) in unexposed individuals. There is a high degree of intraindividual variation in urine mercury levels. The averaging of several urinary mercury determinations may be required (Barregard, 1993).
4) 24-HOUR URINE COLLECTION: A 24-hour urine specimen is preferred if chronic exposure to elemental mercury or mercury salts is suspected (US DHHS, 1992). Spot sample collecting can be used to approximate the 24-hour sample.
5) URINARY MERCURY FOLLOWING DENTAL PROCEDURE: Urinary concentrations of mercury were obtained in normal 5 to 7 year old children before and 9 to 12 days after dental work. Concentrations were 3.83 +/- 2.45 and 5.14 +/- 3.14 microg/L respectively (Khordi-Mood et al, 2001). Results did not correlate with age, sex, weight, or number of fillings placed.
6) SPOT MERCURY LEVELS: Methods of collecting spot samples to closely approximate the 24-hour collection and to avoid contamination are described by Barregard (1993). A first morning void can be used to approximate a 24-hour urine collection.

1) TOTAL MERCURY BODY BURDEN/CHELATION STUDIES: Chelation tests have been used to evaluate the body burden of mercury in individuals with non-specific symptoms who have dental amalgams in an attempt to confirm or refute mercury toxicity. In a small study (n=15), healthy volunteers were given a 30 mg/kg oral loading dose of dimercaptosuccinic acid (DMSA). Pre and post-DMSA urine samples were analyzed for mercury and creatinine. The findings were comparable with the mean concentrations found in previously reported studies with symptomatic subjects. One volunteer had an anaphylactoid response following DMSA administration.
2) Increased urinary excretion of mercury following chelation challenge should not be used as the sole basis for diagnosing mercury poisoning, particularly if further chelation treatment is to be considered (Risher & Amler, 2005).
3) 24 HOUR URINARY DELTA AMINOLEVULINIC ACID (ALA) levels are invariably elevated to 3 to 10 mg/L in chronic poisoning cases. Although urinary levels as high as 2000 mcg/L have been seen without symptoms, behavioral and neurological evaluation should be performed if levels are greater than 100 mcg/L (Adams et al, 1983).
4) TOTAL URINARY PROTEIN levels positively correlated with the level of blood and urinary mercury, and with the exposure duration (Abdelmegid et al, 1993). PROTEINURIA has been reported after acute and chronic mercury vapor exposure (Snodgrass et al, 1981) Rosenmann et al, 1986; Ehrenberg, 1991).
5) URINARY PORPHYRIN PROFILES may reflect renal mercury content and the biological effects of mercury in the kidney. Significant differences in urinary porphyrin levels among mercury exposed dentists, as compared to unexposed dentists, have been reported (Woods et al, 1993). However, Frumkin et al, (2001) could not demonstrate a correlation of exposure with urinary porphyrins in chloralkali workers. Mean precoproporphyrin and coproporphyrin concentrations were 1.5 to 2-fold higher in urine samples from the mercury exposed dentist than from the unexposed dentists, after adjusting for urinary creatinine. Changes in urinary porphyrins correlated better with urinary mercury concentrations when adjustments for urinary creatinine were NOT made (Frumkin et al, 2001).
6) ENZYMURIA is considered to represent renal tubule effects. N-acetyl beta-glucosaminidase (NAG) is a high molecular weight lysosomal enzyme that is a sensitive but nonspecific indicator of early renal injury. Elevations in urinary NAG levels have been associated with chronic low level mercury exposure (Rosenmann et al, 1986).
7) URINARY INTESTINAL ALKALINE PHOSPHATASE (IAP) is a marker of effects on the S3 segment of the renal proximal tubule, a site of mercury effects. An enzyme-antigen immunoassay with specific monoclonal antibodies to IAP has been developed.

1) HAIR
2) ELECTROPHYSIOLOGICAL TESTING
3) SALIVA
4) CEREBROSPINAL FLUID
5) MONITORING
6) NEUROPSYCHOLOGICAL TESTING

a) Even in patients without a fistula, mercury may remain in the appendix, producing inflammation (Birnbaum, 1947; Sawyer, 1967) and rupture (Crikelair & Hiratzka, 1953).

1) the patient has a history of known decreased GI transit or fistula
2) the patient has a history of inflammatory bowel disease
3) a large amount of mercury is ingested (greater than that contained in a household thermometer).

a) Oral laxatives and a laxative diet were provided, with follow-up radiographic studies to insure passage of the mercury. No symptomology and no increased mercury levels in the blood or urine were detected 6 weeks after the ingestion.

a) A procedure for determination of mercury in hair by cold vapor atomic absorption spectrometry with a new reaction vessel is suited for use with a large number of samples (Pineau et al, 1990).

a) The lower limit of detection was 10 mcg/mL in simulated stomach contents (soup) (Winstanley et al, 1987). This method may not detect mercury at quantities near a normal value.

a) Atomic absorption, gas chromatography, and reverse-phase high-performance liquid chromatography, are other methods which can be used to speciate the type of mercury in biological samples (IARC, 1993; Sallsten et al, 1994; Aks et al, 1995).
b) Other analytical methods typically used to quantitate mercury in biological tissues include neutron activation analysis, inductively coupled plasma emission spectrometry, and spark source spectrometry (IARC, 1993).
c) Simultaneous determination of inorganic, monomethyl, and total mercury can be accomplished in biological samples by digestion in methanolic potassium hydroxide, followed by ethylation and gas chromatography with cold vapor atomic fluorescence spectrometry (CVAFS). Limits of detection are 1.3 pg inorganic mercury and 0.6 pg monomethyl mercury (Liang et al, 1994).

A) Any symptomatic patient (dyspnea, hypoxia, wheezes, gastrointestinal complaints) should be admitted to the intensive care unit. Patients with chronic exposure should be removed from exposure and chelated if symptomatic; this may require admission.

A) (Caravati et al, 2008).

A) Consult a toxicologist for assistance in managing patients with mercury toxicity.

A) The following patients should be referred to a healthcare facility for observation and treatment: patients with suspected self-harm, abuse, or malicious use of elemental mercury; patients with symptoms of acute (eg, cough, dyspnea, chest pain) or chronic (eg, rash, tremor, weight loss) exposure to elemental mercury; exposure to recently heated (eg, stove top, oven, furnace) elemental mercury; patients exposed to documented high air mercury concentrations; patients who ingested more mercury than in a household fever thermometer or those with abdominal pain after ingestion; patients with elemental mercury deposited or injected into soft tissue. Observe patients with inhalation exposure for 6 to 12 hours for respiratory disease progression. The results of blood and urine mercury concentrations (usually require an outside laboratory analysis) will not influence acute care. (Caravati et al, 2008).

1) 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.

1) Whole bowel irrigation may assist in cases of large volume ingestion, prolonged retention, mucosal inflammation, or fistula. Surgical removal is almost never needed.
2) Liquid mercury released in the gastrointestinal tract will generally pass through without producing toxicity. An x-ray should probably be obtained to document its course. Elemental mercury will appear round, with a diameter of less than 1 mm to 3 mm (Martijn et al, 1990). These droplets may become smaller as they progress through the intestinal tract. Dental amalgam mercury is irregular in shape.

1) While activated charcoal is known to adsorb mercuric chloride, it is not known if it adsorbs elemental mercury. Activated charcoal and laxatives have been used in some cases of retained elemental mercury in the gastrointestinal tract (McKinney, 1999; Martijn et al, 1990).

1) Consider in patients at risk for poisoning after ingestion of elemental mercury (large ingestion, prolonged retention, inflammation of the GI mucosa, known fistula etc). Consider whole bowel irrigation in these cases.

1) Rarely, mercury may get hung up in the intestine and may require surgical removal (Cantor, 1951).

1) INGESTION: Ingestion usually does not result in acute toxicity since elemental mercury is poorly absorbed. Obtain an x-ray to document its presence and course. Whole bowel irrigation may assist in cases of large volume ingestion, prolonged retention, mucosal inflammation, or fistula. Surgical removal is almost never needed. Postural drainage or suctioning may aid in the removal of aspirated elemental mercury.
2) INHALATION: Inhalation is the prime source of significant toxicity, especially after vaporization from heating or vacuuming spills. Ventilate the area for 15 minutes and pick up mercury globules with cardboard or duct tape. If vacuuming is required, discard the bag in 2 sealed plastic bags immediately after use. Thermometers contain about 500 mg of mercury and can cause significant injury if vaporized by vacuuming. Move the patient to fresh air. Monitor for respiratory distress and hypoxia. Give 100% humidified oxygen, intubate, and assist ventilation as needed. Administer beta-2 adrenergic agonists for bronchospasm. Severe pulmonary toxicity may mandate admission to an intensive care unit for meticulous supportive care and respiratory management.
3) INTRAVENOUS or INTRAMUSCULAR: IV or IM injection usually requires only supportive care.
4) DIFFERENTIAL DIAGNOSIS: Pheochromocytoma; Kawasaki's disease; brucellosis; Creutzfeldt-Jakob disease (Tang et al, 2015; Sasan et al, 2012).

1) 24-hour urinary mercury concentration is the best marker for chronic exposure (a patient should abstain from eating seafood for a week or the placement of mercury amalgams for several weeks prior to collection). Whole blood mercury concentration may be useful for acute exposure. Specimen collection method is important to avoid contamination. A laboratory should use trace element collection tubes for blood samples and acid-washed containers for a 24-hour urine collection. Mercury levels of 10 mcg/L for whole blood and 20 mcg/L for urine typically reflect background exposure.
2) Monitor serum electrolytes, renal function, glucose, urinalysis and liver enzymes in symptomatic patients.
3) Monitor chest radiograph in patients with pulmonary symptoms.
4) Specific urine markers for renal injury should include beta-2 microglobulin, microalbuminuria, and retinol binding protein in symptomatic patients.
5) Postchelation mercury levels should not be utilized as the sole basis for the diagnosis of mercury poisoning and subsequent treatment. This is especially true if no baseline, prechelation concentration was measured.

1) Intraoperative removal of ingested elemental mercury is usually unnecessary and presents risks. Appendiceal mercury without signs of appendicitis is NOT an indication for intraoperative mercury removal. Peritoneal spillage of mercury may result as a risk of operative procedures.

1) Acute inhalation exposure to mercury vapor can produce local effects on the pulmonary system as well as systemic toxicity and elevated urine and blood mercury concentrations (Levin et al, 1988). Chelation may be required.
2) ACRODYNIA: Nifedipine 0.2 mg/kg four times daily initially, increasing to 0.2 mg/kg six times daily while monitoring blood pressure has been used to alleviate the pinkish skin color, extremity pain, anorexia, and proteinuria seen with acrodynia resulting from mercury poisoning (Ozsoylu, 1993).
3) PAIN MANAGEMENT: Severe neuropathic pain has been treated with a combination of carbamazepine (20 mg/kg per day) and pyridoxine (300 mg/day) (Karagol et al, 1998). The mechanism of pain relief of carbamazepine, a sodium-dependent channel blocker, appears to be longer-lasting decrease of repetitive discharges, increase of firing threshold and decreased hyperexcitability.

1) SUMMARY

1) EFFICACY
2) SUCCIMER/DOSE/ADMINISTRATION
3) MONITORING PARAMETERS
4) SUCCIMER/ADVERSE EFFECTS: The following adverse events have occurred in children and adults during clinical trials: nausea, vomiting and diarrhea; transient liver enzyme elevations; rash, pruritus; drowsiness and paresthesia. Events reported infrequently include: sore throat, rhinorrhea, mucosal vesicular eruption, thrombocytosis, eosinophilia, and mild to moderate neutropenia (Prod Info CHEMET(R) oral capsules, 2011).
5) ODOR: Succimer has a sulfurous odor that may be evident in the patient's breath or urine (Prod Info CHEMET(R) oral capsules, 2005).
6) HYPERTHERMIA: One adult developed acute severe hyperthermia associated with hypotension; rechallenge resulted in hyperthermia with shaking chills and hypertension (Marcus et al, 1991).
7) AVAILABLE FORMS: Succimer (Chemet (R)), 100 mg capsules (Prod Info CHEMET(R) oral capsules, 2011).

1) D-penicillamine has been shown to increase urinary mercury excretion in patients with acute and chronic poisoning from elemental mercury (Snodgrass et al, 1981; Yang et al, 1994; Ambre et al, 1977).
2) USUAL ADULT DOSE
3) USUAL PEDIATRIC DOSE
4) ADVERSE REACTIONS
5) DURATION OF THERAPY
6) CAUTIONS
7) PREGNANCY

1) DOSE: Oral N-acetyl penicillamine (NAP) 250 mg to 500 mg, 4 times a day for 6 to 10 days (30 mg/kg/day in children) has been associated with increased urinary mercury excretion and clinical improvement in patients with toxicity from exposure to elemental mercury (Kark et al, 1971; Hryhorczuk et al, 1982; Gledhill & Hopkins, 1972). NAP is still considered experimental.

1) DIMERCAPROL/BAL IN OIL: INDICATIONS: Used for the treatment of mercury (inorganic and elemental), arsenic, and gold poisoning. It is also used in combination with Edetate Calcium Disodium injection to treat patients with severe lead poisoning (Prod Info BAL In Oil intramuscular injection, 2008). Dimercaprol is contraindicated in methyl mercury poisoning (Howland, 2002; Clarkson, 1990).
2) MILD ARSENIC OR GOLD POISONING: DOSE: 2.5 mg/kg 4 times daily for 2 days, 2 times on the third day, and once daily thereafter for 10 days. SEVERE ARSENIC OR GOLD POISONING: DOSE: 3 mg/kg every 4 hours for 2 days, 4 times on the third day, then twice daily thereafter for 10 days. Administered by deep intramuscular injection only (Prod Info BAL In Oil intramuscular injection, 2008).
3) MERCURY POISONING: DOSE: 5 mg/kg initially, then 2.5 mg/kg 1 or 2 times daily for 10 days. Administered by deep intramuscular injection only (Prod Info BAL In Oil intramuscular injection, 2008).
4) ACUTE LEAD ENCEPHALOPATHY: DOSE: 4 mg/kg is given alone in the first dose and thereafter at 4-hour intervals with Edetate Calcium Disodium injection administered at a separate site. For less severe poisoning, dimercaprol dose can be decreased to 3 mg/kg after the first dose. Administered by deep intramuscular injection only. Continue the treatment for 2 to 7 days depending on clinical response (Prod Info BAL In Oil intramuscular injection, 2008). Therapy is generally switched to a less toxic oral chelator as soon as tolerated.
5) ADVERSE EFFECTS: Common effects include pain at the injection site and fever (especially in children). Other effects include hypertension, tachycardia, nausea, vomiting, headache, burning sensations of the mouth and throat, a sensation of constriction in the throat, chest, or hands, conjunctivitis, lacrimation, salivation, tingling of the extremities, diaphoresis, abdominal pain, and anxiety. Dimercaprol injection contains peanut oil. Avoid in patients with peanut allergy (Prod Info BAL In Oil intramuscular injection, 2008). Adverse effects are dose related; they develop in 1% of patients receiving 2.5 mg/kg every 4 to 6 hours, 14% of patients receiving 4 mg/kg every 4 to 6 hours and 65% of patients receiving 5 mg/kg every 4 to 6 hours (Eagle & Magnuson, 1946).
6) PRECAUTIONS: It is generally contraindicated in patients with hepatic insufficiency, with the exception of postarsenical jaundice (Prod Info BAL In Oil intramuscular injection, 2008). May cause hemolysis in G6PD deficient patients. BAL metal chelate disassociates in acid environment; urinary alkalinization is usually recommended. Do not administer with iron therapy as BAL iron complex may cause vomiting (Howland, 2002).
7) LABORATORY: Monitor urine mercury excretion during chelation therapy to assess the effects of therapy.
8) EFFICACY: Dimercaprol therapy was associated with increased urinary mercury excretion and decreased blood mercury levels in a 25-year-old male who injected elemental mercury intravenously (Murray & Hedgepeth, 1988).
9) RENAL FAILURE

1) DMPS/INDICATIONS: Chelating agent for heavy metal toxicities associated with arsenic, bismuth, copper, lead and mercury (Blanusa et al, 2005).
2) DMPS/DOSING
3) SOURCES
4) EFFICACY
5) Ashton et al (1992) reported a patient who injected approximately 270 grams of metal, was treated for 4 years, and survived. Blood mercury concentration was over 1600 mcg/L; urine levels over 73,500 mcg/L.
6) Administration of 300 mg of DMPS orally increased mean urinary mercury excretion of volunteers with dental amalgams from 0.7 to 17.2 mcg (Aposhian et al, 1992). DMPS has been shown to increase urinary mercury excretion after exposure to mercurous chloride and elemental mercury (Gonzales-Ramirez et al, 1995; Maiorino et al, 1996; Gonzales-Ramirez et al, 1998; Torres-Alanis et al, 1995).
7) ADVERSE REACTIONS

1) N-acetylcysteine (15 mg/kg/day) and chelation therapy were used in 21 children with mercury exposure and high mercury blood or urine concentrations. After about 2 weeks of therapy, all blood and urine mercury concentrations of 20 patients were in the reference range. One patient required about one month of continued chelation therapy (Akyildiz et al, 2012).

1) ONSET: Onset of acute lung injury after toxic exposure may be delayed up to 24 to 72 hours after exposure in some cases.
2) NON-PHARMACOLOGIC TREATMENT: The treatment of acute lung injury is primarily supportive (Cataletto, 2012). Maintain adequate ventilation and oxygenation with frequent monitoring of arterial blood gases and/or pulse oximetry. If a high FIO2 is required to maintain adequate oxygenation, mechanical ventilation and positive-end-expiratory pressure (PEEP) may be required; ventilation with small tidal volumes (6 mL/kg) is preferred if ARDS develops (Haas, 2011; Stolbach & Hoffman, 2011).
3) FLUIDS: Crystalloid solutions must be administered judiciously. Pulmonary artery monitoring may help. In general the pulmonary artery wedge pressure should be kept relatively low while still maintaining adequate cardiac output, blood pressure and urine output (Stolbach & Hoffman, 2011).
4) ANTIBIOTICS: Indicated only when there is evidence of infection (Artigas et al, 1998).
5) EXPERIMENTAL THERAPY: Partial liquid ventilation has shown promise in preliminary studies (Kollef & Schuster, 1995).
6) CALFACTANT: In a multicenter, randomized, blinded trial, endotracheal instillation of 2 doses of 80 mL/m(2) calfactant (35 mg/mL of phospholipid suspension in saline) in infants, children, and adolescents with acute lung injury resulted in acute improvement in oxygenation and lower mortality; however, no significant decrease in the course of respiratory failure measured by duration of ventilator therapy, intensive care unit, or hospital stay was noted. Adverse effects (transient hypoxia and hypotension) were more frequent in calfactant patients, but these effects were mild and did not require withdrawal from the study (Wilson et al, 2005).
7) However, in a multicenter, randomized, controlled, and masked trial, endotracheal instillation of up to 3 doses of calfactant (30 mg) in adults only with acute lung injury/ARDS due to direct lung injury was not associated with improved oxygenation and longer term benefits compared to the placebo group. It was also associated with significant increases in hypoxia and hypotension (Willson et al, 2015).

1) Mercury droplets may be absorbed after conjunctival contact (Grant, 1986). Exposed eyes should be immediately irrigated with copious amounts of room temperature water for at least 15 minutes, occasionally lifting upper and lower eyelids.
2) If irritation, pain, swelling, lacrimation, or photophobia persist after 15 minutes of irrigation, an ophthalmologic examination should be considered.

a) PERITONEAL EXPOSURE
b) SMELTING, AMALGAM HANDLING
c) AMALGAM EXPOSURE, DENTAL WORKERS
d) EXPOSURE FROM INJECTION, IMPLANTATION

a) INGESTION
b) SMELTER, ENVIRONMENTAL EXPOSURE
c) SPILLS, OTHER ENVIRONMENTAL

1) The urine and blood mercury levels of 8 family members, who were exposed to mercury vapors as a result of home gold ore processing, were as follows (Solis et al, 2000):
2) Two days following exposure to an elemental mercury spill, the blood mercury levels of 8 adolescents ranged from less than 4 mcg/L to 13 mcg/L (Anon, 2005).
3) ADULTS
4) CHILDREN

a) Adopted Value

1) TCLo- (INHALATION)HUMAN:
2) TCLo- (INHALATION)MOUSE:
3) TCLo- (INHALATION)RAT:

1) Organomercurials and inorganic mercury salts are more commonly associated with ACUTE toxicity (mercury toxicosis) in animals than exposure to elemental mercury (Osweiler & Hook, 1986).
2) Muscle incoordination, ataxia, hyperesthesia, tremor, seizures, coma, skin and hair changes, and gastrointestinal disburbances (diarrhea, vomiting, anorexia) with subsequent fluid and electrolyte losses have been reported (Beasley et al, 1990).
3) SUBACUTE OR CHRONIC TOXICITY is more common, after exposure periods of several days or longer. Neurologic, GI, renal, and dermal effects are seen (Beasley et al, 1990).

1) Clinical signs of mercury toxicosis (associated chiefly with organomercurials and inorganic mercury salts) may include stomatitis, salivation, hemorrhagic or necrotic enteritis, decreased appetite, weakness, and hematuria. Skin and hair changes may be noted. Severe neurological effects may also occur in cattle following organomercury exposure (Osweiler & Hook, 1986).

1) Clinical signs of acute or subacute mercury toxicosis due principally to organomercurials and inorganic mercury salts include stomatitis, salivation, vomiting (in swine), hemorrhagic or necrotic enteritis, decreased appetite, weakness, and hematuria. White pigs may display erythema. Other skin and hair changes may be noted. Severe neurological effects have also been associated with organic mercury exposure in swine (Osweiler & Hook, 1986).

1) Specific decontamination is not generally required following ingestion of elemental mercury unless the mercury remains in the gastrointestinal tract for a prolonged period of time. The following recommendations are principally intended for inorganic or organic mercury exposure.
2) Begin treatment immediately.
3) Keep animal warm.
4) Sample vomitus, blood, urine, and feces for analysis.
5) If skin exposure has occurred, wash animal thoroughly with a mild detergent and flush with copious amounts of water.
6) ANIMAL POISON CONTROL CENTERS

1) MAINTAIN VITAL FUNCTIONS: Secure airway, supply oxygen, and begin supportive fluid therapy if necessary.

1) SMALL ANIMALS
2) LARGE ANIMALS

1) Specific decontamination is not generally required following ingestion of elemental mercury unless the mercury remains in the gastrointestinal tract for a prolonged period of time. The following recommendations are principally intended for inorganic or organic mercury exposure.

1) Emesis or gastric lavage followed by activated charcoal, 20% sodium thiosulfate (0.5 to 3 g), egg white, or tannic acid (200 to 500 mg in 30 to 60 mL water).
2) Dimercaprol (BAL) 3 mg/kg IM every 4 hours days 1 and 2, four times daily on day 3, followed by twice daily on days 4 through 10. d-Penicillamine 11 mg/kg four times daily for 7 to 10 days, orally.

1) Adsorbant. Dimercaprol (BAL): 3 mg/kg IM. Repeat every 4 hours for 2 days, then four times daily on 3rd day, then twice daily for 10 days until recovery. Supportive fluid and electrolyte therapy.

1) METALLIC MERCURY - Only 0.01% is absorbed via the GI tract so elemental mercury is fairly low in toxicity when ingested. If it becomes imbedded in tissues (as may occur if a rectal thermometer breaks while inserted) it may cause toxicity (Beasley et al, 1990).
2) INORGANIC MERCURY - Causes toxicity in the horse at a dose of 8 to 10 grams. Chronic toxicity may result from ingestion of 0.4 milligram/kilogram/day over several weeks in horses (Beasley et al, 1990).
3) ALKYL MERCURIC COMPOUNDS (SATURATED HYDROCARBONS) - Methyl and ethyl mercury are the most toxic forms of mercury. All forms of mercury sequestered in living organisms are converted by anaerobic bacteria into methyl mercury. This is also the form of mercury found in eggs as residue, regardless of the form of mercury ingested by the bird (Beasley et al, 1990).

A) GENERAL TREATMENT

A) GASTRIC DECONTAMINATION

1) Inorganic mercury is well-absorbed from the lungs, but only 7% to 15% is absorbed through the skin and GI tract. Mercury salts can also bind to gut mucosa (Beasley et al, 1990).
2) Elemental mercury can be absorbed via gut mucosa.
3) Organic mercurials are absorbed via all routes, including dermal (Beasley et al, 1990).