a) Organic mercury compounds contain mercury with a covalent bond to at least one carbon atom (Klaassen, 1990). Most of the organic mercury compounds are crystals, granules, scales or powders, which may be incorporated into other preparations. Some organic mercury compounds (e.g., dimethylmercury, methyl mercury) are volatile (IARC, 1993; Proctor et al, 1989). Exposure to vapors, particles, dusts or aerosols can occur.

a) Organic mercury compounds can be further divided into three classes (Gosselin et al, 1984; Sax & Lewis, 1987; Bryson, 1989):

a) Organic mercurials can be subclassified based on the ease with which the organic moiety dissociates (in the body) from the anion to yield inorganic mercury (Bryson, 1989).

a) The Food and Drug Administration (FDA) has advised pregnant women, women who plan to become pregnant, nursing mothers, and young children to avoid eating large fish known to contain high mercury concentrations (eg; shark, swordfish, king mackerel, tilefish) with reported mean mercury concentrations of 0.73 to 1.45 ppm (Ruha et al, 2009; Knobeloch et al, 2006). In one case series, mercury concentrations were reported in the following fish: Lake superior trout (less than 0.02 mcg/g); Lake superior whitefish (less than 0.02 mcg/g); farm-raised salmon (0.05 mcg/g); farm-raised trout (0.05 mcg/g); imported seabass (up to 0.7 mcg/g); panfish (up to 0.58 mcg/g); walleye (up to 3.1 mcg/g); bass (up to 1.7 mcg/g); Northern pike (up to 1.9 mcg/g); perch (0.049 mcg/g); canned tuna (up to 0.85 mcg/g); bluegill (up to 0.53 mcg/g); brook trout (0.016 mcg/g) (Knobeloch et al, 2006).
b) MINAMATA DISEASE: From 1932 until 1968, a factory in Minamata, Japan, discharged mercury and methylmercury contaminated waste directly into Minamata bay and the Yatsushiro Sea. Although in 1959, Minamata disease was determined to be methylmercury poisoning from consuming contaminated fish and shellfish, the factory continued to discharge mercury contaminated waste until 1968(Takaoka et al, 2008).

a) Thiomersal has been used in vaccines as a preservative (Pichichero et al, 2002).
b) HEPATITIS VACCINE: Elevated mercury concentrations after a single dose of hepatitis B vaccine containing thiomersal were observed in preterm and term infants. Overall, a significantly higher mean mercury concentration was observed for the preterm group compared with the term group (mean +/- SD, 7.36 +/- 4.99 mcg/L vs 2.24 +/- 0.58 mcg/L; p less than 0.01) (Stajich et al, 2000).

1) Trace amounts of organic mercury found in vaccine preservatives (thimerosal) have not been associated with cognitive delay or other neurologic toxicity.

1) OVERDOSE: Organic mercury may be absorbed by any route. Once toxicity develops from organic mercury, the effects are largely permanent, and generally outcome is poor after significant overdose. Partial improvement has been observed in some mildly symptomatic children though severely poisoned individuals have not been recovered.
2) MILD TO MODERATE TOXICITY: Delayed neurotoxicity is the hallmark of organic mercury exposure. Acute ingestions may be associated with nausea and vomiting. Symptoms may include fatigue, headaches, cognitive delays, tremor, and paraesthesias. Chronic exposure may lead to withdrawn behavior with irritability (erethism).
3) SEVERE TOXICITY: Neurotoxicity is the manifestation of severe organic mercury poisoning.
4) NEUROLOGIC: Effects of poisoning may be latent for days to months depending upon the compound and the dose of the exposure. Dimethylmercury is the most toxic of the organic mercurials and even minute dermal exposures may lead to rapidly progressive cerebellar deficits, coma, and subsequent death. Methylmercury is more common; it is the form found in fish. Trace amounts of methylmercury found in fish, even in large consumption, have not been associated with cognitive delay or other neurologic toxicity. Ingestion of organic mercurials may lead to paresthesias, headaches, tremor, ataxia, dysarthria. visual field constriction, blindness, dementia, paralysis, coma, and death. Congenital toxicity is characterized by low birth weight, decreased muscle tone, developmental delay, seizure disorders, deafness, blindness, spasticity.
5) CARDIOVASCULAR: Organic mercurials rarely cause cardiovascular toxicity. Hypotension and cardiac dysrhythmias are possible.
6) RESPIRATORY: Respiratory symptoms are rare. Inhalation may lead to respiratory distress and respiratory collapse has been reported due to sensorimotor neuropathy.
7) RENAL: Renal tubular dysfunction may occur but the majority of organic mercury is not cleared through the kidney making renal toxicity less common when compared to inorganic mercurials. Renal effects have been more commonly observed with aryl (eg, phenylmercuric salts) and alkoxyalkyl (eg, methoxyethyl mercury) compounds.
8) GASTROINTESTINAL: Acute ingestion of large amounts of organic mercury may lead to nausea and vomiting. Gastrointestinal disturbances are more common with phenyl mercuric salts, methoxyethyl salts and other aryl and alkoxyalkyl compounds.
9) DERMATOLOGY: Dermatitis may occur though is more common with inorganic mercury exposures. Contact dermatitis from topical organic mercury antiseptics is the most common dermatologic manifestation.

1) Profound adverse effects on the developing child or nursing infant can occur if there is maternal exposure to organic mercury. Pediatric exposure may result in impaired intellectual and motor development, in addition to the effects typically observed in adults.

1) Methyl mercury and other alkylmercurials chiefly affect the neurological system, and are less likely to produce gastrointestinal effects.

1) Treatment is symptomatic and supportive. If significant exposure has occurred, chelation therapy should be started as soon as possible, prior to development of symptoms. Breastfeeding should be halted immediately.

1) Supportive care is the mainstay of care. If significant exposure has occurred, chelation therapy should be started as soon as possible, prior to development of symptoms.

1) PREHOSPITAL: Dermal exposures should be washed off with soap and water. No other prehospital decontamination is indicated. Organic mercury spills should be contained and cleaned by qualified hazardous material abatement crews.
2) HOSPITAL: Most presentations are subacute or chronic exposures making gastrointestinal decontamination ineffective. However, given the dismal outcomes and limited therapeutic options, aggressive gastrointestinal decontamination including gastric lavage, activated charcoal and whole bowel irrigation is recommended for acute ingestions. Breastfeeding mothers should continue to pump breast milk and discard.

1) Airway management may be necessary if a patient progresses to coma, if there is respiratory depression due to sensorimotor neuropathy, or if significant pneumonitis is present.

1) None.

1) Unithiol (2,3-dimercaptopropanol-sulfonic acid, DMPS) is available in Europe and through compounding pharmacies in the United States. It is a water-soluble analog of BAL, and can be given orally or parenterally. For patients with severe poisoning or large exposures, the parenteral unithiol should be the initial chelator if it is available, 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 three 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. There is limited data suggesting that oral succimer (10 mg/kg every 8 hours for 5 days then twice daily for 2 weeks) can reduce mercury levels in the tissues. D-penicillamine (500 mg twice daily for 12 weeks) should be considered the second-line agent. Patients should be treated for 14 days or until there is no mercury detected in the urine. Dimercaprol (BAL; British Anti Lewisite) is CONTRAINDICATED because it increases brain organic mercury concentrations.

1) Hemodialysis, hemoperfusion, and exchange perfusion do not remove significant amounts of mercury after subacute or chronic organic mercury exposure. Hemodialysis in combination with L-cysteine infusion into the arterial blood has been shown to increase mercury clearance in chronic methylmercury intoxication, (L-cysteine converts methylmercury into a diffusible form) but it has not known if this improves outcomes.

1) HOME CRITERIA: Patients with chronic exposures can be referred to outpatient healthcare providers for evaluation. Unintentional pediatric ingestions of mercurochrome can generally be managed in the home without gastrointestinal decontamination.
2) OBSERVATION CRITERIA: Asymptomatic or minimally symptomatic patients with chronic exposures already in healthcare facilities may be observed and referred to neurology or toxicology outpatient providers. All patients with acute exposures should be referred to a healthcare facility.
3) ADMISSION CRITERIA: All patients with an exposure to dimethylmercury should be admitted. All acute ingestions should be admitted. Patients with moderate or severe neurologic toxicity felt to be secondary to organic mercury warrant inpatient evaluation for neurology and toxicology consultation, whole blood quantification, and evaluation for possible chelation.
4) CONSULT CRITERIA: All cases with organic mercury toxicity should involve a toxicology and neurology consultants.

1) Failure to fully appreciate the toxicity of significant organic mercury exposures during the latent phase may lead to delayed recognition of toxicity. Measurement of urine mercury when concerned for methylmercury toxicity is inappropriate since it is primarily cleared through the biliary tract resulting in a proportionally low urine mercury level. This may give false re-assurance when a low concentration is obtained.

1) The organic mercurials are absorbed more completely (more than 90%) from the gastrointestinal tract than any other form of mercury because they are more lipid soluble. This lipid solubility allows passage across the blood-brain-barrier and the placenta. It is also concentrated in red-blood-cells. Organic mercurials are eliminated primarily through the biliary tract, then fecally with a significant amount of enterohepatic recirculation. Less than 10% is cleared renally. Blood half-life is approximately 70 days.

1) Chronic arsenic poisoning may yield muscle weakness; however, the associate dermatologic effects are more prominent than in organic mercury poisoning. Chronic bismuth toxicity may result in a similar progressive neurotoxicity though, dermal changes are more common and black stools would be expected with chronic ingestion of bismuth. Medical etiologies such as progressive multi-focal leukoencephalopathy and cerebrovascular accidents should be considered.

1) Dermal exposure to dimethylmercury should be treated with immediate hospitalization and chelation therapy.
2) DECONTAMINATION: Remove contaminated clothing and wash exposed area thoroughly with soap and water for 10 to 15 minutes. A physician may need to examine the area if irritation or pain persists (Burgess et al, 1999).
3) Take precautions to avoid exposure of health care professionals and other individuals.
4) SYSTEMIC EFFECTS

1) Respiratory distress associated with laryngeal obstruction occurred in an adult 30 hours after self-medication of a sore throat with a thiomersal-containing throat spray (Maibach, 1975). Delayed hypersensitization to thiomersal was the suspected cause; patch testing to thiomersal was strongly positive.
2) Intense dyspnea and other effects suggestive of anaphylactic hypersensitivity occurred in a man 3 minutes after topical application of a mercurochrome- containing antiseptic to abraded skin. Patch tests were positive (Torres & De Corres, 1985).

1) Irritation of the eyes and skin around the eyes may result from contact with highly concentrated solutions of some phenylmercuric salts (Grant & Schuman, 1993).
2) THIMEROSAL in eye drops and contact lens solutions may produce eye irritation in hypersensitive individuals (Grant & Schuman, 1993).

1) MERCURIALENTIS: As reviewed by Grant (1986), long term use of eyedrops which contain phenylmercuric acetate (0.001%) or phenylmercuric nitrate as preservatives have produced lens discoloration.
2) ALTERED LENS TRANSPARENCY has resulted from long term use of eyedrops containing 0.002% phenylmercuric acetate (Grant & Schuman, 1993).

1) Atypical band keratopathy or corneal calcification have been reported from the long term use (average of 10 years) of pilocarpine eyedrops which contained phenylmercuric nitrate (Grant & Schuman, 1993).
2) Corneal injury has resulted from the use of eyedrops which contained high concentrations of phenylmercuric salts.
3) Corneal opacification and vascularization has occurred with the exposure of rats and guinea pigs to eyedrops containing 0.1% HYDRARGAPHEN (PHENYLMERCURIC DINAPHTHYL-METHANEDISULFONATE). An ophthalmic preparation containing 0.033% hydrargaphen has been used in humans without apparent serious adverse effects (Grant & Schuman, 1993).

1) Minor ptosis, irregular nystagmus, jerky visual tracking, and other disturbed eye movements occasionally have been observed (Gosselin et al, 1984; Grant & Schuman, 1993; Davis et al, 1994). Electro-oculography has been useful in detecting abnormal movements (Grant & Schuman, 1993).

1) Occupational inhalational exposure to organic mercury fungicides, ingestion of foods contaminated with methyl mercury, and dermal exposure to dimethylmercury has produced concentric constriction of the visual fields as a result of mercury neurotoxicity (Bakir et al, 1980; Grant & Schuman, 1993; Davis et al, 1994; Nierenberg et al, 1998; Siegler et al, 1999).
2) The constriction may progress considerably over a 2 week period, despite cessation of exposure. Spontaneous recovery of visual field deficits rarely occurs (Grant & Schuman, 1993).

1) Blindness has resulted from ingestion of ethyl or methyl mercury contaminated food, and chronic occupational inhalation exposure to organic mercury compounds (Bakir et al, 1980; Davis et al, 1994; Amin-Zaki et al, 1978; Grant & Schuman, 1993). Spontaneous recovery of central vision may occur in some cases. Deficits in peripheral vision (visual field constriction) are less likely to resolve.
2) Maternal exposure during pregnancy to foods contaminated with methylmercury has resulted in blindness in the neonate (Bakir et al, 1980).
3) HISTOPATHOLOGICAL FINDINGS

1) Retinal edema, chorioretinal atrophy (p-chloromercuribenzoate, in vitro) and slight retinal toxicity from systemic absorption (p-chloromercuribenzoate, rabbit) have been reported (Grant & Schuman, 1993).

1) P-CHLOROMERCURIBENZOATE AND P-CHLOROMERCURIBENZENE SULFONATE have impaired aqueous outflow in an in vitro study (Grant & Schuman, 1993).

1) Outbreaks of methylmercury poisoning due to consumption of foods contaminated with methyl and/or ethyl mercury has resulted in hearing loss and deafness as a result of neurotoxic effects of mercury (Nagi & Yassin, 1974; Bakir et al, 1980). Prenatal exposure also resulted in impaired hearing (Bakir et al, 1980). Dermal exposure to dimethylmercury resulted in mild to moderate sensorineural hearing loss (Nierenberg et al, 1998).

1) A 53-year-old woman developed stomatitis, tremors, and tinnitus. Mercury levels from blood and urine samples were 125 mcg/L and 24 mcg/L, respectively. The patient was consuming up to two fish meals (particularly swordfish) daily 6 or 7 days per week over a period of several years. It is believed that the patient's excessive consumption of fish was the source of mercury exposure. She was advised to substantially reduce her consumption of fish; however, she was lost to follow-up(Risher, 2004).

1) Phenylmercuric salts and other aryl and alkoxyalkyl mercury compounds are converted in vivo to inorganic mercury. Effects similar to inorganic mercury compounds may occur (US DHHS, 1992; Gosselin et al, 1984; Bryson, 1989). Inorganic mercury salts have produced shock and vascular collapse. Organic mercury compounds are generally less corrosive than the inorganic salts (Klaassen, 1990).

1) A few incidences of bradycardia or death due to cardiac dysrhythmias following the intravenous injection of organic mercurials (salyrgan, mercupurin) have been reported (Barker et al, 1942; Brown et al, 1942).
2) Tachycardia, fibrillation, cyanosis, cardiac standstill and death were reported within 3 to 30 minutes of infusion. Bradycardia, cyanosis and seizure activity occurred in one nonfatal case (Brown et al, 1942).
3) Serious preexisting cardiac, renal or other diseases were present in all cases. Cardiac monitoring did not appear to have been conducted during some of these incidences.
4) One study concluded that deaths following injection of mercurial diuretics were more likely due to fluid and electrolyte imbalances, diuresis induced digitalis toxicity, or were idiosyncratic (DeGraff & Nadler, 1942).

1) WITH POISONING/EXPOSURE

1) WITH POISONING/EXPOSURE

1) CASE REPORT: A 44-year-old man required mechanical ventilation for 3 days because of a severe ascending sensorimotor peripheral neuropathy after ingesting 5 grams of Thiomersal (Pfab et al, 1996).

1) Profound adverse effects on the developing child or nursing infant can occur if there is maternal exposure to organic mercury. Pediatric exposure may result in impaired intellectual and motor development, in addition to the effects typically observed in adults.

1) WITH POISONING/EXPOSURE

1) Cerebellar signs of ataxia, loss of coordination and speech and tremor have been reported after ingestion of food contaminated with methyl or ethyl mercury (Nagi & Yassin, 1974; Zhang, 1984; McKeown-Eyssen et al, 1983; Bakir et al, 1980; Davis et al, 1994) and following inhalation of vapors from phenylmercuric ammonium acetate (O'Carroll et al, 1995) and following toxic dermal exposures to dimethylmercury (Siegler et al, 1999).
2) Chronic ingestion of merthiolate by an adult for an unknown duration resulted in agitation and other neurologic effects in a fatal case (Nascimento et al, 1990).
3) Dysmetria, dystaxic handwriting, wide based gait, and scanning speech developed after dermal exposure to dimethylmercury (Nierenberg et al, 1998).
4) CASE REPORT: In cases of methylmercury poisoning, gliosis of the cerebellar cortices predominates. The cerebellum is always affected, with damage consisting of loss of granule and Golgi cells. A few drops of dimethylmercury on the skin have resulted in profound effects on the cerebellum with massive Purkinje cell loss and eventual death (9 months after exposure) in one patient (Siegler et al, 1999).

1) Paresthesias, fatigue, motor weakness, hyperreflexia, diminished muscle tone and spasticity may be observed with moderately severe ingestions (Zhang, 1984; McKeown-Eyssen et al, 1983; Nagi & Yassin, 1974; Cinca et al, 1979; Bakir et al, 1980).
2) Hemiparesis, quadriplegia, and proprioception loss has also been documented in children exposed to methyl mercury contaminated pork (Davis et al, 1994). Increased muscle tone has also been reported in infants who were exposed prenatally to methyl mercury (Bakir et al, 1980).
3) CASE REPORT: A 44-year-old man developed an autonomic and ascending peripheral axonal sensorimotor polyneuropathy 6 days after ingesting 5 grams of Thiomersal (Pfab et al, 1996). He required mechanical ventilation for 3 days.
4) CASE REPORT: A 64-year-old fisherman from Minamata City, Japan presented with numbness of the feet and speech disturbance. Ten years after the initial presentation, neurological examination revealed slight constriction of visual fields on the temporal side, muscular rigidity, increased tendon reflexes. tremor of the fingers, dysgraphia, adiadochokinesis, labyrinthine deafness, hypesthesia, hypalgesia, dysesthesia in the hands and below the knees, a mask-like face, and dyskinesia. Minamata disease (methylmercury poisoning) was suspected, and a sural nerve biopsy revealed endoneurial fibrosis and regenerated myelin sheaths. A month later he died of massive hemorrhage from gastroduodenal ulcer. At autopsy, the dorsal roots and sural nerve revealed endoneurial fibrosis, loss of nerve fibers, and presence of Bungner's hands. Wallerian degeneration of the fasciculus gracilis (Goll's tract) in the spinal cord with relative preservation of neurons in sensory ganglia was observed (Eto et al, 2002).

1) WITH POISONING/EXPOSURE

1) Anxiety, agitation, irrational fears, impulsiveness and headache occurred in a man exposed to phenylmercuric ammonium acetate vapors (O'Carroll et al, 1995).

1) Multiple sclerosis has been hypothetically associated with chronic organic mercury exposure. Research to date reportedly has not adequately supported this hypothesis (Clausen, 1993).
2) Other forms of mercury have been associated with a neurological syndrome resembling amyotrophic lateral sclerosis or Lou Gehrig Disease (Adams et al, 1983). The peripheral effects involve a dying-back axonopathy, followed by demyelination. General loss of brain function may also occur (FOLKL & KONIG, 1983).

1) Muscle rigidity, jerky myoclonic movements and choreoathetotic movements have been observed in individuals exposed to methyl mercury contaminated food (Skerfving & Vostal, 1972; Bakir et al, 1980; Davis et al, 1994) and in an adult who ingested merthiolate on a long-term basis (Nascimento et al, 1990).

1) Hyperactive deep tendon reflexes have been observed in children exposed to methyl mercury (Davis, 1994).

1) Seizures and coma are seen with severe toxicity (Nagi & Yassin, 1974; Cinca et al, 1979; Bakir et al, 1980; Davis et al, 1994).
2) CASE REPORT: A 44-year-old man developed delirium progressing to coma 11 days after ingesting 5 grams of Thiomersal (Pfab et al, 1996).

1) VISUAL/AUDITORY EFFECTS: Constriction of the visual fields, blindness, optic atrophy, mydriasis, and hearing impairment or deafness have been reported with more severe intoxication (Zhang, 1984; McKeown-Eyssen et al, 1983; Nagi & Yassin, 1974; Cinca et al, 1979; Bakir et al, 1980; Clarkson, 1990; Marsh et al, 1987; Davis et al, 1994; Nierenberg et al, 1998; Siegler et al, 1999).
2) Specific damage occurs in the cerebellum and the visual cortex following toxic exposures (Langford & Ferner, 1999). Visual field defects are common and are persistent following organic mercury exposures (Korogi et al, 1998). VISUAL CORTEX ATROPHY has been detected upon autopsy of an individual chronically exposed by inhalation to a methyl mercury in a fungicide (Grant & Schuman, 1993).

1) Severe dysarthria (inability to articulate) has been reported in 19 out of 26 pediatric cases who had developed mercury intoxication after consuming bread prepared from wheat which had been dusted with a methyl mercury fungicide (Nagi & Yassin, 1974). Dysarthria was also reported in an adult who chronically ingested merthiolate (Nascimento et al, 1990).

1) More severe poisonings have resulted in hearing impairment or deafness. Dimethylmercury poisoning has been reported to result in compromise of the auditory neural system, with minimal effect on the sensory (cochlear) mechanism in one fatal case of a dermal exposure. The patient was shown to have relatively good hearing sensitivity for pure tones bilaterally. An abnormal bilateral auditory brain stem response was apparent (Musiek & Hanlon, 1999).

1) Delayed motor and speech development has occurred in infants born to mothers who were exposed to methylmercury during pregnancy (Marsh et al, 1987).

1) Other effects which have been observed following extreme chronic pediatric exposure, or as a result of prenatal exposure include somnolence or agitation, lethargy and weak cry (Davis et al, 1994).

1) Methyl mercury and other alkylmercurials chiefly affect the neurological system, and are less likely to produce gastrointestinal effects.

1) METHYLMERCURY compounds are almost 100% absorbed in the gastrointestinal tract (Manahan, 1991). Aryl and long chain alkyl compounds are also well absorbed, but to a lesser extent than methyl mercury.

1) Nausea, vomiting, abdominal pain and diarrhea may occur (Skerfving & Vostal, 1972; US DHHS, 1992; Pfab et al, 1996). Higher doses may result in an exposure-related colitis (Langford & Ferner, 1999). Symptoms (nausea, diarrhea) may be delayed (a few weeks) and may be persistent for several months following an acute toxic exposure (Siegler et al, 1999).
2) Nausea and diarrhea for 3 months occurred in an adult who chronically ingested merthiolate (Nascimento et al, 1990).

1) Acute or chronic poisoning with organic mercury may result in hepatic enzyme disturbances (Langford & Ferner, 1999).

1) Proteinuria and increased urinary mercury levels have been measured in workers exposed to organomercurial seed dressings. The urinary mercury levels did not correlate well with proteinuria (Taylor et al, 1969).
2) Albuminuria has been reported as a result of ethyl mercury poisoning, skin exposure to phenyl mercury acetate, and inhalation of methoxyethyl mercury silicate (Skerfving & Vostal, 1972).

1) Nephrotic syndrome developed in a patient who inhaled a methoxyethyl mercury compound (Skerfving & Vostal, 1972).

1) Renal insufficiency has occurred in infants as a result of omphalocele treatment with mercurochrome (Debray et al, 1979).
2) CASE REPORT: A 44-year-old man developed polyuric acute renal failure with glycosuria, proteinuria, beta-2-microglobulinuria and a peak serum creatinine of 2.4 mg/dL after ingesting 5 grams of Thiomersal (Pfab et al, 1996).

1) Renal tubular necrosis may occur. Renal effects have been more commonly observed with aryl (e.g. phenylmercuric salts) and alkoxyalkyl (e.g. methoxyethyl mercury) compounds (Gosselin et al, 1984; Bryson, 1989).

1) Metabolic acidosis has occurred in an infant following omphalocele treatment with mercurochrome which resulted in renal insufficiency (Debray et al, 1979).

1) Organic mercury compounds can be absorbed through the skin (Manahan, 1991; Yeh et al, 1978; Nierenberg et al, 1998). Elevated mercury levels and toxicity have occurred in infants with omphaloceles which were treated with organic mercurial antiseptics (Fagan et al, 1977; Nascimento et al, 1990).

1) Phenylmercuric salts (acetate, nitrate) in concentrations of 0.1% and higher are primary irritants. Initially, erythema and burning appear, followed by vesicles within 48 hours (Morris, 1960; Koby, 1972).
2) CASE REPORT: A man who had been sprayed with a mixture of equal parts of phenylmercuric acetate (12% by weight), glacial acetic acid and benzene (benzol) developed second degree burns (Goldwater et al, 1964).
3) Methoxyethyl mercury silicate produces local skin irritation. Concentrated methoxyethyl mercury acetate solutions have produced blisters on the skin of animals (Skerfving & Vostal, 1972).

1) Skin contact with methyl mercury, ethyl mercury, phenyl mercury compounds, and tolyl mercury compounds have produced dermatitis and eczema (Skerfving & Vostal, 1972).
2) ALLERGY: A positive reaction to 0.01% phenylmercuric acetate, and a contact urticaria syndrome consisting of urticaria, facial edema, and bronchospasm have been reported (Torresani et al, 1993). Positive skin reactions to sodium ethyl mercury salicylate (Merthiolate(R), Thimerosal) have occurred (Skerfving & Vostal, 1972; Wilson et al, 1981; Aberer et al, 1990).

1) ACRODYNIA, a particular form of hypersensitization to mercurials has been seen in children of 4 months to 4 years. This reaction involves generalized body rash, chills, profuse perspiration, desquamation of the palms and soles, photophobia, irritability, sleeplessness, leg cramps, and swelling of the cheeks, nose, hands, and feet (HSDB, 1990; (Gosselin et al, 1984).
2) CASE REPORT: Acrodynia developed in a 10-year-old boy 10 days after the inside of his home was painted with interior latex paint which contained phenylmercuric acetate at levels 3 times those recommended by the EPA (Agocs et al, 1990; CDC, 1990).

1) WITH POISONING/EXPOSURE

1) Sensitization can occur (Skerfving & Vostal, 1972; Wilson et al, 1981; Aberer et al, 1990). Anaphylaxis is rare (Torres & De Corres, 1985).
2) Acute laryngeal obstruction requiring emergency tracheostomy occurred in an adult 30 hours after the use of a thiomersal-containing throat spray to treat a minor sore throat. Patch testing to thiomersal was positive (Maibach, 1975).
3) Intense dyspnea, giddiness, upper body flushing and exanthema developed in a man 3 minutes after topical application of a mercurochrome-containing antiseptic to abraded skin. Patch tests to inorganic and organic mercury compounds were positive (Torres & De Corres, 1985).

1) WBC ABNORMAL

1) Abnormalities reported on CT in patients with fetal methylmercury poisoning include sulcal and mild ventricular enlargement, underdevelopment of cerebellar matter and lobe size, and simplified gyral patterns. Findings suggest that developmental defects result from cortical and subcortical lesions (Hamada et al, 1993).

1) In one study, prenatal exposure from contaminated seafood was associated with an increased risk of neurodevelopmental deficit (Steuerwald et al, 2000).
2) Children exposed in utero to organic mercury in the Minamata epidemic developed cerebral palsy, chorea, ataxia, tremors, seizures, and profound mental retardation (Winship, 1985). The organ most sensitive to gestational exposure is the central nervous system (Aschner, 2001; Myers & Davidson, 2000).
3) Iraqi children exposed in utero to methylmercury from contaminated grain developed irritability, increased reflexes, visual and hearing impairment, motor and mental retardation (Bakir et al, 1980).

1) CASE SERIES - A series of 81 infant-mother pairs were evaluated for identification of a dose-response relationship between methylmercury concentrations in single strands of maternal hair and observed effects in the child. The women had, during pregnancy, consumed bread made from methylmercury treated seed. Children of women with higher exposures to methylmercury during gestation were at greater risk for the development of neurologic findings and developmental delays. No mercury concentrations were measured in the children (Marsh et al, 1987).
2) Neurobehavioral effects may occur in children of mothers exposed to methylmercury if maternal mercury concentration in hair is greater than 6 micrograms/gram (30 nanomoles/gram), which correlates to a blood concentration of approximately 24 micrograms/liter (120 nanomoles/Liter) (Grandjean et al, 1994).

1) One study evaluated the risk of very preterm birth in relation to mercury concentrations among women with low to moderate exposure. Maternal hair mercury concentrations ranged from 0.01 to 2.50 mcg/g (mean, 0.29 mcg/g; median, 0.23 mcg/g). The mean mercury concentrations increased as levels of fish consumption increased. The consumption of canned fish, bought fish, and sport-caught fish and total fish consumption were each positively associated with maternal hair mercury concentrations. Overall, women who delivered before 35 weeks' gestation were more likely to have hair mercury concentrations at or above the 90th percentile (equal to 0.55 mcg/g or greater) compared with women delivering at term, even after adjusting for maternal characteristics and fish consumption (adjusted odds ration equal to 3; 95% confidence interval, 1.3 to 6.7) (Xue et al, 2007).

1) In one study, mercury cord and maternal blood concentrations at delivery were correlated with psychomotor status of infants (1-year-old; n=233) whose mothers were exposed to varying amounts of mercury during pregnancy. Total mean mercury concentration in blood (GM) for infants with normal neurocognitive performance was lower than observed in the group with delayed performance (GM = 0.52 mcg/L vs 0.75 mcg/L; p = 0.010). In cord blood, GM was lower in the normal group than in the group with delayed performance (GM, 0.85 mcg/L vs 1.05 mcg/L; p = 0.07). It was concluded that children with mercury concentrations greater than 0.80 mcg/L in cord blood or greater than 0.50 mcg/L in maternal blood had a significantly greater probability of delayed psychomotor or mental performance (Jedrychowski et al, 2006).

1) A study was conducted to determine the incidence of abnormal pregnancies during a period of low methylmercury contamination compared with heavy contamination in 2 areas in Japan. There was a significant increase in stillbirth, spontaneous abortion, hydatidiform mole and extrauterine pregnancy in both areas during the period of heavy contamination, compared with the low methylmercury contamination period (Itai et al, 2004).

1) Davidson et al (1998) reported NO adverse effects in the offspring of mothers in Seychelles with methylmercury hair levels 10 to 20 times higher than United States mothers due to consumption of more fish. Children were followed up to 66 months of age. The mean maternal total hair mercury level was 6.8 ppm; mean total hair mercury level was 6.5 ppm for children at 66 months of age (Davidson et al, 1998). A later report by the same authors concluded that no significant associations were observed between prenatal methylmercury exposure and any of the repeatedly measured endpoints (global cognition (a measure of developmental quotient or IQ); reading, mathematics scholastic achievement, social behavior, and memory) (Davidson et al, 2006).

1) Breast milk of mothers poisoned by methylmercury contaminated food contained mercury at a concentration of 5% of that found in blood (Bakir et al, 1973).
2) Methylmercury is transferred to human breast milk and distributed in nursing infants in a dose-related fashion, as determined by analysis of mercury levels in infants' hair in a fishing community (Grandjean et al, 1994).
3) No adverse effects on infant development during the first year of life were reported despite elevated hair-mercury levels in infants who ingested breast milk from mothers with elevated hair-mercury and who also were likely to have mercury exposure during gestation (Grandjean et al, 1995).
4) Neurobehavioral development was assessed in children who were exposed to methylmercury prenatally and during breastfeeding and compared with children exposed prenatally and not breastfed. At 7 years of age, breastfeeding was associated with a slightly better neuropsychological performance on most tests. Children who were breastfed for more than 4 months had significantly better scores on the WISC-R Block Designs and the Boston Naming Test (Jensen et al, 2005).
5) 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).
6) ANIMAL STUDIES

1) IARC Classification

1) Borderline excess lung cancer incidence was seen in Norwegian chloralkali workers who had been exposed and monitored for mercury (Ellingsen et al, 1993).

1) Mercury at 5 ppm in the drinking water was not carcinogenic in mice (Schroeder & Mitchener, 1975).

a) Mercury produces clastogenic effects in eukaryotic cells, and organic mercury compounds can inhibit the spindle mechanisms of chromosomes in a manner which favors the production of aneuploidy and/or polyploidy. Organic mercury may produce dominant lethal effects (IARC, 1993).

a) Studies of humans chronically exposed to foods contaminated with methyl mercury have reported the presence or absence of increased sister chromatid exchange rates, chromosomal aberrations, and aneuploidy in the lymphocytes (IARC, 1993).
b) POSITIVE - Micronuclei were elevated in peripheral lymphocytes of fishermen eating a high-mercury seafood diet (Franchi et al, 1994).

a) Studies of lymphocytes from workers exposed to organic mercury compounds have been largely inconclusive or negative with respect to the production of chromosomal aberrations, aneuploidy, micronuclei and sister chromatid exchange rates (IARC, 1993).
b) Increased sister chromatid exchange rates were associated with exposure to phenylmercuric acetate (1 study) and increased chromosomal aberrations were associated with exposure to a mixture of methyl mercury chloride, ethyl mercury chloride, and mercuric chloride (1 study). Weakly positive increases in aneuploidy associated with exposure to phenyl mercury compounds was reported in 1 study (IARC, 1993).
c) In most human studies, the specific organic mercury compounds were not identified, and the dose to which exposure occurred was not known.

a) One study evaluated the genotoxic effects of mercury nitrate, methylmercury chloride, and phenylmercury acetate in cultured human lymphocytes. Phenylmercury acetate (3 to 30 mcM) and methylmercury chloride (20 mcM) significantly increased the frequency of sister chromatid exchange (SCE) and endoreduplication. In contrast, all concentrations of mercury nitrate did not cause a significant increase in SCE frequency, but at the concentrations of 30 mcM, it significantly increased the frequency of endoreduplicated mitosis. Overall, at equivalent toxic concentration, PMA was about 3- or 5-fold more effective in increasing SCEs and endoreduplication than methylmercury chloride and mercury nitrate, respectively (Lee et al, 1997).
b) CHROMOSOMAL ABERRATIONS or the absence of chromosomal aberrations have been reported in various animal studies. Chromosomal aberrations and SPINDLE DISTURBANCES have been induced by methyl mercury hydroxide, methoxyethyl mercury chloride, dimethyl mercury, ethylmercury chloride and phenylmercuric chloride in cultured human lymphocytes and other mammalian cells. CHROMOSOMAL ABERRATIONS have also been produced in larvae and newt embryos (IARC, 1993).
c) DOMINANT LETHAL MUTATION has been reported in studies of rats exposed to methyl mercury chloride. Evidence of dominant lethal mutation has not been clearly produced in mice (IARC, 1993).
d) Positive and negative evidence of GENE MUTATION has been reported in cultured Chinese hamster V79 cells. Sex-linked recessive lethal mutations have been produced in Drosophila melanogaster following exposure to methylmercury hydroxide (IARC, 1993).
e) ANEUPLOIDY was produced in Drosophila melanogaster by methyl mercury chloride, methyl mercury hydroxide,phenylmercuric hydroxide and phenyl mercury acetate (IARC, 1993).

1) Obtain whole blood mercury levels in acute exposures. Obtain baseline BUN, creatinine and electrolytes.
2) Blood analysis is useful for identifying acute exposure (Barregard, 1993) and may reflect the body burden of methylmercury.
3) NORMAL WHOLE BLOOD MERCURY CONCENTRATION: Whole blood mercury levels rarely exceed 1.5 mcg/dL in unexposed individuals (US DHHS, 1992). In acute situations, elevation of blood-mercury level to ranges of 25 to 50 mcg/dL (1246.2 to 2492.5 nmol/L) precede elevations in urinary excretion because of the body's capacity to store mercury (Cherian, 1978).
4) CONCENTRATION AT WHICH SYMPTOMS MAY OCCUR: Symptoms of toxicity may occur at blood mercury concentrations of 5 ug/dL or greater. Symptoms do not always correlate with blood mercury levels.
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 renal effects (Ellingsen et al, 1993).

1) The following procedures should be ordered: 24 hour urine collection for long-chain aryl or alkyl mercury compounds (eg; phenylmercury), creatinine and urinalysis. Urinary mercury levels are NOT useful for determining methylmercury (a short-chain alkyl mercury compound) exposure, since approximately 90% of methyl mercury is excreted via the bile into the feces.
2) URINARY MERCURY is the best biological marker for chronic ELEMENTAL, INORGANIC, OR LONG-CHAIN ARYL OR ALKYL (eg; phenylmercury) mercury exposure. Urinary mercury concentrations are also useful for assessing the response to chelation therapy.
3) LIMITATIONS: Urinary mercury levels are NOT useful for determining methylmercury (a short-chain alkyl mercury compound) exposure, since approximately 90% of methyl mercury is excreted via the bile into the feces (US DHHS, 1992) as inorganic mercury, after undergoing demethylation by microorganisms in the gut (Smith et al, 1994). Blood mercury concentration is a better determinant of total body methylmercury (Sue, 1994).
4) The patient should avoid seafood consumption for several days to a week prior to urine collection, as many types of seafood contain organic mercury.
5) NORMAL URINARY MERCURY CONCENTRATION: Urinary mercury concentrations in unexposed adults are usually less than 20 mcg/L (US DHHS, 1992).
6) CONCENTRATION AT WHICH SYMPTOMS MAY OCCUR: Signs and symptoms of toxicity may begin to occur at urinary mercury concentrations of 20 to 100 mcg/L. Urinary mercury levels, however, often do NOT correlate with clinical signs and symptoms of toxicity.
7) 24-HOUR URINE COLLECTION: There is a high degree of intraindividual variation in urine mercury levels. The averaging of several urinary mercury determinations may be required (Barregard, 1993).
8) SPOT MERCURY LEVELS: Spot sample collecting can be used to approximate the 24-hour sample (Barregard, 1993). A first morning void is often used.

1) 24 HOUR URINARY DELTA AMINOLEVULINIC ACID (ALA) levels are elevated to 3 to 10 mg/L in chronic mercury 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).
2) Urinary measurements of proteins (Abdelmegid et al, 1993; Snodgrass et al, 1981; Rosenmann et al, 1986) Ehrenberg, 1991), porphyrin profiles (Woods et al, 1993), N-acetyl beta-glucosaminidase (NAG) and NAG isoenzymes (Rosenmann et al, 1986; Ellingsen et al, 1993), beta(2)-microglobulin (US DHHS, 1992; Sue, 1994), and intestinal alkaline phosphatase (Verpooten et al, 1992) have been used in attempts to identify early effects of organic or inorganic mercury exposure.

1) HAIR
2) TOENAILS
3) MRI
4) BIOPSY AND AUTOPSY
5) ELECTROPHYSIOLOGICAL TESTING
6) NEUROPSYCHOLOGCIAL TESTING
7) OTHER

a) Winfield et al (1994) describe adaptation of a cold vapor atomic fluorescence spectrometric method, which enables detection of very low levels of total mercury, and can differentiate between inorganic and organic mercury (Winfield et al, 1994).
b) Thin-layer and gas chromatographic methods can also distinguish between organic and inorganic mercury in biological samples (IARC, 1993; Sue, 1994).

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). Cold vapor atomic absorption spectrometry can differentiate between inorganic and organic mercury.

a) This method is useful for monitoring chronic exposure to low levels of elemental mercury vapor, and can be adapted in order to differentiate organic mercury from inorganic mercury (Winfield et al, 1994).

a) The CSF mercury concentrations were very low, but correlated with plasma concentrations of mercury. The plasma concentrations of mercury appeared to provide a better indication of exposure than CSF mercury.

A) All patients with an exposure to dimethylmercury should be admitted. All acute ingestions should be admitted. Patients with moderate or severe neurologic toxicity felt to be secondary to organic mercury warrant inpatient evaluation for neurology and toxicology consultation, whole blood quantification, and evaluation for possible chelation.

A) Patients with chronic exposures can be referred to outpatient healthcare providers for evaluation.
B) Unintentional pediatric ingestions of mercurochrome can be managed in the home without gastrointestinal decontamination. In a retrospective series of 2250 cases of mercurochrome exposure (96 percent unintentional, 93.6 percent ingestions, 84.4 percent children) most patients remained asymptomatic. Minor manifestations (nausea, vomiting, abdominal pain, diarrhea) developed in 3.3 percent of patients and moderate manifestations developed in 7 patients (0.4%). Most patients (95.8 percent) were treated with dilution or irrigation only (Bryan & Krenzelok, 1996).

A) All cases with organic mercury toxicity should involve a toxicology and neurology consultants.

A) Asymptomatic or minimally symptomatic patients with chronic exposures already in healthcare facilities may be observed and referred to neurology or toxicology outpatient providers. All patients with acute exposures should be referred to a healthcare facility.

1) CHARCOAL ADMINISTRATION
2) CHARCOAL DOSE

1) INDICATIONS: Consider gastric lavage with a large-bore orogastric tube (ADULT: 36 to 40 French or 30 English gauge tube {external diameter 12 to 13.3 mm}; CHILD: 24 to 28 French {diameter 7.8 to 9.3 mm}) after a potentially life threatening ingestion if it can be performed soon after ingestion (generally within 60 minutes).
2) PRECAUTIONS:
3) LAVAGE FLUID:
4) COMPLICATIONS:
5) CONTRAINDICATIONS:

1) A basic metabolic panel including renal function tests should be followed since toxicity may be delayed.
2) Whole blood mercury levels are the preferred diagnostic test. Blood should be collected in a trace heavy metal free container approved by the appropriate reference laboratory. The whole blood mercury should be speciated to inorganic and organic fractions. Patients should abstain from fish meals for 1 week prior to testing. Levels of 10 to 15 mcg/L are common in patients eating several fish meals per week. Levels over 200 mcg/L have been associated with symptoms.
3) Hair testing is useful in documenting a remote exposure only, but it has no role in quantification of the exposure.
4) Obtain 24-hour urine collection for long-chain aryl or alkyl mercury compounds (eg, phenylmercury). Urinary mercury levels are NOT useful for determining methylmercury (a short-chain alkyl mercury compound) exposure, since approximately 90% of methyl mercury is cleared through biliary and gastrointestinal tract.
5) Chest x-ray should be obtained for inhalational exposures. Serial visual field testing and neuropsychiatric testing is useful for chronic toxicity monitoring.

1) Chelation should be performed with one of the following drugs in severe poisonings. For patients with severe poisoning, intravenous unithiol is the preferred initial chelator if it is available (available in Europe and through compounding pharmacies in the US).
2) All of the effective complexing agents administered to facilitate removal of mercury from the body contain sulfhydryl groups (Clarkson, 1990).

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) ADVERSE REACTIONS

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).
8) CASE REPORT: A 48-year-old woman developed severe neurotoxicity 5 months after allegedly spilling several drops of dimethyl mercury on her hand while wearing protective gloves. Succimer increased urinary mercury excretion from 257 mcg/24 hours to 39,800 mcg/24 hours but did not affect clinical outcome (Nierenberg et al, 1998).

1) EFFICACY
2) USUAL ADULT DOSE
3) USUAL PEDIATRIC DOSE
4) ADVERSE REACTIONS
5) DURATION OF THERAPY
6) CAUTIONS
7) PREGNANCY
8) IMPAIRED RENAL FUNCTION

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 (Kark et al, 1971; Hryhorczuk et al, 1982; Gledhill & Hopkins, 1972).
2) AVAILABILITY: NAP is still considered experimental and is not generally available as a medicinal preparation.
3) EFFICACY

1) THIOL RESIN - EFFICACY

1) BAL therapy has been shown to increase brain mercury levels in experimental animal models of methyl mercury (Berlin et al, 1965; Zimmer & Carter, 1979) and phenylmercuric acetate poisoning (Berlin & Rylander, 1964). It is CONTRAINDICATED in methyl mercury poisoning (Clarkson, 1990).

1) NAC therapy has been shown to reduce methyl mercury-induced fetal mortality and teratogenicity in rodent models (Ornagi et al, 1993).
2) Dialysis performed with n-acetylcysteine infused into the blood as it entered the dialyzer at a rate to produce a 10 millimolar concentration, produced a mean dialysance of 13 milliliters/minute and was associated with a 40-fold increase in urinary mercury excretion in a patient with acute methyl mercury ingestion (Lund et al, 1984).
3) STUDY: Methyl mercury poisoned mice were administered NAC in their drinking water (10 mg/mL) starting at 48 hours after poisoning. NAC-treated mice excreted from 47% to 54% of the radio-labelled mercury in their urine over the next 48 hours, as compared to 4% to 10% excretion in untreated mice. Excretion of inorganic mercury was not affected by oral NAC (Ballatori et al, 1998).

1) Treat pulmonary irritation and systemic effects.
2) Inhalation of alkyl mercury compounds may produce irritation of the mucous membranes. The irritation generally disappears shortly after cessation of exposure (Skerfving & Vostal, 1972).
3) Inhalation of some volatile organic mercury compounds may produce systemic toxicity. Phenyl mercury acetate containing latex paint may release mercury vapors (Agocs et al, 1990; CDC, 1990).

1) PULMONARY FUNCTION: Mild interstitial lung disease has been noted in acute mercury vapor exposure. Pulmonary function tests and chest x-ray may be of value in patients with significant exposure.

1) DECONTAMINATION: Remove contaminated clothing and jewelry and place them in plastic bags. Wash exposed areas with soap and water for 10 to 15 minutes with gentle sponging to avoid skin breakdown. A physician may need to examine the area if irritation or pain persists (Burgess et al, 1999).

1) In cases of significant exposure prehospital decontamination should occur outside the medical facility if possible since the wash may contaminate medical personnel and cause them to become poisoned.
2) Remove all contaminated clothing, seal into bags, and treat as hazardous waste. The person performing decontamination may be protected by wearing rubber gloves, disposable shoe covers, and a rubber apron.
3) All medical personnel should wear protective clothing, including respirators if significant amounts of dust are present, to prevent secondary contamination.

1) APPLICATION
2) DEBRIDEMENT
3) TREATMENT
4) TETANUS PROPHYLAXIS

1) Carefully observe patients with SKIN exposure for the development of any systemic signs or symptoms

a) In a retrospective series of 2250 cases of mercurochrome exposure 96% unintentional, 93.6% ingestions, 84.4% children most patients remained asymptomatic. Minor manifestations (nausea, vomiting, abdominal pain, diarrhea) developed in 3.3% of patients and moderate manifestations developed in 7 patients (0.4%). Most patients (95.8%) were treated with dilution or irrigation only. Unintentional pediatric ingestions of mercurochrome can be managed in the home without gastrointestinal decontamination (Bryan & Krenzelok, 1996).
b) There is little published information concerning the range of toxicity for many consumer products which contain organic mercury (Baselt, 2000; Gosselin et al, 1984).
c) One source rated the following mercury compounds extremely toxic: phenylmercuric salts of organic acids (eg, acetate, salicylate, oleate, benzoate, phthalate, and gluconate), methoxyethylmercuric chloride, ethyl and methyl mercuric chlorides, and ethyl and methyl mercuric phosphates. The oral lethal dose in adult humans is estimated as 5 to 50 mg/kg (Gosselin et al, 1984).

a) An adolescent developed mild clinical effects (nausea, vomiting, abdominal pain and dizziness) with elevated blood and urine mercury levels after ingesting 20 milliliters of a 2% solution of mercurochrome (Magarey, 1993).
b) An adult developed severe effects (hemorrhagic gastritis, renal failure, polyneuropathy) but survived with intensive medical therapy and chelation after ingesting 5 grams of Thiomersal (Pfab et al, 1996).

a) DIMETHYLMERCURY: An accidental spill of several drops of dimethylmercury onto the gloved hand of a female chemist resulted in the onset of diarrhea and nausea 2 months later which persisted for 3 months, then was followed by severe CNS toxicity, with profound effects on the cerebellum and eventual death, about 5 to 6 months post-exposure. Estimated initial body burden of mercury was approximately 1,344 mg (Siegler et al, 1999).
b) DIMETHYLMERCURY: A 48-year-old woman developed severe neurotoxicity 5 months after allegedly spilling several drops of dimethylmercury on her hand while wearing protective gloves. She died 10 months after exposure despite chelation therapy. The estimated absorbed dose (extrapolated from blood levels at presentation) was 1334 mg, or 0.44 mL of liquid dimethylmercury (Nierenberg et al, 1998).

a) Ingestion of 20 mL of 2% Merbromin by an adolescent resulted in nausea, vomiting, abdominal pain, dizziness and elevated blood mercury levels in a 15-year-old female (Magarey, 1993).
b) A 44-year-old man developed polyuric acute renal failure, coma, ascending sensorimotor neuropathy and respiratory failure after ingesting 5 grams of Thiomersal (Pfab et al, 1996).

a) Some organic mercury compounds are volatile and will produce toxic vapors. Examples of these compounds include methyl mercury, dimethyl mercury, ethyl mercuric chloride (chloroethylmercury) and ethyl mercury phosphate. Inhalation of aerosols, dusts or particulates may also result in adverse effects.
b) Proteinuria and subtle neurological and psychological effects have occurred following exposure to airborne mercury concentrations of 0.01 mg/m3 (US DHHS, 1992).
c) The American Conference of Governmental Industrial Hygienists (ACGIH) has recommended a threshold limit value (Time Weighted Average, TWA) of 0.01 mg/m3 for alkyl mercury compounds, and of 0.1 mg/m(3) for aryl compounds (ACGIH, 1994).
d) The OSHA permissible exposure limit (Time Weighted Average, TWA) for organo alkyl mercury compounds is 0.01 mg/m(3). The TWA is the average airborne concentration to which a WORKER may be exposed in any 8 hour shift of a 40 hour work week. This concentration should not be exceeded (OSHA, 1992).

a) METHYLMERCURY: A single acute ingestion of 45 mg of methyl mercury resulted in whole blood levels of 1930 and 1007 nanograms/mL 2 and 24 hours after ingestion but did not result in symptoms of toxicity (Lund et al, 1984).
b) ANTISEPTIC MATERIALS (Thimerosal, Merthiolate, Acetomeroctol, and Merbromin) can be absorbed and can cause symptoms. A 15-year-old female ingested 20 mL of 2% Merbromin and presented 17 hours post ingestion with nausea, vomiting, abdominal pain, and dizziness. Mercury blood levels two days post ingestion were 412.0 nmol/L. The patient recovered (Magarey, 1993).
c) One source report survival by an adult after ingesting 5 grams of Thiomersal. The man presented at the hospital 1 hour after ingestion with nausea and vomiting. Hemorrhagic erosive gastritis, elevated blood mercury levels, tubular renal failure, CNS and peripheral neuropathy resembling Guillian-Barre developed during hospitalization. The patient's survival was tentatively attributed to spontaneous emesis which occurred 15 minutes after ingestion. Chelation and intensive supportive therapy were provided (Pfab et al, 1996).
d) The maximum allowable contaminant level set by the EPA for mercury in drinking water is 2 ppb or 2 mcg/L. The FDA will allow up to 1 ppm of mercury in fish, and 2 ppb (2 mcg/L) in bottled drinking water. The WHO guideline for maximum drinking water concentration of mercury is 1 ppb or 1 mcg/L (US DHHS, 1992).

a) Some organic mercury compounds are volatile and will produce toxic vapors. Examples of these compounds include methyl mercury, dimethyl mercury, ethyl mercuric chloride (chloroethylmercury) and ethyl mercury phosphate. Inhalation of aerosols, dusts or particulates may also result in adverse effects.
b) PHENYLMERCURIC ACETATE: A survey of 74 people living in 19 houses newly-painted with an interior latex paint containing phenylmercuric acetate (median=3.8 millimoles of mercury/liter) showed elevated mercury levels in the air (median=10 nanomoles/cubic meter; range of less than 0.5 to 49.9) and in the urine (median=4.7 nanomoles/millimole of creatinine; range of 1.4 to 66.5) (Agocs et al, 1990). There was no clinical information provided except for the mention of acrodynia in a 4-year-old boy.
c) Alkyl mercury air concentrations which are considered by the National Institute for Occupational Safety and Health immediately dangerous to life or health (IDLH) are 10 mg/m3 (US DHHS, 1990).

a) DIMETHYLMERCURY: A 29-year-old man spilled 1 to 2 mL of dimethylmercury onto his nitrile double gloved hand. After the removal of his glove, 2 decontamination showers, and chelation therapy with succimer (initially 900 mg [10 mg/kg] twice daily and then 500 mg 3 times daily) on hospital day 1, he was discharged the next day. Laboratory results revealed a serum mercury concentration of 4 mcg/L. On a follow-up visit a week later, his neurologic exam was normal and his chelation therapy was switched to DMPS (600 mg 3 times daily; 6.82 mg/kg). At that time, his spot urine mercury was 11 mcg/g creatinine. On week 3, his 24-hour urine collection was 7 mcg/g creatinine. He never developed any symptoms and continued to take DMPS for 3 weeks. His chelation therapy was discontinued after his final serum mercury concentration reached 2 mcg/L (Salinger et al, 2015).

a) ETHYL MERCURY: A 38-year-old woman with Guillain-Barre syndrome was accidentally exposed to high levels of thimerosal (ethyl mercury), a column disinfectant used during a protein A Immunoadsorption treatment. The single acute exposure due to equipment operational errors resulted in a maximum serum mercury level of 2.25 mcg/mL. Ten days after the exposure, chelation therapy was initiated with DMSA 600 mg three times daily for 30 days. The patient did not develop any short or long term clinical effects from the thimerosal exposure (Koch & Trapp, 2006).

1) BLOOD MERCURY LEVELS IN THE US
2) MERCURY CONCENTRATIONS AND THIOMERSAL-CONTAINING VACCINES
3) CASE REPORTS
4) SPECIFIC SUBSTANCE

a) Adopted Value

1) 44,300 mcg/m(3) for 8H (RTECS , 2001)
2) 150 mcg/m(3) for 46D (RTECS , 2001)

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) Muscle incoordination, ataxia, hyperesthesia, tremor, seizures, and coma may occur in some animals. Unusual weight loss may occur as a result of diarrhea and anorexia.
2) ACUTE SYNDROME - Acute syndrome is marked by gastrointestinal signs including vomiting and diarrhea which may lead to fluid and electrolyte losses (Beasley et al, 1990).
3) CHRONIC SYNDROME - Chronic syndrome is more common, after exposure periods of several days or longer. Neurologic, GI, renal, and dermal effects are seen (Beasley et al, 1990).

1) 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) 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) ALKYL MERCURIC COMPOUNDS - 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) Organic mercurials are absorbed via all routes, including dermal (Beasley et al, 1990).