Contact Us    Contact Us     |     Feedback
MOBILE VIEW  | 

MERCURIC ACETATE

Export To Excel

Classification   |    Detailed evidence-based information

Substances Included Synonyms

Therapeutic Toxic Class

    A) Mercuric acetate is an inorganic mercury compound.

Specific Substances

    A) No Synonyms were found in group or single elements
    1.2.1) MOLECULAR FORMULA
    1) C4-H6-O4.Hg

Available Forms Sources

    A) FORMS
    1) Mercuric acetate is an inorganic mercury compound. It occurs as white crystals, scales, or powder with a mild, vinegar-like odor (HSDB, 1993).
    B) USES
    1) It is used for mercuration of organic compounds, in the absorption of ethylene, and as a chemical intermediate and catalyst (EPA, 1985; Budavari, 1989). Mercuric acetate has been used as a model compound to study the effects of inorganic mercury in experimental animals (Gale, 1981).

Overview

Life Support

    A) This overview assumes that basic life support measures have been instituted.

Clinical Effects

    0.2.1) SUMMARY OF EXPOSURE
    A) Mercuric acetate has been used as a model compound to study the toxicity of inorganic mercury.
    B) Mercury compounds can be absorbed by inhalation and through the skin. The principal concerns from acute inorganic mercury poisoning are sudden, profound circulatory collapse with tachycardia, hypotension and peripheral vasoconstriction, vomiting, and bloody diarrhea. Renal failure usually develops within 24 hours and may be life-threatening.
    C) Mercuric salts are corrosive and nephrotoxic. Salivation, metallic taste, abdominal pain, seizures, proteinuria, nephrotic syndrome (oliguria and anuria) may occur. Circulatory collapse, bloody diarrhea, and acute renal failure have been reported following peritoneal lavage with mercuric chloride.
    D) The brain is the critical organ for chronic inorganic mercury poisoning. TREMOR and psychological changes encompassing increased irritability and sensitivity, xenophobia, insomnia, hallucinations, and mania. Eventually there is spongeous degeneration of the brain with loss of many higher functions.
    E) When mercury poisoning is suspected in critically ill patients, chelation therapy should be started regardless of the form of mercury causing toxicity.
    0.2.3) VITAL SIGNS
    A) Sudden and profound circulatory collapse with tachycardia, weak and shallow pulse, hypotension and peripheral vasoconstriction can occur from ingestion of inorganic mercurials (HSDB , 1990).
    0.2.4) HEENT
    A) Mercuric acetate is irritating to the eyes.
    0.2.5) CARDIOVASCULAR
    A) Profound circulatory collapse, with tachycardia and hypotension, can occur from acute exposure to inorganic mercurials.
    0.2.6) RESPIRATORY
    A) Severe and potentially lethal pulmonary edema has been reported from inhalation of large amounts of elemental mercury. Mercuric salts could potentially act in a similar manner.
    0.2.7) NEUROLOGIC
    A) Peripheral neuropathy and brain damage can occur even from acute exposures.
    0.2.8) GASTROINTESTINAL
    A) Vomiting, nausea, bloody diarrhea, and edema of the upper GI tract have occurred from ingestion of inorganic mercurial compounds.
    0.2.9) HEPATIC
    A) Liver necrosis may occur.
    0.2.10) GENITOURINARY
    A) Oliguria, anuria, and renal failure may occur within 24 hours of an acute exposure to inorganic mercurials.
    0.2.14) DERMATOLOGIC
    A) Mercuric acetate may be a primary irritant or corrosive.
    0.2.20) REPRODUCTIVE
    A) At the time of this review, no studies were found on the possible reproductive effects of mercuric acetate in humans.
    B) ANIMAL STUDIES - Mercuric acetate produced resorptions and abnormalities in hamsters.
    0.2.21) CARCINOGENICITY
    A) At the time of this review, no data were available to assess the carcinogenic potential of this agent.
    0.2.22) OTHER
    A) Mercuric acetate can be toxic by inhalation, ingestion, and skin contact.

Laboratory Monitoring

    A) Obtain whole blood mercury levels, 24 hour urine collection for mercury, baseline BUN, creatinine, urinalysis and electrolytes.
    B) NORMAL RANGE - Mercury levels rarely exceed 1.5 mcg/dL.
    C) Normal urine excretion without chelation therapy rarely exceeds 50 mcg/24hrs of mercury.

Treatment Overview

    0.4.2) ORAL/PARENTERAL EXPOSURE
    A) Mercury salts may be corrosive but GI perforation is not common. The role of gastric decontamination is unclear
    B) ACTIVATED CHARCOAL: Administer charcoal as a slurry (240 mL water/30 g charcoal). Usual dose: 25 to 100 g in adults/adolescents, 25 to 50 g in children (1 to 12 years), and 1 g/kg in infants less than 1 year old.
    C) GASTRIC LAVAGE: Consider after ingestion of a potentially life-threatening amount of poison if it can be performed soon after ingestion (generally within 1 hour). Protect airway by placement in the head down left lateral decubitus position or by endotracheal intubation. Control any seizures first.
    1) CONTRAINDICATIONS: Loss of airway protective reflexes or decreased level of consciousness in unintubated patients; following ingestion of corrosives; hydrocarbons (high aspiration potential); patients at risk of hemorrhage or gastrointestinal perforation; and trivial or non-toxic ingestion.
    D) Perform chelation in symptomatic patients.
    1) SUCCIMER: INITIAL DOSE: 10 mg/kg or 350 mg/m(2) every 8 hours orally for 5 days, then increase interval to every 12 hours for next 14 days; repeat course(s) if indicated. A minimum of 2 weeks between courses is recommended, unless the patient's symptoms or blood concentrations indicate a need for more prompt treatment.
    2) D-PENICILLAMINE: Use only if less toxic agents not available or not tolerated. USUAL DOSE: ADULT: 1 to 1.5 g/day given orally in 4 divided doses. CHILD: 15 to 30 mg/kg/day in 3 to 4 divided doses. Initially, a small dose may be given to minimize side effects and then increased gradually (eg, 25% of the desired dose in week 1, 50% in week 2, and the full dose by week 3). Avoid if penicillin allergic. Monitor for proteinuria, hematuria, rash, leukopenia, thrombocytopenia.
    3) BAL (Dimercaprol): Is indicated for patients with severe gastrointestinal symptoms or patients in renal failure. Administer 3 to 5 mg/kg/dose every 4 hours IM for the first 48 hours, then 2.5 to 3 mg/kg every 6 hours for the second 48 hours, then every 12 hours for 7 additional days.
    4) DMPS: A chelating agent, available in Europe, for the treatment of arsenic, bismuth, lead, copper, and mercury toxicity. ADULT DOSE: IV: DAY 1: 250 mg every 3 to 4 hours (1500 to 2000 mg total); DAY 2: 250 mg every 4 to 6 hours (1000 to 1500 mg total); DAY 3: 250 mg every 6 to 8 hours (750 to 1000 mg total); DAY 4: 250 mg every 8 to 12 hours (500 to 750 mg total); SUBSEQUENT DAYS: 250 mg every 8 to 24 hours (250 to 750 mg total). ORAL: ACUTE TOXICITY: 1200 to 2400 mg/day in equally divided doses (100 to 200 mg 12 times daily); CHRONIC TOXICITY: 300 to 400 mg/day orally (in single doses of 100 to 200 mg). The dose may be increased in severe toxicity.
    E) Monitor volume status, hematocrit, urine output and renal function tests.
    F) HEMODIALYSIS should be considered early in severe cases, with diminishing urine output following chelation. The BAL-mercury complex is dialyzable.
    0.4.4) EYE EXPOSURE
    A) DECONTAMINATION: Remove contact lenses and irrigate exposed eyes with copious amounts of room temperature 0.9% saline or water for at least 15 minutes. If irritation, pain, swelling, lacrimation, or photophobia persist after 15 minutes of irrigation, the patient should be seen in a healthcare facility.
    B) Take precautions to avoid exposure of health care professionals and other individuals.
    C) Observe for development of clinical signs and symptoms and follow treatment recommendations in DERMAL EXPOSURE where appropriate.
    0.4.5) DERMAL EXPOSURE
    A) OVERVIEW
    1) 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).
    2) Take precautions to avoid exposure of health care professionals and other individuals.
    3) SYSTEMIC EFFECTS
    a) Some chemicals can produce systemic poisoning by absorption through intact skin. Carefully observe patients with dermal exposure for the development of any systemic signs or symptoms and administer symptomatic treatment as necessary.
    b) Administration of chelators may be required. Provide supportive care.

Range Of Toxicity

    A) The average lethal acute dose of inorganic mercurials is approximately 1 gram. There is no adequate test to determine the body burden of mercury.

Clinical Effects

Summary Of Exposure

    A) Mercuric acetate has been used as a model compound to study the toxicity of inorganic mercury.
    B) Mercury compounds can be absorbed by inhalation and through the skin. The principal concerns from acute inorganic mercury poisoning are sudden, profound circulatory collapse with tachycardia, hypotension and peripheral vasoconstriction, vomiting, and bloody diarrhea. Renal failure usually develops within 24 hours and may be life-threatening.
    C) Mercuric salts are corrosive and nephrotoxic. Salivation, metallic taste, abdominal pain, seizures, proteinuria, nephrotic syndrome (oliguria and anuria) may occur. Circulatory collapse, bloody diarrhea, and acute renal failure have been reported following peritoneal lavage with mercuric chloride.
    D) The brain is the critical organ for chronic inorganic mercury poisoning. TREMOR and psychological changes encompassing increased irritability and sensitivity, xenophobia, insomnia, hallucinations, and mania. Eventually there is spongeous degeneration of the brain with loss of many higher functions.
    E) When mercury poisoning is suspected in critically ill patients, chelation therapy should be started regardless of the form of mercury causing toxicity.

Vital Signs

    3.3.1) SUMMARY
    A) Sudden and profound circulatory collapse with tachycardia, weak and shallow pulse, hypotension and peripheral vasoconstriction can occur from ingestion of inorganic mercurials (HSDB , 1990).
    3.3.4) BLOOD PRESSURE
    A) CIRCULATORY COLLAPSE - Sudden and profound circulatory collapse with tachycardia, hypotension and peripheral vasoconstriction can occur from acute inorganic mercury poisoning.

Heent

    3.4.1) SUMMARY
    A) Mercuric acetate is irritating to the eyes.
    3.4.3) EYES
    A) WITH POISONING/EXPOSURE
    1) IRRITATION - Mercuric acetate is a strong irritant (Sax & Lewis, 1987).
    2) MERCURIALENTIS - Brown deposits of mercury in the lens cause opacity (Clayton & Clayton, 1981).
    3) VISUAL DEFECTS - Narrowing of the visual field and increase in the size of the blind spot are ophthalmic signs of chronic exposure to mercury ad its inorganic salts (Gmyrya et al, 1970).
    4) INCREASED RETINAL EXCITABILITY - Mercuric acetate induced increased excitability in the retina of cats injected subcutaneous with up to 0.25 mg/kg every other day for up to 4 weeks (Gitter et al, 1988).
    3.4.6) THROAT
    A) WITH POISONING/EXPOSURE
    1) CORROSION - Metallic taste, foul breath, loosening of the teeth, burning and intense salivation occur from oral exposure to inorganic mercury salts, as they are corrosive.
    2) Excessive salivation and gingivitis occur with chronic poisoning from inorganic mercurials (HSDB , 1990).

Cardiovascular

    3.5.1) SUMMARY
    A) Profound circulatory collapse, with tachycardia and hypotension, can occur from acute exposure to inorganic mercurials.
    3.5.2) CLINICAL EFFECTS
    A) HYPOTENSIVE EPISODE
    1) WITH POISONING/EXPOSURE
    a) Sudden and profound circulatory collapse with tachycardia, hypotension and peripheral vasoconstriction can occur from acute inorganic mercury poisoning.

Respiratory

    3.6.1) SUMMARY
    A) Severe and potentially lethal pulmonary edema has been reported from inhalation of large amounts of elemental mercury. Mercuric salts could potentially act in a similar manner.
    3.6.2) CLINICAL EFFECTS
    A) ACUTE LUNG INJURY
    1) WITH POISONING/EXPOSURE
    a) Severe and potentially fatal pulmonary edema can occur from inhalation of mercury (ILO, 1983).

Neurologic

    3.7.1) SUMMARY
    A) Peripheral neuropathy and brain damage can occur even from acute exposures.
    3.7.2) CLINICAL EFFECTS
    A) CENTRAL NERVOUS SYSTEM FINDING
    1) WITH POISONING/EXPOSURE
    a) Mercury crosses the blood-brain barrier (Blum & Manzo, 1985).
    B) SECONDARY PERIPHERAL NEUROPATHY
    1) WITH POISONING/EXPOSURE
    a) A neurological syndrome resembling amyotrophic lateral sclerosis (Lou Gehrig disease) can occur even from acute exposure to mercury and its salts (Adams et al, 1983). The peripheral effects involve a dying-back axonopathy, followed by demyelinization. General loss of brain function may also occur (Folkl & Konig, 1983).

Gastrointestinal

    3.8.1) SUMMARY
    A) Vomiting, nausea, bloody diarrhea, and edema of the upper GI tract have occurred from ingestion of inorganic mercurial compounds.
    3.8.2) CLINICAL EFFECTS
    A) VOMITING
    1) WITH POISONING/EXPOSURE
    a) Vomiting along with nausea and bloody diarrhea may occur from ingestion or inhalation of inorganic mercury salts (Clayton & Clayton, 1981).
    B) EDEMA
    1) WITH POISONING/EXPOSURE
    a) Edema of the upper GI tract may occur.

Hepatic

    3.9.1) SUMMARY
    A) Liver necrosis may occur.
    3.9.2) CLINICAL EFFECTS
    A) HEPATIC NECROSIS
    1) WITH POISONING/EXPOSURE
    a) Liver necrosis may occur.

Genitourinary

    3.10.1) SUMMARY
    A) Oliguria, anuria, and renal failure may occur within 24 hours of an acute exposure to inorganic mercurials.
    3.10.2) CLINICAL EFFECTS
    A) KIDNEY DISEASE
    1) WITH POISONING/EXPOSURE
    a) A large amount of the mercurial salt will become localized to the kidney producing a generalized increase in the permeability of the tubular epithelium; nephrotic syndrome occurs with oliguria and anuria requiring dialysis. Diagnosis should be based on elevated urinary excretion of mercury.
    B) RENAL FAILURE SYNDROME
    1) WITH POISONING/EXPOSURE
    a) Renal failure usually develops within 24 hours and is associated with albuminuria, epithelial cell casts, hematuria, glycosuria, and aminoaciduria. Studies in rats and mice indicate that mercuric acetate can produce renal toxicity (HSDB , 1990).
    b) A transient increase in the activity of urinary gamma-glutamyl transferase activity was an indicator of nephrotoxicity in rats given a single IP injection of mercuric acetate at 1 mg Hg/kg (Dierickx, 1981).

Dermatologic

    3.14.1) SUMMARY
    A) Mercuric acetate may be a primary irritant or corrosive.
    3.14.2) CLINICAL EFFECTS
    A) DERMATITIS
    1) WITH POISONING/EXPOSURE
    a) Mercuric acetate may be a primary irritant or corrosive. Dermatitis with or without vesication may be produced (HSDB , 1990).

Reproductive

    3.20.1) SUMMARY
    A) At the time of this review, no studies were found on the possible reproductive effects of mercuric acetate in humans.
    B) ANIMAL STUDIES - Mercuric acetate produced resorptions and abnormalities in hamsters.
    3.20.2) TERATOGENICITY
    A) SUMMARY
    1) Organic mercury compounds are human teratogens. Methyl mercury caused fetal Minimata disease in Japan; phenylmercuric acetate contaminated pork consumed by American Indians, and methyl mercury-treated grain was consumed in Iraq. In all these cases, prenatal exposures were associated with severe or fatal neurological defects (Baranski, 1981).
    2) The effects of exposure to inorganic mercury are less clear. Mercury is available to the fetus (Lauwerys, 1978; Tsuchiya et al, 1984; Lien et al, 1983; pp 505-509).
    B) CASE REPORTS
    1) A 3-month-old developed cataracts, anemia, and renal dysfunction resulting from mercury exposure during fetal life and the 1 month lactation period due to the extensive use of inorganic mercury containing soap by the mother (Lauwerys et al, 1987).
    C) CASE SERIES
    1) 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 following an incident where methyl-mercury-treated seed grain was used in daily preparation of home baked bread and then consumed by the pregnant woman. 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 levels were obtained in the children (Marsh et al, 1987).
    D) ANIMAL STUDIES
    1) Fetotoxicity has been observed in the rat. In the hamster, fetotoxicity, post-implantation mortality, change in litter size and specific developmental abnormalities in homeostasis, the body wall, the central nervous, craniofacial, cardiovascular and musculoskeletal systems have been observed (RTECS , 1990; HSDB , 1990).
    2) Mercuric acetate given as a single dose of 15 mg/kg on day 8 of gestation induced cleft palate, hydrocephalus, increased resorptions, malformed hearts in various strains of hamsters (Gale, 1981). Heart defects were the most prominent malformations (Gale, 1980).
    3) Mercuric acetate was most active for inducing increased resorptions in the hamster by the following routes (in decreasing order): IP, IV, SC, and oral (Gale, 1974).
    4) The embryotoxic effects of mercuric acetate were prevented by zinc (Gale, 1984).
    3.20.3) EFFECTS IN PREGNANCY
    A) PLACENTAL BARRIER
    1) SUMMARY
    a) All forms of mercury move freely across the placenta, and fetal concentrations are at least as high as those in the mother (HSDB , 1990). Mercuric acetate crossed the placenta in hamsters (Gale & Hanlon, 1976).
    B) CASE REPORT
    1) A case of acute mercury inhalation toxicity occurred in a pregnant woman. Twenty-six days after the exposure the child was born without clinical abnormalities, but with serum blood levels comparable with the mother's (Lien et al, 1983).
    C) ABORTION
    1) Increased spontaneous abortions, and menstrual dysfunction, have been reported in women exposed to mercury (Goncharuk, 1971; Panova & Ivanova, 1976; Goncharuk, 1977; Marinova, 1973).
    3.20.4) EFFECTS DURING BREAST-FEEDING
    A) BREAST MILK
    1) Mercury is found in human breast milk (Mattison, 1983). Oral absorption of mercury is greater in infants than in adults (Barlow & Sullivan, 1982). A level of 4 mcg/L in breast milk is considered dangerous for infants (Mattison, 1983).
    B) ABSORPTION
    1) A correlation between total mercury concentrations measured in the hair of nursing neonates and their mothers was found to be significant (Gonzalez et al, 1985).

Carcinogenicity

    3.21.1) IARC CATEGORY
    A) IARC Carcinogenicity Ratings for CAS1600-27-7 (International Agency for Research on Cancer (IARC), 2016; International Agency for Research on Cancer, 2015; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010a; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2008; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2007; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2006; IARC, 2004):
    1) IARC Classification
    a) Listed as: Mercuric acetate
    b) Carcinogen Rating: 2B
    1) The agent (mixture) is possibly carcinogenic to humans. The exposure circumstance entails exposures that are possibly carcinogenic to humans. This category is used for agents, mixtures and exposure circumstances for which there is limited evidence of carcinogenicity in humans and less than sufficient evidence of carcinogenicity in experimental animals. It may also be used when there is inadequate evidence of carcinogenicity in humans but there is sufficient evidence of carcinogenicity in experimental animals. In some instances, an agent, mixture or exposure circumstance for which there is inadequate evidence of carcinogenicity in humans but limited evidence of carcinogenicity in experimental animals together with supporting evidence from other relevant data may be placed in this group.
    3.21.2) SUMMARY/HUMAN
    A) At the time of this review, no data were available to assess the carcinogenic potential of this agent.
    3.21.3) HUMAN STUDIES
    A) LACK OF INFORMATION
    1) At the time of this review, no data were available to assess the carcinogenic potential of this agent.
    B) ANIMAL STUDIES
    1) Mercury was not carcinogenic in mice at a level of 5 ppm in the drinking water (Schroeder & Mitchener, 1975).

Genotoxicity

    A) Mercuric acetate induced mutations in mouse cells. Mercuric ion has induced DNA strand breaks and cross links, and sister chromatid exchanges.

Laboratory Monitoring

Monitoring Parameters Levels

    4.1.1) SUMMARY
    A) Obtain whole blood mercury levels, 24 hour urine collection for mercury, baseline BUN, creatinine, urinalysis and electrolytes.
    B) NORMAL RANGE - Mercury levels rarely exceed 1.5 mcg/dL.
    C) Normal urine excretion without chelation therapy rarely exceeds 50 mcg/24hrs of mercury.
    4.1.2) SERUM/BLOOD
    A) BLOOD/SERUM CHEMISTRY
    1) Normal whole blood mercury levels rarely exceed 1.5 mcg/dL in unexposed individuals. Normal levels are approximately 0.5 mcg/dL (Skerfving, 1972). Levels of 4 to 220 mcg/dL have been lethal (HSDB , 1990).
    2) Most commonly used analytical methods do not distinguish between inorganic and organic mercury in the blood (Zenz, 1988). 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). Specific analysis of inorganic mercury in the blood did correlate with the level of exposure in workers exposed chronically (Yoshida, 1985).
    3) In acute exposures, 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 et al, 1978).
    4) Blood mercury levels did not correlate with indicators of toxicity in chronically exposed workers (Rosenman et al, 1986).
    4.1.3) URINE
    A) URINARY LEVELS
    1) Normal urine excretion rarely exceeds 15 mcg/L (74.7 nmol/L) in unexposed individuals. Normal levels are approximately 0.5 mcg/L, with the upper limit of normality being 20 mcg/L (Clayton & Clayton, 1981). Levels of 0.1 to 0.5 mg Hg/L (100 to 500 mcg/L) are considered significantly elevated (Sittig, 1985).
    2) Spot urine levels are inconsistent due to diurnal variation. The interpretation of these levels is most accurate when samples are taken at the same time of day and corrected for creatinine. Because proteinuria and glycosuria cause specific gravity changes, correction using this method is less accurate than the creatinine method. Patients with kidney damage should be excluded (Calder et al, 1984).
    3) Monitoring of spot urine mercury levels did correlate with occurrence of neuropsychological toxicity and motor nerve conduction velocity in 42 chronically exposed workers (Rosenman et al, 1986).
    4) Urine 24-hour delta ALA levels are invariably elevated to the ranges of 3 to 10 mg/liter in chronic poisoning cases. Although urinary levels as high as 2000 mcg/L have been seen without symptoms, levels greater than 100 mcg/L may need careful behavioral and neurological evaluation (Adams et al, 1983).
    5) Workers chronically exposed to mercury vapor exhibited preclinical renal toxicity at spot urine mercury levels of greater than 50 mcg/g creatinine (Roels et al, 1985).
    6) Collection of a 24-hour urine sample, followed by challenge with D-penicillamine for 4 days, has been used to document mercury body burden (Ishihara et al, 1974).
    4.1.4) OTHER
    A) OTHER
    1) MONITORING
    a) If respiratory tract irritation is present, monitor arterial blood gases and chest x-ray.
    2) ELECTROPHYSIOLOGICAL TESTING
    a) Nerve conduction velocity studies in workers chronically exposed to inorganic mercury are informative for evaluation of mercury toxicity. Slowing of the median motor nerve correlated with both increased blood and urine mercury levels and an increased number of neurologic symptoms (Singer et al, 1987).
    3) PULMONARY FUNCTION TESTS
    a) If respiratory tract irritation is present, it may be useful to monitor pulmonary function tests.

Radiographic Studies

    A) CHEST RADIOGRAPH
    1) If respiratory tract irritation is present, monitor chest x-ray.

Treatment

Life Support

    A) Support respiratory and cardiovascular function.

Monitoring

    A) Obtain whole blood mercury levels, 24 hour urine collection for mercury, baseline BUN, creatinine, urinalysis and electrolytes.
    B) NORMAL RANGE - Mercury levels rarely exceed 1.5 mcg/dL.
    C) Normal urine excretion without chelation therapy rarely exceeds 50 mcg/24hrs of mercury.

Oral Exposure

    6.5.2) PREVENTION OF ABSORPTION
    A) GASTRIC DECONTAMINATION
    1) Inorganic mercury salts may produce severe gastric erosion (Sauder et al, 1988). The role of gastric decontamination is unclear.
    2) Abdominal x-ray may be useful in evaluating the need for gastric lavage.
    B) ACTIVATED CHARCOAL
    1) CHARCOAL ADMINISTRATION
    a) Consider administration of activated charcoal after a potentially toxic ingestion (Chyka et al, 2005). Administer charcoal as an aqueous slurry; most effective when administered within one hour of ingestion.
    2) CHARCOAL DOSE
    a) Use a minimum of 240 milliliters of water per 30 grams charcoal (FDA, 1985). Optimum dose not established; usual dose is 25 to 100 grams in adults and adolescents; 25 to 50 grams in children aged 1 to 12 years (or 0.5 to 1 gram/kilogram body weight) ; and 0.5 to 1 gram/kilogram in infants up to 1 year old (Chyka et al, 2005).
    1) Routine use of a cathartic with activated charcoal is NOT recommended as there is no evidence that cathartics reduce drug absorption and cathartics are known to cause adverse effects such as nausea, vomiting, abdominal cramps, electrolyte imbalances and occasionally hypotension (None Listed, 2004).
    b) ADVERSE EFFECTS/CONTRAINDICATIONS
    1) Complications: emesis, aspiration (Chyka et al, 2005). Aspiration may be complicated by acute respiratory failure, ARDS, bronchiolitis obliterans or chronic lung disease (Golej et al, 2001; Graff et al, 2002; Pollack et al, 1981; Harris & Filandrinos, 1993; Elliot et al, 1989; Rau et al, 1988; Golej et al, 2001; Graff et al, 2002). Refer to the ACTIVATED CHARCOAL/TREATMENT management for further information.
    2) Contraindications: unprotected airway (increases risk/severity of aspiration) , nonfunctioning gastrointestinal tract, uncontrolled vomiting, and ingestion of most hydrocarbons (Chyka et al, 2005).
    C) GASTRIC LAVAGE
    1) CAUTION: Progressive pulmonary distress, leading to fatal cardiopulmonary arrest, was attributed to aspiration of mercury during unprotected gastric lavage following a large overdose of mercuric chloride. Elective tracheal intubation should be considered prior to performance of gastric lavage (McLauchlan, 1991).
    2) 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).
    a) Consider lavage more than 60 minutes after ingestion of sustained-release formulations and substances known to form bezoars or concretions.
    3) PRECAUTIONS:
    a) SEIZURE CONTROL: Is mandatory prior to gastric lavage.
    b) AIRWAY PROTECTION: Place patients in the head down left lateral decubitus position, with suction available. Patients with depressed mental status should be intubated with a cuffed endotracheal tube prior to lavage.
    4) LAVAGE FLUID:
    a) Use small aliquots of liquid. Lavage with 200 to 300 milliliters warm tap water (preferably 38 degrees Celsius) or saline per wash (in older children or adults) and 10 milliliters/kilogram body weight of normal saline in young children(Vale et al, 2004) and repeat until lavage return is clear.
    b) The volume of lavage return should approximate amount of fluid given to avoid fluid-electrolyte imbalance.
    c) CAUTION: Water should be avoided in young children because of the risk of electrolyte imbalance and water intoxication. Warm fluids avoid the risk of hypothermia in very young children and the elderly.
    5) COMPLICATIONS:
    a) Complications of gastric lavage have included: aspiration pneumonia, hypoxia, hypercapnia, mechanical injury to the throat, esophagus, or stomach, fluid and electrolyte imbalance (Vale, 1997). Combative patients may be at greater risk for complications (Caravati et al, 2001).
    b) Gastric lavage can cause significant morbidity; it should NOT be performed routinely in all poisoned patients (Vale, 1997).
    6) CONTRAINDICATIONS:
    a) Loss of airway protective reflexes or decreased level of consciousness if patient is not intubated, following ingestion of corrosive substances, hydrocarbons (high aspiration potential), patients at risk of hemorrhage or gastrointestinal perforation, or trivial or non-toxic ingestion.
    6.5.3) TREATMENT
    A) CHELATION THERAPY
    1) Chelation should be performed with one of the following drugs in severe poisonings.
    2) All of the effective complexing agents administered to facilitate removal of mercury from the body contain sulfhydryl groups (Clarkson, 1990).
    B) DIMERCAPROL
    1) INDICATION
    a) If the patient is severely symptomatic or cannot tolerate oral chelation. BAL therapy may be judiciously continued despite renal failure since a major fraction of this complex is excreted in bile and the BAL mercury complex is cleared by dialysis.
    2) DOSE
    a) 3 to 5 milligrams/kilogram/dose every 4 hours by deep intramuscular injection the first 2 days; 2.5 to 3 milligrams/kilogram/dose intramuscularly every 6 hours for 2 days; then 2.5 to 3 milligrams/kilogram/dose every 12 hours for a week intramuscularly.
    3) EFFICACY
    a) BAL has been shown to increase mercury excretion in the urine, bile and feces, decrease the body burden of mercury, and decrease mortality in animal models of inorganic mercury poisoning (Yonaga & Morita, 1980; (Kojima et al, 1989) Nielsen & Anderson, 1991; Magos, 1967). BAL increased distribution of mercury to the brain in some animal models of inorganic mercury poisoning (Aaseth et al, 1982) Nielsen & Anderson, 1991).
    b) BAL therapy in patients with acute inorganic mercury ingestion has been associated with clinical improvement or the failure to develop severe toxicity (Singer et al, 1994; (Pesce et al, 1977; Longcope et al, 1946) Stack et al, 1983; (Suzuki et al, 1992; Wang et al, 1992). Changes in mercury excretion were not evaluated in these cases.
    c) HEMODIALYSIS: The BAL mercury complex is cleared by hemodialysis (Guinta et al, 1983).
    d) PERITONEAL DIALYSIS: BAL therapy and peritoneal dialysis was associated with mercury clearance rates of 0.57 to 2.38 milliliters/minute in an adult who developed acute renal failure after ingesting mercury bichloride (Lowenthal et al, 1974).
    1) Dialysate mercury concentrations without BAL therapy were undetectable in a child with renal failure after ingesting inorganic mercury. When BAL therapy was begun, dialysate mercury concentrations ranged form 2.9 to 33 micrograms/Liter (Kahn et al, 1977).
    4) LABORATORY
    a) Monitor urine mercury excretion during chelation therapy to assess the effects of therapy.
    5) ADVERSE EFFECTS
    a) Adverse reaction such as urticaria may respond to diphenhydramine. Persistent hyperpyrexia is common in children getting BAL. Hypertension is possible and should be monitored. CNS stimulation may occur.
    C) PENICILLAMINE
    1) USUAL ADULT DOSE
    a) 1 to 1.5 g/day given orally in 4 divided doses (Nelson, 2011).
    2) USUAL PEDIATRIC DOSE
    a) 15 to 30 mg/kg/day in 3 to 4 divided doses. Initially, a small dose may be given to minimize side effects and then increased gradually (eg, 25% of the desired dose in week 1, 50% in week 2, and the full dose by week 3) (Caravati, 2004; Prod Info DEPEN(R) titratable oral tablets, 2009).
    3) ADVERSE REACTIONS
    a) COMMON SIDE EFFECTS/CHRONIC DOSING: Fever, anorexia, nausea, vomiting, diarrhea, abdominal pain, proteinuria, and myalgia(Prod Info DEPEN(R) titratable oral tablets, 2009).
    1) SERIOUS ADVERSE EFFECTS: Nephrotic syndrome, hypersensitivity reactions, leukopenia, thrombocytopenia, aplastic anemia, agranulocytosis, cholestatic hepatitis, and various autoimmune responses (Prod Info DEPEN(R) titratable oral tablets, 2009; Feehally et al, 1987; Kay, 1986).
    4) DURATION OF THERAPY
    a) Administer d-penicillamine for 3 to 10 days with monitoring of urinary excretion of mercury. If urine mercury falls rapidly, body burden is probably small. Wait 10 days and repeat after a baseline collection to determine if there is a rise on re-chelation therapy indicating further body burden.
    b) Repeated courses of D-penicillamine may be required. Regular follow-up of blood and urine mercury levels will establish need for treatment.
    5) CAUTIONS
    a) Patients allergic to penicillin products may have cross-sensitivity to penicillamine (Prod Info DEPEN(R) titratable oral tablets, 2009).
    b) Monitor for proteinuria and hematuria; heavy metals may also cause renal toxicity (Prod Info DEPEN(R) titratable oral tablets, 2009).
    c) Monitor CBC with differential, platelet count, and hepatic enzymes (Prod Info DEPEN(R) titratable oral tablets, 2009).
    d) CROSS-REACTIVITY: The use of penicillamine in a patient with penicillin allergy is controversial.
    1) While positive penicillamine skin tests have been reported in 2.5 to 10% of patients with history of penicillin allergy, the risk of rash or anaphylaxis in these patients is unknown. One such patient did not react when challenged with oral penicillamine (Bell & Graziano, 1983).
    6) PREGNANCY
    a) Penicillamine is considered FDA pregnancy category D(Prod Info CUPRIMINE(R) oral capsules, 2004); it should be avoided if possible in pregnant patients.
    b) Use of penicillamine throughout pregnancy has been associated with connective tissue abnormalities, hydrocephalus, cerebral palsy, cardiac and great vessel anomalies, webbing of fingers and toes, and arthrogryposis multipex (Linares et al, 1979; Solomon et al, 1977; Anon, 1981; Beck et al, 1981; Rosa, 1986). However, the teratogenic effect when used in low doses or for short periods of time, as in metal chelation, has yet to be determined.
    7) IMPAIRED RENAL FUNCTION
    a) Anuria or other evidence of renal dysfunction makes therapy with d-penicillamine dangerous since the main route of elimination of this complex is renal.
    8) EFFICACY
    a) Penicillamine has been shown to increase mercury excretion in urine and bile and decrease body burden of mercury in animal models of inorganic mercury poisoning (Kojima et al, 1989; Yonaga & Morita, 1981).
    b) Penicillamine increased urinary excretion of mercury in a child who ingested mercuric chloride (Seidel, 1980).
    D) SUCCIMER
    1) SUCCIMER/DMSA/EFFICACY
    a) DMSA has been shown to increase urinary mercury excretion, decrease total body, brain and renal mercury levels, and decrease nephrotoxicty, in animal models of inorganic mercury poisoning (Gale et al, 1993) (Aaseth et al, 1982) (Nielsen & Andersen, 1991).
    b) Blood mercury levels fell from 12.2 micrograms/deciliter to 8 micrograms/deciliter after 7 days of DMSA therapy (1 gram TID) in a 35-year-old man with mercurous perchlorate burns (Stremski et al, 1994).
    2) SUCCIMER/DOSE/ADMINISTRATION
    a) PEDIATRIC: Initial dose is 10 mg/kg or 350 mg/m(2) orally every 8 hours for 5 days (Prod Info CHEMET(R) oral capsules, 2011).
    1) The dosing interval is then increased to every 12 hours for the next 14 days. A repeat course may be given if indicated by elevated blood levels. A minimum of 2 weeks between courses is recommended, unless blood lead concentrations indicate the need for prompt retreatment.
    2) Succimer capsule contents may be administered mixed in a small amount of food (Prod Info CHEMET(R) oral capsules, 2011).
    b) ADULT: Succimer is not FDA approved for use in adults, however it has been shown to be safe and effective when used to treat adults with poisoning from a variety of heavy metals (Fournier et al, 1988). Initial dose is 10 mg/kg or 350 mg/m(2) orally every 8 hours for 5 days (Prod Info CHEMET(R) oral capsules, 2011).
    1) The dosing interval then is increased to every 12 hours for the next 14 days. A repeat course may be given if indicated by elevated blood levels. A minimum of 2 weeks between courses is recommended, unless the patient's symptoms or blood concentrations indicate a need for more prompt treatment (Prod Info CHEMET(R) oral capsules, 2011).
    3) MONITORING PARAMETERS
    a) The manufacturer recommends monitoring liver enzymes and complete blood count with differential and platelet count prior to the start of therapy and at least weekly during therapy (Prod Info CHEMET(R) oral capsules, 2011).
    b) Succimer therapy did not worsen preexisting borderline abnormal liver enzyme levels in a prospective evaluation of 15 children with lead poisoning (Kuntzelman & Angle, 1992).
    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) Succimer has a sulfurous odor that may be evident in the patients' breath and urine (Prod Info, 1991a).
    E) N-ACETYL-PENICILLAMINE
    1) DOSE
    a) Oral NAP, 250 milligrams to 500 milligrams, 4 times a day for 6 to 10 days (30 milligrams/kilogram/day in children).
    2) EFFICACY
    a) NAPA has been shown to decrease mortality and body burden of mercury in animal models of inorganic mercury poisoning ( Nielsen & Andersen, 1991).
    3) AVAILABILITY
    a) NAP is still considered experimental. It is available as a chemical from Aldrich Chemical Co in Milwaukee, Wisconsin. Phone (414) 273-3850.
    F) UNITHIOL
    1) DMPS/INDICATIONS: Chelating agent for heavy metal toxicities associated with arsenic, bismuth, copper, lead and mercury (Blanusa et al, 2005).
    2) DMPS/DOSING
    a) ACUTE TOXICITY
    1) ADULT ORAL DOSE:
    a) 1200 to 2400 mg/day in equally divided doses (100 to 200 mg 12 times daily) (Prod Info DIMAVAL(R) oral capsules, 2004).
    2) ADULT INTRAVENOUS DOSE (Arbeitsgruppe BGVV, 1996; Prod Info Dimaval(R) intravenous intramuscular injection solution, 2013):
    a) If oral DMPS therapy is not feasible or in severe toxicity, it may be given intravenously.
    b) ADMINISTRATION: DMPS should be injected immediately after breaking open the ampule and should not be mixed with other solutions. DMPS should be injected slowly over 3 to 5 minutes. The opened ampules cannot be reused.
    c) First 24 hours: 250 mg intravenously every 3 to 4 hours (1500 to 2000 mg total).
    d) Day two: 250 mg intravenously every 4 to 6 hours (1000 to 1500 mg total).
    e) Day three: 250 mg intravenously every 6 to 8 hours (750 to 1000 mg total).
    f) Day four: 250 mg intravenously every 8 to 12 hours (500 to 750 mg total).
    g) Subsequent days: 250 mg intravenously every 8 to 24 hours (250 to 750 mg total).
    h) Depending on the patient's clinical status, therapy may be changed to the oral route.
    3) PEDIATRIC ORAL DOSE (Arbeitsgruppe BGVV, 1996; Blanusa et al, 2005):
    a) There are insufficient clinical data regarding the pediatric use of DMPS. It should be used only if medically necessary.
    b) Initial dose: 20 to 30 mg/kg/day orally in many equal divided doses.
    c) Maintenance dose: 1.5 to 15 mg/kg/day.
    4) PEDIATRIC INTRAVENOUS DOSE (Arbeitsgruppe BGVV, 1996; Blanusa et al, 2005; Prod Info Dimaval(R) intravenous intramuscular injection solution, 2013):
    a) There are insufficient clinical data regarding the pediatric use of DMPS. It should be used only if medically necessary.
    b) If oral DMPS therapy is not feasible or in severe toxicity, it may be given intravenously.
    c) ADMINISTRATION: DMPS should be injected immediately after breaking open the ampule and should not be mixed with other solutions. DMPS should be injected slowly over 3 to 5 minutes. The opened ampules cannot be reused.
    d) First 24 hours: 5 mg/kg intravenously every four hours (total 30 mg/kg).
    e) Day two: 5 mg/kg intravenously every six hours (total 20 mg/kg).
    f) Days three and four: 5 mg/kg intravenously every 8 to 24 hours (total 5 to 15 mg/kg).
    b) CHRONIC TOXICITY
    1) ADULT DOSE
    a) 300 to 400 mg/day orally (in single doses of 100 to 200 mg). The dose may be increased in severe toxicity (Arbeitsgruppe BGVV, 1996; Prod Info DIMAVAL(R) oral capsules, 2004).
    c) DMPS/ADVERSE REACTIONS
    1) Chills, fever, and allergic skin reactions such as itching, exanthema or maculopapular rash are possible (Hla et al, 1992; Prod Info DIMAVAL(R) oral capsules, 2004). Cardiovascular effects such as hypotension, nausea, dizziness or weakness may occur with too rapid injection of DMPS. Hypotensive effects are irreversible at very high doses (300 mg/kg) (Prod Info DIMAVAL(R) oral capsules, 2004; Prod Info Dimaval(R) intravenous intramuscular injection solution, 2013).
    3) SOURCES
    a) DMPS is not FDA-approved, but is available outside of the US from Heyl Chem-pharm Fabrik in Germany (Prod Info Dimaval(R) intravenous intramuscular injection solution, 2013; Prod Info DIMAVAL(R) oral capsules, 2004). In the US it may be obtained from some compounding pharmacies.
    4) EFFICACY
    a) Ashton et al (1992) reported one patient who ingested over 10 grams of mercury. He developed 10 days of renal failure, but survived.
    b) Toet et al (1992, 1994) reported the use of DMPS in a case of mercury chloride ingestion. Initial blood and urine levels were 14,300 and 36,000 micrograms per liter, respectively. Intravenous DMPS was used initially, followed by oral use for 4 weeks. The patient recovered without sequelae. Hemodialysis performed with the patient was receiving DMPS, and mercury could not be detected in the dialysate (dialysis clearance less than 1 milliliter/minute).
    c) Intravenous DMPS, 250 milligrams every 4 to 12 hours for 14 days, followed by oral DMPS (Dimaval), 100 milligrams three times per day for 5 weeks and then reduced to 100 milligrams daily, were successfully used to treat an adolescent who had ingested 2 grams of mercury chloride and developed acute renal failure during BAL treatment (Gricar et al, 1994).
    1) Diuresis and increased urinary mercury excretion occurred during DMPS treatment. Blood mercury level at the start of DMPS was 3730 micrograms per liter and was 105 micrograms per liter when discharged 47 days after hospital admission (Gricar et al, 1994).
    d) In animal models of inorganic mercury poisoning DMPS has been shown to increase survival, reduce nephrotoxicity, increase urinary and fecal mercury elimination, and decrease tissue mercury levels, particularly in brain and kidney (Zalups et al, 1991) Nielsen & Andersen, 1991; Gale et al, 1993).
    5) ADVERSE REACTIONS
    a) SKIN REACTIONS: Urticaria, maculopapular rash, and erythema multiforme (Hla et al, 1992).
    G) ACETYLCYSTEINE
    1) N-acetyl cysteine has been shown to protect against mercury-induced nephrotoxicity in animal models of inorganic mercury poisoning (Girardi & Elias, 1991).

Inhalation Exposure

    6.7.1) DECONTAMINATION
    A) Move patient from the toxic environment to fresh air. Monitor for respiratory distress. If cough or difficulty in breathing develops, evaluate for hypoxia, respiratory tract irritation, bronchitis, or pneumonitis.
    B) OBSERVATION: Carefully observe patients with inhalation exposure for the development of any systemic signs or symptoms and administer symptomatic treatment as necessary.
    C) INITIAL TREATMENT: Administer 100% humidified supplemental oxygen, perform endotracheal intubation and provide assisted ventilation as required. Administer inhaled beta-2 adrenergic agonists, if bronchospasm develops. Consider systemic corticosteroids in patients with significant bronchospasm (National Heart,Lung,and Blood Institute, 2007). Exposed skin and eyes should be flushed with copious amounts of water.
    D) Remove all contaminated clothing, seal into bags, and treat as hazardous waste. Medical personnel should wear adequate protective clothing to prevent secondary contamination.
    6.7.2) TREATMENT
    A) SUPPORT
    1) Acute inhalation exposure to mercury compounds can produce local effects on the pulmonary system and can produce elevated urine mercury concentrations (Levin et al, 1988). Chelation may be required.
    2) Move patient from the toxic environment to fresh air. Monitor for respiratory distress. If cough or difficulty in breathing develops, evaluate for hypoxia, respiratory tract irritation, bronchitis, or pneumonitis.
    3) OBSERVATION: Carefully observe patients with inhalation exposure for the development of any systemic signs or symptoms and administer symptomatic treatment as necessary.
    4) INITIAL TREATMENT: Administer 100% humidified supplemental oxygen, perform endotracheal intubation and provide assisted ventilation as required. Administer inhaled beta-2 adrenergic agonists, if bronchospasm develops. Consider systemic corticosteroids in patients with significant bronchospasm (National Heart,Lung,and Blood Institute, 2007). Exposed skin and eyes should be flushed with copious amounts of water.
    B) Treatment should include recommendations listed in the ORAL EXPOSURE section when appropriate.

Eye Exposure

    6.8.1) DECONTAMINATION
    A) DECONTAMINATION: Remove contact lenses and irrigate exposed eyes with copious amounts of room temperature 0.9% saline or water for at least 15 minutes. If irritation, pain, swelling, lacrimation, or photophobia persist after 15 minutes of irrigation, the patient should be seen in a healthcare facility.
    B) Remove all contaminated clothing, seal into bags, and treat as hazardous waste. All medical personnel should wear protective clothing, including respirators if significant amounts of dust are present, to prevent secondary contamination.
    6.8.2) TREATMENT
    A) OBSERVATION REGIMES
    1) DECONTAMINATION: Remove contact lenses and irrigate exposed eyes with copious amounts of room temperature 0.9% saline or water for at least 15 minutes. If irritation, pain, swelling, lacrimation, or photophobia persist after 15 minutes of irrigation, the patient should be seen in a healthcare facility.
    B) SUPPORT
    1) Observe for development of clinical signs and symptoms and follow treatment recommendations in DERMAL EXPOSURE where appropriate.
    C) Treatment should include recommendations listed in the ORAL EXPOSURE section when appropriate.

Dermal Exposure

    6.9.1) DECONTAMINATION
    A) DERMAL DECONTAMINATION
    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).
    B) PREVENT SECONDARY EXPOSURES
    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.
    6.9.2) TREATMENT
    A) BURN OF SKIN
    1) APPLICATION
    a) These recommendations apply to patients with MINOR chemical burns (FIRST DEGREE; SECOND DEGREE: less than 15% body surface area in adults; less than 10% body surface area in children; THIRD DEGREE: less than 2% body surface area). Consultation with a clinician experienced in burn therapy or a burn unit should be obtained if larger area or more severe burns are present. Neutralizing agents should NOT be used.
    2) DEBRIDEMENT
    a) After initial flushing with large volumes of water to remove any residual chemical material, clean wounds with a mild disinfectant soap and water.
    b) DEVITALIZED SKIN: Loose, nonviable tissue should be removed by gentle cleansing with surgical soap or formal skin debridement (Moylan, 1980; Haynes, 1981). Intravenous analgesia may be required (Roberts, 1988).
    c) BLISTERS: Removal and debridement of closed blisters is controversial. Current consensus is that intact blisters prevent pain and dehydration, promote healing, and allow motion; therefore, blisters should be left intact until they rupture spontaneously or healing is well underway, unless they are extremely large or inhibit motion (Roberts, 1988; Carvajal & Stewart, 1987).
    3) TREATMENT
    a) TOPICAL ANTIBIOTICS: Prophylactic topical antibiotic therapy with silver sulfadiazine is recommended for all burns except superficial partial thickness (first-degree) burns (Roberts, 1988). For first-degree burns bacitracin may be used, but effectiveness is not documented (Roberts, 1988).
    b) SYSTEMIC ANTIBIOTICS: Systemic antibiotics are generally not indicated unless infection is present or the burn involves the hands, feet, or perineum.
    c) WOUND DRESSING:
    1) Depending on the site and area, the burn may be treated open (face, ears, or perineum) or covered with sterile nonstick porous gauze. The gauze dressing should be fluffy and thick enough to absorb all drainage.
    2) Alternatively, a petrolatum fine-mesh gauze dressing may be used alone on partial-thickness burns.
    d) DRESSING CHANGES:
    1) Daily dressing changes are indicated if a burn cream is used; changes every 3 to 4 days are adequate with a dry dressing.
    2) If dressing changes are to be done at home, the patient or caregiver should be instructed in proper techniques and given sufficient dressings and other necessary supplies.
    e) Analgesics such as acetaminophen with codeine may be used for pain relief if needed.
    4) TETANUS PROPHYLAXIS
    a) The patient's tetanus immunization status should be determined. Tetanus toxoid 0.5 milliliter intramuscularly or other indicated tetanus prophylaxis should be administered if required.
    B) SUPPORT
    1) Carefully observe patients with SKIN exposure for the development of any systemic signs or symptoms.
    C) Treatment should include recommendations listed in the ORAL EXPOSURE section when appropriate.

Enhanced Elimination

    A) HEMODIALYSIS
    1) Hemodialysis has not been shown to reduce a significant amount of the total body burden following acute ingestion (Sauder et al, 1988), but should be considered early in severely symptomatic patients with diminished urine output following chelation therapy with BAL (Lund et al, 1984). The BAL-mercury complex is water soluble and dialyzable (Giunta, 1983). It has also been used to treat patients in acute renal failure after ingestion of mercuric chloride (Agarwal et al, 1993).
    2) Hemodialysis removed 81 micrograms of mercury per 24 hours in a 23-year-old woman who ingested 7 grams of mercuric chloride 23 hours prior to institution of dialysis (McLauchlan, 1991).
    B) PERITONEAL DIALYSIS
    1) In an adult who developed acute renal failure after ingesting mercury bichloride, BAL therapy and peritoneal dialysis was associated with mercury clearance rates of 0.57 to 2.38 milliliters/minute (Lowenthal et al, 1974).
    2) In a child with renal failure after ingesting inorganic mercury, dialysate mercury concentrations without BAL therapy were undetectable. When BAL therapy was begun dialysate mercury concentrations ranged form 2.9 to 33 micrograms/Liter (Kahn et al, 1977).
    C) EXTRACORPOREAL REGIONAL COMPLEXING HEMODIALYSIS
    1) ERCH (Extracorporeal Regional Complexing Hemodialysis), using DMSA via arterial infusion, produced a 10-fold increase in dialysate mercury concentrations compared to BAL plus conventional dialysis.
    a) The total amount of mercury removed (1,189 mg) was less than 0.1 percent of the estimated ingested dose (1,425 milligrams) of mercuric chloride, and the patient died 28 days postingestion.
    2) The procedure was delayed until 6 days postingestion. It is possible that efficacy would have been greater if initiated earlier (Kostyniak et al, 1990).
    D) HEMOFILTRATION
    1) Hemofiltration, begun on the fourth day after overdose of 7 grams of mercuric chloride, removed 1.926 milligrams of mercury per 24 hours (McLauchlan, 1991).
    E) PLASMA EXCHANGE
    1) Six plasma exchanges performed between the 7th and 14th day removed only 17 milligrams of mercury in 27-year-old man following an ingestion of 6 grams of mercury chloride (Sauder et al, 1988).
    2) Plasma exchange, performed 23 hours after ingestion of 7 grams of mercuric chloride, removed 3.812 milligrams of mercury (McLauchlan, 1991).

Range Of Toxicity

Summary

    A) The average lethal acute dose of inorganic mercurials is approximately 1 gram. There is no adequate test to determine the body burden of mercury.

Minimum Lethal Exposure

    A) ACUTE
    1) The average lethal dose for inorganic mercuric salts is about 1 gram (Baselt, 1988).

Maximum Tolerated Exposure

    A) ROUTE OF EXPOSURE
    1) Atmospheric levels exceeding 0.01 milligram/cubic meter organic mercury may be toxic. Maximum tolerated oral concentrations are unknown; acute toxicity occurred following absorption of 60 to 90 milliliters of mercurial fungicides. The daily "safe" limit for methylmercury contaminated fish is 0.03 milligram.
    2) A single acute ingestion of 45 milligrams of methylmercury resulted in whole blood levels of 1930 and 1007 nanograms/milliliter 2 and 24 hours after ingestion, but did not result in symptoms of toxicity (Lund et al, 1984).

Workplace Standards

    A) ACGIH TLV Values for CAS1600-27-7 (American Conference of Governmental Industrial Hygienists, 2010):
    1) Not Listed

    B) NIOSH REL and IDLH Values for CAS1600-27-7 (National Institute for Occupational Safety and Health, 2007):
    1) Not Listed

    C) Carcinogenicity Ratings for CAS1600-27-7 :
    1) ACGIH (American Conference of Governmental Industrial Hygienists, 2010): Not Listed
    2) EPA (U.S. Environmental Protection Agency, 2011): Not Listed
    3) IARC (International Agency for Research on Cancer (IARC), 2016; International Agency for Research on Cancer, 2015; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010a; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2008; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2007; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2006; IARC, 2004): 2B ; Listed as: Mercuric acetate
    a) 2B : The agent (mixture) is possibly carcinogenic to humans. The exposure circumstance entails exposures that are possibly carcinogenic to humans. This category is used for agents, mixtures and exposure circumstances for which there is limited evidence of carcinogenicity in humans and less than sufficient evidence of carcinogenicity in experimental animals. It may also be used when there is inadequate evidence of carcinogenicity in humans but there is sufficient evidence of carcinogenicity in experimental animals. In some instances, an agent, mixture or exposure circumstance for which there is inadequate evidence of carcinogenicity in humans but limited evidence of carcinogenicity in experimental animals together with supporting evidence from other relevant data may be placed in this group.
    4) NIOSH (National Institute for Occupational Safety and Health, 2007): Not Listed
    5) MAK (DFG, 2002): Not Listed
    6) NTP (U.S. Department of Health and Human Services, Public Health Service, National Toxicology Project ): Not Listed

    D) OSHA PEL Values for CAS1600-27-7 (U.S. Occupational Safety, and Health Administration (OSHA), 2010):
    1) Not Listed

Toxicity Information

    7.7.1) TOXICITY VALUES
    A) References: RTECS, 2003
    1) LD50- (INTRAPERITONEAL)MOUSE:
    a) 6500 mcg/kg
    2) LD50- (ORAL)MOUSE:
    a) 23,900 mcg/kg
    3) LD50- (ORAL)RAT:
    a) 40,900 mcg/kg
    4) LD50- (SKIN)RAT:
    a) 570 mg/kg

Physicochemical

Physical Characteristics

    A) White, scales or powder; crystals or crystalline powder with a mild vinegar odor (Budavari, 1989).

Molecular Weight

    A) 318.17 (Budavari, 1989)

References

General Bibliography

    1) 40 CFR 372.28: Environmental Protection Agency - Toxic Chemical Release Reporting, Community Right-To-Know, Lower thresholds for chemicals of special concern. National Archives and Records Administration (NARA) and the Government Printing Office (GPO). Washington, DC. Final rules current as of Apr 3, 2006.
    2) 40 CFR 372.65: Environmental Protection Agency - Toxic Chemical Release Reporting, Community Right-To-Know, Chemicals and Chemical Categories to which this part applies. National Archives and Records Association (NARA) and the Government Printing Office (GPO), Washington, DC. Final rules current as of Apr 3, 2006.
    3) 49 CFR 172.101 - App. B: Department of Transportation - Table of Hazardous Materials, Appendix B: List of Marine Pollutants. National Archives and Records Administration (NARA) and the Government Printing Office (GPO), Washington, DC. Final rules current as of Aug 29, 2005.
    4) 49 CFR 172.101: Department of Transportation - Table of Hazardous Materials. National Archives and Records Administration (NARA) and the Government Printing Office (GPO), Washington, DC. Final rules current as of Aug 11, 2005.
    5) 62 FR 58840: Notice of the National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances - Proposed AEGL Values, Environmental Protection Agency, NAC/AEGL Committee. National Archives and Records Administration (NARA) and the Government Publishing Office (GPO), Washington, DC, 1997.
    6) 65 FR 14186: Notice of the National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances - Proposed AEGL Values, Environmental Protection Agency, NAC/AEGL Committee. National Archives and Records Administration (NARA) and the Government Publishing Office (GPO), Washington, DC, 2000.
    7) 65 FR 39264: Notice of the National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances - Proposed AEGL Values, Environmental Protection Agency, NAC/AEGL Committee. National Archives and Records Administration (NARA) and the Government Publishing Office (GPO), Washington, DC, 2000.
    8) 65 FR 77866: Notice of the National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances - Proposed AEGL Values, Environmental Protection Agency, NAC/AEGL Committee. National Archives and Records Administration (NARA) and the Government Publishing Office (GPO), Washington, DC, 2000.
    9) 66 FR 21940: Notice of the National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances - Proposed AEGL Values, Environmental Protection Agency, NAC/AEGL Committee. National Archives and Records Administration (NARA) and the Government Publishing Office (GPO), Washington, DC, 2001.
    10) 67 FR 7164: Notice of the National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances - Proposed AEGL Values, Environmental Protection Agency, NAC/AEGL Committee. National Archives and Records Administration (NARA) and the Government Publishing Office (GPO), Washington, DC, 2002.
    11) 68 FR 42710: Notice of the National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances - Proposed AEGL Values, Environmental Protection Agency, NAC/AEGL Committee. National Archives and Records Administration (NARA) and the Government Publishing Office (GPO), Washington, DC, 2003.
    12) 69 FR 54144: Notice of the National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances - Proposed AEGL Values, Environmental Protection Agency, NAC/AEGL Committee. National Archives and Records Administration (NARA) and the Government Publishing Office (GPO), Washington, DC, 2004.
    13) AIHA: 2006 Emergency Response Planning Guidelines and Workplace Environmental Exposure Level Guides Handbook, American Industrial Hygiene Association, Fairfax, VA, 2006.
    14) Aaseth J, Alexander J, & Raknerud N: Treatment of mercuric chloride poisoning with dimercaptosuccininc acid and diuretics: preliminary studies. J Toxicol - Clin Toxicol 1982; 19:173-186.
    15) Adams CR, Ziegler DK, & Lin JT: Mercury intoxication stimulating amyotrophic lateral sclerosis. JAMA 1983; 250:642-643.
    16) Agarwal SK, Tiwari SC, & Dash SC: Spectrum of poisoning requiring haemodialysis in a tertiary care hospital in India. Internat J Artif Organs 1993; 16:20-22.
    17) American Conference of Governmental Industrial Hygienists : ACGIH 2010 Threshold Limit Values (TLVs(R)) for Chemical Substances and Physical Agents and Biological Exposure Indices (BEIs(R)), American Conference of Governmental Industrial Hygienists, Cincinnati, OH, 2010.
    18) Anon: Cutis laxa and other congenital defects with penicillamine, ADR Highlights (Division of drug experience), Rockville, MD, 1981, pp 1-4-81-21.
    19) Arbeitsgruppe BGVV: Allgemeine und spezielle Massnahmen bei Vergiftungen und bei Drogennotfaellen. Empfehlungen der Kommission "Erkennung und Behandlung von Vergiftungen", Bundesinstituts fuer gesundheitlichen Verbraucherschutz und Veterinaermedizin, Berlin, Germany, 1996.
    20) Arlauskas A, Baker RSU, & Bonin AM: Mutagenicity of metal ions in bacteria. Environ Res 1985; 36:379-388.
    21) Baglan RJ et al: Proc Ann NSF Trace Contam Conf, 1st Iss Conf; 730802:505-509, 1974.
    22) Barlow SM & Sullivan FM: Reproductive Hazards of Industrial Chemicals, Academic Press, London, England, 1982, pp 386-406.
    23) Baselt RC: Biological Monitoring Methods for Industrial Chemicals, 2nd ed, PSG Publishing Company, Littleton, MA, 1988, pp 198-204.
    24) Beck RB, Rosenbaum KN, & Byers PH: Ultrastructural findings in fetal penicillamine syndrome, 14th March of Dimes Ann Birth Defects Conf, San Diego, CA, 1981.
    25) Bell CL & Graziano FM: The safety of administration of penicillamine to penicillin-sensitive individuals. Arthritis Rheum 1983; 26:801-803.
    26) Blanusa M, Varnai VM, Piasek M, et al: Chelators as antidotes of metal toxicity: therapeutic and experimental aspects. Curr Med Chem 2005; 12(23):2771-2794.
    27) Budavari S: The Merck Index, 11th ed, Merck & Co, Inc, Rahway, NJ, 1989, pp 923-924.
    28) Burgess JL, Kirk M, Borron SW, et al: Emergency department hazardous materials protocol for contaminated patients. Ann Emerg Med 1999; 34(2):205-212.
    29) CHRIS : CHRIS Hazardous Chemical Data. US Department of Transportation, US Coast Guard. Washington, DC (Internet Version). Edition expires 1990; provided by Truven Health Analytics Inc., Greenwood Village, CO.
    30) Calder IM, Kelman GR, & Mason H: Diurnal variations in urinary mercury excretion. Human Toxicol 1984; 3:463-467.
    31) Cantoni O, Christie NT, & Robison SH: Characterization of DNA lesions produced by HgCl2 in cell culture systems. Chem-Biol Interact 1984; 49:209-224.
    32) Caravati EM, Knight HH, & Linscott MS: Esophageal laceration and charcoal mediastinum complicating gastric lavage. J Emerg Med 2001; 20:273-276.
    33) Caravati EM: D-Penicillamine. In: Dart RC, ed. Medical Toxicology, Lippincott Williams & Wilkins, Philadelphia, PA, 2004.
    34) Carvajal HF & Stewart CE: Emergency management of burn patients: the first few hours. Emerg Med Reports 1987; 8:129-136.
    35) Chyka PA, Seger D, Krenzelok EP, et al: Position paper: Single-dose activated charcoal. Clin Toxicol (Phila) 2005; 43(2):61-87.
    36) Clayton GD & Clayton FE: Patty's Industrial Hygiene and Toxicology, Vol 2A, Toxicology, 3rd ed, John Wiley & Sons, New York, NY, 1981, pp 1769-1792.
    37) DFG: List of MAK and BAT Values 2002, Report No. 38, Deutsche Forschungsgemeinschaft, Commission for the Investigation of Health Hazards of Chemical Compounds in the Work Area, Wiley-VCH, Weinheim, Federal Republic of Germany, 2002.
    38) Dierickx PJ: Urinary gamma-glytayl transferase as an indicator of acute nephrotoxicity in rats. Arch Toxicol 1981; 47:209-215.
    39) EPA: EPA chemical profile on mercuric acetate, Environmental Protection Agency, Washington, DC, 1985.
    40) EPA: Search results for Toxic Substances Control Act (TSCA) Inventory Chemicals. US Environmental Protection Agency, Substance Registry System, U.S. EPA's Office of Pollution Prevention and Toxics. Washington, DC. 2005. Available from URL: http://www.epa.gov/srs/.
    41) ERG: Emergency Response Guidebook. A Guidebook for First Responders During the Initial Phase of a Dangerous Goods/Hazardous Materials Incident, U.S. Department of Transportation, Research and Special Programs Administration, Washington, DC, 2004.
    42) Elliot CG, Colby TV, & Kelly TM: Charcoal lung. Bronchiolitis obliterans after aspiration of activated charcoal. Chest 1989; 96:672-674.
    43) FDA: Poison treatment drug product for over-the-counter human use; tentative final monograph. FDA: Fed Register 1985; 50:2244-2262.
    44) Fawer RF, De Ribaupieere Y, & Guillemin MP: Measurement of hand tremor induced by industrial exposure to metallic mercury. Br J Ind Med 1983; 40:204-208.
    45) Feehally J, Wheeler DC, Mackay EH, et al: Recurrent acute renal failure with interstitial nephritis due to D-penicillamine. Renal Failure 1987; 10:55-57.
    46) Finkel AJ: Hamilton and Hardy's Industrial Toxicology, 4th ed, John Wright, PSG Inc, Boston, MA, 1983, pp 93-104.
    47) Fisher AA: Reply (Letter). Arch Dermatol 1972; 106:129.
    48) Folkl H & Konig P: Poisoning with elementary mercury: attempted suicide by inhalation of vapors from the heated metal (German). Wiener Klin Woch 1983; 95:580-584.
    49) Fournier L, Thomas G, & Garnier R: 2,3-dimercaptosuccinic acid treatment of heavy metal poisoning in humans. Med Toxicol 1988; 3:499-504.
    50) Gale TF & Hanlon DP: The permeability of the Syrian hamster placenta to mercury. Environ Res 1976; 12:26-31.
    51) Gale TF: Cardiac and non-cardiac malformation produced by mercury in hamsters. Bull Environ Contam Toxicol 1980; 25:726-732.
    52) Gale TF: Embryopathic effects of different routes of administration of mercuric acetate in the hamster. Environ Res 1974; 8:207-213.
    53) Gale TF: The amelioration of mercury-induced embryotoxic effects by simultaneous treatment with zinc. Environ Res 1984; 35:405-412.
    54) Gale TF: The embryotoxic response produced by inorganic mercury in different strains of hamsters. Environ Res 1981; 24:152-161.
    55) Girardi G & Elias MM: Effectivelness of N-acetylcysteine in protecting against mercuric chloride-induced nephrotoxicity. Toxicology 1991; 67:155-164.
    56) Gmyrya AI, Fomicheva LV, & Prokopenko VI: Changes in the organ of vision and their prophylaxis in workers producing mercury and coke chemical plant workers. Oftalmol Zh 1970; 25:570-573.
    57) Golej J, Boigner H, Burda G, et al: Severe respiratory failure following charcoal application in a toddler. Resuscitation 2001; 49:315-318.
    58) Goncharuk GA: Gig Tr Prof Zabol 1971; 7:73-75.
    59) Goncharuk GA: Gig Tr Prof Zabol 1977; 5:17-20.
    60) Gonzalez MJ, Rico MC, & Hernandez LM: Mercury in human hair: a study of residents in Madrid, Spain. Arch Environ Health 1985; 40:225-228.
    61) Graff GR, Stark J, & Berkenbosch JW: Chronic lung disease after activated charcoal aspiration. Pediatrics 2002; 109:959-961.
    62) Gricar M, Jamsek M, & Mozina M: Toxicokinetics of mercury in HgCl2 poisoning, treated with prolonged use of intravenous DMPS (Abstract), EAPCCT XVI International Congress, Vienna, Austria, 1994.
    63) HSDB : Hazardous Substances Data Bank. National Library of Medicine. Bethesda, MD (Internet Version). Edition expires 1990; provided by Truven Health Analytics Inc., Greenwood Village, CO.
    64) Harris CR & Filandrinos D: Accidental administration of activated charcoal into the lung: aspiration by proxy. Ann Emerg Med 1993; 22:1470-1473.
    65) Haynes BW Jr: Emergency department management of minor burns. Top Emerg Med 1981; 3:35-40.
    66) Hla KK, Ashton CE, & Henry JA: Adverse effects from 2,3-dimercaptopropane sulphonate (DMPS) (abstract), EAPCCT, XV Congress, Istanbul, Turkey, 1992, pp 13.
    67) IARC Working Group on the Evaluation of Carcinogenic Risks to Humans : IARC Monographs on the Evaluation of Carcinogenic Risks to Humans: 1,3-Butadiene, Ethylene Oxide and Vinyl Halides (Vinyl Fluoride, Vinyl Chloride and Vinyl Bromide), 97, International Agency for Research on Cancer, Lyon, France, 2008.
    68) IARC Working Group on the Evaluation of Carcinogenic Risks to Humans : IARC Monographs on the Evaluation of Carcinogenic Risks to Humans: Formaldehyde, 2-Butoxyethanol and 1-tert-Butoxypropan-2-ol, 88, International Agency for Research on Cancer, Lyon, France, 2006.
    69) IARC Working Group on the Evaluation of Carcinogenic Risks to Humans : IARC Monographs on the Evaluation of Carcinogenic Risks to Humans: Household Use of Solid Fuels and High-temperature Frying, 95, International Agency for Research on Cancer, Lyon, France, 2010a.
    70) IARC Working Group on the Evaluation of Carcinogenic Risks to Humans : IARC Monographs on the Evaluation of Carcinogenic Risks to Humans: Smokeless Tobacco and Some Tobacco-specific N-Nitrosamines, 89, International Agency for Research on Cancer, Lyon, France, 2007.
    71) IARC Working Group on the Evaluation of Carcinogenic Risks to Humans : IARC Monographs on the Evaluation of Carcinogenic Risks to Humans: Some Non-heterocyclic Polycyclic Aromatic Hydrocarbons and Some Related Exposures, 92, International Agency for Research on Cancer, Lyon, France, 2010.
    72) IARC: List of all agents, mixtures and exposures evaluated to date - IARC Monographs: Overall Evaluations of Carcinogenicity to Humans, Volumes 1-88, 1972-PRESENT. World Health Organization, International Agency for Research on Cancer. Lyon, FranceAvailable from URL: http://monographs.iarc.fr/monoeval/crthall.html. As accessed Oct 07, 2004.
    73) ICAO: Technical Instructions for the Safe Transport of Dangerous Goods by Air, 2003-2004. International Civil Aviation Organization, Montreal, Quebec, Canada, 2002.
    74) ILO: Encyclopaedia of Occupational Health and Safety, 3rd ed, Vol 1. Parmeggiani L (Ed), International Labour Organization, Geneva, Switzerland, 1983.
    75) International Agency for Research on Cancer (IARC): IARC monographs on the evaluation of carcinogenic risks to humans: list of classifications, volumes 1-116. International Agency for Research on Cancer (IARC). Lyon, France. 2016. Available from URL: http://monographs.iarc.fr/ENG/Classification/latest_classif.php. As accessed 2016-08-24.
    76) International Agency for Research on Cancer: IARC Monographs on the Evaluation of Carcinogenic Risks to Humans. World Health Organization. Geneva, Switzerland. 2015. Available from URL: http://monographs.iarc.fr/ENG/Classification/. As accessed 2015-08-06.
    77) Ishihara N, Shiojima S, & Suzuki T: Selective enhancement of urinary organic mercury excretion by D-penicillamine. Br J Ind Med 1974; 31:245-249.
    78) Kahn A, Denis R, & Blum D: Accidental ingestion of mercuric sulphate in a 4-year-old child. Clin Peds 1977; 10:956-958.
    79) Kay A: European league against rheumatism study of adverse reactions to D-penicillamine. Br J Rheumatol 1986; 25:193-198.
    80) Kershaw TG, Dhahir PH, & Clarkson TW: The relationship between blood levels and dose of methylmercury in man. Arch Environ Health 1980; 35:28-35.
    81) Kojima S, Shimada H, & Kiyozumi M: Comparative effects of chelating agents on distribution, excretion, and renal toxicity of inorganic mercury in rats. Research Comm Chem Path Pharmacol 1989; 64:471-484.
    82) Kostyniak PJ, Greizerstein HB, & Goldstein J: Extracorporeal regional complexing haemodialysis treatment of acute inorganic mercury intoxication. Human Toxicol 1990; 9:137-141.
    83) Kuntzelman DR & Angle CR: Abnormal liver function in childhood lead poisoning unaffected by DMSA (Abstract). Vet Hum Toxicol 1992; 34:355.
    84) Lach H, Dziubek K, & Krawczyk S: Influence of chronic doses of mercuric acetate and lead acetate on the number and activity of Gomori-positive Glial cells in the mouse brain. ACTA Biol Acad Sci Hung 1977; 28:367-373.
    85) Lauwerys R, Bonnier CH, & Evrard PH: Prenatal and early postnatal intoxication by inorganic mercury resulting from the maternal use of mercury containing soap. Human Toxicol 1987; 6:253-256.
    86) Lauwerys R, Roels H, & Genet P: Fertility of male workers exposed to mercury vapor or to manganese dust: a questionnaire study. Am J Ind Med 1985; 7:171-176.
    87) Lauwerys R: Environ Res 1978; 15:278-289.
    88) Levin M, Jacobs J, & Polos PG: Acute mercury poisoning and mercurial pneumonitis from gold ore purification. Chest 1988; 94:554-556.
    89) Lien DC, Todoruk DN, & Rajani HR: Accidental inhalation of mercury vapor: respiratory and toxicologic consequences. Canad Med Assoc J 1983; 129:591-595.
    90) Linares A, Zarranz JJ, & Rodrigues-Alarcon J: Reversible cutis laxa due to maternal d-penicillamine treatment. Lancet 1979; 2:43.
    91) Longcope WT, Luetscher JA, & Calkins E: Clinical uses of 2,3-dimercaptopropanol (BAL). XI. The treatment of acute mercury poisoning by BAL. J Clin Invest 1946; 25:557-567.
    92) Lowenthal DT, Chardo F, & Reidenberg MM: Removal of mercury by peritoneal dialysis. Arch Int Med 1974; 134:139-141.
    93) Lund ME, Clarkson TW, & Berlin M: Treatment of acute methylmercury ingestion by hemodialysis with N-acetylcysteine infusion and 2,3-dimercaptopropane sulfonate. Clin Toxicol 1984; 22:31-49.
    94) Mabille V, Roels H, & Jacquet P: Cytogenetic examination of leukocytes of workers exposed to mercury vapor. Internat Arch Occup Environ Health 1984; 53:257-260.
    95) Marcus S, Okose P, & Jennis T: Untoward effects of oral dimercaptosuccinic acid in the treatment for lead poisoning (Abstract). Vet Hum Toxicol 1991; 33:376.
    96) Marinova: Prob Askush I Ginek 1973; 1:75.
    97) Marsh DO, Clarkson TW, & Cox C: Fetal methylmercury poisoning. Relationship between concentration in single strands of maternal hair and child effects. Arch Neurol 1987; 44:1017-1022.
    98) Marzin DR & Phi HV: Study of the mutagenicity of metal derivatives with Salmonella typhimurium TA 102. Mutat Res 1985; 155:49-51.
    99) Matheson DS, Clarkson TW, & Gelfand EW: Mercury toxicity (acrodynia) induced by long-term injection of gammaglobulin. J Pediatrics 1980; 97:153-55.
    100) Mattison DR: Reproductive Toxicology, Alan R Liss, Inc, New York, NY, 1983, pp 259-281.
    101) McFarland RB & Reigel H: J Occup Med 1978; 20:532-534.
    102) McLauchlan GA: Acute mercury poisoning. Anaesthesia 1991; 46:110-112.
    103) Montaldi A, Zentilin L, & Venier P: Interaction of nitrilotriacetic acid with heavy metals in the induction of sister chromatid exchanges in cultured mammalian cells. Environ Mutagen 1985; 7:381-390.
    104) Morimoto K, Iijima S, & Koijumi A: Selenite prevents the induction of sister-chromatid exchanges by methyl mercury and mercuric chloride in human whole-blood cultures. Mutat Res 1982; 102:183-192.
    105) Moylan JA: Burn care after thermal injury. Top Emerg Med 1980; 2:39-52.
    106) NFPA: Fire Protection Guide to Hazardous Materials, 13th ed., National Fire Protection Association, Quincy, MA, 2002.
    107) NRC: Acute Exposure Guideline Levels for Selected Airborne Chemicals - Volume 1, Subcommittee on Acute Exposure Guideline Levels, Committee on Toxicology, Board on Environmental Studies and Toxicology, Commission of Life Sciences, National Research Council. National Academy Press, Washington, DC, 2001.
    108) NRC: Acute Exposure Guideline Levels for Selected Airborne Chemicals - Volume 2, Subcommittee on Acute Exposure Guideline Levels, Committee on Toxicology, Board on Environmental Studies and Toxicology, Commission of Life Sciences, National Research Council. National Academy Press, Washington, DC, 2002.
    109) NRC: Acute Exposure Guideline Levels for Selected Airborne Chemicals - Volume 3, Subcommittee on Acute Exposure Guideline Levels, Committee on Toxicology, Board on Environmental Studies and Toxicology, Commission of Life Sciences, National Research Council. National Academy Press, Washington, DC, 2003.
    110) NRC: Acute Exposure Guideline Levels for Selected Airborne Chemicals - Volume 4, Subcommittee on Acute Exposure Guideline Levels, Committee on Toxicology, Board on Environmental Studies and Toxicology, Commission of Life Sciences, National Research Council. National Academy Press, Washington, DC, 2004.
    111) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for 1,2,3-Trimethylbenzene (Proposed). United States Environmental Protection Agency. Washington, DC. 2006k. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020d68a&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    112) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for 1,2,4-Trimethylbenzene (Proposed). United States Environmental Protection Agency. Washington, DC. 2006m. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020d68a&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    113) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for 1,2-Butylene Oxide (Proposed). United States Environmental Protection Agency. Washington, DC. 2008d. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648083cdbb&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    114) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for 1,2-Dibromoethane (Proposed). United States Environmental Protection Agency. Washington, DC. 2007g. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=09000064802796db&disposition=attachment&contentType=pdf. As accessed 2010-08-18.
    115) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for 1,3,5-Trimethylbenzene (Proposed). United States Environmental Protection Agency. Washington, DC. 2006l. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020d68a&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    116) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for 2-Ethylhexyl Chloroformate (Proposed). United States Environmental Protection Agency. Washington, DC. 2007b. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648037904e&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    117) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Acrylonitrile (Proposed). United States Environmental Protection Agency. Washington, DC. 2007c. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648028e6a3&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    118) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Adamsite (Proposed). United States Environmental Protection Agency. Washington, DC. 2007h. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020fd29&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    119) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Agent BZ (3-quinuclidinyl benzilate) (Proposed). United States Environmental Protection Agency. Washington, DC. 2007f. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=09000064803ad507&disposition=attachment&contentType=pdf. As accessed 2010-08-18.
    120) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Allyl Chloride (Proposed). United States Environmental Protection Agency. Washington, DC. 2008. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648039d9ee&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    121) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Aluminum Phosphide (Proposed). United States Environmental Protection Agency. Washington, DC. 2005b. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020c5ed&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    122) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Arsenic Trioxide (Proposed). United States Environmental Protection Agency. Washington, DC. 2007m. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=0900006480220305&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    123) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Automotive Gasoline Unleaded (Proposed). United States Environmental Protection Agency. Washington, DC. 2009a. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=0900006480a7cc17&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    124) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Biphenyl (Proposed). United States Environmental Protection Agency. Washington, DC. 2005j. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=09000064801ea1b7&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    125) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Bis-Chloromethyl Ether (BCME) (Proposed). United States Environmental Protection Agency. Washington, DC. 2006n. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648022db11&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    126) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Boron Tribromide (Proposed). United States Environmental Protection Agency. Washington, DC. 2008a. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=09000064803ae1d3&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    127) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Bromine Chloride (Proposed). United States Environmental Protection Agency. Washington, DC. 2007d. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648039732a&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    128) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Bromoacetone (Proposed). United States Environmental Protection Agency. Washington, DC. 2008e. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=09000064809187bf&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    129) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Calcium Phosphide (Proposed). United States Environmental Protection Agency. Washington, DC. 2005d. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020c5ed&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    130) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Carbonyl Fluoride (Proposed). United States Environmental Protection Agency. Washington, DC. 2008b. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=09000064803ae328&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    131) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Carbonyl Sulfide (Proposed). United States Environmental Protection Agency. Washington, DC. 2007e. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648037ff26&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    132) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Chlorobenzene (Proposed). United States Environmental Protection Agency. Washington, DC. 2008c. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=09000064803a52bb&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    133) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Cyanogen (Proposed). United States Environmental Protection Agency. Washington, DC. 2008f. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=09000064809187fe&disposition=attachment&contentType=pdf. As accessed 2010-08-15.
    134) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Dimethyl Phosphite (Proposed). United States Environmental Protection Agency. Washington, DC. 2009. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=0900006480a7cbf3&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    135) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Diphenylchloroarsine (Proposed). United States Environmental Protection Agency. Washington, DC. 2007l. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020fd29&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    136) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Ethyl Isocyanate (Proposed). United States Environmental Protection Agency. Washington, DC. 2008h. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648091884e&disposition=attachment&contentType=pdf. As accessed 2010-08-15.
    137) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Ethyl Phosphorodichloridate (Proposed). United States Environmental Protection Agency. Washington, DC. 2008i. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=0900006480920347&disposition=attachment&contentType=pdf. As accessed 2010-08-15.
    138) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Ethylbenzene (Proposed). United States Environmental Protection Agency. Washington, DC. 2008g. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=09000064809203e7&disposition=attachment&contentType=pdf. As accessed 2010-08-15.
    139) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Ethyldichloroarsine (Proposed). United States Environmental Protection Agency. Washington, DC. 2007j. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020fd29&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    140) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Germane (Proposed). United States Environmental Protection Agency. Washington, DC. 2008j. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=0900006480963906&disposition=attachment&contentType=pdf. As accessed 2010-08-15.
    141) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Hexafluoropropylene (Proposed). United States Environmental Protection Agency. Washington, DC. 2006. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=09000064801ea1f5&disposition=attachment&contentType=pdf. As accessed 2010-08-15.
    142) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Ketene (Proposed). United States Environmental Protection Agency. Washington, DC. 2007. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020ee7c&disposition=attachment&contentType=pdf. As accessed 2010-08-15.
    143) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Magnesium Aluminum Phosphide (Proposed). United States Environmental Protection Agency. Washington, DC. 2005h. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020c5ed&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    144) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Magnesium Phosphide (Proposed). United States Environmental Protection Agency. Washington, DC. 2005g. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020c5ed&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    145) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Malathion (Proposed). United States Environmental Protection Agency. Washington, DC. 2009k. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=09000064809639df&disposition=attachment&contentType=pdf. As accessed 2010-08-15.
    146) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Mercury Vapor (Proposed). United States Environmental Protection Agency. Washington, DC. 2009b. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=0900006480a8a087&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    147) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Methyl Isothiocyanate (Proposed). United States Environmental Protection Agency. Washington, DC. 2008k. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=0900006480963a03&disposition=attachment&contentType=pdf. As accessed 2010-08-15.
    148) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Methyl Parathion (Proposed). United States Environmental Protection Agency. Washington, DC. 2008l. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=0900006480963a57&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    149) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Methyl tertiary-butyl ether (Proposed). United States Environmental Protection Agency. Washington, DC. 2007a. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=09000064802a4985&disposition=attachment&contentType=pdf. As accessed 2010-08-15.
    150) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Methylchlorosilane (Proposed). United States Environmental Protection Agency. Washington, DC. 2005. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020c5f4&disposition=attachment&contentType=pdf. As accessed 2010-08-15.
    151) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Methyldichloroarsine (Proposed). United States Environmental Protection Agency. Washington, DC. 2007i. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020fd29&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    152) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Methyldichlorosilane (Proposed). United States Environmental Protection Agency. Washington, DC. 2005a. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020c646&disposition=attachment&contentType=pdf. As accessed 2010-08-15.
    153) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Nitrogen Mustard (HN1 CAS Reg. No. 538-07-8) (Proposed). United States Environmental Protection Agency. Washington, DC. 2006a. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020d6cb&disposition=attachment&contentType=pdf. As accessed 2010-08-15.
    154) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Nitrogen Mustard (HN2 CAS Reg. No. 51-75-2) (Proposed). United States Environmental Protection Agency. Washington, DC. 2006b. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020d6cb&disposition=attachment&contentType=pdf. As accessed 2010-08-15.
    155) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Nitrogen Mustard (HN3 CAS Reg. No. 555-77-1) (Proposed). United States Environmental Protection Agency. Washington, DC. 2006c. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020d6cb&disposition=attachment&contentType=pdf. As accessed 2010-08-15.
    156) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Nitrogen Tetroxide (Proposed). United States Environmental Protection Agency. Washington, DC. 2008n. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648091855b&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    157) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Nitrogen Trifluoride (Proposed). United States Environmental Protection Agency. Washington, DC. 2009l. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=0900006480963e0c&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    158) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Parathion (Proposed). United States Environmental Protection Agency. Washington, DC. 2008o. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=0900006480963e32&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    159) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Perchloryl Fluoride (Proposed). United States Environmental Protection Agency. Washington, DC. 2009c. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=0900006480a7e268&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    160) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Perfluoroisobutylene (Proposed). United States Environmental Protection Agency. Washington, DC. 2009d. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=0900006480a7e26a&disposition=attachment&contentType=pdf. As accessed 2010-08-15.
    161) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Phenyl Isocyanate (Proposed). United States Environmental Protection Agency. Washington, DC. 2008p. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648096dd58&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    162) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Phenyl Mercaptan (Proposed). United States Environmental Protection Agency. Washington, DC. 2006d. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020cc0c&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    163) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Phenyldichloroarsine (Proposed). United States Environmental Protection Agency. Washington, DC. 2007k. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020fd29&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    164) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Phorate (Proposed). United States Environmental Protection Agency. Washington, DC. 2008q. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648096dcc8&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    165) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Phosgene (Draft-Revised). United States Environmental Protection Agency. Washington, DC. 2009e. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=0900006480a8a08a&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    166) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Phosgene Oxime (Proposed). United States Environmental Protection Agency. Washington, DC. 2009f. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=0900006480a7e26d&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    167) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Potassium Cyanide (Proposed). United States Environmental Protection Agency. Washington, DC. 2009g. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=0900006480a7cbb9&disposition=attachment&contentType=pdf. As accessed 2010-08-15.
    168) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Potassium Phosphide (Proposed). United States Environmental Protection Agency. Washington, DC. 2005c. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020c5ed&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    169) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Propargyl Alcohol (Proposed). United States Environmental Protection Agency. Washington, DC. 2006e. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020ec91&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    170) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Selenium Hexafluoride (Proposed). United States Environmental Protection Agency. Washington, DC. 2006f. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020ec55&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    171) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Silane (Proposed). United States Environmental Protection Agency. Washington, DC. 2006g. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020d523&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    172) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Sodium Cyanide (Proposed). United States Environmental Protection Agency. Washington, DC. 2009h. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=0900006480a7cbb9&disposition=attachment&contentType=pdf. As accessed 2010-08-15.
    173) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Sodium Phosphide (Proposed). United States Environmental Protection Agency. Washington, DC. 2005i. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020c5ed&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    174) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Strontium Phosphide (Proposed). United States Environmental Protection Agency. Washington, DC. 2005f. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020c5ed&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    175) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Sulfuryl Chloride (Proposed). United States Environmental Protection Agency. Washington, DC. 2006h. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020ec7a&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    176) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Tear Gas (Proposed). United States Environmental Protection Agency. Washington, DC. 2008s. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648096e551&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    177) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Tellurium Hexafluoride (Proposed). United States Environmental Protection Agency. Washington, DC. 2009i. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=0900006480a7e2a1&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    178) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Tert-Octyl Mercaptan (Proposed). United States Environmental Protection Agency. Washington, DC. 2008r. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648096e5c7&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    179) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Tetramethoxysilane (Proposed). United States Environmental Protection Agency. Washington, DC. 2006j. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020d632&disposition=attachment&contentType=pdf. As accessed 2010-08-17.
    180) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Trimethoxysilane (Proposed). United States Environmental Protection Agency. Washington, DC. 2006i. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020d632&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    181) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Trimethyl Phosphite (Proposed). United States Environmental Protection Agency. Washington, DC. 2009j. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=0900006480a7d608&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    182) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Trimethylacetyl Chloride (Proposed). United States Environmental Protection Agency. Washington, DC. 2008t. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648096e5cc&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    183) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Zinc Phosphide (Proposed). United States Environmental Protection Agency. Washington, DC. 2005e. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020c5ed&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    184) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for n-Butyl Isocyanate (Proposed). United States Environmental Protection Agency. Washington, DC. 2008m. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=09000064808f9591&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    185) National Heart,Lung,and Blood Institute: Expert panel report 3: guidelines for the diagnosis and management of asthma. National Heart,Lung,and Blood Institute. Bethesda, MD. 2007. Available from URL: http://www.nhlbi.nih.gov/guidelines/asthma/asthgdln.pdf.
    186) National Institute for Occupational Safety and Health: NIOSH Pocket Guide to Chemical Hazards, U.S. Department of Health and Human Services, Centers for Disease Control and Prevention, Cincinnati, OH, 2007.
    187) National Research Council : Acute exposure guideline levels for selected airborne chemicals, 5, National Academies Press, Washington, DC, 2007.
    188) National Research Council: Acute exposure guideline levels for selected airborne chemicals, 6, National Academies Press, Washington, DC, 2008.
    189) National Research Council: Acute exposure guideline levels for selected airborne chemicals, 7, National Academies Press, Washington, DC, 2009.
    190) National Research Council: Acute exposure guideline levels for selected airborne chemicals, 8, National Academies Press, Washington, DC, 2010.
    191) Nelson LS: Copper. In: Nelson LS, Hoffman RS, Lewin NA, et al, eds. Goldfrank's Toxicologic Emergencies, 9th ed. McGraw Hill Medical, New York, NY, 2011, pp 1256-1265.
    192) None Listed: Position paper: cathartics. J Toxicol Clin Toxicol 2004; 42(3):243-253.
    193) O'Donaghue JL: Neurotoxicology of Industrial and Commercial Chemicals, Volume 1, CRC Press, Boca Raton, FL, 1985, pp 159-169.
    194) Ohlson CG & Hogstedt C: Parkinson's disease and occupational exposure to organic solvents, agricultural chemicals and mercury -- a case-referent study. Scand J Work Environ Health 1981; 7:252-256.
    195) Panova Z & Ivanova S: Akush I Ginek 1976; 15:133-17.
    196) Pesce AJ, Hanenson I, & Sethi K: B2 Microglobulinuria in a patient with nephrotoxicity secondary to mercuric chloride ingestion. Clin Toxicol 1977; 11:309-315.
    197) Piikivi L, Hanninen H, & Martelin T: Psychological performance and long-term exposure to mercury vapors. Scand J Work Environ Health 1984; 10:35-41.
    198) Pollack MM, Dunbar BS, & Holbrook PR: Aspiration of activated charcoal and gastric contents. Ann Emerg Med 1981; 10:528-529.
    199) Popescu HI, Negru L, & Lancranjan I: Chromosome aberrations induced by occupational exposure to mercury. Arch Environ Health 1979; 34:461-463.
    200) Product Information: CHEMET(R) oral capsules, succimer oral capsules. Ovation Pharmaceuticals,Inc, Deerfield, IL, 2005.
    201) Product Information: CHEMET(R) oral capsules, succimer oral capsules. Lundbeck Inc. (per Manufacturer), Deerfield, IL, 2011.
    202) Product Information: CUPRIMINE(R) oral capsules, penicillamine oral capsules. Merck & Co,Inc, Whitehouse Station, NJ, 2004.
    203) Product Information: DEPEN(R) titratable oral tablets, penicillamine titratable oral tablets. Meda Pharmaceuticals Inc, Somerset, NJ, 2009.
    204) Product Information: DIMAVAL(R) oral capsules, (RS)-2,3-bis(sulphanyl)propane-1-sulphonic acid, sodium salt-monohydrate oral capsules. Heyl Chemisch-pharmazeutische Fabrik GmbH & Co., 2004.
    205) Product Information: Dimaval(R) intravenous intramuscular injection solution, 2,3-Bis(sulfanyl)propane-1-sulfonic acid intravenous intramuscular injection solution. Heyl Chem.-pharm. Fabrik (per manufacturer), Berlin, Germany, 2013.
    206) RTECS : Registry of Toxic Effects of Chemical Substances. National Institute for Occupational Safety and Health. Cincinnati, OH (Internet Version). Edition expires 1990; provided by Truven Health Analytics Inc., Greenwood Village, CO.
    207) RTECS : Registry of Toxic Effects of Chemical Substances. National Institute for Occupational Safety and Health. Cincinnati, OH (Internet Version). Edition expires 1993; provided by Truven Health Analytics Inc., Greenwood Village, CO.
    208) Rau NR, Nagaraj MV, Prakash PS, et al: Fatal pulmonary aspiration of oral activated charcoal. Br Med J 1988; 297:918-919.
    209) Roberts JR: Minor burns (Pt II). Emerg Med Ambulatory Care News 1988; 10:4-5.
    210) Roels H, Gennart JP, & Lauwerys R: Surveillance of workers exposed to mercury vapour: validation of a previously proposed biological threshold limit value for mercury concentration in urine. Am J Ind Med 1985; 7:45-71.
    211) Rosa FW: Teratogen update: penicillamine. Teratology 1986; 33:127-131.
    212) Rosenman KD, Valciukas JA, & Glickman L: Sensitive indicators of inorganic mercury toxicity. Arch Environ Health 1986; 41:208-215.
    213) Ross WD & Sholito MC: ACTA Psych Scand 1983; 67:100-104.
    214) Sauder P, Livardjani F, & Jaeger A: Acute mercury chloride intoxication: effects of hemodialysis and plasma exchange on mercury kinetics. Clin Toxicol 1988; 26:189-197.
    215) Sax NI & Lewis RJ: Dangerous Properties of Industrial Materials, 7th ed, Van Nostrand Reinhold Company, New York, NY, 1989, pp 2190.
    216) Sax NI & Lewis RJ: Hawley's Condensed Chemical Dictionary, 11th ed, Van Nostrand Reinhold Company, New York, NY, 1987, pp 741.
    217) Schroeder HA & Mitchener M: Life-term effects of mercury, methyl mercury, and nine other trace metals on mice. J Nutr 1975; 105:452-458.
    218) Seidel J: Acute mercury poisoning after polyvinyl alcohol preservative ingestion. Pediatrics 1980; 66:132-143.
    219) Sherlock J, Hislop J, & Newton D: Elevation of mercury in human blood from controlled chronic ingestion of methylmercury in fish. Human Toxicol 1984; 3:117-131.
    220) Singer R, Valciukas JA, & Rosenman KD: Peripheral neurotoxicity in workers exposed to inorganic mercury compounds. Arch Environ Health 1987; 42:181-184.
    221) Sittig M: Handbook of Toxic and Hazardous Chemicals and Carcinogens, 2nd ed, Noyes Publications, Park Ridge, NJ, 1985, pp 570-571.
    222) Smith PJ: Br J Ind Med 1983; 40:413-419.
    223) Solomon L, Abrams G, & Dinner M: Neonatal abnormalities associated with d-penicillamine treatment during pregnancy. N Engl J Med 1977; 296:54.
    224) Stremski E, Yousif J, & Furbee B: Mercurous perchlorate burns producing elevated blood mercury (Hg) levels, treatment with dimercaptosuccinate (DMSA) (Abstract), North American Congress of Clinical Toxicology-94, Salt Lake City, UT, 1994, pp 26-1994.
    225) Suzuki T, Hongo T, & Matsuo N: An acute mercuric mercury poisoning: chemical speciation of hair mercury shows a peak of inorganic mercury value. Human Exp Toxicol 1992; 11:53-57.
    226) Tsuchiya H, Mitani K, & Dodama K: Placental transfer of heavy metals in normal pregnant Japanese women. Arch Environ Health 1984; 39:11-17.
    227) U.S. Department of Energy, Office of Emergency Management: Protective Action Criteria (PAC) with AEGLs, ERPGs, & TEELs: Rev. 26 for chemicals of concern. U.S. Department of Energy, Office of Emergency Management. Washington, DC. 2010. Available from URL: http://www.hss.doe.gov/HealthSafety/WSHP/Chem_Safety/teel.html. As accessed 2011-06-27.
    228) U.S. Department of Health and Human Services, Public Health Service, National Toxicology Project : 11th Report on Carcinogens. U.S. Department of Health and Human Services, Public Health Service, National Toxicology Program. Washington, DC. 2005. Available from URL: http://ntp.niehs.nih.gov/INDEXA5E1.HTM?objectid=32BA9724-F1F6-975E-7FCE50709CB4C932. As accessed 2011-06-27.
    229) U.S. Environmental Protection Agency: Discarded commercial chemical products, off-specification species, container residues, and spill residues thereof. Environmental Protection Agency's (EPA) Resource Conservation and Recovery Act (RCRA); List of hazardous substances and reportable quantities 2010b; 40CFR(261.33, e-f):77-.
    230) U.S. Environmental Protection Agency: Integrated Risk Information System (IRIS). U.S. Environmental Protection Agency. Washington, DC. 2011. Available from URL: http://cfpub.epa.gov/ncea/iris/index.cfm?fuseaction=iris.showSubstanceList&list_type=date. As accessed 2011-06-21.
    231) U.S. Environmental Protection Agency: List of Radionuclides. U.S. Environmental Protection Agency. Washington, DC. 2010a. Available from URL: http://www.gpo.gov/fdsys/pkg/CFR-2010-title40-vol27/pdf/CFR-2010-title40-vol27-sec302-4.pdf. As accessed 2011-06-17.
    232) U.S. Environmental Protection Agency: List of hazardous substances and reportable quantities. U.S. Environmental Protection Agency. Washington, DC. 2010. Available from URL: http://www.gpo.gov/fdsys/pkg/CFR-2010-title40-vol27/pdf/CFR-2010-title40-vol27-sec302-4.pdf. As accessed 2011-06-17.
    233) U.S. Environmental Protection Agency: The list of extremely hazardous substances and their threshold planning quantities (CAS Number Order). U.S. Environmental Protection Agency. Washington, DC. 2010c. Available from URL: http://www.gpo.gov/fdsys/pkg/CFR-2010-title40-vol27/pdf/CFR-2010-title40-vol27-part355.pdf. As accessed 2011-06-17.
    234) U.S. Occupational Safety and Health Administration: Part 1910 - Occupational safety and health standards (continued) Occupational Safety, and Health Administration's (OSHA) list of highly hazardous chemicals, toxics and reactives. Subpart Z - toxic and hazardous substances. CFR 2010 2010; Vol6(SEC1910):7-.
    235) U.S. Occupational Safety, and Health Administration (OSHA): Process safety management of highly hazardous chemicals. 29 CFR 2010 2010; 29(1910.119):348-.
    236) United States Environmental Protection Agency Office of Pollution Prevention and Toxics: Acute Exposure Guideline Levels (AEGLs) for Vinyl Acetate (Proposed). United States Environmental Protection Agency. Washington, DC. 2006. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020d6af&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    237) Vale JA, Kulig K, American Academy of Clinical Toxicology, et al: Position paper: Gastric lavage. J Toxicol Clin Toxicol 2004; 42:933-943.
    238) Vale JA: Position Statement: gastric lavage. American Academy of Clinical Toxicology; European Association of Poisons Centres and Clinical Toxicologists. J Toxicol Clin Toxicol 1997; 35:711-719.
    239) Verschaeve L, Kirsch Volders M, & Susanne C: Genetic damage induced by occupationally low mercury exposure. Environ Res 1976; 12:306-316.
    240) Wang RY, Henry GC, & Fine J: Mercuric chloride poisonings from stool fixative ingestion (Abstract). Vet Human Toxicol 1992; 34:341.
    241) Winstanley R, Patel I, & Fischer E: The determination of toxic metals in simulated stomach contents by energy dispersive x-ray fluorescence analysis and a fatal case of mercury poisoning. Forens Sci Internat 1987; 35:181-187.
    242) Yonaga T & Morita K: Comparison of the effect of N-(2,3-dimercaptopropyl) phthalamidic acid, DL-penicillamine and dimercaprol on the excretion and tissue retention of mercury in mice. Toxicol Appl Pharmacol 1981; 57:197-207.
    243) Yoshida M: Relation of mercury exposure to elemental mercury levels in the urine and blood. Scand J Work Environ Health 1985; 11:33-37.
    244) Zalups RK, Gelein RM, & Cernichiari E: DMPS as a rescue agent for the nephropathy induced by mercuric chloride. J Pharmacol Exp Ther 1991; 256:1-10.
    245) Zenz C: Occupational Medicine, 2nd ed, Year Book Medical Publishers, Inc, Chicago, IL, 1988, pp 187-188.