Contact Us    Contact Us     |     Feedback
MOBILE VIEW  | 

GALLIUM ARSENIDE

Export To Excel

Classification   |    Detailed evidence-based information

Substances Included Synonyms

Therapeutic Toxic Class

    A) Gallium arsenide contains 48.2% gallium and 51.8% arsenic and is considered an intermetallic compound (Bingham et al, 2001).

Specific Substances

    1) Gallium Arsenide
    2) Gallium Monoarsenide
    3) Gallium Monoarsenide (GaAs)
    4) Molecular Formula: AS-GA
    5) CAS 13-3-00-0

Available Forms Sources

    A) FORMS
    1) Gallium arsenide (GaAs) occurs as dark grey crystals with a metallic sheen which are prepared by allowing a mixture of arsenic and hydrogen vapor to pass over gallium(III) oxide at a temperature of 600 degrees (Budavari, 1996).
    2) It is available as single crystals, as ingots, as a highly purified electronic grade polycrystalline, and as alloys with gallium phosphide or indium arsenide (Lewis, 1993; HSDB , 2001).
    B) SOURCES
    1) Gallium metal is found widely in the earth's lithosphere, with the mineral germanite sulfide as the richest source (Bingham et al, 2001).
    2) There may be as much as 15 grams of gallium per ton of the lithosperic material (Clayton & Clayton, 1994).
    3) Gallium metal is also found in zinc blends, clays, feldspars, coals, the ores of chromium, manganese, and iron, bauxite, and some tin ores, and may be recovered from by-products in alumina or zinc production and during aluminum refining operations (Bingham et al, 2001).
    C) USES
    1) Gallium arsenide is the most widely used gallium compound. It operates beyond the cutoff frequencies of other diodes, and is used extensively in microelectronics industry because of its photovoltaic properties. It is used in LEDs (light-emitting diodes used for telephone dials), lasers, laser windows, and photodetectors and in the photoelectronic transmission of data by optical fibers. Its estimated that 35,000 kilograms of gallium will be used annually in the microelectrics industry (Bingham et al, 2001).
    2) It is the material of choice for semiconductors in devices such as millimeter wave and microwave telecommunications systems, and ultrafast supercomputers (Webb et al, 1984).
    3) Gallium arsenide is used in medical lasers and is finding applications in transistors for military electronics equipment (infrared emitters) such as radar-jamming devices, microwave devices, solar cells and semiconductor applications (transistors, solar cells, lasers) (Cowen, 1986; Abergel et al, 1984; HSDB , 2001; Bingham et al, 2001).

Overview

Life Support

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

Clinical Effects

    0.2.1) SUMMARY OF EXPOSURE
    A) Gallium arsenide is poorly absorbed from the gastrointestinal tract. Acute toxicity is unlikely and has not been reported. Gallium arsenide components are used in the semiconductor industry and are unlikely to produce acute symptoms.
    B) Chronic toxicity is possible from occupational exposure, but has not been reported. Any anticipated toxicity would most likely be due to the arsenic component.
    1) Chronic health effects due to inorganic arsenic include: primarily cancers {i.e., lung cancer}, perforation of the nasal septum, laryngitis, pharyngitis, bronchitis, peripheral neuropathy, and encephalopathy.
    2) Dermatologic exposure to inorganic arsenic has resulted in hyperkeratosis of the palms and skin cancer.
    C) Under certain conditions arsine gas may be liberated from gallium arsenide.
    D) For further information on arsenic and arsine gas please refer to the ARSENIC or ARSINE managements.
    0.2.5) CARDIOVASCULAR
    A) Dysrhythmias including ventricular fibrillation, ECG changes, and myocardial dysfunction may occur with arsenic poisoning.
    0.2.6) RESPIRATORY
    A) Direct lung injury, pulmonary edema, or fibrosis may occur, based on experimental animal studies.
    0.2.7) NEUROLOGIC
    A) Peripheral neuropathy may develop.
    0.2.8) GASTROINTESTINAL
    A) Nausea, vomiting, diarrhea, and abdominal pain may occur.
    0.2.9) HEPATIC
    A) Gallium arsenide altered hepatic biochemical function in rats, but is only considered a moderate effect of exposure.
    B) Hepatomegaly and jaundice may rarely occur with arsenic poisoning.
    0.2.10) GENITOURINARY
    A) Alterations in renal enzyme function have been reported following gallium arsenide exposure in animals; renal failure may occur after arsenic or arsine poisoning.
    0.2.11) ACID-BASE
    A) Gallium has induced acidosis in rabbits.
    0.2.12) FLUID-ELECTROLYTE
    A) Hemolysis from arsine poisoning may result in hyperkalemia, while gallium has caused hypokalemia in experimental animals. Gastrointestinal fluid losses and "third spacing" in acute arsenic poisoning may lead to hypovolemia and shock.
    0.2.13) HEMATOLOGIC
    A) Gallium has caused bone marrow depression. Anemia may be seen in arsenic poisoning.
    B) Arsine poisoning causes intravascular hemolysis and renal failure.
    C) Gallium arsenide inhibited the heme biosynthetic pathway in rats.
    0.2.14) DERMATOLOGIC
    A) Gallium has induced rash, itching, and edema.
    B) Mee's lines in the fingernails are characteristic of arsenic exposure.
    0.2.15) MUSCULOSKELETAL
    A) Muscle cramping has occurred with arsenic poisoning.
    0.2.17) METABOLISM
    A) Gallium arsenide increased serum corticosterone levels in mice.
    B) Arsenic interferes with metabolic energy production.
    0.2.19) IMMUNOLOGIC
    A) Gallium arsenide is an immunosuppressant.
    0.2.20) REPRODUCTIVE
    A) Gallium arsenide is not an animal teratogen.
    0.2.21) CARCINOGENICITY
    A) No data were available to assess the carcinogenic potential specifically of gallium arsenide.
    B) Arsenic is a confirmed human carcinogen; the IARC has considered that there is sufficient evidence for the carcinogenicity of inorganic compounds in humans.

Laboratory Monitoring

    A) Arsenic blood and spot urine levels are generally not as useful or reliable as 24 hour urine collections for arsenic excretion.

Treatment Overview

    0.4.2) ORAL/PARENTERAL EXPOSURE
    A) 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.
    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) Monitor complete blood count, serum electrolytes, liver and renal functions, and cardiac status carefully.
    D) HYPOTENSION: Infuse 10 to 20 mL/kg isotonic fluid. If hypotension persists, administer dopamine (5 to 20 mcg/kg/min) or norepinephrine (ADULT: begin infusion at 0.5 to 1 mcg/min; CHILD: begin infusion at 0.1 mcg/kg/min); titrate to desired response.
    E) The role of chelation therapy in gallium arsenide poisoning is controversial and unclear.
    1) CHELATION THERAPY: Symptomatic patients who are unable to tolerate oral medication should be treated with BAL 3 to 5 mg/kg/dose IM every 4 hours until gastrointestinal symptoms subside. At that point switch to an oral chelator. Stop chelation therapy when urine arsenic excretion falls below 50 mcg/24 hours.
    2) Dimercaptosuccinic acid (DMSA; Succimer) and 2,3-dimercapto-1-propanesulphonic acid sodium salt (DMPS, Dimaval(R)) have also been used to treat arsenic poisoning, but there has been a limited amount of information regarding its use.
    a) 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.
    b) 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.
    3) 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.
    F) Hemodialysis can be used both to treat renal failure and may remove some arsenic during renal failure.
    0.4.3) INHALATION EXPOSURE
    A) INHALATION: Move patient to fresh air. Monitor for respiratory distress. If cough or difficulty breathing develops, evaluate for respiratory tract irritation, bronchitis, or pneumonitis. Administer oxygen and assist ventilation as required. Treat bronchospasm with an inhaled beta2-adrenergic agonist. Consider systemic corticosteroids in patients with significant bronchospasm.
    B) Administer 100% humidified supplemental oxygen with assisted ventilation if required.
    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) EXPOSURE TO GALLIUM ARSENIDE LASERS: Refer for thorough ophthalmic examination. Treat as a thermal burn.
    0.4.5) DERMAL EXPOSURE
    A) OVERVIEW
    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).

Range Of Toxicity

    A) The minimum lethal and maximum tolerated human exposures to gallium arsenide have not been established.

Clinical Effects

Summary Of Exposure

    A) Gallium arsenide is poorly absorbed from the gastrointestinal tract. Acute toxicity is unlikely and has not been reported. Gallium arsenide components are used in the semiconductor industry and are unlikely to produce acute symptoms.
    B) Chronic toxicity is possible from occupational exposure, but has not been reported. Any anticipated toxicity would most likely be due to the arsenic component.
    1) Chronic health effects due to inorganic arsenic include: primarily cancers {i.e., lung cancer}, perforation of the nasal septum, laryngitis, pharyngitis, bronchitis, peripheral neuropathy, and encephalopathy.
    2) Dermatologic exposure to inorganic arsenic has resulted in hyperkeratosis of the palms and skin cancer.
    C) Under certain conditions arsine gas may be liberated from gallium arsenide.
    D) For further information on arsenic and arsine gas please refer to the ARSENIC or ARSINE managements.

Heent

    3.4.3) EYES
    A) PHOTOPHOBIA and blindness were found in rats administered lethal doses of various gallium salts. Rabbits, dogs, and goats did not develop these effects (Grant & Schuman, 1993).
    B) LACK OF EFFECT - No human cases of photophobia or blindness have been reported following exposure to gallium arsenide (Bingham et al, 2001).
    C) GALLIUM ARSENIDE LASER BURNS - Retinal burns of the eye may occur from exposure to the beam of a gallium arsenide laser (Adams et al, 1974).
    3.4.5) NOSE
    A) IRRITATION - Inhalation of arsenic may cause a sensation of burning, dryness, and constriction of the oral and nasal cavities (Gosselin et al, 1984).
    B) Chronic exposure to inorganic arsenic can result in perforation of the nasal septum, laryngitis, and pharyngitis (pp 472-504).
    3.4.6) THROAT
    A) IRRITATION - Inhalation of arsenic may cause a sensation of burning, dryness, and constriction of the oral and nasal cavities (Gosselin et al, 1984).
    B) Chronic exposure to inorganic arsenic can result in perforation of the nasal septum, laryngitis, and pharyngitis (pp 472-504).

Cardiovascular

    3.5.1) SUMMARY
    A) Dysrhythmias including ventricular fibrillation, ECG changes, and myocardial dysfunction may occur with arsenic poisoning.
    3.5.2) CLINICAL EFFECTS
    A) CONDUCTION DISORDER OF THE HEART
    1) ARSENIC COMPOUNDS - Dysrhythmias including ventricular fibrillation, prolongation of the QT interval, T-wave abnormalities, and myocardial dysfunction contributing to shock have been described in poisoning with other arsenic compounds, especially with chronic exposure (Schoolmeester & White, 1980).
    2) LACK OF EFFECT
    a) At the time of this review, ECG changes have not been reported in gallium arsenide-exposed humans (Bingham et al, 2001).

Respiratory

    3.6.1) SUMMARY
    A) Direct lung injury, pulmonary edema, or fibrosis may occur, based on experimental animal studies.
    3.6.2) CLINICAL EFFECTS
    A) SMELL OF BREATH - FINDING
    1) GARLIC ODOR - The breath may have a garlic odor in arsenic or arsine poisoning; a garlic odor occurs when gallium arsenide is moistened (Schoolmeester & White, 1980; Gosselin et al, 1984; Bingham et al, 2001).
    B) DISORDER OF RESPIRATORY SYSTEM
    1) Chronic exposure to inorganic arsenic can result in bronchitis and lung cancer in some cases (pp 472-504).
    3.6.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) SUMMARY
    a) In animal studies, the respiratory tract is the primary organ system for toxicity following chronic and subchronic gallium arsenide exposure (Bingham et al, 2001)
    2) RESPIRATORY DISORDER
    a) DIRECT LUNG INJURY - Rats administered gallium arsenide by the intratracheal route developed large clusters of gallium arsenide deposits that were being phagocytized by alveolar macrophages 14 days after exposure (Webb et al, 1986). Another study conducted in a similar manner indicated that histopathologic changes of multifocal proliferative alveolitis were present in exposed rats (Harrison, 1986).
    b) A marked thickening of the alveolar walls from pneumatocyte hyperplasia and interstitial pneumonia was found (Webb et al, 1986). Atelectasis and alveolar wall fibrosis were noted in some animals (Webb et al, 1986). No pulmonary edema was observed (Webb et al, 1986).
    c) These authors speculated that gallium arsenide might lead to pulmonary fibrosis (Webb et al, 1986). Exactly how the pathology observed from this mode of exposure relates to workers inhaling gallium arsenide fumes is unclear.
    d) Smaller particles of gallium arsenide (5.82 microns mean volume diameter) were more toxic than larger particles (12.67 microns) in inducing pulmonary responses in rats (Webb et al, 1987).

Neurologic

    3.7.1) SUMMARY
    A) Peripheral neuropathy may develop.
    3.7.2) CLINICAL EFFECTS
    A) SECONDARY PERIPHERAL NEUROPATHY
    1) A single patient exposed by inhalation to gallium trifluoride developed a mild radial nerve palsy with pain and weakness which resolved over about 3 months (Clayton & Clayton, 1994). This effect has not been reported from gallium arsenide exposure.
    2) Severe peripheral neuropathy developed in one patient exposed by the inhalation and dermal routes to the pentavalent arsenic compound monosodium methyl arsenate during an aerial spraying operation (Hessl & Berman, 1982). Peripheral neuropathy is a common finding in severe arsenic poisoning (Schoolmeester & White, 1980).

Gastrointestinal

    3.8.1) SUMMARY
    A) Nausea, vomiting, diarrhea, and abdominal pain may occur.
    3.8.2) CLINICAL EFFECTS
    A) DRUG-INDUCED GASTROINTESTINAL DISTURBANCE
    1) Anorexia, nausea, and vomiting have developed in humans given a mixture of gallium-72 and stable gallium (Clayton & Clayton, 1994). These effects were felt to be due partly to radiation and partly to the effects of the gallium itself (Clayton & Clayton, 1994).
    2) Vomiting, abdominal pain and cramps, diarrhea, and nausea were frequent findings in patients who became symptomatic after ingesting sodium arsenate (Kersjes et al, 1987).
    3) Gastrointestinal fluid losses and "third spacing" in arsenic poisoning may lead to dehydration, hypovolemia, and hypotension (Gosselin et al, 1984).
    3.8.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) GASTROINTESTINAL DISORDER
    a) Experimental animals administered lethal or near lethal doses of various gallium salts have developed vomiting, diarrhea, anorexia, and bloody stools. Rapid weight loss may also occur following injections of certain gallium salts (Bingham et al, 2001).
    b) In animal studies, oral administration of gallium arsenide was less toxic than intratracheal instillation (up to 1000 mg/kg in rats resulted in no acute effects), and resulted in only mild diarrhea and constipation (Bingham et al, 2001).

Hepatic

    3.9.1) SUMMARY
    A) Gallium arsenide altered hepatic biochemical function in rats, but is only considered a moderate effect of exposure.
    B) Hepatomegaly and jaundice may rarely occur with arsenic poisoning.
    3.9.2) CLINICAL EFFECTS
    A) LIVER DAMAGE
    1) ARSENIC EXPOSURE - Hepatotoxicity with hepatomegaly and jaundice, occasionally progressing to ascites may rarely occur in chronic arsenic poisoning (Gosselin et al, 1984).
    3.9.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) HEPATIC FUNCTION ABNORMAL
    a) SUMMARY - In rat studies, oral doses of gallium arsenide altered hepatic enzyme function (i.e., an increase in serum aspartate aminotransferase activity, gamma-glutamyltranspeptidase, and hepatic malondialdehyde). The studies suggested that gallium arsenide had only a moderate effect on liver function as compared to immunologic or hematologic systems (Bingham et al, 2001).
    b) Subacute oral administration of gallium arsenide (50 to 200 mg/kg 5 days/week for 3 weeks) inhibited delta-aminolevulinic acid dehydratase (d-ALAD) activity in blood, reduced glutathione levels, and increased zinc protoporphyrin (ZP) levels in rats (Flora, 1996).

Genitourinary

    3.10.1) SUMMARY
    A) Alterations in renal enzyme function have been reported following gallium arsenide exposure in animals; renal failure may occur after arsenic or arsine poisoning.
    3.10.2) CLINICAL EFFECTS
    A) CRUSH SYNDROME
    1) ARSENIC-
    a) Acute tubular necrosis may occur in arsenic poisoning (Schoolmeester & White, 1980).
    3.10.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) RENAL ENZYMES ABNORMAL
    a) Increases in renal alkaline phosphatase activity and urinary protein excretion have been reported in male albino rats exposed to a single oral dose of gallium arsenide (100, 200, or 500 mg/kg). Moderate effects are anticipated following renal exposure (Flora et al, 1998; Bingham et al, 2001).
    2) RENAL FAILURE
    a) GALLIUM SALTS -
    1) Lethal or near-lethal doses of various gallium salts administered to dogs have produced renal injury similar to that caused by mercury, with elevated blood urea nitrogen and red blood cells, hyaline and granular casts, and albumin in the urine (Clayton & Clayton, 1994).
    2) Late deaths in these dogs were thought to be due to renal failure (Clayton & Clayton, 1994).
    b) Rabbit experiments with gallium citrate have given similar results (Clayton & Clayton, 1994).

Acid-Base

    3.11.1) SUMMARY
    A) Gallium has induced acidosis in rabbits.
    3.11.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) ACIDOSIS
    a) In rabbits administered gallium citrate, uncompensated acidosis was observed (Clayton & Clayton, 1994).

Hematologic

    3.13.1) SUMMARY
    A) Gallium has caused bone marrow depression. Anemia may be seen in arsenic poisoning.
    B) Arsine poisoning causes intravascular hemolysis and renal failure.
    C) Gallium arsenide inhibited the heme biosynthetic pathway in rats.
    3.13.2) CLINICAL EFFECTS
    A) MYELOSUPPRESSION
    1) GALLIUM - Bone marrow depression with lymphopenia, leukopenia, thrombocytopenia, and anemia was noted in humans administered a combination of gallium-72 and stable gallium (Clayton & Clayton, 1994).
    a) The main cause of the bone marrow depression was thought to be radiation, although gallium itself was probably contributory (Clayton & Clayton, 1994).
    B) ANEMIA
    1) ARSENIC - Blood dyscrasias including anemia, leukopenia, and mild thrombocytopenia have been reported in arsenic poisoning (Schoolmeester & White, 1980).
    3.13.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) HEMATOLOGIC ABNORMALITIES
    a) GALLIUM ARSENIDE - In animal studies, the hematologic and the immunological system appear to be the most frequently affected by gallium arsenide exposure. A dose-dependent inhibition of erythrocyte delta-aminolevulinic acid dehydratase (d-ALAD) was reported after a single intratracheal dose (Bingham et al, 2001).
    2) ANEMIA
    a) HEME BIOSYNTHESIS - Subacute oral administration of gallium arsenide (50 to 200 mg/kg 5 days/week for 3 weeks) inhibited delta-aminolevulinic acid dehydratase (d-ALAD) activity in blood of rats (Flora, 1996).
    b) This inhibition appears to be due to the gallium component, which may displace the zinc cofactor from the enzyme (Goering et al, 1988).

Dermatologic

    3.14.1) SUMMARY
    A) Gallium has induced rash, itching, and edema.
    B) Mee's lines in the fingernails are characteristic of arsenic exposure.
    3.14.2) CLINICAL EFFECTS
    A) ERUPTION
    1) Folliculitis, maculopapular rash, itching, or subcutaneous or cutaneous edema was noted in humans administered a combination of gallium-72 and stable gallium (Clayton & Clayton, 1994).
    a) These effects cleared in a few days after cessation of gallium injections, and were felt to be due to the gallium itself and not radiation (Clayton & Clayton, 1994).
    b) These effects have not been reported after gallium arsenide exposure.
    B) MEE'S LINE
    1) White transverse bands across the fingernails and toenails (Mees lines) may occur 4 to 6 weeks after arsenic exposure (Schoolmeester & White, 1980).

Musculoskeletal

    3.15.1) SUMMARY
    A) Muscle cramping has occurred with arsenic poisoning.
    3.15.2) CLINICAL EFFECTS
    A) INCREASED MUSCLE TONE
    1) Cramping of skeletal muscles may occur in arsenic poisoning (Schoolmeester & White, 1980).

Immunologic

    3.19.1) SUMMARY
    A) Gallium arsenide is an immunosuppressant.
    3.19.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) IMMUNE SYSTEM DISORDER
    a) Gallium arsenide suppresses function of all cell types involved with the immune response in mice (Burns et al, 1994). T-cell proliferation in response to sheep red blood cells was suppressed in mice (Burns & Munson, 1993a).
    b) Gallium arsenide inhibited production of interleukins IL-2, IL-4, IL-5 and IL-6 in mice. Addition of IL-2 reversed the inhibition of T-cell proliferation by gallium arsenide (Burns & Munson, 1993b).
    c) Immunosuppression caused by gallium arsenide appears to be due mainly to the arsenic component (Burns et al, 1991).
    d) In a study of male albino rats given a single oral dose of gallium arsenide (100, 200 or 500 mg/kg), most immunological indices were altered with all three doses, and remained elevated even at day 21. Unlike other clinical effects, alterations were more likely to occur at days 7 and 21 (Flora et al, 1998).

Reproductive

    3.20.1) SUMMARY
    A) Gallium arsenide is not an animal teratogen.
    3.20.2) TERATOGENICITY
    A) EMBRYOTOXICITY
    1) Gallium arsenide was not teratogenic by the inhalation exposure route in mice or rats at levels up to 75 mg/m(3). However, embryolethality, fetal growth retardation, and some variations (mainly sternebral defects) were increased (Mast et al, 1991).
    B) CONGENITAL ANOMALY
    1) Sodium arsenate and arsenite have been reported to be teratogenic in chickens, mice, rats, and hamsters, but not in sheep (Council on Scientific Affairs, 1985).
    2) No adverse human reproductive effects or human teratogenicity have been reported with long-term use or exposure to arsenicals at permissible exposure limits (Council on Scientific Affairs, 1985).
    3.20.3) EFFECTS IN PREGNANCY
    A) LACK OF INFORMATION
    1) At the time of this review, no information was available to assess the potential effects during pregnancy or lactation specifically of gallium arsenide.

Carcinogenicity

    3.21.1) IARC CATEGORY
    A) IARC Carcinogenicity Ratings for CAS1303-00-0 (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: Gallium arsenide
    b) Carcinogen Rating: 1
    1) The agent (mixture) is carcinogenic to humans. The exposure circumstance entails exposures that are carcinogenic to humans. This category is used when there is sufficient evidence of carcinogenicity in humans. Exceptionally, an agent (mixture) may be placed in this category when evidence of carcinogenicity in humans is less than sufficient but there is sufficient evidence of carcinogenicity in experimental animals and strong evidence in exposed humans that the agent (mixture) acts through a relevant mechanism of carcinogenicity.
    3.21.2) SUMMARY/HUMAN
    A) No data were available to assess the carcinogenic potential specifically of gallium arsenide.
    B) Arsenic is a confirmed human carcinogen; the IARC has considered that there is sufficient evidence for the carcinogenicity of inorganic compounds in humans.
    3.21.3) HUMAN STUDIES
    A) CARCINOMA
    1) At the time of this review, no data were available to assess the carcinogenic potential specifically of gallium arsenide (Bingham et al, 2001).
    2) During the production of gallium arsenide, potential toxicity is derived from elemental inorganic arsenic in its trivalent form which is a confirmed human carcinogen. It is associated with lung, skin, and liver tumors (Harrison, 1986; pp 285-294). The IARC has considered that there is sufficient evidence for the carcinogenicity of inorganic arsenic compounds in humans (Bingham et al, 2001).
    3) Long-term arsenic exposure has been associated with respiratory tract and skin cancers, cancers of the nasopharynx, stomach, colon, kidney, ureter, bladder, prostate, and liver, as well as leukemia and lymphoma (Schoolmeester & White, 1980). However, except for leukemias and lymphomas, chronic exposure of experimental animals to arsenic compounds has failed to result in these cancers, and the exact role of arsenic in carcinogenesis is presently undefined (Schoolmeester & White, 1980).

Laboratory Monitoring

Monitoring Parameters Levels

    4.1.1) SUMMARY
    A) Arsenic blood and spot urine levels are generally not as useful or reliable as 24 hour urine collections for arsenic excretion.
    4.1.2) SERUM/BLOOD
    A) BLOOD/SERUM CHEMISTRY
    1) Arsenic blood levels are quite variable and not often considered useful in either diagnosis or assessing therapy. The utility of arsenic blood levels in assessing patients with gallium arsenide exposure is unknown. Normal blood arsenic levels in humans range from 0.002 to 0.062 mg/L (2 to 62 mcg/L or 0.2 to 6.2 mcg/dL) with a mean of 0.003 to 0.005 mg/L (3 to 5 mcg/L or 0.3 to 0.5 mcg/dL) (Baselt, 2000).
    2) Monitor complete blood count, serum electrolytes, and liver and renal functions in serious exposures.
    3) Gallium was not found in the blood of experimental animals administered gallium arsenide by the oral and intratracheal routes (Webb et al, 1984; Webb et al, 1986).
    a) While gallium can be measured by a variety of techniques (Clayton & Clayton, 1994), at present, there does not seem to be any utility in attempting to measure gallium blood levels in patients with gallium arsenide exposure.
    b) Alterations in blood delta-aminolevulinic acid dehydratase (d-ALAD) have been reported in experimental studies after single intratracheal doses of gallium arsenide; a microcytic anemia with an erythrocytosis and increased zinc protoporphyrin/heme ratios have also been reported in rat studies (Bingham et al, 2001).
    B) ACID/BASE
    1) Baseline arterial blood gases should be obtained in patients with respiratory tract irritation after arsine or gallium arsenide exposure.
    C) HEMATOLOGIC
    1) Monitor complete blood count in serious exposures.
    4.1.3) URINE
    A) URINARY LEVELS
    1) Arsenic urine levels might be useful in assessing patients with gallium arsenide exposure. Urine arsenic levels in unexposed humans ranged from 0.01 to 0.30 mg/L (10 to 300 mcg/L or 1 to 30 mcg/dL) (Baselt, 2000).
    2) Asymptomatic workers employed in applying arsenical herbicides had urine arsenic levels ranging from 0.07 to 2.50 mg/L (70 to 2,500 mcg/L or 7 to 250 mcg/dL) (Baselt, 2000).
    3) While spot urine specimens have been suggested as a guide to therapy in pentavalent arsenic exposures (Grande et al, 1987), many authors feel that spot urine specimens are not valid and consider only quantitative 24 hour total urine arsenic excretion values reliable for diagnosis and management of therapy.
    4) Even with chelation, a normal individual will usually not have more than 50 mcg/24 hours urine output of arsenic (Abdelghani et al, 1986).
    B) URINALYSIS
    1) Monitor urinalysis in serious exposures. The primary urinary metabolites of inorganic arsenic are the methylated derivatives dimethylarsinic acid (DMA) and monmethylarsinic acid (MMA). (It is currently considered the method of choice for biologic monitoring of workers exposed to urinary arsenic because the levels obtained are not influenced by the presence of organic arsenic from certain foods (i.e., marine origin)). Urinary arsenic levels, DMA and MMA in the urine can be used to evaluate exposure (Harrison, 1986; Bingham et al, 2001).
    2) WORKPLACE STANDARD - Total urinary arsenic levels >50 mcg/L should be repeated; employees should be instructed to refrain from all sources of dietary arsenic before retesting (Harrison, 1986).
    3) Hemoglobinuria is often an early sign of hemolysis in arsine poisoning (Gosselin et al, 1984; HSDB , 2001).
    4.1.4) OTHER
    A) OTHER
    1) PULMONARY FUNCTION TESTS
    a) Pulmonary function tests might be useful in assessing symptomatic patients following gallium arsenide fume inhalation (Bingham et al, 2001).

Radiographic Studies

    A) ABDOMINAL RADIOGRAPH
    1) Arsenic is radiopaque and may be noted on abdominal radiographs after ingestion; it is not known whether gallium arsenide is also radiopaque (Bingham et al, 2001).
    B) CHEST RADIOGRAPH
    1) Patients with arsine exposure or respiratory tract irritation after exposure to gallium arsenide should have a baseline chest x-ray (Bingham et al, 2001).

Treatment

Life Support

    A) Support respiratory and cardiovascular function.

Patient Disposition

    6.3.1) DISPOSITION/ORAL EXPOSURE
    6.3.1.5) OBSERVATION CRITERIA/ORAL
    A) Any patient with significant gallium arsenide exposure should have follow-up care provided. Urine screening (see above) is suggested for initially asymptomatic patients with significant exposure.
    6.3.3) DISPOSITION/INHALATION EXPOSURE
    6.3.3.1) ADMISSION CRITERIA/INHALATION
    A) Patients with respiratory tract irritation after inhalation of gallium arsenide fumes and those exposed to arsine generated from gallium arsenide should be admitted to the hospital.
    6.3.3.5) OBSERVATION CRITERIA/INHALATION
    A) Any patient with significant gallium arsenide exposure should have follow-up care provided. Urine screening (see above) is suggested for initially asymptomatic patients with significant exposure.

Monitoring

    A) Arsenic blood and spot urine levels are generally not as useful or reliable as 24 hour urine collections for arsenic excretion.

Oral Exposure

    6.5.2) PREVENTION OF ABSORPTION
    A) 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).
    B) GASTRIC LAVAGE
    1) INDICATIONS: Consider gastric lavage with a large-bore orogastric tube (ADULT: 36 to 40 French or 30 English gauge tube {external diameter 12 to 13.3 mm}; CHILD: 24 to 28 French {diameter 7.8 to 9.3 mm}) after a potentially life threatening ingestion if it can be performed soon after ingestion (generally within 60 minutes).
    a) Consider lavage more than 60 minutes after ingestion of sustained-release formulations and substances known to form bezoars or concretions.
    2) 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.
    3) 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.
    4) 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).
    5) 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) HYPOTENSIVE EPISODE
    1) SUMMARY
    a) Infuse 10 to 20 milliliters/kilogram of isotonic fluid and keep the patient supine. If hypotension persists, administer dopamine or norepinephrine. Consider central venous pressure monitoring to guide further fluid therapy.
    2) DOPAMINE
    a) DOSE: Begin at 5 micrograms per kilogram per minute progressing in 5 micrograms per kilogram per minute increments as needed (Prod Info dopamine hcl, 5% dextrose IV injection, 2004). If hypotension persists, dopamine may need to be discontinued and a more potent vasoconstrictor (eg, norepinephrine) should be considered (Prod Info dopamine hcl, 5% dextrose IV injection, 2004).
    b) CAUTION: If ventricular dysrhythmias occur, decrease rate of administration (Prod Info dopamine hcl, 5% dextrose IV injection, 2004). Extravasation may cause local tissue necrosis, administration through a central venous catheter is preferred (Prod Info dopamine hcl, 5% dextrose IV injection, 2004).
    3) NOREPINEPHRINE
    a) PREPARATION: 4 milligrams (1 amp) added to 1000 milliliters of diluent provides a concentration of 4 micrograms/milliliter of norepinephrine base. Norepinephrine bitartrate should be mixed in dextrose solutions (dextrose 5% in water, dextrose 5% in saline) since dextrose-containing solutions protect against excessive oxidation and subsequent potency loss. Administration in saline alone is not recommended (Prod Info norepinephrine bitartrate injection, 2005).
    b) DOSE
    1) ADULT: Dose range: 0.1 to 0.5 microgram/kilogram/minute (eg, 70 kg adult 7 to 35 mcg/min); titrate to maintain adequate blood pressure (Peberdy et al, 2010).
    2) CHILD: Dose range: 0.1 to 2 micrograms/kilogram/minute; titrate to maintain adequate blood pressure (Kleinman et al, 2010).
    3) CAUTION: Extravasation may cause local tissue ischemia, administration by central venous catheter is advised (Peberdy et al, 2010).
    B) MONITORING OF PATIENT
    1) Monitor complete blood count, serum electrolytes, renal, hepatic, and cardiac functions carefully.
    C) HEMOLYSIS
    1) If hemolysis occurs secondary to release of ARSINE from gallium arsenide Early aggressive fluid replacement is the mainstay of therapy and may help prevent renal insufficiency. Diuretics such as mannitol or furosemide may be needed to maintain urine output. Urinary alkalinization is NOT routinely recommended.
    2) Vigorous fluid replacement with 0.9% saline is necessary even if there is no evidence of dehydration. Strive to maintain a urine output of at least 2 to 3 mL/kg/hour. In severe cases 500 milliliters of fluid per hour may be required for the first several days. Monitor fluid input and urine output, plus insensible losses. Monitor for evidence of fluid overload; monitor serum electrolytes, and renal function tests.
    3) Alkalinization of the urine is not routinely recommended as it has never been documented to reduce nephrotoxicity and may cause complications such as alkalemia, hypocalcemia, and hypokalemia.
    D) HEMODIALYSIS
    1) Hemodialysis may be necessary if renal failure occurs. An arsenic dialysance of 76 to 87 milliliters/minute was noted in two patients with renal failure secondary to sodium arsenite poisoning (Vaziri et al, 1980).
    E) FLUID/ELECTROLYTE BALANCE REGULATION
    1) Monitor fluid status carefully. Administer enough fluids to maintain blood pressure and an adequate urine output of 1 to 2 mL/kg/hour. In severe arsenic poisonings, "third spacing," dehydration, and resultant hypovolemia are common.
    F) CHELATION THERAPY
    1) INDICATIONS: Some authors have recommended beginning chelation therapy even in asymptomatic patients with pentavalent arsenic ingestion if a spot urine arsenic level is 200 mcg/L or greater (Kersjes et al, 1987).
    2) This recommendation was based on a study of 57 patients with only 7 patients who became symptomatic, although approximately 80% of these 57 patients received chelation therapy (Kersjes et al, 1987).
    3) The necessity for or value of chelation therapy in patients ingesting arsenic who remain asymptomatic based solely on a spot urine arsenic level is presently undetermined.
    4) Chelation therapy is controversial or often not recommended in arsine poisoning. Its role in gallium arsenide poisoning is unclear. Consider chelation in patients with clinical and/or laboratory evidence of arsenic poisoning.
    5) BAL/DIMERCAPROL
    a) DIMERCAPROL/BAL IN OIL: INDICATIONS: Used for the treatment of mercury (inorganic and elemental), arsenic, and gold poisoning. It is also used in combination with Edetate Calcium Disodium injection to treat patients with severe lead poisoning (Prod Info BAL In Oil intramuscular injection, 2008). Dimercaprol is contraindicated in methyl mercury poisoning (Howland, 2002; Clarkson, 1990).
    b) MILD ARSENIC OR GOLD POISONING: DOSE: 2.5 mg/kg 4 times daily for 2 days, 2 times on the third day, and once daily thereafter for 10 days. SEVERE ARSENIC OR GOLD POISONING: DOSE: 3 mg/kg every 4 hours for 2 days, 4 times on the third day, then twice daily thereafter for 10 days. Administered by deep intramuscular injection only (Prod Info BAL In Oil intramuscular injection, 2008).
    c) MERCURY POISONING: DOSE: 5 mg/kg initially, then 2.5 mg/kg 1 or 2 times daily for 10 days. Administered by deep intramuscular injection only (Prod Info BAL In Oil intramuscular injection, 2008).
    d) ACUTE LEAD ENCEPHALOPATHY: DOSE: 4 mg/kg is given alone in the first dose and thereafter at 4-hour intervals with Edetate Calcium Disodium injection administered at a separate site. For less severe poisoning, dimercaprol dose can be decreased to 3 mg/kg after the first dose. Administered by deep intramuscular injection only. Continue the treatment for 2 to 7 days depending on clinical response (Prod Info BAL In Oil intramuscular injection, 2008). Therapy is generally switched to a less toxic oral chelator as soon as tolerated.
    e) ADVERSE EFFECTS: Common effects include pain at the injection site and fever (especially in children). Other effects include hypertension, tachycardia, nausea, vomiting, headache, burning sensations of the mouth and throat, a sensation of constriction in the throat, chest, or hands, conjunctivitis, lacrimation, salivation, tingling of the extremities, diaphoresis, abdominal pain, and anxiety. Dimercaprol injection contains peanut oil. Avoid in patients with peanut allergy (Prod Info BAL In Oil intramuscular injection, 2008). Adverse effects are dose related; they develop in 1% of patients receiving 2.5 mg/kg every 4 to 6 hours, 14% of patients receiving 4 mg/kg every 4 to 6 hours and 65% of patients receiving 5 mg/kg every 4 to 6 hours (Eagle & Magnuson, 1946).
    f) PRECAUTIONS: It is generally contraindicated in patients with hepatic insufficiency, with the exception of postarsenical jaundice (Prod Info BAL In Oil intramuscular injection, 2008). May cause hemolysis in G6PD deficient patients. BAL metal chelate disassociates in acid environment; urinary alkalinization is usually recommended. Do not administer with iron therapy as BAL iron complex may cause vomiting (Howland, 2002).
    6) SUCCIMER
    a) SUCCIMER/DOSE/ADMINISTRATION
    1) 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).
    a) 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.
    b) Succimer capsule contents may be administered mixed in a small amount of food (Prod Info CHEMET(R) oral capsules, 2011).
    2) 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).
    a) 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).
    b) MONITORING PARAMETERS
    1) 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).
    2) Succimer therapy did not worsen preexisting borderline abnormal liver enzyme levels in a prospective evaluation of 15 children with lead poisoning (Kuntzelman & Angle, 1992).
    c) 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).
    d) ODOR: Succimer has a sulfurous odor that may be evident in the patient's breath or urine (Prod Info CHEMET(R) oral capsules, 2005).
    e) HYPERTHERMIA: One adult developed acute severe hyperthermia associated with hypotension; rechallenge resulted in hyperthermia with shaking chills and hypertension (Marcus et al, 1991).
    f) AVAILABLE FORMS: Succimer (Chemet (R)), 100 mg capsules (Prod Info CHEMET(R) oral capsules, 2011).
    7) PENICILLAMINE
    a) USUAL ADULT DOSE
    1) 1 to 1.5 g/day given orally in 4 divided doses (Nelson, 2011).
    b) USUAL PEDIATRIC DOSE
    1) 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).
    c) Patients allergic to penicillin products may have cross-sensitivity to penicillamine (Prod Info DEPEN(R) titratable oral tablets, 2009).
    d) Monitor for proteinuria and hematuria; heavy metals may also cause renal toxicity (Prod Info DEPEN(R) titratable oral tablets, 2009).
    e) Monitor CBC with differential, platelet count, and hepatic enzymes (Prod Info DEPEN(R) titratable oral tablets, 2009).
    f) 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).
    g) Penicillamine is considered FDA pregnancy category D(Prod Info CUPRIMINE(R) oral capsules, 2004); it should be avoided if possible in pregnant patients.
    h) 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.
    8) DMPS
    a) DMPS/INDICATIONS: Chelating agent for heavy metal toxicities associated with arsenic, bismuth, copper, lead and mercury (Blanusa et al, 2005).
    b) DMPS/DOSING
    1) ACUTE TOXICITY
    a) ADULT ORAL DOSE:
    1) 1200 to 2400 mg/day in equally divided doses (100 to 200 mg 12 times daily) (Prod Info DIMAVAL(R) oral capsules, 2004).
    b) ADULT INTRAVENOUS DOSE (Arbeitsgruppe BGVV, 1996; Prod Info Dimaval(R) intravenous intramuscular injection solution, 2013):
    1) If oral DMPS therapy is not feasible or in severe toxicity, it may be given intravenously.
    2) 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.
    3) First 24 hours: 250 mg intravenously every 3 to 4 hours (1500 to 2000 mg total).
    4) Day two: 250 mg intravenously every 4 to 6 hours (1000 to 1500 mg total).
    5) Day three: 250 mg intravenously every 6 to 8 hours (750 to 1000 mg total).
    6) Day four: 250 mg intravenously every 8 to 12 hours (500 to 750 mg total).
    7) Subsequent days: 250 mg intravenously every 8 to 24 hours (250 to 750 mg total).
    8) Depending on the patient's clinical status, therapy may be changed to the oral route.
    c) PEDIATRIC ORAL DOSE (Arbeitsgruppe BGVV, 1996; Blanusa et al, 2005):
    1) There are insufficient clinical data regarding the pediatric use of DMPS. It should be used only if medically necessary.
    2) Initial dose: 20 to 30 mg/kg/day orally in many equal divided doses.
    3) Maintenance dose: 1.5 to 15 mg/kg/day.
    d) PEDIATRIC INTRAVENOUS DOSE (Arbeitsgruppe BGVV, 1996; Blanusa et al, 2005; Prod Info Dimaval(R) intravenous intramuscular injection solution, 2013):
    1) There are insufficient clinical data regarding the pediatric use of DMPS. It should be used only if medically necessary.
    2) If oral DMPS therapy is not feasible or in severe toxicity, it may be given intravenously.
    3) 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.
    4) First 24 hours: 5 mg/kg intravenously every four hours (total 30 mg/kg).
    5) Day two: 5 mg/kg intravenously every six hours (total 20 mg/kg).
    6) Days three and four: 5 mg/kg intravenously every 8 to 24 hours (total 5 to 15 mg/kg).
    2) CHRONIC TOXICITY
    a) ADULT DOSE
    1) 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).
    3) DMPS/ADVERSE REACTIONS
    a) 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).
    c) SOURCES
    1) 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.
    d) CASE REPORTS
    1) 2,3 dimercapto-1-propanesulphonic acid sodium salt (DMPS, Dimaval (R)), was associated with increased urinary arsenic elimination and rapid neurological improvement in a 33-year-old female with a 1.5 year history of multisystem illness (i.e., peripheral neuropathy, pancytopenia, ventricular tachycardia, gastrointestinal complaints, skin rash, nail changes, and a fetal death), which was secondary to arsenic poisoning.
    a) The patient was initially treated with meso-2,3-dimercaptosuccinic acid (DMSA) and did not respond, but arsenic diuresis and neurological improvement occurred after receiving 2,3-dimercapto-1-propanesulphonic acid sodium salt (DMPS) {250 mg intravenously every 4 hours (not available in the U.S.; obtained by the German manufacturer for compassionate use). Neurological symptoms began to improve after 48 hours. Therapy was continued for 12 days and the patient was able to be successfully extubated; at 1-year follow-up the patient had only residual mild weakness and paresthesiae which was controlled with amitriptyline (Wax & Thornton, 2000).
    2) A 42-year-old man was acutely exposed to arsenic and chromium after dermal exposure to tannalysing fluid and was successfully treated with DMPS (100 mg 6 times daily for 14 days) and had a rapid decline in urine arsenic levels; he was discharged at 7 days with no permanent sequelae (Routledge et al, 1998).
    e) CASE SERIES - In a small study, chronically exposed individuals with inorganic arsenic poisoning (found in their drinking water), with increased urinary levels of monomethylarsonous acid (MMA), were evaluated following DMPS administration. The results indicated that a complex formed by DMPS and MMA inhibited MMA methyltransferase by competing with endogenous ligands that form a water soluble chelate or complex which was excreted in the urine. The authors were uncertain as to whether DMPS formed a metal chelate (heterocyclic ring structure) or complex (linear structure) with MMA (Aposhian et al, 2000).
    9) There is some debate about the role of chelation therapy in arsine poisoning, where preservation of renal function from deposition of red blood cell breakdown products has priority. BAL does not protect against the subsequent development of hemolysis, even when given soon after exposure (Gosselin et al, 1984). However, arsenic is recovered with chelation in arsine poisoning.
    10) NEUROPATHY: Early administration (within the first 18 hours of exposure) of BAL may be effective in preventing arsenical neuropathy (Gosselin et al, 1984). Peripheral neuropathy (combined sensory and motor) may respond to BAL or D-penicillamine therapy if treated early after initial manifestations (Schoolmeester & White, 1980).
    a) However, chelation therapy has not prevented the development of arsenical peripheral neuropathy in all reported cases.
    G) APLASTIC ANEMIA
    1) Aplastic anemia may occur in arsenic poisoning (Gosselin et al, 1984) and may respond to D-penicillamine and oxymetholone.
    H) EXCHANGE TRANSFUSION
    1) Exchange transfusion has been suggested to remove red cell breakdown products in arsine poisoning (Gosselin et al, 1984).

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.
    6.7.2) TREATMENT
    A) OXYGEN
    1) Administer 100 percent supplemental humidified oxygen with assisted ventilation as required to patients with respiratory tract irritation.
    B) MONITORING OF PATIENT
    1) Follow arterial blood gases and chest x-ray in patients with significant inhalation exposure or respiratory tract irritation.
    2) Pulmonary function tests might be useful to assess and monitor patients with significant inhalation exposure or respiratory tract irritation.
    C) ARSINE POISONING
    1) If a patient may have been exposed to ARSINE GAS liberated from gallium arsenide:
    a) see arsine management for more information -
    b) Baseline urinalysis, serum electrolytes, and complete blood count should be obtained.
    c) If hemoglobinuria is present, maintain adequate urine output with aggressive hydration and diuretics if necessary.
    d) Exchange transfusion has been suggested to remove red blood cell breakdown products.
    e) HEMODIALYSIS: may not only treat renal failure if it occurs, but may increase arsenic removal.
    f) CHELATION THERAPY - may not prevent hemolysis and its place in the treatment of arsine poisoning is controversial and generally not recommended.
    D) ACUTE LUNG INJURY
    1) ONSET: Onset of acute lung injury after toxic exposure may be delayed up to 24 to 72 hours after exposure in some cases.
    2) NON-PHARMACOLOGIC TREATMENT: The treatment of acute lung injury is primarily supportive (Cataletto, 2012). Maintain adequate ventilation and oxygenation with frequent monitoring of arterial blood gases and/or pulse oximetry. If a high FIO2 is required to maintain adequate oxygenation, mechanical ventilation and positive-end-expiratory pressure (PEEP) may be required; ventilation with small tidal volumes (6 mL/kg) is preferred if ARDS develops (Haas, 2011; Stolbach & Hoffman, 2011).
    a) To minimize barotrauma and other complications, use the lowest amount of PEEP possible while maintaining adequate oxygenation. Use of smaller tidal volumes (6 mL/kg) and lower plateau pressures (30 cm water or less) has been associated with decreased mortality and more rapid weaning from mechanical ventilation in patients with ARDS (Brower et al, 2000). More treatment information may be obtained from ARDS Clinical Network website, NIH NHLBI ARDS Clinical Network Mechanical Ventilation Protocol Summary, http://www.ardsnet.org/node/77791 (NHLBI ARDS Network, 2008)
    3) FLUIDS: Crystalloid solutions must be administered judiciously. Pulmonary artery monitoring may help. In general the pulmonary artery wedge pressure should be kept relatively low while still maintaining adequate cardiac output, blood pressure and urine output (Stolbach & Hoffman, 2011).
    4) ANTIBIOTICS: Indicated only when there is evidence of infection (Artigas et al, 1998).
    5) EXPERIMENTAL THERAPY: Partial liquid ventilation has shown promise in preliminary studies (Kollef & Schuster, 1995).
    6) CALFACTANT: In a multicenter, randomized, blinded trial, endotracheal instillation of 2 doses of 80 mL/m(2) calfactant (35 mg/mL of phospholipid suspension in saline) in infants, children, and adolescents with acute lung injury resulted in acute improvement in oxygenation and lower mortality; however, no significant decrease in the course of respiratory failure measured by duration of ventilator therapy, intensive care unit, or hospital stay was noted. Adverse effects (transient hypoxia and hypotension) were more frequent in calfactant patients, but these effects were mild and did not require withdrawal from the study (Wilson et al, 2005).
    7) However, in a multicenter, randomized, controlled, and masked trial, endotracheal instillation of up to 3 doses of calfactant (30 mg) in adults only with acute lung injury/ARDS due to direct lung injury was not associated with improved oxygenation and longer term benefits compared to the placebo group. It was also associated with significant increases in hypoxia and hypotension (Willson et al, 2015).
    E) Treatment should include recommendations listed in the ORAL EXPOSURE section when appropriate.

Eye Exposure

    6.8.1) DECONTAMINATION
    A) EYE IRRIGATION, ROUTINE: 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, an ophthalmologic examination should be performed (Peate, 2007; Naradzay & Barish, 2006).
    6.8.2) TREATMENT
    A) INJURY DUE TO LASER
    1) Eye exposure to the beam of a gallium arsenide laser can cause ocular damage appearing as an irregular thermal burn lesion of the pigment epithelium and outer retina (Adams et al, 1974).
    2) Persons exposed to the beam of a gallium arsenide laser should have a thorough ophthalmic examination and follow-up.
    B) 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 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).

Enhanced Elimination

    A) HEMODIALYSIS
    1) If renal failure occurs, hemodialysis may be used both to treat the renal failure and to remove arsenic complexed to either BAL or D-penicillamine (Gosselin et al, 1984).

Range Of Toxicity

Summary

    A) The minimum lethal and maximum tolerated human exposures to gallium arsenide have not been established.

Minimum Lethal Exposure

    A) GENERAL/SUMMARY
    1) The minimum human lethal exposure to gallium arsenide has not been determined (Bingham et al, 2001).
    2) Arsenic trioxide may be released from gallium arsenide after absorption (Webb et al, 1984; Webb et al, 1986). The usual lethal dose of arsenic trioxide for an adult human is 200 to 300 mg (Gosselin et al, 1984).
    3) Arsine gas may be released from gallium arsenide under certain conditions. Exposure to 250 ppm of arsine gas for 30 minutes is usually fatal (Bingham et al, 2001).

Maximum Tolerated Exposure

    A) SPECIFIC SUBSTANCE
    1) GALLIUM - The only reported human toxicity from gallium compounds was in a woman exposed to gallium trifluoride fumes, but the concentration of the fumes were not provided (Clayton & Clayton, 1994).
    a) Humans administered intravenous gallium-72 at doses of 10 to 100 microcuries mixed with stable gallium at unspecified doses have developed gastrointestinal symptoms, itching and rashes, and bone marrow depression (Clayton & Clayton, 1994).
    2) ARSENIC - Acute ingestion of between 9 and 14 mg of arsenic trioxide caused classic gastrointestinal signs and symptoms of arsenic poisoning in a 16-month-old child (Watson et al, 1981).
    3) ARSENIC - The single oral toxic dose of arsenic trioxide may range from 5 to 50 mg (Bingham et al, 2001). Estimates of oral toxic doses of various arsenic compounds range from 1 mg to 10 grams.
    4) ARSINE - Arsine gas may be released from gallium arsenide under certain conditions (Sax, 1984; Bingham et al, 2001). Exposure to 3 to 10 ppm of arsine gas can produce symptomatic poisoning in a few hours, and experimental animals exposed to 0.5 to 2 ppm developed changes in the blood over a few days (ACGIH, 1991).
    B) CHRONIC TOXICITY-
    1) At the time of this review, there are no reports of chronic human toxicity from gallium arsenide (Bingham et al, 2001).

Serum Plasma Blood Concentrations

    7.5.2) TOXIC CONCENTRATIONS
    A) TOXIC CONCENTRATION LEVELS
    1) GENERAL
    a) BLOOD -
    1) Arsenic blood levels are quite variable and not often considered useful in either diagnosis or assessing therapy. The utility of arsenic blood levels in assessing patients with gallium arsenide exposure is unknown.
    2) Normal blood arsenic levels in humans range from 0.002 to 0.062 mg/L (2 to 62 mcg/L or 0.2 to 6.2 mcg/dL) with a mean of 0.003 to 0.005 mg/L (3 to 5 mcg/L or 0.3 to 0.5 mcg/dL) (Baselt, 1982).
    b) URINE -
    1) Arsenic urine levels might be useful in assessing patients with gallium arsenide exposure. Urine arsenic levels in unexposed humans ranged from 0.01 to 0.30 mg/L (10 to 300 mcg/L or 1 to 30 mcg/dL) (Baselt, 2000).
    2) Asymptomatic workers employed in applying arsenical herbicides had urine arsenic levels ranging from 0.07 to 2.50 mg/L (70 to 2,500 mcg/L or 7 to 250 mcg/dL) (Baselt, 2000).
    3) While spot urine specimens have been suggested as a guide to therapy in pentavalent arsenic exposures (Grande et al, 1987), many authors feel that spot urine specimens are not valid and consider only quantitative 24 hour total urine arsenic excretion values reliable for diagnosis and management of therapy.
    4) Even with chelation, a normal individual will usually not have more than 50 mcg/24 hours urine output of arsenic (Abdelghani et al, 1986).

Workplace Standards

    A) ACGIH TLV Values for CAS1303-00-0 (American Conference of Governmental Industrial Hygienists, 2010):
    1) Editor's Note: The listed values are recommendations or guidelines developed by ACGIH(R) to assist in the control of health hazards. They should only be used, interpreted and applied by individuals trained in industrial hygiene. Before applying these values, it is imperative to read the introduction to each section in the current TLVs(R) and BEI(R) Book and become familiar with the constraints and limitations to their use. Always consult the Documentation of the TLVs(R) and BEIs(R) before applying these recommendations and guidelines.
    a) Adopted Value
    1) Gallium arsenide
    a) TLV:
    1) TLV-TWA: 0.0003 mg/m(3)
    2) TLV-STEL:
    3) TLV-Ceiling:
    b) Notations and Endnotes:
    1) Carcinogenicity Category: A3
    2) Codes: R
    3) Definitions:
    a) A3: Confirmed Animal Carcinogen with Unknown Relevance to Humans: The agent is carcinogenic in experimental animals at a relatively high dose, by route(s) of administration, at site(s), of histologic type(s), or by mechanism(s) that may not be relevant to worker exposure. Available epidemiologic studies do not confirm an increased risk of cancer in exposed humans. Available evidence does not suggest that the agent is likely to cause cancer in humans except under uncommon or unlikely routes or levels of exposure.
    b) R: Respirable fraction; see Appendix C, paragraph C (of TLV booklet).
    c) TLV Basis - Critical Effect(s): LRT irr
    d) Molecular Weight: 144.64
    1) For gases and vapors, to convert the TLV from ppm to mg/m(3):
    a) [(TLV in ppm)(gram molecular weight of substance)]/24.45
    2) For gases and vapors, to convert the TLV from mg/m(3) to ppm:
    a) [(TLV in mg/m(3))(24.45)]/gram molecular weight of substance
    e) Additional information:

    B) NIOSH REL and IDLH Values for CAS1303-00-0 (National Institute for Occupational Safety and Health, 2007):
    1) Not Listed

    C) Carcinogenicity Ratings for CAS1303-00-0 :
    1) ACGIH (American Conference of Governmental Industrial Hygienists, 2010): A3 ; Listed as: Gallium arsenide
    a) A3 :Confirmed Animal Carcinogen with Unknown Relevance to Humans: The agent is carcinogenic in experimental animals at a relatively high dose, by route(s) of administration, at site(s), of histologic type(s), or by mechanism(s) that may not be relevant to worker exposure. Available epidemiologic studies do not confirm an increased risk of cancer in exposed humans. Available evidence does not suggest that the agent is likely to cause cancer in humans except under uncommon or unlikely routes or levels of exposure.
    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): 1 ; Listed as: Gallium arsenide
    a) 1 : The agent (mixture) is carcinogenic to humans. The exposure circumstance entails exposures that are carcinogenic to humans. This category is used when there is sufficient evidence of carcinogenicity in humans. Exceptionally, an agent (mixture) may be placed in this category when evidence of carcinogenicity in humans is less than sufficient but there is sufficient evidence of carcinogenicity in experimental animals and strong evidence in exposed humans that the agent (mixture) acts through a relevant mechanism of carcinogenicity.
    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 CAS1303-00-0 (U.S. Occupational Safety, and Health Administration (OSHA), 2010):
    1) Not Listed

Toxicity Information

    7.7.1) TOXICITY VALUES
    A) ANIMAL DATA
    1) LD50- (INTRAPERITONEAL)MOUSE:
    a) 4700 mg/kg (RTECS, 2001)

Pharmacology Toxicology

Toxicologic Mechanism

    A) With intratracheal administration of gallium arsenide in rats, systemic absorption was essentially confined to the arsenic component (Webb et al, 1984; Webb et al, 1986). Direct lung injury was produced by the inhalation route, and the authors of these studies speculated that gallium arsenide might cause pulmonary fibrosis (Webb et al, 1984; Webb et al, 1986).
    B) Systemic toxicity in human exposures would most likely be due to the arsenic component of gallium arsenide (Bingham et al, 2001). The toxicity of arsenic is due to a reversible combination with sulfhydryl groups and resultant inhibition of various enzyme systems, with the sulfhydryl cofactor, dihydrolipoate, the principle site of this inhibition (Schoolmeester & White, 1980; Bingham et al, 2001).
    1) This inhibition disrupts the Krebs cycle and thus oxidative phosphorylation with depletion of cellular energy stores, interruption of numerous cellular metabolic systems, and eventually produces cell death (Schoolmeester & White, 1980; Bingham et al, 2001).
    C) Other enzymes such as monoamine oxidase, lipase, arginase, cholinesterase, and adenyl cyclase are also inhibited by arsenic (Schoolmeester & White, 1980; Bingham et al, 2001). "Arsenolysis" with substitution of arsenic ions for phosphate ions in various reactions can lead to the formation of unstable, spontaneously decomposing end products.
    1) A loss of high energy phosphate bonds can also occur and may be the second contributing mechanism to inhibition of oxidative phosphorylation (Schoolmeester & White, 1980).
    2) All these actions of arsenic are more pronounced in the trivalent state than in the pentavalent state (Schoolmeester & White, 1980).
    D) Acute toxicity of gallium can produce transient nausea, and irritate and possibly burn the eyes, nose, and throat. A large exposure can result in skin rash, metallic taste, nausea, and vomiting and may damage the kidneys. Inhalation of gallium can irritate the lungs, resulting in cough/shortness of breath and possibly pulmonary edema leading to death (Bingham et al, 2001).
    1) Intratracheal instillation of 30 to 300 milligrams of gallium arsenide particles in Japanese white rats produced an alteration in lung clearance secondary to proliferative alveolitis and pulmonary edema (Bingham et al, 2001).
    E) In rat studies, the gastrointestinal route was less toxic than intratracheal instillation; orally administered doses of up to 1000 milligrams/kilogram of gallium arsenide resulted in no pathological changes after 14 days. Doses of 10 to 100 milligrams/kilogram were nontoxic to the gastrointestinal system in hamsters, and a 1000 milligrams/kilogram resulted in only mild diarrhea and constipation (Bingham et al, 2001).
    F) Moderate alterations in hepatic and renal tissues have been reported following gallium arsenide exposure in rat studies (Flora et al, 1998).
    G) The immunological and hematological systems were found to be the most vulnerable to the toxic effects of gallium arsenide. It is able to increase blood zinc protoporphyrin and glutathione concentrations, resulting in a decrease in hemoglobin concentration (Flora et al, 1998; Bingham et al, 2001).
    H) Gallium arsenide inhibits the immune response and synthesis of various interleukins in mice. This inhibition can be reversed by the addition of IL-2 (Burns & Munson, 1993b). Gallium arsenide immunosuppression appears to be due mainly to the arsenic component (Burns et al, 1991).
    I) Gallium arsenide appears to inhibit delta-aminolevulinic acid dehydratase (d-ALAD) by displacement of the zinc from the enzyme by the gallium component (Goering et al, 1988).

Physicochemical

Physical Characteristics

    A) Gallium arsenide occurs as cubic crystals with a dark grey metallic sheen (Budavari, 1996).

Molecular Weight

    A) 144.64 (Budavari, 1996)

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) 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.
    5) 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.
    6) 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.
    7) 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.
    8) 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.
    9) 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.
    10) 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.
    11) 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.
    12) ACGIH: Documentation of the Threshold Limit Values and Biological Exposure Indices, 6th ed, Am Conference of Govt Ind Hyg, Inc, Cincinnati, OH, 1991, pp 87-88.
    13) AIHA: 2006 Emergency Response Planning Guidelines and Workplace Environmental Exposure Level Guides Handbook, American Industrial Hygiene Association, Fairfax, VA, 2006.
    14) Abdelghani AA, Anderson AC, & Jaghabir M: Arsenic levels in blood, urine, and hair of workers applying monosodium methanearsonate (MSMA). Arch Environ Health 1986; 41:163-169.
    15) Abergel RP, Meeker CA, & Lam TS: Control of connective tissue metabolism by lasers: Recent developments and future prospects. J Am Acad Dermatol 1984; 11:1142-1150.
    16) Adams DO, Lund DJ, & Shawaluk PD: The nature of chorioretinal lesions produced by the gallium arsenide laser. Invest Opthalmol 1974; 13:471-475.
    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) Aposhian HV, Zheng B, & Aposhian MM: DMPS-arsenic challenge test. II. Modulation of arsenic species, including monomethylarsonous acid (MMA), excreted in human urine. Toxicol Applied Pharmacol 2000; 165:74-83.
    20) 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.
    21) Artigas A, Bernard GR, Carlet J, et al: The American-European consensus conference on ARDS, part 2: ventilatory, pharmacologic, supportive therapy, study design strategies, and issues related to recovery and remodeling.. Am J Respir Crit Care Med 1998; 157:1332-1347.
    22) Baselt RC: Disposition of Toxic Drugs and Chemicals in Man, 2nd ed, Biomedical Publications, Davis, CA, 1982, pp 59-63.
    23) Baselt RC: Disposition of Toxic Drugs and Chemicals in Man, 5th ed, Chemical Toxicology Inst, Foster City, CA, 2000.
    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) Bingham E, Cohrssen B, & Powell CH: Patty's Toxicology - Volume 2: Toxicological issues related to metals: Neurotoxicity and radiation metals and metal compounds, 5th ed, John Wiley & Sons, Inc, New York, NY, 2001.
    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) Brower RG, Matthay AM, & Morris A: Ventilation with lower tidal volumes as compared with traditional tidal volumes for acute lung injury and the acute respiratory distress syndrome. N Eng J Med 2000; 342:1301-1308.
    28) Budavari S: The Merck Index, 12th ed, Merck & Co, Inc, Whitehouse Station, NJ, 1996, pp 738.
    29) Burgess JL, Kirk M, Borron SW, et al: Emergency department hazardous materials protocol for contaminated patients. Ann Emerg Med 1999; 34(2):205-212.
    30) Burns LA & Munson AE: Gallium arsenide selectively inhibits T cell proliferation and alters expression of CD25 (IL-2R/p55). J Pharmacol Exp Ther 1993a; 265:178-186.
    31) Burns LA & Munson AE: Reversal of gallium arsenide-induced suppression of the antibody-forming cell response by vehicle supernatants. II. Nature and identification of reversing factors. J Pharmacol Exp Ther 1993b; 265:150-158.
    32) Burns LA, Sikorski EE, & Saady JJ: Evidence of arsenic as the immunosuppressive component of gallium arsenide. Toxicol Appl Pharmacol 1991; 110:157-169.
    33) Burns LA, Spriggs TL, & Fuchs BA: Gallium arsenide-induced increase in serum corticosterone is not responsible for suppression of the IgM antibody response. J Pharmacol Exp Ther 1994; 268:740-746.
    34) Caravati EM, Knight HH, & Linscott MS: Esophageal laceration and charcoal mediastinum complicating gastric lavage. J Emerg Med 2001; 20:273-276.
    35) Caravati EM: D-Penicillamine. In: Dart RC, ed. Medical Toxicology, Lippincott Williams & Wilkins, Philadelphia, PA, 2004.
    36) Cataletto M: Respiratory Distress Syndrome, Acute(ARDS). In: Domino FJ, ed. The 5-Minute Clinical Consult 2012, 20th ed. Lippincott Williams & Wilkins, Philadelphia, PA, 2012.
    37) Chyka PA, Seger D, Krenzelok EP, et al: Position paper: Single-dose activated charcoal. Clin Toxicol (Phila) 2005; 43(2):61-87.
    38) Clarkson TW: Mercury - an element of mystery (editorial). N Engl J Med 1990; 323:1137-1138.
    39) Clayton GD & Clayton FE: Patty's Industrial Hygiene and Toxicology, Vol 2C, Toxicology, 4th ed, John Wiley & Sons, New York, NY, 1994, pp 1920-1923;2006-2013.
    40) Council on Scientific Affairs: Effects of toxic chemicals on the reproductive system, American Medical Association, Chicago, IL, 1985.
    41) Cowen R: The hidden threat of producing electronic components overseas. National Research Council News Report 1986; 36:26-28.
    42) 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.
    43) 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/.
    44) Eagle H & Magnuson HJ: The systemic treatment of 227 cases of arsenic poisoning (encephalitis, dermatitis, blood dyscrasia, jaundice, fever) with 2,3-dimercaptopropanol (BAL). Am J Syph Gonor Ven Dis 1946; 30:420-441.
    45) Elliot CG, Colby TV, & Kelly TM: Charcoal lung. Bronchiolitis obliterans after aspiration of activated charcoal. Chest 1989; 96:672-674.
    46) FDA: Poison treatment drug product for over-the-counter human use; tentative final monograph. FDA: Fed Register 1985; 50:2244-2262.
    47) 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.
    48) Flora SJS, Kumar P, & Kannan GM: Acute oral gallium arsenide exposure and changes in certain hematological, hepatic, renal and immunological indices at different time intervals in male wistar rats. Toxicol Ltr 1998; 94:103-113.
    49) Flora SJS: Alterations in some hepatic biochemical variables following repeated gallium arsenide administration in rats. Internat Hepatol Commun 1996; 5:97-103.
    50) Fournier L, Thomas G, & Garnier R: 2,3-dimercaptosuccinic acid treatment of heavy metal poisoning in humans. Med Toxicol 1988; 3:499-504.
    51) Goering PL, Maronpot RR, & Fowler BA: Effect of intratracheal gallium arsenide administration on delta-aminolevulinic acid dehydratase in rats: relationship to urinary excretion of aminolevulinic acid. Toxicol Appl Pharmacol 1988; 92:179-193.
    52) Golej J, Boigner H, Burda G, et al: Severe respiratory failure following charcoal application in a toddler. Resuscitation 2001; 49:315-318.
    53) Gosselin RE, Smith RP, & Hodge HC: Clinical Toxicology of Commercial Products, 5th ed, III, Williams & Wilkins, Baltimore, MD, 1984, pp 42-47.
    54) Graff GR, Stark J, & Berkenbosch JW: Chronic lung disease after activated charcoal aspiration. Pediatrics 2002; 109:959-961.
    55) Grande GA, Rogers AA, & Ling LJ: Urine spot test as guide to treatment in acute pentavalent arsenic ingestion. Vet Human Toxicol 1987; 29:73-74.
    56) Grant WM & Schuman JS: Toxicology of the Eye, 4th ed, Charles C Thomas, Springfield, IL, 1993.
    57) Guindo-Nignan M, Garnier R, & Telolahy P: Urinary concentrations of inorganic arsenic, methylarsonic acid and dimethylarsinic acid in workers engaged in the production of gallium arsenide semi-conductors. Arch Mal Prof 1992; 53:375-381.
    58) HSDB : Hazardous Substances Data Bank. National Library of Medicine. Bethesda, MD (Internet Version). Edition expires 2001; provided by Truven Health Analytics Inc., Greenwood Village, CO.
    59) Haas CF: Mechanical ventilation with lung protective strategies: what works?. Crit Care Clin 2011; 27(3):469-486.
    60) Harris CR & Filandrinos D: Accidental administration of activated charcoal into the lung: aspiration by proxy. Ann Emerg Med 1993; 22:1470-1473.
    61) Harrison M: Semiconductor manufacturing hazards. Hazardous Materials Toxicology, Clin Principles of Environmental Hazards, pp 472-504, 1992.
    62) Harrison RJ: Gallium arsenide. Occup Med 1986; 1:49-58.
    63) Hessl SM & Berman E: Severe peripheral neuropathy after exposure to monosodium methyl arsonate. Clin Toxicol 1982; 19:281-287.
    64) Hla KK, Ashton CE, & Henry JA: Adverse effects from 2,3-dimercaptopropane sulphonate (DMPS) (abstract), EAPCCT, XV Congress, Istanbul, Turkey, 1992, pp 13.
    65) Howland MA: Dimercaprol (BAL), in Goldfrank LR, Flomenbaum NE, Lewin NA et al (eds): Goldfrank's Toxicologic Emergencies, 7th ed, McGraw-Hill, New York, NY, 2002.
    66) 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.
    67) 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.
    68) 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.
    69) 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.
    70) 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.
    71) 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.
    72) 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.
    73) 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.
    74) Kay A: European league against rheumatism study of adverse reactions to D-penicillamine. Br J Rheumatol 1986; 25:193-198.
    75) Kersjes MP, Maurer JR, & Trestrail JH: An analysis of arsenic exposures referred to the Blodgett Regional Poison Center. Vet Human Toxicol 1987; 29:75-78.
    76) Kleinman ME, Chameides L, Schexnayder SM, et al: 2010 American Heart Association guidelines for cardiopulmonary resuscitation and emergency cardiovascular care. Part 14: pediatric advanced life support. Circulation 2010; 122(18 Suppl.3):S876-S908.
    77) Kollef MH & Schuster DP: The acute respiratory distress syndrome. N Engl J Med 1995; 332:27-37.
    78) Kuntzelman DR & Angle CR: Abnormal liver function in childhood lead poisoning unaffected by DMSA (Abstract). Vet Hum Toxicol 1992; 34:355.
    79) Lenihan KL, Sheehy JW & Jones JH: Assessment of exposures in gallium arsenide processing: a case study. Hazard Assessment and Control Technology in Semiconductor Industry, pp. 285-294, 1989.
    80) Lewis RJ: Hawley's Condensed Chemical Dictionary, 12th ed, Van Nostrand Reinhold Company, New York, NY, 1993, pp 550-551.
    81) Lewis RJ: Sax's Dangerous Properties of Industrial Materials, 8th ed, Van Nostrand Reinhold Company, New York, NY, 1992.
    82) Linares A, Zarranz JJ, & Rodrigues-Alarcon J: Reversible cutis laxa due to maternal d-penicillamine treatment. Lancet 1979; 2:43.
    83) 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.
    84) Mast TJ, Dill JA, & Greenspan BJ: The developmental toxicity of inhaled gallium arsenide in rodents. Teratology 1991; 43:455-456.
    85) NFPA: Fire Protection Guide to Hazardous Materials, 13th ed., National Fire Protection Association, Quincy, MA, 2002.
    86) NHLBI ARDS Network: Mechanical ventilation protocol summary. Massachusetts General Hospital. Boston, MA. 2008. Available from URL: http://www.ardsnet.org/system/files/6mlcardsmall_2008update_final_JULY2008.pdf. As accessed 2013-08-07.
    87) 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.
    88) 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.
    89) 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.
    90) 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.
    91) Naradzay J & Barish RA: Approach to ophthalmologic emergencies. Med Clin North Am 2006; 90(2):305-328.
    92) 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.
    93) 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.
    94) 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.
    95) 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.
    96) 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.
    97) 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.
    98) 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.
    99) 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.
    100) 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.
    101) 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.
    102) 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.
    103) 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.
    104) 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.
    105) 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.
    106) 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.
    107) 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.
    108) 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.
    109) 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.
    110) 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.
    111) 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.
    112) 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.
    113) 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.
    114) 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.
    115) 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.
    116) 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.
    117) 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.
    118) 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.
    119) 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.
    120) 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.
    121) 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.
    122) 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.
    123) 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.
    124) 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.
    125) 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.
    126) 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.
    127) 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.
    128) 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.
    129) 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.
    130) 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.
    131) 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.
    132) 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.
    133) 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.
    134) 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.
    135) 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.
    136) 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.
    137) 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.
    138) 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.
    139) 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.
    140) 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.
    141) 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.
    142) 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.
    143) 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.
    144) 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.
    145) 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.
    146) 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.
    147) 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.
    148) 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.
    149) 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.
    150) 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.
    151) 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.
    152) 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.
    153) 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.
    154) 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.
    155) 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.
    156) 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.
    157) 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.
    158) 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.
    159) 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.
    160) 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.
    161) 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.
    162) 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.
    163) 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.
    164) 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.
    165) 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.
    166) 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.
    167) 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.
    168) National Research Council : Acute exposure guideline levels for selected airborne chemicals, 5, National Academies Press, Washington, DC, 2007.
    169) National Research Council: Acute exposure guideline levels for selected airborne chemicals, 6, National Academies Press, Washington, DC, 2008.
    170) National Research Council: Acute exposure guideline levels for selected airborne chemicals, 7, National Academies Press, Washington, DC, 2009.
    171) National Research Council: Acute exposure guideline levels for selected airborne chemicals, 8, National Academies Press, Washington, DC, 2010.
    172) 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.
    173) None Listed: Position paper: cathartics. J Toxicol Clin Toxicol 2004; 42(3):243-253.
    174) Peate WF: Work-related eye injuries and illnesses. Am Fam Physician 2007; 75(7):1017-1022.
    175) Peberdy MA , Callaway CW , Neumar RW , et al: 2010 American Heart Association guidelines for cardiopulmonary resuscitation and emergency cardiovascular care science. Part 9: post–cardiac arrest care. Circulation 2010; 122(18 Suppl 3):S768-S786.
    176) Pollack MM, Dunbar BS, & Holbrook PR: Aspiration of activated charcoal and gastric contents. Ann Emerg Med 1981; 10:528-529.
    177) Product Information: BAL In Oil intramuscular injection, dimercaprol intramuscular injection. Akorn, Inc. (per manufacurer), Lake Forest, IL, 2008.
    178) Product Information: CHEMET(R) oral capsules, succimer oral capsules. Ovation Pharmaceuticals,Inc, Deerfield, IL, 2005.
    179) Product Information: CHEMET(R) oral capsules, succimer oral capsules. Lundbeck Inc. (per Manufacturer), Deerfield, IL, 2011.
    180) Product Information: CUPRIMINE(R) oral capsules, penicillamine oral capsules. Merck & Co,Inc, Whitehouse Station, NJ, 2004.
    181) Product Information: DEPEN(R) titratable oral tablets, penicillamine titratable oral tablets. Meda Pharmaceuticals Inc, Somerset, NJ, 2009.
    182) 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.
    183) 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.
    184) Product Information: dopamine hcl, 5% dextrose IV injection, dopamine hcl, 5% dextrose IV injection. Hospira,Inc, Lake Forest, IL, 2004.
    185) Product Information: norepinephrine bitartrate injection, norepinephrine bitartrate injection. Sicor Pharmaceuticals,Inc, Irvine, CA, 2005.
    186) Rau NR, Nagaraj MV, Prakash PS, et al: Fatal pulmonary aspiration of oral activated charcoal. Br Med J 1988; 297:918-919.
    187) Rosa FW: Teratogen update: penicillamine. Teratology 1986; 33:127-131.
    188) Routledge PA, Bialas MC, & Babar I: Blood arsenic and chromium concentrations after dermal exposure to tannalysing fluid and the use of DMPS (abstract). J Toxicol - Clin Toxicol 1998; 36:494-495.
    189) Sax NI: Dangerous Properties of Industrial Materials, 6th ed, Van Nostrand Reinhold Co, New York, NY, 1984.
    190) Schoolmeester WL & White DR: Arsenic poisoning. South Med J 1980; 73:198-208.
    191) Solomon L, Abrams G, & Dinner M: Neonatal abnormalities associated with d-penicillamine treatment during pregnancy. N Engl J Med 1977; 296:54.
    192) Stolbach A & Hoffman RS: Respiratory Principles. In: Nelson LS, Hoffman RS, Lewin NA, et al, eds. Goldfrank's Toxicologic Emergencies, 9th ed. McGraw Hill Medical, New York, NY, 2011.
    193) 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.
    194) 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.
    195) 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-.
    196) 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.
    197) 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.
    198) 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.
    199) 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.
    200) 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-.
    201) U.S. Occupational Safety, and Health Administration (OSHA): Process safety management of highly hazardous chemicals. 29 CFR 2010 2010; 29(1910.119):348-.
    202) 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.
    203) Vale JA, Kulig K, American Academy of Clinical Toxicology, et al: Position paper: Gastric lavage. J Toxicol Clin Toxicol 2004; 42:933-943.
    204) 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.
    205) Vaziri ND, Upham T, & Barton CH: Hemodialysis clearance of arsenic. Clin Toxicol 1980; 17:451-456.
    206) Watson WA, Veltri JC, & Metcalf TJ: Acute arsenic exposure treated with oral D-penicillamine. Vet Human Toxicol 1981; 23:164-166.
    207) Wax PM & Thornton CA: Recovery from severe arsenic-induced peripheral neuropathy with 2,3-dimercapto-1-propanesulphonic acid. Clin Toxicol 2000; 38:777-780.
    208) Webb DR, Sipes IG, & Carter DE: In vitro solubility and in vivo toxicity of gallium arsenide. Toxicol Appl Pharmacol 1984; 76:96-104.
    209) Webb DR, Wilson SE, & Carter DE: Comparative pulmonary toxicity of gallium arsenide, gallium(III) oxide, or arsenic(III) oxide intratracheally instilled into rats. Toxicol Appl Pharmacol 1986; 82:405-416.
    210) Webb DR, Wilson SE, & Carter DE: Pulmonary clearance and toxicity of respirable gallium arsenide particulates intratracheally instilled into rats. Am Ind Hyg Assoc J 1987; 48:660-667.
    211) Willson DF, Truwit JD, Conaway MR, et al: The adult calfactant in acute respiratory distress syndrome (CARDS) trial. Chest 2015; 148(2):356-364.
    212) Wilson DF, Thomas NJ, Markovitz BP, et al: Effect of exogenous surfactant (calfactant) in pediatric acute lung injury. A randomized controlled trial. JAMA 2005; 293:470-476.