ARSENIC

Arsenic is used: in metallurgy for hardening copper, lead, and alloys; in the manufacture of certain types of glass; in pigment production; in pesticides (most often as arsenic trioxide), insecticides, fungicides, and rodenticides; in weed killer; in agriculture as a cotton desiccant; as a by-product in the smelting of copper ores; as a component of electrical devices, and as a dopant material in semiconductor manufacture (Bingham et al, 2001; Budavari, 2000; Hathaway et al, 1996; HSDB , 2001; Lewis, 1998; Zenz, 1994).
ORGANIC: Organic arsenic (melarsoprol) is used to treat the meningoencephalitis stage of African Trypanosomiasis (Anon, 1993; Markell et al, 1992; Gilman et al, 1990; Pepin et al, 1992; Van Voorhis, 1990; Wellde et al, 1989).
Historically, arsenic was used in a tonic known as "Fowler's solution," to treat a variety of illnesses, such as leukemia and psoriasis (Bingham et al, 2001; Harbison, 1998; Zenz, 1994).
It has also been used as a radioactive tracer (an artificial isotope, As) in toxicology (HSDB , 2001).
Arsenic, as arsenic sulfide, is also a component in certain types of hair removal products, known as corrosive arsenic-based depilatory agents (CABD) that have been traditionally used in Iran and India. In Iran, CABD is also referred to as "Vajebi" (Farzaneh et al, 2011).

FORMS

ELEMENTAL: Arsenic is rarely found in its isolated elemental form. More commonly, it is present in mineral species, in alloys, or as an oxide or other compound form (Budavari, 2000).
INORGANIC: As3+ (trivalent or arsenite) and As5+ (pentavalent or arsenate) (Ford, 2006).
GASEOUS: Refer to "ARSINE" document for more information.
METALLOID: Arsenic is a silver-gray or tin-white, shiny, brittle, crystalline and metallic-looking element. It can exist in three allotropic forms: yellow (alpha), black (beta), and gray (gamma) (HSDB , 2001). The amorphous metalloid form (alpha-arsenic) will darken to black (beta-arsenic) and form arsenic trioxide (As2O3) in moist air. When arsenic vapor is cooled suddenly, a yellow type of arsenic which has no metallic properties is formed (Budavari, 2000; Hathaway et al, 1996; Lewis, 1996; NIOSH , 2001).
ORGANIC: Melarsoprol (trypanocidal), parasitic therapy (veterinary), seafood (arsenobetaine) (Ford, 2006).
Arsenic is available commercially in the following grades of purity: Technical, Crude (90-95%), Refined (99%) and Semiconductor (99.999%) (Lewis, 1997).

SOURCES

Arsenic is thought to occur throughout the universe. It is the twentieth most common element in the earth's crust, having a concentration of 1.8 ppm (Baselt, 1997; Bingham et al, 2001; Budavari, 2000; Zenz, 1994).
Arsenic has been found:

In a variety of Asian folk/homeopathic/herbal remedies from China, India, and Iran (Espinoza et al, 1995; Kew et al, 1993; Sheerin et al, 1994; p 5; Hall & Harruff, 1989; Kerr & Saryan, 1986).
In groundwater and drinking water contamination (Endemic hydroarsenicism) in Chile, Taiwan, Mexico, Argentina, Thailand, and India (Mazumder et al, 2001; Rahman et al, 2001; Woollons & Russell-Jones, 1998).
In a wine produced from grapes grown in vineyards treated with an arsenical pesticide (Houser & Vitek, 1979).
In preservatives used by taxidermists (Jensen & Olsen, 1995).
In opium (content as high as 74.1 mcg/100 g) (Datta, 1977).
Contaminated moonshine (contains up to 415 mcg/L of arsenic) (Gerhardt et al, 1980).
In art glass manufacturing (Apostoli et al, 1998).
Sodium arsenic-containing ant poisons (banned by EPA) (Kuslikis et al, 1991).
Seafood, especially shellfish (concentrations range from 2 mg/kg for freshwater fish up to 22 mg/kg for lobsters) (Buchet et al, 1994; Baselt, 2000).
Chromium-copper-arsenate (CCA) used as a wood preservative (exposure to arsenic through airborne dust) (Jensen & Olsen, 1995; Nygren et al, 1992; Peters et al, 1984).

-CLINICAL EFFECTS

GENERAL CLINICAL EFFECTS

USES: Arsenic compounds are used as pesticides and in a variety of occupations (eg, glass/ceramic manufacturing, metallurgy, semiconductor manufacture). However, environmental contamination of groundwater accounts for the majority of modern exposures outside the United States. Organic arsenic (melarsoprol) is used to treat the meningoencephalitis stage of African Trypanosomiasis. Arsenic trioxide is used to treat acute promyelocytic leukemia. Please refer to ARSENIC TRIOXIDE document for more information.

PHARMACOLOGY: Inorganic arsenic reduces cellular apoptosis via damage of mitochondrial membranes and down-regulation of BCL2, a pro-survival protein. Arsenic is actively transported into Trypanosomes by a purine transporter resulting in inhibition of trypanothione production and subsequent parasite lysis.

TOXICOLOGY: Trivalent arsenic (As3+) disrupts oxidative phosphorylation, leading to free radical formation via inhibition of pyruvate dehydrogenase, which subsequently decreases gluconeogenesis due to lack of acetyl-CoA. Pentavalent arsenic may be transformed to arsenic or substitute for inorganic phosphate in glycolysis, leading to uncoupling of oxidative phosphorylation and loss of ATP formation. Chronically, arsenic may cause DNA damage, mutation in the p-53 suppressor gene, and inhibition of DNA repair mechanisms leading to cancer. Arsenic-containing metals are considered nontoxic due to their low solubility. Organic arsenic has relatively low toxicity when compared to the inorganic trivalent and pentavalent forms.

EPIDEMIOLOGY: Toxicity from arsenic is uncommon and major effects are rare.

WITH POISONING/EXPOSURE

ACUTE OVERDOSE: Arsenic compounds are mainly absorbed through the gastrointestinal tract, but some absorption may occur through intact skin or inhalation. Acute arsenic ingestion generally produces signs and symptoms within 30 minutes, but symptoms may be delayed for several hours if ingested with food. Many arsenic compounds are severe irritants of the skin, eye, and mucous membranes; some may be corrosive. Contact produces local hyperemia, followed by vesicular or pustular eruptions. Trivalent compounds are particularly caustic. Acute inhalation exposures have resulted in irritation of the upper respiratory tract.
MILD TO MODERATE TOXICITY: Gastrointestinal symptoms occur rapidly after acute ingestion. Initial signs and symptoms include burning lips, throat constriction, and dysphagia. Excruciating abdominal pain, severe nausea, vomiting, and profuse "rice water-like" diarrhea that may lead to hypovolemia follows these symptoms. In addition, hypovolemia from capillary leakage (third-spacing of fluids) is a common early effect. QTc prolongation may occur. Muscle cramps, facial edema, bronchitis, dyspnea, chest pain, dehydration, intense thirst, and fluid-electrolyte disturbances are also common following significant exposures. A garlic-like odor of the breath and feces may also develop. Subacute toxicity can produce neuropathies, both motor and sensory, and can progress to a Guillain-Barre-like syndrome.
SEVERE TOXICITY: Hypotension and tachycardia are common early signs of severe poisoning. Hypotension may be resistant to fluid resuscitation and multiorgan failure may ensue. Fever and tachypnea may occur. These patients can develop ventricular dysrhythmias, including torsade de pointes. Encephalopathy, seizures, and coma have been reported. Acute renal failure, hemolytic anemia, rhabdomyolysis, and hepatitis may occur several days after ingestion.
CHRONIC TOXICITY: Inhalation is the most common route of exposure in people who work in occupations that use arsenic. The sequence of chronic poisoning involves weakness, anorexia, hepatomegaly, jaundice, and gastrointestinal complaints, followed by conjunctivitis, irritation of the upper respiratory tract, hyperpigmentation, and eczematoid and allergic dermatitis. A hoarse voice and chronic upper respiratory septum is a common result after prolonged inhalation of white arsenic dust or fume. Peripheral nervous system symptoms may include numbness, burning, and tingling of the hands and feet; pain; paresthesias; muscle fasciculations; gross tremors; ataxia; discoloration; and mental confusion. Muscular weakness, limb tenderness, and difficulty walking may follow. The final phase consists of peripheral sensory neuropathy of the hands and feet. Associated motor neuropathy may occur as well. Certain arsenic compounds are known human carcinogens. Chronic exposure in either occupational settings or by drinking contaminated groundwater can cause poisoning and carries an increased risk of skin, lung, bladder, and possibly liver cancers.

POTENTIAL HEALTH HAZARDS - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 152 (ERG, 2004)

Highly toxic, may be fatal if inhaled, swallowed or absorbed through skin.
Contact with molten substance may cause severe burns to skin and eyes.
Avoid any skin contact.
Effects of contact or inhalation may be delayed.
Fire may produce irritating, corrosive and/or toxic gases.
Runoff from fire control or dilution water may be corrosive and/or toxic and cause pollution.

ACUTE CLINICAL EFFECTS

SUMMARY

PHARMACOLOGY: Inorganic arsenic reduces cellular apoptosis via damage of mitochondrial membranes and down-regulation of BCL2, a pro-survival protein. Arsenic is actively transported into Trypanosomes by a purine transporter resulting in inhibition of trypanothione production and subsequent parasite lysis.
TOXICOLOGY: Trivalent arsenic (As3+) disrupts oxidative phosphorylation, leading to free radical formation via inhibition of pyruvate dehydrogenase, which subsequently decreases gluconeogenesis due to lack of acetyl-CoA. Pentavalent arsenic may be transformed to arsenic or substitute for inorganic phosphate in glycolysis, leading to uncoupling of oxidative phosphorylation and loss of ATP formation. Chronically, arsenic may cause DNA damage, mutation in the p-53 suppressor gene, and inhibition of DNA repair mechanisms leading to cancer. Arsenic-containing metals are considered nontoxic due to their low solubility. Organic arsenic has relatively low toxicity when compared to the inorganic trivalent and pentavalent forms.
EPIDEMIOLOGY: Toxicity from arsenic is uncommon and major effects are rare.
ACUTE OVERDOSE: Arsenic compounds are mainly absorbed through the gastrointestinal tract, but some absorption may occur through intact skin or inhalation. Acute arsenic ingestion generally produces signs and symptoms within 30 minutes, but symptoms may be delayed for several hours if ingested with food. Many arsenic compounds are severe irritants of the skin, eye, and mucous membranes; some may be corrosive. Contact produces local hyperemia, followed by vesicular or pustular eruptions. Trivalent compounds are particularly caustic. Acute inhalation exposures have resulted in irritation of the upper respiratory tract.
MILD TO MODERATE TOXICITY: Gastrointestinal symptoms occur rapidly after acute ingestion. Initial signs and symptoms include burning lips, throat constriction, and dysphagia. Excruciating abdominal pain, severe nausea, vomiting, and profuse "rice water-like" diarrhea that may lead to hypovolemia follows these symptoms. In addition, hypovolemia from capillary leakage (third-spacing of fluids) is a common early effect. QTc prolongation may occur. Muscle cramps, facial edema, bronchitis, dyspnea, chest pain, dehydration, intense thirst, and fluid-electrolyte disturbances are also common following significant exposures. A garlic-like odor of the breath and feces may also develop. Subacute toxicity can produce neuropathies, both motor and sensory, and can progress to a Guillain-Barre-like syndrome.
SEVERE TOXICITY: Hypotension and tachycardia are common early signs of severe poisoning. Hypotension may be resistant to fluid resuscitation and multiorgan failure may ensue. Fever and tachypnea may occur. These patients can develop ventricular dysrhythmias, including torsade de pointes. Encephalopathy, seizures, and coma have been reported. Acute renal failure, hemolytic anemia, rhabdomyolysis, and hepatitis may occur several days after ingestion.
CHRONIC TOXICITY: Inhalation is the most common route of exposure in people who work in occupations that use arsenic. The sequence of chronic poisoning involves weakness, anorexia, hepatomegaly, jaundice, and gastrointestinal complaints, followed by conjunctivitis, irritation of the upper respiratory tract, hyperpigmentation, and eczematoid and allergic dermatitis. A hoarse voice and chronic upper respiratory septum is a common result after prolonged inhalation of white arsenic dust or fume. Peripheral nervous system symptoms may include numbness, burning, and tingling of the hands and feet; pain; paresthesias; muscle fasciculations; gross tremors; ataxia; discoloration; and mental confusion. Muscular weakness, limb tenderness, and difficulty walking may follow. The final phase consists of peripheral sensory neuropathy of the hands and feet. Associated motor neuropathy may occur as well. Certain arsenic compounds are known human carcinogens. Chronic exposure in either occupational settings or by drinking contaminated groundwater can cause poisoning and carries an increased risk of skin, lung, bladder, and possibly liver cancers.

CARDIOVASCULAR

CONDUCTION DISORDER OF THE HEART: Ventricular tachycardia, ventricular bigeminy, and ventricular fibrillation have been described after acute arsenic ingestion (Lai et al, 2005; Brayer et al, 1997; Goldsmith, 1980).
TORSADE DE POINTES: QRS morphology of the ventricular dysrhythmia is often consistent with torsade de pointes (Lai et al, 2005; Beckman et al, 1991; Goldsmith, 1980).
ELECTROCARDIOGRAM ABNORMAL: ECG changes have included QT prolongation, left axis deviations, peaked T waves, and also deeply inverted T waves (Lai et al, 2005; Gousios & Adelson, 1959).
MYOCARDITIS: CHRONIC EXPOSURE: Interstitial myocarditis resulting in fatal ventricular arrhythmias has been reported after chronic exposure to arsenic (Hall & Harruff, 1989).
HYPOTENSION: Hypotension and tachycardia are common early signs (Shum et al, 1995; Schoolmeester & White, 1980).
HYPERTENSION: CHRONIC EXPOSURE: A dose-related increased incidence of hypertension was found in a Taiwanese population with chronic arsenic exposure in drinking water (Chen et al, 1995).

DERMATOLOGIC

EXFOLIATIVE DERMATITIS: Skin findings after either acute or chronic arsenic poisoning may include flushing, diaphoresis, diffuse pigmentation, hyperkeratosis of palms and/or soles, peripheral edema, hyperpigmentation, hypopigmentation, leuko-melanoderma, brawny desquamation, and exfoliative dermatitis (Dakeishi et al, 2006; Tsuji et al, 2004; Ahasan, 2001).
NEOPLASM OF SKIN: CHRONIC EXPOSURE: Basal cell and squamous cell cancers of the skin may also be seen years after exposure (Ahasan, 2001; Sass et al, 1993; Renwick et al, 1981).
MEE'S LINES: Transverse white striae of the nails (Mees lines) may be seen after acute or chronic exposure (Duenas-Laita et al, 2005; Sass et al, 1993).

ENDOCRINE

DIABETES MELLITUS: CHRONIC EXPOSURE: A dose-related increase in prevalence of diabetes mellitus has been seen in residents of areas where arsenism is hyperendemic and in workers exposed to arsenic at a copper smelter (Coronado-Gonzalez et al, 2007; Rahman et al, 1998; Rahman & Axelson, 1995).

FLUID ELECTROLYTE

DEHYDRATION: Death in acute arsenic toxicity is often due to loss of fluids and electrolytes. Rapid volume depletion from vomiting, diarrhea, and third spacing of fluids is common (Lai et al, 2005; Hayes, 1982).

GASTROINTESTINAL

Early symptoms within hours following significant exposure to arsenic include abdominal pain, nausea, vomiting, profuse bloody or watery diarrhea (sometimes described as "rice water-like") (Cox & Orledge, 2011; Roth et al, 2011; Majid Cheraghali et al, 2007; Lai et al, 2005; Tsuji et al, 2004; Bartolome et al, 1999; Brayer et al, 1997; Moore et al, 1994a; Quatrehomme et al, 1992), pain in the extremities and muscles, weakness, and flushing of the skin. A sensation of burning and dryness of the oral and nasal cavities may occur.

GENITOURINARY

ACUTE RENAL FAILURE SYNDROME: Oliguria, anuria, hematuria, proteinuria (Majid Cheraghali et al, 2007), acute tubular necrosis, renal failure have occurred following acute arsenic exposure (Lai et al, 2005), and chronic renal insufficiency from cortical necrosis has been described (Gerhardt et al, 1978).

HEENT

Conjunctivitis, photophobia, dimness of vision, diplopia, lacrimation, and sometimes hyperemia, chemosis, and conjunctival hemorrhage may occur (Uede & Furukawa, 2003; Grant, 1993).
PERFORATION OF NASAL SEPTUM: Chronic exposure to trivalent arsenic compounds can cause perforation of the nasal septum (ACGIH, 1996a; OSHA, 1988).

HEMATOLOGIC

HEMOLYSIS: Acute hemolysis may occur after acute arsenic poisoning (Kyle & Pease, 1965).
PANCYTOPENIA: Arsenic can disturb erythropoiesis and myelopoiesis (OSHA, 1988). After either acute or chronic arsenic exposure, pancytopenia may be seen (Rezuke et al, 1991; Kyle & Pease, 1965; Kjeldsberg & Ward, 1972; Bartolome et al, 1999). However, isolated anemia may also be seen.
ERYTHROID HYPERPLASIA: Bone marrow aspirate may demonstrate pronounced erythroid hyperplasia similar to that seen with pernicious anemia (Selzer & Ancel, 1983).
ACUTE LEUKEMIA: CHRONIC EXPOSURE: Aplastic anemia and acute myelogenous leukemia have been described after chronic arsenic exposure (Kjeldsberg & Ward, 1972).
ANEMIA: CHRONIC EXPOSURE: Anemia has also been reported after chronic arsenic exposure (Rahman et al, 2001; Guha Mazumder et al, 1992).
DISSEMINATED INTRAVASCULAR COAGULATION: A 4-month-old developed evidence of disseminated intravascular coagulation within 11.5 hours of ingesting arsenic. He died 36 hours after ingestion despite aggressive chelation and resuscitation(Lai et al, 2005).

HEPATIC

HEPATOCELLULAR DAMAGE: CHRONIC EXPOSURE: Hepatocellular damage after chronic arsenic exposure may be more common than after acute; autopsy data from patients in India known to have liver disease demonstrated higher hepatic arsenic levels than controls (Narang, 1987a).
LIVER ENZYMES ABNORMAL: Mildly elevated AST concentrations (64 to 238 units/L) were reported in 5 of 7 teenagers (ages ranging from 15 to 18 years) who unintentionally ingested an unknown amount of herbicide containing monosodium methylarsonate 24%, mistakenly used as cooking oil. The AST concentrations peaked 3 days postingestion and normalized within 2 weeks (Cox & Orledge, 2011).

MUSCULOSKELETAL

RHABDOMYOLYSIS: Disruption of the normal oxidative intermyofibrillar network (involving type I fibers), perifascicular hypercontracted fibers, increased vacuolization in approximately 30% of fibers, abnormally enlarged mitochondria with loss of cristae, and abundant lipid vacuoles separating the myofibrils has been found on muscle biopsy (Fernandez-Sola et al, 1991).

NEUROLOGIC

COMA: A 4-month-old developed vomiting within 10 minutes of ingesting arsenic. He was comatose within 6 hours of ingestion; he was unresponsive and died 36 hours after ingestion (Lai et al, 2005).
TOXIC ENCEPHALOPATHY: Toxic delirium and encephalopathy are complications of significant acute (Duenas-Laita et al, 2005; Quatrehomme et al, 1992) and chronic (Morton & Caron, 1989) arsenic poisoning. The encephalopathy may be permanent and result in cortical atrophy 1 to 6 months after exposure (Fincher & Koerker, 1987).
PERIPHERAL NEUROPATHY: Physical findings of arsenic neuropathy usually include prominently decreased sensation to touch, pinprick, and temperature, frequently in a stocking and glove distribution (Kelafant et al, 1993); loss of vibration sense is also common; profound muscle weakness and wasting, distal more so than proximal, is also seen (Hahn et al, 2000; Heyman et al, 1956); wrist drop, foot drop, and fasciculations may be seen (Heyman et al, 1956).
CEREBROVASCULAR DISEASE: CHRONIC EXPOSURE: Among a Taiwanese population chronically exposed to high levels of arsenic in drinking water, there was an increased prevalence of cerebrovascular disease, particularly cerebral infarction (Chiou et al, 1997).
DISTURBANCE IN THINKING: A decrease in intellectual function, as measured by a number of different neuropsychiatric tests including the Wechsler Intelligence Scale for Children, the Primary Scale of Intelligence, and the Total Sentence Recall test, has been reported in children following recent exposures to arsenic in drinking water and in food (vonEhrenstein et al, 2007; Wasserman et al, 2007).

RESPIRATORY

BRONCHIECTASIS: CHRONIC EXPOSURE: Bronchiectasis, as identified by high-resolution computed tomography, was reported in individuals following chronic exposure to arsenic in drinking water (Mazumder et al, 2005).
BRONCHITIS: Acute inhalation exposure may result in irritation of the upper respiratory tract (Hathaway et al, 1996; ACGIH, 1996a).
INJURY OF RESPIRATORY SYSTEM: Chronic arsenic exposure due to ingestion of contaminated ground water was studied in 107 subjects. Twenty cases (68.9%) had an obstructive pattern of lung involvement (7 mild; 9 moderate; 4 severe), 8 cases (27.6%) had a mixed obstructive-restrictive pattern and 1 (3.5%) had only a restrictive pattern (Majumdar et al, 2004).

VITAL SIGNS

TEMPERATURE: Less acute arsenic toxicity may cause subnormal body temperatures (Hayes, 1982).
HYPOTENSION: Patients may rapidly become hypotensive after acute arsenic poisoning from third spacing of fluids, diarrhea, or blood loss into the gastrointestinal tract (Schoolmeester & White, 1980).
PULSE: TACHYCARDIA: Patients may become tachycardic secondary to pain, hypovolemia, or cardiac effects of arsenic (Shum et al, 1995).

CHRONIC CLINICAL EFFECTS

As little as 3 to 4 mg of arsenic per day can cause chronic poisoning (HSDB). The trivalent form is eliminated less rapidly than the pentavalent form and can cause cumulative toxicity (HSDB). Chronic arsenic poisoning appears to be more common from nonindustrial exposures; cases of poisoning from ingestion of arsenic-based herbicides are still common (Kelafant et al, 1993).

Evidence for chronic effects from ingestion of arsenic comes from its use in human medicine for the treatment of psoriasis. A peculiar hyperpigmentation of the skin occurs, particularly on the palms of the hands and soles of the feet (Friberg et al, 1986). So-called blackfoot disease (gangrene), anemia, and cirrhosis of the liver (perhaps complicated by alcohol intake in winery workers) have also been reported with chronic arsenic ingestion (ILO, 1983).

Respiratory tract effects can occur from chronic inhalation exposure, including perforation of the nasal septum (ILO, 1983). Effects on the mucous membranes, skin, nervous and circulatory systems (ILO, 1983), hoarseness, and cirrhosis of the liver (ACGIH) have also been reported with chronic inhalation of arsenic compounds. However, cancer of the respiratory tract is the most serious of the various chronic effects.

Arsenic compounds are contact allergens (HSDB) and can cause papular eczema or follicular swelling and pustules, warts, and increased or decreased pigmentation (so-called raindrop pigmentation) which can develop into skin cancer. The skin lesions can be delayed in onset and may occur following exposure by other routes (Friberg et al, 1986). Other effects on the skin are transverse lines in the nails (Mees lines), which appear 4 to 6 weeks after exposure (HSDB).

Similar systemic effects may occur with chronic arsenic poisoning, regardless of the route of exposure. The major target organs for arsenic toxicity are the nerves, heart, blood/bone marrow, and liver. Nervous damage can be both central (encephalopathy) and peripheral (peripheral polyneuropathy) (HSDB). Early symptoms of peripheral nerve damage include pain, numbness, tingling, a pins-and-needles sensation in the extremities, loss of touch sensation, foot or wrist drop, and muscle cramps (HSDB).

Effects on the heart include ECG abnormalities and fibrillation (HSDB). Arsenic can depress formation of all the blood elements in the bone marrow, causing aplastic anemia. Both cirrhosis and cancer of the liver have been reported with chronic arsenic exposure.

In a survey in Bangladesh of 1595 subjects who used wells contaminated with arsenic, results suggest that arsenic exposure may induce hypertension in humans (Hypertension, 1999).

Residents of an area in southern Taiwan, where endogenous arsenic levels in the drinking water are very high, had a 2-fold higher incidence of diabetes mellitus than residents of areas with low concentrations of arsenic in the drinking water. The prevalence of diabetes was related to cumulative arsenic exposure (Lai et al, 1994). Chronic occupational exposure to arsenic has also been associated with diabetes mellitus in a dose-related manner (Rahman & Axelson, 1995).

Slightly elevated odds for diabetes mellitus as a primary or contributing cause of death were seen in Swedish glass workers, who likely would have been exposed to arsenic, as well as other metals (Rahman et al, 1996).

In a survey of 30 United States counties from 1968 to 1984, the risk of vascular disease was elevated in areas where the arsenic content of drinking water was greater than 20 mcg/L (Engel & Smith, 1994).

Arsenic may be a rare example of a chemical carcinogen that is also a co-promoter. An National Institute of Health study showed arsenic enhances the development of skin neoplasms via the chronic stimulation of keratinocyte-derived growth factors (Germolec et al, 1998).

-FIRST AID

FIRST AID AND PREHOSPITAL TREATMENT

PREHOSPITAL: Remove the contaminated clothing and wash the patient thoroughly.

-MEDICAL TREATMENT

LIFE SUPPORT

Support respiratory and cardiovascular function.

SUMMARY

FIRST AID - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 152 (ERG, 2004)

Move victim to fresh air.
Call 911 or emergency medical service.
Give artificial respiration if victim is not breathing.
Do not use mouth-to-mouth method if victim ingested or inhaled the substance; give artificial respiration with the aid of a pocket mask equipped with a one-way valve or other proper respiratory medical device.
Administer oxygen if breathing is difficult.
Remove and isolate contaminated clothing and shoes.
In case of contact with substance, immediately flush skin or eyes with running water for at least 20 minutes.
For minor skin contact, avoid spreading material on unaffected skin.
Keep victim warm and quiet.
Effects of exposure (inhalation, ingestion or skin contact) to substance may be delayed.
Ensure that medical personnel are aware of the material(s) involved and take precautions to protect themselves.

FIRST AID

FIRST AID

The following first aid measures are suggested (National Institute for Occupational Safety and Health, 2007; OSHA, 2000):

EYE EXPOSURE: Immediately wash the eyes with large amounts of water, occasionally lifting the lower and upper lids. Get medical attention immediately. Primary eye protection (spectacles or goggles), as defined by the Occupational Safety and Health Administration (OSHA), should be used when working with this chemical. Face shields should only be worn over primary eye protection.

Contact lens use is not recommended when working with this chemical. If contact lenses are worn, then appropriate eye and face protection devices must be used. OSHA emphasizes that dusty and/or chemical environments may represent an additional hazard to contact lens wearers.

DERMAL EXPOSURE: Immediately wash the contaminated skin with soap and water. If this chemical penetrates the clothing, immediately remove the clothing, wash the skin with soap and water, and get medical attention promptly.
INHALATION EXPOSURE: Move the exposed person to fresh air at once. If breathing has stopped, perform artificial respiration. Keep the affected person warm and at rest. Get medical attention as soon as possible.
ORAL EXPOSURE: If this chemical has been swallowed, get medical attention immediately.
TARGET ORGANS: Liver, kidneys, skin, lungs and lymphatic system [lung and lymphatic cancer] .

GENERAL

Patients with acute arsenic poisoning usually die from hypovolemic shock secondary to vomiting and diarrhea, gastrointestinal tract bleeding, and 'third spacing' of fluids. Fluid replacement is a mainstay of initial treatment.
Another threat to life is cardiac toxicity resulting in arrhythmias or cardiogenic shock. Advanced cardiac support may be required after massive acute arsenic poisoning.

INHALATION EXPOSURE

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.

DERMAL EXPOSURE

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).

EYE EXPOSURE

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.

ORAL EXPOSURE

Activated charcoal does not bind arsenic well.

-RANGE OF TOXICITY

MINIMUM LETHAL EXPOSURE

GENERAL/SUMMARY

Different arsenic compounds may have differing lethal dosages.
Arsine gas at a concentration of 25-50 ppm is believed to be lethal within thirty minutes (Baselt, 2000).
The smallest recorded lethal dose of arsenic is approximately 130 mg (Bingham et al, 2001; OHM/TADS , 2001).
As little as 20 mg of arsenic may produce life-threatening toxicity (Hutton & Christians, 1983; Schoolmeester & White, 1980; Zaloga et al, 1970).
RETROSPECTIVE REVIEW: According to a retrospective review of 155 patients with corrosive arsenic based depilatory (CABD) agent poisoning, 9 patients died following a mean ingestion of 213 +/- 141 g of the CABD powder. While the formulation of these products in not standardized, analysis of CABD has shown that it consists of approximately 25% arsenic sulfide and 65% calcium bicarbonate (Farzaneh et al, 2011).

ADULT

CASE REPORT: A 33-year-old man died from hypovolemia, acute circulatory failure and refractory ventricular dysrhythmias following the ingestion of a wood preservative which contained arsenic pentoxide (45%), chromium trioxide (35%), and cupric oxide (20%). The patient died within several hours of ingestion (Hay et al, 2000).

CHILD

CHILD: One mg/kg of ingested arsenic may be lethal in a child (Alexander, 1964; Woody & Kometani, 1948).
CASE REPORT: A 4-month-old ingested 190 mg (14.6 mg/kg) of arsenic and died 36 hours later despite aggressive resuscitation and chelation (Lai et al, 2005).

MAXIMUM TOLERATED EXPOSURE

ACUTE

SUMMARY

AVERAGE DAILY HUMAN INTAKE OF ARSENIC: 0.025-0.033 mg/kg (in food and water) (Baselt, 2000).
Estimates of acute oral toxic doses of arsenic compounds range from 1 mg to 10 g.
As little as 10 ppm in water may be an acute health hazard (OHM/TADS , 2001).

CASE REPORTS

ADULT

A 30-year-old man survived an ingestion of 6 ounces of "Blue Ball Rat Killer" containing 1.5 percent arsenous oxide (2150 mg metallic arsenic per 6 ounces), ethanol, and intranasal cocaine use with aggressive therapy (fluid resuscitation, chelation therapy, and hemodialysis) (Fesmire et al, 1988).
LACK OF EFFECT: A 32-year-old woman developed only epigastric discomfort and paresthesias in the lower extremities following ingestion of about 2 grams of sodium arsenate; urine arsenic level was 14 mg/L about 13 hours postingestion (Hernandez et al, 1998).
A 45-year-old woman survived an ingestion of sodium arsenite between 8 and 16 g (serum arsenic concentration was 300 mcg/L on admission). Residual quadriplegia did occur (Bartolome et al, 1999).

PEDIATRIC

A 16-year-old girl developed vomiting, agitation, abdominal pain, generalized weakness, and paresthesias after intentionally ingesting up to 240 mL of an herbicide containing 47% monosodium methylarsonate. The patient's condition improved following chelation therapy; however, mild paresthesia in her hands and feet continued to persist at her 6-week follow-up (Roth et al, 2011).
A 3-year-old boy experienced 3 episodes of vomiting after ingesting 5 mL of an herbicide containing 47.6% monosodium methylarsonate. An ECG demonstrated sinus tachycardia (114 bpm). He received dimercaptosuccinic acid for the next 15 days. Other than the initial episodes of vomiting, the patient remained asymptomatic throughout his hospital stay and at his follow-up exam 10 days post-discharge (Roth et al, 2011).

CASE SERIES

PEDIATRIC

A group of Japanese infants (n=381) developed arsenic poisoning after consuming dried milk powder contaminated with arsenic, with the occurrence of a variety of clinical effects, including fever, diarrhea, vomiting, hepatomegaly, abnormal ECG findings, and skin manifestations, including pigmentation, rash, and desquamation, with long-term sequelae of mental retardation and epilepsy. Analysis of the dried milk powder determined that the arsenic concentration to be 4 to 7 mg/L. Based on data from patients whose diet consisted only of the dried milk, and estimating that the critical dose causing the toxicity was approximately 5 cans of milk powder (ie, 5 pounds of dried milk), the total ingested dose of arsenic was calculated to be approximately 60 mg (Dakeishi et al, 2006).

SPECIFIC SUBSTANCE

PENTAVALENT ARSENIC

Trivalent arsenic (arsenite) is more toxic in animals than the pentavalent form (arsenates) by several orders of magnitude. However, significant toxicity may occur with large amounts of pentavalent salts in humans. Pentavalent arsenic may be converted in vivo to trivalent arsenic.
Of 149 cases of sodium arsenate-containing ant killer poisoning, 91 percent were exposed via the bait station. Most cases were children 3-years-old or younger. Symptoms of self-limiting episodes of vomiting and diarrhea were seen in 3 children (Kingston et al, 1989).
Despite trivial or no symptoms (transient emesis) in children with a history of sodium arsenate ant killer ingestion, significant elevations in 24-hour urine arsenic levels occurred, in the range of 3500 to 5350 mcg/L (Scalzo et al, 1989).
Decreases in the hemoglobin and hematocrit values were the only sequelae possibly associated with an acute ingestion of approximately 1.2 g of arsenic as sodium arsenate by a 44-year-old woman (Chan & Matthews, 1990).

CHRONIC

Subjects chronically exposed to arsenic in drinking water at levels between 0.1 and 0.39 mg/L showed no difference in health effects as determined by questionnaire from subjects whose drinking water contained 0.001 mg/L of arsenic (Valentine et al, 1992).
Prolonged ingestion of arsenicals at the rate of 0.04-0.09 mg/kg/day frequently produced mild poisoning (Hayes & Laws, 1991).
The mountaineers of Styria were reported to ingest arsenic once or twice a week as a tonic, and consequently became tolerant of daily doses estimated at 400 mg or more (Hayes & Lawes, 1991).

Carcinogenicity Ratings for CAS7440-38-2 :

ACGIH (American Conference of Governmental Industrial Hygienists, 2010): A1 ; Listed as: Arsenic

A1 :Confirmed Human Carcinogen: The agent is carcinogenic to humans based on the weight of evidence from epidemiologic studies.

ACGIH (American Conference of Governmental Industrial Hygienists, 2010): A1 ; Listed as: Arsenic and inorganic compounds, as As

A1 :Confirmed Human Carcinogen: The agent is carcinogenic to humans based on the weight of evidence from epidemiologic studies.

EPA (U.S. Environmental Protection Agency, 2011): A ; Listed as: Arsenic, inorganic

A : Human Carcinogen.

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: Arsenic and inorganic arsenic compounds

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.

NIOSH (National Institute for Occupational Safety and Health, 2007): Ca ; Listed as: Arsenic (inorganic compounds, as As)

Ca : NIOSH considers this substance to be a potential occupational carcinogen (See Appendix A in the NIOSH Pocket Guide to Chemical Hazards).

NIOSH (National Institute for Occupational Safety and Health, 2007): Not Listed ; Listed as: Arsenic, organic compounds (as As)
MAK (DFG, 2002): Category 1 ; Listed as: Arsenic and inorganic arsenic compounds: Metallic arsenic

Category 1 : Substances that cause cancer in man and can be assumed to make a significant contribution to cancer risk. Epidemiological studies provide adequate evidence of a positive correlation between the exposure of humans and the occurence of cancer. Limited epidemiological data can be substantiated by evidence that the substance causes cancer by a mode of action that is relevant to man.

MAK (DFG, 2002): Category 1 ; Listed as: Arsenic and inorganic arsenic compounds

Category 1 : Substances that cause cancer in man and can be assumed to make a significant contribution to cancer risk. Epidemiological studies provide adequate evidence of a positive correlation between the exposure of humans and the occurence of cancer. Limited epidemiological data can be substantiated by evidence that the substance causes cancer by a mode of action that is relevant to man.

NTP (U.S. Department of Health and Human Services, Public Health Service, National Toxicology Project ): K ; Listed as: Arsenic Compounds, Inorganic

K : KNOWN = Known to be a human carcinogen

TOXICITY AND RISK ASSESSMENT VALUES

EPA IRIS

EPA Risk Assessment Values for CAS7440-38-2 (U.S. Environmental Protection Agency, 2011):

Oral:

Slope Factor: 1.5per mg/kg-day
RfD: 3x10(-4) mg/kg-day

Inhalation:

Unit Risk: 4.3 per mg/m3
RfC:

Drinking Water:

Unit Risk: 5x10(-2) per mg/L

TOXICITY VALUES

References: ITI, 1995 OHM/TADS, 2001 RTECS, 2001
- LD- (ORAL)HUMAN:
- LD- (ORAL)RABBIT:
- LD- (ORAL)RAT:
- LD50- (INTRAPERITONEAL)MOUSE:
- LD50- (ORAL)MOUSE:
- LD50- (ORAL)PIG:
- LD50- (INTRAPERITONEAL)RAT:
- LD50- (ORAL)RAT:
- LDLo- (INTRAPERITONEAL)GUINEA_PIG:
- LDLo- (SUBCUTANEOUS)GUINEA_PIG:
- LDLo- (SUBCUTANEOUS)RABBIT:
- LDLo- (INTRAMUSCULAR)RAT:
- TDLo- (ORAL)HUMAN:
- TDLo- (IMPLANT)RABBIT:
- TDLo- (ORAL)RAT:

-STANDARDS AND LABELS

WORKPLACE STANDARDS

ACGIH TLV Values for CAS7440-38-2 (American Conference of Governmental Industrial Hygienists, 2010):

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.

Adopted Value

Arsenic

TLV:

TLV-TWA: 0.01 mg/m(3)
TLV-STEL:
TLV-Ceiling:

Notations and Endnotes:

Carcinogenicity Category: A1
Codes: BEI
Definitions:

A1: Confirmed Human Carcinogen: The agent is carcinogenic to humans based on the weight of evidence from epidemiologic studies.
BEI: The BEI notation is listed when a BEI is also recommended for the substance listed. Biological monitoring should be instituted for such substances to evaluate the total exposure from all sources, including dermal, ingestion, or non-occupational.

TLV Basis - Critical Effect(s): Lung cancer
Molecular Weight: 74.92

For gases and vapors, to convert the TLV from ppm to mg/m(3):

[(TLV in ppm)(gram molecular weight of substance)]/24.45

For gases and vapors, to convert the TLV from mg/m(3) to ppm:

[(TLV in mg/m(3))(24.45)]/gram molecular weight of substance

Adopted Value

Arsenic and inorganic compounds, as As

TLV:

TLV-TWA: 0.01 mg/m(3)
TLV-STEL:
TLV-Ceiling:

Notations and Endnotes:

Carcinogenicity Category: A1
Codes: BEI
Definitions:

A1: Confirmed Human Carcinogen: The agent is carcinogenic to humans based on the weight of evidence from epidemiologic studies.
BEI: The BEI notation is listed when a BEI is also recommended for the substance listed. Biological monitoring should be instituted for such substances to evaluate the total exposure from all sources, including dermal, ingestion, or non-occupational.

TLV Basis - Critical Effect(s): Lung cancer
Molecular Weight: Varies

For gases and vapors, to convert the TLV from ppm to mg/m(3):

[(TLV in ppm)(gram molecular weight of substance)]/24.45

For gases and vapors, to convert the TLV from mg/m(3) to ppm:

[(TLV in mg/m(3))(24.45)]/gram molecular weight of substance

AIHA WEEL Values for CAS7440-38-2 (AIHA, 2006):

Not Listed

NIOSH REL and IDLH Values for CAS7440-38-2 (National Institute for Occupational Safety and Health, 2007):

Listed as: Arsenic (inorganic compounds, as As)
REL:

TWA:
STEL:
Ceiling: 0.002 mg/m(3) [15-minute]
Carcinogen Listing: (Ca) NIOSH considers this substance to be a potential occupational carcinogen (See Appendix A in the NIOSH Pocket Guide to Chemical Hazards).
Skin Designation: Not Listed
Note(s): See Appendix A,

Listed as: Arsenic, organic compounds (as As)
REL:

TWA: none
STEL:
Ceiling:
Carcinogen Listing: (Not Listed) Not Listed
Skin Designation: Not Listed
Note(s):

IDLH:

IDLH: 5 mg As/m3 (as As)
Note(s): Ca

Ca: NIOSH considers this substance to be a potential occupational carcinogen (See Appendix A).

OSHA PEL Values for CAS7440-38-2 (U.S. Occupational Safety, and Health Administration (OSHA), 2010):

Listed as: Arsenic, inorganic compounds (as As); see 29 CFR 1910.1018
Table Z-1 for Arsenic, inorganic compounds (as As); see 29 CFR 1910.1018:

8-hour TWA:

ppm:

Parts of vapor or gas per million parts of contaminated air by volume at 25 degrees C and 760 torr.

mg/m3:

Milligrams of substances per cubic meter of air. When entry is in this column only, the value is exact; when listed with a ppm entry, it is approximate.

Ceiling Value:
Skin Designation: No
Notation(s): Not Listed

Listed as: Arsenic, organic compounds (as As)
Table Z-1 for Arsenic, organic compounds (as As):

8-hour TWA:

ppm:

Parts of vapor or gas per million parts of contaminated air by volume at 25 degrees C and 760 torr.

mg/m3: 0.5

Milligrams of substances per cubic meter of air. When entry is in this column only, the value is exact; when listed with a ppm entry, it is approximate.

Ceiling Value:
Skin Designation: No
Notation(s): Not Listed

OSHA List of Highly Hazardous Chemicals, Toxics, and Reactives for CAS7440-38-2 (U.S. Occupational Safety and Health Administration, 2010):

Not Listed

ENVIRONMENTAL STANDARDS

EPA CERCLA, Hazardous Substances and Reportable Quantities for CAS7440-38-2 (U.S. Environmental Protection Agency, 2010):

Listed as: Arsenic (D004)
Final Reportable Quantity, in pounds (kilograms):

1 (0.454)

Additional Information: Unlisted Hazardous Wastes Characteristic of Toxicity
Listed as: Arsenic
Final Reportable Quantity, in pounds (kilograms):

1 (0.454)

Additional Information:
Listed as: Arsenic and compounds

Additional Information:
Listed as: Arsenic Compounds (inorganic including arsine)

Additional Information:

EPA CERCLA, Hazardous Substances and Reportable Quantities, Radionuclides for CAS7440-38-2 (U.S. Environmental Protection Agency, 2010):

Not Listed

EPA RCRA Hazardous Waste Number for CAS7440-38-2 (U.S. Environmental Protection Agency, 2010b):

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

EPA SARA Title III, Extremely Hazardous Substance List for CAS7440-38-2 (U.S. Environmental Protection Agency, 2010):

Not Listed

EPA SARA Title III, Community Right-to-Know for CAS7440-38-2 (40 CFR 372.65, 2006; 40 CFR 372.28, 2006):

Listed as: Arsenic Compounds: Includes any unique chemical substance that contains arsenic as part of that chemical's infrastructure
Effective Date for Reporting Under 40 CFR 372.30: 1/1/87
Lower Thresholds for Chemicals of Special Concern under 40 CFR 372.28:

Listed as: Arsenic
Effective Date for Reporting Under 40 CFR 372.30: 1/1/87
Lower Thresholds for Chemicals of Special Concern under 40 CFR 372.28:

DOT List of Marine Pollutants for CAS7440-38-2 (49 CFR 172.101 - App. B, 2005):

Not Listed

EPA TSCA Inventory for CAS7440-38-2 (EPA, 2005):

Listed as: Arsenic

SHIPPING REGULATIONS

SURFACE

DOT -- Table of Hazardous Materials and Special Provisions for UN/NA Number 1558 (49 CFR 172.101, 2005):

Hazardous materials descriptions and proper shipping name: Arsenic

Symbol(s): Not Listed
Hazard class or Division: 6.1

6.1: Poisonous materials. See 49 CFR section 173.132 for definitions.

Identification Number: UN1558
Packing Group: II

II: Packing Group II - indicates the degree of danger presented by the material is medium.

Label(s) required (if not excepted): 6.1

6.1: Poison Inhalation Hazard (inhalation hazard, Zone A or B) or Poison (other than inhalation hazard, Zone A or B; the packing group for a material is indicated in column 5 of the table.).

Special Provisions: IB8, IP2, IP4, T3, TP33

IB8: Authorized IBCs: Metal (11A, 11B, 11N, 21A, 21B, 21N, 31A, 31B and 31N); Rigid plastics (11H1, 11H2, 21H1, 21H2, 31H1 and 31H2); Composite (11HZ1, 11HZ2, 21HZ1, 21HZ2, 31HZ1 and 31HZ2); Fiberboard (11G); Wooden (11C, 11D and 11F); Flexible (13H1, 13H2, 13H3, 13H4, 13H5, 13L1, 13L2, 13L3, 13L4, 13M1 or 13M2).
IP2: When IBCs other than metal or rigid plastics IBCs are used, they must be offered for transportation in a closed freight container or a closed transport vehicle.
IP4: Flexible, fiberboard or wooden IBCs must be sift-proof and water-resistant or be fitted with a sift-proof and water-resistant liner.
T3: Minimum test pressure (bar): 2.65; Minimum shell thickness (in mm-reference steel) (See sxn.178.274(d)): sxn.178.274(d)(2); Pressure-relief requirements (See sxn.178.275(g)): Normal; Bottom opening requirements (See sxn.178.275(d)): sxn.178.275(d)(2).
TP33: The portable tank instruction assigned for this substance applies for granular and powdered solids and for solids which are filled and discharged at temperatures above their melting point which are cooled and transported as a solid mass. Solid substances transported or offered for transport above their melting point are authorized for transportation in portable tanks conforming to the provisions of portable tank instruction T4 for solid substances of packing group III or T7 for solid substances of packing group II, unless a tank with more stringent requirements for minimum shell thickness, maximum allowable working pressure, pressure-relief devices or bottom outlets are assigned in which case the more stringent tank instruction and special provisions shall apply. Filling limits must be in accordance with portable tank special provision TP3. Solids meeting the defnintion of an elevated temperature material must be transported in accordance with the applicable requirements of this subchapter.

Packaging Authorizations (refer to 49 CFR 173.***):

Exceptions: 153
Non-bulk packaging: 212
Bulk packaging: 242

Quantity Limitations:

Passenger aircraft or railcar: 25 kg
Cargo aircraft only: 100 kg

Vessel Stowage Requirements:

Vessel stowage location: A

A: The material may be stowed "on deck" or "under deck" on a cargo vessel and on a passenger vessel.

Vessel stowage other: Not Listed

DOT -- Table of Hazardous Materials and Special Provisions for UN/NA Number 1562 (49 CFR 172.101, 2005):

Hazardous materials descriptions and proper shipping name: Arsenical dust

Symbol(s): Not Listed
Hazard class or Division: 6.1

6.1: Poisonous materials. See 49 CFR section 173.132 for definitions.

Identification Number: UN1562
Packing Group: II

II: Packing Group II - indicates the degree of danger presented by the material is medium.

Label(s) required (if not excepted): 6.1

6.1: Poison Inhalation Hazard (inhalation hazard, Zone A or B) or Poison (other than inhalation hazard, Zone A or B; the packing group for a material is indicated in column 5 of the table.).

Special Provisions: IB8, IP2, IP4, T3, TP33

IB8: Authorized IBCs: Metal (11A, 11B, 11N, 21A, 21B, 21N, 31A, 31B and 31N); Rigid plastics (11H1, 11H2, 21H1, 21H2, 31H1 and 31H2); Composite (11HZ1, 11HZ2, 21HZ1, 21HZ2, 31HZ1 and 31HZ2); Fiberboard (11G); Wooden (11C, 11D and 11F); Flexible (13H1, 13H2, 13H3, 13H4, 13H5, 13L1, 13L2, 13L3, 13L4, 13M1 or 13M2).
IP2: When IBCs other than metal or rigid plastics IBCs are used, they must be offered for transportation in a closed freight container or a closed transport vehicle.
IP4: Flexible, fiberboard or wooden IBCs must be sift-proof and water-resistant or be fitted with a sift-proof and water-resistant liner.
T3: Minimum test pressure (bar): 2.65; Minimum shell thickness (in mm-reference steel) (See sxn.178.274(d)): sxn.178.274(d)(2); Pressure-relief requirements (See sxn.178.275(g)): Normal; Bottom opening requirements (See sxn.178.275(d)): sxn.178.275(d)(2).
TP33: The portable tank instruction assigned for this substance applies for granular and powdered solids and for solids which are filled and discharged at temperatures above their melting point which are cooled and transported as a solid mass. Solid substances transported or offered for transport above their melting point are authorized for transportation in portable tanks conforming to the provisions of portable tank instruction T4 for solid substances of packing group III or T7 for solid substances of packing group II, unless a tank with more stringent requirements for minimum shell thickness, maximum allowable working pressure, pressure-relief devices or bottom outlets are assigned in which case the more stringent tank instruction and special provisions shall apply. Filling limits must be in accordance with portable tank special provision TP3. Solids meeting the defnintion of an elevated temperature material must be transported in accordance with the applicable requirements of this subchapter.

Packaging Authorizations (refer to 49 CFR 173.***):

Exceptions: 153
Non-bulk packaging: 212
Bulk packaging: 242

Quantity Limitations:

Passenger aircraft or railcar: 25 kg
Cargo aircraft only: 100 kg

Vessel Stowage Requirements:

Vessel stowage location: A

A: The material may be stowed "on deck" or "under deck" on a cargo vessel and on a passenger vessel.

Vessel stowage other: Not Listed

ICAO International Shipping Name for UN1558 (ICAO, 2002):

Proper Shipping Name: Arsenic
UN Number: 1558

ICAO International Shipping Name for UN1562 (ICAO, 2002):

Proper Shipping Name: Arsenical dust
UN Number: 1562

LABELS

NFPA

NFPA Hazard Ratings for CAS7440-38-2 (NFPA, 2002):

Not Listed

-HANDLING AND STORAGE

HANDLING

Do not handle broken packages containing arsenic unless wearing appropriate protective clothing (AAR, 2000).

STORAGE

CONTAINER

Protect containers of arsenic against physical damage (ITI, 1995).
Arsenic can be stored in barrels and drums (OHM/TADS , 2001).
The containers should be kept tightly sealed (Sittig, 1991).

ROOM/CABINET RECOMMENDATIONS

Store containers in well-ventilated areas, away from food or food products and combustible materials (ITI, 1995; Sittig, 1991).
Store at ambient temperatures (CHRIS , 2001).

INCOMPATIBILITIES

Arsenic should be stored separately from oxidizers (such as perchlorates, peroxides, permanganates, chlorates and nitrates) and strong acids (such as hydrochloric, nitric and sulfuric acids). Contact will cause violent reactions (Sittig, 1991).
Arsenic will react with nitric acid (Lewis, 1997).
The following compounds will form incandescent reactions with arsenic (NFPA, 1997):
- cesium acetylene carbide, when warmed;
- chromium trioxide;
- iodine pentafluoride;
- rubidium acetylene carbide, when warmed;
- sodium peroxide.
Violent reactions or explosions will result when arsenic is exposed to the following chemicals (NFPA, 1997):
- finely divided bromates of barium, calcium, magnesium, potassium, sodium and zinc;
- bromine pentafluoride, in the cold;
- nitrogen tribromide;
- nitrogen trichloride;
- potassium nitrate, when ignited.
Arsenic burns spontaneously in the presence of gaseous chlorine (NFPA, 1997).
Arsenic ignites upon contact with (NFPA, 1997):
- hypochlorous acid;
- rubidium carbide, when heated;
- silver nitrate, ground in a 10:1 ratio with sublimed arsenic;
- liquid chlorine, at 33 degrees C.
Arsenic is incompatible with (Lewis, 2000):
- bromine azide,
- dirubidium acetylide,
- halogens,
- chloramines,
- silver nitrate,
- chromum trioxide,
- sodium oxide,
- palladium,
- zinc,
- platinum,
- hexafluoroisopropylideneamino lithium.
Arsenic is incompatible with zinc, oxidizing agents, and chemically active metals (CHRIS , 2001).

-PERSONAL PROTECTION

SUMMARY

RECOMMENDED PROTECTIVE CLOTHING - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 152 (ERG, 2004)

Wear positive pressure self-contained breathing apparatus (SCBA).
Wear chemical protective clothing that is specifically recommended by the manufacturer. It may provide little or no thermal protection.
Structural firefighters' protective clothing provides limited protection in fire situations ONLY; it is not effective in spill situations where direct contact with the substance is possible.

Work with arsenic is preferably done in closed systems (ITI, 1995).

Avoid breathing dusts, and fumes from burning arsenic; keep upwind. Avoid bodily contact with arsenic. Do not handle broken packages unless wearing appropriate protective clothing. Wash away any arsenic which may have contacted the body with copious amounts of water or soap and water (AAR, 2000).

Wear full protective clothing when working around arsenic (CHRIS , 2001).

Where there is occupational exposure to arsenic, workers should be provided with suitable protective clothing. This may include underwear, gloves, coveralls, and a hood over the head and neck (HSDB , 2001).

Contaminated clothing should be segregated from any source of potential personal contact (HSDB , 2001).

EYE/FACE PROTECTION

Wear appropriate goggles (AAR, 2000).

Eyewash stations should be present in areas where there is possibility of occupational exposure to arsenic. This is irrespective of the recommendation involving the wearing of eye protection (HSDB , 2001).

Contact lenses should not be worn when working around this material (HSDB , 2001).

RESPIRATORY PROTECTION

Wear a positive pressure self-contained breathing apparatus (SCBA) when fighting fires involving arsenic (AAR, 2000; (CHRIS , 2001).

At conditions above recommended exposure limit, wear a self-contained respirator with a full facepiece and operated in pressure-demand or positive pressure mode (HSDB , 2001).

Refer to 29 CFR 1910.1018 for OSHA respirator standards.

Refer to "Recommendations for respirator selection" in the NIOSH Pocket Guide to Chemical Hazards on TOMES Plus(R) for respirator information.

PROTECTIVE CLOTHING

CHEMICAL PROTECTIVE CLOTHING. Search results for CAS 7440-38-2.

Specific recommendations and test data for this chemical were not found in the available manufacturers' product literature. A complete list of consulted manufacturers and references is presented below.

-PHYSICAL HAZARDS

FIRE HAZARD

SUMMARY

POTENTIAL FIRE OR EXPLOSION HAZARDS - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 152 (ERG, 2004)
- Combustible material: may burn but does not ignite readily.
- Containers may explode when heated.
- Runoff may pollute waterways.
- Substance may be transported in a molten form.
Since arsenic itself does not burn, or burns with difficulty, extinguish fires using an agent suitable for the type of surrounding fire. Use water in flooding quantities as a fog; use foam, dry chemical or CO2 (AAR, 2000 ).
Arsenic burns spontaneously in the presence of gaseous chlorine (NFPA, 1997).
Arsenic ignites upon contact with: hypochlorous acid; rubidium carbide, when heated; silver nitrate, ground in a 10:1 ratio with sublimed arsenic; liquid chlorine, at 33 degrees C (NFPA, 1997).

FLAMMABILITY CLASSIFICATION

NFPA Flammability Rating for CAS7440-38-2 (NFPA, 2002):

Not Listed

FIRE CONTROL/EXTINGUISHING AGENTS

SMALL FIRE PRECAUTIONS - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 152 (ERG, 2004)

Dry chemical, CO2 or water spray.

LARGE FIRE PRECAUTIONS - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 152 (ERG, 2004)

Water spray, fog or regular foam.
Move containers from fire area if you can do it without risk.
Dike fire control water for later disposal; do not scatter the material.
Use water spray or fog; do not use straight streams.

TANK OR CAR/TRAILER LOAD FIRE PRECAUTIONS - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 152 (ERG, 2004)

Fight fire from maximum distance or use unmanned hose holders or monitor nozzles.
Do not get water inside containers.
Cool containers with flooding quantities of water until well after fire is out.
Withdraw immediately in case of rising sound from venting safety devices or discoloration of tank.
ALWAYS stay away from tanks engulfed in fire.
For massive fire, use unmanned hose holders or monitor nozzles; if this is impossible, withdraw from area and let fire burn.

NFPA Extinguishing Methods for CAS7440-38-2 (NFPA, 2002):

Not Listed

Use water in flooding quantities as a fog; use foam, dry chemical or CO2 (AAR, 2000; (Sittig, 1991).

COMBUSTION TOXICITY

Arsenic can be heated to burn in air with a bluish flame, giving off an odor of garlic and dense white fumes of arsenic trioxide (AS2O3) (Budavari, 2000).
When heated, or upon contact with acid or acid fumes (e.g. HNO3), arsenic emits highly toxic fumes, including arsenic gas (the most dangerous form of arsenic) (Budavari, 2000; CHRIS , 2001; Lewis, 1992).

EXPLOSION HAZARD

Arsenic dust is slightly explosive when exposed to flame (Lewis, 2000).

Arsenic should be stored separately from oxidizers (such as perchlorates, peroxides, permanganates, chlorates and nitrates) and strong acids (such as hydrochloric, nitric and sulfuric acids). Contact will cause violent reactions (Sittig, 1991).

Violent reactions or explosions will result when arsenic is exposed to the following chemicals: finely divided bromates of barium, calcium, magnesium, potassium, sodium and zinc; bromine pentafluoride, in the cold; nitrogen tribromide; nitrogen trichloride; potassium nitrate, when ignited (NFPA, 1997).

DUST/VAPOR HAZARD

Inorganic arsenic can react with hydrogen gas to produce highly toxic arsine gas (NIOSH , 2001).

When water reacts with metallic arsenide, toxic arsine gas is produced (Harbison, 1998).

When heated, or upon contact with acid or acid fumes (e.g. HNO3), arsenic emits highly toxic fumes, including arsenic gas (the most dangerous form of arsenic) (Budavari, 2000; Lewis, 2000; OHM/TADS , 2001).

Inhalation of arsine gas can produce rapid death, with massive hemolysis leading to renal failure (Baselt, 2000).

Arsenic dust is flammable when exposed to heat or flame (Lewis, 2000; OHM/TADS , 2001).

Dust is poisonous if inhaled (CHRIS , 2001).

REACTIVITY HAZARD

On contact, arsenic reacts with incandescence with bromine trifluoride (BrF3), chromium trioxide (CrO3), iodine pentafluoride (IF5), nitrosyl fluoride (FNO), and potassium dioxide (KO2). Platinum and arsenic will react on heating and become vividly incandescent (HSDB , 2001; Lewis, 2000; Pohanish & Greene, 1997) Urben, 1999).

Palladium or zinc and arsenic will react on heating with evolution of light and heat (HSDB , 2001) Urben, 1999).

Finely powdered arsenic inflames in gaseous chlorine (Pohanish & Greene, 1997; HSDB , 2001) Urben, 1999).

Rubidium acetylide (Rb2C2) ignites with arsenic (Pohanish & Greene, 1997; HSDB , 2001) Urben, 1999).

A finely divided mixture of arsenic and silver nitrate (AgNO3), with excess nitrate ignited when shaken onto paper (Pohanish & Greene, 1997; HSDB , 2001) Urben, 1999).

Arsenic reacts with powdered aluminum (Al) violently on heating (Lewis, 1996; Pohanish & Greene, 1997) Urben, 1999).

Arsenic reacts violently with ignition with bromine pentafluoride (BrF5) and with chlorine trifluoride (ClF3) at ambient or slightly elevated temperatures (Lewis, 1996; Pohanish & Greene, 1997) Urben, 1999).

Arsenic will initiate a violent and often explosive decomposition of nitrogen trichloride (NCl3) (Lewis, 1996; Pohanish & Greene, 1997) Urben, 1999).

Arsenic explodes on contact with bromine azide (BrN3) and dichlorine oxide (Cl2O); arsenic explodes on grinding in a mortar with solid potassium permanganate (KMnO4); arsenic forms an explosive mixture with sodium peroxide (Na2O2) (Lewis, 1996; Pohanish & Greene, 1997) Urben, 1999).

An explosive compound of arsenic (35 percent sulfuric acid with a high arsenic content) was produced as a surface layer on an exposed iron exterior of a corroded lead-lined ship. Either friction or ignition caused this compound to explode (Urben, 1999).

Inorganic arsenic can react with hydrogen gas to produce highly toxic arsine gas (NIOSH , 2001).

When heated, or on contact with acid or acid fumes, arsenic emits highly toxic fumes (Lewis, 2000).

OHM/TADS lists the following binary reactants for arsenic (OHM/TADS , 2001):

barium bromate,
barium chlorate,
barium iodate,
bromates,
bromine pentafluoride,
bromine trifluoride,
bromoazide,
calcium bromate,
calcium chlorate,
calcium iodate,
cesium acetylene carbide,
chlorates,
chlorine,
chlorine monoxide,
chromium trioxide,
fluorine,
hypochlorous acid,
iodates,
iodine pentafluoride,
magnesium bromate,
magnesium chlorate,
magnesium iodate,
nitrogen tribromide,
nitrogen trichloride,
potassium bromate,
potassium chlorate,
potassium iodate,
potassium nitrate,
potassium permanganate,
potassium peroxide,
rubidium carbide,
rubidium acetylene carbide,
silver nitrate,
sodium bromate,
sodiumchlorate,
sodium iodate,
sodium peroxide,
zinc bromate,
zinc chlorate,
zinc iodate.

EVACUATION PROCEDURES

SUMMARY

Editor's Note: This material is not listed in the Table of Initial Isolation and Protective Action Distances.

SPILL - PUBLIC SAFETY EVACUATION DISTANCES - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 152 (ERG, 2004)

Increase, in the downwind direction, as necessary, the isolation distance of at least 50 meters (150 feet) for liquids and at least 25 meters (75 feet) for solids in all directions.

FIRE - PUBLIC SAFETY EVACUATION DISTANCES - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 152 (ERG, 2004)

If tank, rail car or tank truck is involved in a fire, ISOLATE for 800 meters (1/2 mile) in all directions; also, consider initial evacuation for 800 meters (1/2 mile) in all directions.

PUBLIC SAFETY MEASURES - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 152 (ERG, 2004)

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

MEXICO:

SETIQ:

01-800-00-214-00 in the Mexican Republic;
For calls originating in Mexico City and the Metropolitan Area: 5559-1588;
For calls originating elsewhere, call: 011-52-555-559-1588.

CENACOM:

01-800-00-413-00 in the Mexican Republic;
For calls originating in Mexico City and the Metropolitan Area: 5550-1496, 5550-1552, 5550-1485, or 5550-4885;
For calls originating elsewhere, call: 011-52-555-550-1496, or 011-52-555-550-1552; 011-52-555-550-1485, or 011-52-555-550-4885.

ARGENTINA:

CIQUIME:

0-800-222-2933 in the Republic of Argentina;
For calls originating elsewhere, call: +54-11-4613-1100.

BRAZIL:

PRÓ-QUÍMICA:

0-800-118270 (Toll-free in Brazil);
For calls originating elsewhere, call: +55-11-232-1144 (Collect calls are accepted).

COLUMBIA:

CISPROQUIM:

01-800-091-6012 in Colombia;
For calls originating in Bogotá, Colombia, call: 288-6012;
For calls originating elsewhere, call: 011-57-1-288-6012.

CANADA:

CANUTEC:

613-996-6666 (Collect calls are accepted);
*666 cellular (in Canada only).

UNITED STATES:

CHEMTREC®:

1-800-424-9300 (Toll-free in the U.S., Canada, and the U.S. Virgin Islands);
703-527-3887 for calls originating elsewhere (Collect calls are accepted).

CHEM-TEL, INC.:

1-800-255-3924 (Toll-free in the U.S., Canada, and the U.S. Virgin Islands);
813-248-0585 for calls originating elsewhere (Collect calls are accepted).

INFOTRAC:

1-800-535-5053 (Toll-free in the U.S., Canada, and the U.S. Virgin Islands);
352-323-3500 for calls originating elsewhere (Collect calls are accepted).

3E COMPANY:

1-800-451-8346 (Toll-free in the U.S., Canada, and the U.S. Virgin Islands);
760-602-8703 for calls originating elsewhere (Collect calls are accepted).

NATIONAL RESPONSE CENTER (NRC):

1-800-424-8802 - (24 hours) (Toll-free in the U.S., Canada, and the U.S. Virgin Islands);
202-267-2675 for calls in the District of Columbia.

MILITARY SHIPMENTS:

703-697-0218 - Explosives/ammunition incidents (Collect calls are accepted);
1-800-851-8061 - All other dangerous goods incidents.

NATIONWIDE POISON CONTROL CENTER (United States only):

1-800-222-1222 (Toll-free in the U.S.).

For additional details see the section entitled "WHO TO CALL FOR ASSISTANCE" under the ERG Instructions.
As an immediate precautionary measure, isolate spill or leak area in all directions for at least 50 meters (150 feet) for liquids and at least 25 meters (75 feet) for solids.
Keep unauthorized personnel away.
Stay upwind.
Keep out of low areas.

AIHA ERPG Values for CAS7440-38-2 (AIHA, 2006):

Not Listed

DOE TEEL Values for CAS7440-38-2 (U.S. Department of Energy, Office of Emergency Management, 2010):

Listed as Arsenic
TEEL-0 (units = mg/m3): 0.01
TEEL-1 (units = mg/m3): 0.35
TEEL-2 (units = mg/m3): 2
TEEL-3 (units = mg/m3): 5
Definitions:

TEEL-0: The threshold concentration below which most people will experience no adverse health effects.
TEEL-1: The airborne concentration (expressed as ppm [parts per million] or mg/m(3) [milligrams per cubic meter]) of a substance above which it is predicted that the general population, including susceptible individuals, could experience notable discomfort, irritation, or certain asymptomatic, nonsensory effects. However, these effects are not disabling and are transient and reversible upon cessation of exposure.
TEEL-2: The airborne concentration (expressed as ppm or mg/m(3)) of a substance above which it is predicted that the general population, including susceptible individuals, could experience irreversible or other serious, long-lasting, adverse health effects or an impaired ability to escape.
TEEL-3: The airborne concentration (expressed as ppm or mg/m(3)) of a substance above which it is predicted that the general population, including susceptible individuals, could experience life-threatening adverse health effects or death.

AEGL Values for CAS7440-38-2 (National Research Council, 2010; National Research Council, 2009; National Research Council, 2008; National Research Council, 2007; NRC, 2001; NRC, 2002; NRC, 2003; NRC, 2004; NRC, 2004; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; United States Environmental Protection Agency Office of Pollution Prevention and Toxics, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; 62 FR 58840, 1997; 65 FR 14186, 2000; 65 FR 39264, 2000; 65 FR 77866, 2000; 66 FR 21940, 2001; 67 FR 7164, 2002; 68 FR 42710, 2003; 69 FR 54144, 2004):

Not Listed

NIOSH IDLH Values for CAS7440-38-2 (National Institute for Occupational Safety and Health, 2007):

IDLH: 5 mg As/m3 (as As)
Note(s): Ca

(Ca) NIOSH considers this substance to be a potential occupational carcinogen (See Appendix A).

CONTAINMENT/WASTE TREATMENT OPTIONS

SUMMARY

SPILL OR LEAK PRECAUTIONS - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 152 (ERG, 2004)
- ELIMINATE all ignition sources (no smoking, flares, sparks or flames in immediate area).
- Do not touch damaged containers or spilled material unless wearing appropriate protective clothing.
- Stop leak if you can do it without risk.
- Prevent entry into waterways, sewers, basements or confined areas.
- Cover with plastic sheet to prevent spreading.
- Absorb or cover with dry earth, sand or other non-combustible material and transfer to containers.
- DO NOT GET WATER INSIDE CONTAINERS.
RECOMMENDED PROTECTIVE CLOTHING - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 152 (ERG, 2004)
- Wear positive pressure self-contained breathing apparatus (SCBA).
- Wear chemical protective clothing that is specifically recommended by the manufacturer. It may provide little or no thermal protection.
- Structural firefighters' protective clothing provides limited protection in fire situations ONLY; it is not effective in spill situations where direct contact with the substance is possible.
The treatment or removal of arsenic is complicated by the fact that arsenic exists in multiple valence states. Arsenic can be most effectively removed or stabilized when in its pentavalent form (Leist et al, 2000).
Keep arsenic out of water sources and sewers (AAR, 2000).

WASTE TREATMENT OPTIONS

RECYCLING/RECLAMATION

Arsenic and its compounds should be placed in long-term storage or returned to manufacturers for reprocessing (Sittig, 1991).
Waste management activities associated with material disposition are unique to individual situations. Proper waste characterization and decisions regarding waste management should be coordinated with the appropriate local, state, or federal authorities to ensure compliance with all applicable rules and regulations.

CHEMICAL TREATMENT

Chemical precipitation is applicable for the treatment of aqueous hazardous wastes containing toxic constituents that may be converted to an insoluble form. This includes wastes containing arsenic (Freeman, 1998).
Alum Floc binds arsenic into insoluble form (OHM/TADS , 2001).
Dissolve spilled or leaked arsenic in a minimum amount of concentrated hydrochloric acid; add to water until the appearance of white precipitate. Add 6M-HCl just to dissolve again; saturate with hydrogen sulfide. After filtration, wash the precipitate, dry, package, and return to suppliers (ITI, 1995; OHM/TADS , 2001).
Sewage containing arsenic can be decontaminated using pyrolusite treatment (Sittig, 1991).
Removal of arsenic from wastewater is preferably done through coagulation, normally using iron (Leist et al, 2000).

BIOREMEDIATION

Arsenic (As) tolerant fungi were isolated from As polluted soils. Several strains of the genus Aspergillus fumigatus were found to volatilize arsenic compounds when the arsenic was present in the trivalent state (As(III)) (Hiroki & Yoshiwara, 1993).

-ENVIRONMENTAL HAZARD MANAGEMENT

POLLUTION HAZARD

Arsenic is a naturally occurring element and is found in a number of sulfide ores. It constitutes 5 x 10(-4) percent of the earth's crust. Arsenic can be released to the environment from natural sources, including volcanoes and erosion of mineral deposits. Human activities, e.g. chemical production and use, metal smelting, coal combustion, and waste disposal, result in arsenic releases, causing substantial environmental contamination (HSDB, 2004; ATSDR, 1993).

Native soil concentrations of arsenic are typically in the range of 1.0-40 ppm, and in extreme states, as high as 0.1-500 ppm (Dragun, 1988).
Natural groundwater concentrations of arsenic are typically in the range of <1.0-30 ppm, and in extreme states, as high as 4,000 ppm (Dragun, 1988).

Most human releases of arsenic are to land or soil, primarily from pesticides or solid wastes. Substantial amounts of arsenic are also released to air and water. Arsenic production and use of arsenic-containing products are the major sources of arsenic releases to the air from human activities. Arsenic is released to water by natural weathering processes, by discharge from industrial facilities, by leaching from landfills or soil, and by urban runoffs (ATSDR, 1993).

Arsenic pollution is widespread. Human exposure to both naturally occurring and manufactured arsenic may occur through air, food and water (Bingham et al, 2001).

Although mining activity ceased in 1961, leached mine waste still delivers about 3.5 mg/y of arsenic to Moira Lake in Canada. The arsenic concentration averages about 545 mcg/g in the top sediment and 1000 mcg/g at depths between 23 to 27 cm. Acidification of the overlaying water might release large amounts of arsenic to the lake (Azcue & Nriagu, 1993).

Arsenic content in leachate and runoff from contaminated soil taken from an old wood impregnation plant was studied in a soil-water-sediment freshwater ecosystem constructed in the laboratory. During the four month duration of the experiment, approximately 40 mg (or 0.6%) of the total initial arsenic content of the soil was discharged. Of the total arsenic content, 7.5% remained in the water, 44% settled down to the shallow sediment zone (water depth of 5-30 cm), and 48.5% settled down to the deeper sediment zone (water depth of 80 cm) (Ruokolainen et al, 2000).

Arsenic is a widespread soil contaminant, in part because of past use of arsenic-containing pesticides. Arsenic content of soils in Louisiana ranged from near 0 to 73 mg/kg, with a mean value of 23.2 mg/kg (Ori et al, 1993).

ENVIRONMENTAL FATE AND KINETICS

It is estimated that as much as 210 x 10(5) kg of arsenic is lost to the atmosphere in the vapor state from the land surface each year (Tamaki & Frankenberger, 1992).

WATER

SURFACE WATER
- Arsenic in its 0-oxidation state is rarely found in natural waters. Soluble inorganic arsenate (+5-oxidation state) is most commonly encountered. It is thermodynamically more stable in water than arsenite (+3-oxidation state) (HSDB, 2004)
GROUND WATER
- Oxidation of arsenite (As(III)) was studied in groundwater samples. As(III) quickly converted to As(V) in the presence of ozone, but was slow to do so in the presence of pure oxygen and air. The half-life of As(III) in experimental solution was approximately four minutes for the ozone reaction, two to five days with oxygen and four to nine days for the air (Kim & Nriagu, 2000).

SOIL

TERRESTRIAL
- Arsenic has a high motility in sandy, sandy loam, and loamy sand soils (soil pH 4.2-7.8). Through in soils comprised of silty clay loam and clay, arsenic had a moderate motility (soil pH 4.5-7.0). Low motility was observed in clay and silty clay soils (soil pH 6.2-6.7)(Dragun, 1988).
- The desorption rate for arsenate in soil averages 1.9 mL/g and 1.2 mL/g for arsenite (Dragun, 1988).

ABIOTIC DEGRADATION

Mobility of arsenic in soil varies according to soil type and pH. It can vaporize from the soil to the atmosphere. Plant biouptake is influenced by soil elements, temperature, and plant species. In water, a small percent will dissolve, but the majority will settle to the sediment layers. Acidic waters can solubilize arsenic (Ruokolainen et al, 2000; Azcue & Nriagu, 1993; Tamaki & Frankenberger, 1992; Dragun, 1988).

BIOACCUMULATION

HUMANS

Arsenic is rapidly cleared from the blood in humans (Hayes & Laws, 1991). Arsenic accumulates mostly in the muscle tissues of humans, and is typically excreted in the urine within six days of exposure (Baselt, 2000).
Urine concentrations in persons not exposed to arsenic may range from 0.01 to 0.30 mg/L, while workers exposed to arsenic dust had urine concentrations ranging from 0.02 to 2.00 mg/L (Baselt, 2000).
Concentrations found in the hair of "normal persons" were less than 1.0 mg/kg, whereas concentrations in hair of persons chronically exposed are often between 1 and 5 mg/kg, ranging as high as 47 mg/kg (Baselt, 2000).
The average content in the human body is 3 to 4 mg. This is affected by age and lifestyle, and can vary significantly (Zenz, 1994).
Concentrations of arsenic in the blood of persons exposed to arsenic in drinking water may be up to 60 mcg/As/liter. Non-exposed persons range from 1-4 mcg/As/liter (Hayes & Laws, 1991).

FISH

Arsenic accumulation was examined in conjunction with accumulation of several other heavy metals, organochlorine pesticides (DDTs), hexachlorobenzene (HCB), and hexachlorohexane isomers (HCHs) in marine species from the Ionian and Adriatic Seas. High arsenic levels were found in the fish muscle tissue or the liver of the all fish species tested (teleost and elasmobranch fish species). Highest arsenic levels were measured in muscle tissue samples of Raje spp., Micromesistius poutassou, and Merluccius merluccius. High levels were also found in cephalopod flesh and digestive gland and in the flesh of crustaceans. Levels were low in bivalve molluscs (Marcotrigiano & Storelli, 2003).
- Arsenic Levels in Marine Species (Marcotrigiano & Storelli, 2003):
Arsenic is concentrated to a certain extent in aquatic life (OHM/TADS , 2001).
Fish generally contain lower arsenic levels than other aquatic organisms (HSDB , 2001).
Seafood can contain from 2 mg/kg in freshwater fish, up to 22 mg/kg in lobster (Baselt, 2000).
Marine fish may contain as much as 10 ppm arsenic, freshwater fish approximately 3 ppm (Zenz, 1994).
The fish and invertebrate species living in the Mugu Lagoon, Malibu Lagoon and Ballona Wetlands of southern California were studied in order to assess the extent of metal contamination in these wetlands. Concentrations of arsenic in these biota ranged from 1.0 mcg/g to 8.5 mcg/g (Cohen et al, 2001).
Livers of the fish of the Great Lakes contain from 5.6 to 80 ppb, mainly in the fat fraction (HSDB , 2001).

PLANTS

TERRESTRIAL
- Uptake is influenced by soil elements, temperature and species of plant (HSDB , 2001).
- A study using Indian mustard (Brassica juncea) found that uptake of arsenic by seedlings exposed for two days to 250 mcgM arsenate in axenic hydroponic solution averaged as follows (Ingrid et al, 2000):
- Turnips, growing in a hydroponic environment, were exposed to arsenic in concentrations of 1.0, 2.0, or 5.0 mg/L. Plant uptake of arsenic had a positive correlation to arsenic application. After exposure, both inner root and outer root skin concentrations of arsenic were above the maximum limit set for arsenic content in food crops (1.0 mg/kg). If turnip plants are exposed to a large pulse of arsenic, as growth on contaminated nutrient solutions, they will accumulate residues at levels that are unsafe for animal and human consumption (Carbonell-Barrachina et al, 1999).

MAMMALS

Arsenic is rapidly cleared from the bloodstream, except in rats, where its derivatives bind to hemoglobin (Hayes & Laws, 1991).

OTHER

INVERTEBRATES
- Bioaccumulation of arsenic was studied in aquatic worms, Lumbriculus variegatus. The worms were exposed for 28 days to sediment collected near a sawmill area. Tissue concentrations of arsenic reached 362 mcg/g in these organisms; arsenic was the only wood preservative found to bioaccumulate under test conditions (Lyytikainen et al, 2001).

BIOCONCENTRATION FACTOR

Tilapia (Oreochromis mossambicus): 1394 (mean BCF; intestine) (Liao et al, 2003)
Tilapia (Oreochromis mossambicus): 421 (mean BCF; stomach) (Liao et al, 2003)
Tilapia (Oreochromis mossambicus): 180 (mean BCF; liver) (Carbonell-Barrachina et al, 1999)
Tilapia (Oreochromis mossambicus): 163 (mean BCF; gill) (Liao et al, 2003)
Tilapia (Oreochromis mossambicus): 143 (mean BCF; muscle) (Liao et al, 2003)

ENVIRONMENTAL TOXICITY

FRESHWATER TOXICITY

LC50 - TILAPIA (Oreochromis mossambicus): 69.06 mg/L for 24H (Liao et al, 2003)
LC50 - TILAPIA (Oreochromis mossambicus): 28.68 mg/L for 96H (Liao et al, 2003)
TC - (WATER) BASS: 7.6 ppm for 240H (OHM/TADS , 2001)
TC - (WATER) BLEAK: 2.2 ppm for 72H (OHM/TADS , 2001)
TC - (WATER) CARP: 3.1 ppm for 96H (OHM/TADS , 2001)
TC - (WATER) EEL: 3.1 ppm for 72H (OHM/TADS , 2001)
TC - (WATER) MINNOW: 11.6 ppm for 36H (OHM/TADS , 2001)
TC - (WATER) MINNOW: 60 ppm for 16H (OHM/TADS , 2001)
TC - (WATER) PIKE PERCH: 1.1 ppm for 48H (OHM/TADS , 2001)

SALTWATER TOXICITY

TC - (WATER) CRAB: 4.3 ppm for 264H (OHM/TADS , 2001)

WATERFOWL TOXICITY

0.05 ppm (OHM/TADS , 2001)
LD50 - (ORAL) CHICKEN: 324 mg/kg (OHM/TADS , 2001)
LD50 - (ORAL) FOWL: 6.5 mg/kg (OHM/TADS , 2001)

TERRESTRIAL PLANTS

A field evaluation of the area surrounding a smelter in southwest Montana correlated the concentrations of arsenic and metals in the soils with the vegetative structure and composition as well as with wildlife habitat quality. Concentrations of arsenic and metals in soils were highly enriched surrounding the smelter, and decreased with distance from the smelter and with soil depth, suggesting that the smelter was the source of the enrichment. In enriched areas, there were significant negative correlations between soil arsenic and metals concentrations and the extent of vegetative cover and the vertical diversity of plant species. The native vegetative structure and composition were significantly changed: the evergreen forest was replaced with bare, unvegetated ground; the grasslands species were impoverished and replaced by weed species; and the vertical complexity of the habitat was reduced. Loss of vegetative cover in the affected areas was accompanied by a reduction in the capacity to support indigenous wildlife populations (Galbraith et al, 1995).
Laboratory toxicity tests of soil contaminated with arsenic and metals surrounding a smelter in southwest Montana were performed using site soils from the impacted area. The tests compared germination and growth of alfalfa, lettuce, and wheat between the site soils and reference soils. The degree of phytotoxicity was measured based on the magnitude of difference between germination and growth in the two soils. Based on root growth, length, and mass it was observed that the contaminated site soils exhibited substantial toxicity to the plants: 5% were severely phytotoxic, 55% were highly phytotoxic, 10% were moderately phytotoxic, 20% were mildly phytotoxic, and 10% were nontoxic. Correlations of contaminants in the site soils found that there was a positive correlation between concentrations of As, Cu, Cd, Pb, and Zn and phytotoxicity (Kapustka et al, 1995).

-PHYSICAL/CHEMICAL PROPERTIES

MOLECULAR WEIGHT

74.92 (RTECS , 2001)

DESCRIPTION/PHYSICAL STATE

Arsenic is a silver-gray or tin-white, shiny, brittle, crystalline and metallic-looking element. It can exist in three allotropic forms: yellow (alpha), black (beta), and gray (gamma) (HSDB , 2001).

Rarely is arsenic found in its isolated, elemental form; more commonly, it is present in mineral species, in alloys, or as an oxide or other compound form (Budavari, 2000).

The amorphous metalloid form (alpha-arsenic) will darken to black (beta-arsenic) and form arsenic trioxide (As203) in moist air. When arsenic vapor is cooled suddenly, a yellow modification of arsenic which has no metallic properties is formed. This yellow arsenic can be converted back to the gray arsenic with very short exposure to ultraviolet light (ACGIH, 1996; (Budavari, 2000; Hathaway et al, 1996; Lewis, 1992; Lewis, 1996; NIOSH , 2001).

Arsenic has low thermal and electrical conductivity (ITI, 1995).

It is essentially odorless and tasteless (HSDB , 2001).

However, arsine gas is noted as having a garlic-like odor (Bingham et al, 2001).

VAPOR PRESSURE

1 mmHg (at 372 degrees C) (sublimes) (Lewis, 2000)

61 mmHg (at 500 degrees C) (OHM/TADS , 2001)

SPECIFIC GRAVITY

NORMAL TEMPERATURE AND PRESSURE

(25 degrees C; 77 degrees F and 760 mmHg)
5.778 (at 25/4 degrees C) (Budavari, 2000; ITI, 1995)

TEMPERATURE AND/OR PRESSURE NOT LISTED

Gray crystalline solid: 5.72 (ACGIH, 1996)
1.97 (OHM/TADS , 2001)
Black: 4.7
Yellow: 2.0

DENSITY

NORMAL TEMPERATURE AND PRESSURE

(25 degrees C; 77 degrees F and 760 mmHg)
Metal: 5.73 kg/L (Ashford, 1994; NIOSH , 2001)

FREEZING/MELTING POINT

MELTING POINT

817 degrees C (at 28 atm) (ACGIH, 1991; Bingham et al, 2001; OHM/TADS , 2001)
818 degrees C (at 36 atm) (Budavari, 2000; ITI, 1995)
814 degrees C (at 36 atm) (Lewis, 1997; Lewis, 2000)

BOILING POINT

sublimes at 613 degrees C (ACGIH, 1996; (ITI, 1995; Lewis, 1997; OHM/TADS , 2001)

sublimes at 615 degrees C (760 mmHg) (Ashford, 1994; Budavari, 2000)

sublimes at 612 degrees C (Lewis, 2000)

sublimes at 613 degrees C; 1,135 degrees F; 1076.5 K (CHRIS , 2001)

FLASH POINT

No information found at the time of this review.

SOLUBILITY

IN WATER

Black and gray arsenic are insoluble in water (ACGIH, 1996; (Lewis, 2000).

OTHER

Yellow arsenic is soluble in nitric acid (ACGIH, 1996; (Lewis, 2000).
Arsenic is insoluble in caustic and non-oxidizing acids (Lewis, 1997).
It is dissolved in oxidizing acids (ACGIH, 1996).

OTHER/PHYSICAL

ODOR THRESHOLD

Currently not available (CHRIS , 2002)

DIELECTRIC CONSTANT

10.23 (at 20 degrees C and 60 cycles) (Budavari, 2000)

HEAT OF FUSION

22.4 kcal/g-atom (Budavari, 2000)
6.620 kcal/g-atom (Budavari, 2000)
27,740 J/mol K (latent heat of fusion) (Budavari, 2000)

-REFERENCES

GENERAL BIBLIOGRAPHY

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.

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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.

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.

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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.

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.

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.

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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.

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.

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.

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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.

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.

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.

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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.

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.

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.

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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.

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.

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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.

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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.

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.

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Information to evaluate chemical incidents