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ARSENIC TRIFLUORIDE
CASRN: 7784-35-2
For other data, click on the Table of ContentsHuman Health Effects:
Evidence for Carcinogenicity:
CLASSIFICATION: A; human carcinogen. BASIS FOR CLASSIFICATION: Based on sufficient evidence from human data. An increased lung cancer mortality was observed in multiple human populations exposed primarily through inhalation. Also, increased mortality from multiple internal organ cancers (liver, kidney, lung, and bladder) and an increased incidence of skin cancer were observed in populations consuming drinking water high in inorganic arsenic. HUMAN CARCINOGENICITY DATA: Sufficient. ANIMAL CARCINOGENICITY DATA: Inadequate. /Inorganic Arsenic/
A1. A1= Confirmed human carcinogen. (1993) /Arsenic, elemental and inorganic cmpd (except Arsine), as As/
Classification of carcinogenicity: 1) evidence in humans: sufficient; 2) evidence in animals: limited. Overall summary evaluation of carcinogenic risk to humans is Group 1: Carcinogenic to humans. This evaluation applies to arsenic and arsenic cmpd as a whole and not necessarily to all individual chemicals within the group. /Arsenic and arsenic cmpds/
Human Toxicity Excerpts:
IRRITANT & VESICANT ARSENICAL COMPOUNDS, SUCH AS ARSENIC TRIOXIDE, ARSENIC TRICHLORIDE, & THE ARSENICAL WAR GASES, HAVE BEEN KNOWN TO CAUSE SEVERE DAMAGE TO THE RESPIRATORY SYSTEM UPON INHALATION. SYMPTOMS INCLUDE COUGH, DYSPNEA, & PAIN IN THE CHEST. /ARSENIC COMPD/
/ACUTE POISONING EFFECTS:/ URINE IS SCANTY, ALBUMINOUS, & BLOODY; EVENTUALLY ANURIA MAY OCCUR. ... AS FLUID LOSS PROCEEDS, SYMPTOMS OF SHOCK APPEAR. HYPOXIC CONVULSIONS MAY OCCUR TERMINALLY, & COMA & DEATH ENSUE. IN SEVERE POISONING, DEATH CAN OCCUR WITHIN AN HOUR, BUT THE USUAL INTERVAL IS 24 HR. /ARSENIC/
MOST COMMON EARLY SIGNS OF CHRONIC ARSENIC POISONING ARE ... GARLIC ODOR OF BREATH & PERSPIRATION, EXCESSIVE SALIVATION & SWEATING, STOMATITIS ... /ARSENIC/
/OTHER CHRONIC EFFECTS:/ ... GENERALIZED ITCHING, SORE THROAT, CORYZA, LACRIMATION, NUMBNESS, BURNING OR TINGLING OF EXTREMITIES, DERMATITIS, VITILIGO, & ALOPECIA. /ARSENIC/
/CHRONIC:/ BONE MARROW SERIOUSLY INJURED ... MYELOID TISSUE ... DEPRESSED ... APLASTIC ANEMIA ... /ARSENIC/
The effects of trivalent and pentavalent As on the synthesis of DNA, RNA, and protein in cultured human cells were compared. The clastogenicity of these compounds were also compared. The chromosome-breaking activity in cultured (human) leukocytes was significantly higher for the compounds with trivalent than with pentavalent As. The activity in cultured human skin fibroblasts was similar to that in leukocyte cultures. The colony-forming capacity after exposure to As compounds indicated that trivalent compounds were more toxic than pentavalent compounds. Both trivalent and pentavalent arsenic inhibited DNA and protein synthesis in leukocytes. /Trivalent and pentavalent arsenic/
Arsenicals may act as contact allergens. Thus, low concentrations which ordinarily would not result in local irritation cause allergic reactions (eg folliculitis) in sensitized individuals. /Arsenicals/
The toxicity of arsenical compounds decreases as follows: arsine (-III)> organo-arsine derivatives> arsenites (+III)> arsenoxides> (+III)> arsenates (+V)> pentavalent organic compounds (+V)> arsonium metals (+I)> metallic arsenic (0). /Arsenical compounds/
The wrists are common sites of dermatitis, as are the genitalia if personal hygiene is poor. /Arsenic and arsenic compounds/
Skin, Eye and Respiratory Irritations:
Trivalent arsenic compounds are corrosive to the skin. /Trivalent arsenic compounds/
Drug Warnings:
Food and Environmental Agents: Effect on Breast-Feeding: Reported Sign or Symptom in Infant or Effect on Lactation: Fluorides: None. /from Table 7/
Medical Surveillance:
A periodic sputum cytology examination is recommended for all workers occupationally exposed to inorganic arsenic. The frequency of this procedure should be determined by the responsible medical authority. /Inorganic arsenic/
In pre-employment physical examinations, particular attention should be given to allergic and chronic skin lesions, eye disease, psoriasis, chronic eczematous dermatitis, hyperpigmentation of the skin, keratosis and warts, baseline weight, baseline blood and hemoglobin count, and baseline urinary arsenic determinations. In annual examinations, the worker's general health, weight, and skin condition should be checked, and the worker observed for any evidence of excessive exposure or absorption of arsenic. Chest X-ray and lung function should be evaluated; analysis of the urine, hair, or nails for arsenic should be made every 60 days as long as exposure continues. /Arsenite/
Populations at Special Risk:
Occupations with potential arsenic exposure: farmers, glass makers, and herbicide workers. /Arsenates and arsenites/
Chronic arsenical poisoning due to ingestion is rare and generally confined to patients taking prescribed medications. However, it can be a concomitant of inhaled inorganic arsenic from swallowed sputum and improper eating habits. /Arsenic and arsenic compounds/
Workers may be exposed to airborne arsenic in cutting and sawing operations on wood treated with arsenic-containing preservatives. /Arsenite and arsenate/
Probable Routes of Human Exposure:
... KNOWN TO CAUSE SEVERE DAMAGE TO THE RESPIRATORY SYSTEM UPON INHALATION. /ARSENIC COMPD/
COMPOUNDS OF ARSENIC MAY BE ABSORBED AFTER INGESTION. /ARSENIC COMPD/
... THE SKIN IS POSSIBLE ROUTE OF ABSORPTION OF ARSENIC. /ARSENIC COMPD/
Minimum Fatal Dose Level:
Fatal human dose 70-180 mg. Estimated lethal dose for a 70 kg human as As (III) /Arsenic (III)/
PROBABLE ORAL LETHAL DOSE (HUMAN) IS LESS THAN 5 MG/KG, A TASTE (LESS THAN 7 DROPS) FOR 70 KG PERSON (150 LB). /ARSENITES/
Emergency Medical Treatment:
Emergency Medical Treatment:
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Reserved. Any duplication, replication or redistribution of all or part
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is strictly prohibited.
The following Overview, *** ARSENIC ***, is relevant for this HSDB record chemical. |
| Life Support: |
o This overview assumes that basic life support measures
have been instituted.
|
| Clinical Effects: |
SUMMARY OF EXPOSURE
0.2.1.1 ACUTE EXPOSURE
o Arsenic compounds are absorbed mainly through the GI
tract, but may be absorbed through intact skin or
after inhalation. Hypovolemia from capillary leakage
('third-spacing' of fluids) is a common, serious early
effect.
o Acute arsenic ingestion generally produces signs and
symptoms within 30 minutes, but this may be delayed in
onset for several hours if arsenic is ingested with
food.
1. Initial signs and symptoms of arsenic ingestion
include burning lips, throat constriction and
dysphagia, followed by excruciating abdominal pain,
hemorrhagic gastritis, gastroenteritis, severe nausea,
projectile vomiting, profuse "rice water-like"
diarrhea, with hypovolemia resulting in hypotension
and an irregular pulse.
2. Muscle cramps, facial edema, bronchitis, dyspnea,
chest pain, dehydration, intense thirst, and
fluid-electrolyte disturbances are also common. A
garlic-like odor of the breath and feces may occur.
3. DELAYED EFFECTS - After absorption, arsenic may cause
multi-organ failure by inhibiting
sulfhydryl-containing enzymes within cells.
a. Encephalopathy, with headache, lethargy, mental
confusion, hallucinations, emotional lability,
memory loss and delirium may occur; seizures, stupor,
convulsions, coma, and death may follow within 24
hours of a severe acute exposure.
b. Dysrhythmias (particularly QTc prolongation and
torsade de pointes), cardiomyopathy, ARDS,
hepatitis, rhabdomyolyses, hemolysis, renal failure
may develop over several days. Peripheral
polyneuropathy, bone marrow depression, skin
eruptions, depression of blood cells, alopecia, and
Mees lines may develop days to weeks after acute
exposure. Anemia, leukopenia and thrombocytopenia
are among the hematological abnormalities resulting
from exposure.
c. The delayed effects may lead to systemic collapse,
with severe hypotension, restlessness, convulsions
and coma.
o Many arsenic compounds are severe irritants of the
skin, eye, and mucous membranes, especially of moist
surfaces; 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.
o CHRONIC POISONING - Chronic inhalation of inorganic
arsenic compounds is the most common cause of
occupational poisoning.
1. The sequence of chronic poisoning involves weakness,
anorexia, hepatomegaly, jaundice, and
gastrointestinal complaints, followed by
conjunctivitis, irritation of the throat and
respiratory tract, hyperpigmentation, and eczematoid
and allergic dermatitis.
2. Other effects of chronic exposure include
conjunctivitis with irritation and lacrimation; hair,
skin and nail changes; hyperkeratosis of feet and
hands; and melanosis, with pigment spots in corneal
and conjunctival epithelium.
3. Skin lesions are a common effect, starting as
erythematous, pruritic dermatitis, followed by finely
freckled hyperpigmentation with hypopigmented
maculae. Melanosis also occurs. The skin lesions may
sometimes be pustular, ulcerative, and gangrenous.
4. A hoarse voice and chronic upper respiratory disease
are characteristic in overexposed arsenic workers. A
perforated nasal septum is a common result with
prolonged inhalation of white arsenic dust or fume.
5. CNS symptoms may include numbness, burning, and
tingling of the hands and feet, pain, paresthesias,
tenderness, muscle fasciculations, gross tremors,
ataxia, incoordination, and mental confusion.
Musclular weakness, limb tenderness and difficulty
walking may follow. The final phase consists of
peripheral sensory neuropathy of the hands and feet
and, sometimes, motor paralysis.
o Certain arsenic compounds are known human carcinogens.
Chronic exposure in either occupational settings or
through drinking of contaminated groundwater can cause
poisoning and carries an increased risk of skin, lung,
bladder, and possibly liver cancers.
VITAL SIGNS
0.2.3.1 ACUTE EXPOSURE
o Hypotension and tachycardia are common early signs.
Fever and tachypnea may occur. Hypertension has been
associated with chronic environmental arsenic exposure.
HEENT
0.2.4.1 ACUTE EXPOSURE
o Trivalent arsenic is corrosive to the eyes, mouth, and
mucous membranes. Perforation of the nasal septum can
occur.
CARDIOVASCULAR
0.2.5.1 ACUTE EXPOSURE
o Hypovolemic or hemorrhagic shock, torsades de pointes,
ventricular fibrillation or tachycardia, QTc
prolongation, and T-wave changes may be seen after
acute ingestion. Myocarditis has been reported in
chronic arsenic poisoning.
RESPIRATORY
0.2.6.1 ACUTE EXPOSURE
o Respiratory tract irritation may occur. Cardiogenic or
noncardiogenic pulmonary edema and respiratory failure
may develop in severe poisonings.
NEUROLOGIC
0.2.7.1 ACUTE EXPOSURE
o Altered mental status, seizures, toxic delirium,
encephalopathy, and delayed peripheral neuropathy are
complications of acute arsenic poisoning.
GASTROINTESTINAL
0.2.8.1 ACUTE EXPOSURE
o Acute toxicity results in early symptoms of abdominal
pain, severe vomiting and diarrhea, as well as dryness
of the oral and nasal cavities.
HEPATIC
0.2.9.1 ACUTE EXPOSURE
o Hepatocellular injury occurs rarely after acute
poisoning.
GENITOURINARY
0.2.10.1 ACUTE EXPOSURE
o Hematuria and acute tubular necrosis may occur.
FLUID-ELECTROLYTE
0.2.12.1 ACUTE EXPOSURE
o Rapid volume depletion from vomiting, diarrhea, and
third spacing of fluids is common.
HEMATOLOGIC
0.2.13.1 ACUTE EXPOSURE
o Acute hemolysis and anemia may occur after acute
poisoning. Pancytopenia, aplastic anemia, or leukemia
may occur following chronic exposure. Bone marrow
depression can occur.
DERMATOLOGIC
0.2.14.1 ACUTE EXPOSURE
o Skin findings may include hyperpigmentation, keratoses,
and epidermoid carcinomas. Mee's lines of the nails
are common. Trivalent arsenic compounds are corrosive
to the skin. Arsenic trioxide and pentoxide are
sensitizers.
MUSCULOSKELETAL
0.2.15.1 ACUTE EXPOSURE
o Muscular cramps may occur and progress to
rhabdomyolysis.
REPRODUCTIVE HAZARDS
o Inorganic arsenic crosses the placenta and may result in
spontaneous abortion or stillbirth with either acute or
chronic poisoning.
CARCINOGENICITY
0.2.21.1 IARC CATEGORY
o Chronic therapeutic, occupational, and environmental
arsenic exposure have been associated with lung,
bladder, skin, and other cancers in humans.
GENOTOXICITY
o Arsenic induced DNA damage in human cells.
|
| Laboratory: |
o Monitor CBC, serum electrolytes, urinalysis, spot urine
arsenic, a 24 hour urinary arsenic collection, liver and
renal function tests, and a blood arsenic level in
symptomatic patients. A chelated or nonchelated 24 hour
urinary arsenic collection exceeding 100 mcg is usually
abnormal.
o Obtain an ECG and institute continuous cardiac monitoring
in symptomatic patients.
o An abdominal x-ray should be obtained in all patients
acutely ingesting arsenic as it is radiopaque. Obtain a
chest radiograph in patients with severe poisoning or
pulmonary effects.
o Initial and periodic biological monitoring and medical
surveillance are required for employees exposed to
arsenic.
|
| Treatment Overview: |
ORAL EXPOSURE
o GASTRIC DECONTAMINATION - Aggressive decontamination
with gastric lavage is recommended. If X-ray
demonstrates arsenic in the lower GI tract, whole bowel
irrigation should be considered. Activated charcoal may
not bind significant amounts, but is recommended until
definitive quantitative data are available. Fluid
repletion should begin as soon as possible.
o GASTRIC LAVAGE: Consider after ingestion of a
potentially life-threatening amount of poison if it can
be performed soon after ingestion (generally within 1
hour). Protect airway by placement in Trendelenburg and
left lateral decubitus position or by endotracheal
intubation. Control any seizures first.
1. CONTRAINDICATIONS: Loss of airway protective reflexes
or decreased level of consciousness in unintubated
patients; following ingestion of corrosives;
hydrocarbons (high aspiration potential); patients at
risk of hemorrhage or gastrointestinal perforation; and
trivial or non-toxic ingestion.
o ACTIVATED CHARCOAL: Administer charcoal as slurry (240
mL water/30 g charcoal). Usual dose: 25 to 100 g in
adults/adolescents, 25 to 50 g in children (1 to 12
years), and 1 g/kg in infants less than 1 year old.
o Monitor vital signs, ECG, and liver and renal function
tests. Maintain high urine output 2 to 3 ml/kg/hr in
patients with hemolysis or rhabdomyolysis, which may
prevent red blood cell breakdown products and myoglobin
from being deposited in the renal tubules.
o CHELATION -
1. BAL - Symptomatic patients unable to tolerate oral
medication should be treated with BAL 3 to 5 mg/kg/dose
IM every 4 to 12 hours. The dose and frequency depend
on the degree of toxicity seen. Higher doses of BAL
invariably cause adverse effects.
2. DMSA - Dimercaptosuccinic acid (DMSA) should be used as
soon as the patient is able to tolerate oral
medication. DOSE: 10 mg/kg every 8 hours for 5 days,
then decrease dosing to every 12 hours for 14 days.
It may be more effective and causes fewer side effects
than BAL.
3. PENICILLAMINE - An alternative in patients able to
tolerate oral medications. DOSE: D-penicillamine 100
mg/kg/day up to 2 g daily in four divided doses.
4. ENDPOINT - In severely ill patients, combined therapy
with both BAL and an oral agent should be considered.
Chelation therapy should be stopped when the urinary
arsenic level falls below 50 mcg per 24 hours. If
renal failure exists, dose of BAL and penicillamine
should be decreased after loading dose.
o FLUID/ELECTROLYTES - Monitor volume status; establish
adequate urine flow of at least 1 to 2 mL/kg/hr.
o X-RAY - Arsenic is radiopaque. Obtain abdominal film
and repeat as necessary to insure that gastric emptying
maneuvers have been effective. A chest radiograph
should also be obtained in patients with pulmonary
symptoms.
|
| Range of Toxicity: |
o Trivalent arsenic (arsenite) is more toxic than
pentavalent arsenic (arsenate). Acute ingestion of more
than 100 mg of inorganic arsenic is likely to cause
significant toxicity. Acute ingestion of 200 mg or more
of arsenic trioxide may be fatal in an adult.
|
Antidote and Emergency Treatment:
TREATMENT OF ARSENIC POISONING IN HANDBOOK OF COMMON POISONING IN CHILDREN AAP/FDA HANDBOOK.
1. FLUSH CONTAMINATED EYES, HAIR & SKIN WITH COPIOUS AMT OF FRESH WATER. 2. IN CASES OF POISONING BY RECENTLY INGESTED (UP TO 6 HR) ARSENICALS: A. INTUBATE STOMACH, ASPIRATE, & LAVAGE WITH 3 L OF /PRC- TAP WATER IN CHILDREN, ISOTONIC SALINE IN ADULTS/ ... /ARSENICALS/
A. USE ALL AVAILABLE PRECAUTIONS TO AVOID ASPIRATION OF VOMITUS: 1) IF VICTIM IS UNCONSCIOUS OR OBTUNDED, IT IS HELPFUL TO INSERT ENDOTRACHEAL TUBE (CUFFED, IF AVAILABLE) PRIOR TO INTUBATION. /ARSENICALS/
A. USE ALL AVAILABLE PRECAUTIONS TO AVOID ASPIRATION OF VOMITUS: 2) KEEP VICTIM'S HEAD BELOW LEVEL OF STOMACH DURING INTUBATION (TRENDELENBURG, OR LEFT LATERAL DECUBITUS, WITH HEAD OF TABLE TIPPED DOWNWARD). KEEP VICTIM'S HEAD TURNED TOWARD THE LEFT. /ARSENICALS/
A. USE ALL AVAILABLE PRECAUTIONS TO AVOID ASPIRATION OF VOMITUS: 3) ASPIRATE THE PHARYNX AS REGULARLY AS POSSIBLE TO REMOVE GAGGED OR VOMITED STOMACH CONTENTS. /ARSENICALS/
B. AFTER LAVAGE, INSTILL /PRC- 30 G ACTIVATED CHARCOAL IN 3-4 OZ OF WATER (CHILDREN), 100 G IN 8-10 OZ OF WATER (ADULTS)/ ... /ARSENICALS/
C. IF DIARRHEA OR COLIC HAVE NOT ENSUED WITHIN AN HOUR OF GASTRIC LAVAGE & CHARCOAL ADMIN, GIVE SODIUM SULFATE AS CATHARTIC (ADULTS, 12 YR & OLDER: 15 G IN 6-8 OZ OF WATER; CHILDREN UNDER 12: 0.2 G/KG BODY WT IN 1-6 OZ OF WATER. /ARSENICALS/
IF ARSENICAL ... INGESTED MORE THAN 48 HR PRIOR TO TREATMENT, OR IF EXCESSIVE ABSORPTION ... OCCURRED OVER EXTENDED PERIOD, /INITIAL/ TREATMENT SHOULD BE LIMITED TO /PRC- CHELATION THERAPY & SUPPORTIVE MEASURES/...PLUS NUTRITIONAL SUPLEMENTS TO RESTORE METABOLIC FUNCTIONS AS PROMPTLY AS POSSIBLE. /ARSENICALS/
ADMIN IV ELECTROLYTE & GLUCOSE SOLN TO MAINTAIN HYDRATION & ACCELERATE TOXICANT EXCRETION. COMBAT SHOCK WITH TRANSFUSIONS OF WHOLE BLOOD, & BY INHALATION OF 100% OXYGEN. CAUTION: MONITOR URINE FLOW VIA CATHETER. /ARSENICALS/
D. MONITOR FLUID BALANCE, BODY WT, &/OR CENTRAL VENOUS PRESSURE TO GUARD AGAINST FLUID OVERLOAD RESULTING FROM ACUTE TUBULAR NECROSIS (ANURIA). E. PROMPTLY ADMIN DIMERCAPROL (BAL, BRITISH ANTILEWISITE, DIMERCAPTOPROPANOL) IM, AS 10% SOLN IN VEGETABLE OIL, TO NEUTRALIZE THE TOXIC ACTION OF ARSENICALS. /ARSENICALS/
E. RECOMMENDED DOSAGE SCHEDULE /FOR BAL/ IS: MILD POISONING DAYS 1 & 2: 2.5 MG/KG Q6H X 8 DOSES; DAY 3: 2.5 MG/KG Q12H X 2 DOSES, SUCCEEDING...DAYS: 2.5 MG/KG.../PRC: EVERY 24 HR/. /ARSENICALS/
E. RECOMMENDED DOSAGE SCHEDULE /FOR BAL IN/ ... SEVERE POISONING: DAYS 1 & 2: 3.0 MG/KG Q4H X 12 DOSES; DAY 3: 3.0 MG/KG Q6H X 4 DOSES: SUCCEEDING ... DAYS: 3.0 MG/KG ... /PRC: EVERY 12 HR/. /ARSENICALS/
E. CAUTION: BAL ... CAN CAUSE TROUBLESOME SIDE EFFECTS (HYPERTENSION, TACHYCARDIA, NAUSEA, HEADACHE, PARESTHESIAE & PAIN, LACRIMATION, SWEATING, ANXIETY & RESTLESSNESS). ALTHOUGH USUALLY NOT SO SEVERE AS TO HANDICAP TREATMENT, THESE MANIFESTATIONS MAY REQUIRE ANTIHISTAMINIC THERAPY ... /ARSENICALS/
F. INTENSE ABDOMINAL PAIN MAY REQUIRE MORPHINE (ADULTS, 12 YR & OLDER: 4-15 MG; CHILDREN UNDER 12: 0.1-0.2 MG/KG). /ARSENICALS/
Animal Toxicity Studies:
Evidence for Carcinogenicity:
CLASSIFICATION: A; human carcinogen. BASIS FOR CLASSIFICATION: Based on sufficient evidence from human data. An increased lung cancer mortality was observed in multiple human populations exposed primarily through inhalation. Also, increased mortality from multiple internal organ cancers (liver, kidney, lung, and bladder) and an increased incidence of skin cancer were observed in populations consuming drinking water high in inorganic arsenic. HUMAN CARCINOGENICITY DATA: Sufficient. ANIMAL CARCINOGENICITY DATA: Inadequate. /Inorganic Arsenic/
A1. A1= Confirmed human carcinogen. (1993) /Arsenic, elemental and inorganic cmpd (except Arsine), as As/
Classification of carcinogenicity: 1) evidence in humans: sufficient; 2) evidence in animals: limited. Overall summary evaluation of carcinogenic risk to humans is Group 1: Carcinogenic to humans. This evaluation applies to arsenic and arsenic cmpd as a whole and not necessarily to all individual chemicals within the group. /Arsenic and arsenic cmpds/
Non-Human Toxicity Excerpts:
PERACUTE ARSENICAL POISONING MAY LEAD TO DEATH SO RAPIDLY THAT ILLNESS IS NEVER OBSERVED. WHEN SYMPTOMS DO MANIFEST THEMSELVES THEY INCL INTENSE ABDOMINAL PAIN, STAGGERING GAIT, COLLAPSE, PARALYSIS & DEATH. /ARSENIC/
IN ACUTE CASES THE MOST PROMINENT SYMPTOMS ARE SALIVATION, THIRST, VOMITION WHERE POSSIBLE, VIOLENT COLIC, WATERY DIARRHEA SOMETIMES HEMORRHAGIC, EXHAUSTION ... /ARSENIC/
/CHRONIC SYMPTOMS:/ ... INDIGESTION, THIRST, WASTING & GENERAL APPEARANCE OF UNTHRIFTINESS, WITH A DRY STARING COAT & BRICK RED COLORATION OF THE VISIBLE MUCOUS MEMBRANES; PULSE IS WEAK & IRREGULAR, BUT TEMPERATURE IS NORMAL. /ARSENIC/
Arsenite showed positive mutagenic effects in an Escherichia coli point mutation assay, and in an Escherichia coli DNA repair assay, but negative results in the dominant lethal assay. /Arsenite/
Both arsenite and arsenate cause embryotoxic and teratogenic effects in albino Swiss-wistar mice (CO-1) with 40 mg/kg ip at days 7-12 of gestation. /Arsenic compd/
Of leghorn chicken embryos injected with arsenate (3 ug/egg) on days 2-4, those treated on day 2 were normal. Of day 3 treated embryos, 21% had abnormalities while 32.5% of day 4 treated embryos had abnormalities. /Arsenic compds/
The effect of phosphates, arsenates, and arsenites on the growth of the As-oxidizing microorganisms Pseudomonas putida and Alcaligenes eutrophus was studied in the presence of yeast extract, glucose, fish peptone agar, sodium citrate, sodium acetate, and sodium lactate. The toxic effect of arsenates could be reduced by the addition of phosphates. Phosphates caused the highest inhibitory effect on the growth or arsenite-oxidizing bacteria. /Arsenites and arsenates/
Acute toxicity of arsenite and arsenate to hydrobiont, mosquito larvae, and rat was widely different. In a 28-day study, the degree of toxicity of As (III) and As (V) was nearly equal. The chronic toxicodynamic indicators of both As compd were similar. The effective concn of arsenite and arsenate is 0.05 mg/kg, and 0.01 mg/kg is the min ED for these As compd. Among the gonadotoxic effects examd, both arsenite and arsenate had no effect on acid and osmotic resistance of spermatocytes and size of the gonads. The erythrocyte number in the blood, corproporphyrin excretion in the urine, and activity of aspartate aminotransferase in the blood serum underwent similar charges by arsenite and arsenate. Thus, the valence of As has no effect on its toxicity. /Arsenites and arsenates/
Inorganic arsenic (V) was slightly more toxic than arsenic (III) to rainbow trout, but arsenic (III) was nearly twice as toxic to the fathead minnow and Daphnia magna. /Arsenic (III) and arsenic (V)/
Arsenic (V) is more toxic than arsenic (III) to the amphipod, Ampelisca abdita, whose Species Mean Acute Values are 4,610 ug/L for arsenic (V) and 8,227 ug/L for arsenic (III). /Arsenic (III) and arsenic (V)/
The effects of certain monovalent (Ag1+ and Li1+), divalent (Hg2+, Cu2+, Zn2+, Co2+, Fe2+, Pb2+, Mn2+, Sn2+, Ni2+, and Se2+) and trivalent (Fe3+, As3+, and Al3+) metals on a mitochondrial prepn of K+-stimulated-p-nitrophenyl phosphatase from rat brain were studied. Except for salts of Ni2+, Se2+, and Li2+, which did not produce 50% inhibition, all of the metals examd were potent inhibitors of the enzyme with a 150 value of 490 muM for As3+. ... Salts of Ag+ and Li+ were the most toxic for this enzyme. All metals showed concn dependent inhibition except Li+. The order of their potency was Ag1+ > Hg2+ > Cu2+ > Cd2+ > Zn2+ > Co > Fe2+ > Pb2+ > Fe3+ > Mn2+ > As3+ > Sn2+ > Al3+ > Ni2+ > Se2+ > Li1+. /Arsenite/
Dysfunction of the blood-brain barrier was indicated in rats fed arsenite at a concn of 500 mg/kg ... in a cereal diet for 35 days. /Arsenite/
Arsenic (III) increased albinism in channel catfish. /Arsenic (III)/
Cladophora sp (alga) 2,320 ug/L/2 wk, toxic effect: 100% kill. /Arsenite/
Spirogyra sp (alga) 2,320 ug/L/2 wk, toxic effect: 100% kill. /Arsenite/
Zygnema sp (alga) 2,320 ug/L/2 wk, toxic effect: 100% kill. /Arsenite/
Potomageton sp (submerged plant) 2,320 ug/L/1 mo, toxic effect: 95% kill. /Arsenite/
Non-Human Toxicity Values:
LD50 mouse oral 11.2 ppm/96 hr /Arsenite/
LD50 rat oral 11.2 ppm/96 hr /Arsenite/
LC50 Carassius auratus (goldfish, juvenile) 18,618 ug/l/336 hr /Arsenite/
LC50 Carassius auratus (goldfish, embryo-larval) 490 ug/l/7 days /Arsenite/
Ecotoxicity Values:
LC50 Penaeus seliferus (white shrimp, juvenile) 24,700 ug/l/96 hr /Arsenite/
LC100 Oncorhynchus gorbuscha (pink salmon) 12,307 ug/l/96 hr; 7,195 ug/l/day /Arsenite/
LC50 Oncorhynchus keta (chum salmon) 8,330 ug/l/48 hr /Arsenite/
LC50 Daphnia magna (cladoceran) 2,850 ug/l/3 wk /Arsenite/
LT50 Lepomis cyanellus (green sunfish) 60,000 ug/l/678 hr at 10 deg C; 60,000 ug/l/210 hr at 20 deg C; 60,000 ug/l/124 hr at 30 deg C; 30,000 ug/l/527 hr at 20 deg C; 30,000 ug/l/209 hr at 30 deg C /Arsenite/
LT50 Leopomis cyanellus (green sunfish, juvenile) 40,000 ug/l/39 hr /Arsenite/
LC50 Nereis diversicolor (polychaete worm) >14,500 ug/l/192 hr /Arsenite/
LC50 Notropois hudsonicus (spottail shiner) 27,000 ug/l/72 hr /Arsenite/
LC50 Pimephales promelas (fathead minnow, juvenile) 10,556 ug/l/336 hr /Arsenite/
LC50 Pimephales promelas (fathead minnow) 82,400 ug/l/96 hr /Arsenite/
LC50 Lepomis macrochirus (bluegill, juvenile) 18,328 ug/l/336 hr /Arsenite/
LC50 Lepomis macrochirus (bluegill, fingerling) 290 ug/l/48 hr /Arsenite/
LC50 Gastrophryne carolinensis (toad, embryo-larval) 40 ug/l/7 days /Arsenite/
LC50 Salmo gairdneri (rainbow trout) 540 ug/l/28 days /Arsenite/
LC50 Salvelinus fontinalis (brook trout) 10,440 ug/l/262 hr /Arsenite/
LC50 bay scallop 3,490 ug/l/96 hr /Arsenite/
LC50 American oyster 7,500 ug/l/48 hr /Arsenite/
LC50 Daphnia magna 4,340 ug/l/96 hr /Arsenic (III)/
Metabolism/Pharmacokinetics:
Metabolism/Metabolites:
SOME PENTAVALENT ARSENICALS ARE PARTLY REDUCED IN VIVO TO THE TRIVALENT FORM. HOWEVER, THE REDOX EQUILIBRIA IN VIVO FAVOR OXIDATION, & TRIVALENT ARSENIC IS SLOWLY OXIDIZED IN THE BODY TO THE PENTAVALENT STATE. /ARSENIC COMPD/
... IN VIVO METHYLATION OF INORG ARSENIC HAS BEEN DEMONSTRATED BOTH IN ANIMALS & HUMANS /BY TRANSFORMATION OF TRIVALENT TO PENTAVALENT STATE/. THE MAJOR FORM OF ARSENIC IN URINE OF BOTH EXPOSED & UNEXPOSED HUMANS IS DIMETHYLARSINIC ACID. METHYLARSONIC ACID & INORG ARSENIC ARE ALSO PRESENT BUT IN LOWER CONCN. /ARSENIC COMPD/
The toxicity of products formed as a result of bacterial (Pseudomonas putida and Alcaligenes eutrophus) oxidation of arsenites is significantly greater than that of the corresponding amounts of mineral arsenates. According to the toxicity on the investigated materials, the toxicity of these compounds may be equated with that of trivalent As compd, sometimes even higher. /Arsenites and arsenates/
When a 30 yr old man was given wine with 50 ug trivalent and 13 ug pentavalent arsenic, the major excreted form in urine, in 61 hours, was dimethylarsinic acid (50%). Trivalent and pentavalent arsenic each accounted for 8 percent and methyl arsenic acid for 14 percent.
Absorption, Distribution & Excretion:
COMPOUNDS OF ARSENIC MAY BE ABSORBED AFTER INGESTION OR BY INHALATION. /ARSENIC COMPD/
FOLLOWING INTRAVENOUS INJECTION OR ABSORPTION INTO THE BLOOD, MOST OF THE INORGANIC ARSENIC IS BOUND TO THE GLOBIN OF HEMOGLOBIN IN ERYTHROCYTES; ARSENIC IS ALSO BOUND TO SERUM PROTEINS. /ARSENIC/
SYSTEMIC TOXIC EFFECTS HAVE RESULTED FROM OCCUPATIONAL ACCIDENTS WHERE ARSENIC ACID OR ARSENIC TRICHLORIDE ... SPLASHED ON WORKERS, INDICATING THAT THE SKIN IS POSSIBLE ROUTE OF ABSORPTION OF ARSENIC. AFTER ABSORPTION BY THE LUNGS OR IN THE GI TRACT, ARSENIC IS TRANSPORTED BY THE BLOOD TO OTHER PARTS OF BODY. /ARSENIC COMPD/
ARSENIC IS STORED MAINLY IN LIVER, KIDNEY, WALL OF GI TRACT, SPLEEN, & LUNG. MUCH SMALLER AMT ... IN MUSCLE & NEURAL TISSUE. BECAUSE OF HIGH SULFHYDRYL CONTENT OF KERATIN, HIGH CONCN OF ARSENIC ARE FOUND IN HAIR & NAILS. DEPOSITION IN HAIR STARTS WITHIN 2 WK AFTER ADMIN & ARSENIC STAYS FIXED AT THIS SITE FOR YEARS. /ARSENIC/
/ARSENIC/ ... IS ALSO DEPOSITED IN BONE & RETAINED THERE FOR LONG PERIODS. ARSENIC READILY CROSSES THE PLACENTAL BARRIER, & FETAL DAMAGE HAS BEEN REPORTED IN ANIMALS & HUMAN BEINGS. /ARSENIC COMPD/
ARSENIC IS NOT FOUND IN MILK. /ARSENIC/
IN THE HUMAN FETUS...INCREASING ARSENIC LEVELS /WERE REPORTED/ WITH LENGTH OF PREGNANCY. THE ARSENIC LEVELS IN BONE, LIVER, SKIN & BRAIN WERE 2-4 TIMES HIGHER IN NEWBORN BABIES COMPARED TO 7-MONTH-OLD FETUSES. /ARSENIC/
THE FRACTION OF A DOSE OF TRIVALENT ARSENICAL THAT IS ABSORBED IS EXCRETED SLOWLY. WHILE ARSENIC IS ELIMINATED BY MANY ROUTES (FECES, URINE, SWEAT, MILK, HAIR, SKIN, LUNG), MOST IS EXCRETED IN URINE & FECES. ARSENITE SALTS ARE EXCRETED MAINLY IN THE FECES. /TRIVALENT ARSENIC/
IT MAY TAKE 10 DAYS FOR COMPLETE ELIMINATION OF ARSENITE AFTER A SINGLE DOSE & UP TO 70 DAYS AFTER REPEATED ADMIN. THIS SLOW EXCRETION IS THE BASIS FOR THE CUMULATIVE TOXIC ACTION OF ARSENIC. /ARSENITE/
The distribution of 74-As-labeled arsenate and arsenite in pregnant mice and a monkey has been studied by autoradiography and gamma counting of isolated tissues, and their in vitro toxicity to a chondrogenic system has been investigated. With both arsenic forms, given as single iv injections to the mother, the 74-As-arsenic appeared to pass the mouse placenta relatively freely and approximately to the same extent. The retention time in maternal tissues including the placenta was, ... around three times longer with arsenite than with arsenate. In early gestation, high activity was registered in the embryonic neuroepithelium, which correlates well with reported CNS malformations in rodents. In late gestation, the distribution pattern was more like that in the adults. Accumulation in skin and squamous epithelia of the upper gastrointestinal tract (oral cavity, esophagus, and esophageal region of stomach) dominated the distribution picture, especially at a long survival interval. Arsenate, but not arsenite, showed affinity for the calcified areas of the skeleton. A marmoset monkey in late gestation receiving arsenite showed a somewhat lower rate of placental transfer than the mice. Skin and liver had the highest concn (at 8 hr), both in mother and fetuses. This species is known not to methylate arsenic, resulting in stronger binding and longer retention times of arsenic as compared with other species. The stronger binding in maternal tissues may possibly explain the lower rate of placental transfer. Arsenite was shown to inhibit cartilage formation in a chick limb bud mesenchymal spot culture system (ED50 approximately 5-10 uM), while arsenate seemed to be without effect at concn up to 200 uM (highest tested). Arsenate, however, showed a potentiation of the arsenite toxicity. /Arsenite and arsenate/
The absorption of orally administered 74-As-labelled trivalent and pentavalent arsenic (checked as to valence state at the time of exposure) has been studied in mice. The elimination of arsenic with feces during the first 48 hr was 6-9% of the dose (0.4 or 4 mg/kg body weight) for both valence forms. As about the same fecal elimination of arsenic was seen after subcutaneous administration, the results indicate almost complete initial absorption from the gastrointestinal tract following oral administration. /Arsenite and arsenate/
Methylated arsenic has been detected in the urine of cows and dogs fed arsenate or arsenite. When the dogs were fed doses of about 1.0 mg As/kg body weight of either valence form for 5 days, approximately equal amounts of inorganic and methylated arsenic were excreted in the urine. The cows produced about 3 times as much methylated arsenic as inorganic arsenic in their urine. /Arsenite and arsenate/
In human subjects ingesting arsenite in amounts ranging from 125-1,000 ug/day for 5 days, it was calculated that a steady state condition for excretion occurred within 5 days. With steady state, 60% of daily intake is excreted daily.
Biological Half-Life:
THE BIOLOGICAL T/2 OF ARSENIC IN RATS AFTER A SINGLE EXPOSURE IS LONG (ABOUT 60 DAYS) DUE TO ACCUM ARSENIC IN BLOOD. IN OTHER ANIMALS & IN HUMANS MAJOR PART ... IS ELIMINATED AT MUCH HIGHER RATE. 3 DIFFERENT PHASES ... IN URINARY EXCRETION IN MAN AFTER 1 IV INJECTION OF ... ARSENITE ... T/2 OF ABOUT 2 HR, 8 HR & 8 DAYS. /ARSENITE/
Mechanism of Action:
Enzyme sensitivity to arsenite toxicity: 2X10-4 M arsenite caused 100% inhibition of pyruvate dehydrogenase. /Arsenite/
Enzyme sensitivity to arsenite toxicity: 0.7X10-3 M arsenite causes 48% inhibition of adenylate cyclase. /Arsenite/
Although various classes of enzymes are sensitive to arsenite, the oxidizing enzyme systems appear to be particularly vulnerable, including: pyruvate oxidase, D-amino acid oxidase, 2-glutamic acid oxidase, monoamine oxidase, liver choline oxidase, and glucose oxidase. /Arsneite/
Arsenite is known to be a potent inhibitor of chicken liver xanthine dehydrogenase and related molybdoflavoproteins and probably interacts with the molybdenum center in these enzymes. /Arsenite/
The trivalent form can chemically interfere directly with enzyme action via formation of arsenic-sulfur bonds with those thiol groups which participate in either enzyme structure or function. /Trivalent arsenic/
TRIVALENT ARSENICALS ... ARE REGARDED PRIMARILY AS SULFHYDRYL REAGENTS. AS SUCH, THEY INHIBIT MANY ENZYMES. THE PYRUVATE DEHYDROGENASE SYSTEM IS ESPECIALLY SENSITIVE TO TRIVALENT ARSENICALS BECAUSE OF THEIR INTERACTION WITH TWO SULFHYDRYL GROUPS OF LIPOIC ACID TO FORM A STABLE SIX-MEMBERED RING ... /ARSENITE/
Interactions:
The effect of the chelating agent dimercaprol (BAL) on the embryotoxic and teratogenic effects of arsenite (As3+) was determined. BAL (sc,30 mg/kg) was administered to pregnant CD-1 mice, either 8 and 4 hr prior to or 4 and 8 hr after a 12 mg/kg ip dose of arsenite; other females received a single sc injection of 60 mg/kg BAL concurrently with the arsenite. Treatments were given on gestation day 9 or 12 (copulation plug = day 1). Controls received sc corn oil or ip H2O, with or without arsenite or BAL. Arsenite treatment caused gross and skeletal malformations and prenatal deaths, while controls were unaffected when BAL was given prior to arsenite on Day 9, incidences of prenatal mortality and skeletal malformation were significantly diminished and on day 12, BAL protected against fetocidal effects of arsenite when given concurrently with the arsenite. According to these results, BAL is unlikely to have a practical beneficial effect on the arsenite exposed conceptus, because it must be administered prior to the teratogen (or perhaps simultaneously with it) to be effective. /Arsenite/
Pharmacology:
Drug Warnings:
Food and Environmental Agents: Effect on Breast-Feeding: Reported Sign or Symptom in Infant or Effect on Lactation: Fluorides: None. /from Table 7/
Interactions:
The effect of the chelating agent dimercaprol (BAL) on the embryotoxic and teratogenic effects of arsenite (As3+) was determined. BAL (sc,30 mg/kg) was administered to pregnant CD-1 mice, either 8 and 4 hr prior to or 4 and 8 hr after a 12 mg/kg ip dose of arsenite; other females received a single sc injection of 60 mg/kg BAL concurrently with the arsenite. Treatments were given on gestation day 9 or 12 (copulation plug = day 1). Controls received sc corn oil or ip H2O, with or without arsenite or BAL. Arsenite treatment caused gross and skeletal malformations and prenatal deaths, while controls were unaffected when BAL was given prior to arsenite on Day 9, incidences of prenatal mortality and skeletal malformation were significantly diminished and on day 12, BAL protected against fetocidal effects of arsenite when given concurrently with the arsenite. According to these results, BAL is unlikely to have a practical beneficial effect on the arsenite exposed conceptus, because it must be administered prior to the teratogen (or perhaps simultaneously with it) to be effective. /Arsenite/
Minimum Fatal Dose Level:
Fatal human dose 70-180 mg. Estimated lethal dose for a 70 kg human as As (III) /Arsenic (III)/
PROBABLE ORAL LETHAL DOSE (HUMAN) IS LESS THAN 5 MG/KG, A TASTE (LESS THAN 7 DROPS) FOR 70 KG PERSON (150 LB). /ARSENITES/
Environmental Fate & Exposure:
Probable Routes of Human Exposure:
... KNOWN TO CAUSE SEVERE DAMAGE TO THE RESPIRATORY SYSTEM UPON INHALATION. /ARSENIC COMPD/
COMPOUNDS OF ARSENIC MAY BE ABSORBED AFTER INGESTION. /ARSENIC COMPD/
... THE SKIN IS POSSIBLE ROUTE OF ABSORPTION OF ARSENIC. /ARSENIC COMPD/
Environmental Fate:
Aquatic: All of the arsenic halides are covalent compounds that hydrolyze in the presence of water. /Arsenic halides/
Aquatic: In aerobic water, inorganic arsenic (III) is slowly oxidized to arsenic (V) at neutral pH, but the reaction proceeds measurably in several days in strongly alkaline or acidic solutions. /Arsenic (III) and arsenic (V)/
Aquatic: Total As, arsenate and arsenite concn profiles for the water column of Saanich Inlet, an intermittently anoxic fjord located on Vancouver Island, B.C., Canada, were measured using independent analytical techniques for total As and As speciation to evaluate the accuracy of the speciation technique in oxic and anoxic marine environments. Total As profiles indicated a mid-depth minimum to approximately 1.0 ppb above the oxic-anoxic interface and an enrichment in the anoxic zone to approximately 2.0 ppb. This minimum may have been due to advection of As-poor water into Saanich Inlet at mid-depth or As incorporation onto solid phases within a bacteria- and Mn-rich particulate layer located immediately above the oxic-anoxic interface and subsequent removal via sinking particulate material. Ratios of total As to P in the deep, anoxic waters of the basin were similar to those reported for marine algae, suggesting that the enrichment of total As within the anoxic bottom layer may have been due to its release upon organic matter decomposition. Arsenate and arsenite concn vs depth profiles indicated a rapid (but incomplete in a thermodynamic sense) response to the oxic-anoxic interface. The arsenate/arsenite concn ratio was 15/1 in the oxic region of the water column and 1/12 in ferric-ferrous ... interconversions. Measurements of arsenite oxidation rates at near-ambient arsenite concn and temperatures using an 74-As3+ radioactive tracer technique indicated that arsenite oxidation was initially 10-fold faster in seawater taken from the Mn-rich particulate layer at 165 m depth than in seawater collected near the surface at 50 m depth. Addition of antibiotics to seawater from 165 m depth initially suppressed the rate of arsenite oxidation, indicating that it may have been partially microbially mediated. /Arsenate and arsenite/
Aquatic: Elevated As concn were found in groundwater near Canal Fulton, Ohio. The hydrologic and chemical properties of the area were studied to determine the source of the As and evaluate the possibility of a similar problem occurring elsewhere. Two major aquifer systems existed within the study area: the Sharon Sandstone of the upland areas and the outwash sand and gravel deposits of the buried valleys. Groundwater flow was generally from the north but local variations were caused by the Tuscarawas River Valley on the south and west of the study area. Within the study area, there was no evidence for an anthropogenic source of As to the groundwater. Agricultural soils, abandoned underground coal mines, industrial impoundments to the north and an abandoned industrial dump site within the study area were all eliminated as possible sources for the As. The As in Canal Fulton groundwater was entirely inorganic, consisting of about equal parts of arsenate and arsenite. Reduction-oxidation liberated Fe and As to solution. A high correlation between ferrous Fe and total dissolved As supported this model. It was hypothesized that Eh conditions had been lowered in the aquifer by the recent introduction of methane gas or the deposition of a thick layer of till during the last glacial retreat. The methane gas could have been leaking from deep underground storage at the site and reduced oxidized compounds. The deposition of till would have eliminated local recharge of oxygenated waters. /Arsenate and arsenite/
Environmental Bioconcentration:
Aquatic organisms accumulate arsenic but do not biomagnify it. /Arsenic compds/
Selective detection of inorganic and organic As by the solvent extraction method was done with 20 species of marine organisms, including fish, ascidian, holothurian, sea urchin, crustacean, shellfish, cephalopod, polychaete, and seaweed. In all species, inorganic As, which is more highly toxic than organic As, comprised only a small part (0-7%) of the total As; the one exception was in the seaweed, Hizikia fusiforme, in which inorganic As accounted for 60% of the total As. Furthermore, when As in water-sol and fat-sol fractions was detected, the ratio of water-soluble As reached 58-97% of the total As. Especially in the cephalopod (3 species) and fish (6 species), >84% of the total As was found in the water-soluble fraction. Thus, most arsenicals in marine organisms are present in water-soluble organic forms. /Arsenite and arsenate/
Environmental Water Concentrations:
Studies on the molecular forms of arsenical compd have been reported. The concn ratio As (III)/As (V) was found to be 0.18 in some Sargasso sea water. Fluctuations in the As (III)/As (V) ratio from 0.02 to 0.09 in the saline water of Naragansett Bay appeared to be associated with phytoplankton activity. Sea water samples off Southern California also exhibited a variable As (III)/As (V) ratio, again associated with biological activity. In some instances, the As (III) concn exceeded those of As (V). The same type of biological activity was observed in natural fresh waters. It is evident that the presence of arsenic (III) compd is the result of some reductive activity, which could be either biological or a non-biological effect of dissolved organic matter on arsenic (V). /Arsenite and arsenate/
Water from two groundwater supplies with very high levels of arsenic (224 and 280 mg/L) was analyzed and it was found that about 50% was present as arsenic (III). In a groundwater fed stream, 26% of the total arsenic (0.08 mg/L) was in the form of trivalent arsenic. Arsenic speciation has also been performed on well water samples from an area in Alaska containing high levels of arsenic. In 5 samples containing arsenic concn ranging from 0.52 to 3.6 mg/L, between 3% and 39% of the arsenic present was trivalent, the rest being pentavalent. /Arsenite/
Atmospheric Concentrations:
Workers may be exposed to airborne arsenic in cutting and sawing operations on wood treated with arsenic-containing preservatives. Concn of arsenic in air were found to be 0.043-0.36 mg/cu m originating from the sawing of wood treated with copper, chromium, and arsenic salts. The duration of measurement was 100 min. Only about 5% of the dust particles (on a mass basis) were less than 10 um. /Arsenite and arsenate/
Food Survey Values:
Wine contains high levels of arsenite from reduction during fermentation. Wine made from the musk contains even higher levels of arsenite than normal. /Arsenite/
Environmental Standards & Regulations:
TSCA Requirements:
Reported in EPA TSCA Inventory, 1983.
Atmospheric Standards:
Listed as a hazardous air pollutant (HAP) generally known or suspected to cause serious health problems. The Clean Air Act, as amended in 1990, directs EPA to set standards requiring major sources to sharply reduce routine emissions of toxic pollutants. EPA is required to establish and phase in specific performance based standards for all air emission sources that emit one or more of the listed pollutants. Arsenic trifluoride is included on this list.
Clean Water Act Requirements:
The procedures described in the "Guidelines for Deriving Numerical National Water Quality Criteria for the Protection of Aquatic Organisms and Their Uses" indicate that, except possibly where a locally important species is very sensitive, freshwater aquatic organisms should not be affected adversely if the four-day average concn of arsenic (III) does not exceed 190 ug/L more than once every three years and if the one-hour average concn does not exceed 360 ug/L more than once every three years. /Arsenic (III)/
Federal Drinking Water Standards:
EPA 50 ug/l /Arsenic/
State Drinking Water Guidelines:
(AZ) ARIZONA 50 ug/l /Arsenic/
FDA Requirements:
FDA lists permissible levels of arsenic in food as follows: muscle meats, 0.5 ppm; edible meat by-products, 1.0 ppm; eggs, 0.5 ppm. /Inorganic arsenic compd/
Allowable Tolerances:
Tolerances for residues of arsenic-containing pesticides in fruits and vegetables (0.35-7 mg/kg), field crops (cotton, 0.7-2.8 mg/kg), and livestock (cattle and horses, 0.7-2.7 mg/kg). /Arsenic containing pesticides/
Chemical/Physical Properties:
Molecular Formula:
As-F3
Molecular Weight:
131.91
Color/Form:
OILY LIQUID
MOBILE LIQUID
Colorless
Boiling Point:
57.8 DEG C
Melting Point:
-5.95 DEG C
Density/Specific Gravity:
2.73 AT 15 DEG C/15 DEG C
Solubilities:
SOL IN ETHANOL, ETHER, BENZENE, AMMONIUM HYDROXIDE
Vapor Pressure:
100 MM HG AT 13.2 DEG C
Other Chemical/Physical Properties:
DECOMP IN WATER
MELTING POINT ALSO REPORTED AS -8.5 DEG C, BOILING POINT AS 63 DEG C; HYDROLYZED BY WATER; ETCHES GLASS
Aquatic: The pH of aqueous solutions appears to be the major factor in the relative stability of either valency form. It was found that trivalent arsenic in solutions at pH of 7.0 or 9.6 were oxidized to the extent of 70-90% within one week, compared to 25% conversion at pH 4.8. ... Rapid oxidation of As (III) /occurred/ in aqueous solution at room temperature, while storage at 4 deg C showed little conversion. /Trivalent arsenic/
It is not possible to separately measure total recoverable arsenic (III) and total recoverable arsenic (V). /Arsenic (III) and arsenic (V)/
Chemical Safety & Handling:
DOT Emergency Guidelines:
Health: 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. /Arsenic compound, solid, NOS/
Fire or explosion: 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. /Arsenic compound, solid, NOS/
Public safety: CALL Emergency Response Telephone Number on Shipping Paper first. If Shipping Paper not available or no answer, refer to appropriate telephone number listed on the inside back cover. Isolate spill or leak area immediately for at least 25 to 50 meters (80 to 160 feet) in all directions. Keep unauthorized personnel away. Stay upwind. Keep out of low areas. /Arsenic compound, solid, NOS/
Protective clothing: Wear positive pressure self-contained breathing apparatus (SCBA). Wear chemical protective clothing which is specifically recommended by the manufacturer. Structural firefighters' protective clothing is recommended for fire situations ONLY; it is not effective in spill situations. /Arsenic compound, solid, NOS/
Evacuation: Spill: See the Table of Initial Isolation and Protective Action Distances for highlighted substances. For non-highlighted substances, increase, in the downwind direction, as necessary, the isolation distance shown under "PUBLIC SAFETY". Fire: 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. /Arsenic compound, solid, NOS/
Fire: Small fires: Dry chemical, CO2 or water spray. Large fires: 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. Do not use straight streams. Fire involving tanks or car/trailer loads: 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 the ends of tanks. For massive fire, use unmanned hose holders or monitor nozzles; if this is impossible, withdraw from area and let fire burn. /Arsenic compound, solid, NOS/
Spill or leak: 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. /Arsenic compound, solid, NOS/
First aid: Move victim to fresh air. Call emergency medical care. Apply artificial respiration if victim is not breathing. Do not use mouth-to-mouth method if victim ingested or inhaled the substance; induce 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. /Arsenic compound, solid, NOS/
Skin, Eye and Respiratory Irritations:
Trivalent arsenic compounds are corrosive to the skin. /Trivalent arsenic compounds/
Hazardous Reactivities & Incompatibilities:
REACTION OF ARSENIC TRIFLUORIDE WITH PHOSPHORUS TRIOXIDE IS VERY VIOLENT.
SEE ARSENIC COMPD. ...ON CONTACT WITH ACIDS OR ACID FUMES, EMITS HIGHLY TOXIC FUMES... /ARSENIC COMPD/
With hexafluoroisopropylideneaminolithium: Interaction of the lithium derivative with a range of chloro- and fluoro- derivatives of arsenic ... during warming to 25 deg C tended to be violently exothermic in absence of solvent.
Hazardous Decomposition:
WHEN HEATED ... EMITS HIGHLY TOXIC FUMES OF /ARSENIC AND HYDROGEN FLUORIDE/.
Protective Equipment & Clothing:
(1) Where there is occupational exposure to inorganic arsenic compounds, protective clothing shall be provided by the employers. This may include underwear, gloves, coveralls, and a hood over the head and neck.
Preventive Measures:
Due to potential skin irritation associated with respirator use and arsenic dust exposure, workmen shall be permitted to leave the work area every 2 hours to wash their face and to obtain a clean respirator. /Inorganic arsenic/
Employees exposed to arsenic shall be provided with separate lockers or other storage facilities for street clothes and for work clothes. /Inorganic arsenic/
Employees exposed to arsenic shall wash their hands and exposed skin before eating or smoking during the work shift. No food shall be permitted in areas where arsenic is handled, processed, or stored. Employees shall not smoke in areas where arsenic is handled, processed, or stored. /Inorganic arsenic/
(1) Protective clothing shall be changed at least daily at the end of the shift. (2) Work clothing shall not be taken home by employees. (3) The employer shall ensure that precautions necessary to protect laundry personnel are observed when solid protective clothing is laundered. /Inorganic arsenic/
Air from the exhaust ventilation system shall not be recirculated into work areas, and necessary measures shall be taken to ensure that the discharge outdoors will not produce a health hazard to humans or animals. /Inorganic arsenic/
Shower baths shall be cleaned following use after each work shift. /Inorganic arsenic/
Stability/Shelf Life:
FUMES IN AIR
Shipment Methods and Regulations:
No person may /transport,/ offer or accept a hazardous material for transportation in commerce unless that person is registered in conformance ... and the hazardous material is properly classed, described, packaged, marked, labeled, and in condition for shipment as required or authorized by ... /the hazardous materials regulations (49 CFR 171-177)./
The International Maritime Dangerous Goods Code lays down basic principles for transporting hazardous chemicals. Detailed recommendations for individual substances and a number of recommendations for good practice are included in the classes dealing with such substances. A general index of technical names has also been compiled. This index should always be consulted when attempting to locate the appropriate procedures to be used when shipping any substance or article.
Storage Conditions:
MAY BE STORED IN IRON VESSELS.
May be stored in iron vessels.
Cleanup Methods:
Both arsenate and arsenite can be removed from the water column by coprecipitation or adsorption onto iron oxides. Arsenate species can also be removed by adsorption onto aluminum hydroxide and clays, while arsenite is readily adsorbed onto metal sulfides. /Arsenate and arsenite/
Occupational Exposure Standards:
OSHA Standards:
The employer shall assure that no employee is exposed to inorganic arsenic at concentrations greater than 10 ug/cu m averaged over any 8-hr period. /Arsenic, inorganic cmpd, as As/
Threshold Limit Values:
8 hr Time weighted Avg (TWA) 0.01 mg/cu m /Arsenic, elemental & inorganic cmpd (except Arsine), as As/
A1. A1= Confirmed human carcinogen. /Arsenic, elemental and inorganic cmpd (except Arsine), as As/
BEI (Biological Exposure Index): Inorganic arsenic metabolites in urine, end of workweek 50 ug/g creatinine. The determinant is usually present in a significant amt in biological specimens collected from subjects who have not been occupationally exposed. Such background levels are incl in the BEI value. /Arsenic and soluble compounds including arsine/
Excursion Limit Recommendation: Excursions in worker exposure levels may exceed three times the TLV-TWA for no more than a total of 30 min during a work day, and under no circumstances should they exceed five times the TLV-TWA, provided that the TLV-TWA is not exceeded.
Manufacturing/Use Information:
Major Uses:
CHEM INT FOR FLUORINE COMPOUNDS; CATALYST FOR FLUORINATIONS
Arsenic trifluoride is used ... in ion implantation (qv), and in synthesis of arsenic pentafluoride.
Component used in wood treatment products for weather and fungal resistance. /Metal arsenates and arsenites/.
Manufacturers:
Pennwalt Corporation, Hq, Pennwalt Building, Three Parkway, Philadelphia, PA 19102, (215) 587-7000; Chemicals Group; Subsidiary: Ozark-Mahoning Company, 1870 S Boulder Ave, Tulsa, OK 74119, (918) 585-2661
Methods of Manufacturing:
PROBABLY REACTION OF FLUORINE AND ARSENIC
[RUSSELL ET AL, J AM CHEM SOC 63, 2825 (1941); WOOLF, GREENWOOD, J CHEM SOC 2200 (1950); HOFFMAN, INORG SYN 4 151 (1953); KWASNIK IN HANDBOOK OF PREPARATIVE INORG CHEMISTRY VOL I, G BRAUER, ED (ACADEMIC PRESS, NY, 2ND ED 197 (1963))].
Arsenic trifluoride can be prepared by fluorination of arsenic (III) oxide with sulfuric acid and calcium fluoride, or with hydrofluoric acid or fluorosulfuric acid.
General Manufacturing Information:
The arsenites (trivalent) are the least stable of the arsenicals and are the most toxic to insects and plants and have been used chiefly as the toxicants in baits. The arsenates (pentavalent), although less insecticidal, are more stable and safer to plants and are favored as general-purpose stomach poisons. /Arsenates and arsenites/
Formulations/Preparations:
Wood treating compound with good weather resistance, low mammalian toxicity, and good resistance to fungal attack and water penetration. ... A suitable formulation was comprised of creosote 26.6%, pole oil 33.3%, NH4OH 40.5% (contg 5% As salts). /Arsenic salts/
Even commercially available isotopes of pentavalent arsenic have been shown to contain up to 98% of trivalent arsenic. /Arsenite and arsenate/
U. S. Production:
(1972) ND
(1975) ND
U. S. Imports:
(1972) ND
(1975) ND
U. S. Exports:
(1972) ND
(1975) ND
Laboratory Methods:
Clinical Laboratory Methods:
The radioactive tracer technique was used for studying the extraction and predicting the best conditions of separation of arsenic halides by organic solvents of different natures. Sulfuric acid was found to enhance the extraction of arsenic halides. Stomach and liver samples were used. /Arsenic halides/
Vol 1. Monitoring method: Analyte: arsenic; Matrix: Blood; Range: 0.016-0.6 ug/ml in 1 ml of blood; procedure: Anodic stripping voltammetry. /Arsenic/
The detn of traces of metals in the ... samples is preferably carried out by electrothermal at adsorption spectrophotometry (ET-AAS). Each matrix requires a specific anal program. For example, less than or equal to 12 trace elements can be detd semiautomatically in hairs after HN03 digestion. Not only toxic trace metals are examd, but also other traces which may interfere with these in the biol system. /Arsenites and arsenates/
Analytic Laboratory Methods:
ANALYTE: ARSENIC; MATRIX: AIR; RANGE: 0.198-0.903 MG/CU M; PROCEDURE: FLAMELESS ATOMIC ABSORPTION. /ARSENIC/
WATER SAMPLE, SILVER DIETHYLDITHIOCARBAMATE METHOD: [BALLINGO ET AL; J AMER WATER WORKS ASSOC 54:1424 (1962)]. /ARSENIC/
25.000-25.020. SPECTROPHOTOMETRIC DETERMINATION OF ARSENIC IN FOODS. /ARSENIC/
Sampling Procedures:
Air: The dusts and fumes of inorganic arsenic compounds can be collected on a cellulose membrane filter with a pore size of 5 um or less. /Inorganic arsenic compounds/
Special References:
Special Reports:
NIOSH; Criteria Document: Arsenic (1975) DHEW Pub. NIOSH 75-149
Nat'l Research Council Canada; Effects of Arsenic in the Canadian Environment (1978) NRCC No. 15391
USEPA; Ambient Water Quality Criteria Doc: Arsenic (1980) EPA 440/5-80-021
USEPA; Ambient Water Quality Criteria Doc: Arsenic (1984) EPA 440/5-84-033
WHO; Environ Health Criteria: Arsenic (1978)
DHHS/FDA; Guidance Document for Arsenic in Shellfish (1993)
Synonyms and Identifiers:
Related HSDB Records:
425 [ARSENIC TRIBROMIDE] (Analog)
422 [ARSENIC TRICHLORIDE] (Analog)
420 [ARSENIC TRIIODIDE] (Analog)
Synonyms:
ARSENIC FLUORIDE [ASF3]
**PEER REVIEWED**
ARSENOUS FLUORIDE
**PEER REVIEWED**
ARSENOUS TRIFLUORIDE
**PEER REVIEWED**
TL 156
**PEER REVIEWED**
TRIFLUOROARSINE
**PEER REVIEWED**
Formulations/Preparations:
Wood treating compound with good weather resistance, low mammalian toxicity, and good resistance to fungal attack and water penetration. ... A suitable formulation was comprised of creosote 26.6%, pole oil 33.3%, NH4OH 40.5% (contg 5% As salts). /Arsenic salts/
Even commercially available isotopes of pentavalent arsenic have been shown to contain up to 98% of trivalent arsenic. /Arsenite and arsenate/
RTECS Number:
NIOSH/CG5775000
Administrative Information:
Hazardous Substances Databank Number: 421
Last Revision Date: 20010808
Update History:
Field Update on 08/08/2001, 1 field added/edited/deleted.
Field Update on 05/16/2001, 1 field added/edited/deleted.
Complete Update on 03/24/2000, 1 field added/edited/deleted.
Complete Update on 02/08/2000, 1 field added/edited/deleted.
Complete Update on 02/02/2000, 1 field added/edited/deleted.
Complete Update on 11/18/1999, 1 field added/edited/deleted.
Complete Update on 09/21/1999, 1 field added/edited/deleted.
Complete Update on 08/26/1999, 1 field added/edited/deleted.
Complete Update on 05/04/1999, 1 field added/edited/deleted.
Complete Update on 03/29/1999, 1 field added/edited/deleted.
Complete Update on 02/11/1999, 1 field added/edited/deleted.
Complete Update on 11/23/1998, 1 field added/edited/deleted.
Complete Update on 11/12/1998, 1 field added/edited/deleted.
Complete Update on 06/02/1998, 1 field added/edited/deleted.
Complete Update on 02/25/1998, 1 field added/edited/deleted.
Complete Update on 10/17/1997, 1 field added/edited/deleted.
Complete Update on 08/11/1997, 1 field added/edited/deleted.
Complete Update on 05/08/1997, 1 field added/edited/deleted.
Complete Update on 04/01/1997, 2 fields added/edited/deleted.
Complete Update on 02/11/1997, 1 field added/edited/deleted.
Complete Update on 01/24/1997, 1 field added/edited/deleted.
Complete Update on 10/12/1996, 1 field added/edited/deleted.
Complete Update on 06/21/1996, 2 fields added/edited/deleted.
Complete Update on 06/07/1996, 1 field added/edited/deleted.
Complete Update on 05/10/1996, 1 field added/edited/deleted.
Complete Update on 03/21/1996, 1 field added/edited/deleted.
Complete Update on 01/19/1996, 1 field added/edited/deleted.
Complete Update on 07/17/1995, 1 field added/edited/deleted.
Complete Update on 05/26/1995, 1 field added/edited/deleted.
Complete Update on 03/16/1995, 2 fields added/edited/deleted.
Complete Update on 03/10/1995, 4 fields added/edited/deleted.
Field Update on 01/25/1995, 1 field added/edited/deleted.
Field Update on 12/21/1994, 1 field added/edited/deleted.
Field Update on 11/03/1994, 1 field added/edited/deleted.
Field Update on 11/02/1994, 1 field added/edited/deleted.
Complete Update on 09/16/1994, 1 field added/edited/deleted.
Complete Update on 08/18/1994, 2 fields added/edited/deleted.
Field Update on 08/17/1994, 1 field added/edited/deleted.
Complete Update on 05/05/1994, 1 field added/edited/deleted.
Complete Update on 03/25/1994, 1 field added/edited/deleted.
Complete Update on 10/28/1993, 1 field added/edited/deleted.
Complete Update on 08/07/1993, 1 field added/edited/deleted.
Field update on 12/12/1992, 1 field added/edited/deleted.
Complete Update on 12/03/1992, 1 field added/edited/deleted.
Complete Update on 01/23/1992, 1 field added/edited/deleted.
Complete Update on 10/22/1990, 3 fields added/edited/deleted.
Field Update on 02/10/1989, 1 field added/edited/deleted.
Complete Update on 03/08/1988, 2 fields added/edited/deleted.
Complete Update on 10/03/1986