Dimercaprol

124.23

124.22

1732058

200-433-7

760094|39515|4646

2810

DTXSID5040461

Viscous oily liquid|Colorless

V - Various

29309070

22.2

0.16 (est)

Clear colorless to slightly yellow Liquid

1.2385 g/cm³ @ Temp: 25 °C

77 °C

140 °C

>230 °F

n20/D 1.573(lit.)

H2O: 87 g/L (25 ºC)

2-8°C

7.4 hPa (100 °C)

4.3 (Air = 1)

Peritoneal-rat LD50: 105 mg/kg; oral-mouse LD50: 217 mg/kg

Flammable; burning produces toxic sulfur oxide fumes; patients use side effects; bleeding, dermatitis, redness and swelling of the skin

Pungent offensive odor of mercaptans

8.62(at 25 °C)

Henry's Law constant = 9.39X10-9 atm-cu m/mol at 25 °C (est)

8.62 (at 25 °C)|pKa1 = 8.62; pKa2 = 10.57 at 25 °C

Wt/vol conversion: 5.07 mg/cu m = 1 ppm|Readily oxidized; unstable in aqueous solutions|Hydroxyl radical reaction rate constant = 1.01X10-10 cu cm/molec-sec at 25 °C (est)

Moderately soluble in water with decomposition [Hawley].

Alcohols and Polyols

2,3-DIMERCAPTO-1-PROPANOL forms highly stable chelates with a variety of metal ions. (NTP, 1992) Organosulfides are incompatible with acids, diazo and azo compounds, halocarbons, isocyanates, aldehydes, alkali metals, nitrides, hydrides, and other strong reducing agents. Reactions with these materials generate heat and in many cases hydrogen gas. Many of these compounds may liberate hydrogen sulfide upon decomposition or reaction with an acid.

III

6.1

UN 2810 6.1/PG 3

3

22-36/37/38-36/38

26-36-24/25-23

UB2625000

Xn,Xi

Ventilated, low temperature and dry; stored separately from warehouse food

Stable. Combustible. Incompatible with strong oxidizing agents, many metals.

P261-P301 + P310-P305 + P351 + P338

H301-H315-H319-H335

SRP: Expired or waste pharmaceuticals shall carefully take into consideration applicable DEA, EPA, and FDA regulations. It is not appropriate to dispose by flushing the pharmaceutical down the toilet or discarding to trash. If possible return the pharmaceutical to the manufacturer for proper disposal being careful to properly label and securely package the material. Alternatively, the waste pharmaceutical shall be labeled, securely packaged and transported by a state licensed medical waste contractor to dispose by burial in a licensed hazardous or toxic waste landfill or incinerator.|SRP: At the time of review, regulatory criteria for small quantity disposal are subject to significant revision, however, household quantities of waste pharmaceuticals may be managed as follows: Mix with wet cat litter or coffee grounds, double bag in plastic, discard in trash.

The Approved Drug Products with Therapeutic Equivalence Evaluations List identifies currently marketed prescription drug products, including dimercaprol, approved on the basis of safety and effectiveness by FDA under sections 505 of the Federal Food, Drug, and Cosmetic Act.

This chemical is probably combustible. (NTP, 1992)

|Danger|H301 (94%): Toxic if swallowed [Danger Acute toxicity, oral]|P261, P264, P270, P271, P272, P280, P301+P310, P302+P352, P304+P340, P305+P351+P338, P312, P321, P330, P332+P313, P333+P313, P337+P313, P362, P363, P403+P233, P405, and P501|Aggregated GHS information provided by 50 companies from 9 notifications to the ECHA C&L Inventory. Each notification may be associated with multiple companies.

Fires involving this material can be controlled with a dry chemical, carbon dioxide or Halon extinguisher. (NTP, 1992)

Excerpt from ERG Guide 153 [Substances - Toxic and/or Corrosive (Combustible)]: 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. SPILL: Increase, in the downwind direction, as necessary, the isolation distance shown above. 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. (ERG, 2016)

SMALL SPILLS AND LEAKAGE: If you spill this chemical, FIRST REMOVE ALL SOURCES OF IGNITION. Then, use absorbent paper to pick up all liquid spill material. Seal the absorbent paper, as well as any of your clothing which may be contaminated, in a vapor-tight plastic bag for eventual disposal. Wash any surfaces you may have contaminated with a soap and water solution. Do not reenter the contaminated area until the Safety Officer (or other responsible person) has verified that the area has been properly cleaned. STORAGE PRECAUTIONS: You should store this material in a refrigerator. STORE AWAY FROM SOURCES OF IGNITION. (NTP, 1992)

RECOMMENDED RESPIRATOR: Where the neat test chemical is weighed and diluted, wear a NIOSH-approved half face respirator equipped with an organic vapor/acid gas cartridge (specific for organic vapors, HCl, acid gas and SO2) with a dust/mist filter. (NTP, 1992)

SRP: The scientific literature for the use of contact lenses by industrial workers is inconsistent. The benefits or detrimental effects of wearing contact lenses depend not only upon the substance, but also on factors including the form of the substance, characteristics and duration of the exposure, the uses of other eye protection equipment, and the hygiene of the lenses. However, there may be individual substances whose irritating or corrosive properties are such that the wearing of contact lenses would be harmful to the eye. In those specific cases, contact lenses should not be worn. In any event, the usual eye protection equipment should be worn even when contact lenses are in place.

Dimercaprol may cause eye irritation.

highly toxic

The intramuscular LD50 in rats is approximately 105 mg/kg; intraperitoneally 140 mg/kg. The intraperitoneal LD80 in mice is approximately 125 mg/kg. Dimercaprol has been shown in animal experiments to increase brain deposition of arsenite, organic mercury compounds and increase the toxicity of cadmium and lead. Dimercaprol has been shown to induce seizure in animal studies and also is nephrotoxic.|IDENTIFICATION: Dimercaprol is a therapeutic compound developed as an antidote against the vesicant arsenic was gases such as Lewisite. It is clear to slightly yellow liquid with a pungent odor of mercaptan. It is slightly soluble in water and vegetable oils. Arachis or peanut oil is used in pharmaceutical preparations. It is miscible in alcohol, benzyl benzoate, ether, methyl alcogol and other solvents. Dimercaprol is useful in the treatment of arsenic (organic and inorganic), gold and inorganic mercury poisoning. HUMAN EXPOSURE: The main risks are hypertension, tachycardia, cardiovascular collapse, convulsions, excitation, hyperglycemia and hypoglycemia. Special care should be taken in case of oliguria, hypertension and impaired hepatic function when the antidote is administered. The target organs are the kidneys, the cardiovascular and central nervous systems. The clinical effects are nausea, vomiting, headache, burning sensation of the lips, throat, mouth and eyes; lacrimation and salivation; sweating, rhinorrhea and burning sensation of the penis; a feeling of constriction or pain in the throat or chest, muscle pains and spasms and tingling of the skin of the hands; abdominal pain, anxiety, nervousness and weakness, uticaria and hyperpyrexia. Pain and sterile abscesses can result. Irritation of the skin and mucous membranes can be observed after local contact. This drug should always be administered as soon as possible by deep IM injection and never by IV or SC routes. Dimercaprol is well tolerated in children. The drug cannot be used in poisonings due to iron, cadmium, tellurium, selenium, vanadium and uranium. It is contraindicated in poisonings due to elemental mercury vapor, because it can further increase the metal in the brain. This drug should not be administered in case of renal and hepatic insufficiency and patients with hypertension. Dermal absorption is possible. Peak concentrations in the blood are obtained 30-60 min after IM injection. Dimercaprol is a lipophilic drug, it penetrates rapidly in intracellular spaces. The highest concentrations are found in the liver, kidneys, brain and small intestine. Glucuronic acid conjugates are excreted by the kidneys. Iron therapy should be given 24 hr or more after the last dose of dimercaprol. It should not be administered at the same time. Breath may smell like odor of a mercaptan. Hemolytic anemia was reported in individuals with G6PD deficiency. In children, dimercaprol may induce a transient reduction in polymorphonuclear leukocytes. ANIMAL STUDIES: In animal studies, the biological half life was short and metabolic degradation and renal excretion is complete within 6-24 hr. In animals a lethal dose of dithiols causes convulsions and severe spasm of the abdominal muscles shortly before death occurs. After injection of sublethal amounts of dimercaprol, the animals become apathetic and develop lacrimation, edema of the conjunctiva, blepharospasms, salivation and vomiting. With increasing doses they develop ataxia, analgesia, muscle tremor, nystagmus, tonic and clonic convulsions and death results during coma. In cats following an IV injection cardiovascular depression as indicated by a fall in systemic and pulmonary artery pressure. After repeated local applications in animals, sensitization dermatitis may develop. Chronic effects in animals include fatty degeneration of the liver and impairment of liver function. In animals, chronic parenteral administration increases white blood cell count by 30%. This drug induced malformations of the skeletal system, growth retardation and increased embryo lethality.

In clinical trials conducted in children with Wilson disease, serum aminotransferase levels generally improved or were stable during treatment with dimercaprol. There have been no clinical reports of acute liver injury with jaundice attributed to dimercaprol. Patients with Wilson disease typically have mild-to-moderate serum aminotransferase elevations and may have signs and symptoms of cirrhosis. Improvement in liver injury in Wilson disease typically requires months to years of treatment. The apparent lack of hepatotoxicity of dimercaprol may be due to the infrequency of its use, the typically short courses of therapy and the prominence of other side effects that limit its more prolonged administration.

...GUINEA PIGS ACUTELY POISONED BY IM INJECTION OF TELLURIUM OXIDE SHOWED SEVERE LESIONS OF KIDNEYS & LIVER & HIGHER MORTALITY RATE WHEN RECEIVING BAL...|Dimercaprol forms a toxic complex with iron, cadmium, selenium, or uranium. Iron therapy should not be given concurrently with dimercaprol, and it has been suggested that iron therapy be deferred until at least 24 hours after the last dose of dimercaprol.|Dimercaprol is a compound used in the treatment of mercury intoxication, however with low therapeutic efficacy. It is assumed that dimercaprol acts by reactivating target sulfhydryl-containing proteins. In the present investigation we studied the inhibitory effect of mercuric chloride treatment (3 days with 2.3 or 4.6 mg/kg HgCl2, sc) in mice on cerebral. renal and hepatic delta-aminolevulinate dehydratase (ALA-D) activity, and a possible reversal of the effect of mercury by dimercaprol (0.25 mmol/kg, 24 hr after the last mercury injection). Mercuric chloride did not inhibit cerebral delta-aminolevulinate dehydratase at the doses injected. Dimercaprol treatment did not restore the normal enzyme activity of the liver after the 25% inhibition caused by 4.6 mg/kg HgCl2. In the kidney, dimercaprol enhanced the inhibitory effect of 4.6 mg/kg mercuric chloride (from 35% after mercury treatment alone to 65% after mercury plus dimercaprol treatment). Mercury content increased in kidney after exposure to 2.3 or 4.6 mg/kg and the levels attained were higher than in any other organ. Mercury accumulated in liver only after exposure to 4.6 mg/kg HgCl2. and dimercaprol further increased mercury deposition. Dimercaprol treatment also increased the levels of mercury in brain of animals exposed to 4.6 mg/kg HgCl2. The enzymes from all sources presented similar sensitivity to the combined effect of HgCl2 and dimercaprol in vitro. In the absence of preincubation, 0-500 uM dimercaprol potentiated the inhibitory effect of HgCl2 on delta-aminolevulinate dehydratase activity. In the presence of preincubation, and 100 and 250 uM dimercaprol enhanced delta-aminolevulinate dehydratase sensitivity to mercury, whereas 500 uM dimercaprol partially protected the enzyme from mercury inhibition. Dimercaprol (500 uM) inhibited renal and hepatic delta-aminolevulinate dehydratase when preincubated with the enzymes. These data suggested that the dimercaprol-Hg complex may have a more toxic effect on delta-aminolevulinate dehydratase activity than Hg2+. Furthermore, the present data show that dimercaprol did not act by reactivating mercury-inhibited sulfhydryl-containing delta-aminolevulinate dehydratase, and that indeed it may have an inhibitory effect per se depending on the tissue.|Dimercaprol decreases insulin effectiveness by reducing disulfide bridges.

LD50 Mouse ip 125 mg/kg (approx)|LD50 Rat ip 140 mg/kg (approx)|LD50 Rat intramuscular 105 mg/kg (approx)

Dimercaprol has been reported to induce hemolysis (which may be severe) in individuals with glucose-6-phosphate dehydrogenase deficiency. Therefore, high-risk individuals should be screened for this deficiency, and susceptible patients should be monitored for hemolysis during therapy with dimercaprol.|Dimercaprol is contraindicated in patients with impaired hepatic function, except those with postarsenical jaundice. Dimercaprol also is contraindicated in individuals with known hypersensitivity to peanuts, since the injection is only available as a solution in peanut oil.|BAL in Oil Ampules is formulated with peanut oil. Peanut oil may cause allergic reactions in some individuals. Physicians should use caution in prescribing BAL in Oil Ampules for peanut-sensitive patients. Medication and equipment necessary to treat allergic reactions should be available if the product is administered to peanut-allergic patients

NIOSH (NOES Survey 1981-1983) has statistically estimated that 1,112 workers (572 of these were female) were potentially exposed to dimercaprol in the US(1).

For the treatment of arsenic, gold and mercury poisoning. Indicated in acute lead poisoning when used concomitantly with edetate calcium disodium (DB00974).|FDA Label

Dimercaprol, or British anti-Lewisite (BAL), is a parenterally administered heavy metal chelating agent that is used to treat arsenic, gold, copper and mercury poisoning. Dimercaprol has not been associated with serum enzyme elevations during therapy or with cases of clinically apparent liver injury with jaundice, but its general use has been quite limited.

Chelating Agents

Antidotes; Chelating Agents|Dimercaprol is the antidote of choice in the treatment of acute arsenic (except arsine), mercury, or gold poisoning resulting from ingestion of salts of these metals or following overdosage of therapeutic agents containing these metals. Dimercaprol administration should be accompanied by appropriate supportive measures and is most effective when administered early in the course of the poisoning. In the treatment of acute poisoning by mercury salts, dimercaprol is most effective if administered within 1-2 hours following ingestion, since extensive mercury-induced renal damage cannot be reversed. Dimercaprol is not effective in the treatment of poisonings resulting from monoalkyl mercury compounds, and the drug is only minimally effective in chronic mercury poisoning. Although dimercaprol is usually of no value in the treatment of hypersensitivity reactions to mercury compounds, mercury-induced acrodynia (pink disease) in infants and children responds to treatment with dimercaprol. Dimercaprol is usually effective in the treatment of chronic poisoning from inorganic or organic arsenicals, but may be of little value if aplastic anemia, hemorrhagic encephalitis, or jaundice has developed. In one patient who experienced protein-loss enteropathy in association with arsenic poisoning, hypoproteinemia and edema improved following dimercaprol therapy. The drug is ineffective in the treatment of poisoning resulting from arsine gas (AsH3). Gold-induced dermatitis and gold-induced thrombocytopenia may improve following dimercaprol therapy. /Use included in US product label/|Dermatologic or ocular manifestations of arsenic poisoning have been effectively treated with topical dimercaprol ointment or oil solution, respectively. /Use NOT included in US product label/|Although dimercaprol chelates lead, other agents (e.g., edetate calcium disodium (calcium EDTA), succimer) generally are preferred for the management of most cases of moderate lead poisoning. However, dimercaprol is useful as an adjunct to edetate calcium disodium and concomitant administration of the drugs is preferred, at least initially, in the management of patients with severe lead poisoning (blood lead concentrations exceeding 70 ug/dL) and/or in those with acute lead encephalopathy (which occurs most often in children). Concomitant administration of dimercaprol and edetate calcium disodium increases the rate of excretion of lead, lowers mortality, and may lower the incidence of brain damage as compared with the use of edetate calcium disodium alone; however, such concomitant therapy does not completely eliminate the risk of permanent severe residual brain damage. Since lead encephalopathy occurs only rarely in adults, experience with the use of the combination in these patients is limited; however, use of dimercaprol and edetate calcium disodium has resulted in prompt relief of symptoms in a few adults with lead encephalopathy. Although concomitant therapy with dimercaprol and edetate calcium disodium also has been recommended in symptomatic patients with blood lead concentrations less than 70 ug/dL, the American Academy of Pediatrics currently states that the toxicity of dimercaprol and the current availability of alternative drugs mandate its use only in the most serious cases of lead poisoning (i.e., blood lead concentrations exceeding 70 ug/dL or when symptoms suggestive of encephalopathy are present). Edetate calcium disodium generally is used alone (i.e., without dimercaprol) in asymptomatic patients with blood lead concentrations of 45-70 ug/dL. ... Dimercaprol is not useful in acute poisonings resulting from alkyl lead compounds (e.g., tetraethyl lead). /Use included in US product label/|For more Therapeutic Uses (Complete) data for Dimercaprol (9 total), please visit the HSDB record page.

Dimercaprol is potentially nephrotoxic. Since the chelate dissociates in acid medium, the urine should be kept alkaline during dimercaprol therapy to protect the kidneys. Dimercaprol should be used with caution and/or the dosage reduced in patients with oliguria. If acute renal failure develops during therapy, the drug should be discontinued or used very cautiously because serum concentrations of dimercaprol may reach toxic levels.|Adverse effects of dimercaprol are usually mild and transitory and occur in about one-half of patients who receive an IM dose of 5 mg/kg. If the dose of dimercaprol exceeds 5 mg/kg, most patients will experience vomiting, seizures, and stupor or coma which may begin within 30 minutes after injection and usually subside in 1-6 hours. Prophylactic or therapeutic administration of ephedrine or an antihistamine may prevent or relieve many of the mild adverse effects of dimercaprol. The most frequent adverse effect, a rise in systolic and diastolic blood pressure which is dose related and may be accompanied by tachycardia, may appear 15-30 minutes following the injection and blood pressure usually returns to normal within 2 hours. Frequently pain and occasionally sterile abscesses occur at the injection site, particularly if the drug is not administered deep IM.|Other adverse effects that may occur include nausea, vomiting, headache, sweating, and a feeling of constriction (or pain) in the throat, chest, or hands which may be accompanied by anxiety, nervousness or restlessness, and weakness. Muscular aches and pains, muscle spasms, tingling of extremities, and abdominal pain have also been reported.|Dimercaprol has a strong odor and imparts an unpleasant mercaptan-like odor to the patient's breath. The drug may also produce a burning sensation of the lips, mouth, throat, eyes, and penis, and pain in the teeth. Blepharal spasm, conjunctivitis, lacrimation, rhinorrhea, and salivation may also occur. When the drug is applied topically, it produces erythema and edema.|For more Drug Warnings (Complete) data for Dimercaprol (16 total), please visit the HSDB record page.

Due to its oily nature, dimercaprol is not absorbed orally and its administration requires a deep intra-muscular injection that is extremely painful and allergenic. It was found to mobilize and relocate lead to the brain, increasing its neurotoxic effects. Despite that fact that dimercaprol increases cadmium excretion, there is an associated increase in kidney cadmium concentration. Because of this, dimercaprol must be avoided in patients with cadmium toxicity.

Chemicals that bind to and remove ions from solutions. Many chelating agents function through the formation of COORDINATION COMPLEXES with METALS. (See all compounds classified as Chelating Agents.)

After intra-muscular injection.|Urine.|Because it is a lipophilic drug, dimercaprol penetrates rapidly the intracellular spaces. The highest concentrations are found in the liver, kidneys, brain and small intestine. Due to its lipophilic characteristic, the complexes formed with mercury and other metals may be redistributed into sensitive cells in the brain following dimercaprol treatment.|It is readily absorbed through the skin after topical application. Percutaneous absorption in rats and humans equals 3 millimol (124 mg)/sq cm per hour.|Following absorption, dimercaprol is distributed to all tissues (mainly in the intracellular space) including the brain, with highest concentrations in the liver and kidneys.|Following IM injection of therapeutic doses of dimercaprol, peak blood concentrations are attained in 30-60 minutes. Dimercaprol is slowly absorbed through the skin following topical application.|Dimercaprol is not absorbed orally. It is rapidly absorbed after intramuscular injection and persists for at least 12 hours. Approximately 80% of the dose is absorbed after 1 hours and 90% after 6 hours. Maximal blood concentrations are attained within 1 hour. Hepatic metabolism (by glucuronidation) and excretion are essentially complete within 4 hours. Dimercaprol is the only commonly used chelating agent that readily crosses cellular membranes; as a result, the concentration in certain organs (liver, kidney, small intestine) can be up to five times that in the blood.

... Metabolic degradation and excretion are essentially complete within 4 hours.|Dimercaprol not excreted as dimercaprol-metal complex is quickly metabolized by the liver and excreted as an inactive product in the urine.

The drug has a short half life.

The sulfhydryl groups of dimercaprol form complexes with certain heavy metals thus preventing or reversing the metallic binding of sulfhydryl-containing enzymes. The complex is excreted in the urine.|Dimercaprol is much more effective when given as soon as possible after exposure to the metal because it is more effective in preventing inhibition of sulfhydryl enzymes than in reactivating them. Dimercaprol antagonizes the biological actions of metals that form mercaptides with essential cellular sulfhydryl groups, principally arsenic, gold, and mercury. It also is used in combination with CaNa2EDTA to treat lead poisoning, especially when evidence of lead encephalopathy exists. Intoxication by selenites, which also oxidize sulfhydryl enzymes, is not influenced by dimercaprol|The pharmacological actions of dimercaprol result from formation of chelation complexes between its sulfhydryl groups and metals. The molecular properties of the dimercaprol-metal chelate have considerable practical significance. With metals such as mercury, gold, and arsenic, the strategy is to attain a stable complex to promote elimination of the met al. Dissociation of the complex and oxidation of dimercaprol can occur in vivo. Furthermore, the sulfur-metal bond may be labile in the acidic tubular urine, which may increase delivery of metal to renal tissue and increase toxicity. The dosage regimen therefore is designed to maintain a concentration of dimercaprol in plasma adequate to favor the continuous formation of the more stable 2:1 (BAL-metal) complex and its rapid excretion. However, because of pronounced and dose-related side effects, excessive plasma concentrations must be avoided. The concentration in plasma therefore must be maintained by repeated fractional dosage until the offending metal can be excreted.|Ca2+ is involved in the regulation of a variety of physiological processes, but a persistent increase in free cytosolic Ca2+ concentrations may contribute to cell injury. Dimercaprol (BAL) is a compound used in the treatment of mercury intoxication, but presents low therapeutic efficacy. The molecular mechanism responsible for the BAL toxicity is poorly known. In the present study, the effect of BAL and inorganic and organic mercury on Ca2+ transport by Ca2+-ATPases located in the sarco/endoplasmic reticulum of fast-skeletal muscle and brain was examined. Ca2+ uptake by brain and fast-skeletal muscle microsomes was inhibited in a dose-dependent manner by Hg2+. The calculated IC50 for Ca2+ uptake inhibition by HgCl2 was 1.05+/-0.09 microM (n = 8) for brain and 0.72+/-0.06 microM (n = 9) for muscle. The difference was significant at p < 0.01 (data expressed as mean +/- SD). At a low concentration (1 microM), 2,3-dimer-captopropanol had no effect on Ca2+ uptake by brain or muscle vesicles and did not abolish the inhibition caused by Hg2+. A high concentration of BAL (1 mM) nearly abolished the inhibition caused by 1.75 microM HgCl2 or 6 microM CH3HgCl in skeletal muscle. Surprisingly, at intermediate concentrations (40-100 microM) BAL partially inhibited Ca2+ transport in brain but had no effect on muscle. Furthermore, ATP hydrolysis by brain or muscle microsomes was not inhibited by BAL. These results suggest that in brain microsomes BAL affects in a different way Ca2+ transport and ATP hydrolysis. The increase in BAL concentration observed after toxic administration of this compound to experimental animals may contribute to deregulate Ca2+ homoeostasis and, consequently, to the neurotoxicity of BAL.

SYMPTOMS: Symptoms of exposure to this chemical may include a warm feeling, tingling sensations in the nose, mouth and skin; nausea, vomiting, restlessness, weakness, rapid pulse, rise in blood pressure, tremors, convulsions, tachycardia, headache, feeling of constriction or pain in the throat, chest or hands; conjunctivitis, lachrymation, rhinorrhea, salivation, sweating of the forehead, hands, etc.; abdominal pain and anxiety. ACUTE/CHRONIC HAZARDS: This compound is highly irritating to the skin, eyes and mucous membranes. It is a lachrymator. (NTP, 1992)

EYES: First check the victim for contact lenses and remove if present. Flush victim's eyes with water or normal saline solution for 20 to 30 minutes while simultaneously calling a hospital or poison control center. Do not put any ointments, oils, or medication in the victim's eyes without specific instructions from a physician. IMMEDIATELY transport the victim after flushing eyes to a hospital even if no symptoms (such as redness or irritation) develop. SKIN: IMMEDIATELY flood affected skin with water while removing and isolating all contaminated clothing. Gently wash all affected skin areas thoroughly with soap and water. If symptoms such as redness or irritation develop, IMMEDIATELY call a physician and be prepared to transport the victim to a hospital for treatment. INHALATION: IMMEDIATELY leave the contaminated area; take deep breaths of fresh air. If symptoms (such as wheezing, coughing, shortness of breath, or burning in the mouth, throat, or chest) develop, call a physician and be prepared to transport the victim to a hospital. Provide proper respiratory protection to rescuers entering an unknown atmosphere. Whenever possible, Self-Contained Breathing Apparatus (SCBA) should be used; if not available, use a level of protection greater than or equal to that advised under Protective Clothing. INGESTION: DO NOT INDUCE VOMITING. If the victim is conscious and not convulsing, give 1 or 2 glasses of water to dilute the chemical and IMMEDIATELY call a hospital or poison control center. Be prepared to transport the victim to a hospital if advised by a physician. If the victim is convulsing or unconscious, do not give anything by mouth, ensure that the victim's airway is open and lay the victim on his/her side with the head lower than the body. DO NOT INDUCE VOMITING. IMMEDIATELY transport the victim to a hospital. (NTP, 1992)

/SRP:/ Immediate first aid: Ensure that adequate decontamination has been carried out. If patient is not breathing, start artificial respiration, preferably with a demand valve resuscitator, bag-valve-mask device, or pocket mask, as trained. Perform CPR if necessary. Immediately flush contaminated eyes with gently flowing water. Do not induce vomiting. If vomiting occurs, lean patient forward or place on the left side (head-down position, if possible) to maintain an open airway and prevent aspiration. Keep patient quiet and maintain normal body temperature. Obtain medical attention. /Poisons A and B/|/SRP:/ Basic treatment: Establish a patent airway (oropharyngeal or nasopharyngeal airway, if needed). Suction if necessary. Watch for signs of respiratory insufficiency and assist ventilations if needed. Administer oxygen by nonrebreather mask at 10 to 15 L/min. Monitor for pulmonary edema and treat if necessary ... . Monitor for shock and treat if necessary ... . Anticipate seizures and treat if necessary ... . For eye contamination, flush eyes immediately with water. Irrigate each eye continuously with 0.9% saline (NS) during transport ... . Do not use emetics. For ingestion, rinse mouth and administer 5 mL/kg up to 200 mL of water for dilution if the patient can swallow, has a strong gag reflex, and does not drool ... . Cover skin burns with dry sterile dressings after decontamination ... . /Poisons A and B/|/SRP:/ Advanced treatment: Consider orotracheal or nasotracheal intubation for airway control in the patient who is unconscious, has severe pulmonary edema, or is in severe respiratory distress. Positive-pressure ventilation techniques with a bag valve mask device may be beneficial. Consider drug therapy for pulmonary edema ... . Consider administering a beta agonist such as albuterol for severe bronchospasm ... . Monitor cardiac rhythm and treat arrhythmias as necessary ... . Start IV administration of D5W /SRP: "To keep open", minimal flow rate/. Use 0.9% saline (NS) or lactated Ringer's if signs of hypovolemia are present. For hypotension with signs of hypovolemia, administer fluid cautiously. Watch for signs of fluid overload ... . Treat seizures with diazepam or lorazepam ... . Use proparacaine hydrochloride to assist eye irrigation ... . /Poisons A and B/

/SIGNS AND SYMPTOMS/ Dosage exceeding 5 mg/kg will usually be followed by vomiting, convulsions and stupor, beginning within 30 minutes and subsiding within 6 hours following injection|/SIGNS AND SYMPTOMS/ In humans, the administration of dimercaprol produces a number of side effects that usually are more alarming than serious. Reactions to dimercaprol occur in approximately 50% of subjects receiving 5 mg/kg intramuscularly. The effects of repeated administration of this dose are not cumulative if an interval of at least 4 hours elapses between injections. One of the most consistent responses to dimercaprol is a rise in systolic and diastolic arterial pressures, accompanied by tachycardia. The rise in pressure may be as great as 50 mmHg in response to the second of two doses (5 mg/kg) given 2 hours apart. The pressure rises immediately but returns to normal within 2 hours.|/SIGNS AND SYMPTOMS/ CONTACT...WITH HUMAN EYE CAUSES VERY SEVERE, PERSISTENT STINGING SENSATION, BLEPHAROSPASM, LACRIMATION, & PHOTOPHOBIA FOR AN HOUR OR TWO, BUT NO DAMAGE TO EYE.|/SIGNS AND SYMPTOMS/ The major causes of death are usually related to the cause of poisoning. But Dimercaprol could cause convulsions and coma; irreversible cardiovascular collapse; acidosis and hydroelectrolytic disturbances, renal failure; and secondary consequences of hypertension such as brain injury or cardiac failure.|For more Human Toxicity Excerpts (Complete) data for Dimercaprol (7 total), please visit the HSDB record page.

2,3 Dimercaptopropanol

Dimercaprol is prepared in vegetable oil (peanut or arachis oil) and stabilized with benzyl benzoate.|Grade: USP, as dimercaprol|Parenteral injection, for IM: 100 mg/mL BAL in Oil (with benzyl benzoate 200 mg/mL and peanut oil 700 mg/mL), (Taylor).

1-Propanol, 2,3-dimercapto-: ACTIVE|Although not in current use ... was developed to protect against arsenical war gases (including Lewisite) and has been used as an antidote for exposure to arsenic, mercury, and other heavy metals.

THIN LAYER CHROMATOGRAPHY WAS USED TO SEPARATE & IDENTIFY DIMERCAPROL, ITS BYPRODUCT TRIMERCAPTOPROPANE AND THEIR DEGRADATION PRODUCTS.

GC/MS determination in plasma.

Human Drugs -> FDA Approved Drug Products with Therapeutic Equivalence Evaluations (Orange Book) -> Active Ingredients