COCAINE

BODY PACKING: It is the act of swallowing multiple packets containing an illegal drug in order to smuggle large amounts, usually across international borders. Fatal cocaine poisoning may occur with the rupture of a single package (Souka, 1999).
COCAINE-FILLED CONDOMS: "Body packers" may ingest cocaine wrapped in condoms or other latex material. Each condom may contain 5 to 7 g of cocaine hydrochloride (85% to 99% pure) and may be adulterated with lidocaine 1% to 15% (McCarron & Wood, 1983).
SMUGGLING: Cocaine may be found in food products imported from coca-producing countries. Smugglers may poison a whole or partial shipment of food, which may later enter distribution.

STRUCTURE: Cocaine powder wrapped in cellophane and three or four layers of latex (condoms or toy balloons), tied with a non-absorbable ligature.

BODY STUFFERS hastily ingest cocaine packets to evade law enforcement officials. Leaking from these poorly wrapped packets can produce mild to severe cocaine toxicity (June et al, 2000; Eng et al, 1999).
PONY MALTA: A Colombian soft drink primarily sold in Hispanic neighborhoods in the USA has been used as a vehicle for cocaine smuggling. Bottles were found to contain an average of 30 g of cocaine each and deaths have been reported from consumption of this adulterated product (Martz et al, 1991).
COCA PASTE: Is the most widely used form of cocaine in South America. It is smoked and behaves like free cocaine. It may contain greater than 5% manganese, other alkaloids, and gasoline residue components (ElSohly, 1991).
LOCAL ANESTHESIA: Cocaine toxicity has been reported in children receiving topical adrenaline and cocaine for local anesthesia (Barnett, 1998). While this is most commonly reported when large doses are used on mucous membranes, it has also been reported after dermal application.

FORMS

Cocaine is available legally in this country as either the free-base which is soluble in organic solvents or as the hydrochloride salt which is water soluble. Both forms are white, crystalline powders. Cocaine is used clinically in 4% to 11.8% solutions for topical and nasopharyngeal anesthesia.
HEALTH FOOD TEAS: Cocaine has been detected in "decocainized tea leaves" and in health food stores as "Health Inca Tea" or "Mate de Coca" (Siegel et al, 1986; Floren & Small, 1993).

The concentration of cocaine is identical to that found in untreated cultivated coca leaves (0.13% to 0.68%, or about 4.8 to 5.7 mg per tea bag).
Benzoylecgonine has been detected in the urine of persons drinking these teas. One patient drank an infusion of 80 tea bags and developed classic cocaine toxicity (Siegel et al, 1986).
Jackson et al (1991) studied four males who ingested one cup each of Health Inca Tea. Each tea bag contained 4.8 mg of cocaine. Maximum urinary benzoylecgonine concentrations ranged from 1.4 to 2.8 mg/L, occurring from 4 to 11 hours postingestion (Jackson et al, 1991).

FREE-BASING

Free-base is prepared by treating cocaine hydrochloride with a basic solution (baking soda, sodium hydroxide or ammonia). The precipitated free alkaloid is filtered or dissolved in ether and then removed by drying. These procedures result in 37% to 96% recovery.

Cocaine free-base is usually smoked in a water pipe. Heat from a lighter or matches is applied to volatilize the cocaine for inhalation. Usually only 1% to 5% of the original amount of cocaine remains intact in the smoke, although some street methods may produce more than 67%.
When sprinkled onto tobacco or in marijuana cigarettes, the pyrolysis product contains about 6% cocaine. Free-basing is also known as base balling or smoking "base".
NOTE: Smoking "base" may also refer to smoking of coca paste (pasta, bazooka, cocaine base, basuco), a crude extract of the coca leaf treated with sulfuric acid and then precipitated with sodium carbonate, which contains 40% to 85% cocaine sulfate (Siegel, 1984).

Cocaine smoked in the United States is relatively pure compound of cocaine alkaloid, also known as free-base. Street "free-base" is not easily distinguished from cocaine base by the user who may buy either compound. Free-base kits are readily available to convert cocaine hydrochloride to cocaine alkaloid and to remove the compounds with which it is often adulterated.
A form of pre-converted free-base cocaine, known as "crack" is widely available. Crack is prepared by mixing the hydrochloride salt with baking soda and water and heating to form a "rock", which is then smoked.
In combination with heroin, it is known as a "speedball." More recently several cases have been reported where "Spinhalers(R)" have been used to aid in the nasal inhalation of cocaine.

ADULTERANTS

Street cocaine is often impure. The content of pure cocaine ranges from 10% to 50% (most commonly 15% to 20%). Some street samples were 40% to 60% pure (Gold & Verebey, 1984). In an 11-year survey (1973-1983) of anonymous samples submitted for analysis, 39% were cut with adulterants, and 24% were cut with diluents or sugars (commonly mannitol and inositol and less commonly lactose, glucose, or sucrose). TABLE 1 summarizes the types of adulterants found. TABLE 1 COMMON ADULTERANTS (Messinger, 1984)1973-1975:Lidocaine, procaine, tetracaine, benzocaine, caffeine, ephedrine1976:In addition to above: amphetamine, methamphetamine, benzoylecgonine (decomposition product) acetaminophen, phenacetin, salicylamide, heroin, opioids, quinine1977-1979:In addition to above: niacinamide, methaqualone1980:In addition to above: antipyrine1981:In addition to above: dibucaine, diethylpropion1982:In addition to above: ascorbic acid, theophylline1983:Most frequent adulterants: ephedrine, phenylpropanolamine, niacinamide, lidocaine, tetracaine, mannitol, inositol1984:Lidocaine, procaine, lactose, phencyclidine, diethylpropion, antipyrine, magnesium sulfate (Schnoll et al, 1984)

Crack cocaine adulterated with phenytoin in order to lower cost or augment intoxication has resulted in phenytoin toxicity in 5 patients (Katz et al, 1992).

An HPLC-DAD method was developed and successfully used to detect caffeine, lidocaine, phenacetin, benzocaine, and diltiazem as adulterants in cocaine samples seized in Brazil between 2007 and 2012. At least one of the adulterants was present in 45.2% of 115 samples (n=52), with caffeine being the most frequently detected adulterant (in 43 samples). Phenacetin was found in 5 samples and diltiazem was found in only one sample. The cocaine samples included cocaine paste, cocaine base, and cocaine hydrochloride, with cocaine contents ranging from undetectable to 97.2% (Floriani et al, 2014).
LEVAMISOLE/CASE REPORTS

Severe agranulocytosis (ANC 0 X10(9)/L) and fever have been reported in several patients with a history of cocaine use. Urine toxicology testing detected the presence of cocaine (or its metabolite) and levamisole. All patients recovered following G-CSF and antibiotic therapy. It is suspected that the cocaine used by these patients had been adulterated with levamisole (Zhu et al, 2009). Other effects that may occur as a result of using cocaine adulterated with levamisole include allergic reactions (difficulty breathing, swelling of lips, tongue, or face, and hives), confusion, loss of consciousness, extreme fatigue, memory loss, muscle weakness, paresthesias, seizures, and speech disturbances (Kinzie, 2009).
Neutropenia and retiform purpura, characterized by purpuric macules, papules, and plaques on the pinna, earlobes, cheeks, trunk, and extremities, have been reported in two patients with histories of cocaine use. Urine toxicology screens of both patients confirmed the presence of cocaine. Although the presence of levamisole was unconfirmed, the authors speculate that levamisole contamination may be the causative agent (Waller et al, 2010).

BRODIFACOUM: Severe coagulopathy was reported in a patient who smoked "crack" cocaine that was mixed with brodifacoum, a rodenticide. The patient, a 37-year-old man, presented to the emergency department with epistaxis of several hours in duration. Laboratory data revealed a prothrombin time of 65.8 sec (normal range 9.7 to 12.5), an international normalized ratio of 5.8, and an activated partial-thromboplastin time of 46.4 sec (normal range 21 to 30.6). Toxicologic analysis of a serum sample from the patient indicated a brodifacoum serum level of 680 ng/mL. With supportive therapy, the patient recovered (Waien et al, 2001).
BENZOCAINE: A 34-year-old man, who ingested a packet of cocaine, developed seizures approximately 1 hour after presenting to the emergency department. The patient's skin was blue in color, arterial blood gas analysis revealed a PaO2 of 65.1 kPa and a true fraction of hemoglobin bound to oxygen of 82.5%, and the patient's blood was dark in color. Co-oximetry determined the methemoglobin concentration of 13.8%, indicating methemoglobinemia. Urine mass spectrometry confirmed the presence of cocaine, phenytoin, lidocaine, and benzocaine. It is suspected that the seizures and the methemoglobinemia were the result of ingesting benzocaine-adulterated cocaine (Chakladar et al, 2010).

SUBSTITUTES: In an 11-year survey (1973-1983) of anonymous samples submitted for analysis, other substances were frequently substituted for cocaine. By 1983, only 61% of submitted samples actually contained cocaine. TABLE 2 summarizes the types of substitutes seen.

TABLE 2 COMMON SUBSTITUTES (Messinger, 1984)
1973-1975:	Lidocaine, procaine, tetracaine, benzocaine, caffeine, ephedrine, amobarbital, PCP, heroin, other opioids, LSD
1976:	In addition to above: methapyrilene, acetaminophen, salicylamide, phenacetin, heroin, other opioids
1977:	In addition to above: ketamine, methaqualone
1983:	Most frequent substitutes: ephedrine, phenylpropanolamine, niacinamide, lidocaine, tetracaine, mannitol, inositol
1984:	Caffeine, ephedrine, lidocaine, procaine, phencyclidine, antipyrine, diphenhydramine, methamphetamine, phenacetin, aminopyrine, quinine, salicylate
	(Schnoll et al, 1984)

COCAINE LOOK ALIKES: Many cocaine look-alikes are available on the market under various trade names including Cocoa Leaf, Coco Snow, Crystal Caine, Base-O-Caine, Florida Snow, Milky Trails, Pro Crystal, Pseudo Caine, Real Caine, Repro Crystals, Rock Crystal, Suma Caine, Synth Coke, Toot, Ultra Caine, and White Lady (Rehrig, 1982).

Look-alikes generally contain sympathomimetics (phenylpropanolamine, ephedrine), caffeine, and a local anesthetic (eg, benzocaine, tetracaine, lidocaine) (Rehrig, 1982).

-CLINICAL EFFECTS

GENERAL CLINICAL EFFECTS

USES: Cocaine is used as a topical vasoconstrictor for otolaryngology procedures. The most common clinical scenario with cocaine involves abuse for its psychostimulant effects.

ADULTERANTS: Caffeine, lidocaine, phenacetin, benzocaine, diltiazem, and levamisole have been detected as adulterants in cocaine.

PHARMACOLOGY: The psychostimulant effects of cocaine are due to blockade of reuptake of monoamine (dopamine, norepinephrine, and serotonin) in CNS neurons. The net effect is CNS excitation and an increase in sympathetic nervous system activity. Decreased reuptake of norepinephrine may cause vasoconstriction. The direct cardiac effects of cocaine are due to antagonism of voltage-gated sodium channels in cardiomyocytes.

TOXICOLOGY: Increased sympathetic activity may cause hallucinations, seizures, hypertension, and agitation. Vasospasm may cause cerebral or cardiac ischemia and may contribute to hypertension. These effects may occur with recreational doses of cocaine. Cardiac sodium channel antagonism only occurs with cocaine overdose and will delay intracardiac conduction, causing decreased myocardial function and triggering dysrhythmias. Absorption occurs after injection, ingestion, insufflation, or topical application.

EPIDEMIOLOGY: Cocaine use is common. Cocaine intoxication is frequently associated with emergency department presentation for related complaints (chest pain) or indirectly related complaints (trauma). Severe toxicity is less common. Body stuffers (patients who rapidly ingest small to moderate amounts of cocaine in an attempt to avoid arrest) are common. Body packers (patients who ingest large quantities of cocaine in an attempt to smuggle the cocaine for later distribution) are occasionally seen in locations where international travel is common.

WITH POISONING/EXPOSURE

MILD TO MODERATE TOXICITY: Patients may develop anxiety, hallucinations, chest pain, hypertension, palpitations, or agitation. In some cases, recreational doses of cocaine may cause cardiac or cerebral ischemia.
SEVERE TOXICITY: Patients with severe toxicity may present with either seizures or severe agitation. If uncontrolled, this may progress to severe hyperthermia, rhabdomyolysis, acute renal failure, hepatic injury, coagulopathy, and decreased myocardial function. Severe intoxication may progress rapidly to dysrhythmias and cardiovascular collapse.
ROUTES OF ADMINISTRATION (eg, intranasal, oral, rectal, IV, inhaled, or intravaginal) have been associated with clinical toxicity.

Effects usually develop quickly (within a few minutes to an hour) and are of short duration, although delayed, prolonged effects have been reported after rupture of cocaine-filled condoms in the gastrointestinal tract.

LEVAMISOLE ADULTERATION: A large percentage of cocaine bulk shipments entering the United States have been found to be adulterated with levamisole. Multiple cases of levamisole toxicity (eg, agranulocytosis, neutropenia, vasculitis, retiform purpura) have been reported in patients using cocaine adulterated with levamisole. Refer to the LEVAMISOLE management for further information.

Editor's Note: An ERG guide with information appropriate to this material does not exist.

ACUTE CLINICAL EFFECTS

SUMMARY

PHARMACOLOGY: The psychostimulant effects of cocaine are due to blockade of reuptake of monoamine (dopamine, norepinephrine, and serotonin) in CNS neurons. The net effect is CNS excitation and an increase in sympathetic nervous system activity. Decreased reuptake of norepinephrine may cause vasoconstriction. The direct cardiac effects of cocaine are due to antagonism of voltage-gated sodium channels in cardiomyocytes.
TOXICOLOGY: Increased sympathetic activity may cause hallucinations, seizures, hypertension, and agitation. Vasospasm may cause cerebral or cardiac ischemia and may contribute to hypertension. These effects may occur with recreational doses of cocaine. Cardiac sodium channel antagonism only occurs with cocaine overdose and will delay intra-cardiac conduction, causing decreased myocardial function and triggering dysrhythmias. Absorption occurs after injection, ingestion, insufflation, or topical application.
EPIDEMIOLOGY: Cocaine use is common. Cocaine intoxication is frequently associated with emergency department presentation for related complaints (chest pain) or indirectly related complaints (trauma). Severe toxicity is less common. Body stuffers (patients who rapidly ingest small to moderate amounts of cocaine in an attempt to avoid arrest) are common. Body packers (patients who ingest large quantities of cocaine in an attempt to smuggle the cocaine for later distribution) are occasionally seen in locations where international travel is common.
ADULTERANTS: Caffeine, lidocaine, phenacetin, benzocaine, diltiazem, and levamisole have been detected as adulterants in cocaine
MILD TO MODERATE TOXICITY: Patients may develop anxiety, hallucinations, chest pain, hypertension, palpitations, or agitation. In some cases, recreational doses of cocaine may cause cardiac or cerebral ischemia.
SEVERE TOXICITY: Patients with severe toxicity may present with either seizures or severe agitation. If uncontrolled, this may progress to severe hyperthermia, rhabdomyolysis, acute renal failure, hepatic injury, coagulopathy, and decreased myocardial function. Severe intoxication may progress rapidly to dysrhythmias and cardiovascular collapse.
ROUTES OF ADMINISTRATION: (eg, intranasal, oral, rectal, IV, inhaled, or intravaginal) have been associated with clinical toxicity. Effects usually develop quickly (within a few minutes to an hour) and are of short duration, although delayed, prolonged effects have been reported after rupture of cocaine-filled condoms in the gastrointestinal tract.
LEVAMISOLE ADULTERATION: A large percentage of cocaine bulk shipments entering the United States have been found to be adulterated with levamisole. Multiple cases of levamisole toxicity (eg, agranulocytosis, neutropenia, vasculitis, retiform purpura) have been reported in patients using cocaine adulterated with levamisole. Refer to the LEVAMISOLE management for further information.

ACID-BASE

ACIDOSIS: Severe metabolic acidosis has been reported along with seizures, agitation, and hypotension (Stevens et al, 1994; Jonsson et al, 1983). Acidemia has been reported to contribute to conduction delays, dysrhythmias, and depressed myocardial contractility in patients with cocaine toxicity. Correction of acidemia through supportive care measures such as hyperventilation, sedation, active cooling, and sodium bicarbonate may improve the outcome of cardiac conduction disorders (Wang, 1999).

CARDIOVASCULAR

CARDIOVASCULAR EFFECTS: Severe cardiovascular effects including myocardial ischemia and infarction, arrhythmias, cardiomyopathy, aortic dissection, and endocarditis may develop with acute or chronic cocaine abuse. Sudden cardiac death has been reported (Havlik & Nolte, 2000; Rump et al, 1995; Willens et al, 1994).
SUDDEN DEATH: Struggling during attempts to restrain or arrest them, agitated cocaine-intoxicated patients experienced sudden death (Mirchandani et al, 1994).
AORTIC INJURY: Aortic dissection and rupture have been reported following cocaine use (Sherzoy et al, 1994; Cohle & Lie, 1992; Fisher & Holroyd, 1992).
MYOCARDIAL INFARCTION: After cocaine use, myocardial infarction (MI) may occur even in young patients without risk factors or preexisting cardiac pathology (Qureshi et al, 2001; Havlik & Nolte, 2000; Weber et al, 2000). MI is not uncommon and cannot be reliably predicted or excluded; therefore, all patients presenting with cocaine-related chest pain should be evaluated for possible MI (Feldman et al, 2000; Weber et al, 2000; Hollander et al, 1992). An MI may occur acutely up to 2 weeks after the last cocaine use (Levine & Nishikawa, 1991).
DYSRHYTHMIAS: Sinus tachycardia is the most common finding. Other cocaine-associated dysrhythmias include supraventricular tachycardia (Merigian et al, 1994), PVCs, bigeminy (Orr & Jones, 1968), accelerated ventricular rhythm (Benchimol et al, 1978), ventricular tachycardia (Merigian, 1993), bradycardia (Tanen et al, 2000; Havlik & Nolte, 2000), and ventricular fibrillation (Havlik & Nolte, 2000; Anon, 1979).
VASOCONSTRICTION AND ANGINA: Cocaine induces vasoconstriction in both diseased and nondiseased coronary arteries (Brogan et al, 1992).
MYOCARDITIS: Cocaine-related myocarditis with lymphocytic or eosinophilic infiltrates has been reported (Virmani et al, 1988; Isner et al, 1986; Simpson & Edwards, 1986).
ENDOCARDITIS: IV cocaine abuse was associated with endocarditis more frequently than other IV drugs of abuse; most patients were concurrently using heroin (Chambers et al, 1987).
CARDIOMYOPATHY: Cardiomyopathy has been attributed to cocaine abuse (Chokshi et al, 1989; Karch & Billingham, 1988; Wiener et al, 1986). A study of 30 chronic cocaine abusers revealed increased left ventricular mass on ECG as compared with controls (Brickner, 1991).
DEEP VENOUS THROMBOSIS: An increased incidence of upper extremity deep venous thrombosis has been noted in cocaine abusers (Lisse et al, 1989).
HYPERTENSIVE EPISODE: Moderate doses result in a dose-related increase in heart rate and blood pressure (Havlik & Nolte, 2000; Resnick & Schwartz, 1977; Fennell et al, 1976). With larger doses, hypotension may occur following the loss of sympathetic tone before the onset of a tachyarrhythmia.
MEDIASTINAL EMPHYSEMA: INHALATIONAL EFFECTS: Pneumomediastinum and pneumopericardium may be seen after cocaine inhalation. The practice of inhaling drug crystals or vapors and then applying positive ventilatory pressure has been associated with clinical presentation of pneumopericardium (Adrouny & Magnusson, 1985).

DERMATOLOGIC

GANGRENE: In one case, a 43-year-old woman who had no history of vascular disease developed gangrene of both hands and legs that necessitated digital and above-knee amputations, following repeated use of crack cocaine (Dhawan & Wang, 2007).
STEVENS-JOHNSON SYNDROME: In one case, a 26-year-old man developed Stevens-Johnson syndrome 3 days after cocaine snorting. There were multiple erosions up to 2 cm on his cheeks, tongue, lips, penile glans, and inner aspect of the foreskin. He also exhibited ocular signs, including conjunctival vasculitis as seen in erythema exudativum multiforme (Hofbauer et al, 2000).
SCLERODERMA: Scleroderma may be associated with the use of cocaine (Kilaru et al, 1991; Kerr, 1989).

ENDOCRINE

HYPERPROLACTINEMIA: Withdrawal from cocaine may result in hyperprolactinemia (Cocores et al, 1986).

GASTROINTESTINAL

VASCULAR INSUFFICIENCY OF INTESTINE: Intestinal ischemia following cocaine ingestion, injection, or crack use has been described (Sudhakar et al, 1997; Jawahar et al, 1997). Complications observed include splenic infarction (Novielli & Chambers, 1991), intestinal perforations (Muniz & Evans, 2001), mechanical bowel obstruction (impacted or ruptured cocaine packets) (Mustard et al, 1992; Freudenberger et al, 1990; Cregler & Mark, 1986), and necrosis of the distal ileum and the entire colon and rectum resulting in resection (Wang et al, 1992).
GASTRIC ULCER: Perforated gastric ulcers related to crack use have been reported in young men (Abramson et al, 1989; Abramson et al, 1991).
PNEUMOPERITONEUM: Pneumoperitoneum has been reported after smoking crack cocaine (Uva, 1997).

GENITOURINARY

RENAL FAILURE: Renal failure is presumably secondary to myoglobinuria and rhabdomyolysis and is common in severe overdoses (Van der Woude, 2000; Lucatello et al, 1992; Enriquez et al, 1991).
RENAL INFARCTION: Cases of renal infarction have been reported after nasal inhalation of cocaine (Saleem et al, 2001; Sharff, 1984).
GLOMERULONEPHRITIS: Antiglomerular basement membrane antibody-mediated glomerulonephritis has been reported (Van der Woude, 2000a).
INTERSTITIAL NEPHRITIS: Acute interstitial nephritis has been reported (Wojciechowski et al, 2008; Van der Woude, 2000a; Alvarez et al, 1999).
PRIAPISM: After topical application of cocaine to the glans penis, priapism has been observed (Rodriguez-Blasquez et al, 1990).
ABNORMAL SEXUAL FUNCTION: Decreased libido, impotence, unexplained breast development, galactorrhea, amenorrhea, and sexual dysfunction have been reported in chronic cocaine abusers (Cocores et al, 1986).

HEENT

EYES

RETINAL ARTERY THROMBOSIS: Visual loss secondary to central retinal artery occlusion and spasm have been reported with chronic IV cocaine abuse and following crack use (Libman et al, 1993; Hoffman & Reimer, 1993; Wallace et al, 1992).
CRACK EYE: Chemosis, hyperemia in association with corneal epithelial defects, lacrimation, pain, and photophobia have been reported. Microbial keratitis may complicate the syndrome of crack eye (Miller & Sherman, 2009; Strominger et al, 1990).
CORNEAL ULCERS: Both fungal and bacterial corneal ulcers as well as sterile epithelial defects have been reported after crack cocaine abuse (Miller & Sherman, 2009; Sachs et al, 1993).

NOSE: EFFECTS ON NASAL MUCOSA: Used intranasally, cocaine may cause nasal congestion, hyperemia, irritation, mucosal thickening, ulceration, infection, granulomas, septal perforation, or aspiration of the detached nasal septum (Sevinsky et al, 1995; Libby et al, 1992; Chow et al, 1990).
THROAT:

OROPHARYNGEAL INJURY: Thermal injuries to the upper airway leading to epiglottitis, laryngeal injury, and mucosal necrosis have been reported after smoking crack or freebase cocaine (Bezmalinovic et al, 1988; Savitt & Colagiovanni, 1991; Savitt & Colagiovanni, 1991).
DENTAL EROSIONS have been seen after chronic application of cocaine to the nasal or oral mucosa. Destruction of both enamel and dentin may be seen (Krutchkoff et al, 1990).

HEMATOLOGIC

DISSEMINATED INTRAVASCULAR COAGULATION: Disseminated intravascular coagulation may be seen in severe poisoning cases, often associated with hyperthermia, rhabdomyolysis, renal failure, and hepatic dysfunction (Silva et al, 1991; Bauwens et al, 1989; Campbell, 1988).

HEPATIC

TOXIC HEPATITIS: Fatal hepatitis B infection has been reported in crack abusers whose sexual partners included IV drug abusers (Estroff et al, 1986).
LIVER DAMAGE: Hepatic injury with elevations of alanine aminotransferase, aspartate aminotransferase, and alkaline phosphatase is common (Kothur et al, 1991; Silva et al, 1991; Gubbins et al, 1990). Hepatic necrosis (centrilobular, midzonal, and panlobar) has been reported in severe overdose (Radin, 1993; Silva et al, 1991; Perino et al, 1987).

METABOLIC

DEFICIENCY OF CHOLINESTERASE: Patients with lower plasma cholinesterase levels may be predisposed to more severe cocaine toxicity (Hoffman et al, 1992).

MUSCULOSKELETAL

Rhabdomyolysis is common with cocaine toxicity. Muscle symptoms do not predict increases in CPK levels (Havlik & Nolte, 2000; Van der Woude, 2000; Hoffman et al, 1992).

NEUROLOGIC

SEIZURE: Generalized tonic-clonic, partial motor, and partial complex seizure have all been reported (Havlik & Nolte, 2000; Lora-Tamayo et al, 1994; Mott et al, 1994). Seizures may be recurrent, and status epilepticus has been reported, particularly in children (Tanen et al, 2000; Winbery et al, 1998; Merigian et al, 1994).
INTRACRANIAL HEMORRHAGE: Intracranial hemorrhage (intracerebral or subarachnoid) has been described secondary to cocaine abuse (McEvoy et al, 2000; Daras et al, 1994; Ramadan et al, 1991).
HEADACHE: After cocaine use, headache may occur. Severe headache may be seen with occlusive or hemorrhagic stroke (Levine et al, 1990).
DISTURBANCE IN THINKING: Cortical areas are affected first, with effects progressing caudally. Mental status changes range from euphoria, excitement, restlessness, and anxiety to delirium and acute paranoid psychosis (Mott et al, 1994; Post, 1975).
VASCULITIS: Biopsy-confirmed cerebral vasculitis has been associated with cocaine abuse (Morrow & McQuillen, 1993; Fredericks et al, 1991; Krendel et al, 1990).
CEREBROVASCULAR DISEASE: Cocaine abuse may be associated with cerebral atrophy (Pascual-Leone et al, 1991).
DELIRIUM: The cocaine-associated agitated delirium syndrome is composed of 4 components that appear in sequence: hyperthermia, delirium with agitation, respiratory arrest, and death. These patients usually have low to moderate cocaine blood levels (Wetli et al, 1996).

PSYCHIATRIC

PSYCHOSIS: In any abuser, including the elderly, psychosis may develop (Namboudir & Young, 1991). An incidence of 53% was reported in an evaluation of 55 users (Brady et al, 1991).
EATING DISORDER: Bulimia and anorexia nervosa are prevalent in cocaine abusers (Jonas et al, 1987).
DRUG WITHDRAWAL: Prolonged heavy cocaine use may cause a withdrawal syndrome characterized by dysphoria, fatigue, vivid unpleasant dreams, insomnia or hypersomnia, increased appetite, and psychomotor retardation or agitation (Mendelson & Mello, 1996).
DELUSIONS OF PERSECUTION: Transient paranoid states have been reported with cocaine use (Satel & Edell, 1991) and may be associated with violent behavior (Cordess & Murray, 1991).

RESPIRATORY

APNEA: The initial effect is an increase in rate and depth of respiration followed by rapid shallow breathing that may deteriorate to a Cheyne-Stokes pattern with larger doses (Chiu et al, 1986). Respiratory arrest may follow (Wetli et al, 1996; Schwartz & Oderda, 1980).
PULMONARY INFARCTION: Pulmonary infarction has been reported Following crack use (Delaney & Hoffman, 1991).
ACUTE LUNG INJURY: ACUTE EXPOSURE: Pulmonary edema is a common finding at autopsy (Lora-Tamayo et al, 1994; Finkle & McCloskey, 1978) and has been reported clinically in association with crack cocaine smoking and IV cocaine use (Restrepo et al, 2007; Wilson & Hobbs, 1993; Kline & Hirasuna, 1990).
BRONCHOSPASM: Dyspnea, pleuritic chest pain, bronchospasm, and wheezing have been associated with smoking freebase or snorting cocaine in patients with or without a history of asthma (Restrepo et al, 2007; Krantz et al, 1993; Rubin & Neugarten, 1990).
INTERSTITIAL PNEUMONITIS: Interstitial pneumonitis has been associated with crack cocaine smoking (O'Donnell et al, 1991).
PNEUMOTHORAX: Pneumomediastinum and/or pneumothorax following crack smoking (Restrepo et al, 2007; Bernasko et al, 1997; Uva, 1997) and snorting or smoking of alkaloidal cocaine have been reported (Torre & Barberis, 1998; Christou et al, 1990; Lieberman et al, 1990).
PULMONARY HYPERTENSION: Hypertrophy of the pulmonary vasculature was associated with cocaine-smoking deaths. Cocaine also has a direct effect on pulmonary vascular smooth muscle constriction (Albertson et al, 1995; Robertson et al, 1976).
HEMOPTYSIS: Hemoptysis, black sputum, pleuritic chest pain, impaired pulmonary diffusion capacity, and acute alveolar hemorrhage have been associated with smoking freebase cocaine (Restrepo et al, 2007; Tashkin et al, 1992; Murray et al, 1988).

VITAL SIGNS

FEVER: Hyperthermia is common and life-threatening and may be due to increased muscular activity, vasoconstriction, and perhaps a direct effect on the hypothalamus (Tanen et al, 2000; Wetli et al, 1996; Bauwens et al, 1989). It is often associated with rhabdomyolysis, seizures, and renal failure (Saleem et al, 2001; Merigian et al, 1994; Hoffman et al, 1992).

CHRONIC CLINICAL EFFECTS

Chronic exposure to cocaine can induce tolerance to cardiovascular and subjective effects (Prakash & Das G, 1993), which can lead to inadvertent overdose (Fischman et al, 1985). The stimulant effects do not show tolerance, however (Abel, 1989).

Chronic inhalation of cocaine can lead to nasal irritation, infection, ulceration, granulomas, and perforation of the nasal septum (Libby et al, 1992; Chow et al, 1990; Daggett et al, 1990; Becker & Hill, 1988; Schweitzer, 1986; Schwartz & Oderda, 1980; Rappolt et al, 1976). Nasal allergies may be intensified, and asthma may develop (Snyder & Snyder, 1985). Chronic application of cocaine to the nasal or oral mucosa can cause erosion of dental enamel (Krutchkoff et al, 1990).

Symptoms of chronic cocaine abuse include insomnia, anorexia, restlessness, weight loss, paranoia, violent outbursts, unrivaled fatigue, lapses in attention, inability to concentrate, situational sexual impotency, severe depression, and toxic psychosis (Anon, 1984; Gay, 1982; DiMaio & Garriott, 1978; Post, 1975). There are at least 2 known cases of unmasking or exacerbation of myasthenia gravis by cocaine (Daras et al, 1996).

Withdrawal symptoms that occur after binging or chronic use include severe mental depression, anxiety, irritability, paranoia, and intense craving for cocaine (Gawin & Kleber, 1986).

-FIRST AID

FIRST AID AND PREHOSPITAL TREATMENT

Activated charcoal is not recommended due to rapid absorption of cocaine and the risk of seizures.

-RANGE OF TOXICITY

MINIMUM LETHAL EXPOSURE

ROUTE OF EXPOSURE

TOPICAL

Fatalities have been reported after application of 25 mg of cocaine to the mucous membranes (Gay, 1982), nasal applications of 400 mg (pp 8-14), and topical tracheobronchial application with 200 mg or less in 6 cases (pp 8-14).
Death was reported in a 7.5-month-old girl who received 10 mL of TAC solution (cocaine 1180 mg, tetracaine 50 mg, and epinephrine 5 mg) for wound anesthesia of an upper lip laceration. Contact with nasal mucosa may have increased absorption (blood concentration, 11.9 mg/L) (Dailey, 1988).

BODY PACKERS

Death was reported in 5 cases in which a single plastic bag or balloon filled with cocaine was ingested. The amount was unspecified in 4 cases, and estimated to be 1 ounce in 1 case (Introna & Smialek, 1989).

CASE REPORTS

PEDIATRIC

Fatality in 16 infants (aged 2 weeks to 10 months) has been associated with passive exposure to freebase (crack) cocaine smoke (Mirchandani et al, 1991).

MAXIMUM TOLERATED EXPOSURE

GENERAL/SUMMARY

Addicts have been reported to use up to 10 g a day without experiencing serious acute toxicity.

CASE REPORTS

Topical tracheal application of 30 mg to a 14-month-old child resulted in mydriasis, hyperactivity, hyperventilation, and tachycardia (Schou et al, 1987).
Serious toxicity and seizures developed in a 6-month-old child after application of 2 mL of TAC solution (cocaine 236 mg) to the hard palate. The infant made a complete recovery (Tipton et al, 1989).
A 6.2-kg infant developed opisthotonus and dystonic movements, tachycardia, and tachypnea after receiving 2 drops of a 4% cocaine solution in the nares (at least 4 mg cocaine) (Schubert & Wason, 1992).

Carcinogenicity Ratings for CAS50-36-2 :

ACGIH (American Conference of Governmental Industrial Hygienists, 2010): Not Listed
EPA (U.S. Environmental Protection Agency, 2011): Not Listed
IARC (International Agency for Research on Cancer (IARC), 2016; International Agency for Research on Cancer, 2015; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010a; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2008; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2007; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2006; IARC, 2004): Not Listed
NIOSH (National Institute for Occupational Safety and Health, 2007): Not Listed
MAK (DFG, 2002): Not Listed
NTP (U.S. Department of Health and Human Services, Public Health Service, National Toxicology Project ): Not Listed

TOXICITY AND RISK ASSESSMENT VALUES

EPA IRIS

EPA Risk Assessment Values for CAS50-36-2 (U.S. Environmental Protection Agency, 2011):

Not Listed

TOXICITY VALUES

Reference: RTECS, 1999
- LD50- (INTRAVENOUS)DOG:
- LD50- (SUBCUTANEOUS)GUINEA_PIG:
- LD50- (INTRAPERITONEAL)MOUSE:
- LD50- (INTRAVENOUS)MOUSE:
- LD50- (ORAL)MOUSE:
- LD50- (SUBCUTANEOUS)MOUSE:
- LD50- (INTRAVENOUS)RABBIT:
- LD50- (INTRAPERITONEAL)RAT:
- LD50- (INTRAVENOUS)RAT:
- LD50- (SUBCUTANEOUS)RAT:
- LDLo- (INTRAVENOUS)CAT:
- LDLo- (SUBCUTANEOUS)CAT:
- LDLo- (SUBCUTANEOUS)CATTLE:
- LDLo- (SUBCUTANEOUS)CHICKEN:
- LDLo- (SUBCUTANEOUS)DOG:
- LDLo- (INTRAVENOUS)GUINEA_PIG:
- LDLo- (ORAL)HUMAN:
- LDLo- (ORAL)RABBIT:
- LDLo- (SUBCUTANEOUS)RABBIT:
- TCLo- (INHALATION)HUMAN:
- TDLo- (INTRAPLEURAL)HUMAN:
- TDLo- (INTRAVENOUS)HUMAN:
- TDLo- (ORAL)HUMAN:

-STANDARDS AND LABELS

WORKPLACE STANDARDS

ACGIH TLV Values for CAS50-36-2 (American Conference of Governmental Industrial Hygienists, 2010):

Not Listed

AIHA WEEL Values for CAS50-36-2 (AIHA, 2006):

Not Listed

NIOSH REL and IDLH Values for CAS50-36-2 (National Institute for Occupational Safety and Health, 2007):

Not Listed

OSHA PEL Values for CAS50-36-2 (U.S. Occupational Safety, and Health Administration (OSHA), 2010):

Not Listed

OSHA List of Highly Hazardous Chemicals, Toxics, and Reactives for CAS50-36-2 (U.S. Occupational Safety and Health Administration, 2010):

Not Listed

ENVIRONMENTAL STANDARDS

EPA CERCLA, Hazardous Substances and Reportable Quantities for CAS50-36-2 (U.S. Environmental Protection Agency, 2010):

Not Listed

EPA CERCLA, Hazardous Substances and Reportable Quantities, Radionuclides for CAS50-36-2 (U.S. Environmental Protection Agency, 2010):

Not Listed

EPA RCRA Hazardous Waste Number for CAS50-36-2 (U.S. Environmental Protection Agency, 2010b):

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

EPA SARA Title III, Extremely Hazardous Substance List for CAS50-36-2 (U.S. Environmental Protection Agency, 2010):

Not Listed

EPA SARA Title III, Community Right-to-Know for CAS50-36-2 (40 CFR 372.65, 2006; 40 CFR 372.28, 2006):

Not Listed

DOT List of Marine Pollutants for CAS50-36-2 (49 CFR 172.101 - App. B, 2005):

Not Listed

EPA TSCA Inventory for CAS50-36-2 (EPA, 2005):

Not Listed

LABELS

NFPA

NFPA Hazard Ratings for CAS50-36-2 (NFPA, 2002):

Not Listed

-PERSONAL PROTECTION

SUMMARY

Editor's Note: An ERG guide with information appropriate to this material does not exist.

PROTECTIVE CLOTHING

CHEMICAL PROTECTIVE CLOTHING. Search results for CAS 50-36-2.

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

-PHYSICAL HAZARDS

FIRE HAZARD

SUMMARY

Editor's Note: An ERG guide with information appropriate to this material does not exist.

FLAMMABILITY CLASSIFICATION

NFPA Flammability Rating for CAS50-36-2 (NFPA, 2002):

Not Listed

FIRE CONTROL/EXTINGUISHING AGENTS

Editor's Note: An ERG guide with information appropriate to this material does not exist.

NFPA Extinguishing Methods for CAS50-36-2 (NFPA, 2002):

Not Listed

EVACUATION PROCEDURES

SUMMARY

Editor's Note: An ERG guide with information appropriate to this material does not exist.

AIHA ERPG Values for CAS50-36-2 (AIHA, 2006):

Not Listed

DOE TEEL Values for CAS50-36-2 (U.S. Department of Energy, Office of Emergency Management, 2010):

Not Listed

AEGL Values for CAS50-36-2 (National Research Council, 2010; National Research Council, 2009; National Research Council, 2008; National Research Council, 2007; NRC, 2001; NRC, 2002; NRC, 2003; NRC, 2004; NRC, 2004; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; United States Environmental Protection Agency Office of Pollution Prevention and Toxics, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; 62 FR 58840, 1997; 65 FR 14186, 2000; 65 FR 39264, 2000; 65 FR 77866, 2000; 66 FR 21940, 2001; 67 FR 7164, 2002; 68 FR 42710, 2003; 69 FR 54144, 2004):

Not Listed

NIOSH IDLH Values for CAS50-36-2 (National Institute for Occupational Safety and Health, 2007):

Not Listed

CONTAINMENT/WASTE TREATMENT OPTIONS

SUMMARY

Editor's Note: An ERG guide with information appropriate to this material does not exist.

SMALL LEAK/SPILL

Editor's Note: An ERG guide with information appropriate to this material does not exist.

LARGE LEAK/SPILL

Editor's Note: An ERG guide with information appropriate to this material does not exist.

-PHYSICAL/CHEMICAL PROPERTIES

MOLECULAR WEIGHT

Cocaine hydrochloride: 339.81

Alkaloidal cocaine: 303.35

DESCRIPTION/PHYSICAL STATE

Bitter taste; produces a numbing sensation of the tongue and lips

FREEZING/MELTING POINT

MELTING POINT

Cocaine hydrochloride: 195 degrees C
Cocaine sulfate: 195 degrees C
Cocaine alkaloid or free-base: 98 degrees C (Windholz, 1983)

SOLUBILITY

IN ORGANIC SOLVENTS

Cocaine hydrochloride or sulfate are very soluble in water.

OTHER

The free alkaloid is fat soluble.

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GENERAL BIBLIOGRAPHY

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40 CFR 372.65: Environmental Protection Agency - Toxic Chemical Release Reporting, Community Right-To-Know, Chemicals and Chemical Categories to which this part applies. National Archives and Records Association (NARA) and the Government Printing Office (GPO), Washington, DC. Final rules current as of Apr 3, 2006.

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65 FR 14186: Notice of the National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances - Proposed AEGL Values, Environmental Protection Agency, NAC/AEGL Committee. National Archives and Records Administration (NARA) and the Government Publishing Office (GPO), Washington, DC, 2000.

65 FR 39264: Notice of the National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances - Proposed AEGL Values, Environmental Protection Agency, NAC/AEGL Committee. National Archives and Records Administration (NARA) and the Government Publishing Office (GPO), Washington, DC, 2000.

65 FR 77866: Notice of the National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances - Proposed AEGL Values, Environmental Protection Agency, NAC/AEGL Committee. National Archives and Records Administration (NARA) and the Government Publishing Office (GPO), Washington, DC, 2000.

66 FR 21940: Notice of the National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances - Proposed AEGL Values, Environmental Protection Agency, NAC/AEGL Committee. National Archives and Records Administration (NARA) and the Government Publishing Office (GPO), Washington, DC, 2001.

67 FR 7164: Notice of the National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances - Proposed AEGL Values, Environmental Protection Agency, NAC/AEGL Committee. National Archives and Records Administration (NARA) and the Government Publishing Office (GPO), Washington, DC, 2002.

68 FR 42710: Notice of the National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances - Proposed AEGL Values, Environmental Protection Agency, NAC/AEGL Committee. National Archives and Records Administration (NARA) and the Government Publishing Office (GPO), Washington, DC, 2003.

69 FR 54144: Notice of the National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances - Proposed AEGL Values, Environmental Protection Agency, NAC/AEGL Committee. National Archives and Records Administration (NARA) and the Government Publishing Office (GPO), Washington, DC, 2004.

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