Contact Us    Contact Us     |     Feedback
MOBILE VIEW  | 

LSD

Export To Excel

Classification   |    Detailed evidence-based information

Substances Included Synonyms

Therapeutic Toxic Class

    A) Lysergic acid diethylamide (LSD), an indole derivative, chemically resembles serotonin and acts as a non-selective serotonin agonist, with strong hallucinogenic effects.

Specific Substances

    1) LSD
    2) 9,10-didehydro-N,N-diethyl-6-
    3) methylergoline-8,beta-carboxamide
    4) Acid
    5) Beast
    6) Ben
    7) Blotter
    8) Blue caps
    9) Blue drops
    10) Brain buster
    11) Brown caps
    12) California sunshine
    13) Cubes
    14) D-lsd
    15) D-Lysergic acid diethylamide
    16) Delysid(R)
    17) Diethylamid kyseliny lysergove (Czech)
    18) Ergoline-8-beta-carboxamide,9,10-didehydro-N,N-
    19) diethyl-6-methyl
    20) Ergoline-8-carboxamide,9,10-didehydro-N,N-diethyl-
    21) 6-methyl-,(8beta)
    22) Face melter
    23) Ghost
    24) Green caps
    25) Hawk
    26) Heavenly blue
    27) LSD 25
    28) Lysergamid
    29) Lysergamide,N,N-diethyl-
    30) Lysergaure diethylamid
    31) Lysergic acid diethylamide
    32) Lysergide
    33) Lysergsaurediethylamid
    34) Microdot
    35) NN-diethyl-D-lysergamide
    36) Orange wedges
    37) Paper acid
    38) Pearly gates
    39) Pink drops
    40) Purple haze
    41) Purple wedges
    42) Royal Blue
    43) Sunshine
    44) Wedding bells
    45) White lightning
    46) Window Pane
    47) Yellow caps
    48) Yellow drops
    49) CAS 50-37-3
    1.2.1) MOLECULAR FORMULA
    1) C20-H25-N3-O

Available Forms Sources

    A) FORMS
    1) Substance can be the form of powder, tablet, capsule, in a sugar cube, or a drop of LSD solution evaporated on filter or blotting paper ("blotter acid" or "postage stamps") (Brown & Braden, 1987; Ellenhorn, 1997; Kulberg, 1986; Kulig, 1990).
    2) Sometimes LSD is incorporated into a square of gelatin ("windowpane") (Brown & Braden, 1987; Kulig, 1990).
    3) ADULTERATED PRODUCT: Quite frequently, LSD is "cut" before sale with other drugs or substances such as sugar. Strychnine, phencyclidine (PCP), cocaine, and caffeine all are used as adulterants of LSD.
    a) NBOMe Series: During 2013, there were reports that drugs in the NBOMe class were being sold as LSD. Due to the ease of procuring and counterfeiting NBOMe as LSD, some substance abusers may be unknowingly consuming substances from the NBOMe series. NBOMe intoxication is potentially much more severe than LSD and may include the following adverse events: seizures, metabolic acidosis, elevated creatine kinase, acute renal injury and death. (See PHENETHYLAMINE DESIGNER DRUGS-N-BENZYL SERIES management as indicated) (Ninnemann & Stuart, 2013).
    4) Delysid(R) is a white, base unstable crystalline solid (Shulgin, 1980).
    B) SOURCES
    1) LSD or its derivatives are said to be found in the seeds of the morning glory family (Ipomoea violacea, Rivea corymbosa) and preparations of these have been ingested by amateur thrill seekers (Gosselin et al, 1984).
    2) LSD was believed to be the ingredient in the parasitic fungus Claviceps purpurea and in the Convolvulaceae plant family, both of which were used in religious rites (Ellenhorn & Barceloux, 1988).
    C) USES
    1) LSD was once proposed as an analgesic in terminal patients, an aid in psychotherapy, and as an adjunct to the treatment of alcoholism, opioid addiction, sexual abnormalities, autism, and sociopathy (Ellenhorn & Barceloux, 1988; Gilman et al, 1996).

Overview

Life Support

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

Clinical Effects

    0.2.1) SUMMARY OF EXPOSURE
    A) USES: Lysergic acid diethylamide (LSD) is a hallucinogenic substance first synthesized in 1938. The d-isomer is the extremely potent hallucinogen while the l-isomer appears to be inactive. LSD was originally introduced as a drug for psychiatric use under the trade name of Delysid, but it has since been prohibited as a Schedule 1 substance in the United States. It is abused recreationally for its hallucinogenic effects. A closely related but less active compound, lysergic acid amide, is found naturally in the seeds of the morning glory and the Hawaiian baby wood rose. It is generally used orally, but it has also been used intravenously. There are also reports of patients who have snorted LSD.
    B) TOXICOLOGY: Although its mechanism of action is not exactly understood, it is known that LSD acts as a partial/full agonist at serotonin (5-HT) receptors.
    C) EPIDEMIOLOGY: LSD trafficking and abuse have decreased significantly since the year 2000; however, there are still hundreds of exposures reported every year to poison centers. Deaths and serious outcomes are usually due to trauma-related injuries rather than drug effects.
    D) WITH POISONING/EXPOSURE
    1) Ingestion of LSD causes alterations in cognition, resulting in auditory and visual hallucinations, behavioral changes, paranoia, mood fluctuations, and acute psychotic reactions. Within the first hour of ingestion, patients may experience feelings of tension, lightheadedness, mydriasis, twitching, flushing, tachycardia, hypertension and hyperreflexia. Perceptual changes may start after 30 minutes and include the aforementioned hallucinations and distortions of color, distance, shape, time, and synesthesias. Starting 2 to 12 hours from ingestion, the patient may experience euphoria, mood swings, feelings of depersonalization, derealization, and loss of body image. "Flashbacks" and panic reactions occur unpredictably and can occur even years after exposure. Injection of LSD causes similar symptoms. Seizures can develop in patients with severe toxicity. Rhabdomyolysis has also been reported.
    2) DRUG INTERACTIONS: Serotonin syndrome may develop if LSD is taken with other serotonergic drugs.
    0.2.3) VITAL SIGNS
    A) Hypertension or hypotension, tachycardia, tachypnea, and hyperthermia may occur.
    0.2.4) HEENT
    A) Mydriasis is frequently reported. Lacrimation may also occur.
    B) Impaired perception of color and other visual functions, persistent or recurrent visual illusions and halos around objects have been reported.
    0.2.6) RESPIRATORY
    A) Tachypnea and bronchoconstriction may occur at high doses.
    0.2.8) GASTROINTESTINAL
    A) Vomiting, diarrhea, salivation, and anorexia may occur.
    B) Retroperitoneal fibrosis has been associated with chronic LSD use.
    0.2.10) GENITOURINARY
    A) Rhabdomyolysis and renal failure have been reported, but are probably result from seizures and coma. Uterine contractions may occur. LSD is not normally nephrotoxic but has been linked to retroperitoneal fibrosis.
    0.2.13) HEMATOLOGIC
    A) Poor clot formation and retraction have been noted to occur early and to resolve spontaneously; leukocytosis is possible.
    0.2.15) MUSCULOSKELETAL
    A) Muscle rigidity has been seen as a result of LSD associated neuroleptic malignant syndrome.
    0.2.20) REPRODUCTIVE
    A) LSD has been implicated in teratogenicity, although the causative agent is not always clear and there is no consistency of findings.

Laboratory Monitoring

    A) Plasma and urine LSD levels are measurable and quantified by various techniques but are not clinically useful or readily available. LSD is not detected on most routine drug screens.
    B) Monitor total CK levels and renal function in patients with severe agitation, prolonged seizures or coma.
    C) Severely agitated patients may need cardiac monitoring, especially after receiving chemical sedation.
    D) A careful neurologic exam and head CT may be merited in patients with altered mental status.

Treatment Overview

    0.4.2) ORAL/PARENTERAL EXPOSURE
    A) MANAGEMENT OF MILD TO MODERATE TOXICITY
    1) For mild to moderate toxicity, treatment is largely supportive. This includes the use of benzodiazepines, such as lorazepam or diazepam, for anxiety or agitation.
    B) MANAGEMENT OF SEVERE TOXICITY
    1) Activated charcoal is generally of little value as LSD is rapidly absorbed from the gastrointestinal tract. Patients with severe agitation should be sedated with benzodiazepines, such as lorazepam or diazepam. Patients with prolonged agitation may develop rhabdomyolysis, which should be treated with aggressive fluid hydration.
    C) DECONTAMINATION
    1) PREHOSPITAL: Secondary to rapid absorption, the value of gastrointestinal decontamination is very limited. Decontamination is generally NOT recommended after recreational ingestions.
    2) HOSPITAL: In general, decontamination is not indicated for this overdose, but may be considered for massive overdoses that present early. Activated charcoal could be considered if the patient is awake and cooperative and if the ingestion was relatively recent. There is no role for the use of lavage, whole bowel irrigation or multiple doses of charcoal.
    D) AIRWAY MANAGEMENT
    1) Respiratory arrest has occurred in hospitalized LSD overdose, but is quite rare. In general, there is no reason to intubate a patient early.
    E) ANTIDOTE
    1) None.
    F) RHABDOMYOLYSIS
    1) Administer sufficient 0.9% saline to maintain urine output of 2 to 3 mL/kg/hr. Monitor input and output, serum electrolytes, CK, and renal function. Diuretics may be necessary to maintain urine output. Urinary alkalinization is NOT routinely recommended.
    G) ENHANCED ELIMINATION
    1) Due to its short half-life and a few serious medical reactions, hemoperfusion, hemodialysis, and peritoneal dialysis have not been used for LSD intoxication.
    H) PATIENT DISPOSITION
    1) HOME CRITERIA: Patients with mild symptoms after recreational doses may be observed at home. However, any patients with any concerns or with altered mental status may benefit from medical attention.
    2) OBSERVATION CRITERIA: Symptomatic patients who have any concerns or about whom others are concerned should be sent to a healthcare facility. In addition, patients with altered mental status may need to be observed for 12 hours or longer until they are clearly improved with normal mental status.
    3) ADMISSION CRITERIA: Severely symptomatic patients with abnormal vital signs or alterations in mental status should be admitted; however, this is rare. Due to extreme agitation, these patients may require significant sedation, necessitating ICU admissions.
    4) CONSULT CRITERIA: Patients admitted to the ICU may benefit from intensivist involvement. Patients may also benefit from psychiatric consultation after their acute toxicity resolves. Poison centers should be called on all exposures, and toxicologists may help give clinical guidance for a patient's toxicity.
    I) PITFALLS
    1) LSD is often "cut" with other drugs or substances, such as sugar, strychnine, phencyclidine, cocaine, and caffeine. Thus, toxicity may be caused by adulterated samples and not from LSD itself.
    J) TOXICOKINETICS
    1) Onset of action usually occurs within 30 to 90 minutes after ingestion. Symptoms may last for an extended period of time, and begin to clear after about 12 hours. LSD behaves according to a two compartment open model, with an average elimination half-life of 3 to 4 hours. LSD undergoes extensive hepatic metabolism via N-demethylation, N-deethylation, and hydroxylation to inactive metabolites. Only a small fraction is excreted in urine unchanged. It is highly protein bound (90%) and has a low volume of distribution (0.28 L/kg). It has a pKa of 7.8.
    K) DIFFERENTIAL DIAGNOSIS
    1) Differential diagnosis includes other drugs and substances that can cause hyperstimulation and/or psychosis, such as stimulants like cocaine or phencyclidine. Hallucinogenic substances may also have a similar presentation. Other causes of acute psychotic breaks should also be on the differential.
    0.4.6) PARENTERAL EXPOSURE
    A) Treatment of parenteral exposures is similar to oral exposures.

Range Of Toxicity

    A) TOXICITY: Typical recreational doses of the tartrate salt form are in the range of 25 to 250 mcg. Minimal lethal doses in humans range from 0.2 to 1 mg/kg; however, deaths are usually due to trauma that is secondary to hallucinations/altered perceptions rather than due to the direct actions of the drug.
    B) A single 100 to 400 mcg dose of LSD can produce an altered state of consciousness. Doses as low as 35 mcg can be hallucinogenic.

Clinical Effects

Vital Signs

    3.3.1) SUMMARY
    A) Hypertension or hypotension, tachycardia, tachypnea, and hyperthermia may occur.
    3.3.3) TEMPERATURE
    A) HYPERTHERMIA has been reported (Klock et al, 1975) Friedman & Hirsch, 1971; (Rosenberg et al, 1986; Maslanka & Scott, 1992).

Heent

    3.4.1) SUMMARY
    A) Mydriasis is frequently reported. Lacrimation may also occur.
    B) Impaired perception of color and other visual functions, persistent or recurrent visual illusions and halos around objects have been reported.
    3.4.3) EYES
    A) MYDRIASIS: Large pupils that remain reactive to light are common (Williams & Erickson, 2000; (Blaho et al, 1997; Ianzito et al, 1972; Maslanka & Scott, 1992; Al-Assmar, 1999).
    B) LACRIMATION may also occur in overdose (Caldwell & Sever, 1974).
    C) VISUAL ILLUSIONS including shimmering of images, streaking of moving objects, color distortion, and moving objects appearing as a consecutive series of stationary images have been reported (Williams & Erickson, 2000; (Levi & Miller, 1990). These persisted or recurred after periods of drug abstinence and in the absence of neurologic ophthalmic disease.
    1) Continuous visual disturbances were described in a 15-year-old male with a 1 year history of frequent LSD abuse (Kaminer & Hrecznyj, 1991). These consisted of colored-dot patterns, a trail of white, and halos around the borders of objects which occurred continuously in addition to intermittent visual and auditory hallucinations and persisted for one year despite LSD abstinence.
    D) IMPAIRED VISUAL FUNCTION: Depressed critical flicker frequencies and reduced sensitivity to light during dark adaptation were reported among past users of LSD (Abraham & Wolf, 1988).
    E) IMPAIRED COLOR PERCEPTION lasting as long as 2 years postingestion have been reported among chronic LSD users (Ellenhorn & Barceloux, 1988).
    F) NYSTAGMUS: has been reported following ingestion of 12 seeds of the Hawaiian baby woodrose, which contains LSD (Al-Assmar, 1999).

Cardiovascular

    3.5.2) CLINICAL EFFECTS
    A) HYPERTENSIVE EPISODE
    1) LSD can induce either mild hypertension or hypotension, depending on the predominant form of autonomic excitation, but pressure usually remains normal (Blaho et al, 1997; Klock et al, 1975; Kulig, 1990; Maslanka & Scott, 1992).
    2) CASE REPORT: An 18-year-old male ingested 12 seeds of Argyreia nervosa, commonly called Hawaiian baby woodrose, and subsequently developed hypertension (BP 170/90 mmHg). Four to eight of these seeds are equal to 10,100 micrograms of LSD (Al-Assmar, 1999).
    B) HYPOTENSIVE EPISODE
    1) LSD can induce either mild hypertension or hypotension, depending on the predominant form of autonomic excitation, but pressure usually remains normal (Klock et al, 1975; Kulig, 1990; Maslanka & Scott, 1992).
    C) TACHYARRHYTHMIA
    1) Tachycardia has been noted, especially in frightened children (Berrens et al, 2010; Blaho et al, 1997; Ianzito et al, 1972; Caldwell & Sever, 1974; Maslanka & Scott, 1992).
    2) Tachycardia was reported (110 beats/minute) in an 18-year-old male who ingested 12 seeds of Argyreia nervosa, commonly called Hawaiian baby woodrose. Four to eight of these seeds are equal to 10,100 micrograms of LSD (Al-Assmar, 1999).

Respiratory

    3.6.1) SUMMARY
    A) Tachypnea and bronchoconstriction may occur at high doses.
    3.6.2) CLINICAL EFFECTS
    A) HYPERVENTILATION
    1) At high doses, tachypnea and bronchiolar smooth muscle constriction may occur (Blaho et al, 1997; Ianzito et al, 1972; Caldwell & Sever, 1974; Samuelsson, 1974).
    B) APNEA
    1) Severe toxicity may result in coma, seizures, and respiratory arrest (Klock et al, 1975; Kulberg, 1986).

Neurologic

    3.7.2) CLINICAL EFFECTS
    A) NEUROTOXICITY
    1) SYMPATHOMIMETIC SYMPTOMS: Initially, sympathomimetic symptoms are seen including mydriasis (pupils remain reactive to light), piloerection, weakness, dizziness, paresthesias, diaphoresis, and restlessness (Caldwell & Sever, 1974; Al-Assmar, 1999).
    B) INCREASED MUSCLE TONE
    1) Skeletal muscle tension, tremor, hyperreflexia, and incoordination can develop (Mace, 1979). Muscle weakness and ataxia have been reported (Samuelsson, 1974).
    C) SEIZURE
    1) Hyperthermia, seizures, coma, and respiratory arrest have been reported with doses of LSD in excess of 1 mg (Klock et al, 1975; Fisher & Ungerleider, 1967). Status epilepticus is rare (Ellenhorn & Barceloux, 1988).
    2) VISUAL SEIZURES: Kaminer et al (1991) have hypothesized that posthallucinogen perception disorder (PHPD) occurs within the lateral geniculate nucleus of the thalamus and represents episodes of visual seizures. These visual seizures are visual flashbacks characterized by illusions of movement and halos around objects and may occur for up to several months or years after the last exposure.
    D) VASOSPASM
    1) CEREBRAL ARTERY SPASM has been reported in concentration ranges which parallel its "therapeutic" dose (Altura & Altura, 1981).
    2) CASE REPORT: A 19-year-old intravenous LSD and heroin abuser developed diffuse cerebral angiitis manifesting as nuchal rigidity and global aphasia (Lignelli & Buchheit, 1971).
    3) CASE REPORT: A 24-year-old woman who abused LSD and "diet pills" (phenylpropanolamine?) presented with seizures, headache, and small artery occlusive changes on cerebral angiography (Rumbaugh et al, 1971).
    4) CASE REPORT: A 14-year-old boy who ingested 4 LSD capsules presented with seizures, left-sided spasticity and hemiplegia, left-sided homonymous hemianopsia, conjugate eye deviation to the right, and progressive narrowing of the internal carotid artery with complete obstruction at the carotid siphon (Sobel et al, 1971).
    5) CASE REPORT: A 20-year-old woman presented with headache, nausea, vomiting, left-sided weakness, and occlusion of the right internal carotid artery (Lieberman et al, 1974).
    E) DISTURBANCE IN THINKING
    1) It is possible that repeated use of LSD can induce subtle deficits in the capacity for abstract thinking (Gilman et al, 1990).
    F) NEUROLEPTIC MALIGNANT SYNDROME
    1) Neuroleptic malignant syndrome has been associated with the use of LSD (Behan et al, 1991).
    2) A 21-year-old man developed bilateral extrapyramidal rigidity, hyperpyrexia, a fluctuating level of consciousness, and elevated liver enzymes following ingestion of large amounts of ethanol and 1 LSD tablet. Dantrolene 25 mg 3 times daily produced immediate resolution of symptoms (Bakheit et al, 1990; Behan et al, 1991).

Gastrointestinal

    3.8.1) SUMMARY
    A) Vomiting, diarrhea, salivation, and anorexia may occur.
    B) Retroperitoneal fibrosis has been associated with chronic LSD use.
    3.8.2) CLINICAL EFFECTS
    A) VOMITING
    1) Nausea and vomiting may occur at high doses (Caldwell & Sever, 1974).
    B) LOSS OF APPETITE
    1) Anorexia may occur (Sax & Lewis, 1989).
    C) DIARRHEA
    1) Diarrhea has been reported (Klock et al, 1975).
    D) EXCESSIVE SALIVATION
    1) Increased salivation may occur in overdose (Caldwell & Sever, 1974).
    E) RETROPERITONEAL FIBROSIS
    1) CASE REPORT: A 37-year-old male, with a past history of chronic LSD use, presented with abdominal pain, diarrhea, and weight loss. An abdominal CT scan and subsequent surgery revealed a calcified, fibrotic mesenteric mass partially obstructing a segment of the duodenum. Six months later, an abdominal CT scan revealed another mesenteric mass with similar symptoms. Prednisone, 60 mg daily was initiated and 4 months later, the mass decreased in size, although the patient's abdominal pain persisted (Berk et al, 1999).

Hepatic

    3.9.2) CLINICAL EFFECTS
    A) LIVER ENZYMES ABNORMAL
    1) Liver enzymes may be transiently elevated (Berrens et al, 2010; Bakheit et al, 1990).

Genitourinary

    3.10.1) SUMMARY
    A) Rhabdomyolysis and renal failure have been reported, but are probably result from seizures and coma. Uterine contractions may occur. LSD is not normally nephrotoxic but has been linked to retroperitoneal fibrosis.
    3.10.2) CLINICAL EFFECTS
    A) RENAL FAILURE SYNDROME
    1) Rhabdomyolysis and renal failure have been reported, but are probably due to effects (seizures, coma) of LSD, and not a direct effect of the drug. Oliguria, elevated muscle enzymes, hypotension and death have been reported (Mercieca & Brown, 1984).
    B) UTERINE SPASM
    1) Uterine muscles may constrict with LSD overdose (Caldwell & Sever, 1974; Rothlin, 1957).
    C) RETROPERITONEAL FIBROSIS
    1) LSD is not considered as a nephrotoxic agent, but has been linked to retroperitoneal fibrosis, like its congener methysergide (Stecker et al, 1974).

Hematologic

    3.13.1) SUMMARY
    A) Poor clot formation and retraction have been noted to occur early and to resolve spontaneously; leukocytosis is possible.
    3.13.2) CLINICAL EFFECTS
    A) LEUKOCYTOSIS
    1) Leukocytosis is possible (Hentschel et al, 2000) Williams & Erickson, 2000; (Garson & Robson, 1969; Cohen et al, 1967).
    B) BLOOD COAGULATION PATHWAY FINDING
    1) Eight patients with massive LSD overdose developed poor clot formation and retraction which resolved within 8 hours (Klock et al, 1975).
    2) Bleeding times may be abnormal immediately after massive LSD overdoses but prothrombin times, partial thromboplastin times, and platelet counts are usually normal (Klock et al, 1975).

Dermatologic

    3.14.2) CLINICAL EFFECTS
    A) EXCESSIVE SWEATING
    1) Diaphoresis is common (Williams & Erickson, 2000; (Ellenhorn & Barceloux, 1988; Al-Assmar, 1999).
    B) PILOERECTION
    1) Piloerection may develop (Caldwell & Sever, 1974).

Musculoskeletal

    3.15.1) SUMMARY
    A) Muscle rigidity has been seen as a result of LSD associated neuroleptic malignant syndrome.
    3.15.2) CLINICAL EFFECTS
    A) INCREASED MUSCLE TONE
    1) Behan et al (1991) hypothesize that muscle rigidity, seen in LSD associated neuroleptic malignant syndrome, is centrally-mediated. A cycle of excessive and sustained muscle contraction, followed by hyperpyrexia occurs and results in muscle damage. Muscle biopsy shows focal necrosis, generalized edema and possibly intense irregular contraction of the fibers. Rhabdomyolysis may develop.
    B) RHABDOMYOLYSIS
    1) WITH POISONING/EXPOSURE
    a) CASE REPORT: A 25-year-old man developed agitation and rhabdomyolysis after taking 3 doses (unknown quantity) of LSD. Laboratory results showed a peak CK of 359,000 Units/L (30 hours after presentation), elevated aminotransferases (AST 730 units/L and ALT 137 Units/L), and normal BUN and serum creatinine levels. Urine toxicology screen was positive for tetrahydrocannabinol and negative for other drugs such as PCP, benzodiazepines, cocaine, and amphetamines. Assay for LSD was not performed. Following supportive care, he recovered gradually and was discharged after 6 days (Berrens et al, 2010).

Endocrine

    3.16.2) CLINICAL EFFECTS
    A) HYPERGLYCEMIA
    1) Hyperglycemia may occur (Caldwell & Sever, 1974).

Immunologic

    3.19.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) IMMUNE SYSTEM DISORDER
    a) IN VITRO EFFECTS: LSD concentrations of 100 micromoles suppressed B-lymphocyte proliferation, T-lymphocyte effector function, and the production of cytokines IL-2, IL-4, and IL-6 in studies involving murine cells. Natural Killer cell activities were enhanced at LSD concentrations between 0.0001 to 0.1 micromoles and depressed at 100 micromoles.
    1) The authors conclude that the immune system may be affected by LSD concentrations which can occur in human exposures (House et al, 1994).

Reproductive

    3.20.1) SUMMARY
    A) LSD has been implicated in teratogenicity, although the causative agent is not always clear and there is no consistency of findings.
    3.20.2) TERATOGENICITY
    A) CONGENITAL ANOMALY
    1) There are a number of cases of reported LSD teratogenicity. The causative agent is not always clear and there is no consistency of findings (Walker & Helz, 1971; Pilapil et al, 1973; Eller & Morton, 1970) Smart & Batemen, 1968; (TERIS , 2000).
    2) Rare congenital abnormalities such as anophthalmia, true limb aplasia, and multiple cerebral and cerebellar malformations have been reported in children whose mothers had used LSD, but other factors were not ruled out (Apple & Bennett, 1974; Bogdanoff et al, 1972; Margolis & Martin, 1980).
    3) Although there is no strong evidence of teratogenic action by LSD in man, the 13 cases of limb defects and 18 cases of CNS and/or ocular defects indicate the need for continued surveillance (TERIS , 2000; Long, 1972; Schardein, 1993).
    4) LSD has been implicated in increased limb defects (68) and central nervous system and ocular abnormalities (42), but the evidence is not convincing. It is unlikely that a major teratogenic effect would have been missed during the widespread use of LSD in the 1970s (Koren, 1990).
    3.20.3) EFFECTS IN PREGNANCY
    A) UTERINE DISORDER
    1) LSD causes uterine contraction (Caldwell & Sever, 1974; Rothlin, 1957).
    B) ABORTION
    1) The incidence of abortions and fetal abnormalities appears to be higher among women who use illicit LSD but the effects of pure LSD on pregnancy and the fetus remain uncertain (Gilman et al, 1990; Jacobson & Berlin, 1972; McGlothlin et al, 1970).
    C) PREGNANCY CATEGORY
    LSDC
    Reference: Briggs et al, 1998

Carcinogenicity

    3.21.1) IARC CATEGORY
    A) IARC Carcinogenicity Ratings for CAS50-37-3 (International Agency for Research on Cancer (IARC), 2016; International Agency for Research on Cancer, 2015; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010a; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2008; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2007; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2006; IARC, 2004):
    1) Not Listed

Genotoxicity

    A) CHROMOSOMAL ABNORMALITIES - In vitro chromosomal abnormalities have been reported (Mace, 1979; Muneer, 1978; Cohen et al, 1967).
    B) SPERM CHROMOSOMAL ABNORMALITIES - Estop et al (1991) studied sperm from 7 healthy males, including one individual with a prior history of LSD use. A low percentage of abnormalities in chromosome number and chromosome structural were present in the sperm of all study participants. Prior LSD use was not apparently associated with greater chromosomal abnormalities.
    1) The small sample size prevents any conclusion regarding possible LSD effects, but does indicate that chromosomal abnormalities are present in the sperm of healthy males with no known exposure to genotoxic substances.

Summary Of Exposure

    A) USES: Lysergic acid diethylamide (LSD) is a hallucinogenic substance first synthesized in 1938. The d-isomer is the extremely potent hallucinogen while the l-isomer appears to be inactive. LSD was originally introduced as a drug for psychiatric use under the trade name of Delysid, but it has since been prohibited as a Schedule 1 substance in the United States. It is abused recreationally for its hallucinogenic effects. A closely related but less active compound, lysergic acid amide, is found naturally in the seeds of the morning glory and the Hawaiian baby wood rose. It is generally used orally, but it has also been used intravenously. There are also reports of patients who have snorted LSD.
    B) TOXICOLOGY: Although its mechanism of action is not exactly understood, it is known that LSD acts as a partial/full agonist at serotonin (5-HT) receptors.
    C) EPIDEMIOLOGY: LSD trafficking and abuse have decreased significantly since the year 2000; however, there are still hundreds of exposures reported every year to poison centers. Deaths and serious outcomes are usually due to trauma-related injuries rather than drug effects.
    D) WITH POISONING/EXPOSURE
    1) Ingestion of LSD causes alterations in cognition, resulting in auditory and visual hallucinations, behavioral changes, paranoia, mood fluctuations, and acute psychotic reactions. Within the first hour of ingestion, patients may experience feelings of tension, lightheadedness, mydriasis, twitching, flushing, tachycardia, hypertension and hyperreflexia. Perceptual changes may start after 30 minutes and include the aforementioned hallucinations and distortions of color, distance, shape, time, and synesthesias. Starting 2 to 12 hours from ingestion, the patient may experience euphoria, mood swings, feelings of depersonalization, derealization, and loss of body image. "Flashbacks" and panic reactions occur unpredictably and can occur even years after exposure. Injection of LSD causes similar symptoms. Seizures can develop in patients with severe toxicity. Rhabdomyolysis has also been reported.
    2) DRUG INTERACTIONS: Serotonin syndrome may develop if LSD is taken with other serotonergic drugs.

Laboratory Monitoring

Monitoring Parameters Levels

    4.1.1) SUMMARY
    A) Plasma and urine LSD levels are measurable and quantified by various techniques but are not clinically useful or readily available. LSD is not detected on most routine drug screens.
    B) Monitor total CK levels and renal function in patients with severe agitation, prolonged seizures or coma.
    C) Severely agitated patients may need cardiac monitoring, especially after receiving chemical sedation.
    D) A careful neurologic exam and head CT may be merited in patients with altered mental status.
    4.1.2) SERUM/BLOOD
    A) BLOOD/SERUM CHEMISTRY
    1) Monitor CK levels and renal function tests in patients with severe agitation, or prolonged seizures or coma.
    4.1.3) URINE
    A) URINARY LEVELS
    1) LSD is not detected on most routine toxicology screens.
    2) Urine may be positive for LSD up to 120 hours after ingestion (Baselt, 2000).

Methods

    A) IMMUNOASSAY
    1) LSD can be determined/detected both quantitatively and qualitatively by radioimmunoassay (RIA) which can be sensitive to levels of 0.1 ng/mL (Ellenhorn & Barceloux, 1997; (Stead et al, 1986).
    2) Altunkaya & Smith (1990) have evaluated the Coat-a-Count radioimmunoassay kit for urinary LSD (Diagnostic Products Corporation) and found it satisfactory in analyzing LSD in urine, serum, hemolyzed whole blood and stomach contents. Preliminary extraction of LSD from the samples is not normally necessary.
    B) CHROMATOGRAPHY
    1) Fluorometric thin-layer chromatographic (TLC) and high-performance liquid chromatographic (HPLC) methods may also be used to detect plasma LSD levels as low as 0.5 ng/mL (Ellenhorn, 1997; Smith & Robinson, 1985).
    2) Instrumental high-performance thin-layer chromatographic (HPTLC) methodology has been developed for the detection of LSD in urine. LSD levels less than 1 mcg/L urine can be detected (Blum et al, 1990).
    3) A GC/MS method which involves the formation of the N-trifluroacetyl derivative and utilizes a fused-silica, dimethylsilicone capillary column is far more sensitive and specific than thin-layer chromatography (Gold & Dackis, 1986; Papac & Foltz, 1989; Papac & Foltz, 1990).
    4) RIA screening combined with HPLC and fluorescence detection can quantify both blood and urine LSD levels (Twitchett et al, 1978). RIA with a detection limit of 0.1 ng/mL and HPLC with a limit of 0.5 ng/mL were positive, respectively, in 14 and 11 of 18 patients clinically diagnosed to have LSD intoxication. Both were 100% specific (McCarron et al, 1990).
    5) Highly sensitive quantification of urinary LSD has been accomplished through direct coupling of immunoaffinity chromatography to an ion-spray mass spectrometer. High flow-rates (up to 10 ml/min) can be used on a protein G column allowing large sample volumes (4 ml or greater) to be analyzed in less than 20 minutes (Rule & Henion, 1992).
    6) Bergemann et al (1999) described an HPLC and fluorescence detection method for determination of LSD levels in whole blood and urine. The detection limit, using this method, was 0.05 ng/mL.
    7) White et al (1999) described a method using high-performance liquid chromatography with isotope dilution mass spectrometry (IDMS), with either a deuterated analog of LSD or methylsergide as the internal standard. When compared with methylsergide, using the LSD analog as the internal standard improved the accuracy and reproducibility of the measurement.
    8) The value of these techniques lies in the ability to rule out other toxicants.

Treatment

Life Support

    A) Support respiratory and cardiovascular function.

Patient Disposition

    6.3.1) DISPOSITION/ORAL EXPOSURE
    6.3.1.1) ADMISSION CRITERIA/ORAL
    A) SUMMARY: Severely symptomatic patients with abnormal vital signs or alterations in mental status should be admitted; however, this is rare. Due to extreme agitation, these patients may require significant sedation, necessitating ICU admissions.
    B) Persons suffering from an acute overdose or those undergoing a "bad trip" (panic reaction) may require hospitalization (Klock et al, 1975). Psychotic episodes or flashbacks sometimes occur long after LSD ingestion; such episodes may also drive the victim to seek medical attention. Admission is necessary only (Kulig, 1990; Leikin et al, 1989):
    1) For severely intoxicated patients.
    2) If the patient does not regain insight or control of own thoughts or impulses.
    3) If the Emergency Department cannot observe the patient for an adequate period of time.
    4) If the patient is a suicide risk.
    5) If the diagnosis is truly in question.
    6.3.1.2) HOME CRITERIA/ORAL
    A) Patients with mild symptoms after recreational doses may be observed at home. However, any patients with any concerns or with altered mental status may benefit from medical attention.
    6.3.1.3) CONSULT CRITERIA/ORAL
    A) Patients admitted to the ICU may benefit from intensivist involvement. Patients may also benefit from psychiatric consultation after their acute toxicity resolves. Poison centers should be called on all exposures, and toxicologists may help give clinical guidance for a patient's toxicity.
    6.3.1.5) OBSERVATION CRITERIA/ORAL
    A) Symptomatic patients who have any concerns or about whom others are concerned should be sent to a healthcare facility. In addition, patients with altered mental status may need to be observed for 12 hours or longer until they are clearly improved with normal mental status.

Monitoring

    A) Plasma and urine LSD levels are measurable and quantified by various techniques but are not clinically useful or readily available. LSD is not detected on most routine drug screens.
    B) Monitor total CK levels and renal function in patients with severe agitation, prolonged seizures or coma.
    C) Severely agitated patients may need cardiac monitoring, especially after receiving chemical sedation.
    D) A careful neurologic exam and head CT may be merited in patients with altered mental status.

Oral Exposure

    6.5.1) PREVENTION OF ABSORPTION/PREHOSPITAL
    A) PREHOSPITAL: Secondary to rapid absorption, the value of gastrointestinal decontamination is very limited. Decontamination is generally NOT recommended after recreational ingestions.
    6.5.2) PREVENTION OF ABSORPTION
    A) SUMMARY
    1) In general, decontamination is not indicated for this overdose, but may be considered for massive overdoses that present early. Activated charcoal could be considered if the patient is awake and cooperative and if the ingestion was relatively recent. There is no role for the use of lavage, whole bowel irrigation or multiple doses of charcoal.
    2) Attempts at gut decontamination may intensify behavior abnormalities (Ellenhorn, 1997; Haddad et al, 1998).
    3) Gastric decontamination may be necessary in multiple drug ingestions and in massive overdoses of patients who present early in the course of intoxication (Haddad et al, 1998; Kulig, 1990).
    B) ACTIVATED CHARCOAL
    1) Consider activated charcoal after large ingestions (Kulig, 1990).
    2) CHARCOAL ADMINISTRATION
    a) Consider administration of activated charcoal after a potentially toxic ingestion (Chyka et al, 2005). Administer charcoal as an aqueous slurry; most effective when administered within one hour of ingestion.
    3) CHARCOAL DOSE
    a) Use a minimum of 240 milliliters of water per 30 grams charcoal (FDA, 1985). Optimum dose not established; usual dose is 25 to 100 grams in adults and adolescents; 25 to 50 grams in children aged 1 to 12 years (or 0.5 to 1 gram/kilogram body weight) ; and 0.5 to 1 gram/kilogram in infants up to 1 year old (Chyka et al, 2005).
    1) Routine use of a cathartic with activated charcoal is NOT recommended as there is no evidence that cathartics reduce drug absorption and cathartics are known to cause adverse effects such as nausea, vomiting, abdominal cramps, electrolyte imbalances and occasionally hypotension (None Listed, 2004).
    b) ADVERSE EFFECTS/CONTRAINDICATIONS
    1) Complications: emesis, aspiration (Chyka et al, 2005). Aspiration may be complicated by acute respiratory failure, ARDS, bronchiolitis obliterans or chronic lung disease (Golej et al, 2001; Graff et al, 2002; Pollack et al, 1981; Harris & Filandrinos, 1993; Elliot et al, 1989; Rau et al, 1988; Golej et al, 2001; Graff et al, 2002). Refer to the ACTIVATED CHARCOAL/TREATMENT management for further information.
    2) Contraindications: unprotected airway (increases risk/severity of aspiration) , nonfunctioning gastrointestinal tract, uncontrolled vomiting, and ingestion of most hydrocarbons (Chyka et al, 2005).
    6.5.3) TREATMENT
    A) MONITORING OF PATIENT
    1) Plasma and urine LSD levels are measurable and quantified by various techniques but are not clinically useful or readily available. LSD is not detected on most routine drug screens.
    2) Monitor total CK levels and renal function in patients with severe agitation, prolonged seizures or coma.
    3) Severely agitated patients may need cardiac monitoring, especially after receiving chemical sedation.
    4) A careful neurologic exam and head CT may be merited in patients with altered mental status.
    B) PSYCHOMOTOR AGITATION
    1) Benzodiazepines are generally effective in controlling agitation and combativeness (Williams & Erickson, 2000) (Blaho et al, 1997; Miller et al, 1992).
    a) INDICATION
    1) If patient is severely agitated, sedate with IV benzodiazepines.
    b) DIAZEPAM DOSE
    1) ADULT: 5 to 10 mg IV initially, repeat every 5 to 20 minutes as needed (Brophy et al, 2012; Prod Info diazepam IM, IV injection, 2008; Manno, 2003).
    2) CHILD: 0.1 to 0.5 mg/kg IV over 2 to 5 minutes; up to a maximum of 10 mg/dose. May repeat dose every 5 to 10 minutes as needed (Loddenkemper & Goodkin, 2011; Hegenbarth & American Academy of Pediatrics Committee on Drugs, 2008).
    c) LORAZEPAM DOSE
    1) ADULT: 2 to 4 mg IV initially; repeat every 5 to 10 minutes as needed (Manno, 2003).
    2) CHILD: 0.05 to 0.1 mg/kg IV over 2 to 5 minutes, up to a maximum of 4 mg/dose; may repeat in 5 to 15 minutes as needed (Brophy et al, 2012; Loddenkemper & Goodkin, 2011; Hegenbarth & American Academy of Pediatrics Committee on Drugs, 2008).
    d) Extremely large doses of benzodiazepines may be required in patients with severe intoxication in order to obtain adequate sedation. Titrate dose to clinical response and monitor for hypotension, CNS and respiratory depression, and the need for endotracheal intubation.
    2) CHLORDIAZEPOXIDE: Given at a dose of 50 to 100 milligrams in an adult, may be an alternative in an uncooperative patient (Kulig, 1990; Strassman, 1984).
    3) CHLORPROMAZINE
    a) Because of the possibility of simultaneous ingestion of other drugs such as dimethyltryptamine (DMT) along with the LSD, subsequent injection of a phenothiazine such as chlorpromazine can induce marked hypotension, sedation, potentiation of anticholinergic effects, and extrapyramidal reactions (Ellenhorn, 1997).
    b) Chlorpromazine can also lower the seizure threshold (Gilman et al, 1996). This may precipitate seizures, especially if the LSD has been cut with a CNS stimulant such as strychnine.
    c) Chlorpromazine may be used in doses of 50 to 100 mg, but effectiveness may be only partial until recovery occurs spontaneously (Ellenhorn, 1997).
    4) PSYCHOLOGIC ASSISTANCE may be helpful in "talking down" some patients who are undergoing a "bad trip". Reassurance by a psychiatrist, psychologist, or a trusted friend may be helpful in ameliorating the acute anxiety state (Ellenhorn, 1997; Gilman et al, 1996).
    5) Provide a quiet, dimly lit room for such therapy. Restraints imposed on patients suffering from LSD-induced psychotic anxiety state tend to worsen that state (Ellenhorn, 1997).
    6) HALOPERIDOL: May be given at doses of 5 to 10 milligrams intramuscularly or 10 to 20 milligrams orally, administered hourly as necessary in cases of extreme agitation or hallucinosis (Kulig, 1990; Leikin et al, 1989; Strassman, 1984; Miller et al, 1992). Although the manufacturers advocate against intravenous administration, this route has been recommended by some authors (Kulig, 1990; Prod Info Haldol(R), haloperidol, 1990).
    7) DROPERIDOL: A 24-year-old male, who became agitated, confused, tachycardic, hypertensive, and diaphoretic approximately 30 minutes after ingesting LSD, received droperidol 5 mg IV in the field. Within 5 minutes, the patient developed respiratory distress, requiring mechanical ventilation, and muscle rigidity, along with continued hypertension (154/92 mmHg), tachycardia (157 beats/min), and fever (38.6 degrees C), prompting a diagnosis of serotonin syndrome. The patient recovered with supportive care (Heard et al, 1999).
    a) The authors speculate that droperidol administration may have initiated the patient's respiratory distress and muscle rigidity and may have exacerbated the patient's symptoms secondary to LSD ingestion, and; therefore, do NOT recommend the administration of droperidol for sedation in patients exhibiting symptoms that are consistent with the diagnosis of serotonin syndrome.
    C) PSYCHOTIC DISORDER
    1) LSD psychosis requires treatment with neuroleptics (Leikin et al, 1989).
    2) Lisansky et al (1984) recommend drug-free observation of LSD psychosis for several days, using only minor tranquilizers if necessary, and then treating any clinical symptoms which develop.
    3) Drug therapy has included haloperidol, phenothiazines, ECT, tricyclic antidepressants, monoamine oxidase inhibitors, and lithium (Leikin et al, 1989; Strassman, 1984).
    4) L-5-HYDROXYTRYPTOPHAN (5-HTP) 400 milligrams/day and 100 milligrams/day of the carbidopa may reverse the symptoms of LSD-psychosis (Abraham, 1983). However, this regimen may cause eosinophilia-myalgia syndrome (Kulig, 1990).
    a) In a randomized, placebo-controlled double-blind crossover study, L-5-hydroxytryptophan (5-HTP) reversed the psychosis in a 23-year-old male who had developed psychotic symptoms following the use of LSD (Abraham, 1983).
    b) L-hydroxytryptophan is not recommended by some authors because of the potential for development of eosinophilia-myalgia syndrome (CDC, 1990; Chiba et al, 1990; Clauw et al, 1990; Golden, 1990; Kulig, 1990; Martin et al, 1990; Medsger, 1990; Swygert et al, 1990).
    c) There may be a possible role for serotonin-S2 receptor antagonists in the treatment of LSD-induced psychoses. Meert & Clincke (1992) have studied the effects of ritanserin, a serotonin-S2 antagonist, on rats with various chemical addictions and found an antagonism of the discriminative stimulus properties of LSD.
    1) Theoretically, it would seem reasonable to assume that serotonin-S2 receptor antagonists, such as risperidone or ketanserin, which are currently available in the United States, may be effective in the treatment of LSD-induced psychoses (Glennon, 1990).
    D) FLASHBACKS
    1) Psychotherapy and benzodiazepines as in ACUTE ANXIETY above may be indicated (Ellenhorn, 1997; Leikin et al, 1989).
    2) Other drugs used with variable success in the control of flashbacks include haloperidol, chlorpromazine, and phenytoin (Leikin et al, 1989).
    3) Patients should be instructed to avoid stress, antihistamines, marijuana, fatigue, and other known precipitating factors.
    E) NEUROLEPTIC MALIGNANT SYNDROME
    1) Neuroleptic malignant syndrome may be successfully managed with intravenous or oral dantrolene sodium, or bromocriptine in conjunction with cooling and other supportive care (May et al, 1983; Mueller et al, 1983; Leikin et al, 1987; Schneider, 1991; Barkin, 1992).
    a) DANTROLENE LOADING DOSE: 2.5 milligrams/kilogram, to a maximum of 10 milligrams/kilogram intravenously (Barkin, 1992).
    b) DANTROLENE MAINTENANCE DOSE: 2.5 milligrams/kilogram intravenously every 6 hours (Barkin, 1992); 1 milligram/kilogram orally every 12 hours, up to 50 milligrams/dose has also been successful (May et al, 1983).
    c) BROMOCRIPTINE DOSE: 5 milligrams three times a day orally (Mueller et al, 1983).
    d) NON-PHARMACOLOGIC METHODS: Rapid cooling, hydration, and serial assessment of respiratory, cardiovascular, renal and neurologic function, and fluid status are used in conjunction with drug therapy and discontinuation of the neuroleptic agent (Knight & Roberts, 1986).
    F) RHABDOMYOLYSIS
    1) SUMMARY: Early aggressive fluid replacement is the mainstay of therapy and may help prevent renal insufficiency. Diuretics such as mannitol or furosemide may be added if necessary to maintain urine output but only after volume status has been restored as hypovolemia will increase renal tubular damage. Urinary alkalinization is NOT routinely recommended.
    2) Initial treatment should be directed towards controlling acute metabolic disturbances such as hyperkalemia, hyperthermia, and hypovolemia. Control seizures, agitation, and muscle contractions (Erdman & Dart, 2004).
    3) FLUID REPLACEMENT: Early and aggressive fluid replacement is the mainstay of therapy to prevent renal failure. Vigorous fluid replacement with 0.9% saline (10 to 15 mL/kg/hour) is necessary even if there is no evidence of dehydration. Several liters of fluid may be needed within the first 24 hours (Walter & Catenacci, 2008; Camp, 2009; Huerta-Alardin et al, 2005; Criddle, 2003; Polderman, 2004). Hypovolemia, increased insensible losses, and third spacing of fluid commonly increase fluid requirements. Strive to maintain a urine output of at least 1 to 2 mL/kg/hour (or greater than 150 to 300 mL/hour) (Walter & Catenacci, 2008; Camp, 2009; Erdman & Dart, 2004; Criddle, 2003). To maintain a urine output this high, 500 to 1000 mL of fluid per hour may be required (Criddle, 2003). Monitor fluid input and urine output, plus insensible losses. Monitor for evidence of fluid overload and compartment syndrome; monitor serum electrolytes, CK, and renal function tests.
    4) DIURETICS: Diuretics (eg, mannitol or furosemide) may be needed to ensure adequate urine output and to prevent acute renal failure when used in combination with aggressive fluid therapy. Loop diuretics increase tubular flow and decrease deposition of myoglobin. These agents should be used only after volume status has been restored, as hypovolemia will increase renal tubular damage. If the patient is maintaining adequate urine output, loop diuretics are not necessary (Vanholder et al, 2000).
    5) URINARY ALKALINIZATION: Alkalinization of the urine is not routinely recommended, as it has never been documented to reduce nephrotoxicity, and may cause complications such as hypocalcemia and hypokalemia (Walter & Catenacci, 2008; Huerta-Alardin et al, 2005; Brown et al, 2004; Polderman, 2004). Retrospective studies have failed to demonstrate any clinical benefit from the use of urinary alkalinization (Brown et al, 2004; Polderman, 2004; Homsi et al, 1997).
    6) MANNITOL/INDICATIONS
    a) Osmotic diuretic used in the management of rhabdomyolysis and myoglobinuria (Zimmerman & Shen, 2013).
    7) RHABDOMYOLYSIS/MYOGLOBINURIA
    a) ADULT: TEST DOSE: (for patients with marked oliguria or those with inadequate renal function) 0.2 g/kg IV as a 15% to 25% solution infused over 3 to 5 minutes to produce a urine flow of at least 30 to 50 mL/hr; a second test dose may be given if urine flow does not increase within 2 to 3 hours. The patient should be reevaluated if there is inadequate response following the second test dose (Prod Info MANNITOL intravenous injection, 2009). TREATMENT DOSE: 50 to 100 g IV as a 15% to 25% solution may be used. The rate should be adjusted to maintain urinary output at 30 to 50 mL/hour (Prod Info mannitol IV injection, urologic irrigation, 2006) OR 300 to 400 mg/kg or up to 100 g IV administered as a single dose (Prod Info MANNITOL intravenous injection, 2009).
    b) PEDIATRIC: Dosing has not been established in patients less than 12 years of age(Prod Info Mannitol intravenous injection, 2009). TEST DOSE (for patients with marked oliguria or those with inadequate renal function): 0.2 g/kg or 6 g/m(2) body surface area IV as a 15% to 25% solution infused over 3 to 5 minutes to produce a urine flow of at least 30 to 50 mL/hr; a second test dose may be given if urine flow does not increase; TREATMENT DOSE: 0.25 to 2 g/kg or 60 g/m(2) body surface area IV as a 15% to 20% solution over 2 to 6 hours; do not repeat dose for persistent oliguria (Prod Info MANNITOL intravenous injection, 2009).
    8) ADVERSE EFFECTS
    a) Fluid and electrolyte imbalance, in particular sodium and potassium; expansion of the extracellular fluid volume leading to pulmonary edema or CHF exacerbations(Prod Info MANNITOL intravenous injection, 2009).
    9) PRECAUTION
    a) Contraindicated in well-established anuria or impaired renal function not responding to a test dose, pulmonary edema, CHF, severe dehydration; caution in progressive oliguria and azotemia; do not add to whole blood for transfusions(Prod Info Mannitol intravenous injection, 2009); enhanced neuromuscular blockade observed with tubocurarine(Miller et al, 1976).
    10) MONITORING PARAMETERS
    a) Renal function, urine output, fluid balance, serum potassium, serum sodium, and serum osmolality (Prod Info Mannitol intravenous injection, 2009).
    G) FLUID/ELECTROLYTE BALANCE REGULATION
    1) Monitor fluid and electrolyte balance closely.
    H) SEROTONIN SYNDROME
    1) SUMMARY
    a) Benzodiazepines are the mainstay of therapy. Cyproheptadine, a 5-HT antagonist, is also commonly used. Severe cases have been managed with benzodiazepine sedation and neuromuscular paralysis with non-depolarizing agents(Claassen & Gelissen, 2005).
    2) HYPERTHERMIA
    a) Control agitation and muscle activity. Undress patient and enhance evaporative heat loss by keeping skin damp and using cooling fans.
    b) MUSCLE ACTIVITY: Benzodiazepines are the drug of choice to control agitation and muscle activity. DIAZEPAM: ADULT: 5 to 10 mg IV every 5 to 10 minutes as needed, monitor for respiratory depression and need for intubation. CHILD: 0.25 mg/kg IV every 5 to 10 minutes; monitor for respiratory depression and need for intubation.
    c) Non-depolarizing paralytics may be used in severe cases.
    3) CYPROHEPTADINE
    a) Cyproheptadine is a non-specific 5-HT antagonist that has been shown to block development of serotonin syndrome in animals (Sternbach, 1991). Cyproheptadine has been used in the treatment of serotonin syndrome (Mills, 1997; Goldberg & Huk, 1992). There are no controlled human trials substantiating its efficacy.
    b) ADULT: 12 mg initially followed by 2 mg every 2 hours if symptoms persist, up to a maximum of 32 mg in 24 hours. Maintenance dose 8 mg orally repeated every 6 hours (Boyer & Shannon, 2005).
    c) CHILD: 0.25 mg/kg/day divided every 6 hours, maximum dose 12 mg/day (Mills, 1997).
    4) HYPERTENSION
    a) Monitor vital signs regularly. For mild/moderate asymptomatic hypertension, pharmacologic intervention is usually not necessary.
    5) HYPOTENSION
    a) Administer 10 to 20 mL/kg 0.9% saline bolus and place patient supine. Further fluid therapy should be guided by central venous pressure or right heart catheterization to avoid volume overload.
    b) Pressor agents with dopaminergic effects may theoretically worsen serotonin syndrome and should be used with caution. Direct acting agents (norepinephrine, epinephrine, phentolamine) are theoretically preferred.
    c) NOREPINEPHRINE
    1) PREPARATION: Add 4 mL of 0.1% solution to 1000 mL of dextrose 5% in water to produce 4 mcg/mL.
    2) INITIAL DOSE
    a) ADULT: 2 to 3 mL (8 to 12 mcg)/minute.
    b) ADULT or CHILD: 0.1 to 0.2 mcg/kg/min. Titrate to maintain adequate blood pressure.
    3) MAINTENANCE DOSE
    a) 0.5 to 1 mL (2 to 4 mcg)/minute.
    6) SEIZURES
    a) DIAZEPAM
    1) MAXIMUM RATE: Administer diazepam IV over 2 to 3 minutes (maximum rate: 5 mg/min).
    2) ADULT DIAZEPAM DOSE: 5 to 10 mg initially, repeat every 5 to 10 minutes as needed. Monitor for hypotension, respiratory depression and the need for endotracheal intubation. Consider a second agent if seizures persist or recur after diazepam 30 milligrams.
    3) PEDIATRIC DIAZEPAM DOSE: 0.2 to 0.5 mg/kg, repeat every 5 minutes as needed. Monitor for hypotension, respiratory depression and the need for endotracheal intubation. Consider a second agent if seizures persist or recur after diazepam 10 milligrams in children over 5 years or 5 milligrams in children under 5 years of age.
    4) RECTAL USE: If an intravenous line cannot be established, diazepam may be given per rectum (not FDA approved), or lorazepam may be given intramuscularly.
    b) LORAZEPAM
    1) MAXIMUM RATE: The rate of IV administration of lorazepam should not exceed 2 mg/min (Prod Info Ativan(R), 1991).
    2) ADULT LORAZEPAM DOSE: 2 to 4 mg IV. Initial doses may be repeated in 10 to 15 minutes, if seizures persist (Prod Info ATIVAN(R) injection, 2003).
    3) PEDIATRIC LORAZEPAM DOSE: 0.1 mg/kg IV push (range: 0.05 to 0.1 mg/kg; maximum dose 4 mg); may repeat dose in 5 to 10 minutes if seizures continue. It has also been given rectally at the same dose in children with no IV access (Sreenath et al, 2009; Chin et al, 2008; Wheless, 2004; Qureshi et al, 2002; De Negri & Baglietto, 2001; Mitchell, 1996; Appleton, 1995; Giang & McBride, 1988).
    c) RECURRING SEIZURES
    1) If seizures cannot be controlled with diazepam or recur, give phenobarbital or propofol.
    d) PHENOBARBITAL
    1) SERUM LEVEL MONITORING: Monitor serum levels over next 12 to 24 hours for maintenance of therapeutic levels (15 to 25 mcg/mL).
    2) ADULT PHENOBARBITAL LOADING DOSE: 600 to 1200 mg of phenobarbital IV initially (10 to 20 mg/kg) diluted in 60 mL of 0.9% saline given at 25 to 50 mg/minute.
    3) ADULT PHENOBARBITAL MAINTENANCE DOSE: Additional doses of 120 to 240 mg may be given every 20 minutes.
    4) MAXIMUM SAFE ADULT PHENOBARBITAL DOSE: No maximum safe dose has been established. Patients in status epilepticus have received as much as 100 mg/min until seizure control was achieved or a total dose of 10 mg/kg.
    5) PEDIATRIC PHENOBARBITAL LOADING DOSE: 15 to 20 mg/kg of phenobarbital intravenously at a rate of 25 to 50 mg/min.
    6) PEDIATRIC PHENOBARBITAL MAINTENANCE DOSE: Repeat doses of 5 to 10 mg/kg may be given every 20 minutes.
    7) MAXIMUM SAFE PEDIATRIC PHENOBARBITAL DOSE: No maximum safe dose has been established. Children in status epilepticus have received doses of 30 to 120 mg/kg within 24 hours. Vasopressors and mechanical ventilation were needed in some patients receiving these doses.
    8) NEONATAL PHENOBARBITAL LOADING DOSE: 20 to 30 mg/kg IV at a rate of no more than 1 mg/kg/min in patients with no preexisting phenobarbital serum levels.
    9) NEONATAL PHENOBARBITAL MAINTENANCE DOSE: Repeat doses of 2.5 mg/kg every 12 hours may be given; adjust dosage to maintain serum levels of 20 to 40 mcg/mL.
    10) MAXIMUM SAFE NEONATAL PHENOBARBITAL DOSE: Doses of up to 20 mg/kg/min up to a total of 30 mg/kg have been tolerated in neonates.
    11) CAUTION: Adequacy of ventilation must be continuously monitored in children and adults. Intubation may be necessary with increased doses.
    7) CHLORPROMAZINE
    a) Chlorpromazine is a 5-HT2 receptor antagonist that has been used to treat cases of serotonin syndrome (Graham, 1997; Gillman, 1996). Controlled human trial documenting its efficacy are lacking.
    b) ADULT: 25 to 100 mg intramuscularly repeated in 1 hour if necessary.
    c) CHILD: 0.5 to 1 mg/kg repeated as needed every 6 to 12 hours not to exceed 2 mg/kg/day.
    8) NOT RECOMMENDED
    a) BROMOCRIPTINE: It has been used in the treatment of neuroleptic malignant syndrome but is NOT RECOMMENDED in the treatment of serotonin syndrome as it has serotonergic effects (Gillman, 1997). In one case the use of bromocriptine was associated with a fatal outcome (Kline et al, 1989).

Enhanced Elimination

    A) EXTRACORPOREAL ELIMINATION
    1) Because of the short half-life and few serious medical reactions, hemoperfusion, hemodialysis, and peritoneal dialysis have not been used for LSD intoxication (Ellenhorn, 1997).

Abstracts

Case Reports

    A) ACUTE EFFECTS
    1) Bakheit et al (1990) report the case of a 21-year-old male presenting to the ED unconscious following alcohol and LSD ingestion a few hours earlier. Presentation included marked bilateral extrapyramidal rigidity and bilateral extensor plantar responses. Pulse rate was 100/min and blood pressure 120/70 mm Hg. No other signs of toxicity were present on admission.
    a) His condition over the following days included fluctuating levels of consciousness and low grade fever. Transient visual hallucinations developed on day 2. Slurred speech and hypokinesia were notable. Laboratory values included elevated liver function tests, increased CPK, and increased ESR. Urine myoglobin was negative. Muscle biopsy revealed conspicuous contraction banding of fibers.
    b) Neuroleptic malignant syndrome was diagnosed. Treatment with oral dantrolene was initiated, and the patient made a full recovery by day 12.

Range Of Toxicity

Summary

    A) TOXICITY: Typical recreational doses of the tartrate salt form are in the range of 25 to 250 mcg. Minimal lethal doses in humans range from 0.2 to 1 mg/kg; however, deaths are usually due to trauma that is secondary to hallucinations/altered perceptions rather than due to the direct actions of the drug.
    B) A single 100 to 400 mcg dose of LSD can produce an altered state of consciousness. Doses as low as 35 mcg can be hallucinogenic.

Therapeutic Dose

    7.2.1) ADULT
    A) GENERAL
    1) Minimum effective dose - 25 micrograms (Gilman et al, 1996).
    2) PSYCHEDELIC DOSE - 100 to 750 micrograms, with as much as 1000 to 3000 micrograms in some studies (Louria, 1968).
    3) Usual street dose - 50 to 300 micrograms (Gilman et al, 1996).
    4) 30 micrograms/kilogram may produce intense depersonalization and derealization (Cohen et al, 1967).
    5) Intravenously, 50 to 500 micrograms have been given (Louria, 1968).

Minimum Lethal Exposure

    A) GENERAL/SUMMARY
    1) Estimates of average lethal doses in humans range from 0.2 to 1 mg/kg (Hoffer, 1965) Leiken et al, 1989).
    2) Deaths from LSD are usually due to trauma occurring during hallucinations with altered perceptions rather than due to the drug itself (Ellenhorn & Barceloux, 1988).
    3) Witnessed respiratory arrest in hospitalized LSD overdoses indicates that death can occur after LSD use (Gosselin et al, 1984; Ellenhorn & Barceloux, 1988).
    B) CASE REPORTS
    1) Two deaths have been directly attributed to LSD overdoses, both with laboratory documentation of LSD levels in body fluids and tissues in the absence of evidences for other causes of death (Fysh et al, 1985; Griggs & Ward, 1977).
    C) ANIMAL DATA
    1) An elephant has been killed by a 300-mg (0.1 mg/kg) intramuscular injection (West et al, 1962).

Maximum Tolerated Exposure

    A) CASE REPORTS
    1) Doses of 20 micrograms/kilogram have been survived but the psychic disturbances are profound and may have permanent sequelae (Gosselin et al, 1984).
    2) Humans have ingested up to 1 milligram/kilogram safely (Haddad & Winchester, 1990).

Serum Plasma Blood Concentrations

    7.5.2) TOXIC CONCENTRATIONS
    A) TOXIC CONCENTRATION LEVELS
    1) CONCENTRATION LEVEL
    a) Dose of 2 micrograms/kilogram intravenously = 9.5 nanograms/milliliter in plasma 5 minutes after, and dropping to 1 nanogram/milliliter at 8 hours (Aghajanian & Bing, 1964).
    b) Dose of 600 micrograms orally (35-year-old) = 2 nanograms/milliliter in plasma at 30 minutes, 1.9 nanogram/milliliter at 1 hour and 1 nanogram/milliliter at 4 hours (Widdop, 1974).
    c) Dose of 500 micrograms orally (17-year-old) = 4.2 nanograms/milliliter in plasma 2 hours postingestion (Widdop, 1974).
    d) Dose of 200 to 400 micrograms orally in adults = urine levels of 0 to 55 nanograms/milliliter 24 hours postingestion (Taunton-Rigby et al, 1973).
    e) A 25-year-old man who died 16 hours postadmission had an antemortem plasma LSD level of 14.8 ng/mL and a postmortem level of 4.8 ng/mL (Fysh et al, 1985).
    f) 2 of 8 patients who insufflated massive doses of LSD presented with coma, vomiting, sympathomimetic signs, and admission plasma LSD levels of 6.6 and 11.6 ng/mL (Klock et al, 1975). Another patient with catatonia, hyperreflexia, and fixed mydriasis had an admission plasma LSD level of 16 ng/mL.
    g) A 28-year-old man with hallucinations but without gastrointestinal symptoms had an admission plasma LSD level of 2.1 ng/mL (Ellenhorn & Barceloux, 1988).

Workplace Standards

    A) ACGIH TLV Values for CAS50-37-3 (American Conference of Governmental Industrial Hygienists, 2010):
    1) Not Listed

    B) NIOSH REL and IDLH Values for CAS50-37-3 (National Institute for Occupational Safety and Health, 2007):
    1) Not Listed

    C) Carcinogenicity Ratings for CAS50-37-3 :
    1) ACGIH (American Conference of Governmental Industrial Hygienists, 2010): Not Listed
    2) EPA (U.S. Environmental Protection Agency, 2011): Not Listed
    3) IARC (International Agency for Research on Cancer (IARC), 2016; International Agency for Research on Cancer, 2015; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010a; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2008; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2007; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2006; IARC, 2004): Not Listed
    4) NIOSH (National Institute for Occupational Safety and Health, 2007): Not Listed
    5) MAK (DFG, 2002): Not Listed
    6) NTP (U.S. Department of Health and Human Services, Public Health Service, National Toxicology Project ): Not Listed

    D) OSHA PEL Values for CAS50-37-3 (U.S. Occupational Safety, and Health Administration (OSHA), 2010):
    1) Not Listed

Toxicity Information

    7.7.1) TOXICITY VALUES
    A) LD50- (INTRAPERITONEAL)MOUSE:
    1) 50 mg/kg ((RTECS, 2000))

Pharmacology Toxicology

Toxicologic Mechanism

    A) HALLUCINOGENESIS -
    1) LSD, an indolealkylamine, acts on multiple sites at the CNS, but its best studied effects are the agonistic actions at presynaptic receptors for 5-hydroxytryptamine (5-HT) in the midbrain (Gilman et al, 1996).
    a) Various hypotheses regarding the mechanisms of LSD actions have been reviewed by Agahajanian (1972). One hypothesis is that LSD prevents the inhibitory effects of serotonin on the next neurons in the chain. The results could include increased electrical firing of neurons in the brain with associated distortions of perception and thought. Other authors contend that the postsynaptic serotonin receptors are more affected than the presynaptic ones (Kuhn et al, 1978).
    b) With inhibition or displacement of serotonin, there is disinhibition of sensory and higher cortical function neurons for which serotonin is an inhibitory neurotransmitter (Kulig, 1990). The increased electrical firing of neurons cause perceptual and thought distortions.
    c) The inhibitory effects of LSD on raphe (5-HT) neurons can account for its hallucinogenic effects but this has to be verified because of contradictory animal studies (Gilman et al, 1996; Kulig, 1990).
    d) LSD and related agents act selectively at 5-HT2 receptors either as agonists or partial agonists (Gilman et al, 1996; Titeler et al, 1988).
    e) At the locus ceruleus, LSD decreases spontaneous activity but enhances activation by peripheral stimuli (Gilman et al, 1996).
    f) Potentiation of the excitomodulatory effect of serotonin in the facial motor nucleus and possibly in the nucleaus accumbens is the postulated hallucinatory mechanism of LSD (Leikin et al, 1989). The hallucinatory effects are propagated and sustained also with the inhibition of the dorsal and medial raphe neurons.
    g) Burris et al (1991) have demonstrated in animal studies that +LSD, but not its nonhallucinogenic congeners, is a 5-HT(1C) receptor agonist. These receptors may have a role in mediating the psychoactive effects of LSD.
    h) Penington & Fox (1994) have demonstrated in rat neurons that LSD mimicks the actions of 5-HT. LSD significantly suppresses calcium current in a dose-dependent manner and activates a potassium conductance. LSD may activate 5-HT(1A) receptors of the dorsal raphe nucleus, causing inhibition of 5-HT release. Reduction of competition between 5-HT and LSD for the postsynaptic 5-HT receptors may play a role in the hallucinogenic effects of LSD.
    i) LSD binds to areas of the hippocampus, corpus striatum, cerebral cortex, and, to a much lesser extent, cerebellum (Ellenhorn & Barceloux, 1988) 1997).
    j) Animal studies show increased spontaneous potentials in the retina, optic nerve, and visual cortex generated with toxic LSD levels in the optic tracts and lateral geniculate bodies (McLane & Carroll, 1986).
    k) Behavioral changes induced by LSD correlate accurately with changes in intracellular serotonin concentration (Louria, 1968).
    2) The probable agonist/antagonist effect of LSD on postsynaptic dopamine receptors and the physiologic significance of this mechanism have yet to be established (Ellenhorn & Barceloux, 1988; Kulig, 1990).
    3) The etiology of flashbacks is unknown. Theories have related flashbacks to a "visual seizure" phenomenon due to LSD effects on the lateral geniculate nucleus but others believe that it is a function of the normal memory process and should be classified as an atypical dissociative disorder (Leikin et al, 1989)
    B) TOLERANCE -
    1) LSD is more potent than 5-HT in stimulating phosphoinositide hydrolysis mediated by 5-HT2 receptors but the maximum response to LSD is only 25% of that to 5-HT (Gilman et al, 1996). This down regulation of receptors may account for the rapid development of tolerance to LSD and related agents.
    2) The neurochemical basis for tolerance involve changes within the central nervous system rather than increased peripheral metabolism and appear to operate at a site other than that mediating behavioral effects (Trulson & Crisp, 1982) 1983).
    3) A high degree of tolerance to the behavioral effects develops after 3 to 4 daily doses (Gilman et al, 1996). However, the drug is most commonly used sporadically and after 3 to 4 days of abstinence, preexisting sensitivity to the drug returns (Caldwell & Sever, 1974).
    4) Cross-tolerance with other hallucinogens, such as mescaline or psilocybin, has been noted (Appel & Freedman, 1968) but none between LSD and amphetamines or between LSD-like drugs and scopolamine (Gilman et al, 1996).
    C) WITHDRAWAL - A withdrawal syndrome does not occur upon abrupt discontinuation of LSD use and signs of physical dependence have not been seen (Gilman et al, 1996; Gosselin et al, 1984).
    D) BLEEDING DISORDERS - Abnormal clotting and poor clot retraction may be due to the inhibition of serotonin-induced platelet aggregation (Ellenhorn & Barceloux, 1988).

Physicochemical

Physical Characteristics

    A) LSD is colorless, odorless, and tasteless (Haddad et al, 1998; Mace, 1979).

Molecular Weight

    A) 323.42

References

General Bibliography

    1) 40 CFR 372.28: Environmental Protection Agency - Toxic Chemical Release Reporting, Community Right-To-Know, Lower thresholds for chemicals of special concern. National Archives and Records Administration (NARA) and the Government Printing Office (GPO). Washington, DC. Final rules current as of Apr 3, 2006.
    2) 40 CFR 372.65: Environmental Protection Agency - Toxic Chemical Release Reporting, Community Right-To-Know, Chemicals and Chemical Categories to which this part applies. National Archives and Records Association (NARA) and the Government Printing Office (GPO), Washington, DC. Final rules current as of Apr 3, 2006.
    3) 49 CFR 172.101 - App. B: Department of Transportation - Table of Hazardous Materials, Appendix B: List of Marine Pollutants. National Archives and Records Administration (NARA) and the Government Printing Office (GPO), Washington, DC. Final rules current as of Aug 29, 2005.
    4) 62 FR 58840: Notice of the National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances - Proposed AEGL Values, Environmental Protection Agency, NAC/AEGL Committee. National Archives and Records Administration (NARA) and the Government Publishing Office (GPO), Washington, DC, 1997.
    5) 65 FR 14186: Notice of the National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances - Proposed AEGL Values, Environmental Protection Agency, NAC/AEGL Committee. National Archives and Records Administration (NARA) and the Government Publishing Office (GPO), Washington, DC, 2000.
    6) 65 FR 39264: Notice of the National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances - Proposed AEGL Values, Environmental Protection Agency, NAC/AEGL Committee. National Archives and Records Administration (NARA) and the Government Publishing Office (GPO), Washington, DC, 2000.
    7) 65 FR 77866: Notice of the National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances - Proposed AEGL Values, Environmental Protection Agency, NAC/AEGL Committee. National Archives and Records Administration (NARA) and the Government Publishing Office (GPO), Washington, DC, 2000.
    8) 66 FR 21940: Notice of the National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances - Proposed AEGL Values, Environmental Protection Agency, NAC/AEGL Committee. National Archives and Records Administration (NARA) and the Government Publishing Office (GPO), Washington, DC, 2001.
    9) 67 FR 7164: Notice of the National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances - Proposed AEGL Values, Environmental Protection Agency, NAC/AEGL Committee. National Archives and Records Administration (NARA) and the Government Publishing Office (GPO), Washington, DC, 2002.
    10) 68 FR 42710: Notice of the National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances - Proposed AEGL Values, Environmental Protection Agency, NAC/AEGL Committee. National Archives and Records Administration (NARA) and the Government Publishing Office (GPO), Washington, DC, 2003.
    11) 69 FR 54144: Notice of the National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances - Proposed AEGL Values, Environmental Protection Agency, NAC/AEGL Committee. National Archives and Records Administration (NARA) and the Government Publishing Office (GPO), Washington, DC, 2004.
    12) AIHA: 2006 Emergency Response Planning Guidelines and Workplace Environmental Exposure Level Guides Handbook, American Industrial Hygiene Association, Fairfax, VA, 2006.
    13) Abraham HD & Wolf E: Visual function in past users of LSD: Psychophysical findings. J Abnorm Psychol 1988; 4:443-447.
    14) Abraham HD: L-5-hydroxytryptophan for LSD-induced psychosis. Am J Psychiatry 1983; 140:456-458.
    15) Aghajanian GK & Bing OHL: Persistence of lysergic acid diethylamide in the plasma of human subjects. Clin Pharmacol Ther 1964; 5:611-614.
    16) Al-Assmar SE: The seeds of the Hawaiian baby woodrose are a powerful hallucinogen. Arch Intern Med 1999; 159:2090.
    17) Altura BT & Altura BM: Phencyclidine lyseric acid diethylamide, and mescaline: cerebral artery spasms and hallucinogenic activity. Science 1981; 212:1051-1052.
    18) American Conference of Governmental Industrial Hygienists : ACGIH 2010 Threshold Limit Values (TLVs(R)) for Chemical Substances and Physical Agents and Biological Exposure Indices (BEIs(R)), American Conference of Governmental Industrial Hygienists, Cincinnati, OH, 2010.
    19) Apple DJ & Bennett TO: Multiple systemic and ocular malformations associated with maternal LSD usage. Arch Ophthalmol 1974; 92:301-303.
    20) Appleton R: Lorazepam vs diazepam in the acute treatment of epileptic seizures and status epilepticus.. Dev Med Child Neuro 1995; 37:682-688.
    21) Axelrod J, Brady RO, & Witkop B: The distribution and metabolism of lysergic acid diethylamine. Ann Acad Sci 1957; 66:435-444.
    22) Bakheit AMO, Behan PO, & Prach AT: A syndrome identical to the neuroleptic malignant syndrome induced by LSD and alcohol. Br J Addiction 1990; 85:150-151.
    23) Barkin RM: Pediatric Emergency Medicine, Mosby YearBook, St Louis, MO, 1992, pp 500.
    24) Baselt RC: Disposition of Toxic Drugs and Chemicals in Man, 5th ed, Chemical Toxicology Institute, Foster City, CA, 2000.
    25) Behan WMH, Bakheit AMO, & Behan PO: The muscle findings in the neuroleptic malignant syndrome associated with lysergic acid diethylamide. J Neurol Neurosurg Psychiatry 1991; 54:741-743.
    26) Berk SI, LeBlond RF, & Hodges KB: A mesenteric mass in a chronic LSD user (letter). Amer J Med 1999; 107:188-189.
    27) Berrens Z, Lammers J, & White C: Rhabdomyolysis After LSD Ingestion. Psychosomatics 2010; 51(4):356-356.
    28) Blacha C, Schmid MM, Gahr M, et al: Self-inflicted testicular amputation in first lysergic acid diethylamide use. J Addict Med 2013; 7(1):83-84.
    29) Blaho K, Merigian K, & Wingery S: Clinical pharmacology of lysergic acid diethylamine: case reports and review of the treatment of intoxication. Am J Therapeutics 1997; 4:211-221.
    30) Blum LM, Carenzo EF, & Rieders F: Determination of lysergic acid diethylamide (LSD) in urine by instrumental high-performance thin-layer chromatography. J Analytical Tox 1990; 14:285-287.
    31) Bogdanoff B, Rorke LB, & Tanoff M: Brain and eye abnormalities. Am J Dis Child 1972; 123:145-148.
    32) Boyer EW & Shannon M: The serotonin syndrome. N Eng J Med 2005; 352(11):1112-1120.
    33) Brophy GM, Bell R, Claassen J, et al: Guidelines for the evaluation and management of status epilepticus. Neurocrit Care 2012; 17(1):3-23.
    34) Brown CV, Rhee P, Chan L, et al: Preventing renal failure in patients with rhabdomyolysis: do bicarbonate and mannitol make a difference?. J Trauma 2004; 56(6):1191-1196.
    35) Brown RT & Braden NJ: Hallucinogens. Pediatr Clin North Am 1987; 34:341-347.
    36) CDC: Analysis of L-tryptophan for the etiology of eosinophilia-myalgia syndrome. CDC: MMWR 1990; 39:589-591.
    37) Caldwell J & Sever PS: The biochemical pharmacology of abused drugs. 1. Amphetamines, cocaine, and LSD. Clin Pharmacol Ther 1974; 16(4):625-638.
    38) Camp NE: Drug- and toxin-induced Rhabdomyolysis. J Emerg Nurs 2009; 35(5):481-482.
    39) Chiba S, Miyagawak K, & Tanaka T: Tryptophan-associated eosinophilia-myalgia syndrome and pancreatitis. Lancet 1990; 336:121.
    40) Chin RF , Neville BG , Peckham C , et al: Treatment of community-onset, childhood convulsive status epilepticus: a prospective, population-based study. Lancet Neurol 2008; 7(8):696-703.
    41) Chyka PA, Seger D, Krenzelok EP, et al: Position paper: Single-dose activated charcoal. Clin Toxicol (Phila) 2005; 43(2):61-87.
    42) Claassen JAHR & Gelissen HPMM: The serotonin syndrome (letter). N Eng J Med 2005; 352(23):2455.
    43) Clauw DJ, Nashel DJ, & Umhau A: Tryptophan-associated eosinophilic connective tissue disease. JAMA 1990; 263:1502-1506.
    44) Cohen MM, Hirschhorn K, & Frosch WA: In vivo and in vitro chromosomal damage induced by LSD-25. N Engl J Med 1967; 277:1043-1049.
    45) Criddle LM: Rhabdomyolysis. Pathophysiology, recognition, and management. Crit Care Nurse 2003; 23(6):14-22, 24-26, 28.
    46) DFG: List of MAK and BAT Values 2002, Report No. 38, Deutsche Forschungsgemeinschaft, Commission for the Investigation of Health Hazards of Chemical Compounds in the Work Area, Wiley-VCH, Weinheim, Federal Republic of Germany, 2002.
    47) De Negri M & Baglietto MG: Treatment of status epilepticus in children. Paediatr Drugs 2001; 3(6):411-420.
    48) Decker WJ & Brandes WB: LSD misadventure in middle age. J Forensic Sci 1978; 23:3-4.
    49) EPA: Search results for Toxic Substances Control Act (TSCA) Inventory Chemicals. US Environmental Protection Agency, Substance Registry System, U.S. EPA's Office of Pollution Prevention and Toxics. Washington, DC. 2005. Available from URL: http://www.epa.gov/srs/.
    50) Ellenhorn MJ & Barceloux DG: Medical Toxicology: Diagnosis and Treatment of Human Poisoning, Elsevier, New York, NY, 1988.
    51) Ellenhorn MJ: Medical Toxicology: Diagnosis and Treatment of Human Poisoning, 2nd ed, Williams and Wilkins, Baltimore, MD, 1997.
    52) Eller JL & Morton JM: Bizarre deformities in offspring of user of lysergic acid diethylamide. N Engl J Med 1970; 283:395-397.
    53) Elliot CG, Colby TV, & Kelly TM: Charcoal lung. Bronchiolitis obliterans after aspiration of activated charcoal. Chest 1989; 96:672-674.
    54) Erdman AR & Dart RC: Rhabdomyolysis. In: Dart RC, Caravati EM, McGuigan MA, et al, eds. Medical Toxicology, 3rd ed. Lippincott Williams & Wilkins, Philadelphia, PA, 2004, pp 123-127.
    55) FDA: Poison treatment drug product for over-the-counter human use; tentative final monograph. FDA: Fed Register 1985; 50:2244-2262.
    56) Fisher D & Ungerleider J: Grand mal seizures following ingestion of LSD. California Med 1967; 106:210-211.
    57) Fysh RR, Oon MCH, & Robinson KN: A fatal poisoning with LSD. Forensic Sci Int 1985; 28:109-113.
    58) Garson OM & Robson MK: Studies in a patient with acute leukemia after lysergide treatment. Br Med J 1969; 2:800-2.
    59) Giang DW & McBride MC : Lorazepam versus diazepam for the treatment of status epilepticus. Pediatr Neurol 1988; 4(6):358-361.
    60) Gillman PK: Ecstasy, serotonin syndrome and the treatment of hyperpyrexia (letter). MJA 1997; 167:109-111.
    61) Gillman PK: Successful treatment of serotonin syndrome with chlorpromazine (letter). MJA 1996; 165:345.
    62) Gilman AG, Hardman JG, & Limbird LE: Goodman and Gilman's The Pharmacological Basis of Therapeutics, 9th ed, McGraw-Hill, New York, NY, 1996.
    63) Gilman AG, Rall TW, & Nies AS: Goodman and Gilman's The Pharmacological Basis of Therapeutics, 8th ed, Pergamon Press, New York, NY, 1990.
    64) Glennon RA: Do classical hallucinogens act as 5-HT2 agonists or antagonists?. Neuropsychopharmacology 1990; 3:509-517.
    65) Gold MS & Dackis CA: Role of the laboratory in the evaluation of suspected drug abuse. J Clin Psychiatry 1986; 1 (suppl):17-23.
    66) Goldberg RJ & Huk M: Serotonin syndrome from trazodone and buspirone (letter). Psychosomatics 1992; 33:235-236.
    67) Golden RL: Eosinophilia-myalgia syndrome and L-tryptophan. N Y State J Med 1990; 90:512-513.
    68) Golej J, Boigner H, Burda G, et al: Severe respiratory failure following charcoal application in a toddler. Resuscitation 2001; 49:315-318.
    69) Gosselin RE, Smith RP, & Hodge HC: Clinical Toxicology of Commercial Products, 5th ed, Williams & Wilkins, Baltimore, MD, 1984.
    70) Graff GR, Stark J, & Berkenbosch JW: Chronic lung disease after activated charcoal aspiration. Pediatrics 2002; 109:959-961.
    71) Graham PM: Successful treatment of the toxic serotonin syndrome with chlorpromazine (letter). Med J Australia 1997; 166:166-167.
    72) Griggs E & Ward M: LSD-toxicity: a suspected cause of death. J Ky Med Assoc 1977; 75:172-173.
    73) HSDB : Hazardous Substances Data Bank. National Library of Medicine. Bethesda, MD (Internet Version). Edition expires 2000; provided by Truven Health Analytics Inc., Greenwood Village, CO.
    74) Haddad LM & Winchester JF: Clinical Management of Poisoning and Drug Overdosage, 2nd ed, WB Saunders Co, Philadelphia, PA, 1990.
    75) Haddad LM, Shannon MW, & Winchester JF: Clinical Management of Poisoning and Drug Overdose, 3rd ed, WB Saunders Co, Philadelphia, PA, 1998.
    76) Harris CR & Filandrinos D: Accidental administration of activated charcoal into the lung: aspiration by proxy. Ann Emerg Med 1993; 22:1470-1473.
    77) Heard K, Daly FFS, & O'Malley G: Respiratory distress after use of droperidol for agitation (letter). Ann Emerg Med 1999; 34:410.
    78) Hegenbarth MA & American Academy of Pediatrics Committee on Drugs: Preparing for pediatric emergencies: drugs to consider. Pediatrics 2008; 121(2):433-443.
    79) Hentschel H, Bergmann I, & Lampe J: Two cases of ingestion of hawaiian baby wood rose (Argyreia nervosa) (abstract). J Toxicol Clin Toxicol 2000; 38:234.
    80) Hoffer A: D-Lysergic acid diethylamide (LSD): a review of its present status. Clin Pharmcol Ther 1965; 6:183-255.
    81) Homsi E, Barreiro MF, Orlando JM, et al: Prophylaxis of acute renal failure in patients with rhabdomyolysis. Ren Fail 1997; 19(2):283-288.
    82) House RV, Thomas PT, & Bhargava HN: Immunological consequences of in vitro exposure to lysergic acid diethylamide (LSD). Immunopharmacology & Immunotoxicology 1994; 16:23-40.
    83) Huerta-Alardin AL, Varon J, & Marik PE: Bench-to-bedside review: Rhabdomyolysis -- an overview for clinicians. Crit Care 2005; 9(2):158-169.
    84) IARC Working Group on the Evaluation of Carcinogenic Risks to Humans : IARC Monographs on the Evaluation of Carcinogenic Risks to Humans: 1,3-Butadiene, Ethylene Oxide and Vinyl Halides (Vinyl Fluoride, Vinyl Chloride and Vinyl Bromide), 97, International Agency for Research on Cancer, Lyon, France, 2008.
    85) IARC Working Group on the Evaluation of Carcinogenic Risks to Humans : IARC Monographs on the Evaluation of Carcinogenic Risks to Humans: Formaldehyde, 2-Butoxyethanol and 1-tert-Butoxypropan-2-ol, 88, International Agency for Research on Cancer, Lyon, France, 2006.
    86) IARC Working Group on the Evaluation of Carcinogenic Risks to Humans : IARC Monographs on the Evaluation of Carcinogenic Risks to Humans: Household Use of Solid Fuels and High-temperature Frying, 95, International Agency for Research on Cancer, Lyon, France, 2010a.
    87) IARC Working Group on the Evaluation of Carcinogenic Risks to Humans : IARC Monographs on the Evaluation of Carcinogenic Risks to Humans: Smokeless Tobacco and Some Tobacco-specific N-Nitrosamines, 89, International Agency for Research on Cancer, Lyon, France, 2007.
    88) IARC Working Group on the Evaluation of Carcinogenic Risks to Humans : IARC Monographs on the Evaluation of Carcinogenic Risks to Humans: Some Non-heterocyclic Polycyclic Aromatic Hydrocarbons and Some Related Exposures, 92, International Agency for Research on Cancer, Lyon, France, 2010.
    89) IARC: List of all agents, mixtures and exposures evaluated to date - IARC Monographs: Overall Evaluations of Carcinogenicity to Humans, Volumes 1-88, 1972-PRESENT. World Health Organization, International Agency for Research on Cancer. Lyon, FranceAvailable from URL: http://monographs.iarc.fr/monoeval/crthall.html. As accessed Oct 07, 2004.
    90) Ianzito BM, Liskow B, & Stewart MA: Reaction to LSD in a two-year-old child. J Pediatr 1972; 80:643-45.
    91) International Agency for Research on Cancer (IARC): IARC monographs on the evaluation of carcinogenic risks to humans: list of classifications, volumes 1-116. International Agency for Research on Cancer (IARC). Lyon, France. 2016. Available from URL: http://monographs.iarc.fr/ENG/Classification/latest_classif.php. As accessed 2016-08-24.
    92) International Agency for Research on Cancer: IARC Monographs on the Evaluation of Carcinogenic Risks to Humans. World Health Organization. Geneva, Switzerland. 2015. Available from URL: http://monographs.iarc.fr/ENG/Classification/. As accessed 2015-08-06.
    93) Jackson TW & Hornfeldt CS: Seizure activity following recreational LSD use in patients treated with lithium and fluoxetine (Abstract). Vet Hum Toxicol 1991; 33:387.
    94) Jacobson CB & Berlin CH: Possible reproductive detriment in LSD users. JAMA 1972; 222:1367-1373.
    95) Kaminer Y & Hrecznyj B: Lysergic acid diethylamide-induced chronic visual disturbances in an adolescent. J Nervous & Mental Dis 1991; 179:173-174.
    96) Klepfisz A & Racy J: Homicide and LSD. Jama 1973; 223:429-30.
    97) Kline SS, Mauro LS, & Scala-Barnett DM: Serotonin syndrome versus neuroleptic malignant syndrome as a cause of death. Clin Pharmac 1989; 8:510-514.
    98) Klock JC, Boerner U, & Becker CE: Coma, hyperthermia and bleeding associated with massive LSD overdose. Clin Toxicol 1975; 8:191-203.
    99) Knight ME & Roberts RJ: Phenothiazine and butyrophenone intoxication in children. Pediatr Clin North Am 1986; 33:299-309.
    100) Koren G: Maternal-Fetal Toxicology; A Clinicians' Guide, Marcel Dekker, Inc, New York, NY, 1990.
    101) Kuhn DM, White FJ, & Appel JB: The descriminative stimulus properties of LSD: mechanisms of action. Neuropharmacology 1978; 17:257-263.
    102) Kulberg A: Substance abuse: clinical identification and management. Pediatr Clin N Am 1986; 33:325-361.
    103) Kulig K: LSD. Emerg Med Clin North Am 1990; 8:551-558.
    104) Leikin JB, Baron S, & Engle J: Treatment of neuroleptic malignant syndrome with diphenhydramine (abstract). Vet Hum Toxicol 1987; 29:480.
    105) Leikin JB, Krantz AJ, & Zell-Lanter M: Clinical features and management of intoxication due to hallucinogenic drugs. Med Toxicol Adverse Drug Exp 1989; 4:324-350.
    106) Levi L & Miller NR: Visual illusions associated with previous drug abuse. J Clin Neuro Ophthalmol 1990; 10:103-110.
    107) Lieberman AN, Bloom W, & Koshore PS: Carotid artery occlusion following ingestion of LSD. Stroke 1974; 5:213-215.
    108) Lignelli GJ & Buchheit WA: Letter to the editor. N Engl J Med 1971; 284:112-113.
    109) Loddenkemper T & Goodkin HP: Treatment of Pediatric Status Epilepticus. Curr Treat Options Neurol 2011; Epub:Epub.
    110) Long SY: Does LSD induce chromosomal damage and malformations? A review of literature. Teratology 1972; 6:75-90.
    111) Louria DB: Lysergic acid diethylamide. 1968; 278:435-38.
    112) Mace S: LSD. Clin Toxicol 1979; 15:219-224.
    113) Manno EM: New management strategies in the treatment of status epilepticus. Mayo Clin Proc 2003; 78(4):508-518.
    114) Margolis S & Martin L: Anophthalmia in an infant of parents using LSD. Ann Ophthalmol 1980; 12:1378-1381.
    115) Markel H, Lee A, & Holmes RD: LSD flashback syndrome exacerbated by selective serotonin reuptake inhibitor antidepressants in adolescents. J Pediatr 1994; 125:817-819.
    116) Martin RW, Duffy J, & Engel AG: The clinical spectrum of the eosinophilia-myalgia syndrome associated with L-tryptophan ingestion. Ann Intern Med 1990; 113:124-134.
    117) Maslanka AM & Scott SK: LSD overdose in an eight-month-old boy. J Emerg Med 1992; 10:481-483.
    118) May DC, Morris SW, & Stewart RM: Neuroleptic malignant syndrome: response to dantrolene sodium. Ann Int Med 1983; 98:183-184.
    119) McCarron MM, Walberg CB, & Baselt RC: Confirmation of LSD intoxication by analysis of serum and urine. J Anal Toxicol 1990; 14:165-167.
    120) McGlothlin WH, Sparkes RS, & Arnold DO: Effect of LSD on human pregnancy. JAMA 1970; 212:1483-1487.
    121) McLane NJ & Carroll DM: Ocular manifestations of drug abuse. Surv Ophthalmol 1986; 30:298-313.
    122) Medsger TA: Tryptophan-induced eosinophilia-myalgia syndrome. N Engl J Med 1990; 322:926-928.
    123) Mercieca J & Brown EA: Acute renal failure due to rhabdomyolysis associated with use of a strait jacket in lysergide intoxication. Br Med J 1984; 288:1949-1950.
    124) Miller PL, Gay GR, & Ferris KC: Treatment of acute, adverse psychedelic reactions: "I've tripped and I can't get down". J Psychoactive Drugs 1992; 24:277-279.
    125) Miller RD, Sohn YJ, & Matteo RS: Enhancement of d-tubocurarine neuromuscular blockade by diuretics in man. Anesthesiology 1976; 45:442-445.
    126) Mills KC: Serotonin syndrome: a clinical update. Med Toxicol 1997; 13:763-783.
    127) Milman DH: An untoward reaction to accidental ingestion of LSD in a 5-year-old girl. JAMA 1967; 201:143-146.
    128) Mitchell WG: Status epilepticus and acute repetitive seizures in children, adolescents, and young adults: etiology, outcome, and treatment. Epilepsia 1996; 37(S1):S74-S80.
    129) Morris GN & McGee PT: Anaesthesia and past use of LSD. Can J Anaesth 1995; 42:177-179.
    130) Mueller PS, Vester JW, & Fermaglich J: Neuroleptic malignant syndrome: successful treatment with bromocriptine. JAMA 1983; 249:386-388.
    131) Muneer RS: Effects of LSD on human chromosomes. Mutat Res 1978; 51:403-410.
    132) NFPA: Fire Protection Guide to Hazardous Materials, 13th ed., National Fire Protection Association, Quincy, MA, 2002.
    133) NRC: Acute Exposure Guideline Levels for Selected Airborne Chemicals - Volume 1, Subcommittee on Acute Exposure Guideline Levels, Committee on Toxicology, Board on Environmental Studies and Toxicology, Commission of Life Sciences, National Research Council. National Academy Press, Washington, DC, 2001.
    134) NRC: Acute Exposure Guideline Levels for Selected Airborne Chemicals - Volume 2, Subcommittee on Acute Exposure Guideline Levels, Committee on Toxicology, Board on Environmental Studies and Toxicology, Commission of Life Sciences, National Research Council. National Academy Press, Washington, DC, 2002.
    135) NRC: Acute Exposure Guideline Levels for Selected Airborne Chemicals - Volume 3, Subcommittee on Acute Exposure Guideline Levels, Committee on Toxicology, Board on Environmental Studies and Toxicology, Commission of Life Sciences, National Research Council. National Academy Press, Washington, DC, 2003.
    136) NRC: Acute Exposure Guideline Levels for Selected Airborne Chemicals - Volume 4, Subcommittee on Acute Exposure Guideline Levels, Committee on Toxicology, Board on Environmental Studies and Toxicology, Commission of Life Sciences, National Research Council. National Academy Press, Washington, DC, 2004.
    137) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for 1,2,3-Trimethylbenzene (Proposed). United States Environmental Protection Agency. Washington, DC. 2006k. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020d68a&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    138) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for 1,2,4-Trimethylbenzene (Proposed). United States Environmental Protection Agency. Washington, DC. 2006m. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020d68a&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    139) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for 1,2-Butylene Oxide (Proposed). United States Environmental Protection Agency. Washington, DC. 2008d. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648083cdbb&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    140) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for 1,2-Dibromoethane (Proposed). United States Environmental Protection Agency. Washington, DC. 2007g. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=09000064802796db&disposition=attachment&contentType=pdf. As accessed 2010-08-18.
    141) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for 1,3,5-Trimethylbenzene (Proposed). United States Environmental Protection Agency. Washington, DC. 2006l. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020d68a&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    142) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for 2-Ethylhexyl Chloroformate (Proposed). United States Environmental Protection Agency. Washington, DC. 2007b. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648037904e&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    143) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Acrylonitrile (Proposed). United States Environmental Protection Agency. Washington, DC. 2007c. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648028e6a3&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    144) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Adamsite (Proposed). United States Environmental Protection Agency. Washington, DC. 2007h. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020fd29&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    145) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Agent BZ (3-quinuclidinyl benzilate) (Proposed). United States Environmental Protection Agency. Washington, DC. 2007f. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=09000064803ad507&disposition=attachment&contentType=pdf. As accessed 2010-08-18.
    146) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Allyl Chloride (Proposed). United States Environmental Protection Agency. Washington, DC. 2008. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648039d9ee&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    147) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Aluminum Phosphide (Proposed). United States Environmental Protection Agency. Washington, DC. 2005b. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020c5ed&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    148) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Arsenic Trioxide (Proposed). United States Environmental Protection Agency. Washington, DC. 2007m. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=0900006480220305&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    149) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Automotive Gasoline Unleaded (Proposed). United States Environmental Protection Agency. Washington, DC. 2009a. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=0900006480a7cc17&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    150) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Biphenyl (Proposed). United States Environmental Protection Agency. Washington, DC. 2005j. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=09000064801ea1b7&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    151) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Bis-Chloromethyl Ether (BCME) (Proposed). United States Environmental Protection Agency. Washington, DC. 2006n. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648022db11&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    152) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Boron Tribromide (Proposed). United States Environmental Protection Agency. Washington, DC. 2008a. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=09000064803ae1d3&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    153) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Bromine Chloride (Proposed). United States Environmental Protection Agency. Washington, DC. 2007d. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648039732a&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    154) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Bromoacetone (Proposed). United States Environmental Protection Agency. Washington, DC. 2008e. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=09000064809187bf&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    155) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Calcium Phosphide (Proposed). United States Environmental Protection Agency. Washington, DC. 2005d. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020c5ed&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    156) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Carbonyl Fluoride (Proposed). United States Environmental Protection Agency. Washington, DC. 2008b. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=09000064803ae328&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    157) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Carbonyl Sulfide (Proposed). United States Environmental Protection Agency. Washington, DC. 2007e. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648037ff26&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    158) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Chlorobenzene (Proposed). United States Environmental Protection Agency. Washington, DC. 2008c. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=09000064803a52bb&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    159) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Cyanogen (Proposed). United States Environmental Protection Agency. Washington, DC. 2008f. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=09000064809187fe&disposition=attachment&contentType=pdf. As accessed 2010-08-15.
    160) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Dimethyl Phosphite (Proposed). United States Environmental Protection Agency. Washington, DC. 2009. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=0900006480a7cbf3&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    161) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Diphenylchloroarsine (Proposed). United States Environmental Protection Agency. Washington, DC. 2007l. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020fd29&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    162) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Ethyl Isocyanate (Proposed). United States Environmental Protection Agency. Washington, DC. 2008h. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648091884e&disposition=attachment&contentType=pdf. As accessed 2010-08-15.
    163) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Ethyl Phosphorodichloridate (Proposed). United States Environmental Protection Agency. Washington, DC. 2008i. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=0900006480920347&disposition=attachment&contentType=pdf. As accessed 2010-08-15.
    164) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Ethylbenzene (Proposed). United States Environmental Protection Agency. Washington, DC. 2008g. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=09000064809203e7&disposition=attachment&contentType=pdf. As accessed 2010-08-15.
    165) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Ethyldichloroarsine (Proposed). United States Environmental Protection Agency. Washington, DC. 2007j. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020fd29&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    166) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Germane (Proposed). United States Environmental Protection Agency. Washington, DC. 2008j. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=0900006480963906&disposition=attachment&contentType=pdf. As accessed 2010-08-15.
    167) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Hexafluoropropylene (Proposed). United States Environmental Protection Agency. Washington, DC. 2006. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=09000064801ea1f5&disposition=attachment&contentType=pdf. As accessed 2010-08-15.
    168) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Ketene (Proposed). United States Environmental Protection Agency. Washington, DC. 2007. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020ee7c&disposition=attachment&contentType=pdf. As accessed 2010-08-15.
    169) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Magnesium Aluminum Phosphide (Proposed). United States Environmental Protection Agency. Washington, DC. 2005h. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020c5ed&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    170) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Magnesium Phosphide (Proposed). United States Environmental Protection Agency. Washington, DC. 2005g. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020c5ed&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    171) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Malathion (Proposed). United States Environmental Protection Agency. Washington, DC. 2009k. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=09000064809639df&disposition=attachment&contentType=pdf. As accessed 2010-08-15.
    172) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Mercury Vapor (Proposed). United States Environmental Protection Agency. Washington, DC. 2009b. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=0900006480a8a087&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    173) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Methyl Isothiocyanate (Proposed). United States Environmental Protection Agency. Washington, DC. 2008k. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=0900006480963a03&disposition=attachment&contentType=pdf. As accessed 2010-08-15.
    174) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Methyl Parathion (Proposed). United States Environmental Protection Agency. Washington, DC. 2008l. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=0900006480963a57&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    175) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Methyl tertiary-butyl ether (Proposed). United States Environmental Protection Agency. Washington, DC. 2007a. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=09000064802a4985&disposition=attachment&contentType=pdf. As accessed 2010-08-15.
    176) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Methylchlorosilane (Proposed). United States Environmental Protection Agency. Washington, DC. 2005. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020c5f4&disposition=attachment&contentType=pdf. As accessed 2010-08-15.
    177) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Methyldichloroarsine (Proposed). United States Environmental Protection Agency. Washington, DC. 2007i. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020fd29&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    178) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Methyldichlorosilane (Proposed). United States Environmental Protection Agency. Washington, DC. 2005a. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020c646&disposition=attachment&contentType=pdf. As accessed 2010-08-15.
    179) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Nitrogen Mustard (HN1 CAS Reg. No. 538-07-8) (Proposed). United States Environmental Protection Agency. Washington, DC. 2006a. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020d6cb&disposition=attachment&contentType=pdf. As accessed 2010-08-15.
    180) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Nitrogen Mustard (HN2 CAS Reg. No. 51-75-2) (Proposed). United States Environmental Protection Agency. Washington, DC. 2006b. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020d6cb&disposition=attachment&contentType=pdf. As accessed 2010-08-15.
    181) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Nitrogen Mustard (HN3 CAS Reg. No. 555-77-1) (Proposed). United States Environmental Protection Agency. Washington, DC. 2006c. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020d6cb&disposition=attachment&contentType=pdf. As accessed 2010-08-15.
    182) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Nitrogen Tetroxide (Proposed). United States Environmental Protection Agency. Washington, DC. 2008n. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648091855b&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    183) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Nitrogen Trifluoride (Proposed). United States Environmental Protection Agency. Washington, DC. 2009l. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=0900006480963e0c&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    184) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Parathion (Proposed). United States Environmental Protection Agency. Washington, DC. 2008o. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=0900006480963e32&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    185) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Perchloryl Fluoride (Proposed). United States Environmental Protection Agency. Washington, DC. 2009c. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=0900006480a7e268&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    186) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Perfluoroisobutylene (Proposed). United States Environmental Protection Agency. Washington, DC. 2009d. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=0900006480a7e26a&disposition=attachment&contentType=pdf. As accessed 2010-08-15.
    187) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Phenyl Isocyanate (Proposed). United States Environmental Protection Agency. Washington, DC. 2008p. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648096dd58&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    188) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Phenyl Mercaptan (Proposed). United States Environmental Protection Agency. Washington, DC. 2006d. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020cc0c&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    189) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Phenyldichloroarsine (Proposed). United States Environmental Protection Agency. Washington, DC. 2007k. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020fd29&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    190) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Phorate (Proposed). United States Environmental Protection Agency. Washington, DC. 2008q. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648096dcc8&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    191) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Phosgene (Draft-Revised). United States Environmental Protection Agency. Washington, DC. 2009e. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=0900006480a8a08a&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    192) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Phosgene Oxime (Proposed). United States Environmental Protection Agency. Washington, DC. 2009f. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=0900006480a7e26d&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    193) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Potassium Cyanide (Proposed). United States Environmental Protection Agency. Washington, DC. 2009g. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=0900006480a7cbb9&disposition=attachment&contentType=pdf. As accessed 2010-08-15.
    194) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Potassium Phosphide (Proposed). United States Environmental Protection Agency. Washington, DC. 2005c. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020c5ed&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    195) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Propargyl Alcohol (Proposed). United States Environmental Protection Agency. Washington, DC. 2006e. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020ec91&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    196) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Selenium Hexafluoride (Proposed). United States Environmental Protection Agency. Washington, DC. 2006f. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020ec55&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    197) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Silane (Proposed). United States Environmental Protection Agency. Washington, DC. 2006g. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020d523&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    198) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Sodium Cyanide (Proposed). United States Environmental Protection Agency. Washington, DC. 2009h. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=0900006480a7cbb9&disposition=attachment&contentType=pdf. As accessed 2010-08-15.
    199) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Sodium Phosphide (Proposed). United States Environmental Protection Agency. Washington, DC. 2005i. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020c5ed&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    200) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Strontium Phosphide (Proposed). United States Environmental Protection Agency. Washington, DC. 2005f. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020c5ed&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    201) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Sulfuryl Chloride (Proposed). United States Environmental Protection Agency. Washington, DC. 2006h. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020ec7a&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    202) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Tear Gas (Proposed). United States Environmental Protection Agency. Washington, DC. 2008s. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648096e551&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    203) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Tellurium Hexafluoride (Proposed). United States Environmental Protection Agency. Washington, DC. 2009i. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=0900006480a7e2a1&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    204) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Tert-Octyl Mercaptan (Proposed). United States Environmental Protection Agency. Washington, DC. 2008r. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648096e5c7&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    205) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Tetramethoxysilane (Proposed). United States Environmental Protection Agency. Washington, DC. 2006j. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020d632&disposition=attachment&contentType=pdf. As accessed 2010-08-17.
    206) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Trimethoxysilane (Proposed). United States Environmental Protection Agency. Washington, DC. 2006i. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020d632&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    207) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Trimethyl Phosphite (Proposed). United States Environmental Protection Agency. Washington, DC. 2009j. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=0900006480a7d608&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    208) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Trimethylacetyl Chloride (Proposed). United States Environmental Protection Agency. Washington, DC. 2008t. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648096e5cc&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    209) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Zinc Phosphide (Proposed). United States Environmental Protection Agency. Washington, DC. 2005e. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020c5ed&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    210) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for n-Butyl Isocyanate (Proposed). United States Environmental Protection Agency. Washington, DC. 2008m. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=09000064808f9591&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    211) National Institute for Occupational Safety and Health: NIOSH Pocket Guide to Chemical Hazards, U.S. Department of Health and Human Services, Centers for Disease Control and Prevention, Cincinnati, OH, 2007.
    212) National Research Council : Acute exposure guideline levels for selected airborne chemicals, 5, National Academies Press, Washington, DC, 2007.
    213) National Research Council: Acute exposure guideline levels for selected airborne chemicals, 6, National Academies Press, Washington, DC, 2008.
    214) National Research Council: Acute exposure guideline levels for selected airborne chemicals, 7, National Academies Press, Washington, DC, 2009.
    215) National Research Council: Acute exposure guideline levels for selected airborne chemicals, 8, National Academies Press, Washington, DC, 2010.
    216) Ninnemann A & Stuart GL: The NBOMe series: a novel, dangerous group of hallucinogenic drugs. J Stud Alcohol Drugs 2013; 74(6):977-978.
    217) None Listed: Position paper: cathartics. J Toxicol Clin Toxicol 2004; 42(3):243-253.
    218) Papac DI & Foltz RL: Gas chromatography/mass spectrometry of LSD in human plasma. Toxicologist 1989; 9:9.
    219) Papac DI & Foltz RL: Measurement of lysergic acid diethylamide (LSD) in human plasma by gas chromatography/negative ion chemical ionization mass spectrometry. J Analytical Tox 1990; 14:189-190.
    220) Pilapil UR, Harp RA, & Ehrhard OE: LSD and cyanotic congenital heart disease. J Am Med Women's Assoc 1973; 28:131-132.
    221) Polderman KH: Acute renal failure and rhabdomyolysis. Int J Artif Organs 2004; 27(12):1030-1033.
    222) Pollack MM, Dunbar BS, & Holbrook PR: Aspiration of activated charcoal and gastric contents. Ann Emerg Med 1981; 10:528-529.
    223) Product Information: ATIVAN(R) injection, lorazepam injection. Baxter Healthcare Corporation, Deerfield, IL, 2003.
    224) Product Information: Haldol(R), haloperidol. McNeil Pharmaceutical, Spring House, PA, 1990.
    225) Product Information: MANNITOL intravenous injection, mannitol intravenous injection. Hospira, Inc. (per DailyMed), Lake Forest, IL, 2009.
    226) Product Information: Mannitol intravenous injection, mannitol intravenous injection. American Regent, Inc. (per DailyMed), Shirley, NY, 2009.
    227) Product Information: diazepam IM, IV injection, diazepam IM, IV injection. Hospira, Inc (per Manufacturer), Lake Forest, IL, 2008.
    228) Product Information: mannitol IV injection, urologic irrigation, mannitol IV injection, urologic irrigation. Abraxis Pharmaceutical Products, Schaumburg, IL, 2006.
    229) Qureshi A, Wassmer E, Davies P, et al: Comparative audit of intravenous lorazepam and diazepam in the emergency treatment of convulsive status epilepticus in children. Seizure 2002; 11(3):141-144.
    230) RTECS : Registry of Toxic Effects of Chemical Substances. National Institute for Occupational Safety and Health. Cincinnati, OH (Internet Version). Edition expires 2000; provided by Truven Health Analytics Inc., Greenwood Village, CO.
    231) Rau NR, Nagaraj MV, Prakash PS, et al: Fatal pulmonary aspiration of oral activated charcoal. Br Med J 1988; 297:918-919.
    232) Ray O: Drugs, Society, and Human Behavior, Mosby, St Louis, MO, 1974.
    233) Rosenberg J, Pentel P, & Pond S: Hyperthermia associated with drug intoxication. Cr Care Med 1986; 14:964-969.
    234) Rothlin E: Pharmacology of lysergic acid diethylamine and some of its related compounds. J Pharm Pharmacol 1957; 9:569-587.
    235) Rule GS & Henion JD: Determination of drugs from urine by on-line immuno- affinity chromatography-high-performance liquid chromatography-mass spectrometry. J Chromatography 1992; 582:103-112.
    236) Rumbaugh CL, Bergerson RT, & Fang HCH: Cerebral angiographic changes in drug abuse patients. Radiology 1971; 101:335-344.
    237) Samuelsson BO: LSD intoxication in a two-year-old child. Acta Paediatr Scand 1974; 63:797-798.
    238) Sax NI & Lewis RJ: Dangerous Properties of Industrial Materials, 7th ed, Van Nostrand Reinhold Co, New York, NY, 1989.
    239) Schardein JL: Chemically Induced Birth Defects, Marcel Dekker Inc, New York, 1993.
    240) Schneider SM: Neuroleptic malignant syndrome: controversies in treatment. Am J Emerg Med 1991; 9:360-362.
    241) Shulgin AT: Profiles of psychedelic drugs. 9. LSD J Psychedelic Drugs 1980; 12:173-174.
    242) Siddik ZH, Barnes RD, & Dring LG: The fate of lysergic acid di14Cethylamide (14CLSD) in the rat. Biochem Soc Trans 1975; 3:290.
    243) Smith RN & Robinson K: Body fluid levels of lysergide (LSD). Forensic Sci Int 1985; 28:229-237.
    244) Sobel J, Esponas OA, & Friedman SA: Carotid artery obstruction following LSD capsule ingestion. Arch Intern Med 1971; 127:290-291.
    245) Sreenath TG, Gupta P, Sharma KK, et al: Lorazepam versus diazepam-phenytoin combination in the treatment of convulsive status epilepticus in children: A randomized controlled trial. Eur J Paediatr Neurol 2009; Epub:Epub.
    246) Stead AH, Watton J, & Goddard CP: The development and evaluation of a I125 radioimmunoassay for the measurement of LSD in body fluids. Forensic Sci Int 1986; 32:49-60.
    247) Stecker JF Jr, Rawls HP, & Devine CJ: Retroperitoneal fibrosis and ergot derivatives. J Urol 1974; 112:30-32.
    248) Sternbach H: The serotonin syndrome. Am J Psychiatr 1991; 148:705-713.
    249) Strassman RJ: Adverse reactions to psychedelic drugs: a review of the literature. J Nerv Mental Dis 1984; 172:577-595.
    250) Swygert LA, Maes EF, & Sewell LE: Eosinophilia myalgia syndrome: results of national surveillance. JAMA 1990; 264:1698-1703.
    251) TERIS : The Teratogen Information System. University of Washington. Seattle, WA (Internet Version). Edition expires 2000; provided by Truven Health Analytics Inc., Greenwood Village, CO.
    252) Taunton-Rigby A, Sher SE, & Kelley PR: Lysergic acid diethylamide: radioimmunoassy. Science 1973; 181:165-166.
    253) Titeler M, Lyon RA, & Glennon RA: Radioligand binding evidence implicates the brain 5-HT2 receptor as a site of action for LSD and phenylisopropylamine hallucinogens. Psychopharmacology 1988; 94:213-216.
    254) Trulson ME & Crisp T: Lack of synergism and cross-tolerance between tactile stimulus and LSD-induced limb flickering in the cat. Pharmacol Biochem Behav 1982; 17:589-591.
    255) Twitchett PJ, Fletcher SM, & Sullivan AT: Analysis of LSD in human body fluids by high performance liquid chromatography, fluorescence spectroscopy and radioimmunoassay. J Chromatogr 1978; 150:73-84.
    256) U.S. Department of Energy, Office of Emergency Management: Protective Action Criteria (PAC) with AEGLs, ERPGs, & TEELs: Rev. 26 for chemicals of concern. U.S. Department of Energy, Office of Emergency Management. Washington, DC. 2010. Available from URL: http://www.hss.doe.gov/HealthSafety/WSHP/Chem_Safety/teel.html. As accessed 2011-06-27.
    257) U.S. Department of Health and Human Services, Public Health Service, National Toxicology Project : 11th Report on Carcinogens. U.S. Department of Health and Human Services, Public Health Service, National Toxicology Program. Washington, DC. 2005. Available from URL: http://ntp.niehs.nih.gov/INDEXA5E1.HTM?objectid=32BA9724-F1F6-975E-7FCE50709CB4C932. As accessed 2011-06-27.
    258) U.S. Environmental Protection Agency: Discarded commercial chemical products, off-specification species, container residues, and spill residues thereof. Environmental Protection Agency's (EPA) Resource Conservation and Recovery Act (RCRA); List of hazardous substances and reportable quantities 2010b; 40CFR(261.33, e-f):77-.
    259) U.S. Environmental Protection Agency: Integrated Risk Information System (IRIS). U.S. Environmental Protection Agency. Washington, DC. 2011. Available from URL: http://cfpub.epa.gov/ncea/iris/index.cfm?fuseaction=iris.showSubstanceList&list_type=date. As accessed 2011-06-21.
    260) U.S. Environmental Protection Agency: List of Radionuclides. U.S. Environmental Protection Agency. Washington, DC. 2010a. Available from URL: http://www.gpo.gov/fdsys/pkg/CFR-2010-title40-vol27/pdf/CFR-2010-title40-vol27-sec302-4.pdf. As accessed 2011-06-17.
    261) U.S. Environmental Protection Agency: List of hazardous substances and reportable quantities. U.S. Environmental Protection Agency. Washington, DC. 2010. Available from URL: http://www.gpo.gov/fdsys/pkg/CFR-2010-title40-vol27/pdf/CFR-2010-title40-vol27-sec302-4.pdf. As accessed 2011-06-17.
    262) U.S. Environmental Protection Agency: The list of extremely hazardous substances and their threshold planning quantities (CAS Number Order). U.S. Environmental Protection Agency. Washington, DC. 2010c. Available from URL: http://www.gpo.gov/fdsys/pkg/CFR-2010-title40-vol27/pdf/CFR-2010-title40-vol27-part355.pdf. As accessed 2011-06-17.
    263) U.S. Occupational Safety and Health Administration: Part 1910 - Occupational safety and health standards (continued) Occupational Safety, and Health Administration's (OSHA) list of highly hazardous chemicals, toxics and reactives. Subpart Z - toxic and hazardous substances. CFR 2010 2010; Vol6(SEC1910):7-.
    264) U.S. Occupational Safety, and Health Administration (OSHA): Process safety management of highly hazardous chemicals. 29 CFR 2010 2010; 29(1910.119):348-.
    265) United States Environmental Protection Agency Office of Pollution Prevention and Toxics: Acute Exposure Guideline Levels (AEGLs) for Vinyl Acetate (Proposed). United States Environmental Protection Agency. Washington, DC. 2006. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020d6af&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    266) Upshall DG & Wailling DG: The determination of LSD in human plasma following oral administration. Clin Chim Acta 1972; 36:67-73.
    267) Vanholder R, Sever MS, Erek E, et al: Rhabdomyolysis. J Am Soc Nephrol 2000; 11(8):1553-1561.
    268) Wagner JG, Aghajanian GK, & Bing OHL: Correlation of performance test scores with "tissue concentrations" of lysergic acid diethylamide in human subjects. Clin Pharmacol Ther 1968; 9:635-638.
    269) Walker FA & Helz T: Presumptive teratogenicity of "street" LSD (abstract). J Pediatr 1971; 78:1059.
    270) Walter LA & Catenacci MH: Rhabdomyolysis. Hosp Physician 2008; 44(1):25-31.
    271) West L, Pierce CM, & Thomas WD: Lysergic acid diethylamide: its effects on a male asiatic elephant. Science 1962; 138:1100-1103.
    272) Wheless JW : Treatment of status epilepticus in children. Pediatr Ann 2004; 33(6):376-383.
    273) Widdop B: The detection of LSD in biological fluids. Bull Int Assoc Forensic Toxicol 1974; 7:6-7.
    274) Zimmerman JL & Shen MC: Rhabdomyolysis. Chest 2013; 144(3):1058-1065.