Light yellow resinous oilBrown amorphous semi-solid, viscous oil or chunky golden yellow solid
Löslichkeit
2.8 mg/L at 73 °F (NTP, 1992)In water, 2.8 mg/L at 23 °CEssentially insoluble in water1 part in 1 part of alcohol1 part in 1 part of acetone1 part in 3 parts of glycerol. In 0.15M sodium chloride, 0.77 mg/L at 23 °C. Soluble in fixed oils.2.63e-03 g/LAcetonitrile: 50 mg/mlDMF: 50 mg/mlDMF: PBS (pH 7.2)(1:3): 250 µg/mlDMSO: 60 mg/mlEthanol: 35 mg/mlMethanol: 30 mg/ml2.8mg/L(23 ºC)
Human Drugs
Breast FeedingLactationMilk, HumanCannabinoidsStreet DrugsAntiemeticsFDA approved drugs -> Active ingredientPharmaceuticals
Siedepunkt
392 °F at 0.02 mmHg (NTP, 1992)BP: 200 °C at 0.02 mm Hgbp0.02 200°
Decomposition
When heated to decomposition it emits acrid smoke and irritating fumes.
Schmelzpunkt
200 °C<25 °C
Optical Rotation
Specific optical rotation: -150.5 deg at 20 °C/D (concentration = 0.53% in chloroform)
Physical Description
1-trans-delta-9-tetrahydrocannabinol appears as brown amorphous semi-solid, viscous oil or chunky golden yellow solid. (NTP, 1992)Light yellow oil[Merck Index] Brown semi-solid, viscous liquid, or golden yellow solid[CAMEO] Odorless resinous oil[MSDSonline]
Dichte
1.0536 (rough estimate)
Brechungsindex
1.5404 (estimate)
Flammpunkt
14 °C
Lagerbedingungen
2-8°C
Aggregatzustand
ethanol solution
pKa (Säurekonstante)
pKa 10.6 (Uncertain)
Henry-Konstante
4.1×101 mol/(m3Pa) at 25℃, HSDB (2015)
BCS Class
2/4
CAS Datenbank
1972-08-3
EPA chemische Informationen
Tetrahydrocannabinol (1972-08-3)
Sicherheit & Vorschriften
GHS-Einstufung
WarningH302 (100%): Harmful if swallowed [Warning Acute toxicity, oral]P203, P264, P270, P273, P280, P301+P317, P318, P330, P405, and P501 (click each P-code to see the statement)Aggregated GHS information provided per 92 reports by companies from 7 notifications to the ECHA C&L Inventory. Each notification may be associated with multiple companies.
Regulatorische Informationen
DEA schedule II controlled substanceDEA schedule III controlled substanceRegulation (EC) No 178/2002 (amended)Delta-9-tetrahydrocannabinol: Does not have an individual approval but may be used as a component in a product covered by a group standard. It is not approved for use as a chemical in its own right.
Brandgefahren
Flash point data for this chemical are not availablehowever, it is probably combustible. (NTP, 1992)
Gesundheitsgefahren
SYMPTOMS: Exposure to this compound may cause euphoria, relaxation, sleepiness, short term memory impairmentdeterioration of ability to perform memory-dependent goal-oriented behavior, and loss of balance. Higher doses can cause hallucinations, delusions, paranoia, confusion, altered time sense, anxiety, nausea, vomiting, ataxia, stupor, coma, cardiovascular effects and redness of the eyes.
Gefahrenübersicht
Emergency treatment: Plants- marijuanaLow level exposures cause mild euphoria and somnolence. Higher level exposures cause short term memory impairment, mood alterations, and decreased motor coordination. [HSDB] A respiratory tract irritant[MSDSonline]
FDA-Anforderungen
Schedule I shall consist of the drugs and other substances, by whatever official name, common or usual name, chemical name, or brand name designated, listed in this section. Each drug or substance has been assigned the DEA Controlled Substances Code Number set forth opposite it. ... Unless specifically excepted or unless listed in another schedule, any material, compound, mixture, or preparation, which contains any quantity of the following hallucinogenic substances, or which contains any of its salts, isomers, and salts of isomers whenever the existence of such salts, isomers, and salts of isomers is possible within the specific chemical designation (for purposes of this paragraph only, the term "isomer" includes the optical, position and geometric isomers). Tetrahydrocannabinols (DEA Code Number: 7370) are included on this list. Meaning tetrahydrocannabinols naturally contained in a plant of the genus Cannabis (cannabis plant), as well as synthetic equivalents of the substances contained in the cannabis plant, or in the resinous extractives of such plant, and/or synthetic substances, derivatives, and their isomers with similar chemical structure and pharmacological activity to those substances contained in the plant, such as the following: 1 cis or trans tetrahydrocannabinol, and their optical isomers
Anwendungen & Verwendung
Beschreibung
Tetrahydrocannabinol (THC) is the main active compound in marijuana. It comes from the plant Cannabis sativa (cannabis), which is a dioecious (monoecious varieties do exist) annual herb naturally found in many tropic and temperate regions of the world. Many varieties of cannabis exist, and two related species (Cannabis indica and Cannabis ruderalia) are main sources of THC. Cannabis sativa is also known as hemp, although this name is not unique to the species; its stem is a source of fiber that has been used throughout history for hundreds of applications including rope, twine, paper, and cloth. Hemp seeds are edible and high in protein. The seeds are also a source of fatty oil that can be used for food, cosmetics, medicines, and as a fuel source. Cannabis contains chemicals called cannabinoids; of the 60 cannabinoids found in Cannabis, one is THC, , which is the psychoactive ingredient in marijuana. Marijuana is produced from the leaves and fl owers of cannabis, and hashish is a resin collected from the female fl owers. The THC content, which determines the effect of cannabis drugs, varies with plant structure, variety, and preparation. Buds and fl owers specifically cultivated for drug use have greater THC content than leaves. THC content may vary from a few tenths of a percent to more than 10%, but good quality marijuana has a THC content of approximately 10%, and good hashish and hashish oils generally have THC contents between 30% and 80%.
History
THC was first isolated from hashish in 1964 by Raphael Mechoulam (1930–) and Yehiel Gaoni at the Weizmann Institute. In the early 1990s, the specific brain receptors affected by THC were identified. These receptors are activated by a cannabinoid neurotransmitter called arachidonylethanolamide, known as anandamide. Anandamide was named by Mechoulam using ananda, which is the Sanskrit word for ecstasy. Anandamide is thought to be associated with memory, pain, depression, and appetite. THC is able to attach to and activate anandamide receptors. These receptors are actually called THC receptors rather than anandamide receptors because researchers discovered that THC attaches to these receptors before anandamide was discovered. The areas of the brain with the most THC receptors are the cerebellum, the cerebral cortex, and the limbic system. This is why marijuana affects thinking, memory, sensory perception, and coordination.
Verwenden
It is the principal active constituent of cannabis. Agonist at CB1 and CB2 cannabinoid receptors. Antiemetic; appetite stimulant. Controlled substance (hallucinogen).
6 cis or trans tetrahydrocannabinol, and their optical isomers
and 3, 4 cis or trans tetrahydrocannabinol, and its optical isomers. (Since nomenclature of these substances is not internationally standardized, compounds of these structures, regardless of numerical designation of atomic positions covered.) /Tetrahydrocannabinols/
Schedule I shall consist of the drugs and other substances, by whatever official name, common or usual name, chemical name, or brand name designated, listed in this section. Each drug or substance has been assigned the DEA Controlled Substances Code Number set forth opposite it. ... Unless specifically excepted or unless listed in another schedule, any material, compound, mixture, or preparation, which contains any quantity of the following hallucinogenic substances, or which contains any of its salts, isomers, and salts of isomers whenever the existence of such salts, isomers, and salts of isomers is possible within the specific chemical designation (for purposes of this paragraph only, the term "isomer" includes the optical, position and geometric isomers). Marihuana (DEA Code Number: 7360) is included on this list. /Marihuana/
Schedule II shall consist of the drugs and other substances, by whatever official name, common or usual name, chemical name, or brand name designated, listed in this section. Each drug or substance has been assigned the DEA Controlled Substances Code Number set forth opposite it. ... Hallucinogenic substances. Dronabinol [(-)-delta-9-trans tetrahydrocannabinol] in an oral solution in a drug product approved for marketing by the U.S. Food and Drug Administration (DEA Code Number: 7365) is included on this list. /Dronabinol/
Schedule III shall consist of the drugs and other substances, by whatever official name, common or usual name, chemical name, or brand name designated, listed in this section. Each drug or substance has been assigned the DEA Controlled Substances Code Number set forth opposite it. ... Hallucinogenic substances. (1) Dronabinol (synthetic) in sesame oil and encapsulated in a soft gelatin capsule in a U.S. Food and Drug Administration approved product - /DEA Code Number:/ 7369. [Some other names for dronabinol: (6aR-trans)-6a,7,8,10a-tetrahydro-6,6,9-trimethyl-3-pentyl-6H-dibenzo[b,d]pyran-1-ol] or (-)-delta-9-(trans)-tetrahydrocannabinol]. /Dronabinol/
The Approved Drug Products with Therapeutic Equivalence Evaluations identifies currently marketed prescription drug products, including dronabinol, approved on the basis of safety and effectiveness by FDA under sections 505 of the Federal Food, Drug, and Cosmetic Act. /Dronabinol/
Reaktive Gruppe
Ethers
Special Reports
DHHS/NIDAResearch Monograph Series 79: Structure-Activity Relationships of the Cannabinoids p.177 (1987) DHHS Pub No. (ADM)90-1534Research Monograph Series 14: Marijuana Research Findings p.130 (1976) DHHS Pub No. (ADM)81-1168Research Monograph Series 50: Cocaine: Pharmacology Effects and Treatment of Abuse (1984) DHHS Pub No. ADM(87)-1326Research Monograph Series 52: Testing Drugs for Physical Dependence Potential and Abuse Liability (1984) DHHS Pub No. (ADM)87-1332For more Special Reports (Complete) data for delta 9-Tetrahydrocannabinol (13 total), please visit the HSDB record page.
Reactivity Profile
1-TRANS-DELTA-9-TETRAHYDROCANNABINOLis very unstable to light and high temperatures. It should be protected from air during all handling due to its extreme instability. (NTP, 1992). Flammable and/or toxic gases are generated by the combination of alcohols with alkali metals, nitrides, and strong reducing agents. They react with oxoacids and carboxylic acids to form esters plus water. Oxidizing agents convert them to aldehydes or ketones. Alcohols exhibit both weak acid and weak base behavior. They may initiate the polymerization of isocyanates and epoxides.
Air and Water Reactions
Slightly soluble in water.
Hazard Classes and Categories
Acute Tox. 4 (100%)
Brandbekämpfung
Fires involving this compound should be controlled with a dry chemical, carbon dioxide or Halon extinguisher. (NTP, 1992)
Erste Hilfe
EYES: First check the victim for contact lenses and remove if present. Flush victim's eyes with water or normal saline solution for 20 to 30 minutes while simultaneously calling a hospital or poison control center. Do not put any ointments, oils, or medication in the victim's eyes without specific instructions from a physician. IMMEDIATELY transport the victim after flushing eyes to a hospital even if no symptoms (such as redness or irritation) develop.
Lagerbedingungen
Dronabinol Capsules, USP should be packaged in a well-closed container and stored in a refrigerator, 2 to 8 °C (36 to 46 °F). Protect from freezing.When cannabis was stored at -18 °C, 4 °C, and 22 °C, the content of delta 9-tetrahydrocannabinol was reduced by 3.8, 5.3, and 6.9% respectively per year. There was greater deterioration at higher temperature.Substantial amounts of THC (tetrahydrocanabinol) are lost from polystyrene, but not glassvials when samples are stored at room temperature for 4 days and then frozen (-20 °C) for 4 wk.
Freisetung ohne Brand
SMALL SPILLS AND LEAKAGE: Should a spill occur while you are handling this chemical, FIRST REMOVE ALL SOURCES OF IGNITION, then you should dampen the solid spill material with 60-70% ethanol and transfer the dampened material to a suitable container. Use absorbent paper dampened with 60-70% ethanol to pick up any remaining material. Seal the absorbent paper, and any of your clothes, which may be contaminated, in a vapor-tight plastic bag for eventual disposal. Solvent wash all contaminated surfaces with 60-70% ethanol followed by washing with a soap and water solution. Do not reenter the contaminated area until the Safety Officer (or other responsible person) has verified that the area has been properly cleaned.
Entsorgungsverfahren
SRP: Expired or waste pharmaceuticals shall carefully take into consideration applicable DEA, EPA, and FDA regulations. It is not appropriate to dispose by flushing the pharmaceutical down the toilet or discarding to trash. If possible return the pharmaceutical to the manufacturer for proper disposal being careful to properly label and securely package the material. Alternatively, the waste pharmaceutical shall be labeled, securely packaged and transported by a state licensed medical waste contractor to dispose by burial in a licensed hazardous or toxic waste landfill or incinerator.
Personal Protective Equipment (PPE)
RECOMMENDED RESPIRATOR: Where the neat test chemical is weighed and diluted, wear a NIOSH-approved half face respirator equipped with a combination filter cartridge, i.e. organic vapor/acid gas/HEPA (specific for organic vapors, HCl, acid gas, SO2 and a high efficiency particulate filter). (NTP, 1992)
Körperbelastung
delta 9-Tetrahydrocannabinol was detected in 77 of 250 hair samples at <0.02-4.2 ng/mg(1). Cannabio shampoo contained 412 ng/mL of delta 9-tetrahydrocannabinol, delta 9-tetrahydrocannabinol was not detected (detection limit 0.05 ng/mg) in hair samples collected from individuals using this shampoo daily(2). About 70% of delta 9-tetrahydrocannabinol administered orally is excreted as its metabolites with 72 hours in feces and urine, only trace amounts of unmetabolized delta 9-tetrahydrocannabinol were detected in urine(2). Upon smoking cannabis cigarettes containing 1.75 and 3.55% delta 9-tetrahydrocannabinol, blood levels of delta 9-tetrahydrocannabinol were reported as 7 and 18.1 ng/mL, respectively(3). The half-life in blood was 18.7 hours to 4.1 days(3).
Treatment
A potentially serious oral ingestion, if recent, should be managed with gut decontamination. In unconscious patients with a secure airway, instill activated charcoal (30 to 100 g in adults, 1 to 2 g/kg in infants) via a nasogastric tube. A saline cathartic or sorbitol may be added to the first dose of activated charcoal. Patients experiencing depressive, hallucinatory or psychotic reactions should be placed in a quiet area and offered reassurance. Benzodiazepines (5 to 10 mg diazepam po) may be used for treatment of extreme agitation. Hypotension usually responds to Trendelenburg position and IV fluids. Pressors are rarely required. (L1712)
Wechselwirkungen
The cannabinoid receptor agonist delta(9)-tetrahydrocannabinol (THC) enhances the antinociceptive effects of u-opioid receptor agonists, raising the possibility of using a combination of THC and opioids for treating pain. This study examined the effects of noncontingent and contingent administration of THC on intravenous heroin self-administration in rhesus monkeys. Self-administration of different unit doses of heroin (0.0001-0.1 mg/kg/infusion) generated a typical inverted U-shaped dose-response curve. In one experiment (n=4), noncontingent THC (0.1-1.0 mg/kg) dose dependently shifted the heroin dose-response curve downward in three monkeys and slightly leftward in one monkey. In a second experiment (n=4), monkeys could self-administer THC alone (0.0032-0.032 mg/kg/infusion), heroin alone, or a mixture of THC and heroin. THC alone did not maintain responding above that obtained with salinehowever, increasing the THC dose with heroin dose dependently decreased the number of infusions received and the rate of responding, as compared with data that were obtained with heroin alone. These results indicate that THC does not significantly enhance the positive reinforcing effects of heroin, further supporting the view that combining cannabinoid and opioid receptor agonists (e.g., for treating pain) does not increase, and might decrease, the abuse liability of individual drugs.Although it is more common for drug abuse to progress from tobacco to cannabis, in many cases cannabis use develops before tobacco use. Epidemiological evidence indicates that prior cannabis use increases the likelihood of becoming dependent on tobacco. To determine whether this effect might be due to cannabis exposure per se, in addition to any genetic, social, or environmental factors that might contribute, we extended our series of studies on 'gateway drug' effects in animal models of drug abuse. Rats were exposed to THC, the main psychoactive constituent of cannabis, for 3 days (two intraperitoneal injections/day). Then, starting 1 week later, they were allowed to self-administer nicotine intravenously. THC exposure increased the likelihood of acquiring the nicotine self-administration response from 65% in vehicle-exposed rats to 94% in THC-exposed rats. When the price of nicotine was manipulated by increasing the response requirement, THC-exposed rats maintained higher levels of intake than vehicle-exposed rats, indicating that THC exposure increased the value of nicotine reward. These results contrast sharply with our earlier findings that prior THC exposure did not increase the likelihood of rats acquiring either heroin or cocaine self-administration, nor did it increase the reward value of these drugs. The findings obtained here suggest that a history of cannabis exposure might have lasting effects that increase the risk of becoming addicted to nicotine.BACKGROUND: Recently, high-dose oral synthetic delta-9-tetrahydrocannabinol (THC) was shown to alleviate cannabis withdrawal symptoms. The present data describe cannabinoid pharmacokinetics in chronic, daily cannabis smokers who received high-dose oral THC pharmacotherapy and later a smoked cannabis challenge. METHODS: Eleven daily cannabis smokers received 0, 30, 60, or 120 mg/d THC for four 5-day-medication sessions, each separated by 9 days of ad libitum cannabis smoking. On the fifth day, participants were challenged with smoking one 5.9% THC cigarette. Plasma collected on the first and fifth days was quantified by two-dimensional gas chromatography mass spectrometer for THC, 11-hydroxy-THC (11-OH-THC), and 11-nor-9-carboxy-THC (THCCOOH). Linear ranges (ng/mL) were 0.5-100 for THC, 1-50 for 11-OH-THC, and 0.5-200 for THCCOOH. RESULTS: During placebo dosing, THC, 11-OH-THC, and THCCOOH concentrations consistently decreased, whereas all cannabinoids increased dose dependently during active dronabinol administration. THC increase over time was not significant after any dose, 11-OH-THC increased significantly during the 60- and 120-mg/d doses, and THCCOOH increased significantly only during the 120-mg/d dose. THC, 11-OH-THC, and THCCOOH concentrations peaked within 0.25 hours after cannabis smoking, except after 120 mg/d THC when THCCOOH peaked 0.5 hours before smoking. CONCLUSIONS: The significant withdrawal effects noted during placebo dronabinol administration were supported by significant plasma THC and 11-OH-THC concentration decreases. During active dronabinol dosing, significant dose-dependent increases in THC and 11-OH-THC concentrations support withdrawal symptom suppression. THC concentrations after cannabis smoking were only distinguishable from oral THC doses for 1 hour, too short a period to feasibly identify cannabis relapse. THCCOOH/THC ratios were higher 14 hours after overnight oral dronabinol abstinence but cannot distinguish oral THC dosing from the smoked cannabis intake.Methamphetamine (METH) is a potent psychostimulant with neurotoxic properties. Heavy use increases the activation of neuronal nitric oxide synthase (nNOS), production of peroxynitrites, microglia stimulation, and induces hyperthermia and anorectic effects. Most METH recreational users also consume cannabis. Preclinical studies have shown that natural (delta9-tetrahydrocannabinol, delta9-THC) and synthetic cannabinoid CB1 and CB2 receptor agonists exert neuroprotective effects on different models of cerebral damage. Here, we investigated the neuroprotective effect of delta9-THC on METH-induced neurotoxicity by examining its ability to reduce astrocyte activation and nNOS overexpression in selected brain areas. Rats exposed to a METH neurotoxic regimen (4x10 mg/kg, 2 hours apart) were pre- or post-treated with delta9-THC (1 or 3 mg/kg) and sacrificed 3 days after the last METH administration. Semi-quantitative immunohistochemistry was performed using antibodies against nNOS and Glial Fibrillary Acidic Protein (GFAP). Results showed that, as compared to corresponding controls (i) METH-induced nNOS overexpression in the caudate-putamen (CPu) was significantly attenuated by pre- and post-treatment with both doses of delta9-THC (-19% and -28% for 1 mg/kg pre- and post-treated animals-25% and -21% for 3 mg/kg pre- and post-treated animals)(ii) METH-induced GFAP-immunoreactivity (IR) was significantly reduced in the CPu by post-treatment with 1 mg/kg delta9-THC1 (-50%) and by pre-treatment with 3 mg/kg delta9-THC (-53%)(iii) METH-induced GFAP-IR was significantly decreased in the prefrontal cortex (PFC) by pre- and post-treatment with both doses of delta9-THC (-34% and -47% for 1 mg/kg pre- and post-treated animals-37% and -29% for 3 mg/kg pre- and post-treated animals). The cannabinoid CB1 receptor antagonist SR141716A attenuated METH-induced nNOS overexpression in the CPu, but failed to counteract the delta9-THC-mediated reduction of METH-induced GFAP-IR both in the PFC and CPu. Our results indicate that delta9-THC reduces METH-induced brain damage via inhibition of nNOS expression and astrocyte activation through CB1-dependent and independent mechanisms, respectively.For more Interactions (Complete) data for delta 9-Tetrahydrocannabinol (34 total), please visit the HSDB record page.
Gesundheitliche Auswirkungen
The heightened suggestibility and intensified emotions that hallucinogens create can worsen any pre-existing emotional problems. Physical effects of hallucinogen use include dilated pupils, sweating, insomnia, loss of appetite, tremorsand increased body temperature, heart rate and blood pressure.
Hepatotoxicity
Serum aminotransferase elevations during dronabinol therapy were reported to occur in 6% of treated patients compared to 4.3% in controls who receiving cancer chemotherapy. The aminotransferase elevations were transient, mild-to-moderate in severity, and not associated with symptoms or jaundice. There have been no convincing cases of clinically apparent liver injury attributable to dronabinol published in the literature and, thus, significant liver injury from dronabinol must be exceeding rare, if it occurs at all.
Ökotoxizitätswerte
LD50Species: Danio rerio (Zebra danio) embryo 10 stageConditions: freshwater, staticConcentration: 2000-5000 ug/L for 6-9 days /99.5% purity formulation/
Umweltverhalten
TERRESTRIAL FATE: Based on a classification scheme(1), an estimated Koc value of 330,000(SRC), determined from a structure estimation method(2), indicates that delta 9-tetrahydrocannabinol is expected to be immobile in soil(SRC). Volatilization of delta 9-tetrahydrocannabinol from moist soil surfaces is not expected(SRC) given an estimated Henry's Law constant of 2.4X10-7 atm-cu m/mole(SRC), using a fragment constant estimation method(2). delta 9-Tetrahydrocannabinol is not expected to volatilize from dry soil surfaces(SRC) based upon an estimated vapor pressure of 4.8X10-8 mm Hg at 25 °C(SRC), determined from a fragment constant method(2). Biodegradation data in soil were not available(SRC, 2017).AQUATIC FATE: Based on a classification scheme(1), an estimated Koc value of 330,000(SRC), determined from a structure estimation method(2), indicates that delta 9-tetrahydrocannabinol is expected to adsorb to suspended solids and sediment(SRC). Volatilization from water surfaces is not expected(3) based upon an estimated Henry's Law constant of 2.4X10-7 atm-cu m/mole(SRC), developed using a fragment constant estimation method(2). delta 9-Tetrahydrocannabinol is not expected to undergo hydrolysis in the environment due to the lack of functional groups that hydrolyze under environmental conditions(3). According to a classification scheme(4), an estimated BCF of 18,000(SRC), from its log Kow of 6.97(5) and a regression-derived equation(2), suggests the potential for bioconcentration in aquatic organisms is very high, provided the compound is not metabolized by the organism(SRC). Biodegradation data in water were not available(SRC, 2017).ATMOSPHERIC FATE: According to a model of gas/particle partitioning of semivolatile organic compounds in the atmosphere(1), delta 9-tetrahydrocannabinol, which has an estimated vapor pressure of 4.6X10-8 mm Hg at 25 °C(SRC), determined from a fragment constant method(2), will exist in both the vapor and particulate phases in the ambient atmosphere. Vapor-phase delta 9-tetrahydrocannabinol is degraded in the atmosphere by reaction with photochemically-produced hydroxyl radicals(SRC)the half-life for this reaction in air is estimated to be 75 minutes(SRC), calculated from its rate constant of 3.1X10-10 cu cm/molecule-sec at 25 °C(SRC) that was derived using a structure estimation method(2). The rate constant for the vapor-phase reaction of delta 9-tetrahydrocannabinol with ozone has been estimated as 4.3X10-16 cu cm/molecule-sec at 25 °C(SRC) that was derived using a structure estimation method(2). This corresponds to an atmospheric half-life of about 38 minutes at an atmospheric concentration of 7X10+11 ozone molecules per cu cm(3). Particulate-phase delta 9-tetrahydrocannabinol may be removed from the air by wet and dry deposition(SRC). delta 9-Tetrahydrocannabinol absorb light at a maximum wavelength of 283 nm(4) and, therefore, may be susceptible to direct photolysis by sunlight(SRC).
Lebensmitteluntersuchungswerte
Cannibus plants are used in some oils, noodles, crackers and teathese products may contain delta 9-tetrahydrocannabinol at <1%(1).
Unerwünschte Wirkungen
Neurotoxin - Other CNS neurotoxinThe most commonly reported adverse effects of THC usage that necessitate discontinuation are dysphoria, hallucinations, and paranoia. Other prevalent adverse effects include sedation, confusion, headache, dry mouth, euphoria, and hypotension. In addition, seizures and seizure-like activity have been reported in patients using THC.Hypersensitivity to Dronabinol or Sesame Oil: Clinical staff should monitor patients for signs of hypersensitivity reactions. Reported signs include lip swelling, hive, rash, oral lesions, skin burning, and throat tightness.
Expositionspfade
Oral
Milk Concentrations
Analysis of breast milk in a chronic heavy marijuana user revealed an eightfold accumulation of delta9-THC in breast milk compared with maternal plasma.
Toxizitätsübersicht
IDENTIFICATION AND USE: delta 9-tetrahydrocannabinol (THC, dronabinol) is light yellow resinous oil. This is a Schedule I controlled substance in the USA. The only legal medical application for marijuana is to reduce the adverse effects of chemotherapy for cancer patients, some patients have been given THC to reduce the pressure in the eye from glaucoma. HUMAN STUDIES: An oral dose of 20 mg of delta-9-THC or the smoking of a cigarette containing 2% delta-9-THC produces effects on mood, memory, motor coordination, cognitive ability, sensorium, time sense, and self-perception. Most commonly there is an increased sense of well-being or euphoria, accompanied by feelings of relaxation and sleepiness when subjects are alonewhere users can interact, sleepiness is less pronounced and there is often spontaneous laughter. Short-term memory is impaired, and there is a deterioration in capacity to carry out tasks requiring multiple mental steps to reach a specific goal. High doses of delta 9-THC can induce frank hallucinations, delusions, and paranoid feelings. Thinking becomes confused and disorganizeddepersonalization and altered time sense are accentuated. Anxiety reaching panic proportions may replace euphoria, often as a result of the feeling that the drug-induced state will never end. With high enough doses, the clinical picture is that of a toxic psychosis with hallucinations, depersonalization, and loss of insightthis can occur acutely or only after months of use. Clinical manifestations due to marijuana smoking have included long-term impairment of memory in adolescents, a sixfold increase in the incidence of schizophrenia, cancer of the mouth, jaw, tongue, and lungs in 19- to 30-year olds, fetotoxicity, and nonlymphoblastic leukemia in children of marijuana-smoking mothers. Studies of aircraft pilot performance following the smoking of one cigarette containing 20 mg of THC suggest that impairment of performance can last as long as 24 hours after smoking. The user may be unaware of the drug's influence. Babies born to mothers who smoked marijuana during pregnancy weighed an average of 3.4 ounces less than babies born to a control group of mothers who did not smoke marijuanathere was no statistically significant difference in either gestational age or frequency of congenital abnormalities. ANIMAL STUDIES: There was no evidence of carcinogenic activity of 1-trans-delta 9-tetrahydrocannabinol in male or female rats administered 12.5, 25, or 50 mg/kg. There was equivocal evidence of carcinogenic activity of THC in male and female mice based on the increased incidences of thyroid gland follicular cell adenomas in 125 mg/kg groups. Increased incidences of thyroid gland follicular cell hyperplasia occurred in male and female mice, and increased incidences of hyperplasia and ulcers of the forestomach were observed in male mice. The incidences of mammary gland fibroadenomas and uterine stromal polyps were decreased in dosed groups of female rats, as were the incidences of pancreatic adenomas, pituitary gland adenomas, and interstitial cell adenomas of the testis in dosed male rats and liver neoplasms in dosed mice. In a long-term study (77 days) in rats, oral administration of dronabinol at doses of 30 to 150 mg/sq m reduced ventral prostate, seminal vesicle and epididymal weights and caused a decrease in seminal fluid volume. Decreases in spermatogenesis, number of developing germ cells, and number of Leydig cells in the testis were also observed. However, sperm count, mating success and testosterone levels were not affected. Dronabinol was not genotoxic in the Ames tests, the in vitro chromosomal aberration test in Chinese hamster ovary cells, and the in vivo mouse micronucleus test. It, however, produced a weak positive response in a sister chromatid exchange test in Chinese hamster ovary cells. Cannabinoids exert many effects through activation of G-protein-coupled cannabinoid receptors in the brain and peripheral tissues. Additionally, there is evidence for non-receptor-dependent mechanisms.The median lethal dose (LD50) of THC has been determined in various animal species through oral administration and ranges from 800 to 9000 mg/kg. In humans, there have been no recorded instances of fatal overdoses resulting from acute THC use. However, estimates for a potentially lethal human dose range from 4 to 15 g.The mechanism of action of marinol is not completely understood. It is thought that cannabinoid receptors in neural tissues may mediate the effects of dronabinol and other cannabinoids. Animal studies with other cannabinoids suggest that marinol's antiemetic effects may be due to inhibition of the vomiting control mechanism in the medulla oblongata.
Wassergefährdungsklasse (WGK)
1
UN-Transportnummer
UN 1230 3/PG 2
R-Sätze (R)
11-39/23/24/25-23/24/25
Toxizität
LD50 (sesame oil emulsion) in male rats (mg/kg): 800 orally35.5. i.v.672 i.p. (Rosenkranz)
