Ethyl alcohol, or ethanol, is an intoxicating ingredient found in beer, wine, and liquor. Alcohol is produced by the fermentation of yeast, sugars, and starches.
Alcohol affects every organ in the body. It is a central nervous system depressant that is rapidly absorbed from the stomach and small intestine into the bloodstream. Alcohol is metabolized in the liver by enzymes, however, the liver can only metabolize a small amount of alcohol at a time, leaving the excess alcohol to circulate throughout the body. The intensity of the effect of alcohol on the body is directly related to the amount consumed.
Amphetamine is a Schedule II controlled substance available by prescription (Dexedrine®) and is also available on the illicit market. Amphetamines are a class of potent sympathomimetic agents with therapeutic applications. They are chemically related to the human body’s natural catecholamines: epinephrine and norepinephrine. Acute higher doses lead to enhanced stimulation of the central nervous system and induce euphoria, alertness, reduced appetite, and a sense of increased energy and power. Cardiovascular responses to amphetamines include increased blood pressure and cardiac arrhythmias. More acute responses produce anxiety, paranoia, hallucinations, and psychotic behavior. The effects of amphetamines generally last 2-4 hours following use, and the drug has a half-life of 4-24 hours in the body. About 30% of amphetamines are excreted in the urine in unchanged form, with the remainder as hydroxylated and deaminated derivatives.
Barbiturates were first introduced for medical use in the early 1900s. More than 2,500 barbiturates have been synthesized, and at the height of their popularity, about 50 were marketed for human use. Today, about a dozen are in medical use. Barbiturates produce a wide spectrum of central nervous system depression, from mild sedation to coma, and have been used as sedatives, hypnotics, anesthetics, and anticonvulsants. The primary differences among many of these products are how fast they produce an effect and how long those effects last. Barbiturates are classified as ultrashort, short, intermediate, and long-acting.
The ultrashort-acting barbiturates produce anesthesia within about one minute after intravenous administration. Those in current medical use are the Schedule IV drug methohexital (Brevital®), and the Schedule III drugs thiamyl (Surital®) and thiopental (Pentothal®). Barbiturate abusers prefer the Schedule II short-acting and intermediate-acting barbiturates that include amobarbital (Amyta®), pentobarbital (Nembutal®), secobarbital (Seconal®), and Tuinal (an amobarbital/secobarbital combination product). Other short and intermediate-acting barbiturates are in Schedule III and include butalbital (Fiorina®), butabarbital (Butisol®), talbutal (Lotusate®), and aprobarbital (Alurate®). After oral administration, the onset of action is from 15 to 40 minutes, and the effects last up to six hours. These drugs are primarily used for insomnia and preoperative sedation. Veterinarians use pentobarbital for anesthesia and euthanasia.
Long-acting barbiturates include phenobarbital (Luminal®) and mephobarbital (Mebaral®), both of which are in Schedule IV. Effects of these drugs are realized in about one hour and last for about 12 hours, and are used primarily for daytime sedation and the treatment of seizure disorders.
The benzodiazepine family of depressants is used therapeutically to produce sedation, induce sleep, relieve anxiety and muscle spasms, and to prevent seizures. In general, benzodiazepines act as hypnotics in high doses, anxiolytics in moderate doses, and sedatives in low doses. Of the drugs marketed in the United States that affect central nervous system function, benzodiazepines are among the most widely prescribed medications. Fifteen members of this group are presently marketed in the United States, and about 20 additional benzodiazepines are marketed in other countries. Benzodiazepines are controlled in Schedule IV of the CSA.
Short-acting benzodiazepines are generally used for patients with sleep-onset insomnia (difficulty falling asleep) without daytime anxiety. Shorter-acting benzodiazepines used to manage insomnia include estazolam (ProSom®), flurazepam (Dalmane®), temazepam (Restoril®), and triazolam (Halcion®). Midazolam (Versed®), a short-acting benzodiazepine, is utilized for sedation, anxiety, and amnesia in critical care settings and prior to anesthesia. It is available in the United States as an injectable preparation and as a syrup (primarily for pediatric patients).
Benzodiazepines with a longer duration of action are utilized to treat insomnia in patients with daytime anxiety. These benzodiazepines include alprazolam (Xanax®), chlordiazepoxide (librium®), clorazepate (Tranxene®), diazepam (Valium®), halazepam (Paxipam®), lorzepam (Ativan®), oxazepam (Serax®), prazepam (Centrax®), and quazepam (Doral®). Clonazepam (Klonopin®), diazepam, and clorazepate are also used as anticonvulsants.
Benzodiazepines are classified in the CSA as depressants. Repeated use of large doses or; in some cases, daily use of therapeutic doses of benzodiazepines is associated with amnesia, hostility, irritability, and vivid or disturbing dreams, as well as tolerance and physical dependence. The withdrawal syndrome is similar to that of alcohol and may require hospitalization. Abrupt cessation of benzodiazepines is not recommended and tapering-down the dose eliminates many of the unpleasant symptoms.
Given the millions of prescriptions written for benzodiazepines (about 100 million in 1999), relatively few individuals increase their dose on their own initiative or engage in drug-seeking behavior. Those individuals who do abuse benzodiazepines often maintain their drug supply by getting prescriptions from several doctors, forging prescriptions, or buying diverted pharmaceutical products on the illicit market. Abuse is frequently associated with adolescents and young adults who take benzodiazepines to obtain a “high.” This intoxicated state results in reduced inhibition and impaired judgment. Concurrent use of alcohol or other depressant; with benzodiazepines can be life threatening. Abuse of benzodiazepines is particularly high among heroin and cocaine abusers. A large percentage of people entering treatment for narcotic or cocaine addiction also report abusing benzodiazepines. Alprazolam and diazepam are the two most frequently encountered benzodiazepines on the illicit market.
Flunitrazepam (Rohypnol®) is a benzodiazepine that is not manufactured or legally marketed in the United States, but is smuggled in by traffickers. In the mid-1990s, flunitrazepam was extensively trafficked in Florida and Texas. Known as “rophies,” “roofies,” and “roach,” flunitrazepam gained popularity among younger individuals as a “party” drug. It has also been utilized as a “date rape” drug. In this context, flunitrazepam is placed in the alcoholic drink of an unsuspecting victim to incapacitate them and prevent resistance from sexual assault. The victim is frequently unaware of what has happened to them and often does not report the incident to authorities. A number of actions by the manufacturer of this drug and by government agencies have resulted in reducing the availability and abuse of flunitrazepam in the United States.
Newly Marked Drugs: Zolpidem (Ambien®) and zaleplon (Sonata®) are two relatively new, benzodiazepine-like CNS depressants that have been approved for the short-term treatment of insomnia. Both of these drugs share many of the same properties as the benzodiazepines and are in Schedule IV of the CSA.
Buprenorphine is a semisynthetic opioid analgesic derived from thebain, a component of opium. It has a longer duration of action than morphine when indicated for the treatment of moderate to severe pain, peri-operative analgesia, and opioid dependence. Low doses buprenorphine produces sufficient agonist effect to enable opioid-addicted individuals todiscontinue the misuse of opioids without experiencing withdrawal symptoms. Buprenorphine carries a lower risk of abuse, addiction, and side effects compared to full opioid agonists because of the “ceiling effect,” which means no longer continue to increase with further increases in dose when reaching a plateau at moderate doses. However, it has also been shown that Buprenorphine has abuse potential and may itself cause dependency. Subutex®, and a Buprenorphine/Naloxone combination product, Suboxone®, are the only two forms of Buprenorphine that have been approved by FDA in 2002 for use in opioid addiction treatment. Buprenorphine was rescheduled from Schedule V to Schedule III drug just before FDA approval of Suboxone® and Subutex®.
Cocaine is a powerfully-addictive stimulant that directly affects the brain. Cocaine is not a new drug. In fact, it is one of the oldest known drugs. The pure chemical, cocaine hydrochloride, has been an abused substance for more than 100 years, and coca leaves, the source of cocaine, have been ingested for thousands of years.1
The powdered, hydrochloride salt form of cocaine can be snorted or dissolved in water and injected. Crack is cocaine that has not been neutralized by an acid to make the hydrochloride salt. This form of cocaine comes in a rock crystal that can be heated and its vapors smoked. The term “crack” refers to the crackling sound heard when it is heated.4
Control Status: Today, cocaine is a Schedule II drug under the Controlled Substances Act of 1970, meaning that it has high potential for abuse, but can be administered by a doctor for legitimate medical uses, such as local anesthesia for some eye, ear, and throat surgeries.
Street Names: Blow, nose candy, snowball, tornado, wicky stick, Perico (Spanish)5
Short-term Effects: Cocaine’s effects appear almost immediately after a single dose, and disappear within a few minutes or hours. Taken in small amounts (up to 100 mg), cocaine usually makes the user feel euphoric, energetic, talkative, and mentally alert, especially to the sensations of sight, sound, and touch. It can also temporarily decrease the need for food and sleep. Some users find that the drug helps them perform simple physical and intellectual tasks more quickly, while others experience the opposite effect.6
The duration of cocaine’s immediate euphoric effects depends upon the route of administration. The faster the absorption, the more intense the high. Also, the faster the absorption, the shorter the duration of action. The high from snorting is relatively slow in onset, and may last 15 to 30 minutes, while that from smoking may last 5 to 10 minutes.7
The short-term physiological effects of cocaine include constricted blood vessels; dilated pupils; and increased temperature, heart rate, and blood pressure. Large amounts (several hundred milligrams or more) intensify the user’s high, but may also lead to bizarre, erratic, and violent behavior. These users may experience tremors, vertigo, muscle twitches, paranoia, or, with repeated doses, a toxic reaction closely resembling amphetamine poisoning. Some users of cocaine report feelings of restlessness, irritability, and anxiety. In rare instances, sudden death can occur on the first use of cocaine or unexpectedly thereafter. Cocaine-related deaths are often a result of cardiac arrest or seizures followed by respiratory arrest.8
Long-term Effects: Cocaine is a powerfully addictive drug. Thus, an individual may have difficulty predicting or controlling the extent to which he or she will continue to want or use the drug. Cocaine’s stimulant and addictive effects are thought to be primarily a result of its ability to inhibit the reabsorption of dopamine by nerve cells. Dopamine is released as part of the brain’s reward system, and is either directly or indirectly involved in the addictive properties of every major drug of abuse.9
An appreciable tolerance to cocaine’s high may develop, with many addicts reporting that they seek but fail to achieve as much pleasure as they did from their first experience. Some users will frequently increase their doses to intensify and prolong the euphoric effects. While tolerance to the high can occur, users can also become more sensitive (sensitization) to cocaine’s anesthetic and convulsant effects, without increasing the dose taken. This increased sensitivity may explain some deaths occurring after apparently low doses of cocaine.10
Use of cocaine in a binge, during which the drug is taken repeatedly and at increasingly high doses, leads to a state of increasing irritability, restlessness, and paranoia. This may result in a full-blown paranoid psychosis, in which the individual loses touch with reality and experiences auditory hallucinations.11
1-2. National Institute on Drug Abuse, Research Report – Cocaine Abuse and Addiction, www.nida.nih.gov/researchreports/cocaine/cocaine.html.
3. Drug Enforcement Administration, Office of Diversion Control, www.deadiversion.usdoj.gov/drugs_concern/cocaine/cocaine.htm.
4. National Institute on Drug Abuse, InfoFacts: Crack and Cocaine, www.drugabuse.gov/Infofacts/cocaine.html. Snorting is the process of inhaling cocaine powder through the nose, where it is absorbed into the bloodstream through the nasal tissues. Injecting is the use of a needle to release the drug directly into the bloodstream; any needle use increases a user’s risk of contracting HIV and other blood-borne infections. Smoking involves inhaling cocaine vapor or smoke into the lungs, where absorption into the bloodstream is as rapid as by injection.
5. Office of National Drug Control Policy (ONDCP), Cocaine Street Terms
6-11. National Institute on Drug Abuse, Research Report – Cocaine Abuse and Addiction
Tricyclic antidepressants are commonly used for the treatment of depressive disorders. TCA overdoses can result in profound central nervous system depression, cardiotoxicity and anticholinergic effects. TCA overdose is the most common cause of death from prescription drugs. TCAs are taken orally or sometimes by injection. TCAs are metabolized in the liver. Both TCAs and their metabolites are excreted in urine mostly in the form of metabolites for up to ten days. The DrugCheck® Drug of Abuse Test yields a positive result when the concentration of Tricyclic Antidepressants in urine exceeds 1,000 ng/mL.
Marijuana is the most commonly abused illicit drug in the United States. A dry, shredded green/brown mix of flowers, stems, seeds, and leaves of the plant Cannabis sativa, it usually is smoked as a cigarette (joint, nail), or in a pipe (bong). It also is smoked in blunts, which are cigars that have been emptied of tobacco and refilled with marijuana, often in combination with another drug. It might also be mixed in food or brewed as a tea. As a more concentrated, resinous form it is called hashish and, as a sticky black liquid, hash oil. Marijuana smoke has a pungent and distinctive, usually sweet-and-sour odor.1
The main active chemical in marijuana is THC (delta-9-tetrahydrocannabinol). The membranes of certain nerve cells in the brain contain protein receptors that bind to THC. Once securely in place, THC kicks off a series of cellular reactions that ultimately lead to the high that users experience when they smoke marijuana.2
Control Status: Marijuana is a Schedule I substance under the Controlled Substances Act (CSA). Schedule I drugs are classified as having a high potential for abuse, no currently accepted medical use in treatment in the United States, and a lack of accepted safety for use of the drug or other substance under medical supervision.
Street Names: Grass, pot, weed, bud, Mary Jane, dope, indo, hydro3
Short-term Effects: When marijuana is smoked, its effects begin immediately after the drug enters the brain and last from 1 to 3 hours. If marijuana is consumed in food or drink, the short-term effects begin more slowly, usually in 1/2 to 1 hour, and last longer, for as long as 4 hours. Smoking marijuana deposits several times more THC into the blood than does eating or drinking the drug.4
As THC enters the brain, it causes a user to feel euphoric — or “high” — by acting in the brain’s reward system, areas of the brain that respond to stimuli such as food and drink as well as most drugs of abuse. THC activates the reward system in the same way that nearly all drugs of abuse do, by stimulating brain cells to release the chemical dopamine.5
A marijuana user may experience pleasant sensations, colors and sounds may seem more intense, and time appears to pass very slowly. The user’s mouth feels dry, and he or she may suddenly become very hungry and thirsty. His or her hands may tremble and grow cold. The euphoria passes after awhile, and then the user may feel sleepy or depressed. Occasionally, marijuana use produces anxiety, fear, distrust, or panic.6
Long-term Effects: Someone who smokes marijuana regularly may have many of the same respiratory problems that tobacco smokers do, such as daily cough and phlegm production, more frequent acute chest illnesses, a heightened risk of lung infections, and a greater tendency toward obstructed airways. Cancer of the respiratory tract and lungs may also be promoted by marijuana smoke. Marijuana has the potential to promote cancer of the lungs and other parts of the respiratory tract because marijuana smoke contains 50 percent to 70 percent more carcinogenic hydrocarbons than does tobacco smoke.7
Marijuana’s damage to short-term memory seems to occur because THC alters the way in which information is processed by the hippocampus, a brain area responsible for memory formation. In one study, researchers compared marijuana smoking and nonsmoking 12th-graders’ scores on standardized tests of verbal and mathematical skills. Although all of the students had scored equally well in 4th grade, those who were heavy marijuana smokers, i.e., those who used marijuana seven or more times per week, scored significantly lower in 12th grade than nonsmokers. Another study of 129 college students found that among heavy users of marijuana critical skills related to attention, memory, and learning were significantly impaired, even after they had not used the drug for at least 24 hours.8
1-2. National Institute on Drug Abuse, InfoFacts: Marijuana, April 2006
3. Office of National Drug Control Policy (ONDCP), Marijuana Street Terms
4-6. National Institute on Drug Abuse, Research Report Series—Marijuana Abuse, July 2005
7-8. National Institute on Drug Abuse, Research Report Series—Marijuana Abuse, October 2001
MDMA (3,4-methylenedioxymethamphetamine) is a synthetic, psychoactive drug chemically similar to the stimulant methamphetamine and the hallucinogen mescaline. MDMA is an illegal drug that acts as both a stimulant and psychedelic, producing an energizing effect, as well as distortions in time and perception and enhanced enjoyment from tactile experiences.1
Adolescents and young adults use it to promote euphoria, feelings of closeness, empathy, sexuality and to reduce inhibitions. It is considered a “party drug” and obtained at “rave” or “techno” parties. However, its abuse has expanded, to include other settings outside of the rave scenes, such as a college campus.2
Although MDMA is known universally among users as ecstasy, researchers have determined that many ecstasy tablets contain not only MDMA but also a number of other drugs or drug combinations that can be harmful as well. Adulterants found in MDMA tablets purchased on the street include methamphetamine, caffeine, the over-the-counter cough suppressant dextromethorphan, the diet drug ephedrine, and cocaine. Also, as with many other drugs of abuse, MDMA is rarely used alone. It is not uncommon for users to mix MDMA with other substances, such as alcohol and marijuana.3
Control Status: In the 1980s, MDMA gained popularity as a drug of abuse resulting in its final placement in Schedule I of the Controlled Substances Act (CSA).4
Street Terms: MDMA, Ecstasy, XTC, E, X, Beans, Adams, Hug Drug, Disco Biscuit, Go
Short-term Effects: In high doses, MDMA can interfere with the body’s ability to regulate temperature. On rare but unpredictable occasions, this can lead to a sharp increase in body temperature (hyperthermia), resulting in liver, kidney, and cardiovascular system failure, and death.5
Because MDMA can interfere with its own metabolism (breakdown within the body), potentially harmful levels can be reached by repeated drug use within short intervals.6
Users of MDMA face many of the same risks as users of other stimulants such as cocaine and amphetamines. These include increases in heart rate and blood pressure, a special risk for people with circulatory problems or heart disease, and other symptoms such as muscle tension, involuntary teeth clenching, nausea, blurred vision, faintness, and chills or sweating.7
Almost 60 percent of people who use MDMA report withdrawal symptoms, including fatigue, loss of appetite, depressed feelings, and trouble concentrating.8
Long-term Effects: Research in animals links MDMA exposure to long-term damage to neurons that are involved in mood, thinking, and judgment. A study in nonhuman primates showed that exposure to MDMA for only 4 days caused damage to serotonin nerve terminals that was evident 6 to 7 years later. While similar neurotoxicity has not been definitively shown in humans, the wealth of animal research indicating MDMA’s damaging properties suggests that MDMA is not a safe drug for human consumption.9
1. National Institute on Drug Abuse, InfoFacts: MDMA, May 2006
2. Drug Enforcement Administration, Office of Diversion Control, www.deadiversion.usdoj.gov/drugs_concern/mdma/mdma.htm
3. National Institute on Drug Abuse, Research Report: MDMA (Ecstasy) Abuse, March 2006
4. Drug Enforcement Administration, Drugs of Abuse, 2005
5-7. National Institute on Drug Abuse, InfoFacts: MDMA, May 2006
8. National Institute on Drug Abuse, Research Report: MDMA (Ecstasy) Abuse, March 2006
9. National Institute on Drug Abuse, InfoFacts: MDMA, May 2006
Today, methamphetamine is second only to alcohol and marijuana as the drug used most frequently in many Western and Midwestern states. Seizures of dangerous laboratory materials have increased dramatically — in some states, fivefold. In response, many special task forces and local and Federal initiatives have been developed to target methamphetamine production and use. Legislation and negotiation with earlier source areas for precursor substances have also reduced the availability of the raw materials needed to make the drug.1
Methamphetamine is a highly addictive drug with potent central nervous system stimulant properties. In the 1960s, methamphetamine pharmaceutical products were widely available and extensively diverted and abused. The 1971 placement of methamphetamine into Schedule II of the Controlled Substance Act (CSA) and the removal of methamphetamine injectable formulations from the United States market, combined with a better appreciation for its high abuse potential, led to a drastic reduction in the abuse of this drug. However, a resurgence of methamphetamine abuse occurred in the 1980s and it is currently considered a major drug of abuse. The widespread availability of methamphetamine today is largely fueled by illicit production in large and small clandestine laboratories throughout the United States and illegal production and importation from Mexico. In some areas of the country (especially on the West Coast), methamphetamine abuse has outpaced both heroin and cocaine.2
The drug has limited medical uses for the treatment of narcolepsy, attention deficit disorders, and obesity.3
Control Status: Methamphetamine is in Schedule II of the CSA.
Street Names: Speed, Meth, Ice, Crystal, Chalk, Crank, Tweak, Uppers, Black Beauties, Glass, Bikers Coffee, Methlies Quick, Poor Man’s Cocaine, Chicken Feed, Shabu, Crystal Meth, Stove Top, Trash, Go-Fast, Yaba, and Yellow Bam
Short-term Effects: As a powerful stimulant, methamphetamine, even in small doses, can increase wakefulness and physical activity and decrease appetite. A brief, intense sensation, or rush, is reported by those who smoke or inject methamphetamine. Oral ingestion or snorting produces a long-lasting high instead of a rush, which reportedly can continue for as long as half a day. Both the rush and the high are believed to result from the release of very high levels of the neurotransmitter dopamine into areas of the brain that regulate feelings of pleasure.4
Methamphetamine has toxic effects. In animals, a single high dose of the drug has been shown to damage nerve terminals in the dopamine-containing regions of the brain. The large release of dopamine produced by methamphetamine is thought to contribute to the drug’s toxic effects on nerve terminals in the brain. High doses can elevate body temperature to dangerous, sometimes lethal, levels, as well as cause convulsions.5
Long-term Effects: Long-term methamphetamine abuse results in many damaging effects, including addiction. Addiction is a chronic, relapsing disease, characterized by compulsive drug-seeking and drug use which is accompanied by functional and molecular changes in the brain. In addition to being addicted to methamphetamine, chronic methamphetamine abusers exhibit symptoms that can include violent behavior, anxiety, confusion, and insomnia. They also can display a number of psychotic features, including paranoia, auditory hallucinations, mood disturbances, and delusions (for example, the sensation of insects creeping on the skin, which is called “formication”). The paranoia can result in homicidal as well as suicidal thoughts.6
With chronic use, tolerance for methamphetamine can develop. In an effort to intensify the desired effects, users may take higher doses of the drug, take it more frequently, or change their method of drug intake. In some cases, abusers forego food and sleep while indulging in a form of binging known as a “run,” injecting as much as a gram of the drug every 2 to 3 hours over several days until the user runs out of the drug or is too disorganized to continue. Chronic abuse can lead to psychotic behavior, characterized by intense paranoia, visual and auditory hallucinations, and out-of-control rages that can be coupled with extremely violent behavior.7
Although there are no physical manifestations of a withdrawal syndrome when methamphetamine use is stopped, there are several symptoms that occur when a chronic user stops taking the drug. These include depression, anxiety, fatigue, paranoia, aggression, and an intense craving for the drug.8
In scientific studies examining the consequences of long-term methamphetamine exposure in animals, concern has arisen over its toxic effects on the brain. Researchers have reported that as much as 50 percent of the dopamine-producing cells in the brain can be damaged after prolonged exposure to relatively low levels of methamphetamine. Researchers also have found that serotonin-containing nerve cells may be damaged even more extensively. Whether this toxicity is related to the psychosis seen in some long-term methamphetamine abusers is still an open question.9
1. Hunt, D., S. Kuck, and L. Truitt, Methamphetamine Use: Lessons Learned, final report to the National Institute of Justice, February 2006 (NCJ 209730), available at www.ncjrs.gov/pdffiles1/nij/grants/209730.pdf.
2. Drug Enforcement Administration, Office of Diversion Control, www.deadiversion.usdoj.gov/drugs_concern/meth.htm
3. National Institute on Drug Abuse, Research Report – Methamphetamine Abuse and Addiction, www.drugabuse.gov/ResearchReports/methamph/methamph.html
4-9. Ibid.
German scientists synthesized methadone during World War II because of a shortage of morphine. Although chemically unlike morphine or heroin, methadone produces many of the same effects. Introduced into the United States in 1947 as an analgesic (Dolophinel), it is primarily used today for the treatment of narcotic addiction. It is available in oral solutions, tablets, and injectable Schedule II formulations, and is almost as effective when administered orally as it is by injection.
Methadone’s effects can last up to 24 hours, thereby permitting once-a-day oral administration in heroin detoxification and maintenance programs. High-dose methadone can block the effects of heroin, thereby discouraging the continued use of heroin by addicts under treatment with methadone. Chronic administration of methadone results in the development of tolerance and dependence. The withdrawal syndrome develops more slowly and is less severe but more prolonged than that associated with heroin withdrawal. Ironically, methadone used to control narcotic addiction is frequently encountered on the illicit market and has been associated with a number of overdose deaths.
“Opiates” refers to any drug that is derived from the opium poppy, including the natural products morphine and codeine, and semi-synthetic drugs such as heroin. The term “opioid” is more general, referring to any drug that acts on the opioid receptor. Opioid analgesics comprise a large group of substances that control pain by depressing the central nervous system. Large doses of morphine can produce higher tolerance levels, physiological dependency in users, and may lead to substance abuse. Morphine is excreted unmetabolized, and is also the major metabolic product of codeine and heroin. Morphine is detectable in the urine for several days after an opiate dose.
OxyContin® is a prescription painkiller used for moderate to high pain relief associated with injuries, bursitis, dislocations, fractures, neuralgia, arthritis, lower back pain, and pain associated with cancer.1 OxyContin® contains oxycodone, the medication’s active ingredient, in a timed-release tablet. Oxycodone products have been illicitly abused for the past 30 years.2
Oxycodone is a Schedule II narcotic analgesic and is widely used in clinical medicine. It is marketed either alone as controlled release (OxyContin®) and immediate release formulations (OxyIR®, OxyFast®), or in combination with other nonnarcotic analgesics such as aspirin (Percodan®) or acetaminophen (Percocet®). The introduction in 1996 of OxyContin®, commonly known on the street as OC, OX, Oxy, Oxycotton, Hillbilly heroin, and kicker, led to a marked escalation of its abuse as reported by drug abuse treatment centers, law enforcement personnel, and health care professionals. Although the diversion and abuse of OxyContin® appeared initially in the eastern US, it has now spread to the western US including Alaska and Hawaii. Oxycodone-related adverse health effects increased markedly in recent years. In 2004, Food and Drug Administration (FDA) approved for marketing generic forms of controlled release oxycodone products.3
Control Status: Oxycodone products are in Schedule II of the federal Controlled Substances Act of 1970.4
Street Names: Kicker, OC, Oxy, OX, Blue, Oxycotton, Hillbilly Heroin
Short-term Effects: Pharmacological effects include analgesia, sedation, euphoria, feelings of relaxation, respiratory depression, constipation, papillary constriction, and cough suppression. A 10 mg dose of orally-administered oxycodone is equivalent to a 10 mg dose of subcutaneously administered morphine as an analgesic in a normal population. Oxycodone’s behavioral effects can last up to 5 hours. The drug is most often administered orally. The controlled-release product, OxyContin®, has a longer duration of action (8-12 hours).5
The most serious risk associated with opioids, including OxyContin®, is respiratory depression. Common opioid side effects are constipation, nausea, sedation, dizziness, vomiting, headache, dry mouth, sweating, and weakness. Taking a large single dose of an opioid could cause severe respiratory depression that can lead to death.6
Long-term Effects: As with most opiates, oxycodone abuse may lead to dependence and tolerance. Acute overdose of oxycodone can produce severe respiratory depression, skeletal muscle flaccidity, cold and clammy skin, reduction in blood pressure and heart rate, coma, respiratory arrest, and death.7
Chronic use of opioids can result in tolerance for the drugs, which means that users must take higher doses to achieve the same initial effects. Long-term use also can lead to physical dependence and addiction — the body adapts to the presence of the drug, and withdrawal symptoms occur if use is reduced or stopped. Properly managed medical use of pain relievers is safe and rarely causes clinical addiction, defined as compulsive, often uncontrollable use of drugs. Taken exactly as prescribed, opioids can be used to manage pain effectively.8
1. National Drug Intelligence Center, Information Bulletin: OxyContin® Diversion and Abuse, January 2001
2. Drug Enforcement Administration, Congressional Testimony, Statement by Terrance W. Woodworth, Deputy Director, Officer of Diversion Control, Before the House Committee on Energy and Commerce, Subcommittee on Oversight and Investigations, August 28, 2001
3. DEA Office of Diversion Control, Oxycodone
4-5. Ibid.
6. Partnership for a Drug-Free America
7. DEA Office of Diversion Control, Oxycodone
8. Partnership for a Drug-Free America
Phencyclidine, also known as PCP or Angel Dust, is a hallucinogen that was first marketed as a surgical anesthetic in the 1950s. It was removed from the market because patients receiving it became delirious and experienced hallucinations.
Phencyclidine is used in powder, capsule, and tablet form. The powder is either snorted or smoked after mixing it with marijuana or vegetable matter. Phencyclidine is most commonly administered by inhalation but can be used intravenously, intra-nasally, and orally. After low doses, the user thinks and acts swiftly and experiences mood swings from euphoria to depression. Selfinjurious behavior is one of the devastating effects of Phencyclidine.
PCP can be found in urine within 4 to 6 hours after use and will remain in urine for 7 to 14 days, depending on factors such as metabolic rate, user’s age, weight, activity, and diet.5 Phencyclidine is excreted in the urine as an unchanged drug (4% to 19%) and conjugated metabolites (25% to 30%).
NOTE: Effexor Tablets (venlafaxine hydrochloride) a treatment for depressive, anxiety and social disorder have shown to cause false positive urine results for Phencyclidine (PCP). Positive urine screening should always be confirmed by GCMS.
Propoxyphene (PPX) is a mild narcotic analgesic found in various pharmaceutical preparations, usually as the hydrochloride or napsylate salt. These preparations typically also contain large amounts of acetaminophen, aspirin, or caffeine. Peak plasma concentrations of propoxyphene are achieved from 1 to 2 hours post dose. In the case of overdose, propoxyphene blood concentrations can reach significantly higher levels. In human, propoxyphene is metabolized by N-demethylation to yield norpropoxyphene. Norpropoxyphene has a longer half-life (30 to 36 hours) than parent propoxyphene (6 to 12 hours). The accumulation of norpropoxyphene seen with repeated doses may be largely responsible for resultant toxicity.
